qid
int64
1
194k
question
stringlengths
46
29.5k
answers
listlengths
2
32
date
stringlengths
10
10
metadata
sequencelengths
3
3
18,407
<p>I saw an article on the web comparing the effectiveness of PAs and MDs with regard to minor ailments, with the result that for minor ailments, MDs were no better than PAs. I've tried finding this article again, but have not been able to do so. Can anyone else provide a link to a similar study?</p>
[ { "answer_id": 18423, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p><strong>1.</strong> <a href=\"https://www.hprac.org/en/projects/resources/LiteratureReview_PhysicianAssistants.pdf\" rel=\"nofollow noreferrer\"><strong>Physician Assistants:</strong> A Literature Review (Health Professions Regulatory Advisory Council - HPRAC, 2011\n)</a></p>\n\n<p>The review mentions several studies about the effectiveness of physician assistants.</p>\n\n<hr>\n\n<p><strong>2.</strong> <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3903046/\" rel=\"nofollow noreferrer\">THE CONTRIBUTIONS OF <strong>PHYSICIAN ASSISTANTS</strong> IN PRIMARY CARE SYSTEMS (PubMed, 2012)</a></p>\n\n<blockquote>\n <p>Contemporary studies suggest that PAs can contribute to the successful\n attainment of primary care functions, particularly the provision of\n comprehensive care, accessibility, and accountability.</p>\n</blockquote>\n\n<p><strong>3.</strong> <a href=\"https://www.bmj.com/content/320/7241/1038\" rel=\"nofollow noreferrer\"><strong>Nurse</strong> management of patients with minor illnesses in general practice: multicentre, randomised controlled trial (BMJ, 2000)</a></p>\n\n<blockquote>\n <p>Patients were very satisfied with both nurses and doctors, but they\n were significantly more satisfied with their consultations with nurses\n (mean (SD) score of satisfaction 78.6 (16.0) of 100 points for nurses\n v 76.4 (17.8) for doctors...</p>\n</blockquote>\n\n<hr>\n\n<p><strong>4.</strong> Another one from BMJ, 1995: <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2549167/pdf/bmj00585-0032.pdf\" rel=\"nofollow noreferrer\">Establishing a minor illness <strong>nurse</strong> in a busy general practice</a> </p>\n\n<blockquote>\n <ul>\n <li>The nurse managed 86% of patients without contact with the doctor; half required a prescription signing</li>\n <li>Half of patients required only advice on self care, and 79% did not reconsult</li>\n <li>Practice nurses could successfully manage many patients requesting same day appointments with their general practitioner</li>\n <li>Of 696 consultations in six months, 602 (86%) required no doctor contact. 549 (79%) patients did not reconsult about the episode of\n illness, and 343 (50%) patients were given advice on self care only.\n Trained nurses could diagnose and treat a large proportion of patients\n currently consulting general practitioners about minor illness\n provided that the nurse has immediate access to a doctor.</li>\n </ul>\n</blockquote>\n\n<hr>\n" }, { "answer_id": 18430, "author": "Camille Markham", "author_id": 15491, "author_profile": "https://health.stackexchange.com/users/15491", "pm_score": -1, "selected": false, "text": "<p>Physician assistantsundergo intensive medical training and provide many of the same services as doctors. ... “Like physicians, the exact duties of the PA depend on the type of medical setting in which they work and their level of experience, specialty and the state laws where they practice.\nThat being said...\nPhysician assistants undergo intensive medical training and provide many of the same services as doctors (<a href=\"https://health.usnews.com/health-news/patient-advice/slideshows/10-reasons-to-see-a-physician-assistant\" rel=\"nofollow noreferrer\">https://health.usnews.com/health-news/patient-advice/slideshows/10-reasons-to-see-a-physician-assistant</a>)\nIf you need a scholarly link Google scholar narrows down your search more efficiently and accurately, than most scholarly data bases. Then again Cochrane provides meta-analysis, the highest level of research. Be prepared no matter what data base you utilize to search through the articles provided before finding anything remotely related to the key words you used. </p>\n" } ]
2019/01/13
[ "https://health.stackexchange.com/questions/18407", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15480/" ]
18,411
<p>Your family doctor obviously learned how to diagnose various illnesses, such as the flu, skin conditions (rashes, burns, etc.), etc. </p> <p>I was wondering what textbooks they studied in medical school to learn this? In other words, is there specific textbook(s) that teach you how to diagnose illnesses? </p> <p>It looks like the textbook <em>Current Medical Diagnosis and Treatment</em>, 2018 is the type of thing I'm looking for. It lists various illnesses and has brief descriptions. Is there something more suited for my interests, or is this as good as it gets? I would like something with more detail (detailed symptoms, etc.), including images, if possible.</p> <p>Thank you.</p>
[ { "answer_id": 18413, "author": "practiZ", "author_id": 15382, "author_profile": "https://health.stackexchange.com/users/15382", "pm_score": 4, "selected": true, "text": "<p>There is no specific book that will <em>teach</em> you how to diagnose illnesses. First of all, medicine is an extremely large and complex science, consisting of different specialties, and every one of them has its own large spectrum of knowledge to study (eg. your question - skin conditions are subject of dermatology, flu - infectious diseases etc.). Doctors go through the basics in all fields during their ~6 years studies, and later become specialists only in a particular branch.</p>\n\n<p>Secondly, just knowing the symptoms of a disease won't qualify you for diagnosing. It's a complex process, that involves a set of special skills, such as knowing how to examine a patient, understanding imaging/lab, and so on. </p>\n\n<p>And here comes an important note: most of what I described is not only <em>taught</em> on a basis of medical literature, but also <em>by</em> a mentor who not only is a good specialist themselves, but also knows how to make other people capable of using all this knowledge.</p>\n\n<p>Last but not least, the comment regarding background knowledge is also completely true and is to be taken into account. </p>\n\n<p>Having said all that, I assume that your goal is to get a peek inside how diagnosis works, in this case i'd recommend some \"Introduction to...\" textbooks for different medical specialties, they might be a bit challenging to understand without required theoretical background (eg. histology, physiology etc.) but will give a nice overview of what do those specialties work with.</p>\n" }, { "answer_id": 18432, "author": "Camille Markham", "author_id": 15491, "author_profile": "https://health.stackexchange.com/users/15491", "pm_score": 2, "selected": false, "text": "<p>I had to study pathophysiology. My textbook was called something like advanced pathophysiology. However, I learned a lot about neuropsychiatric conditions by studying a book titled something like pharmacological approaches for the treatment of neuropsychological diseases. I think! Very close if not right on. </p>\n\n<p>What it is in layman's terms and probably in medical school texts, is psych pharm. Or psychiatric pharmacology. </p>\n\n<p>Pathophysiology of disease is great for all types of knowledge and psych pharm is very in depth. </p>\n\n<p>Many physicians, ARNPs, and PAs, learn by internship or clinical practice while in school. This cemented book knowledge together with real life presentations with expert guidance. \nHope that helped. </p>\n\n<p>Let me add the site that provided my online text for my psych pharm class. This text has pathopsysiological texts, pharmacology texts as well as prescribing information. It had some interactive case studies. It is wonderful. <a href=\"https://stahlonline.cambridge.org/\" rel=\"nofollow noreferrer\">https://stahlonline.cambridge.org/</a>\nPerhaps Cambridge University has similar texts that are strictly medical. </p>\n" } ]
2019/01/14
[ "https://health.stackexchange.com/questions/18411", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15483/" ]
18,415
<p>The FLUENTAL® moderator/shifter appears often in the literature surrounding BNCT therapy. Google offers no search results with useful information on how it was made and whom by. </p>
[ { "answer_id": 18419, "author": "Carey Gregory", "author_id": 805, "author_profile": "https://health.stackexchange.com/users/805", "pm_score": 1, "selected": false, "text": "<p><a href=\"https://www.drugs.com/international/fluental.html\" rel=\"nofollow noreferrer\">Fluental</a> is a drug sold in Italy. It's a combination of acetaminophen (paracetamol) and <a href=\"https://www.drugs.com/international/sobrerol.html\" rel=\"nofollow noreferrer\">sobrelol</a>, which is a mucolytic. Basically, it's a cold remedy. It is manufactured by <a href=\"https://www.sanofi.com/\" rel=\"nofollow noreferrer\">Sanofi</a>.</p>\n" }, { "answer_id": 18420, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 2, "selected": false, "text": "<p>After looking (without result!) at loads of pages returned from a Bing search for BNCT, I hit upon searching for:</p>\n\n<blockquote>\n <p><a href=\"https://www.bing.com/search?q=%20FLUENTAL%20moderator&amp;qs=n&amp;form=QBRE&amp;sp=-1&amp;pq=fluental%20moderator&amp;sc=0-18&amp;sk=&amp;cvid=AE6A53394FB447BBB8053908D0688FEC\" rel=\"nofollow noreferrer\">FLUENTAL moderator</a></p>\n</blockquote>\n\n<p>The first reference I looked at was:</p>\n\n<ul>\n<li><a href=\"http://www.npl.co.uk/upload/pdf/20061026_nuc_green_1.pdf\" rel=\"nofollow noreferrer\">Use of TEPCs for characterising BNCT Beams</a></li>\n</ul>\n\n<p>but there is no reference to the manufacturer.</p>\n\n<p>However, the opening chapter of:</p>\n\n<ul>\n<li><a href=\"https://www.vtt.fi/inf/pdf/technology/2014/T156.pdf\" rel=\"nofollow noreferrer\">Chemical aspects on the final disposal of irradiated</a></li>\n</ul>\n\n<p>reads:</p>\n\n<blockquote>\n <p>The Boron Neutron Capture Therapy (BNCT) at VTT utilized the FiR 1 TRIGA reactor as a source for the neutron beam. The fast fission neutrons from the reactor needed to be slowed down to the epithermal energy range (0.5 eV–10 keV) prior to reaching the patient. The epithermal neutrons were produced in a block of FLUENTAL™ set between the the reactor and the patient. <strong>FLUENTAL™ is a patented material that has been developed and produced by VTT (Auterinen &amp; Salmenhaara 2008, Savolainen et al. 2013)</strong>. The composition of FLUENTAL™ is AlF3 (69 w-%), metallic aluminium (30 w-%) and LiF (1 w-%). The manufacturing process is based on a hot isostatic pressing technique, which results in a FLUENTAL™ product consisting of solid blocks with a density of 3 000 kg/m3. The decommissioning of the FiR 1 reactor leaves VTT with two options; to sell it abroad or to dispose of it together with the other decommissioning waste. At present, both options are considered and the final decision will be made at a later stage.</p>\n</blockquote>\n" } ]
2019/01/14
[ "https://health.stackexchange.com/questions/18415", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15485/" ]
18,473
<p>What is the difference between Eisenmenger syndrome and ventricular septal defect? </p> <p>They are both related to a hole between the two ventricles, right?</p>
[ { "answer_id": 18479, "author": "Chris", "author_id": 14056, "author_profile": "https://health.stackexchange.com/users/14056", "pm_score": 4, "selected": true, "text": "<h1>Ventricular septal defect</h1>\n\n<p>A <a href=\"https://emedicine.medscape.com/article/892980-overview\" rel=\"noreferrer\">ventricular septal defect</a> (VSD) is a <a href=\"https://www.merriam-webster.com/dictionary/congenital\" rel=\"noreferrer\">congenital</a> defect of the central wall (septum) of the heart. This septum divides the right ventricle of the heart from the left ventricle.</p>\n\n<p>The right side of the heart receives blood from the head and body (via the vena cava) and pumps it to the lungs to be oxygenated.</p>\n\n<p>The left side of the heart receives oxygenated blood from the lungs and returns it to the body (via the aorta). The left side is at a higher pressure than the right.</p>\n\n<p><strong>Heart anatomy and ventricular septal defect</strong></p>\n\n<p><a href=\"https://i.stack.imgur.com/qUIW7.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/qUIW7.jpg\" alt=\"Heart and VSD\"></a></p>\n\n<p>Note that the right side of the heart is on the left side of the image and vice versa.</p>\n\n<p>A VSD results in oxygenated blood being pushed (or <em>shunted</em>) from the higher pressure left ventricle through the defect to the right ventricle, where it will travel to the lungs again (unnecessarily).</p>\n\n<hr>\n\n<h1>Eisenmenger’s syndrome</h1>\n\n<p><a href=\"https://emedicine.medscape.com/article/154555-overview\" rel=\"noreferrer\">Eisenmenger’s syndrome</a> is a complication that can arise from many untreated heart defects (including VSD).</p>\n\n<p><strong>Pathophysiology of Eisenmenger’s syndrome</strong></p>\n\n<p><a href=\"https://i.stack.imgur.com/oRjxD.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/oRjxD.jpg\" alt=\"Pathophysiology of Eisenmenger’s syndrome\"></a></p>\n\n<p>The left-to-right shunt causes increased blood flow to the lungs, which damages the endothelium (inner lining) of the blood vessels. This results in gradually increasing vascular resistance in the lungs. </p>\n\n<p>Eventually the resistance gets to a point where the pressure in the right ventricle rises above that of the left ventricle across the VSD. As a result, the shunting reverses, so that blood is now moving from right to left.</p>\n\n<p><a href=\"https://i.stack.imgur.com/JioXT.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/JioXT.jpg\" alt=\"Eisenmenger’s syndrome\"></a></p>\n\n<p>This is a problem because blood is now bypassing the lungs, resulting in reduced oxygen availability to the body (<a href=\"https://en.m.wikipedia.org/wiki/Hypoxia_(medical)\" rel=\"noreferrer\">hypoxia</a>).</p>\n\n<p>This can result in cyanosis (blue discolouration due to hypoxia), heart failure, breathlessness, chest pain, fatigue, haemoptysis (coughing blood), collapse and cardiac arrest.</p>\n\n<hr>\n\n<h1>Summary</h1>\n\n<p>In summary, a VSD is a congenital defect of the heart, and Eisenmenger’s syndrome is a potential long-term complication that can arise if it is left untreated.</p>\n\n<hr>\n\n<p>You can read more about the two conditions by following the links.</p>\n\n<p>Images courtesy of the American Medical Association and Mayo Clinic.</p>\n" }, { "answer_id": 18480, "author": "De Novo", "author_id": 14173, "author_profile": "https://health.stackexchange.com/users/14173", "pm_score": 3, "selected": false, "text": "<p>Eisenmenger syndrome is a clinical syndrome. A ventricular septal defect (VSD) is an anatomic lesion. They are related in that Eisenmenger syndrome can be caused by a VSD (among other things).</p>\n<h3>VSD</h3>\n<p>A <a href=\"https://en.wikipedia.org/wiki/Ventricular_septal_defect\" rel=\"noreferrer\">ventricular septal defect</a> is a (typically) congenital opening between the right and left ventricle, caused by a failure of the ventricular septum, or wall between the two ventricles, to fully develop</p>\n<h3>Eisenmenger syndrome</h3>\n<p>Eisenmenger syndrome is a clinical syndrome and disease process in which a (congenital) <a href=\"https://en.wikipedia.org/wiki/Cardiac_shunt\" rel=\"noreferrer\">left to right shunt</a> (from the systemic circulation to the pulmonary circulation) causes the development of pulmonary vascular disease, <a href=\"https://en.wikipedia.org/wiki/Pulmonary_hypertension\" rel=\"noreferrer\">pulmonary hypertension</a>, and eventually a <a href=\"https://en.wikipedia.org/wiki/Cardiac_shunt\" rel=\"noreferrer\">right to left shunt</a>, leading to <a href=\"https://en.wikipedia.org/wiki/Cyanosis\" rel=\"noreferrer\">cyanosis</a> (a bluish discoloration of the skin caused by inadequate oxygenation of blood). The eventual right to left shunt means that blood returning from the systemic veins goes directly through to the systemic arteries without passing through the pulmonary circulation and the lungs. This prevents gas exchange. Ventricular septal defects are the most common cause of Eisenmenger syndrome, but other initial left to right shunts can cause the same syndrome. <a href=\"https://en.wikipedia.org/wiki/Atrial_septal_defect\" rel=\"noreferrer\">Atrial septal defects</a> and a <a href=\"https://en.wikipedia.org/wiki/Patent_ductus_arteriosus\" rel=\"noreferrer\">patent ductus arteriosus</a> are also relatively common causes of Eisenmenger syndrome.</p>\n<p>I've added links to competent Wikipedia articles about some of the terms here, and you can read about Eisenmenger Syndrome, VSDs, and other congenital cardiac shunts in Lilly's Pathophysiology of Heart Disease, Chapter 16, on Congenital Heart Disease.</p>\n" }, { "answer_id": 18496, "author": "rncardio", "author_id": 1477, "author_profile": "https://health.stackexchange.com/users/1477", "pm_score": 2, "selected": false, "text": "<p>Apart from information on differences given in two excellent answers here, there is a major difference in treatment of these two conditions. </p>\n\n<p>Ventricular Septal Defect (VSD) before development of Eisenmenger syndrome can be treated by surgery. Usually the defect is closed using a patch. Closure can sometimes be done without surgery using devices inserted through peripheral arteries or veins. </p>\n\n<p>If the VSD is very small, it may not need any treatment at all apart from preventive measures to be taken at time of other medical and dental procedures. These are required since there may be a risk of infection at the site of VSD from bacteria that may enter the bloodstream during these procedures.</p>\n\n<p>However, once Eisenmenger syndrome (irreversible pulmonary hypertension with reversal of shunt) develops, surgery (or device closure) is no more an option and condition is generally managed by medicines only. </p>\n\n<p>Pregnancy also carries an increased risk in patients with Eisenmenger syndrome while risk is generally not increased in patients who have had VSD successfully closed earlier.</p>\n\n<p>See this American Heart Association (AHA) page: <a href=\"https://www.heart.org/en/health-topics/congenital-heart-defects/about-congenital-heart-defects/ventricular-septal-defect-vsd\" rel=\"nofollow noreferrer\">https://www.heart.org/en/health-topics/congenital-heart-defects/about-congenital-heart-defects/ventricular-septal-defect-vsd</a> for more information (search for 'pulmonary hypertension', since the term 'Eisenmenger syndrome' is not used there).</p>\n\n<p>Treatment/management options are best discussed with treating doctors since many factors have to be taken into account before deciding best course of action.</p>\n" } ]
2019/01/24
[ "https://health.stackexchange.com/questions/18473", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15535/" ]
18,484
<p>My grandpa's specialist has ordered quarterly blood tests for him. Most of LifeLabs' phlebotomists (in Ontario, Canada) venipuncture very painfully. </p> <p>Though he didn't mention algophobia, he chanced on a kinder phlebotomist yesterday who was canny enough to sense his needle phobia and introduced him to the <a href="https://www.reddit.com/r/legaladvice/comments/5l1vx6/can_i_refuse_a_blood_test_as_a_minor_ca/dbsgaxj/" rel="nofollow noreferrer">baby needle</a>, which every phlebotomist in his life (to his memory) failed to do. </p> <p>He already <a href="http://jenniferfulwiler.com/2008/09/4-blood-test-tips-for-needle-phobes/" rel="nofollow noreferrer">drinks much water and gets blood pumping</a>. Thus what else can a phlebotomist do? </p>
[ { "answer_id": 18486, "author": "Kate Gregory", "author_id": 400, "author_profile": "https://health.stackexchange.com/users/400", "pm_score": 2, "selected": false, "text": "<p>Most people do not know that you are an active participant in getting blood drawn or IVs started. The skill differences among those who are poking you include their skill in getting you to do the right thing. My tips:</p>\n\n<ul>\n<li>drink plenty of fluids and avoid caffeine the day of the draw</li>\n<li>keep your arm warm. I leave it in a sweater until the last minute. I also rub the inside of my elbow while waiting for them to get all their tubes ready etc. When I was getting IV treatments they would wrap my arm in a heating pad</li>\n<li>relax, breathe slowly, try not to tense your mouth, in fact try opening your mouth a little. Make sure your entire arm is relaxed except for your hand if they've asked for a fist. This takes practice. Focus on it.</li>\n<li>support your elbow with your other hand to keep it at a good angle and to stop yourself from jerking backwards as the needle goes in</li>\n<li>keep your eyes open. Closing my eyes slows blood flow (learned this from a chemo nurse and would not have believed it but several experiences have shown it is true for me) Don't look at the puncture site or watch the blood if it upsets you. Focus on something behind the poker -- wall art, a clock, their computer, etc.</li>\n<li>tell them to use the smallest needle. If you have scar tissue from a lot of draws and tests, tell them so</li>\n<li>after they swab with alcohol, ask them to wait a moment until it evaporates. The burning sensation you sometimes feel as the needle goes in is alcohol. It's not necessary to endure that, just some pokers don't wait</li>\n<li>if there is a spot that hurts more or that often fails, tell them not to try that spot</li>\n<li>follow their instructions about making a fist etc</li>\n<li>pay attention every time, and when you have a \"good\" draw remember all the things you did, then do them next time whether the poker asks you to or not</li>\n</ul>\n\n<p>I learned these tips from good phlebotomists and nurses. They have dramatically reduced the pain and bruising of both blood draws and IV starts. They also reduce the number of failed attempts. I have had a vein spasm shut once the needle is in, and been walked through a relaxation process that got it to open again. Opening both your eyes and mouth is key to this. Another time, when it spasmed shut with a different person, I convinced them to leave the needle and let me try getting it open. It worked and they said \"I did not know that was possible.\" Neither did I until I learned to do it. </p>\n\n<p>Actively work on learning what you can do to make the pain and difficulty less. People will tell you that you have nothing to do with it, but they're wrong. It's your arm, your muscles, your heart rate and blood pressure. You can make it go better.</p>\n\n<p>[will add links if I find some]</p>\n" }, { "answer_id": 23497, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 0, "selected": false, "text": "<p>This isn't the best suggestion in the time of a respiratory pandemic as we have now with COVID-19 but the cough trick is quite effective at pain reduction during venipuncture</p>\n<blockquote>\n<p>We tested the effectiveness of the cough trick (CT) as a method of pain relief during peripheral venipuncture (VP) in a crossover study. Twenty healthy volunteers were punctured twice in the same hand vein within an interval of 3 wk, once with the CT procedure and once without it. The intensity of pain, hand withdrawal, palm sweating, blood pressure, heart rate, and serum glucose concentration were recorded. The intensity of pain during VP with the CT procedure was less than without it, whereas the other variables changed insignificantly. The easily performed CT was effective in pain reduction during VP, although the mechanism remains unclear.</p>\n<p><strong>Implications:</strong> The effectiveness of a cough trick for pain reduction during peripheral venipuncture was tested in a volunteer study in which each subject served as his own control. The easily performed cough-trick procedure was effective for pain reduction, although the mechanism remains unclear though is blocked by Naloxone. It is more effective than distraction by cognitive-motor tasks.</p>\n</blockquote>\n<p>The cough trick is to turn ones head away from the phlebotomist and cough at the time of venipuncture. It somehow distracts the brain from pain perception.</p>\n<p>Reducing Venipuncture Pain by a Cough Trick: A Randomized Crossover Volunteer Study\n<a href=\"https://pubmed.ncbi.nlm.nih.gov/14742367/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/14742367/</a></p>\n<p><a href=\"https://www.hindawi.com/journals/prm/2019/9459103/\" rel=\"nofollow noreferrer\">https://www.hindawi.com/journals/prm/2019/9459103/</a></p>\n" } ]
2019/01/25
[ "https://health.stackexchange.com/questions/18484", "https://health.stackexchange.com", "https://health.stackexchange.com/users/-1/" ]
18,544
<p>I read an article <a href="https://www.huffingtonpost.com/2015/07/14/dairy-skin-effect_n_7787546.html?guccounter=1" rel="noreferrer">here</a> that says:</p> <blockquote> <p>“There is a very strong correlation between consuming dairy products — such as milk — and acne, skin breakouts and aging.”</p> <p>The reason? Hormones, Bella says. “Most of the cows used in farming are actually pregnant cows. The hormones such as progesterone and insulin growth factors make their way into the milk,” she explains. “When we consume the milk, it leads to increased levels of inflammation, skin breakdown, aging and acne in many people.”</p> </blockquote> <p>It was interesting for me to ask: Can those hormones be alive(active) even when we eat pasteurized milk(boiled milk) and other dairies that I think are derived from the pasteurized milk? </p> <p>I mean won't hormones destroyed after boiling milk? I also like to know can cow hormones have any effects on humans?</p>
[ { "answer_id": 18546, "author": "De Novo", "author_id": 14173, "author_profile": "https://health.stackexchange.com/users/14173", "pm_score": 3, "selected": false, "text": "<p>These are biologically plausible effects supported by moderate quality observational evidence. As a personal aside, I do not believe there is enough evidence for harm to recommend eliminating dairy products from a healthy person's diet. A full discussion of all the evidence for the impact of dairy in diet is beyond the scope of this answer, though, so lets move on to your specific question </p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Sex_steroid\" rel=\"nofollow noreferrer\">Sex steroids</a> are lipid soluble fused ring structures derived from cholesterol, and conserved across many species. They are not inactivated by pasteurization. In addition to being identified in dairy products and in the people who consume them, consumption of dairy products appears to be associated with some expected biological effects in humans, e.g., <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3712661/\" rel=\"nofollow noreferrer\">sperm quality</a>. That linked study as well as the other points are succinctly reviewed in the introduction to <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5699997/\" rel=\"nofollow noreferrer\">this article</a>. </p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Insulin-like_growth_factor_1\" rel=\"nofollow noreferrer\">Insulin like growth factor 1</a> (IGF-1) is a peptide hormone, but has been demonstrated to be active after pasteurization. It is also conserved across species. There is evidence (well summarized in both the narrative review and meta-analysis in <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5400803/\" rel=\"nofollow noreferrer\">this article</a>) for an association between consumption of dairy products, increased levels of circulating IGF-1, and downstream effects of that increased level (e.g., prostate cancer).</p>\n\n<p>You should note that it is not surprising that a hormone produced by another animal would be active in a human. See, <a href=\"https://www.nobelprize.org/prizes/medicine/1923/banting/facts/\" rel=\"nofollow noreferrer\">the 1923 Nobel Prize</a>.</p>\n\n<p>Just to be clear:\n<strong>This answer addresses the specific two questions posed in the OP: are hormones in milk and milk products active after pasteurization, and are cow hormones active in humans. This answer (and the evidence) does NOT provide support for the question, in balance is dairy good or bad for you, and does not address the claims in the linked article (a la a Skeptics.SE question)</strong></p>\n" }, { "answer_id": 18554, "author": "LаngLаngС", "author_id": 11231, "author_profile": "https://health.stackexchange.com/users/11231", "pm_score": 3, "selected": false, "text": "<p>If the main thrust of the question is indeed expressed in the title and tags of the question:</p>\n\n<blockquote>\n <p><strong>Q</strong> “There is a very strong correlation between consuming dairy products — such as milk — and acne, skin breakouts and aging.”</p>\n</blockquote>\n\n<p>Then the jury on that really isn't finished deciding:</p>\n\n<blockquote>\n <p>Is acne related to the ingestion of dairy products? It is not a new idea. It goes back to the early days of the last century and beyond. The counter-claim, that there is no relationship between diet and acne, has reached mythic proportions. It has never been substantiated, but it is repeated as gospel in all major dermatology textbooks. Epstein, commenting on contributions on the subject by Waisman, Bickers, and Rosenberg, trod the middle road. Inexplicably asserting that \"Controlled studies indicate that foods have no effect on acne,\" he nonetheless allowed, \"the patient should receive any assistance that dietary control may impart.\" <strong>In a review of 274 clinical trials of acne, the massive 2001 Evidence Report on the Management of Acne found <em>one</em> solitary paper that mentioned diet, but no trial reported specifically on patients’ diets.</strong></p>\n \n <p>Dairy products have been implicated as a possible factor in the etiology of prostate cancer in several large epidemiological studies, but not in all. The possible influences of dairy hormone in breast cancer are likewise unclear and in need of further definition.<br>\n The next few years will be fascinating for those of us interested in hormones and \"the blight of youth.\" One wonders what the impact will be upon our patients, our practices, and the industries that make milk, hormones, and acne products. Time alone will tell.</p>\n \n <p><a href=\"https://www.jaad.org/article/S0190-9622(04)02500-9/abstract\" rel=\"nofollow noreferrer\">F. William Danby: \"Acne and milk, the diet myth, and beyond\"</a>, J AM ACAD DERMATOL FEBRUARY 2005</p>\n</blockquote>\n\n<p>While it seems very much up for debate to either substantiate whether indeed industrialised milk production schemes result in increased hormone presence in milk sold, whether there is a difference between production methods and 'ingredients' in milk sold, whether this is then true for all dairy products.</p>\n\n<p>Case in point: water soluble pharmacologically active compounds will be greatly reduced in butter and ghee, molecules found in whey greatly reduced in most cheeses, and anything greatly processed is another game entirely. If yeasts, worms, insects bacteria ferment the milk-product, how much of the hormones is reduced by those organisms? –– or amplified?</p>\n\n<p>Milk as is not the main product consumed by most people and all dairy products are clearly not the same. Kefir is different from cheese, fresh or aged, with bacteria or fungi, from whey, from butter, from ghee, from protein-isolate and so on. Given the different profiles for all those products they either have to have something in common across the board or they have to be analysed separately.</p>\n\n<p>It is of course quite interesting to look for evidence that shows how much different modern milk and milk products are compared to just a few decades ago. Be it in nutritional or now even pharmacological profiles. </p>\n\n<p>But to start a comparison with dairy, hypothesising about hormones, then linking that all up to skin disorders seems very premature and theoretical. At least if there are not clear epidemiological indicators of indeed a possible link.</p>\n\n<p>Which suspects would there be to observe in the proposed link between acne and skin?</p>\n\n<p>Only the most prominent are:</p>\n\n<blockquote>\n <p>Prolactin, Somatostatin, Gonadotropin-releasing hormone, Luteinizing hormone, Thyroid-stimulating hormone, Thyreotropin-releasing hormone, Epidermal growth factor, Insulin-like growth factor 1, Insulin-like growth factor 2, Insulin, Vitamin D, Transferrin, Lactoferrin, Prostaglandins</p>\n</blockquote>\n\n<p>Now which of these are contained in fresh milk under which circumstances and therefore concentrations in the first place? How much of this is linked to milking pregnant cows?</p>\n\n<blockquote>\n <p><strong>Acne and milk</strong><br>\n Milk and other dairy products contain more than 60 molecules including prolactin, somatostatin, gonadotropin-releasing hormone, luteinizing hormone, thyroid-stimulating and thyreotropin-releasing hormones, insulin, epidermal growth factor, nerve growth factor, IGF-1 and 2, transforming growth factors, vitamin D, transferrin, lactoferrin and prostaglandins (Koldovsky, 1995). <strong>This makes it difficult to distinguish which of these factors could have an acneigenic effect, especially when this fact is combined with the broad range of dairy products</strong> (Table 25.2, Figure 25.4).<br>\n The most important factor of the ones mentioned above is the insulin-like growth factor. The IGFs are proteins with high sequence similarity to insulin. IGFs are part of a complex system that cells use to communicate with their physiologic environment. <strong>Cow milk contains IGF-1 and -2, even after pasteurization and homogenization, and bovine and human IGF-1 share exactly the same amino acid sequence</strong> (Melnik and Schmitz, 2009). High milk consumption increases IGF-1 levels 10%-20% in adults and 20%-30% in children (Hoppe et al., 2004 a, b) and milk and dairy products raise IGF-1 levels more than dietary proteins such as meat (Hoppe et al., 2005).<br>\n Milk also contains carbohydrates, including lactose, and therefore its consumption produces a glycemic response and an insulinemic response. The insulinemic response to ingested milk is actually three to six times what would be predicted from the carbohydrate load in the milk serving (Ostman et al., 2001). <strong>This happens for skimmed and full-fat milk, but not for cheese</strong> (Holt et al., 1997; Hoyt et al., 2005). <strong>The reasons are not yet understood, but they may</strong> relate to the insulinotropic effects of some of the other multiple hormones that are present in milk (Koldovsky, 1995).\n A glass of milk added to a low glycemic index meal can boost the insulin response up to 300% of the level produced by a high glycemic index meal and cow milk-formula does this even better than human breast milk (Liljeberg and Bjorck, 2001; Lucas et al., 1980). <strong>Different studies suggest that insulin rises in response to the whey component</strong> (20% of milk protein), <strong>whereas casein is responsible for the IGF-1 increase</strong> (Hoppe et al., 2006). Because whey and casein are both involved in stimulating androgen production, there is little point in further differentiating them in dietary restriction, since both should be avoided.</p>\n</blockquote>\n\n<p>If the result of the above is indeed true: \"whey and casein should both be avoided\" then this is still incomplete as to whether it is for example whey-protein itself (essentialist reading) or what's commonly in there (varying by methods of production) as well and surely not encompassing 'all dairy', as butter for example is largely free of both.</p>\n\n<p>Then it remains a stretch to conclude that \"stimulating androgen production\" is just \"all bad/causes acne\" on the one side and on the other side there are other types of causes that are \"stimulating androgen production\": hyperinsulinemia for example, which can also activate or upregulate IGF receptors. </p>\n\n<p>It is simply too simplistic to reduce the focus to just one or a few pathways and \"reason the rest\" from there.</p>\n\n<p>But take note that this is not the sole point of that article. The very next item was about 'glycemic index'. To give more context:</p>\n\n<blockquote>\n <p>Key facts</p>\n \n <ul>\n <li>Androgen excess, peroxisome proliferator-activated receptors and inflammation are the main pathogenetic mechanisms of acne.</li>\n <li>Nutrition seems to play an important role in skin biology and pathology, affecting the onset and clinical manifestation of several dermatologic disorders, including acne.</li>\n <li>The typical Western diet consists of numerous dairy sources and foods with high glycemic indices.</li>\n <li>A study performed by Adebamowo et al. (2005) demonstrated the association between dairy products and acne.</li>\n <li>A study provided by Smith et al. (2007) showed the link between high glycemic load intake of carbohydrates and acne.</li>\n <li>High glycemic carbohydrates and milk appear to raise serum insulin levels, free IGF-1 and insulin resistance, thus contributing to the pathogenesis of acne.</li>\n <li>IGF-1 seems to be the most important acneigenic factor contained in diet.</li>\n <li>At the genomic level, the effects of insulin and IGF-1 are mediated by the nuclear concentration of the transcription factor FoxO1.</li>\n <li>At the promoter level, SREBP-1c expression is suppressed by nuclear FoxO1, which is an important co-repressor of the retinoid X receptor and liver X receptor.</li>\n <li>Dermatologists should be able to include dietary restriction in acne therapy management.</li>\n </ul>\n \n <p>Summary points</p>\n \n <ul>\n <li>Skin reflects individual age, health and beauty.</li>\n <li>Nutritional customs affect several skin diseases including psoriasis, atopic dermatitis and acne. </li>\n <li>Epidemiological studies with milk and dairy products support the association of milk consumption with acne\n onset and clinical course.</li>\n <li>High glycemic load diets are also considered to be involved in acne pathogenesis because of the consequent\n hyperglycemia and hyperinsulinemia.</li>\n <li>Dermatologists should include restrictive dietary management in acne therapy in their daily clinical practice. </li>\n </ul>\n \n <p>A.I. Liakou, C.I. Liakou and C.C. Zouboulis: \"Acne and nutrition\", Victor R. Preedy (Ed): \"Handbook of diet, nutrition and the skin\", Wageningen Academic Publishers, Wageningen, 2012. </p>\n</blockquote>\n\n<p>Note especially that 'dairy' is not unique in containing these molecules, concentrationand consumption patterns have to be observed as well. Dosis facit venenum. But even if the same molecules are measured, the effect may not be same after all, as the milk vs meat example aboive illustrates. And how much of those are even present in milk 'now' compared to 'earlier times' is partly dependent on the alleged production methods of \"pregnant cows\". How much <a href=\"https://skeptics.stackexchange.com/questions/43363/is-the-majority-of-milk-in-industrialized-countries-obtained-from-pregnant-cows\">has that changed</a>? We can hardly know. </p>\n\n<p>One of the more prominent papers investigating a possible link comes sponsored from a food-giant:</p>\n\n<blockquote>\n <p>Bodo C. Melnik: \"Evidence for Acne-Promoting Effects of Milk and Other Insulinotropic Dairy Products\", Clemens RA, Hernell O, Michaelsen KF (eds): Milk and Milk Products in Human Nutrition. Nestlé Nutr Inst Workshop Ser Pediatr Program, vol 67, pp 131–145, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2011. </p>\n</blockquote>\n\n<p>And that is quite a problem. The dairy side sponsoring research to show how \"good it is for you\", and from animal-rights over vegan to frankenfood-companies financing the other side of ideology. All sides looking for evidence that they <em>were</em> right, from the start. This is more like gnosis that science and it is extremely difficult to weed out all the chaff thrown in to the pool of knowledge.</p>\n\n<blockquote>\n <p>A meta-analysis can help inform the debate about the epidemiological evidence on dairy intake and development of acne. A systematic literature search of PubMed from inception to 11 December 2017 was performed to estimate the association of dairy intake and acne in children, adolescents, and young adults in observational studies. We estimated the pooled random effects odds ratio (OR) (95% CI), heterogeneity (I2-statistics, Q-statistics), and publication bias. We included 14 studies (n = 78,529; 23,046 acne-cases/55,483 controls) aged 7–30 years. ORs for acne were 1.25 (95% CI: 1.15–1.36; p = 6.13 × 10−8) for any dairy, 1.22 (1.08–1.38; p = 1.62 × 10−3) for full-fat dairy, 1.28 (1.13–1.44; p = 8.23 × 10−5) for any milk, 1.22 (1.06–1.41; p = 6.66 × 10−3) for whole milk, 1.32 (1.16–1.52; p = 4.33 × 10−5) for low-fat/skim milk, 1.22 (1.00–1.50; p = 5.21 × 10−2) for cheese, and 1.36 (1.05–1.77; p = 2.21 × 10−2) for yogurt compared to no intake. ORs per frequency of any milk intake were 1.24 (0.95–1.62) by 2–6 glasses per week, 1.41 (1.05–1.90) by 1 glass per day, and 1.43 (1.09–1.88) by ≥2 glasses per day compared to intake less than weekly. Adjusted results were attenuated and compared unadjusted. There was publication bias (p = 4.71 × 10−3), and heterogeneity in the meta-analyses were explained by dairy and study characteristics. In conclusion, any dairy, such as milk, yogurt, and cheese, was associated with an increased OR for acne in individuals aged 7–30 years. </p>\n \n <p><strong><em>However, results should be interpreted with caution due to heterogeneity and bias across studies.</em></strong> </p>\n \n <p>Christian R. Juhl et al: \"Dairy Intake and Acne Vulgaris: A Systematic Review and Meta-Analysis of 78,529 Children, Adolescents, and Young Adults\", Nutrients 2018, 10(8), 1049, <a href=\"https://doi.org/10.3390/nu10081049\" rel=\"nofollow noreferrer\">DOI</a></p>\n</blockquote>\n\n<p>So it remains currently at this:</p>\n\n<blockquote>\n <p><a href=\"https://www.webmd.com/skin-problems-and-treatments/acne/features/worst-foods-for-your-skin#1\" rel=\"nofollow noreferrer\">Dairy and Acne</a></p>\n \n <p>There's no definite link between dairy and acne, but there are theories about it.</p>\n</blockquote>\n" }, { "answer_id": 31001, "author": "haz", "author_id": 25043, "author_profile": "https://health.stackexchange.com/users/25043", "pm_score": 1, "selected": false, "text": "<p>Milk is a specialised substance produced by mammals to support development during the infant growth phase. The nutritional content in milk represents a postnatal continuum of the support established during gestation between mother and child with particular emphasis on growth factors.</p>\n<p>Amongst the growth promoting signals in milk is the presence of IGF-1 and exosomes that contain various conserved microRNAs that persist following pasteurisation. The exosomes have evolved to survive digestion and enter the bloodstream. Their miRNA cargo directs pro-growth gene expression.</p>\n<p>Hence bovine milk is favoured amongst bodybuilders and power athletes for its anabolic effect. However, this growth state is mediated by activation of the mTor complex, a pro-aging and pro-oncogenic pathway.</p>\n<p>Unsurprisingly, there is a significant signal in the literature between cancer incidence (colonic, breast and prostate) and dairy consumption albeit with the usual confounding due to lack of distinction between dairy types. In contrast, we see no such ambiguity regarding quality plant based diets.</p>\n<p>In any case, dairy milk is a mTor activator and mTor activation is pro-aging and pro-acne.</p>\n<p>See</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8000710/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8000710/</a></p>\n<p><a href=\"https://www.bmj.com/content/367/bmj.l6204\" rel=\"nofollow noreferrer\">https://www.bmj.com/content/367/bmj.l6204</a></p>\n" } ]
2019/02/01
[ "https://health.stackexchange.com/questions/18544", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15574/" ]
18,653
<p>A leading theory behind the rising allergy and intolerance diagnosis rates is the <a href="https://www.aaaai.org/conditions-and-treatments/library/allergy-library/prevalence-of-allergies-and-asthma" rel="nofollow noreferrer">"hygiene hypothesis."</a> This theory suggests that living conditions in much of the world might be too clean and that kids aren't being exposed to germs that train their immune systems to tell the difference between harmless and harmful irritants.</p> <p>A counter-argument I heard recently on the radio here in the UK (<a href="https://www.bbc.co.uk/sounds/play/m0002hnj" rel="nofollow noreferrer">on this BBC Radio 2 programme - section starting from 42min 40secs </a>) was that you can't say that when in some countries where cholera is high, you cannot safely allow children to play in the mud (from 46min 3secs).</p> <p>When looking at the rise in food allergies, one area which I have been looking at is the constant changes in what should and shouldn't be eaten during pregnancy. Expectant mothers are told not to eat nuts, shellfish, dairy products etc. in order to avoid allergy problems in the baby, yet when you look at the great long <a href="https://www.nhs.uk/conditions/pregnancy-and-baby/foods-to-avoid-pregnant" rel="nofollow noreferrer">list of don't eats</a> provided by the NHS, they even point out that there can be conflicting information given regarding peanuts, because</p> <blockquote> <p>the government previously advised women to avoid eating peanuts if there was a history of allergy – such as asthma, eczema, hay fever and food allergy – in their child's immediate family.</p> <p>This advice has now changed because the latest research has shown no clear evidence that eating peanuts during pregnancy affects the chances of your baby developing a peanut allergy.</p> </blockquote> <p>There are also reports in places such as <a href="https://www.parents.com/baby/health/allergy/food-allergy-facts" rel="nofollow noreferrer">this parenting site</a> where they say that it is fine to eat high allergy foods if you as an expectant mother are not allergic yourself.</p> <p>What is the state of play within medical science regarding this? What <strong>is</strong> the cause of the rise in allergies and food intolerance? Is it purely lack of exposure to potential allergens early in life (including during prenatal development)? <strong>Should</strong> expectant mothers avoid dairy, nuts, shellfish etc. which others are allergic to "just in case"?</p>
[ { "answer_id": 18671, "author": "LаngLаngС", "author_id": 11231, "author_profile": "https://health.stackexchange.com/users/11231", "pm_score": 2, "selected": false, "text": "<p>In general, it seems that there has to be a slight distinction made between a diet during pregnancy and a mother's diet during breast feeding. Overall the available evidence is judged as 'not there' or 'too weak' to make any recommendation to avoid specific antigens.</p>\n<blockquote>\n<p>Evidence is inadequate to advise women to avoid specific foods during pregnancy or breastfeeding to protect their children from allergic diseases like eczema and asthma.</p>\n<p>We included five trials, involving 952 participants. Trials of mothers' avoidance of milk, eggs, and other potentially 'antigenic' foods during pregnancy or breastfeeding, or both, provide inadequate evidence about whether such avoidance helps prevent atopic eczema or asthma in the child. Women who avoided eating these foods gained significantly less weight during pregnancy in the one trial reporting on this outcome, raising the possibility of adverse nutritional effects on the mother or fetus. Finally, one small trial reported an inconclusive response of breastfed infants with atopic eczema when their mothers avoided consumption of cow milk and egg.</p>\n<p>Prescription of an antigen avoidance diet to a high-risk woman during pregnancy is unlikely to reduce substantially her child's risk of atopic diseases, and such a diet may adversely affect maternal or fetal nutrition, or both. Prescription of an antigen avoidance diet to a high-risk woman during lactation may reduce her child's risk of developing atopic eczema, but better trials are needed.</p>\n<p>Dietary antigen avoidance by lactating mothers of infants with atopic eczema may reduce the severity of the eczema, but larger trials are needed.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/22972039\" rel=\"nofollow noreferrer\">Kramer MS, Kakuma R.: &quot;Maternal dietary antigen avoidance during pregnancy or lactation, or both, for preventing or treating atopic disease in the child.&quot;</a> Cochrane Database of Systematic Reviews 2012, Issue 9. Art. No.: CD000133. DOI: 10.1002/14651858.CD000133.pub3</p>\n</blockquote>\n<p>To the contrary, a few studies highlight a possiblly protective effect revealed by correlational outcomes in a prospective study:</p>\n<blockquote>\n<p>Among mothers without P/TN (peanuts/tree nuts) allergy, <strong>higher</strong> peripregnancy <strong>consumption</strong> of P/TN was associated with <strong>lower risk</strong> of P/TN allergy in their offspring. Our study supports the hypothesis that early allergen exposure increases tolerance and lowers risk of childhood food allergy.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed?term=24366539\" rel=\"nofollow noreferrer\">Frazier AL, Camargo CA Jr, Malspeis S, Willett WC, Young MC: &quot;Prospective study of peripregnancy consumption of peanuts or tree nuts by mothers and the risk of peanut or tree nut allergy in their offspring.&quot;</a>, JAMA Pediatr. 2014;168(2):156.</p>\n</blockquote>\n<p>But that is not a universal:</p>\n<blockquote>\n<p>Maternal CM avoidance was associated with lower levels of mucosal-specific IgA levels and the development of CMA in infants.<br />\n(CM = cow's milk; CMA = cow milk allergy)\n<a href=\"https://www.ncbi.nlm.nih.gov/pubmed?term=24164317\" rel=\"nofollow noreferrer\">Järvinen KM1, Westfall JE, Seppo MS, James AK, Tsuang AJ, Feustel PJ, Sampson HA, Berin C.: &quot;Role of maternal elimination diets and human milk IgA in the development of cow's milk allergy in the infants.&quot;</a>, Clin Exp Allergy. 2014 Jan;44(1):69-78. doi: 10.1111/cea.12228.</p>\n</blockquote>\n<p>And if you then compare</p>\n<blockquote>\n<p>High maternal consumption of milk products during pregnancy may protect children from developing CMA, especially in offspring of non-allergic mothers.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed?term=26757832\" rel=\"nofollow noreferrer\">Tuokkola J et al.: &quot;Maternal diet during pregnancy and lactation and cow's milk allergy in offspring.&quot;</a>, Eur J Clin Nutr. 2016 May;70(5):554-9. doi: 10.1038/ejcn.2015.223. Epub 2016 Jan 13.</p>\n</blockquote>\n<p>Then I conclude that we do not know anything certain about this –– but any avoidance scheme seems quite unfounded.</p>\n<p>That is most unfortunate, as mothers were apparently quite shaken by 'scientific' and 'pseudo-scientific' in recent years:</p>\n<blockquote>\n<p>In conclusion, all mothers in the present study restricted at least one type of food without scientific rationale while breastfeeding and more than a third of nursing mothers experienced difficulties with diet restriction. Nursing mothers should be educated on proper diet practices while being warned about unscientific approaches to diet restriction. In recent systematic review, education and emotional support by healthcare providers could enhance breastfeeding). We expect this study will give scientific basis for dietary recommendation to breastfeeding mothers and could promote a breastfeeding.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5383635/\" rel=\"nofollow noreferrer\">Goun Jeong et al.: &quot;Maternal food restrictions during breastfeeding&quot;</a>, Korean J Pediatr. 2017 Mar; 60(3): 70–76.\nPublished online 2017 Mar 27. doi: 10.3345/kjp.2017.60.3.70\nPMCID: PMC5383635</p>\n</blockquote>\n" }, { "answer_id": 18682, "author": "Physicsapproval", "author_id": 15648, "author_profile": "https://health.stackexchange.com/users/15648", "pm_score": 3, "selected": false, "text": "<p>This answer would be for the Hygiene Hypothesis part of the question</p>\n\n<p><strong><em>Epidemiology studies in favour of Hypothesis</em></strong></p>\n\n<blockquote>\n <p>The geographical distribution of allergic and autoimmune diseases is a mirror image of the geographical distribution of various infectious diseases, including HAV, gastrointestinal infections and parasitic infections. <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n \n <p>migration studies have shown that offspring of immigrants coming from a country with a low incidence acquire the same incidence as the host country, as rapidly as the first generation for T1D and MS.  <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n</blockquote>\n\n<p>Eg. :</p>\n\n<ol>\n<li><p>This is well illustrated by the increasing frequency of diabetes in families of immigrants from Pakistan to the United Kingdom or the increased risk of MS in Asian immigrants moving to the United States </p></li>\n<li><p>The prevalence of systemic lupus erythematosus (SLE) is also much higher in African Americans compared to West Africans</p></li>\n</ol>\n\n<blockquote>\n <p>In countries where good health standards do not exist, people are chronically infected by those various pathogens. In those countries, the prevalence of allergic diseases remains low. Interestingly, several countries that have eradicated those common infections see the emergence of allergic and autoimmune diseases.  <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n</blockquote>\n\n<ul>\n<li><p>Proof of principle of the casual relationship between the decline of\ninfectious diseases and an increase of immunological disorders.</p></li>\n<li><p>The answer to this question comes from animal models of autoimmune and allergic diseases and, to a lesser degree, from clinical intervention studies.</p></li>\n<li><p>The incidence of spontaneous T1D is directly correlated with the sanitary conditions of the animal facilities, for both the non-obese diabetic (NOD) mouse and the bio-breeding diabetes-prone (BB-DP) rat : <strong>the lower the infectious burden, the higher the disease incidence</strong> <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a>\nOther examples -</p></li>\n<li><p>infection of NOD mice with a wide variety of bacteria, virus and parasites protects completely (‘clean’ NOD mice) from diabetes </p></li>\n<li><p>mycobacteria (e.g. complete Freund's adjuvant) prevent induction of experimental autoimmune encephalomyelitis and ovalbumin-induced allergic asthma.</p></li>\n</ul>\n\n<blockquote>\n <p>The decline is particularly clear for hepatitis A (HAV), childhood diarrhoea and perhaps even more spectacular for parasitic diseases such as filariasis, onchocercosis, schistosomiasis or other soil-transmitted helminthiasis. <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n \n <p>Epidemiological data of cross-sectional studies revealed that Schistosoma infections have a strong protective effect against atopy, as reviewed recently. Hookworms such as Necator americanus also seem to protect from asthma\n (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434398/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434398/</a>)</p>\n</blockquote>\n\n<ul>\n<li><p>Interestingly, it's been thought that, if parasitic infections if decline, then eosinophils which are involved in allergic reactions and parasitic reactions, may in fact have a role in increased allergy.\n(Ref. Robbins and Cotran- Pathologic basis of diseases)</p></li>\n<li><blockquote>\n <p>It has been shown that helminth eradication increases atopic skin\n sensitization in Venezuela.\n  <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n</blockquote></li>\n</ul>\n\n<p><strong><em>Mechanism of Hygiene Hypothesis:</em></strong>\n <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n\n<ol>\n<li><p><em>Th1 to Th2 deviation</em> - </p>\n\n<ul>\n<li><p>Th1 T cells produce inflammatory cytokines such as IL-2, interferon\n(IFN)-γ and tumour necrosis factor (TNF)-α that are operational in\ncell-mediated immunity (including autoimmune diabetes).</p></li>\n<li><p>In contrast, Th2 T cells that produce IL-4, IL-5, IL-6 and IL-13\ncontribute to IgE production and allergic responses.</p></li>\n<li><p>IL - 5 most potent eosinophil activating cytokine known. Upon activation, eosinophils liberate proteolytic enzymes as well as two unique proteins called major basic protein and eosinophil cationic protein which damage tissue.It is now believed that the late phase reaction is a major cause of symptoms in some type 1 hypersensitivity reactions such as allergic asthma.\n(Ref. Robbins and Cotran- Pathologic basis of diseases)</p></li>\n<li><blockquote>\n <p>IL-4 enhances Th2 differentiation; also promote class switching of B cell to IgE. \n IL-13 enhances IgE production and acts on epithelial cells to stimulate mucus secretion.\n (Ref. Robbins and Cotran- Pathologic basis of diseases)</p>\n</blockquote></li>\n<li><p>IgE is involved in Type-1 Hypersensitivity, and hence it increases\nwill increase HST, like allergic asthma. (Ref. Robbins and Cotran- Pathologic basis of diseases)</p></li>\n<li><p>Given the reciprocal down-regulation of Th1 and Th2 cells, some authors suggested initially that in developed countries the lack of microbial burden in early childhood, which normally favours a strong Th1-biased immunity, redirects the immune response towards a Th2 phenotype and therefore predisposes the host to allergic disorders.</p></li>\n</ul></li>\n</ol>\n\n<p>2.<em>Antigen Competition</em></p>\n\n<ul>\n<li><blockquote>\n <p>The development of strong immune responses against antigens from infectious agents could inhibit responses to ‘weak’ antigens such as autoantigens and allergens. </p>\n</blockquote></li>\n</ul>\n\n<p>(<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828/</a>)</p>\n\n<ol start=\"3\">\n<li><p><em>Immunoregulation</em> </p>\n\n<ul>\n<li>Regulatory T cells which can suppress immune responses distinct from responses against the antigen in question, here antigens expressed by infectious agents (a phenomenon called bystander suppression)</li>\n</ul></li>\n</ol>\n\n<p>4.<em>Non Antigenic Ligand</em></p>\n\n<ul>\n<li><p>A number of experiments indicate that infectious agents can promote protection from allergic diseases through mechanisms independent of their constitutive antigens, leading to stimulation of non-antigen specific receptors. This concept is well illustrated by the example of Toll-like receptors (TLRs)</p></li>\n<li><p>It has also been observed that TLR stimulation could prevent the onset of spontaneous autoimmune diseases such as T1D in NOD.</p></li>\n<li><p>Another mechanism of TLR4 is studied,\nwhere a virus (RSV) which is linked with childhood asthma flips the 'switch' of TLR4. Now LPS a bacterial endotoxin also flips the switch but in a different way.</p>\n\n<ul>\n<li>When this education is lacking or weak, the response to RSV by some critical cells in the immune system’s defence against infections—called “T-cells”—might inadvertently trigger asthma instead of protecting the infant and clearing the infection. How this happens is a mystery that we are trying to solve.\n(Ref.- <a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm</a>)</li>\n</ul></li>\n<li><p>Gene-Environment Interaction\nEg. NOD2 - cytoplasmic sensor of bacteria expressed in Paneth and other intestinal epithelial cells; May control resistance to gut commensal bacteria.</p>\n\n<ul>\n<li>Correlation with Inflammatory Bowel Diseases. (Ref. Robbins and Cotran- Pathologic basis of diseases).</li>\n</ul></li>\n</ul>\n\n<p><em>Hygiene during early childhood/pre-natal</em></p>\n\n<blockquote>\n <p>Graham Rook and colleagues proposed a new explanation for the rise of immune disorders, which Rook called the “old friends” hypothesis. “We realized human beings coevolved with a whole host of organisms, and it was far more likely what was going on was that we were being deprived of organisms on which we are dependent.</p>\n \n <p>Maternal microbes colonize the human gut while babies are in utero, and again as they pass through the birth canal and start breastfeeding. Young children continue amassing microbiota in every contact with family members, while playing outside in the dirt, getting licked by dogs, and sharing toys with friends. The developing immune system takes cues from all of these encounters.</p>\n</blockquote>\n\n<p><strong><em>Recent Thoughts</em></strong></p>\n\n<ul>\n<li><p>To the public, “hygiene” is interpreted as personal cleanliness: washing hands, keeping food clean and fresh, sanitizing the home.<a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">2</a></p></li>\n<li><p>However, because the hypothesis has been largely uncoupled from infections, the idea that we need to be less hygienic is wrong.\n<a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">2</a></p></li>\n<li><p>Relaxing hygiene standards would not reverse the trend but only serve to increase the risks of infectious disease, says Bloomfield.\n<a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">2</a></p></li>\n<li><p>The second major concern among researchers is a lack of evidence demonstrating how to reduce rates of allergic and autoimmune diseases. <a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">2</a></p></li>\n<li><p><em>Although hygiene hypothesis proposes germ exposure but still diseases like Diabetes and Asthma are multifactorial in origin and hygiene may be playing only a part.</em><a href=\"https://www.mayoclinic.org/diseases-conditions/childhood-asthma/expert-answers/hygiene-hypothesis/faq-20058102\" rel=\"nofollow noreferrer\">1</a></p>\n\n<ul>\n<li>Eg. Asthma \n\n<blockquote>\n <p>But preventing asthma isn't as simple as avoiding antibacterial soap, having a big family or spending time on the farm. For one thing, a number of microbes — such as a respiratory syncytial virus (RSV) — may cause asthma rather than prevent it. In addition, infections that might help prevent asthma can cause a number of other health problems. The type of germ isn't the only factor that plays a role, either. The severity of infection and when the infection occurs during childhood also appear to matter.\n (Ref. <a href=\"https://www.mayoclinic.org/diseases-conditions/childhood-asthma/expert-answers/hygiene-hypothesis/faq-20058102\" rel=\"nofollow noreferrer\">https://www.mayoclinic.org/diseases-conditions/childhood-asthma/expert-answers/hygiene-hypothesis/faq-20058102</a>)</p>\n</blockquote></li>\n</ul></li>\n</ul>\n\n<p>More research is needed to understand exactly how childhood germ exposure might help prevent asthma. What we do know is that in children with asthma, exposure to germs is likely to do more harm than good.</p>\n\n<p><strong>Abbreviations</strong></p>\n\n<ul>\n<li><p>HAV - hepatitis A Virus</p></li>\n<li><p>T1D - type 1 diabetes</p></li>\n<li><p>MS- multiple sclerosis</p></li>\n<li><p>NOD - non-obese diabetic</p></li>\n<li><p>HST - hypersensitivity</p></li>\n<li><p>TLR - toll-like receptors</p></li>\n<li><p>LPS - lipopolysaccharide</p></li>\n</ul>\n\n<p><strong>References</strong>:</p>\n\n<ol>\n<li><a href=\"https://www.mayoclinic.org/diseases-conditions/childhood-asthma/expert-answers/hygiene-hypothesis/faq-20058102\" rel=\"nofollow noreferrer\">https://www.mayoclinic.org/diseases-conditions/childhood-asthma/expert-answers/hygiene-hypothesis/faq-20058102</a></li>\n<li><p><a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm</a></p></li>\n<li><p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828/</a></p></li>\n<li><p>Robbins and Cotran- Pathologic basis of diseases</p></li>\n</ol>\n" } ]
2019/02/16
[ "https://health.stackexchange.com/questions/18653", "https://health.stackexchange.com", "https://health.stackexchange.com/users/7951/" ]
18,663
<p>Each cell of a human body contains 46 chromosomes. If so then each cell of a kidney should have a pair of sex chromosomes. <strong>How is it possible that a kidney of a female donor will work on male kidney patient?</strong></p>
[ { "answer_id": 18664, "author": "Nils Pawlik", "author_id": 15665, "author_profile": "https://health.stackexchange.com/users/15665", "pm_score": 4, "selected": false, "text": "<p>The Chromosomes are not the main Factor in this. The immune system (and antibodies) is, this is a bit different. For example females have a higher HLA antigens and therefore rely on more immunsuppressive therapy.</p>\n<p>This Therapy is the thing that makes a transplantation possible, nearly all Organs are incompatible to the body, that means that you always have to give medication to stop the body from attacking the new organ. How much is needed is done via HLA matching (see <a href=\"https://health.ucdavis.edu/transplant/learnabout/learn_hla_type_match.html\" rel=\"noreferrer\">UC Davis (n.d.)</a>), which is quite extensive as a topic, you can read the lkink if you want to dig deeper.\nIn short, depending on the HLA classification you might have a risk to not accept your new organ and therefore your medication will be tailored to the compatibility.</p>\n<p>Also difference between Male/Female in general is comparably small,there are some studies and you can read <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964018/\" rel=\"noreferrer\">Puoti et al (2016)</a> for some differences in survival rates etc.</p>\n<h2>References</h2>\n<p>Puoti, F., Ricci, A., Nanni-Costa, A., Ricciardi, W., Malorni, W., &amp; Ortona, E. (2016). Organ transplantation and gender differences: a paradigmatic example of intertwining between biological and sociocultural determinants. <em>Biology of sex differences, 7</em>(1), 35. doi: <a href=\"https://doi.org/10.1186/s13293-016-0088-4\" rel=\"noreferrer\">10.1186/s13293-016-0088-4</a> pmcid: <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964018/\" rel=\"noreferrer\">4964018</a></p>\n<p>UC Davis (n.d.) <em>HLA Typing/Matching</em> [Online]<br>\nRetrieved from: <a href=\"https://health.ucdavis.edu/transplant/learnabout/learn_hla_type_match.html\" rel=\"noreferrer\">https://health.ucdavis.edu/transplant/learnabout/learn_hla_type_match.html</a></p>\n" }, { "answer_id": 18689, "author": "De Novo", "author_id": 14173, "author_profile": "https://health.stackexchange.com/users/14173", "pm_score": 3, "selected": false, "text": "<p>@NilsPawlik has addressed the issue of a donor/recipient gender mismatch (it's not the most important factor, but it is something to consider). I thought I'd clarify the point about donor/recipient compatibility. </p>\n\n<h2>What makes an organ compatible?</h2>\n\n<p>There are a number different things that make a donor organ work more or less well for a recipient, but each kind of organ has its own challenges. For example, where size matching is not an issue for liver transplants, it is important for heart transplants, and may be a little important for kidney transplants (Schwartz Principles of Surgery, Ch. 11)*. For all solid organ transplants, though, the <em>major</em> driver of organ and tissue compatibility is found in 6 genes on the short arm of chromosome 6.</p>\n\n<h2>Antigens distinguish self from non-self</h2>\n\n<p>All jawed vertebrates have an adaptive immune system and are able to tell the difference between invaders (non-self) and things that are a part of their own body (self). This system works by examining patterns in biological molecules (proteins, sugars, lipids). Those patterns are called antigens. When you transplant an organ from a donor to a recipient, the recipient's immune system will look at the antigens, or patterns, on the cells of the donor organ, and make a decision about whether those cells are part of their body or part of an invader.</p>\n\n<h2>Identifying and responding to antigens involves the entire immune system</h2>\n\n<p>The way the immune system examines and responds to those antigens involves a whole series of important and complicated interactions between many different soluble proteins, receptors, and cells, including antibodies, T-cell receptors, cytokines, macrophages, and more, but the key to predicting which organs will work well is looking at the antigens themselves. </p>\n\n<h2>HLAs determine whether a recipient will recognize a donor organ as self or non-self</h2>\n\n<p>The most important antigens for figuring out whether a human donor organ will be compatible with a human recipient are called Human Leukocyte Antigens (HLA), because they are molecular patterns (antigens) initially discovered on human white blood cells (leukocytes). These antigens are very important functional proteins that play a particular role in the way the immune system works, but for our purposes you can just think of them as being little markers on each cell saying either <em>\"I'm one of you!\"</em>, or <em>\"I'm not one of you!\"</em>. </p>\n\n<p>These markers (human leukocyte antigens) are encoded in the genome. Their genes are found on the short arm of chromosome 6. These genes are part of a group of genes called the Major Histocompatibility Complex (or MHC), because they are a <strong>major</strong> part of determining whether a donor <strong>tissue (histo)</strong> will be <strong>compatible</strong> with a recipient's immune system. </p>\n\n<h2>What kind of a match do you need?</h2>\n\n<p>There are many many many different types of MHC alleles. Because HLAs strongly influence our ability to respond to infection, this variability is a good thing overall, but it makes transplant immunology complicated. Because there are so many different MHC alleles, finding a match can be difficult. Organs are in short supply, though, so rather than waiting for an exact match, the goal is often to <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5141243/\" rel=\"noreferrer\">find a match that is good enough</a>.</p>\n\n<h2>Further Reading</h2>\n\n<p>In addition to the linked articles and the surgical considerations discussed in Schwartz, much of the relevant immunology here is discussed in good detail in the Transplant Immunology subsection of Chapter 11. I also recommend Lauren Sompayrac's little book, How the Immune System Works for either an introduction or review.</p>\n\n<h2>Note</h2>\n\n<p>*Even the mechanisms of immune rejection vary from organ type to organ type. Liver transplants, for example, are not as susceptible to the kind of rejection that is caused by pre-formed antibodies. They are more susceptible to the kind caused by T-cells (again, Schwartz Ch. 11, unless <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4607901/\" rel=\"noreferrer\">you want to see how this is even more complicated</a>)</p>\n" } ]
2019/02/18
[ "https://health.stackexchange.com/questions/18663", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15663/" ]
18,670
<p>The common consensus is that most adults should get 8 hours of sleep a night.</p> <p>However, sleep needs are highly variable, with some people needing more to function properly, and some gaining little benefit past just a few hours. I'm trying to learn more about the statistics here.</p> <p>I'd imagine sleep needs would fit a normal distribution, with a median of around 8 hours and a standard deviation of around an hour. The <a href="https://en.wikipedia.org/wiki/68%E2%80%9395%E2%80%9399.7_rule" rel="noreferrer">empirical rule</a> would then put 68% of adults in the 7-9 hour range, 95% in the 6-10 hour range, and 99.7% in the 5-11 hour range, but that's just a guess.</p> <p>Has this distribution been studied, and where?</p>
[ { "answer_id": 18675, "author": "Laurent R.", "author_id": 15670, "author_profile": "https://health.stackexchange.com/users/15670", "pm_score": 2, "selected": false, "text": "<p>Many well-done newer studies are supporting the theory that quality trumps quantity when it comes to sleep. <a href=\"https://www.lifehack.org/643556/quality-or-quantity-why-dont-you-sleep-on-it\" rel=\"nofollow noreferrer\">This excellent article at lifehack.org</a> lists 12 good sources, including “two studies (which) assessed how sleep quality and quantity affected college students’ health and well-being. The studies concluded that sleep quality was a better predictor for a healthy and happy life and improved well-being than sleep quantity.”</p>\n\n<p>For those who still want it boiled down to a number, here are the numbers the National Sleep Foundation updated in 2015:<a href=\"https://i.stack.imgur.com/lFdO0.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/lFdO0.jpg\" alt=\"https://www.sleepfoundation.org/press-release/national-sleep-foundation-recommends-new-sleep-times\"></a> link: <a href=\"https://www.sleepfoundation.org/press-release/national-sleep-foundation-recommends-new-sleep-times\" rel=\"nofollow noreferrer\">https://www.sleepfoundation.org/press-release/national-sleep-foundation-recommends-new-sleep-times</a></p>\n" }, { "answer_id": 19764, "author": "Vijay Labh", "author_id": 16547, "author_profile": "https://health.stackexchange.com/users/16547", "pm_score": 2, "selected": false, "text": "<p>If you are aged between <strong>26 to 64 year age</strong>, you need minimum <strong>7-9 hours of sleep</strong> (other factors like your physical work, stress plays extra role).</p>\n\n<p>If you are doing more physical hard work, you might need 8-9hrs of sleep, while with desk job, you are with 7hrs of sleep as well.</p>\n\n<p>You can check the National Sleep Foundation data as below for age wise sleeping hours required.\n<a href=\"https://i.stack.imgur.com/vrq6W.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/vrq6W.png\" alt=\"enter image description here\"></a></p>\n\n<p><a href=\"https://www.helpguide.org/articles/sleep/sleep-needs-get-the-sleep-you-need.htm\" rel=\"nofollow noreferrer\">source</a></p>\n" } ]
2019/02/18
[ "https://health.stackexchange.com/questions/18670", "https://health.stackexchange.com", "https://health.stackexchange.com/users/11/" ]
18,672
<p>My brother in law got chickenpox, yet somehow he didn't infect my two nephews, even though they are living together. According to wikipedia, varicella has an infection rate of 90%:</p> <blockquote> <p>Varicella is highly communicable, with an infection rate of 90% in close contacts.</p> </blockquote> <p><a href="https://en.wikipedia.org/wiki/Chickenpox" rel="nofollow noreferrer">https://en.wikipedia.org/wiki/Chickenpox</a></p> <p>He got varicella over a week ago and the children are completely healthy, even though they have not had the disease yet nor are they vaccinated against it.</p> <p>How is this possible? Is the infection rate actually lower, than 90%? Is an outcome like this usual or plausible?</p> <p>edit: they did end up getting sick after all.</p>
[ { "answer_id": 18673, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 5, "selected": false, "text": "<p>If there was close contact, if the 90% rate is accurate, and if occurrence is independent in related individuals, then you would expect 0.10 * 0.10 = 1% of contacts with 2 potentially vulnerable people to result in neither person infected.</p>\n\n<p>1% sounds rare, but <em>rare events happen all the time</em>, and 1% isn't even particularly rare. If you know 100 families, you'd expect this outcome to happen on average in 1 of them.</p>\n\n<p>That's not very unusual and is clearly plausible just from the information you have at hand. As @DeNovo mentioned in a comment, it is also likely that the spread is <em>not</em> independent, because the children share several characteristics: they are related, so they share: </p>\n\n<ul>\n<li>any genetic component to vulnerability </li>\n<li>any characteristics of the father's illness such as the level of virus replicating in the father's lungs</li>\n<li>perhaps the level of actual contact with the father and how well he may be effectively quarantined from the others</li>\n</ul>\n\n<p>Those factors could make the joint probability across the two children closer towards the 10% rate for a single individual: once you know if the first child is infected or not infected, you can make a better guess about the second child based on all the possible shared characteristics of the children or the infected person.</p>\n" }, { "answer_id": 18674, "author": "De Novo", "author_id": 14173, "author_profile": "https://health.stackexchange.com/users/14173", "pm_score": 5, "selected": true, "text": "<p>To add to @BryanKrause's answer re: rare events happen all the time, the children are not out of the woods yet. The mean incubation time for a primary VZV infection (the clinical syndrome known as chicken pox) is 14 days, but often lasts up to 21 days (see Murray Medical Microbiology, Ch. 53). The father is infectious while shedding virus, usually via the lungs. This correlates with the period of time a patient is febrile. I wouldn't say the father didn't infect his children until he has been afebrile for 21 days. </p>\n" }, { "answer_id": 18685, "author": "LаngLаngС", "author_id": 11231, "author_profile": "https://health.stackexchange.com/users/11231", "pm_score": 3, "selected": false, "text": "<p>Apart from not getting infected due to pure chance (as mentioned already) there is one highly probable explanation (<em>explanation</em>, not overall chance).</p>\n<p>People get, but don't show it:</p>\n<p><strong>asymptomatic infection</strong></p>\n<blockquote>\n<p>Asymptomatic infection is unusual, but some cases are so mild, they go unrecognised. The primary viraemic phase is followed by a secondary viraemia to the skin and the mucosal surfaces.</p>\n<p><a href=\"https://www.gponline.com/chickenpox-varicella-zoster-clinical-review/infections-and-infestations/viral-infections/article/1284872\" rel=\"noreferrer\">Chickenpox (varicella zoster) - Clinical Review, GP-online, 2014</a></p>\n</blockquote>\n" } ]
2019/02/18
[ "https://health.stackexchange.com/questions/18672", "https://health.stackexchange.com", "https://health.stackexchange.com/users/6814/" ]
18,766
<p>According to this article below, people who can do more than 40 push-ups have lower risk of heart attack. Is this a valid claim?</p> <p><a href="https://www.sciencealert.com/what-new-science-says-about-men-who-can-do-over-40-push-ups" rel="noreferrer">https://www.sciencealert.com/what-new-science-says-about-men-who-can-do-over-40-push-ups</a></p> <p>EDIT: </p> <p>Actual journal article: <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778" rel="noreferrer">https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778</a></p>
[ { "answer_id": 18767, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 4, "selected": true, "text": "<p>Yes, or at least, that's what this article in a reputable medical journal says and there is no reason to be more skeptical of it than the normal skepticism that any isolated article deserves.</p>\n\n<p>The 10 year IRR they find is 0.04 (95% CI 0.01-0.36), after adjusting for age and BMI, which is a pretty strong effect. The article is not claiming this is the best or most predictive way to estimate risk, they are just pointing out that this might be a simple, no-cost method of assessing physical health (and note that they only tested men, and all of the men are firefighters).</p>\n\n<p>Note that the study does not claim nor should be interpreted as causal: that is, it is unlikely that training to do more push ups has a substantial cardiovascular benefit. Instead, people who can do a large number of push ups for their age are probably among the most physically fit in other ways, too.</p>\n\n<p>I think you can restate the claim to be \"physically fit men have lower risk of heart attack than non-physically fit men of the same age and weight, and # of push ups is a decent estimator of physical fitness\" and stated that way it doesn't sound all that controversial, and that's pretty much how the Science Alert article you linked to describes the results.</p>\n" }, { "answer_id": 18771, "author": "Physicsapproval", "author_id": 15648, "author_profile": "https://health.stackexchange.com/users/15648", "pm_score": 2, "selected": false, "text": "<p>Limitations of the study:<a href=\"https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778\" rel=\"nofollow noreferrer\">(3)</a></p>\n\n<ul>\n<li><p>First, the study assessed the association between push-ups and CVD events. The results do not support push-up capacity as an independent predictor of CVD risk. </p></li>\n<li><p>Second, because the study cohort consisted of middle-aged, occupationally active men, the study results may not be generalizable to women, older or nonactive persons, other occupational groups, or unemployed persons.</p></li>\n</ul>\n\n<p><strong>Previous studies and research</strong><a href=\"https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778\" rel=\"nofollow noreferrer\">(3)</a></p>\n\n<ul>\n<li><p>Cross-sectional studies have incorporated push-ups in the assessment of muscular fitness and its correlation with cardiometabolic risk markers.In those studies, the authors found that a higher level of muscular strength was associated with lower cardiometabolic risk independent of cardiorespiratory fitness in the cohorts observed.</p></li>\n<li><p>Muscular strength has been shown to have an independent protective effect for all-cause mortality and hypertension in healthy males and is inversely associated with metabolic syndrome incidence and prevalence.</p></li>\n</ul>\n\n<p>However, most of those studies were either cross-sectional or conducted with adolescent participants.</p>\n\n<p>Hands down, this article and the research conducted is exceptional and one of it's kind. \nBut one may fail to recognise that \n<strong><em>Heart attack itself is multifactorial disease and that's mentioned in the research paper-</em></strong> </p>\n\n<blockquote>\n <p>The results do not support push-up capacity as an <strong>independent predictor</strong> of CVD risk.\n <a href=\"https://ghr.nlm.nih.gov/primer/mutationsanddisorders/complexdisorders\" rel=\"nofollow noreferrer\">(1)</a>:</p>\n</blockquote>\n\n<ul>\n<li><p>Although complex disorders often cluster in families, they do not have a clear-cut pattern of inheritance. This makes it difficult to determine a person’s risk of inheriting or passing on these disorders.</p></li>\n<li><p>Secondly the other risk factors, just a few mentioned;</p>\n\n<ul>\n<li><p>Hemoglobin A1c</p></li>\n<li><p>Blood Pressure</p></li>\n<li><p>Low‐Density Lipoprotein</p></li>\n<li><p>Type 2 Diabetes Mellitus:</p></li>\n</ul></li>\n</ul>\n\n<p>Are quite well established(traditional risk factors) </p>\n\n<p>In 2016, the American Heart Association released a scientific statement concluding that “CRF should be measured in clinical practice… Indeed, decades of research have produced unequivocal evidence that CRF provides independent and additive morbidity and mortality data that when added to traditional risk factors significantly improves CVD risk prediction.<a href=\"https://www.ahajournals.org/doi/full/10.1161/01.CIR.102.14.1623\" rel=\"nofollow noreferrer\">(2)</a><a href=\"https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778\" rel=\"nofollow noreferrer\">(5)</a></p>\n\n<p>So alternatively <em>physical fitness will help to keep the traditional risk factors within the range or in control</em>,</p>\n\n<p>let's see an example: </p>\n\n<ul>\n<li><p>In men, Cardiorespiratory fitness was indirectly associated with all CHD risk factors among men without CHD. </p></li>\n<li><p>Triglycerides and HDL demonstrated significant higher-order associations with fitness<a href=\"https://www.ahajournals.org/doi/full/10.1161/01.CIR.102.14.1623\" rel=\"nofollow noreferrer\">(2)</a></p></li>\n</ul>\n\n<p><strong>Let's look at another example:</strong></p>\n\n<p>Let's say there's an athlete <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884475/\" rel=\"nofollow noreferrer\">(here)</a>with<a href=\"https://www.heart.org/en/health-topics/cholesterol/causes-of-high-cholesterol/familial-hypercholesterolemia-fh\" rel=\"nofollow noreferrer\"> familial hypercholesterolemia</a></p>\n\n<ul>\n<li><p>Now think, won't the athlete be able to do 40 or may be far more than that.</p></li>\n<li><p>Let's say there's another non-athlete with no history of hypercholesterolemia of same age and sex; he is not able to do even 5 pushups. </p></li>\n<li><p>But now it's quite tricky to think who will have a higher risk, but here it's also important to realize that <strong>this shows how and why multifactorial disease are difficult to screen and treat.</strong></p></li>\n</ul>\n\n<p>The example above may be <strong>rare</strong>, but they do form a part of medicine. In no way I want to prove that this article is far from truth, it's merely the part of a big big story.</p>\n\n<p><strong>This research,</strong></p>\n\n<ul>\n<li><p>Paves a way for new ways of screening just as- self examination of breast in breast cancer is.</p></li>\n<li><p>May also be used in assessing risk in clinics provided keeping in mind the other risk factors.</p></li>\n<li><p>The problem with typical CRF testing is that it’s typically expensive, time-consuming, and requires special personnel this research may help in this aspect. </p></li>\n<li><p>Lastly a greater data is needed and this has to compared to the well established risk factors.</p></li>\n</ul>\n\n<p><strong>Conclusion</strong>: As a risk factor this has strong association but this may be true for one individual (or patient) and may be not for other, as case may be that even a healthy and fit, able to do 40 pushups easily have an heart attack <a href=\"https://www.google.com/amp/s/tonic.vice.com/amp/en_us/article/jpnea7/how-does-someone-as-fit-as-bob-harper-have-a-heart-attack\" rel=\"nofollow noreferrer\">(here)</a></p>\n\n<p><strong>References</strong>:</p>\n\n<p>1:<a href=\"https://ghr.nlm.nih.gov/primer/mutationsanddisorders/complexdisorders\" rel=\"nofollow noreferrer\">https://ghr.nlm.nih.gov/primer/mutationsanddisorders/complexdisorders</a></p>\n\n<p>2:<a href=\"https://www.ahajournals.org/doi/full/10.1161/01.CIR.102.14.1623\" rel=\"nofollow noreferrer\">https://www.ahajournals.org/doi/full/10.1161/01.CIR.102.14.1623</a></p>\n\n<p>3:<a href=\"https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778\" rel=\"nofollow noreferrer\">https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778</a></p>\n\n<p>4:<a href=\"https://www.heart.org/en/health-topics/cholesterol/causes-of-high-cholesterol/familial-hypercholesterolemia-fh\" rel=\"nofollow noreferrer\">https://www.heart.org/en/health-topics/cholesterol/causes-of-high-cholesterol/familial-hypercholesterolemia-fh</a></p>\n\n<p>5:<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884475/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884475/</a></p>\n\n<p>6:<a href=\"https://www.google.com/amp/s/tonic.vice.com/amp/en_us/article/jpnea7/how-does-someone-as-fit-as-bob-harper-have-a-heart-attack\" rel=\"nofollow noreferrer\">https://www.google.com/amp/s/tonic.vice.com/amp/en_us/article/jpnea7/how-does-someone-as-fit-as-bob-harper-have-a-heart-attack</a></p>\n" } ]
2019/03/05
[ "https://health.stackexchange.com/questions/18766", "https://health.stackexchange.com", "https://health.stackexchange.com/users/8973/" ]
18,788
<p>It's said Viagra effects only last around 3-4 hours, and it stay in the body up to 8 hours. </p> <p>So why is the recommendation to not take more than 100mg/daily comes from?</p>
[ { "answer_id": 18792, "author": "Carey Gregory", "author_id": 805, "author_profile": "https://health.stackexchange.com/users/805", "pm_score": 1, "selected": false, "text": "<p>Viagra (sildenafil ) has a half-life of about <a href=\"https://www.drugs.com/pro/sildenafil-injection.html\" rel=\"nofollow noreferrer\">4 hours</a>. It takes five half-lives for a drug to completely leave your system, so the time it takes for Viagra to leave your system is more like 20 hours, not eight. That's probably the reason for the once daily recommendation. </p>\n" }, { "answer_id": 18793, "author": "De Novo", "author_id": 14173, "author_profile": "https://health.stackexchange.com/users/14173", "pm_score": 3, "selected": true, "text": "<blockquote>\n <p>Why is the recommendation to not take more than 100mg/daily?</p>\n</blockquote>\n\n<p>Because that is what the clinical data show. If you take more than 100mg/daily you are at a higher than acceptable risk of undesirable effects.</p>\n\n<p>As to where this information comes from...</p>\n\n<blockquote>\n <p>Where does the recommendation for (anything related to dose for any medication approved by a modern regulatory authority) come from?</p>\n</blockquote>\n\n<p>Initial estimates for dosing are based on preclinical studies of pharmacokinetic and toxicological studies in animals. Final recommendations are based on a series of three general types of clinical trials in human subjects. </p>\n\n<p>Phase I clinical trials establish pharmacokinetic properties, safety and tolerability of a medication, using a range of doses. These data are used to estimate likely effective and safe doses in volunteers with the disease of interest. Sometimes this is described as Phase 0 and Phase I, or Phase Ia and Phase Ib, but traditionally, this is all considered Phase I. </p>\n\n<p>Phase II clinical trials are primarily aimed at efficacy (whether the drug provides a benefit) in volunteers with the disease of interest. Though efficacy is the main concern here, these trials do continue to monitor safety and tolerability, and can collect additional pharmacokinetic data as well. Data from Phase II clinical trials is used to design Phase III clinical trials. The doses tested in Phase III may be adjusted from what was predicted by Phase I.</p>\n\n<p>Phase III trials provide more information about both safety and efficacy, using a much larger number of subjects, typically in multicenter studies. Here again, the research subjects are volunteers with the disease of interest. Once Phase III trials are complete, an application is submitted to the regulatory authority. </p>\n\n<p>The label information, including dose recommendations, is approved by the regulatory authority based on the aggregate data from these studies. </p>\n\n<p>Goodman &amp; Gilman's The Pharmacological Basis of Therapeutics discusses this process in Chapter 1. You can also read about it on <a href=\"https://en.wikipedia.org/wiki/Phases_of_clinical_research\" rel=\"nofollow noreferrer\">Wikipedia</a>, but this is not the best Wikipedia article I've read.</p>\n" } ]
2019/03/08
[ "https://health.stackexchange.com/questions/18788", "https://health.stackexchange.com", "https://health.stackexchange.com/users/767/" ]
18,828
<p>I remember a case where someone apparently had great difficulty perceiving the distance of an object if it was (quickly) travelling towards them. Their depth perception was otherwise fine, but when, for instance, catching a ball, that person could not accurately gauge depth and seemed to rely on guesswork/other cues (size of the object? timing?) to decide when to attempt to catch it. Hand-eye coordination was not a problem, and for slow-moving objects (for instance, rolling a ball across the floor) there was no problem. What is the name of this condition, and what could be likely causes?</p>
[ { "answer_id": 18831, "author": "Jiminy Cricket.", "author_id": 15405, "author_profile": "https://health.stackexchange.com/users/15405", "pm_score": 2, "selected": false, "text": "<p>What you appear to be describing is called <a href=\"https://en.wikipedia.org/wiki/Akinetopsia\" rel=\"nofollow noreferrer\">Akinetopsia</a>.</p>\n\n<p>(Greek: a for \"without\", kine for \"to move\" and opsia for \"seeing\")</p>\n\n<blockquote>\n <p>a neuropsychological disorder in which a patient cannot perceive\n motion in their visual field, despite being able to see stationary\n objects without issue [...]<br>\n There are varying degrees of akinetopsia: from seeing motion as a cinema reel to an inability to discriminate any motion. There is currently no effective treatment or cure for akinetopsia. </p>\n</blockquote>\n\n<p>Causes range from brain lesions to dementia, certain medications such as antidepressants (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/10577608\" rel=\"nofollow noreferrer\">nefazodone</a>) and halucinogens such as LSD. It may be induced artificially by <a href=\"https://www.researchgate.net/publication/21794388_Cerebral_Visual_Motion_Blindness_Transitory_Akinetopsia_Induced_by_Transcranial_Magnetic_Stimulation_of_Human_Area_V5\" rel=\"nofollow noreferrer\">Transcranial magnetic stimulation</a>.</p>\n" }, { "answer_id": 18832, "author": "Jiminy Cricket.", "author_id": 15405, "author_profile": "https://health.stackexchange.com/users/15405", "pm_score": 1, "selected": false, "text": "<p><strong><a href=\"https://www.healthline.com/health/dysmetria\" rel=\"nofollow noreferrer\">Dysmetria</a> is a possibility. (Specifically Ocular Dysmetria)</strong></p>\n<p>It is a type of <a href=\"https://www.medicinenet.com/ataxia/article.htm#what_are_the_different_types_of_ataxia\" rel=\"nofollow noreferrer\">ataxia</a> characterised:</p>\n<blockquote>\n<p>is a lack of coordination of movement typified by the undershoot or\novershoot of intended position</p>\n</blockquote>\n<p>It can occur in the major skeletal muscles and the eyes.</p>\n<p><strong><a href=\"https://en.wikipedia.org/wiki/Dysmetria#Saccadic\" rel=\"nofollow noreferrer\">Ocular Dysmetria</a>:</strong></p>\n<blockquote>\n<p>During eye movements hypometric and hypermetric saccades will occur [...]</p>\n<p>Saccades are the very quick, simultaneous movements made by the eye to\nreceive visual information and shift the line of vision from one\nposition to another. A person depends profoundly on the ability of\nthe accuracy of these movements. The information is received from\nthe retina, is translated into spatial information and is then\ntransferred to motor centers for motor response.</p>\n</blockquote>\n<p>As you might imagine, when tracking a moving object, the person's spacial sense is likely to be recieving garbled input and will not function as well as when an object is stationary.</p>\n<p><strong>Causes:</strong></p>\n<blockquote>\n<p>Lesions in the cerebellum or in the proprioceptive nerves that lead to\nthe cerebellum that coordinate visual, spatial and other sensory\ninformation with motor control.</p>\n<p>Damage to the proprioceptive nerves does not allow the cerebellum to\naccurately judge where the hand, arm, leg, or eye should move.</p>\n</blockquote>\n<p><strong>Causes of the lesions are manfold</strong>; stroke, tumour, <a href=\"https://www.webmd.com/brain/understanding-als-basics#1\" rel=\"nofollow noreferrer\">ALS</a>, or <a href=\"https://www.webmd.com/multiple-sclerosis/default.htm\" rel=\"nofollow noreferrer\">MS</a>.</p>\n<p>I am unable to find treatments specific to the Ocular version, but treatment regimes with <a href=\"https://en.wikipedia.org/wiki/Clonazepam\" rel=\"nofollow noreferrer\">clonazepam</a> or a tailored form of <a href=\"https://www.physiotherapy-treatment.com/frenkel-exercises.html\" rel=\"nofollow noreferrer\">Frenkel exercises</a> - both of which seem to be of benefit to general Dysmetria patients - may come into play.</p>\n" } ]
2019/03/14
[ "https://health.stackexchange.com/questions/18828", "https://health.stackexchange.com", "https://health.stackexchange.com/users/14373/" ]
18,872
<p>If we search the internet, we see plenty of articles </p> <ol> <li><a href="https://ww5.komen.org/BreastCancer/Turmeric.html" rel="nofollow noreferrer">https://ww5.komen.org/BreastCancer/Turmeric.html</a>, </li> <li><a href="https://examine.com/supplements/curcumin/" rel="nofollow noreferrer">https://examine.com/supplements/curcumin/</a>, </li> <li>(Video) <a href="https://www.youtube.com/watch?v=rZJTk9Re3Qc" rel="nofollow noreferrer">https://www.youtube.com/watch?v=rZJTk9Re3Qc</a>, </li> <li>(Video testimonial) <a href="https://www.youtube.com/watch?v=tNdPeR8tSj0" rel="nofollow noreferrer">https://www.youtube.com/watch?v=tNdPeR8tSj0</a>, </li> <li><a href="https://www.fixmanboobs.com.au/the-anti-gynecomastia-powers-of-turmeric/" rel="nofollow noreferrer">https://www.fixmanboobs.com.au/the-anti-gynecomastia-powers-of-turmeric/</a>) claiming that the ingredient curcumin in turmeric is an effective estrogen blocker, and hence can be used to reduce gynecomastia (male breasts).</li> </ol> <p>There're also few studies that're more technical in nature and hard for a person who isn't a medical specialist to understand, e.g. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354546/" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354546/</a></p> <p>So I'd like to know by further existent studies, if turmeric is effective in decreasing estrogen level in male body, and hence reducing male breasts or gynecomastia? Thanks in advance!!</p>
[ { "answer_id": 18984, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p>The following comprehensive scientific sources <strong>do not even mention any relationship between turmeric/curcumin and gynecomastia:</strong></p>\n\n<ul>\n<li><a href=\"https://ww5.komen.org/BreastCancer/Turmeric.html\" rel=\"nofollow noreferrer\">Turmeric, Natural Medicines Comprehensive Database, komen.org</a></li>\n<li><a href=\"https://nccih.nih.gov/health/turmeric/ataglance.htm#hed3\" rel=\"nofollow noreferrer\">Turmeric, National Center for Complementary and Integrative Health</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664031/\" rel=\"nofollow noreferrer\">Curcumin: A Review of Its’ Effects on Human Health, PubMed, 2017</a></li>\n<li><a href=\"https://examine.com/supplements/curcumin/#interactions-with-hormones_estrogen\" rel=\"nofollow noreferrer\">Curcumin, Examine.com, 2015</a></li>\n<li>Google .gov: or .edu: search for <em>turmeric</em> or <em>curcumin</em> + <em>gynecomastia</em></li>\n</ul>\n\n<hr>\n\n<p>The youtube videos and fixmanboobs.com.au site mentioned in the question are not backed up by any references.</p>\n\n<hr>\n\n<p>The <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354546/\" rel=\"nofollow noreferrer\">PubMed article</a> from the question mentions that curcumin can inhibit estrogen receptors and thus decrease estrogen activity but it does not say if this has any health effects.</p>\n\n<hr>\n\n<p><strong>In conclusion,</strong> there seems to be no scientific evidence to support the claim that turmeric/curcumin helps to reduce gynecomastia.</p>\n" }, { "answer_id": 18985, "author": "LаngLаngС", "author_id": 11231, "author_profile": "https://health.stackexchange.com/users/11231", "pm_score": 2, "selected": false, "text": "<p>There seems to be <em>no</em> clear and direct evidence for this.</p>\n<p>But a few angles might be worth exploring:</p>\n<blockquote>\n<p>Molecular Dynamics (MD) simulations found curcumin to be a stable inhibitor of aromatase (Singh et al 2016).</p>\n<p>The prepubertal gynecomastia in males and breast hypertrophy in females are conditions of aromatase excess syndrome (Metwalley and Farghaly 2013).</p>\n<p>Aromatase inhibitors are used as therapy for breast cancer, endometriosis, leiomyoma (fibroid tumors), idiopathic short stature, gynecomastia, and male hypogonadism, as they prevent estrogen formation (Le Ray et al 2012; Pavone and Bulun 2012; Singh 2013; Hero 2016; Blakemore and Naftolin 2016; Miller et al 2016).</p>\n<p><sub>Singh S, Awasthi M, Pandey VP, Dwivedi UN (2016) Plant derived anti-cancerous secondary metabolites as multipronged inhibitor of COX, Topo and aromatase: Molecular modeling and dynamics simulation analyses. J Biomol Struct Dyn 1–65. doi: 10.1080/07391102.2016.1241720</sub></p>\n<p><sub>Metwalley KA, Farghaly HS (2013) Aromatase excess syndrome presenting with prepubertal gynecomastia in an Egyptian child with type 1 neurofibromatosis. Indian J Hum Genet 19:472–4. doi: 10.4103/0971-6866.124379</sub></p>\n<p><sub>Singh SK (2013) Aromatase inhibitors in male sex. Indian J Endocrinol Metab 17:S259-61. doi: 10.4103/2230-8210.119594</sub></p>\n<p><sub>Blakemore J, Naftolin F (2016) Aromatase: Contributions to Physiology and Disease in Women and Men. Physiology (Bethesda) 31:258–69. doi: 10.1152/physiol.00054.2015</sub></p>\n<p>Seema Patel: &quot;Disruption of aromatase homeostasis as the cause of a multiplicity of ailments: A comprehensive review&quot;,The Journal of Steroid Biochemistry and Molecular Biology, Volume 168, April 2017, Pages 19-25 (DOI <a href=\"http://dx.doi.org/doi:10.1016/j.jsbmb.2017.01.009\" rel=\"nofollow noreferrer\">http://dx.doi.org/doi:10.1016/j.jsbmb.2017.01.009</a> <a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0960076017300092\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/abs/pii/S0960076017300092</a>)</p>\n</blockquote>\n<p>This is quite promising, but currently nothing more. Also in light of the multitude (<a href=\"https://www.mayoclinic.org/diseases-conditions/gynecomastia/symptoms-causes/syc-20351793\" rel=\"nofollow noreferrer\">https://www.mayoclinic.org/diseases-conditions/gynecomastia/symptoms-causes/syc-20351793</a>) of possible (<a href=\"https://my.clevelandclinic.org/health/diseases/16227-enlarged-male-breast-tissue-gynecomastia\" rel=\"nofollow noreferrer\">https://my.clevelandclinic.org/health/diseases/16227-enlarged-male-breast-tissue-gynecomastia</a>) causes for this one diagnosis.</p>\n" } ]
2019/03/18
[ "https://health.stackexchange.com/questions/18872", "https://health.stackexchange.com", "https://health.stackexchange.com/users/1180/" ]
18,876
<p>What is the English term for a manufactured pharmaceutical drug of a specific strength and dosage form, i.e. a pill, an ointment etcetera?</p>
[ { "answer_id": 18877, "author": "Nuclear Hoagie", "author_id": 1050, "author_profile": "https://health.stackexchange.com/users/1050", "pm_score": 0, "selected": false, "text": "<p>Most generally, you could call this a <strong><em>dose</em></strong> of a drug. This refers to a specific amount of medication taken at one time. For example, Regular and Extra Strength versions of common painkillers will have different amounts of the active ingredient, so they differ in dose. Dose only refers to the amount of a particular active ingredient, as you can't really compare \"strength\" of different compounds like insulin and aspirin, for example. Generally, higher doses of a drug will have a greater effect (i.e. Extra Strength painkiller is just a higher dose of Regular Strength painkiller).</p>\n" }, { "answer_id": 18878, "author": "August Karlstrom", "author_id": 15888, "author_profile": "https://health.stackexchange.com/users/15888", "pm_score": 2, "selected": false, "text": "<p><em>Drug product</em> seems to be the correct term, see <a href=\"https://biorelevant.com/blog/drug-substance-vs-drug-product/\" rel=\"nofollow noreferrer\">https://biorelevant.com/blog/drug-substance-vs-drug-product/</a>.</p>\n" } ]
2019/03/18
[ "https://health.stackexchange.com/questions/18876", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15888/" ]
18,924
<p>A <a href="http://archives.who.int/eml/expcom/expcom15/applications/sections/Antitrypanosomal.pdf" rel="nofollow noreferrer">WHO document</a>, contains the statement</p> <blockquote> <p>[Melarsoprol] injections must be performed using glass syringes.</p> </blockquote> <p>Why is this the case?</p>
[ { "answer_id": 18925, "author": "ayush", "author_id": 15917, "author_profile": "https://health.stackexchange.com/users/15917", "pm_score": 2, "selected": false, "text": "<p>Since Melarsoprol is insoluble in water, dosage occurs via a 3.6% propylene glycol intravenous injection.</p>\n\n<blockquote>\n <p>As propylene glycol can dissolve plastic, the drug should preferably be administered using a glass syringe (only if sterilisation is reliable), otherwise inject immediately (but slowly) using a plastic syringe (<a href=\"https://medicalguidelines.msf.org/viewport/EssDr/english/melarsoprol-injectable-16682915.html\" rel=\"nofollow noreferrer\">Source</a>).</p>\n</blockquote>\n\n<p>Melarsoprol is sometimes colloquially referred to as \"arsenic in antifreeze\".</p>\n" }, { "answer_id": 18972, "author": "JohnP", "author_id": 64, "author_profile": "https://health.stackexchange.com/users/64", "pm_score": 2, "selected": false, "text": "<p>The reason for it may not be the barrel of the syringe, but the rubber in the stopper which is of a different material. There was a <a href=\"https://www.ncbi.nlm.nih.gov/m/pubmed/6702838/\" rel=\"nofollow noreferrer\">study done on paraldehyde</a> and the affect it had on the plastic in syringes and needle hubs. The pertinent part (Note the time, there was no effect until after at least 3 hours immersion) is below (Emphasis mine).</p>\n\n<blockquote>\n <p>No measurable change in residue weight was noted in any syringes for up to three hours. Compared with the control, there was a significant increase in the average weight of residue in the Glaspak and in the Plastipak syringes at 6, 12, and 24 hours. There was no significant difference in the weight of residue between the Glaspak and Plastipak syringes at those times, however. The amount of residue for the plastic and metal needle hubs was not significantly different. <strong>The source of the extractive residue appeared to be the rubber plunger tip. Since the nature of the extractive material in the residue is not known, paraldehyde should be administered in all-glass syringes if possible; other syringe types can be used only if the drug is administered immediately.</strong></p>\n</blockquote>\n\n<p>So basically, it's possibly erring on the side of caution as they don't know how soon it might start dissolving stuff.</p>\n" } ]
2019/03/24
[ "https://health.stackexchange.com/questions/18924", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15916/" ]
18,955
<p>I had a couple fillings done today at the dentist. One on the top and one on the bottom. The top filling went fine with no issues.</p> <p>For the second filling, the first injection of local anesthesia didn't work at all. After I felt severe pain she did a second injection. This time I noticed some mild effect, but it still hurt severely. A third one didn't help.</p> <p>We persevered and the filling was (painfully) completed. But I'm curious how common this is? and what are the possible causes? </p> <p>I'd never experienced local anesthesia not working before, and I'd be lying if I said it hasn't made me more hesitant to go to the dentist in future due to the fear it wont work again.</p> <p>Note: This is not in anyway me seeking medical advice. I'm just genuinely curious why this might have happened.</p>
[ { "answer_id": 18957, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 3, "selected": false, "text": "<p>This depends on the type of anesthetic used, there are plenty:</p>\n\n<blockquote>\n <p><a href=\"https://en.wikipedia.org/wiki/Local_anesthetic#Types\" rel=\"noreferrer\">Types of anesthetic</a></p>\n</blockquote>\n\n<p>which include:</p>\n\n<ul>\n<li>Esters (Benzocaine, Cyclomethycaine, Propoxycaine)</li>\n<li>Amides (Bupivacaine, Mepivacaine, Trimecaine)</li>\n<li>Naturals (Saxitoxin, Tetrodotoxin, Spilanthol).</li>\n</ul>\n\n<p>This link:</p>\n\n<blockquote>\n <p><a href=\"https://www.dentalfearcentral.org/media/overcome_failed_LA.pdf\" rel=\"noreferrer\">How to overcome failed local anaethesia</a></p>\n</blockquote>\n\n<p>is dental specific, and lists possible causes of local anesthetia failure:</p>\n\n<ul>\n<li>Operator (wrong anaesthetic, poor technique)</li>\n<li>Anatomical (inconsistent foramina, multiple nerve supply, cortial barrier)</li>\n<li>Pathological (reduced jaw opening, inflammation)</li>\n<li>Psychological (fear, anxiety, stress).</li>\n</ul>\n\n<p>Any general statistics won't mean much as it depends very much on the patient's personal condition and the implementation and type of anesthetic used.</p>\n" }, { "answer_id": 18959, "author": "BillDOe", "author_id": 2833, "author_profile": "https://health.stackexchange.com/users/2833", "pm_score": 3, "selected": false, "text": "<p>In addition to JonMark Perry's excellent answer it's also worth noting that many of us aren't wired the same as everyone one else.</p>\n\n<p>When your dentist tries to numb a particular tooth, he or she is trying to numb the particular nerve, or group of nerves, that innervates that tooth. Those nerves may not be in the same location as the next patient. This <a href=\"http://directionsindentistry.net/5-reasons-cant-get-numb-dentist-2/\" rel=\"nofollow noreferrer\">blog</a> by Nicholas Calcaterra DDS mentions this as the fourth of five reasons you may not be numbed. The most pertinent passage: </p>\n\n<blockquote>\n <p><b>4. You’re wired differently</b><br>\n The human body is incredibly variable. People are double jointed. Remember the kid in grade school who could move his ears? Why is Usain Bolt faster then any other human? You get the picture.<br><br>Each person is different! Most people have what I might call “standard anatomy.” This means that the nerves going to your teeth are where you might expect them to be located. But just like Usain Bolt and the kid from fifth grade who could move his ears, some patients have extreme variability with the nerves going to their teeth. We see this most frequently with lower molars.\n Some people may have up to 4 nerves going to their lower molar teeth. This can mean 4 different injections to get them numb! This doesn’t mean your dentist is incompetent – it means you’re wired differently. So if that happens to you, just think about Usain Bolt and the kid from fifth grade who could move his ears.</p>\n</blockquote>\n\n<p>I had the same thing happen to me a very long time ago and just grinned and bore it; it was temporary, after all, and it has never happened since. My dentist then said he just couldn't locate the nerve going to that particular tooth. And in the citation above, if the dentist doesn't get all four of those nerves going to the molar in question, you won't be completely numbed.</p>\n" }, { "answer_id": 31201, "author": "kedaes", "author_id": 25266, "author_profile": "https://health.stackexchange.com/users/25266", "pm_score": -1, "selected": false, "text": "<p>In addition to the excellent answers, there's another, and that's regarding your metabolism. The most commonly used local anesthetics are metabolized by the liver, specifically the P450 system. If you're a fast metabolizer, your body degrades the medication, and its effects, quickly. The opposite is true for a slow metabolizer. As a physician who sutures wounds, I've learned that some patients require a more potent strength of a longer lasting anesthetic than others to get the same effect.</p>\n" } ]
2019/03/30
[ "https://health.stackexchange.com/questions/18955", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15954/" ]
19,049
<p>I read two online articles on the use of probiotics to help maintain balance of gut bacteria when undergoing antibiotic treatment:</p> <ul> <li><a href="https://www.healthline.com/nutrition/what-to-eat-antibiotics" rel="nofollow noreferrer">https://www.healthline.com/nutrition/what-to-eat-antibiotics</a></li> <li><a href="https://blog.bulletproof.com/restore-gut-flora" rel="nofollow noreferrer">https://blog.bulletproof.com/restore-gut-flora</a></li> </ul> <p>I was looking for "weight of the evidence" on whether eating probiotics (pills, yogurt, kimchi, kefir) actually maintains good gut bacteria when one goes on antibiotic treatment.</p> <p>The four cited articles that seemed focus on this are:</p> <ul> <li><a href="https://www.ncbi.nlm.nih.gov/pubmed/25157183" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pubmed/25157183</a></li> <li><a href="https://www.ncbi.nlm.nih.gov/pubmed/22570464" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pubmed/22570464</a></li> <li><a href="https://www.sciencedirect.com/science/article/pii/S1473309906704959" rel="nofollow noreferrer">https://www.sciencedirect.com/science/article/pii/S1473309906704959</a></li> <li><a href="https://www.bmj.com/content/324/7350/1361.full" rel="nofollow noreferrer">https://www.bmj.com/content/324/7350/1361.full</a></li> </ul> <p>There seems to be weak evidence that it helps with diarrhea, and weaker evidence that it helps with the <a href="https://wikipedia.org/wiki/Gut_flora" rel="nofollow noreferrer">gut flora</a> overall (notwithstanding the phrase "reasonable evidence" used in the Wikipedia article). However, it doesn't hurt.</p> <p>Is this a reasonable summary of the current knowledge?</p> <p><strong>NOTE:</strong> This differs from <a href="https://medicalsciences.stackexchange.com/questions/4766/how-to-increase-my-gut-bacteria-are-there-any-drugs-available">another article</a> in that I'm asking not for suggestions or anecdotes, but an assessment of current information.</p>
[ { "answer_id": 19057, "author": "bparn", "author_id": 16043, "author_profile": "https://health.stackexchange.com/users/16043", "pm_score": 2, "selected": false, "text": "<p>Post-Antibiotic Gut Mucosal Microbiome Reconstitution Is Impaired by Probiotics and Improved by Autologous FMT</p>\n\n<p>Published: September 6, 2018 DOI:<a href=\"https://doi.org/10.1016/j.cell.2018.08.047\" rel=\"nofollow noreferrer\">https://doi.org/10.1016/j.cell.2018.08.047</a></p>\n\n<p>Abstract:\nProbiotics are widely prescribed for prevention of antibiotics-associated dysbiosis and related adverse effects. However, probiotic impact on post-antibiotic reconstitution of the gut mucosal host-microbiome niche remains elusive. We invasively examined the effects of multi-strain probiotics or autologous fecal microbiome transplantation (aFMT) on post-antibiotic reconstitution of the murine and human mucosal microbiome niche. Contrary to homeostasis, antibiotic perturbation enhanced probiotics colonization in the human mucosa but only mildly improved colonization in mice. Compared to spontaneous post-antibiotic recovery, probiotics induced a markedly delayed and persistently incomplete indigenous stool/mucosal microbiome reconstitution and host transcriptome recovery toward homeostatic configuration, while aFMT induced a rapid and near-complete recovery within days of administration. In vitro,Lactobacillus-secreted soluble factors contributed to probiotics-induced microbiome inhibition. Collectively, potential post-antibiotic probiotic benefits may be offset by a compromised gut mucosal recovery, highlighting a need of developing aFMT or personalized probiotic approaches achieving mucosal protection without compromising microbiome recolonization in the antibiotics-perturbed host.</p>\n\n<p>My conclusions from reading this abstract: it includes human study. It is not directed specifically to C. diff. It discusses recolonization of the gut microbiome and that recolonization might be necessary for probiotics to be effective for ulcerative colitis.</p>\n" }, { "answer_id": 19060, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 1, "selected": false, "text": "<p><strong><em>PRESCRIBED</em> PROBIOTICS AND ANTIBIOTIC-ASSOCIATED DIARRHEA</strong></p>\n\n<p><strong>There seems to be <em>moderate evidence</em> that probiotic <em>supplements</em> can reduce the risk of antibiotic-associated diarrhea.</strong></p>\n\n<p><a href=\"https://www.cochrane.org/CD006095/IBD_use-probiotics-prevent-clostridium-difficile-diarrhea-associated-antibiotic-use\" rel=\"nofollow noreferrer\">The use of probiotics to prevent Clostridium difficile diarrhea associated with antibiotic use (Cochrane.org, 2017)</a></p>\n\n<blockquote>\n <p>Based on this systematic review and meta-analysis of 31 randomized\n controlled trials including 8672 patients, <em>moderate certainty\n evidence</em> suggests that probiotics are effective for preventing CDAD\n [C. difficile-associated diarrhea after antibiotic use].</p>\n</blockquote>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/29511547\" rel=\"nofollow noreferrer\">Comparative efficacy and tolerability of probiotics for antibiotic-associated diarrhea: Systematic review with network meta-analysis (PubMed, 2018)</a></p>\n\n<blockquote>\n <p>LGG [Lactobacillus rhamnosus GG ] is probably the best option to\n consider when AAD is indicated. L. casei appears to be the most\n efficacious choice when associated with severe C. difficile-related\n cases.</p>\n</blockquote>\n\n<p><a href=\"https://bmcgastroenterol.biomedcentral.com/articles/10.1186/s12876-018-0831-x\" rel=\"nofollow noreferrer\">A practical guide for probiotics applied to the case of antibiotic-associated diarrhea in The Netherlands (BMC Gastroenterology, 2018)</a></p>\n\n<p>After systematic review of available literature, they conclude that:</p>\n\n<blockquote>\n <p>...there is sufficient evidence to make a recommendation for the use\n of specific probiotic products for the prevention of antibiotic\n associated diarrhea. In particular, we provide a three-star\n recommendation for preparations with...the probiotic strain\n Lactobacillus rhamnosus GG.</p>\n</blockquote>\n\n<p><a href=\"https://www.mdpi.com/2079-6382/6/4/21\" rel=\"nofollow noreferrer\">Probiotics for the Prevention of Antibiotic-Associated Diarrhea in Outpatients—A Systematic Review and Meta-Analysis (MDPI, 2017)</a></p>\n\n<blockquote>\n <p>...the overall quality of the included studies was moderate...The\n results suggests that probiotic use may be beneficial in the\n prevention of AAD among <em>outpatients.</em></p>\n</blockquote>\n\n<p><a href=\"https://www.gastrojournal.org/article/S0016-5085(17)30136-1/pdf\" rel=\"nofollow noreferrer\">Timely Use of Probiotics in Hospitalized Adults Prevents Clostridium difficile Infection: A Systematic Review With Meta-Regression Analysis (Gatroenterology, 2017)</a></p>\n\n<blockquote>\n <p>...we found evidence that administration of probiotics closer to the\n first dose of antibiotic reduces the risk of CDI by >50% in\n <em>hospitalized</em> adults.</p>\n</blockquote>\n\n<p><strong><em>COMMERCIAL</em> PROBIOTICS AND OVERALL HEALTH</strong></p>\n\n<p><strong>There seems to be <em>insufficient evidence</em> to claim that commercially available probiotic capsules or foods, such as yogurt, kefir, cheese, sauerkraut, kombucha and kimchi, help in overall health. Even if they \"help with the gut flora overall,\" this dos not already mean they are beneficial for health.</strong> </p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/29267517\" rel=\"nofollow noreferrer\">What do Cochrane systematic reviews say about probiotics as preventive interventions? (PubMed, 2107)</a></p>\n\n<blockquote>\n <p>Despite the marketing and the benefits associated with probiotics,\n there is little scientific evidence supporting the use of probiotics.\n None of the reviews provided any high-quality evidence for prevention\n of illnesses through use of probiotics.</p>\n</blockquote>\n\n<p><a href=\"https://www.bmj.com/content/324/7350/1361.full\" rel=\"nofollow noreferrer\">Probiotics in prevention of antibiotic associated diarrhoea: meta-analysis (theBMJ, 2002)</a></p>\n\n<blockquote>\n <p>Commercially available strains are being marketed in capsules and\n yoghurt based drinks, but their potential benefit needs further\n investigation. It would be wrong to credit the proved benefits of one\n strain to an untested but closely related strain.</p>\n</blockquote>\n" } ]
2019/04/13
[ "https://health.stackexchange.com/questions/19049", "https://health.stackexchange.com", "https://health.stackexchange.com/users/13007/" ]
19,076
<p>I was identified as a glaucoma suspect and told to get rechecked for glaucoma annually. Knowing that glaucoma can move more quickly than that I was spooked and wound up creating my own self test. If this doesn't already exist I'll share my approach as an answer.</p> <p>Is there an existing self test for glaucoma?</p>
[ { "answer_id": 19077, "author": "Ruminator", "author_id": 1268, "author_profile": "https://health.stackexchange.com/users/1268", "pm_score": 3, "selected": true, "text": "<p>Disclaimer: I have no formal medical or vision science training. Please point out any factual errors.</p>\n\n<p>My test is based on the idea that Glaucoma is indicated by pressure on optic nerve, which one may not even be aware of but slowly destroys the nerve (which is actually a bundle of nerves, similar to a huge communications cable) from the outside of the cable in. The effect of this is a gradual loss of vision from the periphery toward the center, forming tunnel vision and eventually total blindness. The mind compensates so the person doesn't even realize that their field of vision is being narrowed until it is too late. </p>\n\n<p>Doctors test for vision loss at the periphery by snapping fingers at the periphery and seeing if the patient can see it.</p>\n\n<p>With my test you simply look straight ahead and raise your arms into a circle around your head, similar to a ballet dancer:</p>\n\n<p><a href=\"https://i.stack.imgur.com/c71ad.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/c71ad.jpg\" alt=\"Starting position\"></a></p>\n\n<p>Slowly move the elbows forward while continuing to look ahead. If you have to move your elbow on either arm significantly forward (consult an eye doctor to \"calibrate\" your elbows) then you may have damage to the periphery of the optic nerve. If so, the further forward, the more the damage.</p>\n\n<p>Damage to the optic nerve is, with current technology progressive and never regressive so acting quickly is of the utmost importance.</p>\n" }, { "answer_id": 23269, "author": "a a", "author_id": 19357, "author_profile": "https://health.stackexchange.com/users/19357", "pm_score": 0, "selected": false, "text": "<p>from</p>\n\n<p><a href=\"https://www.glaucoma.org/glaucoma/glaucoma-and-the-brain\" rel=\"nofollow noreferrer\">https://www.glaucoma.org/glaucoma/glaucoma-and-the-brain</a>.</p>\n\n<p>\"Researchers now view glaucoma as a disease of the brain — a neurodegenerative disease — rather than simply an eye disease. Recent research has shown that the complex connection between the eye and the brain is an important key to the disease.</p>\n\n<p>and more relevant links</p>\n\n<p><a href=\"https://www.bing.com/search?q=Glaucoma+brain+cancer&amp;qs=n&amp;form=QBRE&amp;sp=-1&amp;pq=glaucoma+brain+cancer&amp;sc=1-21&amp;sk=&amp;cvid=F60A28D249C24EC88DCE821B7110D442\" rel=\"nofollow noreferrer\">https://www.bing.com/search?q=Glaucoma+brain+cancer&amp;qs=n&amp;form=QBRE&amp;sp=-1&amp;pq=glaucoma+brain+cancer&amp;sc=1-21&amp;sk=&amp;cvid=F60A28D249C24EC88DCE821B7110D442</a></p>\n" } ]
2019/04/16
[ "https://health.stackexchange.com/questions/19076", "https://health.stackexchange.com", "https://health.stackexchange.com/users/1268/" ]
19,099
<p>"When you are a hammer", the proverb goes, "everything looks like a nail".</p> <p>To my knowledge current apnea testing involves a multitude of sensors that record the position of various parts of the body but do not evaluate the position and motions of the jaw and the number of apnea events indicates either a go/no-go decision about CPAP.</p> <p>However, the location of the jaw can in some cases <a href="https://www.sciencedaily.com/releases/2018/11/181106073233.htm" rel="nofollow noreferrer">be manipulated by a physical appliance</a> resulting in a relatively simple, passive solution.</p> <p>In fact, armed with sufficient data it may be possible to identify currently unidentified jaw and dental problems that might be creating or contributing significantly to the apnea.</p> <p>In addition the collected data may lead to other insights such as a patient shown to be grinding their teeth, resting their jaw on their hand during sleep, etc. </p> <p>I would imagine that all that would be involved is a sensor on the skull (already present) and one (or better yet, three, for each axis) on the jaw.</p> <p>Note: At the heart of this is my suspicion that dental and jaw issues account for a significant part of apnea, confirmed by the efficacy of the new appliance.</p> <p>Related:</p> <p><a href="https://medicalsciences.stackexchange.com/questions/19088/has-a-correlation-between-sleep-apnea-and-grinding-of-teeth-been-identified-or-r">Has a correlation between sleep apnea and grinding of teeth been identified or ruled out?</a></p>
[ { "answer_id": 19077, "author": "Ruminator", "author_id": 1268, "author_profile": "https://health.stackexchange.com/users/1268", "pm_score": 3, "selected": true, "text": "<p>Disclaimer: I have no formal medical or vision science training. Please point out any factual errors.</p>\n\n<p>My test is based on the idea that Glaucoma is indicated by pressure on optic nerve, which one may not even be aware of but slowly destroys the nerve (which is actually a bundle of nerves, similar to a huge communications cable) from the outside of the cable in. The effect of this is a gradual loss of vision from the periphery toward the center, forming tunnel vision and eventually total blindness. The mind compensates so the person doesn't even realize that their field of vision is being narrowed until it is too late. </p>\n\n<p>Doctors test for vision loss at the periphery by snapping fingers at the periphery and seeing if the patient can see it.</p>\n\n<p>With my test you simply look straight ahead and raise your arms into a circle around your head, similar to a ballet dancer:</p>\n\n<p><a href=\"https://i.stack.imgur.com/c71ad.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/c71ad.jpg\" alt=\"Starting position\"></a></p>\n\n<p>Slowly move the elbows forward while continuing to look ahead. If you have to move your elbow on either arm significantly forward (consult an eye doctor to \"calibrate\" your elbows) then you may have damage to the periphery of the optic nerve. If so, the further forward, the more the damage.</p>\n\n<p>Damage to the optic nerve is, with current technology progressive and never regressive so acting quickly is of the utmost importance.</p>\n" }, { "answer_id": 23269, "author": "a a", "author_id": 19357, "author_profile": "https://health.stackexchange.com/users/19357", "pm_score": 0, "selected": false, "text": "<p>from</p>\n\n<p><a href=\"https://www.glaucoma.org/glaucoma/glaucoma-and-the-brain\" rel=\"nofollow noreferrer\">https://www.glaucoma.org/glaucoma/glaucoma-and-the-brain</a>.</p>\n\n<p>\"Researchers now view glaucoma as a disease of the brain — a neurodegenerative disease — rather than simply an eye disease. Recent research has shown that the complex connection between the eye and the brain is an important key to the disease.</p>\n\n<p>and more relevant links</p>\n\n<p><a href=\"https://www.bing.com/search?q=Glaucoma+brain+cancer&amp;qs=n&amp;form=QBRE&amp;sp=-1&amp;pq=glaucoma+brain+cancer&amp;sc=1-21&amp;sk=&amp;cvid=F60A28D249C24EC88DCE821B7110D442\" rel=\"nofollow noreferrer\">https://www.bing.com/search?q=Glaucoma+brain+cancer&amp;qs=n&amp;form=QBRE&amp;sp=-1&amp;pq=glaucoma+brain+cancer&amp;sc=1-21&amp;sk=&amp;cvid=F60A28D249C24EC88DCE821B7110D442</a></p>\n" } ]
2019/04/18
[ "https://health.stackexchange.com/questions/19099", "https://health.stackexchange.com", "https://health.stackexchange.com/users/1268/" ]
19,239
<p>I have been <strong>researching</strong> fish oil supplementation, and one thing that concerns me is that fish oil may contain Vitamin A, which is fat soluble. <a href="https://wikipedia.org/wiki/Hypervitaminosis_A" rel="nofollow noreferrer">Hypervitamintosis A</a> can occur if too much Vitamin A is ingested.</p> <p>For example, <a href="https://healthyeating.sfgate.com/side-effects-many-fish-oil-supplements-10064.html" rel="nofollow noreferrer">this article</a> mentions this as a possibility.</p> <p>I have performed multiple searches, using different terms, and have found <a href="https://www.consumerlab.com/answers/can-combining-vitamin-a-supplements-with-fish-oil-lead-to-a-vitamin-a-overdose/vitamin_A/" rel="nofollow noreferrer">only one web page that claims fish oil does not contain Vitamin A</a>, but it has not a single reference, nor does it say how they reached their conclusion. I learned long ago not to believe the first thing I read, especially when it is not substantiated by any data, even when it's the first result in a search.</p> <p><strong>On average, how much Vitamin A is contained in 1g of fish oil <em>(not cod liver oil)</em>?</strong> I have performed multiple searches, and asked two doctors, one nurse, and have not found the answer.</p> <p>BTW, out of caution, I'll mention that certain oils, such as cod liver oil, can contain <a href="https://www.healthline.com/nutrition/fish-oil-dosage" rel="nofollow noreferrer">high levels of Vitamin A, and are not advised during pregnancy</a>. But for this question, I am only asking about regular fish oil, which is manufactured from the body of the fish, as opposed to the liver.</p>
[ { "answer_id": 19241, "author": "Gordon", "author_id": 13819, "author_profile": "https://health.stackexchange.com/users/13819", "pm_score": 2, "selected": false, "text": "<p>Vitamin A is an important Vitamin in my opinion. See, importance for Children 6-59 months <a href=\"https://www.who.int/elena/titles/vitamina_children/en/\" rel=\"nofollow noreferrer\">https://www.who.int/elena/titles/vitamina_children/en/</a></p>\n\n<p>So age is a consideration. Here is the Pauling Institute article on Vitamin A, Oregon State Univ. <a href=\"https://lpi.oregonstate.edu/mic/vitamins/vitamin-A\" rel=\"nofollow noreferrer\">https://lpi.oregonstate.edu/mic/vitamins/vitamin-A</a> This article also discusses the osteoporosis risk. </p>\n\n<p>How well people convert Beta carotene to Vitamin A is also an issue. Should the government continue to allow beta carotene to stand for Vitamin A in our foodstuffs? Stay tuned. </p>\n\n<p>I would not advise a heavy smoker to ingest too much beta carotene. <a href=\"https://www.ncbi.nlm.nih.gov/m/pubmed/20155614/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/m/pubmed/20155614/</a></p>\n\n<p>If the fish oil supplements contained a significant amount of pre-formed Vitamin A, then believe me it would be listed on the bottle because there is a bit of hysteria about \"hypervitamintosis A\" at present. </p>\n\n<p>(Some young people in America get the idea that if a little preformed Vitamin A helps acne, then a lot of it could help even more, and they may take a lot of the vitamin, without medical supervision, day after day, and this could potentially be a problem.) </p>\n\n<p>The answer regarding supplementation is \"it depends\", on such things as age, medical condition, whether pregnant or not, medications taken and so on. Work with your doctor to find the right level of Vitamin A for you. </p>\n\n<p>Back to fish oil Omega 3 type supplements, I never know whether the oil could be rancid, or whether it could contain an unhealthy level of heavy metals. They can offer health benefits for the right person, particularly if they become a member at a company like Consumer Labs, and follow the information about the good and bad products in this category. Always inform your doctor of the supplements you are taking. </p>\n\n<p>NB Article: Vitamin A and the retina. <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738993/#!po=0.454545\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738993/#!po=0.454545</a> Type 2 Diabetes: <a href=\"https://www.sciencedaily.com/releases/2017/06/170613111649.htm\" rel=\"nofollow noreferrer\">https://www.sciencedaily.com/releases/2017/06/170613111649.htm</a></p>\n" }, { "answer_id": 19242, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p>According to USDA Food Composition Database, 1 gram (or even 100 grams) of fish oil from <a href=\"https://ndb.nal.usda.gov/ndb/foods/show/04594?fgcd=&amp;manu=&amp;format=&amp;count=&amp;max=25&amp;offset=&amp;sort=default&amp;order=asc&amp;qlookup=fish%20oil&amp;ds=&amp;qt=&amp;qp=&amp;qa=&amp;qn=&amp;q=&amp;ing=\" rel=\"nofollow noreferrer\">sardines</a>, <a href=\"https://ndb.nal.usda.gov/ndb/foods/show/04590?fgcd=&amp;manu=&amp;format=&amp;count=&amp;max=25&amp;offset=&amp;sort=default&amp;order=asc&amp;qlookup=fish%20oil&amp;ds=&amp;qt=&amp;qp=&amp;qa=&amp;qn=&amp;q=&amp;ing=\" rel=\"nofollow noreferrer\">herring</a>, <a href=\"https://ndb.nal.usda.gov/ndb/foods/show/04593?fgcd=&amp;manu=&amp;format=&amp;count=&amp;max=25&amp;offset=&amp;sort=default&amp;order=asc&amp;qlookup=fish%20oil&amp;ds=&amp;qt=&amp;qp=&amp;qa=&amp;qn=&amp;q=&amp;ing=\" rel=\"nofollow noreferrer\">salmon</a> and <a href=\"https://ndb.nal.usda.gov/ndb/foods/show/04591?fgcd=&amp;manu=&amp;format=&amp;count=&amp;max=25&amp;offset=&amp;sort=default&amp;order=asc&amp;qlookup=fish%20oil&amp;ds=&amp;qt=&amp;qp=&amp;qa=&amp;qn=&amp;q=&amp;ing=\" rel=\"nofollow noreferrer\">menhaden</a> contains <strong>0 (zero) μg</strong> vitamin A.</p>\n\n<p><a href=\"https://www.nap.edu/read/10026/chapter/6#125\" rel=\"nofollow noreferrer\">Tolerable Upper Intake Levels for Vitamin A (The National Academic Press, 2001)</a></p>\n\n<blockquote>\n <p><strong>Acute toxicity</strong> is characterized by nausea, vomiting, headache, increased cerebrospinal fluid pressure, vertigo, blurred vision,\n muscular incoordination..., and bulging fontanel in infants. These are\n usually transient effects involving single or short-term large doses\n of greater than or equal to <strong>150,000 μg in adults</strong> and\n proportionately less in children.</p>\n \n <p><strong>Chronic toxicity</strong> is usually associated with ingestion of large doses greater than or equal to <strong>30,000 μg/day</strong> <em>for months or years.</em></p>\n</blockquote>\n\n<hr>\n\n<p>According to other sources, such as <a href=\"https://food-nutrition.canada.ca/cnf-fce/serving-portion.do?id=458\" rel=\"nofollow noreferrer\">Canada Nutrient File</a> (you need to click \"generate nutrient profile\") and <a href=\"https://nutritiondata.self.com/facts/fats-and-oils/629/2\" rel=\"nofollow noreferrer\">NutritionData</a>, there is also no vitamin A in fish oil. Not sure how much these databases are different from the USDA one, but you can see there are also no other vitamins and minerals in fish oil; or according to <a href=\"https://nccih.nih.gov/health/omega3/introduction.htm\" rel=\"nofollow noreferrer\">National Center for Complementary and Integrative Health</a>: \"fish oil supplements are the nonvitamin/nonmineral natural products...\" </p>\n\n<p>More sources about vitamin A in fish oil:</p>\n\n<ul>\n<li><a href=\"https://www.drugs.com/fish_oil.html\" rel=\"nofollow noreferrer\">Drugs.com</a> does not even mention vitamin A in fish oil.</li>\n<li><a href=\"https://www.drugbank.ca/drugs/DB13961\" rel=\"nofollow noreferrer\">Drugbank</a> mentions that vitamin A and some other vitamins can be <em>added</em> to <em>some</em> fish oil supplements.</li>\n</ul>\n\n<p>More about vitamin A toxicity:</p>\n\n<p><a href=\"https://ods.od.nih.gov/factsheets/VitaminA-HealthProfessional/\" rel=\"nofollow noreferrer\">Office of Dietary Supplements by NIH.gov</a> mentions some (unreliable) observational studies in which vitamin A in doses as low as 1,500 μg/day have been \"associated\" with side effects.</p>\n\n<p>According to <a href=\"https://lpi.oregonstate.edu/mic/vitamins/vitamin-A#toxicity\" rel=\"nofollow noreferrer\">Linus Pauling Institute</a>, long-term consumption of vitamin A in doses 8,000-10,000 μg/day vitamin A could be toxic.</p>\n" } ]
2019/05/09
[ "https://health.stackexchange.com/questions/19239", "https://health.stackexchange.com", "https://health.stackexchange.com/users/453/" ]
19,310
<p>The medical field is vast and there is a great deal of literature, including textbooks. Is there a clear progression of textbooks that one could go through in order to build knowledge in the medical sciences? For example, in the topics of physiology and biochemistry, how does one determine where to start?</p>
[ { "answer_id": 19314, "author": "DoctorWhom", "author_id": 6776, "author_profile": "https://health.stackexchange.com/users/6776", "pm_score": 3, "selected": true, "text": "<p>Medicine is challenging for many reasons. One major reason is that it takes multiple tiers of knowledge as a foundation prior to being able to even start studying the fundamentals.</p>\n<p>This is how it works in the USA for most schools:</p>\n<h2><strong>FIRST: College or University (after high school, before medical school)</strong></h2>\n<p><strong>Undergraduate level (usually 4 years):</strong></p>\n<ol>\n<li>Math: through advanced algebra and trigonometry, if not done in high school. Calculus may be required to enter med school, but its concepts are not really necessary for medicine unless you plan to do certain advanced research topics. I'd also recommend at least one course in statistics, if not biostatistics as well.</li>\n<li>Physics: minimum 2 semesters. Trig-based should be enough, not necessary for calculus-based.</li>\n<li>Biology: as much as you can get, usually multiple semesters are required. Especially focus on cellular, molecular, genetic. Consider taking mammalian physiology or an undergrad anatomy &amp; physiology class for a solid foundation.</li>\n<li>Chemistry: usually requires 2 semesters of inorganic, 2 of organic, and 1-2 of biochemistry. Biochemistry is the most useful.</li>\n</ol>\n<h2><strong>SECOND: Med school (4 years):</strong></h2>\n<p><strong>The first 2 years are basic sciences,</strong> extremely dense, fast classes:</p>\n<ol>\n<li>Anatomy and histology: goes in depth, including gross anatomy. Example textbooks: Grey's Anatomy, Moore's Clinical Anatomy, Netter's Atlas.</li>\n<li>Normal Physiology: including all systems (e.g. cardiology, pulmonology, endocrinology etc etc). Example textbooks: Boron and Boulpaep, West Pulmonology, Kablunde Cardiology, and other system-based textbooks.</li>\n<li>Pathology: including histopathology and the abnormal of all physiology topics. Example textbook: Robbins &amp; Cotran.</li>\n<li>Public health: usually just an overview, with lots of epidemiology and biostatistics.</li>\n</ol>\n<p><strong>The last 2 years of med school</strong> are clinical rotations plus lectures, reading, and exams on the application of all of the above to clinical situations. Examples of books used are Harrison's Internal Medicine, Case Files and Blueprints for each specialty rotation, etc.</p>\n<h2><strong>THIRD: Residency:</strong></h2>\n<p><strong>You'll do 3 to 7 years of residency in your specialty</strong>, where you practice medicine under supervision with additional lectures, reading, and exams. This is finally when things fully come together.</p>\n<h2><strong>In summary:</strong></h2>\n<p>It's hard to say &quot;read X to get started&quot; without a clear idea of how far into the fundamentals one has gone. There's a reason it takes so many years to study - it's like building a pyramid from the ground up. You can't skip to the top block without building a solid foundation.</p>\n" }, { "answer_id": 19318, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": false, "text": "<p>Examples of books from four basic \"pre-clinical\" subjects:</p>\n\n<ul>\n<li><strong>Anatomy:</strong> Sobotta Atlas of Human Anatomy (<a href=\"https://archive.org/details/SobottaAtlasOfHumanAnatomyVolume1_201611\" rel=\"noreferrer\">entire book, page by page</a>)</li>\n<li><strong>Biology:</strong> Goodman: Medical Cell Biology (<a href=\"https://www.elsevier.com/books/medical-cell-biology/goodman/978-0-12-370458-0\" rel=\"noreferrer\">Google preview</a>)</li>\n<li><strong>Biochemistry:</strong> Lehninger: Principles of Biochemistry (<a href=\"https://www.macmillanlearning.com/catalog//samplechapters/1637_LehningerPreviewandCh5watermarked.pdf\" rel=\"noreferrer\">book overview with a sample chapter about proteins</a>)</li>\n<li><strong>Physiology:</strong> Berne &amp; Levy Physiology (<a href=\"https://www.elsevier.com/books/berne-and-levy-physiology/koeppen/978-0-323-39394-2\" rel=\"noreferrer\">Google preview</a>)</li>\n</ul>\n\n<p>These books are often a part of \"recommended literature\" for medical students at various universities. They are \"complete\" books. They should be easy to understand for everyone who has finished a high school with emphasis on natural sciences. I don't think it makes sense to read any short version of such books to \"get prepared.\"</p>\n\n<p>It is a good idea to get familiar with basic <strong>medical terms.</strong> Examples of online sources:</p>\n\n<ul>\n<li><a href=\"https://www.dmu.edu/medterms/basics/\" rel=\"noreferrer\">Des Moines University</a></li>\n<li><a href=\"https://www.aimseducation.edu/blog/all-essential-medical-terms/\" rel=\"noreferrer\">Aimseducation.edu</a></li>\n<li><a href=\"http://www.mb-guide.org/learn-basic-medical-terminology.html\" rel=\"noreferrer\">MB-Guide</a></li>\n<li><a href=\"https://www.medicinenet.com/medterms-medical-dictionary/article.htm\" rel=\"noreferrer\">Medterms</a> (a huge online medical dictionary)</li>\n</ul>\n" } ]
2019/05/21
[ "https://health.stackexchange.com/questions/19310", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16242/" ]
19,333
<p>EDIT.</p> <p>I am looking for references to serious research articles on the subject, whether confirming or refuting. (Or articles referring to such, but <em>not articles without peer refereed references</em>.)</p> <p>To avoid any confusion, by "serious" I only mean reputable peer refereed journals.</p> <p>Here are some examples of such articles, taken from <a href="https://www.reddit.com/r/C_S_T/comments/6t6wot/oil_pulling_and_why_the_skeptics_are_wrong/" rel="nofollow noreferrer">https://www.reddit.com/r/C_S_T/comments/6t6wot/oil_pulling_and_why_the_skeptics_are_wrong/</a>, (some of which seem to confirm the positive effects of the oil pulling but do not seem to study the specific problem in the question):</p> <p><a href="https://www.johcd.org/doi/pdf/10.5005/johcd-1-1-12" rel="nofollow noreferrer">https://www.johcd.org/doi/pdf/10.5005/johcd-1-1-12</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/27084861" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pubmed/27084861</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/11890570" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pubmed/11890570</a> <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853744/" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3853744/</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/25838632" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pubmed/25838632</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/21911944" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pubmed/21911944</a> <a href="https://www.nature.com/articles/sj.bdj.2012.856?foxtrotcallback=true" rel="nofollow noreferrer">https://www.nature.com/articles/sj.bdj.2012.856?foxtrotcallback=true</a></p> <hr> <p><a href="https://articles.mercola.com/sites/articles/archive/2016/08/03/oil-pulling-benefits.aspx" rel="nofollow noreferrer">Many</a> <a href="https://fashionista.com/2014/03/oil-pulling" rel="nofollow noreferrer">sources</a> recommend to spend 15-20 minutes for oil pulling, however those numbers look randomly chosen with no justification provided. It is conceivable that 15-20 minutes have been chosen by popular practitioners for reasons of their personal comfort, while other sources have simply repeated the figure. It is also conceivable that longer pulling may increase the benefits, even if it feels less comfortable to some practitioners. Or, conversely, are there side effects of any prolonged oil pulling?</p> <p>My question is, where is the science and where are people's personal convenience choices? Has any research been conducted to study effects of the oil pulling over different periods?</p>
[ { "answer_id": 19336, "author": "Chris Rogers", "author_id": 7951, "author_profile": "https://health.stackexchange.com/users/7951", "pm_score": 2, "selected": false, "text": "<p>The study you linked in the comments (<a href=\"https://www.johcd.org/doi/pdf/10.5005/johcd-1-1-12\" rel=\"nofollow noreferrer\">Amith et al., 2007</a>) stated that there were 10 subjects and the subjects were to</p>\n<blockquote>\n<p>Swish approximately 8-10 minutes or till you feel a fullness in your mouth.</p>\n</blockquote>\n<p>The last part of the instructions to the subjects suggests that the feeling of fullness in the mouth could happen before the 8 minute point. Plus the study of 10 subjects is a very small study. Nevertheless, the study points out that there is a potential that oil pulling can help with oral hygiene.</p>\n<p>The point that the study makes is that 10 minutes is enough to obtain any benefit from oil pulling. Whether or not you choose to pull for more time is up to you.</p>\n<p>As pointed out in the comments, <a href=\"https://www.123dentist.com/truth-oil-pulling/\" rel=\"nofollow noreferrer\">the dentistry website you linked</a> indicates that:</p>\n<blockquote>\n<p>There is no official verdict regarding the benefits of oil pulling as there is unfortunately very little research on the topic.</p>\n</blockquote>\n<p>Once there are more (and larger) studies performed, there will be more of a consensus on the subject, therefore creating an official stance on the benefits of oil pulling.</p>\n<p>If you feel that oil pulling helps, there is an indication that 8-10 minutes is enough. If you wish to follow the 15-20 minute suggestion you have seen (or longer) then fine. That is your choice.</p>\n<p>What I would suggest is to speak to your dentist/orthodontist and seek their advice. Their advice will be tailored to your specific needs.</p>\n<h2>References</h2>\n<p>Amith, H. V., Ankola, A. V., &amp; Nagesh, L. (2007). Effect of oil pulling on plaque and gingivitis. <em>J Oral Health Community Dent, 1</em>(1), 12-18. Retrieved from <a href=\"https://www.johcd.org/doi/pdf/10.5005/johcd-1-1-12\" rel=\"nofollow noreferrer\">https://www.johcd.org/doi/pdf/10.5005/johcd-1-1-12</a></p>\n" }, { "answer_id": 19346, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p><strong>Is oil pulling beneficial for oral health?</strong></p>\n\n<p>It may not be possible to make convincing conclusions from <a href=\"https://www.johcd.org/doi/pdf/10.5005/johcd-1-1-12\" rel=\"nofollow noreferrer\">three</a> <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/25838632\" rel=\"nofollow noreferrer\">small</a> <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/21911944\" rel=\"nofollow noreferrer\">studies</a> (linked in the question) about the benefits of oil pulling on oral health, especially when knowing this is an Ayurvedic dental technique and most authors involved in the studies are Indians, so they might be biased for positive results.</p>\n\n<p>A systematic review is usually considered a higher level evidence.</p>\n\n<p>The authors of the following review from the University of Oxford/UK <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/27261981\" rel=\"nofollow noreferrer\">Effect of oil pulling in promoting oro dental hygiene: A systematic review of randomized clinical trials (PubMed, 2016)</a> have concluded:</p>\n\n<blockquote>\n <p>The limited evidence to date from clinical trials suggests that oil\n pulling may have beneficial effects on oro dental hygiene as seen\n for the short period of time investigated.</p>\n</blockquote>\n\n<p>This systematic review included 26 randomized clinical trials, which were short term (10-45 days) and included only 160 participants in total, they \"varied in reporting quality,\" and in 5 studies no effect was observed, which, altogether, is not a very strong evidence.</p>\n\n<p>The authors (mainly from Pakistan and Saudi Arabia) of the following review <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5654187/\" rel=\"nofollow noreferrer\">Oil pulling and importance of traditional medicine in oral health maintenance (PubMed, 2017)</a> have concluded:</p>\n\n<blockquote>\n <p>For modern day practices, oil pulling can be suggested for adjunct\n use, with tooth brushing and flossing, to maintain the standard oral\n health care.</p>\n</blockquote>\n\n<p>According to <a href=\"https://www.mouthhealthy.org/en/az-topics/o/oil-pulling\" rel=\"nofollow noreferrer\">American Dental Association</a>:</p>\n\n<blockquote>\n <p>Currently, there are no reliable scientific studies to show that oil\n pulling reduces cavities, whitens teeth or improves oral health and\n well-being. Based on the lack of scientific evidence, the American\n Dental Association does not recommend oil pulling as a dental hygiene\n practice.</p>\n</blockquote>\n\n<p><strong>Are there any benefits of oil pulling for more than 20 minutes?</strong></p>\n\n<p>I have found no studies that would test this.</p>\n" } ]
2019/05/26
[ "https://health.stackexchange.com/questions/19333", "https://health.stackexchange.com", "https://health.stackexchange.com/users/857/" ]
19,340
<p>Brushing teeth appears to be commonly recommended, but the evidence appears to be anecdotal. Have any randomized prospective trials been done to determine the efficacy of brushing to prevent conditions such as dental caries?</p> <p>I am interested in research that measures dental disease, not merely plaque removal. </p> <hr> <p>A Google Scholar search for "<a href="https://scholar.google.com/scholar?as_vis=1&amp;q=brush%20teeth&amp;hl=en&amp;as_sdt=1,5" rel="nofollow noreferrer">brush teeth</a>" returns articles that:</p> <ul> <li>Compare toothbrushes (eg, traditional vs electronic)</li> <li>Compare toothpastes</li> <li>Test pre-brush mouth washes</li> <li>Editorials/Opinions about brushing</li> <li>Survey attitudes toward brushing</li> <li>Test new vs old toothbrushes</li> <li>Test brush strokes against each other</li> <li>Test different electric toothbrush heads</li> <li>Etc.</li> </ul> <p>Within the first 20 pages, no articles test the efficacy of brushing. Around page 16, results became less relevant to brushing.</p> <hr> <p>I have looked through the list of ADA references that <a href="https://medicalsciences.stackexchange.com/a/19349/14759">JonMark Perry refers to</a>. They don't address brushing vs not or the prevention of dental conditions, such as caries. For instance:</p> <ul> <li><p>The first article, and a few others, are about plaque or biofilm removal, which may or may not be related to dental caries. Since approximately 100% of the population has dental plaque, it's not a useful predictor of dental disease.</p></li> <li><p>Second article is about fluoride levels, not dental caries, or other dental conditions. It also tests brushing duration, rather than brushing vs not brushing.</p></li> <li><p>Several about brush design.</p></li> <li>Some about brush contamination and sanitation.</li> <li>Some about gingival abrasion and recession.</li> </ul>
[ { "answer_id": 19336, "author": "Chris Rogers", "author_id": 7951, "author_profile": "https://health.stackexchange.com/users/7951", "pm_score": 2, "selected": false, "text": "<p>The study you linked in the comments (<a href=\"https://www.johcd.org/doi/pdf/10.5005/johcd-1-1-12\" rel=\"nofollow noreferrer\">Amith et al., 2007</a>) stated that there were 10 subjects and the subjects were to</p>\n<blockquote>\n<p>Swish approximately 8-10 minutes or till you feel a fullness in your mouth.</p>\n</blockquote>\n<p>The last part of the instructions to the subjects suggests that the feeling of fullness in the mouth could happen before the 8 minute point. Plus the study of 10 subjects is a very small study. Nevertheless, the study points out that there is a potential that oil pulling can help with oral hygiene.</p>\n<p>The point that the study makes is that 10 minutes is enough to obtain any benefit from oil pulling. Whether or not you choose to pull for more time is up to you.</p>\n<p>As pointed out in the comments, <a href=\"https://www.123dentist.com/truth-oil-pulling/\" rel=\"nofollow noreferrer\">the dentistry website you linked</a> indicates that:</p>\n<blockquote>\n<p>There is no official verdict regarding the benefits of oil pulling as there is unfortunately very little research on the topic.</p>\n</blockquote>\n<p>Once there are more (and larger) studies performed, there will be more of a consensus on the subject, therefore creating an official stance on the benefits of oil pulling.</p>\n<p>If you feel that oil pulling helps, there is an indication that 8-10 minutes is enough. If you wish to follow the 15-20 minute suggestion you have seen (or longer) then fine. That is your choice.</p>\n<p>What I would suggest is to speak to your dentist/orthodontist and seek their advice. Their advice will be tailored to your specific needs.</p>\n<h2>References</h2>\n<p>Amith, H. V., Ankola, A. V., &amp; Nagesh, L. (2007). Effect of oil pulling on plaque and gingivitis. <em>J Oral Health Community Dent, 1</em>(1), 12-18. Retrieved from <a href=\"https://www.johcd.org/doi/pdf/10.5005/johcd-1-1-12\" rel=\"nofollow noreferrer\">https://www.johcd.org/doi/pdf/10.5005/johcd-1-1-12</a></p>\n" }, { "answer_id": 19346, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p><strong>Is oil pulling beneficial for oral health?</strong></p>\n\n<p>It may not be possible to make convincing conclusions from <a href=\"https://www.johcd.org/doi/pdf/10.5005/johcd-1-1-12\" rel=\"nofollow noreferrer\">three</a> <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/25838632\" rel=\"nofollow noreferrer\">small</a> <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/21911944\" rel=\"nofollow noreferrer\">studies</a> (linked in the question) about the benefits of oil pulling on oral health, especially when knowing this is an Ayurvedic dental technique and most authors involved in the studies are Indians, so they might be biased for positive results.</p>\n\n<p>A systematic review is usually considered a higher level evidence.</p>\n\n<p>The authors of the following review from the University of Oxford/UK <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/27261981\" rel=\"nofollow noreferrer\">Effect of oil pulling in promoting oro dental hygiene: A systematic review of randomized clinical trials (PubMed, 2016)</a> have concluded:</p>\n\n<blockquote>\n <p>The limited evidence to date from clinical trials suggests that oil\n pulling may have beneficial effects on oro dental hygiene as seen\n for the short period of time investigated.</p>\n</blockquote>\n\n<p>This systematic review included 26 randomized clinical trials, which were short term (10-45 days) and included only 160 participants in total, they \"varied in reporting quality,\" and in 5 studies no effect was observed, which, altogether, is not a very strong evidence.</p>\n\n<p>The authors (mainly from Pakistan and Saudi Arabia) of the following review <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5654187/\" rel=\"nofollow noreferrer\">Oil pulling and importance of traditional medicine in oral health maintenance (PubMed, 2017)</a> have concluded:</p>\n\n<blockquote>\n <p>For modern day practices, oil pulling can be suggested for adjunct\n use, with tooth brushing and flossing, to maintain the standard oral\n health care.</p>\n</blockquote>\n\n<p>According to <a href=\"https://www.mouthhealthy.org/en/az-topics/o/oil-pulling\" rel=\"nofollow noreferrer\">American Dental Association</a>:</p>\n\n<blockquote>\n <p>Currently, there are no reliable scientific studies to show that oil\n pulling reduces cavities, whitens teeth or improves oral health and\n well-being. Based on the lack of scientific evidence, the American\n Dental Association does not recommend oil pulling as a dental hygiene\n practice.</p>\n</blockquote>\n\n<p><strong>Are there any benefits of oil pulling for more than 20 minutes?</strong></p>\n\n<p>I have found no studies that would test this.</p>\n" } ]
2019/05/27
[ "https://health.stackexchange.com/questions/19340", "https://health.stackexchange.com", "https://health.stackexchange.com/users/14759/" ]
19,348
<p>Say you go to a doctor and they say -- more or less -- that you are "healthy."</p> <p>What does this mean? Under what circumstances does one fall within these supposed confines?</p> <p>And what would falling under these confines mean in a more deeper outlook? Like if I am "healthy," does that mean I can't be healthier? If I am not healthy enough, could I get healthier then?</p> <p>Many people vaguely use the term healthiness to define a set of rules that must apply to someone, like if someone is disease free or not overweight or etc. But is this just vague?</p> <p>A doctor saying you are healthy doesn't mean you are of utmost health, because how would you know each individual's maximum healthiness potential, if it even exists?</p> <p>I always strive to be as healthy as possible with being on the lookout for new supplements and solutions to any health signs of stresses and such. But what really makes me ponder is how we can confidently dish the term healthy around in an overall manner that isn't particularly individualized.</p> <p>No two different people are necessarily as equally healthy as one another in all possible respects if they're both meeting a particular set of observable standards or tests/procedures/etc.</p> <p>So it makes me think that one can envision health as a perpetually tested standard one must always be working to achieve or progress towards. I don't think anyone can be perfectly healthy or the inverse, but how healthy one can become is the big question. Many people have demonstrated massive differences in their feelings/well being from supplementation, homeopathy, herbs, antioxidants and many other potential undertakings not necessarily relating to consumption. I realize you can feel healthy and not be sometimes, but usually feeling really good and strong is a symbol of good health more often than not.</p> <p>In a sense, does the term "healthy" mean that much? Is there always theoretical improvement of our health regardless, because there is no one size fits all or perfect health analysis?</p>
[ { "answer_id": 19352, "author": "practiZ", "author_id": 15382, "author_profile": "https://health.stackexchange.com/users/15382", "pm_score": 2, "selected": false, "text": "<p>Here's the definition of health according to WHO:</p>\n\n<blockquote>\n <p>Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.</p>\n</blockquote>\n\n<p>As you can see, there are a lot of components to this term, of which some, like absence of disease, can be objectively assessed in a uniform manner, while others may have criteria that vary individually from person to person.</p>\n\n<p><em>Source: <a href=\"https://www.who.int/about/who-we-are/constitution\" rel=\"nofollow noreferrer\">https://www.who.int/about/who-we-are/constitution</a></em></p>\n" }, { "answer_id": 19354, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 0, "selected": false, "text": "<p><em>Being healthy</em> is a <em>term</em> that usually describes the presence of desired states, such as stamina and well-being, and the absence of disease and unpleasant feelings.</p>\n\n<p>A doctor will likely consider you healthy when you do not have any symptoms and signs of known health conditions and when your results of medical investigations are within the normal ranges. The normal or <a href=\"https://en.wikipedia.org/wiki/Reference_range\" rel=\"nofollow noreferrer\">reference ranges</a> of different values (normal blood sodium concentration, normal blood pressure, etc.) have been determined on the basis of the studies that have shown they are <em>least commonly associated with various diseases.</em></p>\n\n<p>When everything appears normal by medical criteria, you can still have a room for improvement. You can be in better relationships, feel better, learn to work more efficiently, etc. On the other hand, if you run faster, does this make you healthier or happier? Health should not be viewed as a goal, but as a tool one can use to achieve personal goals in life. </p>\n" } ]
2019/05/27
[ "https://health.stackexchange.com/questions/19348", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16265/" ]
19,358
<p>It is being constantly claimed, upheld and emphasized that being overweight or, even worse, obese, possesses many and severe health hazards. Overweight and obese people are being repeatedly urged to lose weight. That not losing excess weight is harmful for health seems certain.</p> <p>However, there seems to be one more factor, which, admittedly, comes from my experience in the form of the observation of people surrounding me. Namely, I'd put a hypothesis that working to lose weight causes considerable strain on the psyche. I know a person who had been calm and happy… before she started dieting frantically to lose weight. She managed to lose most of her excess weight and works very hard to keep it that way, nonetheless seeing her as nervous and tired and humorless as she is now and comparing to how I remember her before makes me question if her efforts are worth it. Another example comes from a newspaper article (which, again, I can't now find to link it) about a talk-show host. The article snidely remarked that with her excess weight the host lost all of her funniness she had been esteemed for. Finally: I also read a newspaper article (which I, again, can't find now...) that seemed to confirm my anecdotal and intuitive observations: namely, it claimed that both hunger itself and conscious attempts to suppress hunger and restraining the urge to eat cause considerable stress and lower one's mood.</p> <p>Still, in cases when both weight and stress are discussed together, it seems that it is usually in the context of excess weight causing stress because overweight people tend to have low self-esteem and they tend to be ostracized by their peers. I would, however, ask about this relationship from a different angle:</p> <ul> <li>Can working to lose weight, as opposed to neglecting this, cause considerable stress?</li> <li>Since chronic stress is also widely recognized to be a health hazard, can the costs of being more stressed outweigh the costs of not losing weight? Assume absence of other egregious lifestyle-related risks – that is, our overweight person does not smoke, has some moderate physical activity, is not being bullied for being overweight, does not mostly eat junk food, etc etc.</li> </ul>
[ { "answer_id": 19388, "author": "userJT", "author_id": 15631, "author_profile": "https://health.stackexchange.com/users/15631", "pm_score": -1, "selected": false, "text": "<p>There a none and the reason may be that it would be a hard study to design in a way that would answer the trade-off dilemma. Some answers are so individual that designing a general population study is so difficult that it is not done.</p>\n" }, { "answer_id": 19483, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p><strong>Can working to lose weight, as opposed to neglecting this, cause considerable stress?</strong></p>\n\n<p>Not necessary, according to the following review.</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986493/\" rel=\"nofollow noreferrer\">Diet-Induced Weight Loss Has No Effect on Psychological Stress in Overweight and Obese Adults: A Meta-Analysis of Randomized Controlled Trials (Nutrients, 2018)</a></p>\n\n<blockquote>\n <p>This systematic review and meta-analysis of randomized controlled\n clinical trials showed that <em>weight loss</em> induced by dietary\n restriction in adult overweight and obese men and women <em>does not\n have a beneficial or detrimental effect on self-reported psychological\n stress.</em></p>\n</blockquote>\n\n<p>Still, an obese person who tries to lose weight from wrong reasons (to please someone or to reach some theoretical health goal) or in a wrong way (too fast or by some annoying method) can lose the peace of mind.</p>\n\n<hr>\n\n<p><strong>What is the association between obesity, weight loss and health, according to studies?</strong></p>\n\n<p><em>(Categorization of increased weight based on the body mass index or BMI (weight in kg/height in m squared): overweight = 25-30, grade I obesity = 30-35, grade II obesity = 35-40, grade III obesity = >40.)</em></p>\n\n<p><strong>Obesity as a risk factor for chronic conditions:</strong></p>\n\n<ul>\n<li><strong>All-cause mortality</strong> risk may not increase with BMI 25-30, but may increase <strong>by 30% with BMI >35</strong> (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855514/\" rel=\"nofollow noreferrer\">JAMA, 2013</a> ; <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5401682/\" rel=\"nofollow noreferrer\">Annals of Translational Medicine, 2017</a>).</li>\n<li><strong>Hypertension</strong> risk may increase up to two-fold with BMI 25-30 and <strong>by four-fold with BMI >30</strong> (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3743236/\" rel=\"nofollow noreferrer\">Circulation, 2012</a>).</li>\n<li><strong>Coronary heart disease</strong> risk may increase by 20% with BMI 25-30 and <strong>by 60% with BMI >30</strong> (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/25960160\" rel=\"nofollow noreferrer\">The Lancet Diabetes &amp; Endocrinology, 2015</a> ; <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/26025084\" rel=\"nofollow noreferrer\">Heart, 2015</a>)</li>\n<li>More than 75% individuals with <strong>diabetes type 2</strong> have <strong>BMI >25</strong> (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/23590534\" rel=\"nofollow noreferrer\">Current Diabetes Reviews, 2013</a> ; <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1890993/\" rel=\"nofollow noreferrer\">International Journal of Clinical Practice, 2007</a>).</li>\n<li>The risk of some <strong>cancers</strong> (endometrial, esophageal, gastric, liver) may increase by <strong>two-fold</strong> with obesity (<a href=\"https://www.cancer.gov/about-cancer/causes-prevention/risk/obesity/obesity-fact-sheet\" rel=\"nofollow noreferrer\">National Cancer Institute, 2017</a>).</li>\n<li>The risk of <strong>other conditions,</strong> such as osteoarthritis, gallbladder disease, body pain and difficulty with physical functioning, sleep apnea, depression (<a href=\"https://www.cdc.gov/healthyweight/effects/index.html\" rel=\"nofollow noreferrer\">Centers for Disease Control and Prevention, 2015</a>), fatty liver, pancreatitis and acid reflux (<a href=\"https://www.loc.gov/rr/scitech/SciRefGuides/obesity.html\" rel=\"nofollow noreferrer\">Science Reference Services, 2017</a>) also increases with obesity.</li>\n</ul>\n\n<p><strong>Intentional weight loss and a decreased health risk:</strong></p>\n\n<ul>\n<li><strong>All-cause mortality</strong> may decrease <strong>by up to 33%</strong> with 9-13 kg of weight loss (<a href=\"https://pdfs.semanticscholar.org/c272/0153b4523c02a1bada4f5c224eba8b191c94.pdf\" rel=\"nofollow noreferrer\">Diabetes Care, 2000</a>) or by ~15% with 5.5 kg weigh loss (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4368053/\" rel=\"nofollow noreferrer\">Plos One, 2015</a>); see also <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/29138133\" rel=\"nofollow noreferrer\">BMJ, 2017</a> and <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/15883243\" rel=\"nofollow noreferrer\">The Archives of Internal Medicine, 2005</a>).</li>\n<li>The risk of <strong>heart disease</strong> and <strong>diabetes type 2</strong> may decrease <strong>by 28%</strong> with intentional weight loss <a href=\"https://pdfs.semanticscholar.org/c272/0153b4523c02a1bada4f5c224eba8b191c94.pdf\" rel=\"nofollow noreferrer\">(Diabetes Care, 2000</a>).</li>\n<li><strong>High blood pressure</strong> can decrease by <strong>1 mm Hg</strong> with <strong>1 kg</strong> loss of body weight (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/3070038\" rel=\"nofollow noreferrer\">Journal of Human Hypertension, 1988</a> ; <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/12975389/\" rel=\"nofollow noreferrer\">Hypertension, 2003</a>).</li>\n</ul>\n\n<p>Most studies about weight loss are observational, so it may be difficult to differ between intentional and unintentional weight loss - the later is typically associated with a disease. This is why in several studies weight loss is not associated with health improvement or is even associated with an increased risk of disease (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750037/\" rel=\"nofollow noreferrer\">The Journals of Gerontology, 2007</a> ; <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/20212495b\" rel=\"nofollow noreferrer\">International Journal of Obesity, 2010</a>).</p>\n\n<p><strong>The risks of intentional <em>rapid</em> weight loss:</strong></p>\n\n<ul>\n<li><strong>Gallstones;</strong> in one study, 500 Kcal/day diet was associated with a three-fold greater risk of symptomatic gallstones than 1,200-1,500 Kcal/day diet (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3921672/\" rel=\"nofollow noreferrer\">International Journal of Obesity, 2014</a>).</li>\n<li><strong>Aggressive steatohepatitis</strong> (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5935795/\" rel=\"nofollow noreferrer\">Modern Pathology, 2017</a>)</li>\n</ul>\n\n<hr>\n\n<p><strong>Can the costs of being more stressed outweigh the costs of not losing weight?</strong></p>\n\n<p>It seems that trying to lose weight to improve the quality of life can be more beneficial than just remaining obese.</p>\n" } ]
2019/05/28
[ "https://health.stackexchange.com/questions/19358", "https://health.stackexchange.com", "https://health.stackexchange.com/users/6604/" ]
19,374
<p>Most daily multivitamins have close to 100% of the RDA for each element in the vitamin, and I believe that the nutrients get into your blood in a short time frame.</p> <p>Does this daily spike in vitamins have any known health consequences? It would seem more natural to have them split up into smaller doses and be taken with meals each day.</p> <p>For example, in Japan many vitamins are smaller and designed to be taken a few times over the course of a day. The one-a-day approach most Americans use seems arbitrary and makes me wonder, for example, why we don't take one bigger vitamin every three days (let me ignore the problem of forgetting the day on which we last took vitamins even though it is important here).</p> <p>So are there any health consequences to taking a single multivitamin once a day? Or is a split approach more conducive to absorption and utilization? At what frequency will vitamin blood concentrations start to have unhealthy spikes?</p>
[ { "answer_id": 19384, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": true, "text": "<p>RDA is the recommended dietary allowance. Vitamins and minerals should not cause side effects when you exceed 100% RDA, but they can cause them when you exceed <a href=\"https://ods.od.nih.gov/pubs/conferences/tolerable_upper_intake.pdf\" rel=\"nofollow noreferrer\">\"the tolerable upper intake\" (UI)</a>, which is usually considerably higher than RDA.</p>\n\n<p>According to <a href=\"https://ods.od.nih.gov/factsheets/VitaminC-HealthProfessional/\" rel=\"nofollow noreferrer\">Office of Dietary Supplements</a>, the RDA for vitamin C for adults is 90 mg/day and the UI is 2,000 mg/day. You can also see from the table 2 that a single serving of certain foods can exceed the RDA for vitamin C. Excessive amounts of vitamin C and other water soluble vitamins and minerals are excreted in the urine and the fat-soluble vitamins are stored in the body fat. For a complete list of recommended and upper intakes of all nutrients, you can check these charts on <a href=\"http://nationalacademies.org/hmd/~/media/Files/Report%20Files/2019/DRI-Tables-2019/6_DRIValues_Summary.pdf?la=en\" rel=\"nofollow noreferrer\">nationalacademies.org</a>. They use Dietary Reference Intakes (DRI) instead of RDA, but they are very similar.</p>\n\n<p>Concluding from the big difference between the RDA and UI for most supplements, I don't think you need to split a 100% RDA dose of a supplement into smaller doses to make it \"less harmful.\" Splitting the dose can increase the percent of a supplement that is absorbed, though. For example, RDA for <a href=\"https://ods.od.nih.gov/factsheets/Calcium-HealthProfessional/\" rel=\"nofollow noreferrer\">calcium</a> for adults is 1,300 mg, but the maximal absorption occurs when you take less than 500 mg at once.</p>\n\n<p>Splitting the dose can be more important with prescribed supplements, which usually come in multiple RDA doses. The entire dose of iron can irritate the stomach, calcium can cause constipation, magnesium lose stools, etc. Again, this should not often happen with multivitamins in 100% RDA doses. </p>\n\n<p>Currently, there is no convincing evidence that taking multivitamin supplements would be harmful; healthy people do not need supplements, anyway, and can get all the essential nutrients in appropriate amounts from food (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3309636/\" rel=\"nofollow noreferrer\">PubMed, 2012</a>). </p>\n" }, { "answer_id": 19390, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 2, "selected": false, "text": "<p>In addition to <a href=\"https://medicalsciences.stackexchange.com/a/19384/8728\">Jan's answer</a> it is important to recognize that the biological half-life of most vitamins is quite long, <em>on the order of several days</em>.</p>\n\n<p>This means that you do not really have a spike when you take a multivitamin: the amount of each vitamin already in your body is much higher than the daily intake amount. It is not actually necessary to take the daily recommended intake every day, that's just an amount that, if taken daily, will not result in any long-term deficiencies (assuming otherwise normal absorption/metabolism).</p>\n\n<p>To give an example of one particular vitamin from <a href=\"https://www.ncbi.nlm.nih.gov/books/NBK114313/\" rel=\"nofollow noreferrer\">this book</a>, the estimated body concentration of vitamin B6 is somewhere between 60-160 mg depending on sex and which model they use. Compare this to the recommended daily intake of 1.3 mg (hardly a spike relative to even 60 mg), and the tolerable intake of 100 mg/day (which would indeed be a 'spike', but amounts less than that can be cleared without negative effects in a normal individual).</p>\n" } ]
2019/05/29
[ "https://health.stackexchange.com/questions/19374", "https://health.stackexchange.com", "https://health.stackexchange.com/users/9517/" ]
19,479
<p>I frequently come up with articles about the topic such as this one <a href="https://www.nhs.uk/news/heart-and-lungs/study-says-theres-no-link-between-cholesterol-and-heart-disease/" rel="nofollow noreferrer">https://www.nhs.uk/news/heart-and-lungs/study-says-theres-no-link-between-cholesterol-and-heart-disease/</a>. Now, if there is no link between atherosclerosis and cholesterol then what causes it?</p>
[ { "answer_id": 19384, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": true, "text": "<p>RDA is the recommended dietary allowance. Vitamins and minerals should not cause side effects when you exceed 100% RDA, but they can cause them when you exceed <a href=\"https://ods.od.nih.gov/pubs/conferences/tolerable_upper_intake.pdf\" rel=\"nofollow noreferrer\">\"the tolerable upper intake\" (UI)</a>, which is usually considerably higher than RDA.</p>\n\n<p>According to <a href=\"https://ods.od.nih.gov/factsheets/VitaminC-HealthProfessional/\" rel=\"nofollow noreferrer\">Office of Dietary Supplements</a>, the RDA for vitamin C for adults is 90 mg/day and the UI is 2,000 mg/day. You can also see from the table 2 that a single serving of certain foods can exceed the RDA for vitamin C. Excessive amounts of vitamin C and other water soluble vitamins and minerals are excreted in the urine and the fat-soluble vitamins are stored in the body fat. For a complete list of recommended and upper intakes of all nutrients, you can check these charts on <a href=\"http://nationalacademies.org/hmd/~/media/Files/Report%20Files/2019/DRI-Tables-2019/6_DRIValues_Summary.pdf?la=en\" rel=\"nofollow noreferrer\">nationalacademies.org</a>. They use Dietary Reference Intakes (DRI) instead of RDA, but they are very similar.</p>\n\n<p>Concluding from the big difference between the RDA and UI for most supplements, I don't think you need to split a 100% RDA dose of a supplement into smaller doses to make it \"less harmful.\" Splitting the dose can increase the percent of a supplement that is absorbed, though. For example, RDA for <a href=\"https://ods.od.nih.gov/factsheets/Calcium-HealthProfessional/\" rel=\"nofollow noreferrer\">calcium</a> for adults is 1,300 mg, but the maximal absorption occurs when you take less than 500 mg at once.</p>\n\n<p>Splitting the dose can be more important with prescribed supplements, which usually come in multiple RDA doses. The entire dose of iron can irritate the stomach, calcium can cause constipation, magnesium lose stools, etc. Again, this should not often happen with multivitamins in 100% RDA doses. </p>\n\n<p>Currently, there is no convincing evidence that taking multivitamin supplements would be harmful; healthy people do not need supplements, anyway, and can get all the essential nutrients in appropriate amounts from food (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3309636/\" rel=\"nofollow noreferrer\">PubMed, 2012</a>). </p>\n" }, { "answer_id": 19390, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 2, "selected": false, "text": "<p>In addition to <a href=\"https://medicalsciences.stackexchange.com/a/19384/8728\">Jan's answer</a> it is important to recognize that the biological half-life of most vitamins is quite long, <em>on the order of several days</em>.</p>\n\n<p>This means that you do not really have a spike when you take a multivitamin: the amount of each vitamin already in your body is much higher than the daily intake amount. It is not actually necessary to take the daily recommended intake every day, that's just an amount that, if taken daily, will not result in any long-term deficiencies (assuming otherwise normal absorption/metabolism).</p>\n\n<p>To give an example of one particular vitamin from <a href=\"https://www.ncbi.nlm.nih.gov/books/NBK114313/\" rel=\"nofollow noreferrer\">this book</a>, the estimated body concentration of vitamin B6 is somewhere between 60-160 mg depending on sex and which model they use. Compare this to the recommended daily intake of 1.3 mg (hardly a spike relative to even 60 mg), and the tolerable intake of 100 mg/day (which would indeed be a 'spike', but amounts less than that can be cleared without negative effects in a normal individual).</p>\n" } ]
2019/06/12
[ "https://health.stackexchange.com/questions/19479", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16352/" ]
19,498
<p>When optometrists measure your prescription, they use a machine that switches between different diopters. Except, the lenses on this machine are essentially parallel to the walls and orthogonal to the ground. Whereas, my ears are lower than my eyes, so the 'arms' of my glasses tilt downwards from my eyes to my ears. This means the prescription is kind of bullcrap. Why don't optometrists account for this?</p>
[ { "answer_id": 19500, "author": "Chris Rogers", "author_id": 7951, "author_profile": "https://health.stackexchange.com/users/7951", "pm_score": 1, "selected": false, "text": "<p>Although the tops of your ears maybe below the centre(s) of your eye(s) - you can have one ear lower than the other too - everyone is different. Some may find their ears are above the eye centres.</p>\n\n<p>When receiving your prescription made spectacles you should have them <a href=\"https://www.felixandiris.com/how-to-adjust-glasses.html\" rel=\"nofollow noreferrer\">fitted (adjusted)</a> to fit your specific shape.</p>\n\n<p>The link I provided shows adjustments and slight tweaks you can make yourself and some best done by the opticians.</p>\n\n<p>As well as adjusting the temples for pinching and being too wide &mdash; although if given proper clear advice when choosing your frames, you should have been provided with frames which are the correct width for your face in the first place &mdash; they can be adjusted to accommodate the different ear height by putting a slight bend at the temples either upward or downward.</p>\n" }, { "answer_id": 19521, "author": "kamran", "author_id": 8647, "author_profile": "https://health.stackexchange.com/users/8647", "pm_score": -1, "selected": false, "text": "<p>For measurements the best configuration to avoid errors introduced by slanted, oblique perspective, and misalignment of the axis of your eye lens and the trial lens is what they do.</p>\n\n<p>Later the eyeglass technician has to adjust the angle of handles and the nose rest pads to maintain the correct line up of the lenses.</p>\n\n<p>Contact lenses usually don't have these kinds of issues, unless your eyes corneas have surface bumps or other geometrical issues.</p>\n" } ]
2019/06/15
[ "https://health.stackexchange.com/questions/19498", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16370/" ]
19,532
<p>I am a lay person who wants a broad technical understanding of cancer including a survey of types, their etiologies, epidemiology, treatment modalities, prognoses, and current state of the art research. I have spent hours searching but to my surprise I cannot find a book or documentary or other resource that surveys these topics in spite of the ubiquitous impact of this family of disease. The best I have found is "The Emperor of All Maladies" which is really an historical account, and a few TED talks. Popular books on cancer tend to be aimed at sufferers and an endless litany of miracle cures involving vitamins and diets.</p> <p>I must be overlooking something. How did <strong>you</strong> get up to speed on these diseases? Surely I don't need to go to med school?</p>
[ { "answer_id": 19536, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 1, "selected": false, "text": "<p>You could try the 'For Dummies' range:</p>\n\n<blockquote>\n <p><a href=\"https://www.dummies.com/store-search.html?query=cancer\" rel=\"nofollow noreferrer\">https://www.dummies.com/store-search.html?query=cancer</a></p>\n</blockquote>\n\n<p>which, incidentally, cover a whole range of health issues:</p>\n\n<blockquote>\n <p><a href=\"https://www.dummies.com/health/\" rel=\"nofollow noreferrer\">https://www.dummies.com/health/</a></p>\n</blockquote>\n" }, { "answer_id": 19546, "author": "Fixee", "author_id": 16387, "author_profile": "https://health.stackexchange.com/users/16387", "pm_score": 3, "selected": true, "text": "<p>I've spent a few hours going through the Johns Hopkins short course entitled \"Introduction to the Biology of Cancer\" and which covers almost exactly what I was looking for: major types of cancer (lung, stomach, colon, liver, breast and prostate, but curiously not skin cancer), known causes (spoiler: don't smoke), genetic bases, metastatic process, treatment options, epidemiology, prognoses.</p>\n\n<p>The course uses terms without definition at times, so the student should have a basic understanding of biology (example terms used without definition: \"histology\" and \"allele\"). But that's about it: no chemistry, cellular biology, pathology, statistics, or other background is needed.</p>\n\n<p>My one concern thus far: there seem to be a few misstatements I wouldn't expect from Johns Hopkins professors (and I'm a medical lay person so I could be wrong, but I think it's they who are wrong). Example misstatements:</p>\n\n<ul>\n<li><strong>A variation in nucleotides is called a \"polymorphism\" or a \"single-nucleotide polymorphism\"</strong> (while SNPs are overwhelmingly the most common polymorphisms, there are multiple-nucleotide polymorphisms as well)</li>\n<li><strong>No one else has an exact copy of your DNA</strong> (tell this to an identical twin)</li>\n<li><strong>A \"mutation\" is a detrimental genetic variation that increases the risk of developing a disease</strong> (there are benign mutations (most in fact) as well as beneficial mutations; in fact, beneficial mutations drive the process of evolution)</li>\n</ul>\n\n<p>Am I being too pedantic? Perhaps. Overall, I am deeply grateful I have access to this resource, from experts, for free. The course is available to audit for free through Coursera (<a href=\"https://coursera.org/learn/cancer\" rel=\"nofollow noreferrer\">https://coursera.org/learn/cancer</a>) or you can pay $49 USD if you want to take the exams and get course credit. (I am in no way affiliated with Coursera.)</p>\n" } ]
2019/06/19
[ "https://health.stackexchange.com/questions/19532", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16387/" ]
19,539
<p>CBD-infused shots, beers, and other alcoholic drinks have started to be produced and I have seen claims online that mixing CBD and alcohol can intensify each other’s effects, resulting in changes in mood and behaviour, yet it can help with alcohol addictions.</p> <p>One study of 10 people found that when participants took 200mg of CBD with alcohol, they had significantly lower blood alcohol levels than when they consumed alcohol with a placebo (<a href="https://www.ncbi.nlm.nih.gov/pubmed/120541" rel="nofollow noreferrer">Consroe et al. 1979</a>), however, combining alcohol with CBD caused significant impairments in motor performance and alterations in the perception of time.</p> <blockquote> <p>Compared to placebo, alcohol and alcohol plus CBD, but not CBD alone, produced significant impairments of motor and psychomotor performances, overestimations of time production and subjective responses indicating an accurate self-perception of their intoxication and deficits. The combination of alcohol plus CBD resulted in significantly lower blood alcohol levels compared to alcohol given alone, however, there were few differences observed between the pharmacological effects of the two alcohol conditions.</p> </blockquote> <p><strong>The point I am making is that the study found that although CBD being added to alcohol lowers blood alcohol levels the pharmacological effects of the alcohol remain the same as without CBD.</strong> Although CBD does not have psychoactive effects on its own, it appears to me if I am interpreting the results correctly, that CBD speeds up the metabolization of alcohol, hense lower blood alcohol levels, yet the potency of lower blood alcohol levels is elevated too. Which if you think about it could affect driver blood alcohol testing limits?</p> <p>The last point I made about driver testing is beside the point (in a way), but what I am wondering is <strong>What is the scientific stance on addiction therapy with CBD?</strong></p> <h2>References</h2> <p>Consroe, P., Carlini, E. A., Zwicker, A. P., &amp; Lacerda, L. A. (1979). Interaction of cannabidiol and alcohol in humans. <em>Psychopharmacology, 66</em>(1), 45-50. pmid: <a href="https://www.ncbi.nlm.nih.gov/pubmed/120541" rel="nofollow noreferrer">120541</a></p>
[ { "answer_id": 19536, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 1, "selected": false, "text": "<p>You could try the 'For Dummies' range:</p>\n\n<blockquote>\n <p><a href=\"https://www.dummies.com/store-search.html?query=cancer\" rel=\"nofollow noreferrer\">https://www.dummies.com/store-search.html?query=cancer</a></p>\n</blockquote>\n\n<p>which, incidentally, cover a whole range of health issues:</p>\n\n<blockquote>\n <p><a href=\"https://www.dummies.com/health/\" rel=\"nofollow noreferrer\">https://www.dummies.com/health/</a></p>\n</blockquote>\n" }, { "answer_id": 19546, "author": "Fixee", "author_id": 16387, "author_profile": "https://health.stackexchange.com/users/16387", "pm_score": 3, "selected": true, "text": "<p>I've spent a few hours going through the Johns Hopkins short course entitled \"Introduction to the Biology of Cancer\" and which covers almost exactly what I was looking for: major types of cancer (lung, stomach, colon, liver, breast and prostate, but curiously not skin cancer), known causes (spoiler: don't smoke), genetic bases, metastatic process, treatment options, epidemiology, prognoses.</p>\n\n<p>The course uses terms without definition at times, so the student should have a basic understanding of biology (example terms used without definition: \"histology\" and \"allele\"). But that's about it: no chemistry, cellular biology, pathology, statistics, or other background is needed.</p>\n\n<p>My one concern thus far: there seem to be a few misstatements I wouldn't expect from Johns Hopkins professors (and I'm a medical lay person so I could be wrong, but I think it's they who are wrong). Example misstatements:</p>\n\n<ul>\n<li><strong>A variation in nucleotides is called a \"polymorphism\" or a \"single-nucleotide polymorphism\"</strong> (while SNPs are overwhelmingly the most common polymorphisms, there are multiple-nucleotide polymorphisms as well)</li>\n<li><strong>No one else has an exact copy of your DNA</strong> (tell this to an identical twin)</li>\n<li><strong>A \"mutation\" is a detrimental genetic variation that increases the risk of developing a disease</strong> (there are benign mutations (most in fact) as well as beneficial mutations; in fact, beneficial mutations drive the process of evolution)</li>\n</ul>\n\n<p>Am I being too pedantic? Perhaps. Overall, I am deeply grateful I have access to this resource, from experts, for free. The course is available to audit for free through Coursera (<a href=\"https://coursera.org/learn/cancer\" rel=\"nofollow noreferrer\">https://coursera.org/learn/cancer</a>) or you can pay $49 USD if you want to take the exams and get course credit. (I am in no way affiliated with Coursera.)</p>\n" } ]
2019/06/20
[ "https://health.stackexchange.com/questions/19539", "https://health.stackexchange.com", "https://health.stackexchange.com/users/7951/" ]
19,562
<p>my orthopedist told me I should begin the "Mézières method" for some back problems I have.I looked it up on the Internet to find out what is it but I could not find any research that found it works (i looked it up on google and on google scholar, but I don't know where else to look up). My question is, is there any scientific foundation of this kind of physiotherapy or is it just some alternative medicine like homeopathy or acupuncture?</p>
[ { "answer_id": 19563, "author": "Chris Rogers", "author_id": 7951, "author_profile": "https://health.stackexchange.com/users/7951", "pm_score": 2, "selected": false, "text": "<p>There doesn't seem to be a lot of scientific foundation for it at the moment but <a href=\"https://clinicaltrials.gov/ct2/show/NCT03738306\" rel=\"nofollow noreferrer\">there is a clinical trial</a> on it.</p>\n<p>There is however, one pilot study paper on the effects of 2 physiotherapy programs on pain perception, muscular flexibility, and illness impact (<a href=\"https://www.researchgate.net/profile/B_Fradejas/publication/23719179_Effects_of_2_Physiotherapy_Programs_on_Pain_Perception_Muscular_Flexibility_and_Illness_Impact_in_Women_With_Fibromyalgia_A_Pilot_Study/links/56693b2e08ae9da364ba3f54/Effects-of-2-Physiotherapy-Programs-on-Pain-Perception-Muscular-Flexibility-and-Illness-Impact-in-Women-With-Fibromyalgia-A-Pilot-Study.pdf\" rel=\"nofollow noreferrer\">Valencia et al. 2009</a>). The comparison between kinesiotherapy and active muscular stretching with Global Myofascial Physiotherapy according to the Mézières method found that</p>\n<blockquote>\n<p>Patients had achieved a statistically significant reduction in the severity of the disease and improved their flexibility level by the end of the program, but had returned to initial values after follow-up. Significant differences were not observed between the 2 treatment groups in the initial values or in the results at the end of the program or after the follow-up, so neither program proved better than the other.</p>\n</blockquote>\n<h2>References</h2>\n<p>Valencia, M., Alonso, B., Alvarez, M. J., Barrientos, M. J., Ayán, C., &amp; Sánchez, V. M. (2009). Effects of 2 physiotherapy programs on pain perception, muscular flexibility, and illness impact in women with fibromyalgia: a pilot study. <em>Journal of manipulative and physiological therapeutics, 32</em>(1), 84-92. doi: <a href=\"https://doi.org/10.1016/j.jmpt.2008.07.003\" rel=\"nofollow noreferrer\">10.1016/j.jmpt.2008.07.003</a></p>\n" }, { "answer_id": 19580, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 1, "selected": false, "text": "<p>There doesn't appear to be a lot of actual scientific research on the subject, but you can follow a paper trail for a while:</p>\n\n<p>The Daily Telegraph (an English newspaper) has an <a href=\"https://www.telegraph.co.uk/news/health/4967492/Mezieres-Method-Perfection-isallin-the-body.html\" rel=\"nofollow noreferrer\">article</a> on the subject, and references two people:</p>\n\n<ul>\n<li><a href=\"http://www.positivehealth.com/therapist/joel-carbonnel-alexander-and-mezieres-technique\" rel=\"nofollow noreferrer\">Joel Carbonnel</a></li>\n<li><a href=\"https://www.researchgate.net/scientific-contributions/2127204326_M_Jesel\" rel=\"nofollow noreferrer\">Professor M Jesel</a></li>\n</ul>\n\n<p>The article also states:</p>\n\n<blockquote>\n <p>But in recent years, the University of Strasbourg has taken up the Mézières flag and is developing the therapy under the name Postural Reconstruction.</p>\n</blockquote>\n\n<p>Looking up Postural Reconstruction doesn't get you far either, you arrive at:</p>\n\n<ul>\n<li><a href=\"https://www.britanniabodyworks.com/services/physiotherapy-calgary/postural-reconstruction/https://\" rel=\"nofollow noreferrer\">Britannia Body Works</a></li>\n<li><a href=\"https://www.reconstruction-posturale.com/documentation#articles-et-livres-scientifiques\" rel=\"nofollow noreferrer\">Reconstruction Postural</a></li>\n<li><a href=\"http://www.orthomorphy.co.uk/mezieres/an-overview/\" rel=\"nofollow noreferrer\">Orthomorphy</a></li>\n</ul>\n\n<p>with the only remotely looking scientific article coming from Science Direct:</p>\n\n<blockquote>\n <p><a href=\"https://www.sciencedirect.com/sdfe/pdf/download/eid/1-s2.0-S1779012316303825/first-page-pdf\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/sdfe/pdf/download/eid/1-s2.0-S1779012316303825/first-page-pdf</a></p>\n</blockquote>\n" } ]
2019/06/24
[ "https://health.stackexchange.com/questions/19562", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16407/" ]
19,733
<p>In movies or television, the doctor gets giant heavy clothing iron sized leads. Clashes them together and uses them on the patient that has a flat lined heart and after doing it 1 times per second the patient wakes up.</p> <p>Is it just another dramatic effect? Do doctors/EMT really do this?</p>
[ { "answer_id": 19739, "author": "JohnP", "author_id": 64, "author_profile": "https://health.stackexchange.com/users/64", "pm_score": 4, "selected": true, "text": "<p>While it used to be done, in reality anymore it isn't done as it is possible to damage the equipment by rubbing, and the possibility exists of an accidental discharge between paddles which can be dangerous for everyone around.</p>\n\n<p>In older times, conductive gel was applied directly to the paddles, and doctors/EMT's would rub the paddles together to distribute the gel evenly on the paddles. Now, there are conductive pads that are placed on the patients skin, and the paddles are used against those. </p>\n\n<p><a href=\"https://i.stack.imgur.com/A2MiJ.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/A2MiJ.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Additionally, when you see a flatline on the heart monitor, either the leads have become detached or the patient is in a condition called asystole. Asystole is an absence of any electrical activity in the heart, which means that the defibrillator (Note the name) will not work. When the heart is in a wild jagged line, it is \"fibrillating\", and the paddles work to disrupt that fatal rhythm and restore a normal sinus rhythm.</p>\n" }, { "answer_id": 19742, "author": "Carey Gregory", "author_id": 805, "author_profile": "https://health.stackexchange.com/users/805", "pm_score": 2, "selected": false, "text": "<p>This is additional information for John's otherwise good answer. </p>\n\n<p>Although they're rarely used, it's still common to see paddles on the defibrillators used in EMS at the paramedic level. See those packs on the side of the unit in the photo below? In addition to cables, ECG pads, and defibrillator pads, there are paddles in there along with a tube of conductive gel. I can't ever recall seeing a 12-lead on a paramedic unit that didn't have paddles.</p>\n\n<p><a href=\"https://i.stack.imgur.com/1z3Mw.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/1z3Mw.png\" alt=\"enter image description here\"></a></p>\n\n<p>They're there because EMS doesn't have the luxury of a supply room down the hall. They typically carry extras of all the disposable items, but it's always possible to run out of something because of back-to-back calls, multiple patients, etc. It would be very difficult to explain to your medical director that your patient arrived dead because you ran out of defib pads, and even harder to explain to the family. There can also be situations where pads just can't be used. For example, severe burns to the chest. Pads would tear skin off when they're removed.</p>\n\n<p>There's even a scene showing them being used in this <a href=\"https://youtu.be/YhuMgL2wJ5U?t=65\" rel=\"nofollow noreferrer\">product video</a> (loud volume). </p>\n\n<p>What's not true is the clashing them together part. They're just rubbed against each other to smear the gel evenly on both paddles. There's no clashing. </p>\n" } ]
2019/07/23
[ "https://health.stackexchange.com/questions/19733", "https://health.stackexchange.com", "https://health.stackexchange.com/users/11912/" ]
19,748
<p>It's known that a hormone called TSH (thyroid stimulate hormone) does exist and it's secreted in the pituitary gland. But my question is about a hormone which secreted from the pituitary gland too but it stimulates the <strong>para</strong>thyroid glands. I am asking it because I read <a href="https://www.ncbi.nlm.nih.gov/pubmed/7420044" rel="noreferrer">this article</a> and I'm not sure how the science refers to it currently. </p>
[ { "answer_id": 19925, "author": "Chris", "author_id": 14056, "author_profile": "https://health.stackexchange.com/users/14056", "pm_score": 2, "selected": false, "text": "<p>The pituitary does not have a direct effect on the parathyroid glands.</p>\n\n<blockquote>\n <p>The parathyroid gland and adrenal medulla are not controlled by the\n pituitary but play important roles in calcium metabolism and the\n adrenergic (sympathetic nervous system) function respectively. Source:\n <a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0263931914001598\" rel=\"nofollow noreferrer\">Science Direct</a></p>\n</blockquote>\n\n<p>Although they are located close together, the thyroid and parathyroid glands work independently.</p>\n\n<p>The role of the parathyroid glands is to regulate blood calcium levels. They do this by secreting <a href=\"https://en.m.wikipedia.org/wiki/Parathyroid_hormone\" rel=\"nofollow noreferrer\">parathyroid hormone</a> (PTH) when calcium levels fall, in a negative feedback system.</p>\n\n<p>PTH has the following effects:</p>\n\n<ul>\n<li>Increases release of calcium from bone (by increasing osteoclasts activity)</li>\n<li>Reduces calcium losses in the kidneys</li>\n<li>Increase calcium absorption in the gut</li>\n</ul>\n\n<p>As a result, calcium levels in the blood will be corrected to normal levels.</p>\n\n<p>The hormone <a href=\"https://en.m.wikipedia.org/wiki/Calcitonin\" rel=\"nofollow noreferrer\">calcitonin</a> has the opposite effect of PTH. It is actually secreted by the thyroid gland itself in response to high calcium levels.</p>\n\n<p>Here is a diagram summarising the role of PTH (<a href=\"http://what-when-how.com/acp-medicine/diseases-of-calcium-metabolism-and-metabolic-bone-disease-part-1/\" rel=\"nofollow noreferrer\">source</a>):</p>\n\n<p><a href=\"https://i.stack.imgur.com/mTKfx.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/mTKfx.jpg\" alt=\"Effects of parathyroid hormone\"></a></p>\n\n<p>Here is a basic diagram showing interplaynof parathyroid hormone and calcitonin (<a href=\"http://biology.reachingfordreams.com/biology/endocrine-system/13-thyroid-and-parathyroid-gland-hormons\" rel=\"nofollow noreferrer\">source</a>):</p>\n\n<p><a href=\"https://i.stack.imgur.com/CiiHY.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/CiiHY.png\" alt=\"Parathyroid and calcitonin\"></a></p>\n\n<p>The study you mention relates to cattle and is almost 40 years old. There has been nothing that I can find in human research to suggest the presence of a clinically significant parathyroid-stimulating hormone.</p>\n" }, { "answer_id": 19926, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p>In short: It seems, there is not enough evidence to say that parathyroid-stimulating hormone secreted from the pituitary gland exists in humans. </p>\n\n<p><strong>A) Parathyroid Stimulating Hormone (PTH)</strong></p>\n\n<p>Some texts use the term <strong>parathyroid-stimulating hormone with the acronym PTH</strong> or in a way that suggests they actually meant parathyroid hormone.</p>\n\n<p><a href=\"https://jcs.biologists.org/content/joces/121/21/3581.full.pdf?with-ds=yes\" rel=\"nofollow noreferrer\">Journal of Cell Science (2008)</a>:</p>\n\n<blockquote>\n <p>...and parathyroid hormone-related peptide receptor (PTH1R), whose\n stimulation by <strong>parathyroid stimulating hormone (PTH)</strong> increases the\n intracellular levels of cAMP, IP3, DAG and Ca2+...</p>\n</blockquote>\n\n<p><a href=\"https://www.sciencedirect.com/science/article/pii/S0165032717323893?via%3Dihub\" rel=\"nofollow noreferrer\">Respiratory subtype of panic disorder: Can serum phosphate levels be a possible outcome to group cognitive-behavior therapy? (Journal of Affective Disorders, 2018)</a>:</p>\n\n<blockquote>\n <p>All patients underwent 12 structured sessions of group\n cognitive-behavioral therapy for PD (Otto and Deveney, 2005) and had\n their blood collected at baseline to assess fasting glucose, complete\n blood count, thyroid stimulating hormone, <strong>parathyroid stimulating\n hormone</strong>, ionized calcium, creatinine and phosphate levels.</p>\n</blockquote>\n\n<p><a href=\"https://emedicine.medscape.com/article/1091928-workup\" rel=\"nofollow noreferrer\">Chronic Mucocutaneous Candidiasis Workup (Emedicine, 2017)</a>:</p>\n\n<blockquote>\n <p>Other endocrine screening tests that may be considered include\n follicle-stimulating hormone, luteinizing hormone, prolactin,\n testosterone, <strong>parathyroid-stimulating hormone</strong>, calcium, phosphate,\n magnesium, and short synacthen test.</p>\n</blockquote>\n\n<p><a href=\"https://escholarship.org/content/qt4kq2z97b/qt4kq2z97b.pdf\" rel=\"nofollow noreferrer\">Dermatology Online Journal (2014)</a>:</p>\n\n<blockquote>\n <p>According to current guidelines for high risk patients (i.e. those\n that are genetically confirmed to have MEN-1), annual laboratory\n studies to include calcium, <strong>parathyroid stimulating hormone</strong>,\n prolactin, gastrin...</p>\n</blockquote>\n\n<p><em>^^From this <a href=\"https://www.niddk.nih.gov/health-information/endocrine-diseases/multiple-endocrine-neoplasia-type-1\" rel=\"nofollow noreferrer\">NIDDK article</a>, it is clear that parathyroid hormone is meant above.</em></p>\n\n<hr>\n\n<p><strong>B) Parathyroid Stimulating Hormone (PSH)</strong></p>\n\n<p>I've found a single text that mentions <strong>parathyroid stimulating hormone with the acronym PSH</strong>, in which they clearly suggest it is secreted from the pituitary gland and stimulates the release of parathyroid hormone.</p>\n\n<p><a href=\"https://www.sciencedirect.com/topics/medicine-and-dentistry/intertragic-notch\" rel=\"nofollow noreferrer\">Cranial Endocrine Glands Represented at Intertragic Notch (ScienceDirect, 2014)</a>:</p>\n\n<blockquote>\n <p>103.e Parathyrotrophin Hormones (PSH, Parathyroid-Stimulating Hormone) [IT 2] Location: Found on the most central part of wall of\n intertragic notch, below LM_9.</p>\n \n <p>Function: The parathyroid pituitary hormone PSH regulates parathormone\n release by the parathyroid gland. This point facilitates calcium\n metabolism and reduces muscle tetanus.</p>\n</blockquote>\n\n<p><strong>C)</strong> I haven't found any text in which <strong>parathyroid-stimulating hormone</strong> in <em>humans</em> would be mentioned with the acronym <strong>PTSH</strong> (like in <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/7420044\" rel=\"nofollow noreferrer\">this article</a> linked from the question, which mentions PTSH in <em>cows</em>).</p>\n" } ]
2019/07/24
[ "https://health.stackexchange.com/questions/19748", "https://health.stackexchange.com", "https://health.stackexchange.com/users/7395/" ]
19,770
<p>I've read <a href="https://www.nhs.uk/conditions/obesity/causes/" rel="nofollow noreferrer">https://www.nhs.uk/conditions/obesity/causes/</a> containing the list of many causes of obesity. I'm interested in the numerical distribution, i.e. out of 100 obese people how many eat too many calories, how many have a poor diet and how many don't do enough physical activity. Is data about this available publicly?</p> <p>More specifically, I'd like to get answers to these questions, based on scientific studies:</p> <ul> <li>Out of 100 obese people how many eat more calories than the average healthy, non-obese person of their age and gender?</li> <li>Out of 100 obese people how many have a poorer diet than the average healthy, non-obese person of their age and gender?</li> <li>Out of 100 obese people how many do less physical activity than the average healthy, non-obese person of their age and gender?</li> </ul> <p>By knowing these numbers governments would have a better idea how to fight obesity: e.g. should they promote food with fewer calories, or should they promote physical activity? (However, this is just an example, and in this question I'm interested in the numbers above rather than on the best ways for governments to fight obesity.)</p> <p>I understand that obesity is caused by a combination of factors, and for helping a person become less obese, all factors should be considered personally for them. Nevertheless, I'm still interested in the numbers above.</p> <p>I understand that even these numbers don't paint the full picture, because we don't know e.g. how many of them eat more calories and do less physical activity (at the same time).</p> <p>I also understand that it's possible to eat (a bit) more and not become obese, e.g. if also doing more physical activity.</p> <p>If there are similar factor breakdown numbers available publicly, I'm interested in them.</p>
[ { "answer_id": 19776, "author": "Chris Rogers", "author_id": 7951, "author_profile": "https://health.stackexchange.com/users/7951", "pm_score": 2, "selected": false, "text": "<p>What you are seeking cannot in scientific terms exist. The reason is that obesity is caused by a combination of the issues you are talking about.</p>\n<p>The term &quot;poor diet&quot; is a general term which can mean different things in different circumstances and in different contexts. A diet high in sugars would be very poor for someone who is diabetic, for example, no matter what their weight is.</p>\n<p>As the NHS page you cited points out in simple terms</p>\n<blockquote>\n<p>Obesity is generally caused by eating too much and moving too little.</p>\n</blockquote>\n<p>A poor diet in the context of fighting obesity levels is a diet higher in calories than required.</p>\n<p>If you consume more energy in the form of foods and drink, than you burn off through exercise and physical activity, much of the surplus energy will be stored by the body as fat.</p>\n<p>The energy value of food is measured in units called calories (kcal).</p>\n<p>Generally speaking, the average <strong>physically active</strong> man needs about 2,500 calories a day to maintain a healthy weight, and the average <strong>physically active</strong> woman needs about 2,000 calories a day (See your NHS link).</p>\n<p>If you are more sedentary than the average person, the amount of calories you consume will need to be lower to balance that out.</p>\n<p>Some of calories are burnt off keeping you alive. It's the amount of energy required to maintain basic bodily functions while at rest, such as regulating body temperature, keeping the heart beating, and breathing. This is called the &quot;basal metabolic rate&quot; or BMR and it accounts for about 2/3 of the total calories burned each day.</p>\n<blockquote>\n<p>It's true: just sitting on the couch staring into space requires that you burn some calories (<a href=\"https://www.health.harvard.edu/staying-healthy/burning-calories-without-exercise\" rel=\"nofollow noreferrer\">Harvard Medical School, 2018</a>).</p>\n</blockquote>\n<p>The BMR varies from person to person.</p>\n<blockquote>\n<p>Some people have higher BMRs than others (although this variability is not usually the reason someone is obese or lean). And BMR can vary over time; it may speed up when you're sick or if you've added muscle mass or it may slow down with age or when you're losing weight. In fact, a slowing metabolic rate is one reason dieters have such a hard time continuing to lose weight or tend to regain lost weight. Certain medical conditions (such as thyroid disease) and medications can affect BMR (<a href=\"https://www.health.harvard.edu/staying-healthy/burning-calories-without-exercise\" rel=\"nofollow noreferrer\">Harvard Medical School, 2018</a>).</p>\n</blockquote>\n<p>The remaining calories consumed which is not burnt off at the BMR is what you need to burn off with physical activity, whether it is exercise at a gym or swimming pool, or walking around etc.</p>\n<p>If you burn more calories than you consume, you will lose the excess body fat put on when not exercising.</p>\n<h2>References</h2>\n<p>Harvard Medical School (2018). <em>Burning calories without exercise</em>. Retrieved from: <a href=\"https://www.health.harvard.edu/staying-healthy/burning-calories-without-exercise\" rel=\"nofollow noreferrer\">https://www.health.harvard.edu/staying-healthy/burning-calories-without-exercise</a></p>\n" }, { "answer_id": 19796, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": true, "text": "<p>From the title of the question: What are most probable causes of obesity?</p>\n\n<p>There is a single cause of obesity: greater amount of calories consumed then burned.</p>\n\n<p>From the body of the question: Out of 100 obese people, how many eat more calories, how many are not physically active enough...:</p>\n\n<p>This is not possible to answer because: </p>\n\n<ul>\n<li>High calorie intake alone does not cause obesity. A known US swimmer said that during a certain period he was consuming 8-10,000 calories per day and, apparently, he did not become obese, because of regular training (<a href=\"https://ftw.usatoday.com/2017/06/michael-phelps-diet-12000-calories-myth-but-still-ate-8000-to-10000-quote\" rel=\"nofollow noreferrer\">USA Today</a>).</li>\n<li>A bedridden person with nearly zero physical activity does not become obese if he/she consumes only the amount of calories he/she spends (for example, about 1,500/day).</li>\n<li>The poorest/unhealthiest/most fatty/most sugary diet on the world does not make you obese if it is not hypercaloric, so \"poor diet\" by itself is not a cause but can be a risk factor for obesity.</li>\n<li>Individuals with genetic disorders, such as Down syndrome, become obese only if they consume excessive calories, so genetics alone is not a cause but can be a risk factor for obesity.</li>\n</ul>\n\n<p>Some health organizations that are concerned about public health have made the estimations of the number of overweight/obese individuals by region, sex, etc. They know the risk factors (mentioned above) and they know the trends about how these factors change with time (see below). What they do not know is how many people eat too much and how many do not exercise enough. Such estimations are probably more meaningful on a personal than public level. </p>\n\n<p><strong>Statistics of increased weight at the world level</strong> (<a href=\"https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight\" rel=\"nofollow noreferrer\">World Health Organization, 2016</a>):</p>\n\n<blockquote>\n <ul>\n <li>In 2016, more than 1.9 billion adults (39%), 18 years and older, were overweight. Of these over 650 million (13% of all) were obese.</li>\n <li>Over 340 million children and adolescents aged 5-19 were overweight or obese in 2016.</li>\n <li>41 million children under the age of 5 were overweight or obese in 2016.</li>\n <li>Worldwide obesity has nearly tripled since 1975.</li>\n </ul>\n</blockquote>\n\n<p><em>Overweight: BMI = 25-30; obese = BMI >30. BMI (body mass index) = person's weight in kilograms divided by the square of his height in meters (kg/m2).</em></p>\n\n<p>The following is the closest from what I found about the relationship between calorie intake and the number of obese individuals:</p>\n\n<p><strong>Share of adult men overweight or obese vs. daily supply of calories, 1975 to 2013</strong> (<a href=\"https://ourworldindata.org/obesity\" rel=\"nofollow noreferrer\">Our World in Data</a>):</p>\n\n<p>See <a href=\"https://ourworldindata.org/grapher/share-of-adult-men-overweight-or-obese-vs-daily-supply-of-calories\" rel=\"nofollow noreferrer\">this graph</a>: X axis is daily calorie supply (per capita); Y axis is the percent of overweight or obesity in a country/region. You can see that United States have more than 3,500 calorie supply per capita per day and that more than 70% of their adult males are overweight or obese.</p>\n\n<p>The <strong>trends</strong> of risk factors of obesity, according to <a href=\"https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight\" rel=\"nofollow noreferrer\">World Health Organization</a>:</p>\n\n<blockquote>\n <p>The fundamental cause of obesity and overweight is an energy imbalance\n between calories consumed and calories expended. Globally, there has\n been:</p>\n \n <ul>\n <li>an increased intake of energy-dense foods that are high in fat and</li>\n <li>an increase in physical inactivity due to the increasingly sedentary nature of many forms of work</li>\n </ul>\n</blockquote>\n\n<p>They obviously care only about the <em>trends</em> and not the <em>number</em> of people with increased calorie intake or physical inactivity.</p>\n" }, { "answer_id": 19834, "author": "Count Iblis", "author_id": 856, "author_profile": "https://health.stackexchange.com/users/856", "pm_score": -1, "selected": false, "text": "<p>From both biological plausibility and <a href=\"https://onlinelibrary.wiley.com/doi/abs/10.1002/oby.22556\" rel=\"nofollow noreferrer\">observational evidence</a> one can conclude that Western-style diets are prone to cause obesity due to having an unnaturally high energy density. A problem within the field of nutrition is that biologically unnaturally high energy density diets have become the norm in the civilized world. People who eat a natural diet with a biologically normal energy density can be found in indigenous populations who are isolated from modern civilization, the vast majority of the people in the civilized world don't eat that way. Almost all research on the relation between diet and health involves the diets the people in the civilized world eat. </p>\n\n<p>The gap between these sort of high energy density diet most people in the civilized world eat and a biologically natural low energy density diet is so large that the data of people participating in studies who do eat the latter type of diet would be filtered out as \"implausible outliers\". E.g. many studies use a limit of 1 kg of a single food item as an upper limit. But if you eat 1000 Kcal worth of potatoes you do need to eat 1.3 kg worth of potatoes. That may sound like an impossibly large amount of potatoes to eat, but I (a small guy weighing just 53 kg) regularly eat that amount of potatoes for dinner without problems. Eating large volumes of food is the only way you can get enough calories in the natural world where high energy density foods like cooking oils, butter, cheese etc. don't grow from the trees. </p>\n\n<p>While it seems plausible that only total caloric intake and energy expended due to exercise should be relevant for obesity, we can easily see that there is a problem with biological plausibility here. Consider a group of animals who have a stable body weight who due to some environmental perturbation suddenly need to expend more energy to get their food and the amount of food they get is also a bit less than they used to be getting. If body weight were to be a delicate fine-tuned balance between energy intake and energy expended as a result of exercise, they would starve to death. Even a small imbalance of just 100 Kcal a day less energy intake compared to what's expended would cause a weight loss of 40 kg in 5.5 years. </p>\n\n<p>This calculus must thus be wrong, obviously the fault lies with ignoring feedbacks on the metabolism. As the animal loses weight, it will expend less energy in moving around, but there are also more direct feedback effects. As the fat cells become emptier, they produce different hormones compared to when they were full, and this impacts appetite and it modulates metabolism. A lot is still unknown about such feedbacks on the metabolism, but it's implausible that mammals who burn energy at a fast rate would not modulate their metabolism as a response to their energy reserves, especially at rest when it would affect physical performance the least. </p>\n\n<p>Such feedback mechanisms then keep the body weight stable under natural conditions, they don't only prevent the animal starving to death due to trivial reasons, it also works the other way and and prevent the animal from gaining weight due to eating a bit more on the long term. Weight gain and becoming physically unfit as a consequence is also very dangerous to animals living the wild.</p>\n\n<p>The reason why we are prone to getting obese must then have something to do with our unnatural diet, rather than the energy balance between exercise and calorie intake, unless this energy balance is out of wack much more than what the natural feedback mechanisms can compensate for. The latter cases do occur, our very high energy density foods make it easy to stuff our stomachs with thousands of Kcal worth of food more than would normally fit in there. But most people who complain about gaining weight and try all sorts of diets to lose weight, don't fall into this category.</p>\n\n<p>The typical people who struggle with their weight are people who eat a normal amount of calories, say between 2000 and 2500 Kcal a day, they stop eating before they're full, they feel hungry during the day and try to tolerate that as best as they can not doing that would lead to them gaining weight. So, their problem is that their weight is by far not as stable as that of animals in the wild. The high energy density of the diet plays a direct role on a perception of fullness after a meal but this alone doesn't explain why they need to fine tune the calorie intake to prevent weight gain.</p>\n\n<p>Another relevant property of high energy density foods is that they have a low nutrient density. While we make sure that we do get all the essential vitamins and minerals, we can't be sure whether we get enough to prevent problems that are not acute medical problems, such as the risk of getting obese. One very important component of the diet is fiber. A natural low energy density diet will contain 80 grams of more of fiber per 2500 Kcal. The RDA which takes a high energy density diet where you would get a substantial part of your calories from refined oils as the norm, is 40 grams a day. But most people get only half of that, about 20 grams a day.</p>\n\n<p>What could plausibly go wrong of we eat less than a quarter of the natural amount of fiber our body has evolved to eat? Fibers are food for the intestinal microbes, the lack of fiber <a href=\"https://en.wikipedia.org/wiki/Human_gastrointestinal_microbiota#Obesity_and_metabolic_syndrome\" rel=\"nofollow noreferrer\">has been linked to obesity</a>. The mechanisms proposed in he literature are i.m.o. too simplistic as they appeal to arguments that would bring back the calorie intake finite tuning problem. I.m.o., getting the required amount of fiber allows the body to have a microbiome that it can more easily control to help keep the body weight stable.</p>\n\n<p>As I explained above a stable body weight without having to count calories or count the number of steps you take per day, is essential for long term survival. Mechanisms that keep the body weight stable must thus have evolved. Evolution doesn't care about how exactly such mechanisms are implemented, whether it's purely internally regulated via hormones or via the microbiome with microbes eating more of your food if you eat more. What matters is whether all mechanisms together produce the desired result in a robust way.</p>\n\n<p>The fundamental cause of obesity thus has nothing to do with calorie intake. In fact, putting the blame on calorie intake has led people to reduce portion size which causes people to stick to the extremely unhealthy high energy density diets that cause obesity. To get out of the obesity epidemic we need get the entire population to get gradually used to eating far larger volumes of healthy low energy density foods. </p>\n" } ]
2019/07/27
[ "https://health.stackexchange.com/questions/19770", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16580/" ]
19,774
<p>I need to create easy to read universal list of medical specialties. This goal seems impossible if taking into account subspecialties - in most countries they are pretty different. Since there are no worldwide agreements on how to group specialties, I decided to group it by the medicine branch it belongs to. </p> <p><strong>I need help clarifying what specialties and subspecialties exist, and how they are related.</strong></p> <p>As a basis I took a list of medical branches from wikipedia:</p> <pre><code> Anesthesiology Cardiology Critical care medicine Dentistry Dermatology Emergency medicine Endocrinology Epidemiology First aid Gastroenterology General practice/Family medicine Geriatrics Gynaecology Hematology Hepatology Infectious disease Internal medicine Neurology Nephrology Obstetrics Oncology Ophthalmology Optometry Orthopaedics Otorhinolaryngology Pathology Pediatrics Preventive medicine Psychiatry Pulmonology Radiology Sports medicine Rheumatology Surgery Urology </code></pre> <p>Then I google a list of medical specialties and try to put it all together. This is the first link from google: <a href="https://www.sgu.edu/blog/medical/ultimate-list-of-medical-specialties/" rel="nofollow noreferrer">https://www.sgu.edu/blog/medical/ultimate-list-of-medical-specialties/</a></p> <p>Lets take a look on how do they group <strong>Surgery</strong>:</p> <p><a href="https://i.stack.imgur.com/5Dy6v.png" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/5Dy6v.png" alt="enter image description here"></a></p> <p>They put <strong>Paediatric Surgery</strong> into <strong>Surgery</strong>. Fair enough.</p> <p><a href="https://i.stack.imgur.com/oSrlp.png" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/oSrlp.png" alt="enter image description here"></a> </p> <p>Lets see <strong>Pediatrics</strong> group:</p> <p><a href="https://i.stack.imgur.com/Cwu0E.png" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/Cwu0E.png" alt="enter image description here"></a></p> <p>Almost all specialties constructed as two medical branches joined together: </p> <p><strong>Pediatric Cardiology</strong>, <strong>Pediatric Endocrinology</strong>. Are there any unique specialties in Pediatrics? Why we don't put it into Endocrinology, Cardiology groups? What brach of medicine has more weight when grouping specialties? </p> <p>As I understand, if you are Cardiologist, you can perform Pediatric Cardiology procedures also, and it should be your subspecialty. So for <strong>Surgery</strong> they did right grouping, but for pediatrics, we should leave only those specialties that are unique for this branch of medicine only. </p> <p>And the biggest issue. There are such branches as:</p> <p><strong>Internal medicine</strong></p> <p><strong>General practice/Family medicine</strong></p> <p>Lets take a look at Internal Medicine</p> <p><a href="https://i.stack.imgur.com/zEL3p.png" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/zEL3p.png" alt="enter image description here"></a></p> <p>Almost all specialties just repeat existing medicine branches.</p> <p>Aren't Internal Medicine doctors are more generic? Seems like <code>oncology</code> requires Oncologist, which can have also different areas of expertise, but not Internal Medicine doctor. </p> <p><strong>How can I better conceptualize how specialties and subspecialties are divided up?</strong></p>
[ { "answer_id": 19775, "author": "DoctorWhom", "author_id": 6776, "author_profile": "https://health.stackexchange.com/users/6776", "pm_score": 3, "selected": true, "text": "<p>The best way to answer this would depend on your reason for making the list, which I do not know. Also, I am not sure how to create an international list, as specialties within a country are defined by the training path and board exams, which do differ somewhat between countries. But you do have some misunderstandings on some of the fundamentals of this, and I can at least advise you on those. I can speak from the perspective of the US system.</p>\n\n<h2>The general order of training goes:</h2>\n\n<ol>\n<li>Undergraduate (Bachelor degree)</li>\n<li>Medical School (MD or DO)</li>\n<li>Residency (in a specialty) training by practicing in your field under supervision of \"attending physicians,\" after which you complete a boards exam and are \"board certified\" in that specialty.\n\n<ul>\n<li>After this step you can either apply to enter a FELLOWSHIP or you can go practice in your field independently.</li>\n</ul></li>\n<li>Optional next step: Fellowship (in a subspecialty) where you similarly practice the subspecialty under attendings, and take a boards exam etc.</li>\n</ol>\n\n<p><em>Subspecialties</em> such as Cardiology, Hematology-Oncology, Rheumatology, etc cannot be selected straight out of medical school. You must first complete a residency in Internal Medicine; similarly for Pediatric Cardiology, a residency in Pediatrics.</p>\n\n<p>This list breaks down the specialties from which you can enter specific subspecialties:</p>\n\n<ul>\n<li><a href=\"https://www.abms.org/member-boards/specialty-subspecialty-certificates/\" rel=\"nofollow noreferrer\">https://www.abms.org/member-boards/specialty-subspecialty-certificates/</a></li>\n<li><a href=\"https://www.sgu.edu/blog/medical/ultimate-list-of-medical-specialties/\" rel=\"nofollow noreferrer\">https://www.sgu.edu/blog/medical/ultimate-list-of-medical-specialties/</a></li>\n</ul>\n\n<p>They are too long to copy here, but definitely check it out - it should help a lot to see how it breaks down.</p>\n\n<h2>The specialties referred to as \"generalists\" are NOT the same as GP (General Practice)</h2>\n\n<p>Internal Medicine, Family Medicine, and Pediatrics are specialties. Those residencies are 3 or 4 years long and have a boards exam at the end. An IM, FM, or Peds boarded physician is sometimes referred to as a \"generalist.\" A generalist is NOT the same as a GP (General Practice) physician. </p>\n\n<p><strong>The term \"generalist\" comes from the fact that these specialties practice broadly, rather than focused on a specific narrow field.</strong> FM, IM, and Peds all do learn quite a bit of cardiology, rheumatology, heme-onc, etc and can practice almost everything non-surgical at least at a basic level. But they will refer to a Cardiologist (a subspecialist who spent 3 additional years in a fellowship studying just cardiology AFTER doing 3 years of Internal Medicine) for extremely complex cases, procedures (stents, pacemakers, ablations), and other things not within their scope of practice.</p>\n\n<p>Family Medicine is unique in that it includes adult medicine, pediatric medicine, and basic obstetrics (minus the extensive surgical training that the OB/GYN specialists obtain). From FM you can go to subspecialties like sports med, geriatrics, palliative care, adolescent med... but not cardiology or rheumatology. FM might be considered the broadest specialty of all.</p>\n\n<h2><strong>General Practice</strong> is a special case, and is not a residency (at least not in the USA).</h2>\n\n<p>Internationally, a General Practice physician (GP) functions similarly to a Primary Care Provider in the USA (a PCP, which is generally either IM FM or Peds in the USA), providing \"generalist\" type care of most concerns and chronic disease management, referring to specialists for complex cases etc.</p>\n\n<p>In many countries, it's its own residency. In some, it's what you are after completing the one or two year \"Internship\" type training post-medical-school. Perhaps someone outside the USA can help beef this section up :)</p>\n\n<p>Within the USA, a GP is usually a physician who did a single year of residency (or more, but did not sit for their specialty boards) and applied for a license. They are not boarded in any particular specialty. Many of these have received extensive on-the-job training and are hired to practice in primary care or even in other specialty offices - but aren't boarded.</p>\n\n<h2>When considering medical management of children, they are not just smaller-sized adults.</h2>\n\n<p>That is why all subspecialties branch off of adult medicine (IM) or child medicine (Pediatrics). Slightly different, pediatric surgery (and surgical subspecialties) is usually a subspecialty done AFTER a surgical residency like General Surgery or Orthopedic Surgery.</p>\n\n<h2>There are sometimes multiple ways to arrive at a subspecialty.</h2>\n\n<p>For example, a Pediatric Emergency physician can either go from Emergency Medicine to Peds EM fellowship, or Pediatrics to and EM fellowship. A Geriatrician could have come from either Internal Medicine or Family Medicine. </p>\n\n<h2>Additions:</h2>\n\n<h2>If a doctor is boarded in a subspecialty, then almost certianly she/he is also boarded in a specialty.</h2>\n\n<p>Since a Cardiologist has to go through Internal Medicine to get to Cardiology, the vast majority of them sit for the boards exams for Internal Medicine. </p>\n" }, { "answer_id": 19797, "author": "Patrick Garfjeld Roberts", "author_id": 16599, "author_profile": "https://health.stackexchange.com/users/16599", "pm_score": 2, "selected": false, "text": "<p>To elaborate from a UK perspective, especially regarding two of the comments:</p>\n\n<ol>\n<li>Genera Practitioner is not a “basic level” kind of Doctor in the UK. It has a separate specialist training programme, run by the Royal College of General Practitioners. Broadly, this programme takes about 50% of UK trainees, and produces doctors with a breadth and depth of medical knowledge to manage the primary presentations (the first symptoms a patient seeks help for) of most conditions including medical, surgical and psychiatric pathology. Where they cannot be managed in the community, they refer to specialist (usually hospital based) services. In the UK they have a ‘gate keeper’ role (Google that for lots discussion about how that fits into the UK health system). They are definitely not ‘basic level’, it’s a specialty in its own right. Some General Practitioners also become ‘GPwSI’ (pronounced gypsy), meaning GP with special interest in another specialty e.g. musculoskeletal, cardiology, family planning. They often have an extended role or cross over into some hospital level service provision.</li>\n<li>Not all subspecialties are created equal! There are many ways to become a sleep specialist (in the UK it’s often via Respiratory as well as the route mentioned). ITU can come via anaesthetics and general medicine, breast surgery via general and plastics, hand surgery via Ortho and plastics, spinal surgery via Ortho and Neurosurgery. These ‘interface’ specialties group people with a shared regional interest but bring different skills e.g. the scope of practice for an orthopaedic hand surgeon and a plastic hand surgeons will overlap but not be exactly the same.</li>\n</ol>\n" } ]
2019/07/28
[ "https://health.stackexchange.com/questions/19774", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16582/" ]
19,814
<p>I've heard and read from multiple sources that acne gets worse during the first two weeks of treatment with isotretinoin, but I haven't been able to find an explanation as to why this happens.</p> <p>From the <a href="https://www.aafp.org/afp/2000/1015/p1835.html" rel="nofollow noreferrer">American Academy of Family Physicians</a>:</p> <blockquote> <p>Your acne may get worse when you start using isotretinoin. This usually just lasts for a little while.</p> </blockquote>
[ { "answer_id": 19907, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 0, "selected": false, "text": "<p>This is a concept not unique to <a href=\"https://en.wikipedia.org/wiki/Isotretinoin\" rel=\"nofollow noreferrer\">Isotretinoin</a>, which is that of either:</p>\n\n<ul>\n<li><a href=\"https://en.wikipedia.org/wiki/Desensitization_(medicine)\" rel=\"nofollow noreferrer\">drug sensitivity</a>.</li>\n<li><a href=\"https://en.wikipedia.org/wiki/Drug_allergy\" rel=\"nofollow noreferrer\">drug allergy</a></li>\n<li><a href=\"https://en.wikipedia.org/wiki/Drug_intolerance\" rel=\"nofollow noreferrer\">drug intolerance</a></li>\n</ul>\n\n<p>Drug sensitivity happens as the body reacts to an initial exposure to a drug, before it builds a <a href=\"https://en.wikipedia.org/wiki/Drug_tolerance\" rel=\"nofollow noreferrer\">tolerance</a> to it.</p>\n\n<blockquote>\n <p>A drug allergy is different from an intolerance. A drug intolerance, which is often a milder, non-immune-mediated reaction, does not depend on prior exposure. [WP:Drug Allergy]</p>\n</blockquote>\n" }, { "answer_id": 19969, "author": "Poidah", "author_id": 16700, "author_profile": "https://health.stackexchange.com/users/16700", "pm_score": 3, "selected": true, "text": "<p>Isotretinoin works by reducing the production of the skin's natural oil (sebum) - <a href=\"https://www.netdoctor.co.uk/medicines/skin-hair/a7486/roaccutane-isotretinoin/\" rel=\"nofollow noreferrer\">Netdoctor UK</a>. \nThe half life of isotretinoin is 10-22 hours <a href=\"https://www.semanticscholar.org/paper/A-review-of-three-systemic-retinoids-in-dermatology-Mortazavi-Aghazadeh/5e1d7c4456fa24cff8dd4a87ef768c6fcd85d4ff\" rel=\"nofollow noreferrer\">(Mortazavis et al., 2014)</a>, so it would take about a 5 days to week for the drug to reach steady state. In the meantime as the sebum production reduces, the skin dryness will stimulate the sebum glands to increase production causing a period of short term deterioration due to sebum over-production, before sebum production drops by two to four weeks. Another factor could be is that isotretinoin causes an increase in increase in epidermal cell turnover <a href=\"https://www.researchgate.net/publication/7057374_Epidermal_effects_of_tretinoin_and_isotretinoin_Influence_of_isomerism\" rel=\"nofollow noreferrer\">(Tadini, Gaspar &amp; Campos, 2006)</a>. This can lead to sloughing, peeling, and redness that might make acne appear to be worsening when in fact it is a different skin process altogether.</p>\n\n<p>There is also a more serious complication of starting isotretinoin which is a flare of acne fulminans. Acne fulminans is a severe form of inflammatory acne which usually require steroids resolve. Younger age, male sex and sebaceous retention are significant risk factors for acne fulminans, more specificially if the acne was severe to start with, there is more than 44 facial comedones, 2 facial nodules and presence of truncal acne <a href=\"https://www.jle.com/en/revues/ejd/e-docs/predictive_factors_for_acne_flare_during_isotretinoin_treatment_278096/article.phtml?cle_doc=00043E50\" rel=\"nofollow noreferrer\">(Demircay, Kus &amp; Sur, 2008)</a>. However, now as isotretinoin is started at a lower dose and usually antibiotics and/or steroids are given for those at high risk making acne fulminans a far less common complication. </p>\n\n<p>*References:</p>\n\n<p>Demircay, Z., Sadiye, K., Haydar, S. (2008). <a href=\"https://www.jle.com/en/revues/ejd/e-docs/predictive_factors_for_acne_flare_during_isotretinoin_treatment_278096/article.phtml?cle_doc=00043E50\" rel=\"nofollow noreferrer\">Predictive factors for acne flare during isotretinoin treatment</a>. European Journal of Dermatology. pg 452-6. </p>\n\n<p><sub>\nMortazavi, H., Aghazadeh, N., Ghiasi, M., &amp; Lajevardi, V. (2014). <a href=\"https://www.semanticscholar.org/paper/A-review-of-three-systemic-retinoids-in-dermatology-Mortazavi-Aghazadeh/5e1d7c4456fa24cff8dd4a87ef768c6fcd85d4ff\" rel=\"nofollow noreferrer\">A review of three systemic retinoids in dermatology: Acitretin , isotretinoin and bexarotene.</a> Iranian Journal of Dermatology.\n</sub></p>\n\n<p>Tadini, A., Gaspar, K., &amp; Campos, P. (2006). <a href=\"https://www.researchgate.net/publication/7057374_Epidermal_effects_of_tretinoin_and_isotretinoin_Influence_of_isomerism\" rel=\"nofollow noreferrer\">Epidermal effects of tretinoin and isotretinoin: Influence of isomerism</a>. Die Pharmazie, 61, 453–456.</p>\n" } ]
2019/07/31
[ "https://health.stackexchange.com/questions/19814", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16610/" ]
19,815
<p>So as I understand it, there are two main solutions for male pattern baldness:</p> <p>Finasteride and Minoxidil. </p> <p>Finasteride works by reducing the production of some hormone that is damaging to the follicles, so already I am not a fan since it's a hormone treatment rather than an actual scalp treatment. On the other hand, Minoxidil is a pure scalp treatment. It actually is <em>about</em> your hair and helping it grow.</p> <p>Finasteride is also quite expensive. Minoxidil is far cheaper, since you can buy 3 flasks that will last you several months, while 1 package of Finasteride pills only last 30 days. </p> <p>Finasteride has many (serious) side-effects. There are sexual side-effects, possible risks of prostate cancer, and some men even get boobs. I know the last one is quite rare, but the sexual side-effects are worryingly common. I've read it happens to roughly 5 % of users ... that is <strong>a lot</strong>, in my honest opinion. On the other hand, Minoxidil's worst side-effect is probably some rash or something. </p> <p>So with all this in mind, why in the world would anybody choose Finasteride over Minoxidil? At least one ought to try Minoxidil first, no, and then only go to Finasteride if Minoxidil don't work?</p>
[ { "answer_id": 19907, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 0, "selected": false, "text": "<p>This is a concept not unique to <a href=\"https://en.wikipedia.org/wiki/Isotretinoin\" rel=\"nofollow noreferrer\">Isotretinoin</a>, which is that of either:</p>\n\n<ul>\n<li><a href=\"https://en.wikipedia.org/wiki/Desensitization_(medicine)\" rel=\"nofollow noreferrer\">drug sensitivity</a>.</li>\n<li><a href=\"https://en.wikipedia.org/wiki/Drug_allergy\" rel=\"nofollow noreferrer\">drug allergy</a></li>\n<li><a href=\"https://en.wikipedia.org/wiki/Drug_intolerance\" rel=\"nofollow noreferrer\">drug intolerance</a></li>\n</ul>\n\n<p>Drug sensitivity happens as the body reacts to an initial exposure to a drug, before it builds a <a href=\"https://en.wikipedia.org/wiki/Drug_tolerance\" rel=\"nofollow noreferrer\">tolerance</a> to it.</p>\n\n<blockquote>\n <p>A drug allergy is different from an intolerance. A drug intolerance, which is often a milder, non-immune-mediated reaction, does not depend on prior exposure. [WP:Drug Allergy]</p>\n</blockquote>\n" }, { "answer_id": 19969, "author": "Poidah", "author_id": 16700, "author_profile": "https://health.stackexchange.com/users/16700", "pm_score": 3, "selected": true, "text": "<p>Isotretinoin works by reducing the production of the skin's natural oil (sebum) - <a href=\"https://www.netdoctor.co.uk/medicines/skin-hair/a7486/roaccutane-isotretinoin/\" rel=\"nofollow noreferrer\">Netdoctor UK</a>. \nThe half life of isotretinoin is 10-22 hours <a href=\"https://www.semanticscholar.org/paper/A-review-of-three-systemic-retinoids-in-dermatology-Mortazavi-Aghazadeh/5e1d7c4456fa24cff8dd4a87ef768c6fcd85d4ff\" rel=\"nofollow noreferrer\">(Mortazavis et al., 2014)</a>, so it would take about a 5 days to week for the drug to reach steady state. In the meantime as the sebum production reduces, the skin dryness will stimulate the sebum glands to increase production causing a period of short term deterioration due to sebum over-production, before sebum production drops by two to four weeks. Another factor could be is that isotretinoin causes an increase in increase in epidermal cell turnover <a href=\"https://www.researchgate.net/publication/7057374_Epidermal_effects_of_tretinoin_and_isotretinoin_Influence_of_isomerism\" rel=\"nofollow noreferrer\">(Tadini, Gaspar &amp; Campos, 2006)</a>. This can lead to sloughing, peeling, and redness that might make acne appear to be worsening when in fact it is a different skin process altogether.</p>\n\n<p>There is also a more serious complication of starting isotretinoin which is a flare of acne fulminans. Acne fulminans is a severe form of inflammatory acne which usually require steroids resolve. Younger age, male sex and sebaceous retention are significant risk factors for acne fulminans, more specificially if the acne was severe to start with, there is more than 44 facial comedones, 2 facial nodules and presence of truncal acne <a href=\"https://www.jle.com/en/revues/ejd/e-docs/predictive_factors_for_acne_flare_during_isotretinoin_treatment_278096/article.phtml?cle_doc=00043E50\" rel=\"nofollow noreferrer\">(Demircay, Kus &amp; Sur, 2008)</a>. However, now as isotretinoin is started at a lower dose and usually antibiotics and/or steroids are given for those at high risk making acne fulminans a far less common complication. </p>\n\n<p>*References:</p>\n\n<p>Demircay, Z., Sadiye, K., Haydar, S. (2008). <a href=\"https://www.jle.com/en/revues/ejd/e-docs/predictive_factors_for_acne_flare_during_isotretinoin_treatment_278096/article.phtml?cle_doc=00043E50\" rel=\"nofollow noreferrer\">Predictive factors for acne flare during isotretinoin treatment</a>. European Journal of Dermatology. pg 452-6. </p>\n\n<p><sub>\nMortazavi, H., Aghazadeh, N., Ghiasi, M., &amp; Lajevardi, V. (2014). <a href=\"https://www.semanticscholar.org/paper/A-review-of-three-systemic-retinoids-in-dermatology-Mortazavi-Aghazadeh/5e1d7c4456fa24cff8dd4a87ef768c6fcd85d4ff\" rel=\"nofollow noreferrer\">A review of three systemic retinoids in dermatology: Acitretin , isotretinoin and bexarotene.</a> Iranian Journal of Dermatology.\n</sub></p>\n\n<p>Tadini, A., Gaspar, K., &amp; Campos, P. (2006). <a href=\"https://www.researchgate.net/publication/7057374_Epidermal_effects_of_tretinoin_and_isotretinoin_Influence_of_isomerism\" rel=\"nofollow noreferrer\">Epidermal effects of tretinoin and isotretinoin: Influence of isomerism</a>. Die Pharmazie, 61, 453–456.</p>\n" } ]
2019/08/01
[ "https://health.stackexchange.com/questions/19815", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16611/" ]
19,822
<p>I checked into what ear crystals are made of, and it is Calcium Carbonate. I also checked the main ingredient of the antacid I frequently take for heartburn, and... it is Calcium Carbonate! <strong>My question is: can taking antacids (that have Calcium Carbonate) cause ear crystals to form and grow?</strong></p> <p>I remember from my MRI results, I had some “harmless calcification” in my brain, but they told me it isn’t anything to worry about, it is fairly normal. However, it does seem to lend further credibility to the idea (if it is happening in my brain, why not also my vestibular system). </p> <p><strong>Edit:</strong> To address the concerns in the comments and the answers, I am not seeking medical advice, just wondering if my possible connection of antacids to increased ear crystals is valid. If it is a valid hypothesis, I could follow up with my doctors to see if that is what is happening. This could also help the medical community if it turns out to be a new discovery. I have gone to many doctors and specialists, including two ENT's, and psychologists and no one has been able to properly diagnose me. I appreciate the answers, and will award the bounty to the one I feel is best near the end of the bounty period.</p> <p>This article provides the background for what I am asking: <a href="https://vestibular.org/understanding-vestibular-disorders/types-vestibular-disorders/benign-paroxysmal-positional-vertigo" rel="nofollow noreferrer">https://vestibular.org/understanding-vestibular-disorders/types-vestibular-disorders/benign-paroxysmal-positional-vertigo</a></p>
[ { "answer_id": 19890, "author": "cako", "author_id": 16296, "author_profile": "https://health.stackexchange.com/users/16296", "pm_score": 3, "selected": false, "text": "<p>First of all: This is not an answer related to your described medical condition. Therefore, I will not draw any conclusions regarding your condition.</p>\n\n<p>But, taking calcium carbonate containing antacids is very unlikley a cause for otoconia (\"ear crystals\") to form and/or grow. Actually, the formation of otoconia requires more than just a calcium carbonate source (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/11710459\" rel=\"noreferrer\">1</a>):</p>\n\n<blockquote>\n <p>The fundamental requirements for the production of vertebrate otoconia are availability of calcium and carbonate ions. <strong>However, the activity of these ions in the endolymphatic space is far too low for spontaneous nucleation</strong>. Therefore, mechanisms for localized concentration of the reactants are required, a role typically played in other carbonate-based calcification systems by acidic glycoproteins.</p>\n</blockquote>\n\n<p>Also, the formation of otoconia is a nonrecurring event in the human development (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4482761/\" rel=\"noreferrer\">2</a>):</p>\n\n<blockquote>\n <p>Mammalian otoconia form at late embryonic stages [...].</p>\n</blockquote>\n\n<hr>\n\n<p>References:</p>\n\n<p>(1)\nDevelopment and maintenance of otoconia: biochemical considerations.\n<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/11710459\" rel=\"noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/11710459</a></p>\n\n<p>(2)\nMechanisms of Otoconia and Otolith Development\n<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4482761/\" rel=\"noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4482761/</a></p>\n" }, { "answer_id": 19892, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p>Calcium carbonate from antacids does not appear as calcium carbonate in the ear (or brain). When you take antacids, the gastric acid converts calcium carbonate to calcium chloride.</p>\n\n<blockquote>\n <p>These effect is based on the chemical reaction CaCO3 + 2HCl → CaCl2 +\n H2O + CO2, in which hydrochloric acid and calcium carbonate, the base\n component, form water, carbon dioxide and calcium chloride, therefore\n neutralizing the acid by consuming the H+ radicals (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174013/\" rel=\"nofollow noreferrer\">JCED</a>).</p>\n</blockquote>\n\n<p>When absorbed, calcium chloride appears in the blood as calcium and chloride, the same way as sodium chloride appears as sodium and chloride. </p>\n\n<p><a href=\"https://www.drugs.com/sfx/calcium-carbonate-side-effects.html\" rel=\"nofollow noreferrer\">Drugs.com</a> does not mention any calcium carbonate side effects tat would be related to labyrinth or vertigo.</p>\n\n<p>The search for \"ear crystals\" + \"antacids\" does not give any meaningful results.</p>\n\n<p>If antacids were increasing the risk of ear crystals, this would be clearly mentioned in any serious article about ear crystals. It's not that crystals are formed because of too much calcium carbonate. Crystals are already there, they are part of normal anatomy, so everyone has them, but if they become <em>loose,</em> they can cause dizziness (<a href=\"https://health.clevelandclinic.org/bppv-why-loose-ear-crystals-make-you-dizzy-and-how-to-fix-them/\" rel=\"nofollow noreferrer\">Cleveland Clinic</a>):</p>\n\n<blockquote>\n <p>Three factors make it more likely that ear crystals may loosen:</p>\n \n <ul>\n <li>Age over 65 years</li>\n <li>Head injury</li>\n <li>Viral inner ear infections</li>\n </ul>\n</blockquote>\n\n<p>Anyone who has vertigo that significantly affects his/her life can ask a primary doctor for advice. The doctor may recommend visiting an ENT specialist or neurologist. So, the first step is <strong>to get a proper diagnosis.</strong></p>\n" }, { "answer_id": 19894, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 2, "selected": false, "text": "<p><a href=\"https://en.wikipedia.org/wiki/Otolith\" rel=\"nofollow noreferrer\">Octonium\\Otoliths</a> (also known as ear crystals\\rocks) are a natural part of the <a href=\"https://en.wikipedia.org/wiki/Vestibular_system\" rel=\"nofollow noreferrer\">vestibular system</a>.</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Benign_paroxysmal_positional_vertigo#Cause\" rel=\"nofollow noreferrer\">BPPV</a> is caused by these otoliths coming loose, and so isn't directly related to calcium carbonate intake.</p>\n\n<blockquote>\n <p>BPPV can result from a head injury or simply occur among those who are older. A specific cause is often not found. The underlying mechanism involves a small calcified otolith moving around loose in the inner ear.<br>\n ...<br>\n Within the labyrinth of the inner ear lie collections of calcium crystals known as otoconia or otoliths. In people with BPPV, the otoconia are dislodged from their usual position within the utricle, and migrate over time into one of the semicircular canals (the posterior canal is most commonly affected due to its anatomical position). When the head is reoriented relative to gravity, the gravity-dependent movement of the heavier otoconial debris (colloquially \"ear rocks\") within the affected semicircular canal causes abnormal (pathological) endolymph fluid displacement and a resultant sensation of vertigo. This more common condition is known as canalithiasis. </p>\n</blockquote>\n\n<p>Further research into <a href=\"https://en.wikipedia.org/wiki/Calcium_supplement#Side_effects\" rel=\"nofollow noreferrer\">calcium supplements</a> leads to a hypothesis that they cause <a href=\"https://en.wikipedia.org/wiki/Milk-alkali_syndrome\" rel=\"nofollow noreferrer\">milk-alkali syndrome</a>, which has symptoms similar to BPPV:</p>\n\n<blockquote>\n <p>The most common symptoms (of milk-alkali syndrome) are poor appetite, dizziness, headache, confusion, psychosis, and dry mouth; laboratory tests may show that a person with milk-alkali syndrome has high blood calcium, kidney failure, and metabolic alkalosis.</p>\n</blockquote>\n\n<p>But the basic answer to your question: Can taking antacids (that have Calcium Carbonate) cause ear crystals to form and grow?, is no.</p>\n" } ]
2019/08/01
[ "https://health.stackexchange.com/questions/19822", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16614/" ]
19,823
<p>Dietary fat contains lots of calories, just like carbohydrates.</p> <p>But the metabolic response differs. </p> <p>For example, for ingested fat, the body has a much lower insulin response.</p> <p>Is all the fat you eat metabolised or stored, or does the body have a (protection?) mechanism to respond to large amounts of dietary fat by simply letting it pass straight through?</p>
[ { "answer_id": 19890, "author": "cako", "author_id": 16296, "author_profile": "https://health.stackexchange.com/users/16296", "pm_score": 3, "selected": false, "text": "<p>First of all: This is not an answer related to your described medical condition. Therefore, I will not draw any conclusions regarding your condition.</p>\n\n<p>But, taking calcium carbonate containing antacids is very unlikley a cause for otoconia (\"ear crystals\") to form and/or grow. Actually, the formation of otoconia requires more than just a calcium carbonate source (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/11710459\" rel=\"noreferrer\">1</a>):</p>\n\n<blockquote>\n <p>The fundamental requirements for the production of vertebrate otoconia are availability of calcium and carbonate ions. <strong>However, the activity of these ions in the endolymphatic space is far too low for spontaneous nucleation</strong>. Therefore, mechanisms for localized concentration of the reactants are required, a role typically played in other carbonate-based calcification systems by acidic glycoproteins.</p>\n</blockquote>\n\n<p>Also, the formation of otoconia is a nonrecurring event in the human development (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4482761/\" rel=\"noreferrer\">2</a>):</p>\n\n<blockquote>\n <p>Mammalian otoconia form at late embryonic stages [...].</p>\n</blockquote>\n\n<hr>\n\n<p>References:</p>\n\n<p>(1)\nDevelopment and maintenance of otoconia: biochemical considerations.\n<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/11710459\" rel=\"noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/11710459</a></p>\n\n<p>(2)\nMechanisms of Otoconia and Otolith Development\n<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4482761/\" rel=\"noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4482761/</a></p>\n" }, { "answer_id": 19892, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p>Calcium carbonate from antacids does not appear as calcium carbonate in the ear (or brain). When you take antacids, the gastric acid converts calcium carbonate to calcium chloride.</p>\n\n<blockquote>\n <p>These effect is based on the chemical reaction CaCO3 + 2HCl → CaCl2 +\n H2O + CO2, in which hydrochloric acid and calcium carbonate, the base\n component, form water, carbon dioxide and calcium chloride, therefore\n neutralizing the acid by consuming the H+ radicals (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174013/\" rel=\"nofollow noreferrer\">JCED</a>).</p>\n</blockquote>\n\n<p>When absorbed, calcium chloride appears in the blood as calcium and chloride, the same way as sodium chloride appears as sodium and chloride. </p>\n\n<p><a href=\"https://www.drugs.com/sfx/calcium-carbonate-side-effects.html\" rel=\"nofollow noreferrer\">Drugs.com</a> does not mention any calcium carbonate side effects tat would be related to labyrinth or vertigo.</p>\n\n<p>The search for \"ear crystals\" + \"antacids\" does not give any meaningful results.</p>\n\n<p>If antacids were increasing the risk of ear crystals, this would be clearly mentioned in any serious article about ear crystals. It's not that crystals are formed because of too much calcium carbonate. Crystals are already there, they are part of normal anatomy, so everyone has them, but if they become <em>loose,</em> they can cause dizziness (<a href=\"https://health.clevelandclinic.org/bppv-why-loose-ear-crystals-make-you-dizzy-and-how-to-fix-them/\" rel=\"nofollow noreferrer\">Cleveland Clinic</a>):</p>\n\n<blockquote>\n <p>Three factors make it more likely that ear crystals may loosen:</p>\n \n <ul>\n <li>Age over 65 years</li>\n <li>Head injury</li>\n <li>Viral inner ear infections</li>\n </ul>\n</blockquote>\n\n<p>Anyone who has vertigo that significantly affects his/her life can ask a primary doctor for advice. The doctor may recommend visiting an ENT specialist or neurologist. So, the first step is <strong>to get a proper diagnosis.</strong></p>\n" }, { "answer_id": 19894, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 2, "selected": false, "text": "<p><a href=\"https://en.wikipedia.org/wiki/Otolith\" rel=\"nofollow noreferrer\">Octonium\\Otoliths</a> (also known as ear crystals\\rocks) are a natural part of the <a href=\"https://en.wikipedia.org/wiki/Vestibular_system\" rel=\"nofollow noreferrer\">vestibular system</a>.</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Benign_paroxysmal_positional_vertigo#Cause\" rel=\"nofollow noreferrer\">BPPV</a> is caused by these otoliths coming loose, and so isn't directly related to calcium carbonate intake.</p>\n\n<blockquote>\n <p>BPPV can result from a head injury or simply occur among those who are older. A specific cause is often not found. The underlying mechanism involves a small calcified otolith moving around loose in the inner ear.<br>\n ...<br>\n Within the labyrinth of the inner ear lie collections of calcium crystals known as otoconia or otoliths. In people with BPPV, the otoconia are dislodged from their usual position within the utricle, and migrate over time into one of the semicircular canals (the posterior canal is most commonly affected due to its anatomical position). When the head is reoriented relative to gravity, the gravity-dependent movement of the heavier otoconial debris (colloquially \"ear rocks\") within the affected semicircular canal causes abnormal (pathological) endolymph fluid displacement and a resultant sensation of vertigo. This more common condition is known as canalithiasis. </p>\n</blockquote>\n\n<p>Further research into <a href=\"https://en.wikipedia.org/wiki/Calcium_supplement#Side_effects\" rel=\"nofollow noreferrer\">calcium supplements</a> leads to a hypothesis that they cause <a href=\"https://en.wikipedia.org/wiki/Milk-alkali_syndrome\" rel=\"nofollow noreferrer\">milk-alkali syndrome</a>, which has symptoms similar to BPPV:</p>\n\n<blockquote>\n <p>The most common symptoms (of milk-alkali syndrome) are poor appetite, dizziness, headache, confusion, psychosis, and dry mouth; laboratory tests may show that a person with milk-alkali syndrome has high blood calcium, kidney failure, and metabolic alkalosis.</p>\n</blockquote>\n\n<p>But the basic answer to your question: Can taking antacids (that have Calcium Carbonate) cause ear crystals to form and grow?, is no.</p>\n" } ]
2019/08/01
[ "https://health.stackexchange.com/questions/19823", "https://health.stackexchange.com", "https://health.stackexchange.com/users/9721/" ]
19,882
<p>Granted this question may seem quite specific to me as I'm unsure if the general public have a similar effect to these foods as I do.</p> <p>When I consume basmati rice, 100g provides about 120 calories according to the back of the pack. However that 100g fills me up for a good few hours. But when I consume Avocados, I can eat 2 avocados which consist of 500 calories and still be hungry after.</p> <p>So doesn't this suggest that eating carbs is better for fat loss than dietary fat, as carbs are more filling and less calories dense. However, I see several diets cut out carbs in order to aid with fat loss.</p> <p>I've seen answers from propel suggesting carbs are non-filling whereas fat is, but I've not noticed this.</p> <p>If anyone could please enlighten me on whether carbs are better to consume than fat for fat loss or if fat is better. Or even if neither matters as I just need to find the right balance for a caloric deficit each day.</p>
[ { "answer_id": 19884, "author": "Zui Muss", "author_id": 16676, "author_profile": "https://health.stackexchange.com/users/16676", "pm_score": 3, "selected": true, "text": "<p>One important factor is that you have to be certain that your weight caused not by sickness or disorder, i.e. doctor told you that weight gain caused only by improper food intake.</p>\n\n<p>The short and general answer is that weight control is not directly intuitive link between sugar and \"fat\" intake and outcomes in weight measurements. E.g. wikipedia article on <a href=\"https://en.wikipedia.org/wiki/Glycemic_index#Weight_control\" rel=\"nofollow noreferrer\">Glycemic index</a> gives next suggestion:</p>\n\n<blockquote>\n <p>Dietary replacement of saturated fats by carbohydrates with a low glycemic index may be beneficial for <strong>weight control</strong>, whereas substitution with refined, high glycemic index carbohydrates is not.[20] A Cochrane review found that adoption of low glycemic index (or load) diets by people who are overweight or obese leads to more weight loss (and better fat control) than use of diets involving higher glycemic index/load or other strategies.[21] Benefits were apparent even with low glycemic index/load diets that allow people to eat as much as they like.[21] The authors of the review concluded that \"Lowering the glycaemic load of the diet appears to be an effective method of promoting weight loss and improving lipid profiles and can be simply incorporated into a person's lifestyle.\"[21]</p>\n</blockquote>\n\n<p>As you may have found from same article, most of white rice (and basmati is one of them) is high GI food and hence is NOT good for your weight. </p>\n\n<p>The other factor is cholesterol intake and its impact on your weight. Very short answer is - avoid animal fat and red meat, and rely on plant (olive preferably) oils as source of needed components. Red meat better be substituted by fish and poultry.</p>\n\n<p>That said, ask for appointment to dietologist or nutritionist, as you get confused even on simplistic factors, while you might need professional advise.</p>\n" }, { "answer_id": 19887, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p>Technically, the only thing needed for weight loss is <strong>a caloric deficit.</strong></p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2763382/\" rel=\"nofollow noreferrer\">Comparison of Weight-Loss Diets with Different Compositions of Fat, Protein, and Carbohydrates (NEJM, 2009)</a>:</p>\n\n<blockquote>\n <p>Reduced-calorie diets result in clinically meaningful weight loss\n regardless of which macronutrients they emphasize.</p>\n</blockquote>\n\n<p>The other question is, which foods are most <strong>satiating.</strong></p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359496/\" rel=\"nofollow noreferrer\">Diets with High or Low Protein Content and Glycemic Index for Weight-Loss Maintenance (NEJM, 2010)</a>:</p>\n\n<blockquote>\n <p>In this large European study, <strong>a modest increase in protein content\n and a modest reduction in the glycemic index</strong> led to an improvement\n in study completion and maintenance of weight loss.</p>\n</blockquote>\n\n<p>Here is one <a href=\"https://www.health.harvard.edu/diseases-and-conditions/glycemic-index-and-glycemic-load-for-100-foods\" rel=\"nofollow noreferrer\">list of foods with glycemic index values</a>.</p>\n\n<p>Some reasoning why some macronutrients could be more satiating than others:</p>\n\n<ul>\n<li>Proteins and fats can be more satiating than carbs because they stay in the stomach for a longer time, so they are more filling.</li>\n<li>Slowly absorbed carbohydrates (whole grains and legumes) may be more satiating than the quickly absorbed carbohydrates (plain starch from white bread, rice and cornflakes, and potatoes), again, because they are more filling.</li>\n</ul>\n\n<p>There are a lot of studies about the effect of low-carb/high fat and low-fat/high carbs on the satiety and weight loss, which are, in summary, very confusing, so I won't discuss this further.</p>\n\n<p>These were some theories, what about practice?</p>\n\n<ul>\n<li>Try to find a food pattern that will become your usual long-term diet, not just a temporary weight loss diet. Include foods you like. </li>\n<li>Avoid/limit liquid calories (soda, fruit juice, alcohol) and other \"quick calories\" from sweets, like chocolate, and other energy-dense foods (fast food).</li>\n</ul>\n\n<p>In conclusion, listen your body and do what works for you and do not overthink the macronutrient ratios.</p>\n" }, { "answer_id": 19896, "author": "Zebrafish", "author_id": 15569, "author_profile": "https://health.stackexchange.com/users/15569", "pm_score": 1, "selected": false, "text": "<p>When you eat 100 g of basmati rice and take on 120 calories you've had a \"meal/snack\" that's 1.2 calories/g (calories per gram) in energy density. An avocado might be <a href=\"https://www.verywellfit.com/calories-in-an-avocado-3495640\" rel=\"nofollow noreferrer\">136 grams in weight</a> (without seed) and contain 227 calories. If you eat two avocados then you can calculate that (assuming these numbers are accurate) you've eaten 272 grams (136 g x 2) of avocados and taken on roughly 500 calories of energy. This ends up being an energy density of 1.8 calories/g. What this means is that you can eat 50% more rice (as opposed to avocados, by weight) for the same amount of energy intake. Or another way of thinking of it, if you're eating basmati rice you can eat 150% the weight of the avocados for the same energy intake.</p>\n\n<p>The difference in fat intake will be 42 grams from the avocados and almost none from the rice.</p>\n\n<p>I also hear often that fats and proteins are more filling than carbohydrates, but I can only say that that's something I've \"heard\". I don't know if the research is decisive on this topic.</p>\n\n<p>Also, remember that there are many many different factors to this issue. Just to mention one when it comes to dieting, there's something called the <a href=\"https://en.wikipedia.org/wiki/Specific_dynamic_action\" rel=\"nofollow noreferrer\">\"thermic effect of food\"</a> (also known by a number of other names, including \"food-induced thermogenesis\"). Basically everything you eat requires energy from your body to metabolize that food. You probably would have heard the factoid that eating celery makes your body burn more calories than are contained in the celery, making it a <a href=\"https://en.wikipedia.org/wiki/Negative-calorie_food\" rel=\"nofollow noreferrer\">negative-calorie food</a>. Leaving aside whether this is true or not, this is based on that idea of the thermic effect of food. The thermic effect of eating carbohydrates and fats that is reported will depend on which study you read, and will likely vary on the type of person (what body composition they have, age etc.) and the type of fat you're talking about.</p>\n\n<p>As I said, there are many different factors, including psychological ones about what foods feel more filling to you, but one last one I'll mention is the fact that your two avocados will have about 18 grams of fiber as opposed to a maximum of 2 grams of fiber from the basmati rice. A generally accepted effect of dietary fiber, whether soluble or insoluble is that it:</p>\n\n<blockquote>\n <p>Increases food volume without increasing caloric content to the same extent as digestible carbohydrates, providing satiety which may reduce appetite. <br>\n <a href=\"https://en.wikipedia.org/wiki/Dietary_fiber#Effects_of_fiber_intake\" rel=\"nofollow noreferrer\">Dietary fiber - Effects of fiber intake (Wikipedia article)</a></p>\n</blockquote>\n\n<p>and</p>\n\n<blockquote>\n <p>Aids in achieving healthy weight. High-fiber foods tend to be more filling than low-fiber foods, so you're likely to eat less and stay satisfied longer.<br>\n <a href=\"https://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/fiber/art-20043983\" rel=\"nofollow noreferrer\">mayoclinic.org</a></p>\n</blockquote>\n\n<p>Here is a <a href=\"https://nutritiondata.self.com/\" rel=\"nofollow noreferrer\">good site</a> where you can compare nutrition data of different foods. Just be careful when reading information because cooked and uncooked cereals, such as pasta and rice, have a difference of \"about\" three times in their values (can be more or less, depending how you cook it). </p>\n" } ]
2019/08/11
[ "https://health.stackexchange.com/questions/19882", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16674/" ]
19,904
<p>I <a href="https://www.nih.gov/news-events/nih-research-matters/smoking-bladder-cancer" rel="nofollow noreferrer">read online</a> that smoking could cause bladder damage such as cancer, but I wasn't able to find if the problem is the nicotine or the other additives found in cigarette smoke that causes the damage.</p> <p>Could other sources of smoke (bonfire, paper fire, forest fire, etc) cause the same issues?</p>
[ { "answer_id": 19935, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 0, "selected": false, "text": "<p>According to <a href=\"https://en.wikipedia.org/wiki/Bladder_cancer#Causes\" rel=\"nofollow noreferrer\">Wikipedia</a>, <a href=\"https://en.wikipedia.org/wiki/2-Naphthylamine\" rel=\"nofollow noreferrer\">2-Naphthylamine</a> is the <a href=\"https://en.wikipedia.org/wiki/Carcinogen\" rel=\"nofollow noreferrer\">carcinogen</a> responsible</p>\n\n<blockquote>\n <p>Thirty percent of bladder tumors probably result from occupational exposure in the workplace to carcinogens such as benzidine. <strong>2-Naphthylamine, which is found in cigarette smoke, has also been shown to increase bladder cancer risk</strong>. Occupations at risk are bus drivers, rubber workers, painters, motor mechanics, leather (including shoe) workers, blacksmiths, machine setters, and mechanics.[14][15] Hairdressers are thought to be at risk as well because of their frequent exposure to permanent hair dyes.</p>\n</blockquote>\n\n<p>which is backed up here:</p>\n\n<blockquote>\n <p><a href=\"https://www.cdc.gov/niosh/npg/npgd0442.html\" rel=\"nofollow noreferrer\">https://www.cdc.gov/niosh/npg/npgd0442.html</a></p>\n</blockquote>\n" }, { "answer_id": 19937, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 0, "selected": false, "text": "<p>There is some evidence that <strong>firefighters</strong> are at increased risk of bladder cancer, but more likely of testicular and prostate cancer and non-Hodghkin lymphoma (<a href=\"https://www.ncbi.nlm.nih.gov/books/NBK326822/\" rel=\"nofollow noreferrer\">IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 98.</a>).</p>\n" }, { "answer_id": 19940, "author": "Chris Rogers", "author_id": 7951, "author_profile": "https://health.stackexchange.com/users/7951", "pm_score": 1, "selected": false, "text": "<p>The report you have linked to also states:</p>\n\n<blockquote>\n <p>The composition of cigarettes has also changed in the past few decades. While there have been reductions in tar and nicotine, the concentrations of other cancer-causing compounds have increased.</p>\n</blockquote>\n\n<p>So it does look like the increase in cases may be down to carcinogens other than nicotine and tar, but don't forget that nicotine and tar are still present so they can still have an effect.</p>\n\n<p>The US <a href=\"https://www.cancer.gov/about-cancer/causes-prevention/risk/tobacco/cessation-fact-sheet#r5\" rel=\"nofollow noreferrer\">National Cancer Institute points out</a> that:</p>\n\n<blockquote>\n <p>Of the more than 7,000 chemicals in tobacco smoke, at least 250 are known to be harmful, including hydrogen cyanide, carbon monoxide, and ammonia.</p>\n \n <p>Among the 250 known harmful chemicals in tobacco smoke, at least 69 can cause cancer.</p>\n</blockquote>\n\n<p>They also cited a report of the Surgeon General (<a href=\"http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf\" rel=\"nofollow noreferrer\">US Department of Health and Human Services, 2014</a>). Page 228 has a big list of carcinogens in cigarettes and from page 30 the document describes how the different forms of tobacco burning during smoking creates other carcinogens and harmful materials.</p>\n\n<p>Whilst it is suggested in another answer that 2-Naphthylamine is the cause, <a href=\"https://www.cancer.org/cancer/bladder-cancer/causes-risks-prevention/risk-factors.html\" rel=\"nofollow noreferrer\">arsenic can cause bladder cancers</a> which is also found in cigarette smoke (see page 41 of the Surgeon General's report) so you can't point to just 2-Naphthylamine.</p>\n\n<p>The link above also points out many other factors which can lead to bladder cancer.</p>\n\n<h2>References</h2>\n\n<p>US Department of Health and Human Services. (2014). The health consequences of smoking—50 years of progress: a report of the Surgeon General. Retrieved from: <a href=\"http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf\" rel=\"nofollow noreferrer\">http://www.surgeongeneral.gov/library/reports/50-years-of-progress/full-report.pdf</a></p>\n" } ]
2019/08/15
[ "https://health.stackexchange.com/questions/19904", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16692/" ]
19,963
<p>The UKPDS 50 study suggested that smokers experience <em>lower</em> rates of diabetic retinopathy</p> <blockquote> <p>Somewhat counter-intuitively, smoking status was inversely related to the development of new lesions and to the progression of established retinopathy. This finding is not likely to be chance alone because of the strength of the association. It, however, is at variance with much of the published epidemiology of diabetic retinopathy.</p> <p>There could be quite specific reasons for the effect of smoking that we describe here; perhaps the associ- ation of smoking with lower blood pressure [36] might have accounted for the univariate reduction. The presence of the effect in the multivariate model suggests that there could be an independent effect, perhaps the pharmacological effect of nicotine itself or of one of the many other active compounds found in tobacco smoke.<sup>*</sup><br /> <sup><sub> * Referencing: Solberg Y, Rosner M, Belkin M 1998) The association between cigarette smoking and ocular diseases. Surv Ophthalmol May-Jun 42 6): 535–47.</sub></sup><br /> <sub>–– I. M. Stratton &amp; E. M. Kohner et al.: &quot;UKPDS 50: Risk factors for incidence and progression of retinopathy in Type II diabetes over 6 years from diagnosis&quot;, Diabetologia, 2001) 44: 156–163.</sub><br /> <a href="https://www.researchgate.net/profile/Irene_Stratton/publication/12061775_UKPDS_50_Risk_factors_for_incidence_and_progression_of_retinopathy_in_Type_II_diabetes_over_6_years_from_diagnosis/links/0deec529984412dd76000000/UKPDS-50-Risk-factors-for-incidence-and-progression-of-retinopathy-in-Type-II-diabetes-over-6-years-from-diagnosis.pdf" rel="nofollow noreferrer">Free full-text of the article</a></p> </blockquote> <p><strong>Is anyone aware of any potentially therapeutic compounds in cigarette smoke?</strong></p> <p><em>(please note: I am absolutely not suggesting people should smoke. I'm wondering if - somewhere among the 10,000 harmful chemicals in cigarette smoke - there may be a novel class of compounds which could help treat disease, if it were extracted / purified / synthesised)</em></p>
[ { "answer_id": 19966, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p>In short: In some studies, smoking was associated with reduced risk of retinopathy only in individuals with diabetes type 2, but with an increased risk in those with type 1. In diabetes type 2, nicotine may further increase insulin levels, which may be protective against retinopathy. </p>\n\n<p>In this study <a href=\"https://www.researchgate.net/profile/Irene_Stratton/publication/12061775_UKPDS_50_Risk_factors_for_incidence_and_progression_of_retinopathy_in_Type_II_diabetes_over_6_years_from_diagnosis/links/0deec529984412dd76000000/UKPDS-50-Risk-factors-for-incidence-and-progression-of-retinopathy-in-Type-II-diabetes-over-6-years-from-diagnosis.pdf\" rel=\"nofollow noreferrer\">UKPDS 50: Risk factors for incidence and progression of retinopathy in Type II diabetes over 6 years from diagnosis\", Diabetologia, 2001)</a> they have found an association between diabetic retinopathy and:</p>\n\n<ul>\n<li>High blood glucose levels</li>\n<li>High blood pressure</li>\n<li>Not smoking</li>\n</ul>\n\n<p>The authors of the study concluded:</p>\n\n<blockquote>\n <p>Somewhat counter-intuitively, <strong><em>smoking status was inversely related to\n the development of new lesions and to the progression of established\n retinopathy.</em></strong> This finding is not likely to be chance alone because of\n the strength of the association. <strong><em>It, however, is at variance with\n much of the published epidemiology of diabetic retinopathy.</em></strong></p>\n</blockquote>\n\n<p><strong>Studies with <em>no or mild positive association</em> between smoking and diabetic retinopathy:</strong></p>\n\n<p><a href=\"https://diabetes.diabetesjournals.org/content/26/1/46\" rel=\"nofollow noreferrer\">Diabetes, 1977</a>: \"The numbers of patients with proliferative retinopathy rose with increasing tobacco consumption.\"</p>\n\n<p><a href=\"https://academic.oup.com/aje/article-abstract/118/2/228/48956?redirectedFrom=PDF\" rel=\"nofollow noreferrer\">American Journal of Epidemiology, 1983</a>: \"These data suggest that there is no excess risk of retinopathy in smokers or ex-smokers when contrasted with those who never smoked.\"</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/4085172\" rel=\"nofollow noreferrer\">Diabetes Research, 1985</a>: \"Cigarette smoking was related to retinopathy in men but not in women.\"</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/3758532\" rel=\"nofollow noreferrer\">Diabetologia, 1986</a>: \"Proliferative retinopathy was present in 12.5% of the smoking and in 6.8% of the non-smoking patients [with diabetes type 1].\"</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/2060413\" rel=\"nofollow noreferrer\">Diabetes Care, 1991</a>: \"Smoking is not likely to be an important risk factor for diabetic retinopathy.\"</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/8841303\" rel=\"nofollow noreferrer\">Ophtalmology, 1996</a> \"Cigarette smoking is not a risk factor for the long-term incidence of retinopathy.\"</p>\n\n<p><a href=\"https://www.karger.com/Article/PDF/350813\" rel=\"nofollow noreferrer\">Karger, 2013</a>: \"We found neither a beneficial nor a harmful effect of smoking on long-term incidence\" [in diabetes type 1].</p>\n\n<p><a href=\"https://care.diabetesjournals.org/content/35/3/556\" rel=\"nofollow noreferrer\">Diabetes Care, 2012</a>, <a href=\"https://care.diabetesjournals.org/content/40/3/412\" rel=\"nofollow noreferrer\">Diabetes Care, 2017</a>, <a href=\"https://bmjopen.bmj.com/content/7/9/e016280\" rel=\"nofollow noreferrer\">BMJ, 2017</a>: They don't even mention smoking as a risk factor.</p>\n\n<p><strong>Studies with <em>negative association</em> between smoking and diabetic retinopathy:</strong></p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/6881128\" rel=\"nofollow noreferrer\">American Journal of Epidemiology, 1983</a>: \"In participants diagnosed before age 30, the relative risk for the presence of retinopathy in smokers compared with those who had never smoked was 1.06 (95% confidence limits (CL) 0.97-1.18); <em>in participants diagnosed at 30 years or older it was 0.89.</em>\" </p>\n\n<p><a href=\"https://link.springer.com/article/10.1007%2Fs12020-018-1697-y\" rel=\"nofollow noreferrer\">A meta analysis in Endocrine, 2018</a>: \"Compare with non-smokers, the risk of diabetic retinopathy significantly increased in smokers with type 1 diabetes while <em>significantly decreased in smokers with type 2 diabetes.</em>\"</p>\n\n<p><strong>Possible explanation:</strong> In the study mentioned in the question <a href=\"https://www.researchgate.net/profile/Irene_Stratton/publication/12061775_UKPDS_50_Risk_factors_for_incidence_and_progression_of_retinopathy_in_Type_II_diabetes_over_6_years_from_diagnosis/links/0deec529984412dd76000000/UKPDS-50-Risk-factors-for-incidence-and-progression-of-retinopathy-in-Type-II-diabetes-over-6-years-from-diagnosis.pdf\" rel=\"nofollow noreferrer\">UKPDS 50</a> and in the <a href=\"https://link.springer.com/article/10.1007%2Fs12020-018-1697-y\" rel=\"nofollow noreferrer\">2018 meta analysis</a>, <strong>smoking was negatively associated with retinopaty only in individuals with <em>diabetes type 2.</em></strong> In diabetes type 2 with elevated insulin levels, nicotine could further increases insulin levels (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/8790020\" rel=\"nofollow noreferrer\">Circulation, 1996</a>), which could be protective against retinopathy (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546345/\" rel=\"nofollow noreferrer\">Cell Metabolism, 2014, Fig. 1</a>):</p>\n\n<p><a href=\"https://i.stack.imgur.com/u52oR.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/u52oR.jpg\" alt=\"enter image description here\"></a></p>\n\n<p><strong>PYRAZINES</strong></p>\n\n<p>A part of diabetic retinopathy pathophysiology is that excessive glucose is converted to sorbitol, which is trapped in the retinal cells and damages them (<a href=\"https://www.hindawi.com/journals/isrn/2013/343560/\" rel=\"nofollow noreferrer\">Hindawi</a>). <a href=\"https://tobaccocontrol.bmj.com/content/25/4/444\" rel=\"nofollow noreferrer\">Pyrazines</a>, which appear as additives in tobacco, can stimulate the clearance of sorbitol by converting it to fructose; they can also lower blood glucose and increase insulin levels (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/1970847\" rel=\"nofollow noreferrer\">Metabolism</a>, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3252962/\" rel=\"nofollow noreferrer\">British Journal of Pharmacology</a>), all of which may help prevent retinopathy. Fenugreek is high in pyrazine (<a href=\"https://pubchem.ncbi.nlm.nih.gov/compound/pyrazine\" rel=\"nofollow noreferrer\">PubChem</a>).</p>\n\n<p>In one systematic review of Chinese herbal medicines, including the ones with pyrazine, the authors were not able to make any conclusions about their effectiveness in diabetic retinopathy (<a href=\"http://www.ccmu.edu.cn/docs/20190221143615941927.pdf\" rel=\"nofollow noreferrer\">Cochrane, 2018</a>).</p>\n\n<p><strong>Tetramethylpyrazine (Ligustrazine)</strong></p>\n\n<p>Studies about potential beneits of tetramethylpyrazine on retina.</p>\n\n<ul>\n<li><a href=\"http://www.ccmu.edu.cn/docs/20190221143615941927.pdf\" rel=\"nofollow noreferrer\">Single herbal medicine for diabetic retinopathy (Cochrane, 2018)</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4613279/\" rel=\"nofollow noreferrer\">Tetramethylpyrazine Protects Retinal Capillary Endothelial Cells (TR-iBRB2) against IL-1β-Induced Nitrative/Oxidative Stress (International Journal of Molecular Science, 2015)</a></li>\n<li><a href=\"https://link.springer.com/article/10.1007/s12177-009-9024-8\" rel=\"nofollow noreferrer\">Neural protection by naturopathic compounds—an example of tetramethylpyrazine from retina to brain (Journal of Ocular Biology, Diseases, and Informatics, 2009)</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2675694/\" rel=\"nofollow noreferrer\">Protective effects of tetramethylpyrazine on rat retinal cell cultures (Neurochemistry International, 2008)</a></li>\n<li><a href=\"https://onlinelibrary.wiley.com/doi/full/10.1111/jnc.13970\" rel=\"nofollow noreferrer\">Tetramethylpyrazine nitrone protects retinal ganglion cells against N‐methyl‐d‐aspartate‐induced excitotoxicity (Journal of Neurochemistry, 2017)</a></li>\n</ul>\n" }, { "answer_id": 19971, "author": "Jay K", "author_id": 16735, "author_profile": "https://health.stackexchange.com/users/16735", "pm_score": 2, "selected": false, "text": "<p>I've previously researched the answer to this question. I've inserted my research on this answer below. I'm very interested to hear what you think.</p>\n\n<hr>\n\n<p>Nicotine is a component of cigarette smoke. Nicotine promotes angiogenesis in the laboratory (1), including in human retinal endothelial cells.(2) However, surprisingly “cigarette smoke” inhibits angiogenesis in the laboratory(3) and epidemiological studies suggest smoking is actually protective against developing proliferative diabetic retinopathy.(4) </p>\n\n<p>Pyrazine compounds have been shown to be highly potent inhibitors of angiogenesis and the growth of chorioallantoic membranes (CAM). CAM are vascular membrane found in eggs of birds and reptiles which is analogous to the mammalian placenta.(5, 6)</p>\n\n<p>Tobacco leaf contains very low levels of pyrazines and contains the precursors for pyrazine formation. After the tobacco leaf is roasted, the levels of pyrazines increases dramatically whilst the levels of amino acids in the leaf simultaneously decrease.(7) Pyrazines comprise a very small fraction of cigarette smoke condensate by weight (5-50µg/cig).(7) </p>\n\n<p>Internal documents obtained through litigation reveals cigarette manufacturers have added a range of non-nicotine compounds initially referred to as known as “Super-juice” to cigarettes since approximately 1976.(8) Manufacturers have disclosed that Pyrazine compounds are currently 10 of out of the 599 ingredients in cigarettes. These compounds provided users who smoke “light” cigarettes with the flavor profile of high-tar cigarettes. Pyrazines were may enhance the perceived smoothness of the cigarettes, increasing the tolerability of irritation to the respiratory tract during consumption. Furthermore, pyrazine compounds were may have complex chemosensory effects which appeared to influence the ‘learned behavior’ of consumers, promoting and enhancing consumer acceptance and ongoing usage.(8) </p>\n\n<p>To date, 106 pyrazines are found in either tobacco or tobacco smoke, with 40% of these pyrazine being found in both.(7) </p>\n\n<p>The effect of nicotine and pyrazine on endothelial growth and survival has been compared, confirming that nicotine acts as a growth factor for endothelial cells and pyrazine acts as a death factor for endothelial cells. The following compounds were found to inhibit the growth of endothelial cells: 2-ethylpyridine, 3-ethylpyridine, and pyrazine.(9) </p>\n\n<p>One component of cigarette smoke 2,3,5,6-tetramethylpyrazine (also known as ligustrazine, used in Chinese herbal medicine), has undergone a pharmacokinetic evaluation.(10) It found that tetramethylpyrazine is rapidly absorbed from the nasal mucosa into the systemic circulation, and then crosses the blood–brain barrier (BBB) to reach the cerebral cortex.</p>\n\n<p>In 2005, a group accidentally discovered that various compounds with a pyrazine-pyridine backbone are potent inhibitors of vascular endothelial growth factor receptor-2 (VEGFR2).(11)</p>\n\n<p>Thus, in isolation nicotine promotes angiogenesis of retinal endothelial cells partially via the VEGF pathway. However, cigarette smoke contains not only nicotine but also pyrazine compounds which antagonize VEGF receptors, potently inhibiting the angiogenic drive of nicotine.</p>\n\n<p><a href=\"https://i.stack.imgur.com/SfiOi.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/SfiOi.png\" alt=\"Graphic representatin of the Maillard Browning reaction in the formation of pyrazines\"></a></p>\n\n<p>References</p>\n\n<ol>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/24793809\" rel=\"nofollow noreferrer\">Ma X, Jia Y, Zu S, et al. alpha5 Nicotinic acetylcholine receptor mediates nicotine-induced HIF-1alpha and VEGF expression in non-small cell lung cancer. Toxicology and applied pharmacology 2014;278:172-179.</a></li>\n<li><a href=\"https://iovs.arvojournals.org/article.aspx?articleid=2187889\" rel=\"nofollow noreferrer\">Dom AM, Buckley AW, Brown KC, et al. The α7-nicotinic Acetylcholine Receptor and MMP-2/-9 Pathway Mediate the Proangiogenic Effect of Nicotine in Human Retinal Endothelial Cells. Investigative Ophthalmology &amp; Visual Science 2011;52:4428-4438.</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/12709416\" rel=\"nofollow noreferrer\">Michaud SE, Menard C, Guy LG, Gennaro G, Rivard A. Inhibition of hypoxia-induced angiogenesis by cigarette smoke exposure: impairment of the HIF-1alpha/VEGF pathway. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2003;17:1150-1152.</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/11270671\" rel=\"nofollow noreferrer\">Stratton IM, Kohner EM, Aldington SJ, et al. UKPDS 50: Risk factors for incidence and progression of retinopathy in Type II diabetes over 6 years from diagnosis. Diabetologia 2001;44:156-163.</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2862761/\" rel=\"nofollow noreferrer\">Ivnitski-Steele I, Walker MK. Inhibition of neovascularization by environmental agents. Cardiovascular toxicology 2005;5:215-226.</a></li>\n<li><a href=\"https://academic.oup.com/toxsci/article/75/2/393/1655896\" rel=\"nofollow noreferrer\">Melkonian G, Eckelhoefer H, Wu M, et al. Growth and Angiogenesis Are Inhibited in Vivo in Developing Tissues by Pyrazine and Its Derivatives. Toxicological Sciences 2003;75:393-401.</a></li>\n<li><a href=\"https://www.researchgate.net/publication/294261056_The_Chemical_Components_of_Tobacco_and_Tobacco_Smoke_Second_Edition\" rel=\"nofollow noreferrer\">Rodgman A, Perfetti TA. The Chemical Components of Tobacco and Tobacco Smoke, Second Edition: CRC Press; 2016.</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/26063608\" rel=\"nofollow noreferrer\">Alpert HR, Agaku IT, Connolly GN. A study of pyrazines in cigarettes and how additives might be used to enhance tobacco addiction. Tobacco Control 2016;25:444.</a></li>\n<li><a href=\"https://academic.oup.com/toxsci/article/93/1/82/1651255\" rel=\"nofollow noreferrer\">Yu R, Wu M, Lin S, Talbot P. Cigarette Smoke Toxicants Alter Growth and Survival of Cultured Mammalian Cells. Toxicological Sciences 2006;93:82-95.</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/26579367\" rel=\"nofollow noreferrer\">Meng D, Lu H, Huang S, et al. Comparative pharmacokinetics of tetramethylpyrazine phosphate in rat plasma and extracellular fluid of brain after intranasal, intragastric and intravenous administration. Acta Pharmaceutica Sinica B 2014;4:74-78.</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/16033269\" rel=\"nofollow noreferrer\">Kuo G-H, Prouty C, Wang A, et al. Synthesis and Structure−Activity Relationships of Pyrazine-Pyridine Biheteroaryls as Novel, Potent, and Selective Vascular Endothelial Growth Factor Receptor-2 Inhibitors. Journal of Medicinal Chemistry 2005;48:4892-4909.</a></li>\n</ol>\n\n<hr>\n\n<p>Very interested to get your thoughts on this. Thank you</p>\n" } ]
2019/08/22
[ "https://health.stackexchange.com/questions/19963", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16735/" ]
19,964
<p>I'm not a medical professional. I have just noticed the mention of <a href="https://en.wikipedia.org/wiki/Magnetic_resonance_neurography" rel="nofollow noreferrer">MRN - Magnetic Resonance Neurography</a> as a diagnostic tool for nerve issues. </p> <p>Now, I know that MRN is essentially a kind of MR imaging; but - how can I tell (given a results disk), if I've only been MRIed, whether I've also been MRNed? Or is it the case that MRN actually involves a different procedure physically rather than a different way of processing the information from the MR imager?</p>
[ { "answer_id": 19965, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": false, "text": "<p>If you are going to have a Magnetic Resonance Neurography (MRN), also known as MR Imaging of Peripheral Nerves (PNI) (<a href=\"https://radiology.ucsf.edu/patient-care/services/mr-neurography\" rel=\"noreferrer\">UCSF</a>), a doctor will likely tell you in advance, at least because the investigation may not be covered by your insurance (<a href=\"https://www.neurography.com/frequently-asked-questions-about-mr-neurography-and-the-neurography-institute/\" rel=\"noreferrer\">Neurography Institute</a>).</p>\n\n<p>The MRI and MRN procedures are similar, only that MRN requires more powerful scanners that are usually cylindrical (\"closed\"), while regular MRI scanners can be \"open\" or \"closed\" (<a href=\"https://www.vantagediagnostic.com/single-post/2018/01/19/Closed-MRI-vs-Open-MRI\" rel=\"noreferrer\">images and brief description</a>).</p>\n\n<p>MRN is usually used to check disorders of the nerves that go from the spinal cord to an arm (brachial plexus) or leg (lumbosacral plexus, sciatic nerve) (<a href=\"https://radiology.ucsf.edu/patient-care/services/mr-neurography\" rel=\"noreferrer\">UCSF</a>).</p>\n\n<p>After the investigation, it should be clearly stated in your medical documentation if you had MRI or MRN. </p>\n" }, { "answer_id": 19982, "author": "Chris", "author_id": 14056, "author_profile": "https://health.stackexchange.com/users/14056", "pm_score": 2, "selected": false, "text": "<p><a href=\"https://www.nhs.uk/conditions/mri-scan/\" rel=\"nofollow noreferrer\">Magnetic Resonance Imaging</a> is an umbrella term for any medical imaging technique that makes use of the phenomenon of <a href=\"https://en.wikipedia.org/wiki/Nuclear_magnetic_resonance\" rel=\"nofollow noreferrer\">nuclear magnetic resonance</a>. There are many variants depending on how the scanner is configured and analysed, but all are considered MRI.</p>\n\n<hr>\n\n<p><strong>The basis for the different types of MRI scanning</strong></p>\n\n<p>Much of the following is adapted from <a href=\"https://casemed.case.edu/clerkships/neurology/Web%20Neurorad/MRI%20Basics.htm\" rel=\"nofollow noreferrer\">MRI Basics</a>.</p>\n\n<p>Essentially, the protons in hydrogen atoms in the water that constitutes your body are sensitive to magnetic fields and align when placed in a very powerful magnetic field. Short bursts of radio waves knock them out of alignment. When the protons realign, they emit radio waves again, which is what is detected by the scanner. This frequency data is processed using a <a href=\"https://en.wikipedia.org/wiki/Fourier_transform\" rel=\"nofollow noreferrer\">Fourier transform</a> to get the relative intensity at each point in the plane.</p>\n\n<p>Different variations are possible by altering the frequency and timing of the radio energy pulses applied. This gives various sequences such as <em>T1-weighted</em>, <em>T2-weighted</em>, <em>Fluid Attenuated Inversion Recovery (Flair)</em> and <em>diffusion weighted imaging (DWI), which differentiates tissues based on the movement of water</em>. Each is better at evaluating a particular type of body tissue, distinguishing between certain adjacent tissues or detecting a disease process such as inflammation.</p>\n\n<p>This image shows how the brain would appear under T1, T2 and FLAIR sequences.</p>\n\n<p><a href=\"https://i.stack.imgur.com/RQ8eu.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/RQ8eu.jpg\" alt=\"MRI of brain showing T1, T2 and FLAIR sequences\"></a></p>\n\n<p><a href=\"https://www.insideradiology.com.au/gadolinium-contrast-medium/\" rel=\"nofollow noreferrer\">Gadolinium</a> can be used as a contrast medium, particularly to identify vascular structures. Unlike the radiopaque contrast needed for certain types of plain x-ray or CT, gadolinium (when chelated) is <a href=\"https://en.wikipedia.org/wiki/Paramagnetism\" rel=\"nofollow noreferrer\">paramagnetic</a>.</p>\n\n<p><strong>Types of scanning procedures</strong></p>\n\n<p>There are many types of MRI scan, depending on the anatomical area under investigation and the configuration of the scanner, as detailed above. Here are some examples:</p>\n\n<ul>\n<li><p>Magnetic resonance angiography (MRA) - using MRI to identify the course and potency of blood vessels.</p></li>\n<li><p>Magnetic resonance cholangiopancreatography (MRCP) - used to investigate the biliary tree and pancreas (less invasive than the endoscopic alternative, an <a href=\"https://www.sages.org/publications/patient-information/patient-information-for-ercp-endoscopic-retrograde-cholangio-pancreatography-from-sages/\" rel=\"nofollow noreferrer\">ERCP</a>).</p></li>\n<li><p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/21118531\" rel=\"nofollow noreferrer\">Cardiac MRI</a> - imaging the heart requires pulsed sequences synchronised the the patient's ECG.</p></li>\n<li><p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073717/\" rel=\"nofollow noreferrer\">Functional MRI</a> (fMRI) - this depicts changes in deoxyhemoglobin concentration due to modulation of neural metabolism. It is used to identify metabolically active areas of the brain, as opposed to investigating anatomical pathology. It has been used for studies in neuroscience, surgical planning, for monitoring treatment outcomes.</p></li>\n<li><p><a href=\"https://en.wikipedia.org/wiki/Magnetic_resonance_neurography\" rel=\"nofollow noreferrer\">Magnetic resonance neurography</a> (MRN) - as mentioned in the question, this is an adapted form that is especially good at distinguishing nerves from surrounding tissue by optimising the configuration for the water properties of nerves. This was initially an adapted form of diffusion-weighted imaging that is configured to focus on the fact that water tends to diffuse <em>anisotropically</em> in nerves (it diffuses more prominently in the longitudinal axis, along the length of the nerve). It has been found to be a useful adjunct to other means of assessing peripheral nerves such as nerve conjunction studies and electromyography. See <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/19663545\" rel=\"nofollow noreferrer\">this study</a>.</p></li>\n</ul>\n\n<p>Here is an example image of a magnetic resonance neurography study. It demonstrates the <a href=\"https://en.wikipedia.org/wiki/Brachial_plexus\" rel=\"nofollow noreferrer\">brachial plexus</a>.</p>\n\n<p><a href=\"https://i.stack.imgur.com/uOIba.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/uOIba.jpg\" alt=\"MRN of brachial plexus\"></a></p>\n\n<p>It is likely that an MRN will be done if a nerve needs to be directly assessed (e.g. checking for a specific nerve injury like a nerve root compression of the spine (<a href=\"https://en.wikipedia.org/wiki/Radiculopathy\" rel=\"nofollow noreferrer\">radiculopathy</a>) or <a href=\"https://en.wikipedia.org/wiki/Carpal_tunnel_syndrome\" rel=\"nofollow noreferrer\">carpal tunnel syndrome</a>). MRN would not automatically be performed when imaging a body area for other reasons (e.g. MRI of chest for lung disease etc). It should be clear on the radiologist's report which sequences and configuration were used.</p>\n\n<hr>\n\n<p>In summary, the term MRI covers all types of nuclear magnetic resonance imaging. MRN is one example.</p>\n" } ]
2019/08/22
[ "https://health.stackexchange.com/questions/19964", "https://health.stackexchange.com", "https://health.stackexchange.com/users/8418/" ]
20,087
<p>Some medications are applied topically for a local skin effect, such as:</p> <ul> <li>Topical corticosteroids for eczema or psoriasis, of which approx 2% is absorbed systemically.</li> <li>Topical tretinoin for acne, of which approximately 1 to 2% is absorbed systemically.</li> <li>Topical minoxidil for hair loss, of which approx 1 to 2% is absorbed systemically.</li> </ul> <p>Some medications are applied topically for a regional effect on underlying anatomy, such as:</p> <ul> <li>Topical diclofenac (NSAID) for pain relief and anti-inflammatory treatment of muscle strain or arthritis, of which approximately 6% is absorbed systemically.</li> <li>Topical lidocaine for local pain control (the percentage of systemic absorption varies dramatically depending on formulation and application method).</li> </ul> <p>Some medications are applied topically for systemic effects, such as:</p> <ul> <li>Topical nicotine patch to aid in smoking cessation.</li> <li>Topical birth control patch (estrogen/progesterone) for contraception.</li> <li>Topical fentanyl patch for pain control in hospice / cancer patients.</li> </ul> <p>The bioavailability of topically applied medications is complex, including pH, hydrophobicity, vehicle (gel vs cream vs injection vs patch), and other drug factors - plus the skin factors at the site applied such as thickness of stratum corneum and blood supply.</p> <p>But of all these factors, which have the largest effect of <em>increasing</em> bioavailability, ie systemic absorption of a medication?</p>
[ { "answer_id": 19965, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": false, "text": "<p>If you are going to have a Magnetic Resonance Neurography (MRN), also known as MR Imaging of Peripheral Nerves (PNI) (<a href=\"https://radiology.ucsf.edu/patient-care/services/mr-neurography\" rel=\"noreferrer\">UCSF</a>), a doctor will likely tell you in advance, at least because the investigation may not be covered by your insurance (<a href=\"https://www.neurography.com/frequently-asked-questions-about-mr-neurography-and-the-neurography-institute/\" rel=\"noreferrer\">Neurography Institute</a>).</p>\n\n<p>The MRI and MRN procedures are similar, only that MRN requires more powerful scanners that are usually cylindrical (\"closed\"), while regular MRI scanners can be \"open\" or \"closed\" (<a href=\"https://www.vantagediagnostic.com/single-post/2018/01/19/Closed-MRI-vs-Open-MRI\" rel=\"noreferrer\">images and brief description</a>).</p>\n\n<p>MRN is usually used to check disorders of the nerves that go from the spinal cord to an arm (brachial plexus) or leg (lumbosacral plexus, sciatic nerve) (<a href=\"https://radiology.ucsf.edu/patient-care/services/mr-neurography\" rel=\"noreferrer\">UCSF</a>).</p>\n\n<p>After the investigation, it should be clearly stated in your medical documentation if you had MRI or MRN. </p>\n" }, { "answer_id": 19982, "author": "Chris", "author_id": 14056, "author_profile": "https://health.stackexchange.com/users/14056", "pm_score": 2, "selected": false, "text": "<p><a href=\"https://www.nhs.uk/conditions/mri-scan/\" rel=\"nofollow noreferrer\">Magnetic Resonance Imaging</a> is an umbrella term for any medical imaging technique that makes use of the phenomenon of <a href=\"https://en.wikipedia.org/wiki/Nuclear_magnetic_resonance\" rel=\"nofollow noreferrer\">nuclear magnetic resonance</a>. There are many variants depending on how the scanner is configured and analysed, but all are considered MRI.</p>\n\n<hr>\n\n<p><strong>The basis for the different types of MRI scanning</strong></p>\n\n<p>Much of the following is adapted from <a href=\"https://casemed.case.edu/clerkships/neurology/Web%20Neurorad/MRI%20Basics.htm\" rel=\"nofollow noreferrer\">MRI Basics</a>.</p>\n\n<p>Essentially, the protons in hydrogen atoms in the water that constitutes your body are sensitive to magnetic fields and align when placed in a very powerful magnetic field. Short bursts of radio waves knock them out of alignment. When the protons realign, they emit radio waves again, which is what is detected by the scanner. This frequency data is processed using a <a href=\"https://en.wikipedia.org/wiki/Fourier_transform\" rel=\"nofollow noreferrer\">Fourier transform</a> to get the relative intensity at each point in the plane.</p>\n\n<p>Different variations are possible by altering the frequency and timing of the radio energy pulses applied. This gives various sequences such as <em>T1-weighted</em>, <em>T2-weighted</em>, <em>Fluid Attenuated Inversion Recovery (Flair)</em> and <em>diffusion weighted imaging (DWI), which differentiates tissues based on the movement of water</em>. Each is better at evaluating a particular type of body tissue, distinguishing between certain adjacent tissues or detecting a disease process such as inflammation.</p>\n\n<p>This image shows how the brain would appear under T1, T2 and FLAIR sequences.</p>\n\n<p><a href=\"https://i.stack.imgur.com/RQ8eu.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/RQ8eu.jpg\" alt=\"MRI of brain showing T1, T2 and FLAIR sequences\"></a></p>\n\n<p><a href=\"https://www.insideradiology.com.au/gadolinium-contrast-medium/\" rel=\"nofollow noreferrer\">Gadolinium</a> can be used as a contrast medium, particularly to identify vascular structures. Unlike the radiopaque contrast needed for certain types of plain x-ray or CT, gadolinium (when chelated) is <a href=\"https://en.wikipedia.org/wiki/Paramagnetism\" rel=\"nofollow noreferrer\">paramagnetic</a>.</p>\n\n<p><strong>Types of scanning procedures</strong></p>\n\n<p>There are many types of MRI scan, depending on the anatomical area under investigation and the configuration of the scanner, as detailed above. Here are some examples:</p>\n\n<ul>\n<li><p>Magnetic resonance angiography (MRA) - using MRI to identify the course and potency of blood vessels.</p></li>\n<li><p>Magnetic resonance cholangiopancreatography (MRCP) - used to investigate the biliary tree and pancreas (less invasive than the endoscopic alternative, an <a href=\"https://www.sages.org/publications/patient-information/patient-information-for-ercp-endoscopic-retrograde-cholangio-pancreatography-from-sages/\" rel=\"nofollow noreferrer\">ERCP</a>).</p></li>\n<li><p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/21118531\" rel=\"nofollow noreferrer\">Cardiac MRI</a> - imaging the heart requires pulsed sequences synchronised the the patient's ECG.</p></li>\n<li><p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073717/\" rel=\"nofollow noreferrer\">Functional MRI</a> (fMRI) - this depicts changes in deoxyhemoglobin concentration due to modulation of neural metabolism. It is used to identify metabolically active areas of the brain, as opposed to investigating anatomical pathology. It has been used for studies in neuroscience, surgical planning, for monitoring treatment outcomes.</p></li>\n<li><p><a href=\"https://en.wikipedia.org/wiki/Magnetic_resonance_neurography\" rel=\"nofollow noreferrer\">Magnetic resonance neurography</a> (MRN) - as mentioned in the question, this is an adapted form that is especially good at distinguishing nerves from surrounding tissue by optimising the configuration for the water properties of nerves. This was initially an adapted form of diffusion-weighted imaging that is configured to focus on the fact that water tends to diffuse <em>anisotropically</em> in nerves (it diffuses more prominently in the longitudinal axis, along the length of the nerve). It has been found to be a useful adjunct to other means of assessing peripheral nerves such as nerve conjunction studies and electromyography. See <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/19663545\" rel=\"nofollow noreferrer\">this study</a>.</p></li>\n</ul>\n\n<p>Here is an example image of a magnetic resonance neurography study. It demonstrates the <a href=\"https://en.wikipedia.org/wiki/Brachial_plexus\" rel=\"nofollow noreferrer\">brachial plexus</a>.</p>\n\n<p><a href=\"https://i.stack.imgur.com/uOIba.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/uOIba.jpg\" alt=\"MRN of brachial plexus\"></a></p>\n\n<p>It is likely that an MRN will be done if a nerve needs to be directly assessed (e.g. checking for a specific nerve injury like a nerve root compression of the spine (<a href=\"https://en.wikipedia.org/wiki/Radiculopathy\" rel=\"nofollow noreferrer\">radiculopathy</a>) or <a href=\"https://en.wikipedia.org/wiki/Carpal_tunnel_syndrome\" rel=\"nofollow noreferrer\">carpal tunnel syndrome</a>). MRN would not automatically be performed when imaging a body area for other reasons (e.g. MRI of chest for lung disease etc). It should be clear on the radiologist's report which sequences and configuration were used.</p>\n\n<hr>\n\n<p>In summary, the term MRI covers all types of nuclear magnetic resonance imaging. MRN is one example.</p>\n" } ]
2019/09/16
[ "https://health.stackexchange.com/questions/20087", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15443/" ]
20,101
<p>From what I have read it is not considered effective to screen for ovarian cancer in non-symptomatic women. Would it not be worth doing an ultra-sound scan, then if there are growths found, do a ROMA test?</p>
[ { "answer_id": 20102, "author": "DoctorWhom", "author_id": 6776, "author_profile": "https://health.stackexchange.com/users/6776", "pm_score": 5, "selected": true, "text": "<p>Screening tests are done across the population of asymptomatic people at risk of a disease (e.g. mammogram to look for breast cancer in all women with breasts) to try to catch disease early in its course.</p>\n<p>Diagnostic tests are done when a patient presents with symptoms.</p>\n<p>The <a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0009898114005208\" rel=\"noreferrer\">ROMA test</a> is a diagnostic test done when a woman presents with an adnexal mass, and uses serum markers (CA125, HE4) to stratify the risk of the mass being cervical cancer in that individual. It is generally done after a pelvic ultrasound, and helps guide decisions regarding biopsy etc.</p>\n<p>Currently, most professional organizations including <a href=\"https://jamanetwork.com/journals/jama/fullarticle/2672638\" rel=\"noreferrer\">the USPSTF do NOT recommend screening for ovarian cancer</a>:</p>\n<blockquote>\n<p><strong>Rationale</strong></p>\n<p><strong>Importance</strong> - The age-adjusted incidence of ovarian cancer from\n2010 to 2014 was 11.4 cases per 100,000 women per year.1 Ovarian\ncancer is the fifth most common cause of cancer death among US women\nand the leading cause of death from gynecologic cancer, despite its\nlow incidence.1 Approximately 14,000 women die of ovarian cancer each\nyear in the United States. More than 95% of ovarian cancer deaths\noccur among women 45 years and older.2</p>\n<p><strong>Detection</strong> - The positive predictive value of screening tests for ovarian\ncancer is low, and most women with a positive screening test result do\nnot have ovarian cancer (ie, many women without ovarian cancer will\nhave a false-positive result on screening tests).</p>\n<p><strong>Benefits of Screening</strong> - The USPSTF found adequate evidence that\nscreening with transvaginal ultrasound, testing for the serum tumor\nmarker cancer antigen 125 (CA-125), or a combination of both does not\nreduce ovarian cancer mortality.</p>\n<p><strong>Harms of Screening</strong> - The USPSTF found adequate evidence that screening\nfor ovarian cancer can result in important harms, including many\nfalse-positive results, which can lead to unnecessary surgical\ninterventions in women who do not have cancer. Depending on the type\nof screening test used, the magnitude of harm ranges from moderate to\nsubstantial and reflects the risk for unnecessary diagnostic surgery.\nThe USPSTF found inadequate evidence on the psychological harms of\nscreening for ovarian cancer.</p>\n<p><strong>USPSTF Assessment</strong> - The USPSTF concludes that there is at least moderate\ncertainty that the harms of screening for ovarian cancer outweigh the\nbenefits.</p>\n</blockquote>\n<p>To summarize, screening tests are generally done population-wide when the population-wide benefits of catching early disease <em><strong>outweighs the harms</strong></em> of the testing/treatment done on the <em><strong>false positive cases</strong></em> of those screening tests. Testing and treating a false-positive can have serious or even fatal consequences. The benefits and risks are weighed carefully when deciding whether to screen population-wide.</p>\n<p>Screening for an individual based on their risks (e.g. first degree family members with ovarian cancer, environmental exposures or genetic mutations known to increase risk, etc) is NOT considered population-wide screening, it is something discussed with an individual's physician in their wellness visit, and is based on individual factors.</p>\n<p><strong>Once <em>any</em> test (whether screening or diagnostic) is performed, <em>any positive results ABSOLUTELY MUST be followed up by the physician</em> to discuss risks and benefits of the next steps in diagnosis and/or treatment.</strong> That is why the risks of diagnostics/treatments of false positive results (which occur at least a small % of the time in <em>any</em> test) have to be considered when deciding whether there is more harm or benefit to screening at a population level.</p>\n<p>Without giving an entire lecture on biostatistics... for example, if a screening test were to have a 5% false positive rate, and we screened a population of 1 million women, about 50,000 of those women screened would have a falsely positive result that would result in unnecessary additional tests/treatment. But when considering an individual, many other factors may change the balance of risks/benefits to favor doing testing, so that is why primary care providers are (usually) well trained in both doing and <em>discussing</em> screening tests with patients, to guide each individual in what is best for them.</p>\n" }, { "answer_id": 20107, "author": "rumtscho", "author_id": 193, "author_profile": "https://health.stackexchange.com/users/193", "pm_score": 3, "selected": false, "text": "<p>It's interesting that you picked this one specific example, because it happens to have been <a href=\"https://www.nature.com/articles/s41598-018-35585-z.pdf\" rel=\"nofollow noreferrer\">studied by Gigerenzer</a>, a prominent expert on risk perception. It also showcases that one shouldn't insist all the time of applying \"common sense\" to medicine, since facts show that, counterintuitive as it is to both patients and physicians, the screening does not have benefits. </p>\n\n<p>There is a nice citation in Gigerenzer's paper subsuming the facts: </p>\n\n<blockquote>\n <p>about 3 women in 1,000 in both the screening and the nonscreening group died of ovarian cancer within that time frame, and about 85 in 1,000 in each group of other causes. It further revealed substantial harms within the screening group: 96 women in every 1,000 screened had a false alarm, of whom 32 had their ovaries unnecessarily removed as part of further diagnostic work-up. </p>\n</blockquote>\n\n<p>So, screening for ovarian cancer does not reduce your chances of dying of ovarian cancer (or dying at all - that part is quite important, since one cannot rely on a death certificate correctly stating the reason for death). If you lost a relative to ovarian cancer, it is normal to have thoughts like \"if only she had been tested early enough\", but in reality, that would not have helped. </p>\n\n<p>The problem here is that the scenario of \"test -> detection -> help\" is so firmly rooted in people's ideas about medicine, that the idea of a test which does individually detect a malignancy but is unsuitable for screening just doesn't compute. I recommend reading the full paper (10.1038/s41598-018-35585-z), or try to get hold of some talks by Gigerenzer or his staff, highly interesting stuff. </p>\n\n<p>There are better way of representing this information, and one of them was tested in the paper I cite. I hope you can see easier from it why the screening is not recommended. </p>\n\n<p><a href=\"https://i.stack.imgur.com/Mb2Km.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Mb2Km.png\" alt=\"enter image description here\"></a></p>\n" } ]
2019/09/18
[ "https://health.stackexchange.com/questions/20101", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16864/" ]
20,108
<p>I'm personally not a big fan of recreational drugs, illicit or otherwise, but there's an interesting medical question buried in their use.</p> <p>Why is it that substances that make you feel good tend to be dangerous? The most effective "feel good" drugs — opioids, benzodiazepines, amphetamines, cocaine in all its forms, MDMA, and of course, alcohol — tend to be very dangerous from a medical perspective, with fairly low therapeutic indices and numerous means of causing harm.</p> <p>Sources:</p> <ul> <li>Psychoactive drugs with low <a href="https://en.wikipedia.org/wiki/Therapeutic_index" rel="nofollow noreferrer">therapeutic index</a>: alcohol, cocaine, <a href="https://www.ncbi.nlm.nih.gov/pubmed/21999760" rel="nofollow noreferrer">opioids</a> (heroin, morphine, codeine, methadone), <a href="https://toxnet.nlm.nih.gov/cgi-bin/sis/search/a?dbs%20hsdb:@term%20@DOCNO%203287" rel="nofollow noreferrer">amphetamine</a> and <a href="https://www.ncbi.nlm.nih.gov/pubmed/9255991" rel="nofollow noreferrer">barbiturates</a></li> <li><a href="https://www.nature.com/articles/srep08126" rel="nofollow noreferrer">Margine of exposure of psychoactive drugs</a></li> <li><a href="https://www.researchgate.net/publication/8565872_Comparison_of_acute_lethal_toxicity_of_commonly_abused_psychoactive_substances" rel="nofollow noreferrer">Safety ratio of psychoactive drugs</a> (click: download pdf)</li> <li><a href="https://ncsacw.samhsa.gov/files/TrainingPackage/MOD2/PhysicalandPsychEffectsSubstanceUse.pdf" rel="nofollow noreferrer">Physical and Psychological Effects of Substance Use</a> </li> </ul>
[ { "answer_id": 20102, "author": "DoctorWhom", "author_id": 6776, "author_profile": "https://health.stackexchange.com/users/6776", "pm_score": 5, "selected": true, "text": "<p>Screening tests are done across the population of asymptomatic people at risk of a disease (e.g. mammogram to look for breast cancer in all women with breasts) to try to catch disease early in its course.</p>\n<p>Diagnostic tests are done when a patient presents with symptoms.</p>\n<p>The <a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0009898114005208\" rel=\"noreferrer\">ROMA test</a> is a diagnostic test done when a woman presents with an adnexal mass, and uses serum markers (CA125, HE4) to stratify the risk of the mass being cervical cancer in that individual. It is generally done after a pelvic ultrasound, and helps guide decisions regarding biopsy etc.</p>\n<p>Currently, most professional organizations including <a href=\"https://jamanetwork.com/journals/jama/fullarticle/2672638\" rel=\"noreferrer\">the USPSTF do NOT recommend screening for ovarian cancer</a>:</p>\n<blockquote>\n<p><strong>Rationale</strong></p>\n<p><strong>Importance</strong> - The age-adjusted incidence of ovarian cancer from\n2010 to 2014 was 11.4 cases per 100,000 women per year.1 Ovarian\ncancer is the fifth most common cause of cancer death among US women\nand the leading cause of death from gynecologic cancer, despite its\nlow incidence.1 Approximately 14,000 women die of ovarian cancer each\nyear in the United States. More than 95% of ovarian cancer deaths\noccur among women 45 years and older.2</p>\n<p><strong>Detection</strong> - The positive predictive value of screening tests for ovarian\ncancer is low, and most women with a positive screening test result do\nnot have ovarian cancer (ie, many women without ovarian cancer will\nhave a false-positive result on screening tests).</p>\n<p><strong>Benefits of Screening</strong> - The USPSTF found adequate evidence that\nscreening with transvaginal ultrasound, testing for the serum tumor\nmarker cancer antigen 125 (CA-125), or a combination of both does not\nreduce ovarian cancer mortality.</p>\n<p><strong>Harms of Screening</strong> - The USPSTF found adequate evidence that screening\nfor ovarian cancer can result in important harms, including many\nfalse-positive results, which can lead to unnecessary surgical\ninterventions in women who do not have cancer. Depending on the type\nof screening test used, the magnitude of harm ranges from moderate to\nsubstantial and reflects the risk for unnecessary diagnostic surgery.\nThe USPSTF found inadequate evidence on the psychological harms of\nscreening for ovarian cancer.</p>\n<p><strong>USPSTF Assessment</strong> - The USPSTF concludes that there is at least moderate\ncertainty that the harms of screening for ovarian cancer outweigh the\nbenefits.</p>\n</blockquote>\n<p>To summarize, screening tests are generally done population-wide when the population-wide benefits of catching early disease <em><strong>outweighs the harms</strong></em> of the testing/treatment done on the <em><strong>false positive cases</strong></em> of those screening tests. Testing and treating a false-positive can have serious or even fatal consequences. The benefits and risks are weighed carefully when deciding whether to screen population-wide.</p>\n<p>Screening for an individual based on their risks (e.g. first degree family members with ovarian cancer, environmental exposures or genetic mutations known to increase risk, etc) is NOT considered population-wide screening, it is something discussed with an individual's physician in their wellness visit, and is based on individual factors.</p>\n<p><strong>Once <em>any</em> test (whether screening or diagnostic) is performed, <em>any positive results ABSOLUTELY MUST be followed up by the physician</em> to discuss risks and benefits of the next steps in diagnosis and/or treatment.</strong> That is why the risks of diagnostics/treatments of false positive results (which occur at least a small % of the time in <em>any</em> test) have to be considered when deciding whether there is more harm or benefit to screening at a population level.</p>\n<p>Without giving an entire lecture on biostatistics... for example, if a screening test were to have a 5% false positive rate, and we screened a population of 1 million women, about 50,000 of those women screened would have a falsely positive result that would result in unnecessary additional tests/treatment. But when considering an individual, many other factors may change the balance of risks/benefits to favor doing testing, so that is why primary care providers are (usually) well trained in both doing and <em>discussing</em> screening tests with patients, to guide each individual in what is best for them.</p>\n" }, { "answer_id": 20107, "author": "rumtscho", "author_id": 193, "author_profile": "https://health.stackexchange.com/users/193", "pm_score": 3, "selected": false, "text": "<p>It's interesting that you picked this one specific example, because it happens to have been <a href=\"https://www.nature.com/articles/s41598-018-35585-z.pdf\" rel=\"nofollow noreferrer\">studied by Gigerenzer</a>, a prominent expert on risk perception. It also showcases that one shouldn't insist all the time of applying \"common sense\" to medicine, since facts show that, counterintuitive as it is to both patients and physicians, the screening does not have benefits. </p>\n\n<p>There is a nice citation in Gigerenzer's paper subsuming the facts: </p>\n\n<blockquote>\n <p>about 3 women in 1,000 in both the screening and the nonscreening group died of ovarian cancer within that time frame, and about 85 in 1,000 in each group of other causes. It further revealed substantial harms within the screening group: 96 women in every 1,000 screened had a false alarm, of whom 32 had their ovaries unnecessarily removed as part of further diagnostic work-up. </p>\n</blockquote>\n\n<p>So, screening for ovarian cancer does not reduce your chances of dying of ovarian cancer (or dying at all - that part is quite important, since one cannot rely on a death certificate correctly stating the reason for death). If you lost a relative to ovarian cancer, it is normal to have thoughts like \"if only she had been tested early enough\", but in reality, that would not have helped. </p>\n\n<p>The problem here is that the scenario of \"test -> detection -> help\" is so firmly rooted in people's ideas about medicine, that the idea of a test which does individually detect a malignancy but is unsuitable for screening just doesn't compute. I recommend reading the full paper (10.1038/s41598-018-35585-z), or try to get hold of some talks by Gigerenzer or his staff, highly interesting stuff. </p>\n\n<p>There are better way of representing this information, and one of them was tested in the paper I cite. I hope you can see easier from it why the screening is not recommended. </p>\n\n<p><a href=\"https://i.stack.imgur.com/Mb2Km.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Mb2Km.png\" alt=\"enter image description here\"></a></p>\n" } ]
2019/09/20
[ "https://health.stackexchange.com/questions/20108", "https://health.stackexchange.com", "https://health.stackexchange.com/users/11/" ]
20,124
<p>Traditionally, I knew that when one has a medical emergency that can't wait for a doctor's opinion, you go to the emergency room. Now, I see that there are Urgent Care centers around.</p> <p>So when would one go there vs an actual emergency room? For example, if someone thinks that they're having a heart attack, stroke, should one go to an Urgent care? What if one has a broken bone? Potential appendicitis? </p>
[ { "answer_id": 20128, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 3, "selected": false, "text": "<p>Urgent care is for things that your normal physician could treat, but you are outside their hours or unable to get an appointment within a reasonable time for the condition.</p>\n\n<p>Emergency rooms are for medical emergencies.</p>\n\n<hr>\n\n<p><strong>Examples of things that can be treated in Urgent Care (via the <a href=\"https://healthblog.uofmhealth.org/health-management/urgent-care-vs-emergency-room-whats-difference\" rel=\"nofollow noreferrer\">University of Michigan</a>)</strong>:</p>\n\n<p>Cold/flu, sprained ankle, broken bones in wrist/hand/ankle/foot without severe displacement or skin punctured, sore throat, nausea, minor cuts, eye/ear infection, minor burns</p>\n\n<hr>\n\n<p><strong>Things for which you should go to the ER (or better, call 911/emergency services)</strong>:</p>\n\n<p>Extremely high fever, severe trauma, broken bones severely displaced or puncturing skin, difficulty breathing, heart attack/stroke, uncontrolled bleeding, poisoning, major burns</p>\n\n<hr>\n\n<p>In summary, if you could die, go to the ER. If you have a non-life threatening acute medical issue, urgent care. If in question or unsure, go to the ER.</p>\n" }, { "answer_id": 25703, "author": "Franck Dernoncourt", "author_id": 43, "author_profile": "https://health.stackexchange.com/users/43", "pm_score": 0, "selected": false, "text": "<p>Nice visual summary from the practice <a href=\"https://urgentcarelajolla.com/services/\" rel=\"nofollow noreferrer\">https://urgentcarelajolla.com/services/</a> (ER = Emergency Room):</p>\n<p><a href=\"https://i.stack.imgur.com/RmlJR.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/RmlJR.png\" alt=\"enter image description here\" /></a></p>\n" } ]
2019/09/23
[ "https://health.stackexchange.com/questions/20124", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16882/" ]
20,144
<p><a href="https://i.stack.imgur.com/gdDfj.png" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/gdDfj.png" alt="enter image description here"></a></p> <p>I have a syringe that looks a lot like this. I'm not using it for medical purposes, but rather to create vacuum and pressure in hoses for testing out fuel delivery in small motors. When I look up syringes to buy it usually comes up with what are called "Luer taper", "Luer-Lok" and "Luer-Slip (registered trademarks), or generically "Luer-Lock" and "Luer-Slip". These look very different from the image posted above. If we take a look one example of a "Luer-Slip" syringe, they usually look like this:</p> <p><a href="https://i.stack.imgur.com/SNn0Z.png" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/SNn0Z.png" alt="enter image description here"></a></p> <p>The first problem being (for my purposes) that the syringe tip or opening is larger than I would like, and the second is that it's not tapered. I would ideally need both (tapered and smaller) to jam them into hoses/lines to get a decent seal. </p> <p>Does anyone know what these type of syringes are called? I'm trying to search for them at different places. </p> <p>The one I have and the one in the first image are curved, I don't know if they have a particular name, but I only need a straight one.</p> <p>As another example, here are some sold on eBay:</p> <p><a href="https://i.stack.imgur.com/d7uvv.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/d7uvv.jpg" alt="enter image description here"></a></p> <p>The one on the left is close to what I'm looking for, but I would want a tapered tip beginning from a smaller size at the tip so I can slide it into a tube and get a good seal.</p>
[ { "answer_id": 20145, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 3, "selected": true, "text": "<p>I think you are looking for <a href=\"https://www.google.com/search?q=irrigation+syringe\" rel=\"nofollow noreferrer\">irrigation syringes</a> - I'm familiar only with the curved variety but at least on a google images search I see straight ones as well.</p>\n\n<p>That said, I've always used luer-style syringes with an appropriate fitting when using syringes in an equipment context. Major catalog parts suppliers have plastic and metal fittings with just about every conversion you can imagine. For example, if I were testing hoses, I'd get a hose barb fitting.</p>\n" }, { "answer_id": 20175, "author": "blacksmith37", "author_id": 9688, "author_profile": "https://health.stackexchange.com/users/9688", "pm_score": 1, "selected": false, "text": "<p>There are a variety of syringes listed as \"disposable catheter \" that typically have a tapered straight tip. A common size is 60 ml . The tip is \"universal\" friction fit. I use them for G-tube feeding , they are standard for that application despite the name. I typically use them about 20 times. Then use them for purposes similar to in the question . In quantity of 50 they are available on the net for down to about $ 0.60 each and of course as high a price as you want to pay.There are many brands, I seem to end up with a different one each time.</p>\n" } ]
2019/09/26
[ "https://health.stackexchange.com/questions/20144", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15569/" ]
20,186
<p>Where can I find official documentation on difference between Salt Tablets and Table Salt.</p> <p>Several people online mention that Table Salt is just sodium and less of other minerals whereas Salt Tablets have sodium and more of other elements such as potassium.</p> <p>When I called a Pharmacist he said just the opposite. He said Salt Tablets are just Sodium Chloride whereas Table Salt has sodium and other minerals.</p> <p>And when I asked why does Doctor prescribe Salt Tablets, the pharmacist said because it is harder to measure Table Salt, whereas Tablets are pre-portioned.</p> <p>Where to get official guidance on this?</p>
[ { "answer_id": 20145, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 3, "selected": true, "text": "<p>I think you are looking for <a href=\"https://www.google.com/search?q=irrigation+syringe\" rel=\"nofollow noreferrer\">irrigation syringes</a> - I'm familiar only with the curved variety but at least on a google images search I see straight ones as well.</p>\n\n<p>That said, I've always used luer-style syringes with an appropriate fitting when using syringes in an equipment context. Major catalog parts suppliers have plastic and metal fittings with just about every conversion you can imagine. For example, if I were testing hoses, I'd get a hose barb fitting.</p>\n" }, { "answer_id": 20175, "author": "blacksmith37", "author_id": 9688, "author_profile": "https://health.stackexchange.com/users/9688", "pm_score": 1, "selected": false, "text": "<p>There are a variety of syringes listed as \"disposable catheter \" that typically have a tapered straight tip. A common size is 60 ml . The tip is \"universal\" friction fit. I use them for G-tube feeding , they are standard for that application despite the name. I typically use them about 20 times. Then use them for purposes similar to in the question . In quantity of 50 they are available on the net for down to about $ 0.60 each and of course as high a price as you want to pay.There are many brands, I seem to end up with a different one each time.</p>\n" } ]
2019/10/04
[ "https://health.stackexchange.com/questions/20186", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16937/" ]
20,200
<p><a href="https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html" rel="nofollow noreferrer">According to the CDC</a>, there are reports of more than 1000 patients in the US with vaping-associated lung injuries, and <a href="https://www.nytimes.com/2019/10/08/nyregion/vaping-death.html" rel="nofollow noreferrer">23 deaths</a> have been confirmed. The median age of deceased patients is 49.5 years, while the median age of patients overall is 23 years. The first reported death occurred in Illinois August 23rd 2019.</p> <p>Do any of the following three explanations for this outbreak have factual support?</p> <ol> <li>There is no outbreak. After the first death attributed to vaping, patients with lung disease were asked about their vaping history, whereas before they were not. This explains the rapid rise of reported cases in the last two months. There were similar cases all along, but hospitals changed the questions they asked.</li> <li>Vapers changed the vaping parameters after watching videos like <a href="https://www.youtube.com/watch?v=Syccl7rd3Lk" rel="nofollow noreferrer">this one</a> (8 of the 10 most watched vaping videos on youtube are about vape tricks). During the hot summer months vaping outside, the viscosity of e-liquid was lower, introducing a second change that increased the substance intake through the inhaled aerosol.</li> <li>The onset of the outbreak was so rapid that no change in products, buying behaviour or vaping behaviour could explain it because these things happen over months and years, not weeks. The cause of the outbreak was a firmware upgrade in the vaping devices that led to a change in vaping conditions resulting in harmful substances created while vaping (for example in a vape dry hit).</li> </ol>
[ { "answer_id": 20230, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p>There are some data about possible causes of vaping-related lung damage, the type of the damage and symptoms, but not about the changes in medical history questionnaires, vaping habits or e-cigarette firmware.</p>\n<p>Most commonly associated substances were THC and nicotine containing oils. Most of the investigated samples contained very high amounts of vitamin E.</p>\n<h2>EVIDENCE:</h2>\n<p><strong>Tetrahydrocannabinol (THC)-containing oils</strong> (not smoking or vaping plant matter):</p>\n<p><a href=\"https://www.cdc.gov/mmwr/volumes/68/wr/mm6839e2.htm?s_cid=mm6839e2_w\" rel=\"nofollow noreferrer\">E-cigarette Product Use, or Vaping, Among Persons with Associated Lung Injury — Illinois and Wisconsin, April–September 2019 (CDC.gov, October 4th, 2019)</a>:</p>\n<blockquote>\n<p>Overall, 75 (87%) of 86 interviewed patients reported using\ne-cigarette products containing tetrahydrocannabinol (THC), and 61\n(71%) reported using nicotine-containing products.</p>\n</blockquote>\n<p><a href=\"https://i.stack.imgur.com/BlMEv.gif\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/BlMEv.gif\" alt=\"enter image description here\" /></a></p>\n<p><em>Image: Brands of tetrahydrocannabinol and nicotine products reported by patients with lung damage</em></p>\n<p><a href=\"https://newsnetwork.mayoclinic.org/discussion/vaping-associated-lung-injury-may-be-caused-by-toxic-chemical-fumes-study-fines/\" rel=\"nofollow noreferrer\">Mayo Clinic, October 2nd, 2019</a>:</p>\n<blockquote>\n<p>All of the patients (17) had vaped, and 71% had vaped with marijuana\nor cannabis oils.</p>\n</blockquote>\n<p><strong>Vitamin E acetate:</strong></p>\n<p><a href=\"https://www.health.ny.gov/press/releases/2019/2019-09-05_vaping.htm\" rel=\"nofollow noreferrer\">New York State Department of Health Announces Update on Investigation into Vaping-Associated Pulmonary Illnesses (September, 5th, 2019)</a>:</p>\n<blockquote>\n<p>Laboratory test results showed very high levels of vitamin E\nacetate in nearly all cannabis-containing samples analyzed by the\nWadsworth Center as part of this investigation.</p>\n</blockquote>\n<p>and, according to <a href=\"https://www.governor.ny.gov/news/governor-cuomo-takes-aggressive-action-protect-new-yorkers-harmful-and-addictive-vaping\" rel=\"nofollow noreferrer\">governor.ny.gov</a>:</p>\n<blockquote>\n<p>...The Wadsworth Center has obtained samples of thickeners from these\nthree companies and determined that they are nearly pure vitamin E\nacetate oil.</p>\n</blockquote>\n<p>So, they have found vitamin E acetate in the actual vaping liquids used by the patients and in the thickening agents sold by 3 commercial suppliers.</p>\n<p><strong>Chemical injury of the lungs:</strong></p>\n<p><a href=\"https://newsnetwork.mayoclinic.org/discussion/vaping-associated-lung-injury-may-be-caused-by-toxic-chemical-fumes-study-fines/\" rel=\"nofollow noreferrer\">Mayo Clinic, October 2nd, 2019</a>:</p>\n<blockquote>\n<p>it seems to be some kind of direct chemical injury, similar to\nwhat one might see with exposures to toxic chemical fumes, poisonous\ngases and toxic agents.</p>\n<p>Researchers found no evidence of tissue injury caused by accumulation\nof lipids — fatty substances such as mineral oils.</p>\n<p>We were not surprised by what we found, regarding toxicity,&quot; says Dr.\nLarsen, senior author of the study. &quot;We have seen a handful of cases,\nscattered individual cases, over the past two years where we've\nobserved the same thing, and now we are seeing a sudden spike in\ncases.</p>\n</blockquote>\n<p><strong>Symptoms:</strong></p>\n<p><a href=\"https://www.cdc.gov/media/releases/2019/s0821-cdc-fda-states-e-cigarettes.html\" rel=\"nofollow noreferrer\">CDC.gov, October, 3rd, 2019</a>:</p>\n<blockquote>\n<p>Patients in this investigation have reported symptoms such as: cough,\nshortness of breath, chest pain, nausea, vomiting, diarrhea, fatigue,\nfever, or abdominal pain that have developed over few days to several\nweeks.</p>\n<p>A lung infection does not appear to be causing the symptoms.</p>\n</blockquote>\n<p><strong>In summary,</strong> the cause of vaping-related lung damage is still not known; the only <em>unusual</em> thing they've found so far are high amounts of vitamin E acetate in vaping liquids that probably came from thickening agents.</p>\n" }, { "answer_id": 20388, "author": "LаngLаngС", "author_id": 11231, "author_profile": "https://health.stackexchange.com/users/11231", "pm_score": 3, "selected": true, "text": "<p>While it could still be a mixture of acute reasons: metals, dust, plainly unknown toxins; the underlying reason seems not to be that plant matter is vaped, nor that liquids are vaped.</p>\n\n<p>It also seems not to be causal whether THC or nicotine are in most cases \"associated\" with the disease.</p>\n\n<p>What the fast onset of this disease makes prudent: implicating either THC or nicotine is so highly unlikely as to be an irresponsible claim. It makes no sense to scare people into another moral panic when the exact same substances are tolerated for decades in anyone user when pyrolised (traditional smoking). Note though that adding anything, including THC, to stuff to be <em>inhaled</em> is not 'healthy' per se</p>\n\n<p>What is currently is known is that vaping liquids <em>can</em> be much more dangerous than ordinary smoking.<br>\n<em>But</em> this seems to be caused by additives in uncontrolled, unregulated, often even black-market and refill products. And in these the most likely suspect substance of the now leading theory is:</p>\n\n<blockquote>\n <ul>\n <li><p>Recent CDC laboratory testing of bronchoalveolar lavage (BAL) fluid samples (or samples of fluid collected from the lungs) from 29 patients with EVALI submitted to CDC from 10 states found <strong><em>vitamin E acetate in ALL of the BAL fluid samples.</em></strong> Vitamin E acetate is used as an additive in the production of e-cigarette, or vaping, products. This is the first time that we have detected a potential chemical of concern in biologic samples from patients with these lung injuries.</p></li>\n <li><p>CDC tested for a range of other chemicals that might be found in e-cigarette, or vaping, products, including plant oils, petroleum distillates like mineral oil, MCT oil, and terpenes (which are compounds found in or added to THC products). None of these potential chemicals of concern were detected in the BAL fluid samples tested.</p></li>\n <li><p>This is the first time that we have detected a potential chemical of concern in biologic samples from patients with these lung injuries. These findings provide direct evidence of vitamin E acetate at the primary site of injury within the lungs.</p></li>\n <li><p>These findings complement the <a href=\"https://www.fda.gov/news-events/public-health-focus/lung-illnesses-associated-use-vaping-products\" rel=\"nofollow noreferrer\">ongoing work of FDA</a> and some state public health laboratories to characterize e-liquid exposures and inform the ongoing multistate outbreak.</p></li>\n </ul>\n \n <p>Key Facts about Vitamin E Acetate</p>\n \n <ul>\n <li><p>Vitamin E is a vitamin found in many foods, including vegetable oils, cereals, meat, fruits, and vegetables. It is also available as a dietary supplement and in many cosmetic products, like skin creams.</p></li>\n <li><p>Vitamin E acetate usually does not cause harm when ingested as a vitamin supplement or applied to the skin. However, previous research suggests when vitamin E acetate is inhaled, it may interfere with normal lung functioning.</p></li>\n <li><p>Vitamin E acetate is used as an additive in the production of e-cigarette, or vaping, products, because it resembles THC oil. Vitamin E acetate is also used as a thickening ingredient in e-liquids.</p></li>\n </ul>\n \n <p>–– <a href=\"https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html#what-is-new\" rel=\"nofollow noreferrer\">CDC: Outbreak of Lung Injury Associated with the Use of E-Cigarette, or Vaping, Products (Updated November 8, 2019,)</a></p>\n</blockquote>\n" } ]
2019/10/05
[ "https://health.stackexchange.com/questions/20200", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16873/" ]
20,209
<p>I understand how to evaluate <em>therapeutic</em> studies: basically you compare the results of two groups that were chosen randomly. One group gets the new drug, the other group gets the placebo (or the drug against which the new drug should be tested). Neither the physicians nor the patients know in which group they are (double-blind testing). You can clearly see the results and test the statistical significance (e.g. with a t-test, depending on the study design).</p> <p>I have a problem understanding <em>diagnostic</em> studies. My problem lies in the fact that you do not know "the truth", i.e. whether a patient really has the condition which should be diagnosed. Therefore you use the so-called "gold standard", i.e. the best diagnostic method so far. There is no problem when the new diagnostic method is worse than the gold standard. Yet I think there might be a problem when the new diagnostic method is <em>better</em> than the gold standard! Why? Because the results will be <em>different</em> which would be interpreted as <em>inferior</em>.</p> <p>Let me give you an example: Let's assume that a patient really has some form of cancer, yet the gold standard is not able to detect it. The new method is able to detect it and therefore both tests disagree. Because the gold standard is taken as the <em>reference</em> the new method would get a minus point here... although it was right in the first place!</p> <p><strong>My questions</strong><br> Is my thinking correct? If yes, how do handle this problem in practice? Is there a common term for this kind of problem? If no, where lies my misunderstanding?</p> <p><strong>Edit</strong><br> Perhaps another (more extreme) example is in order: Let's say the gold standard has an accuracy of 50%, i.e. the toss of a coin. If you had a new method with an accuracy of 100% (so the results of this method and "the truth" are the same) and tested it against the gold standard this new method would get an accuracy of only 50% (i.e. the accuracy of the gold standard against "the truth").</p>
[ { "answer_id": 20214, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 0, "selected": false, "text": "<p><a href=\"https://en.wikipedia.org/wiki/Gold_standard_(test)\" rel=\"nofollow noreferrer\">Wikipedia</a> says:</p>\n\n<blockquote>\n <p>Before widespread acceptance of any new test, the former test retains its status as the \"gold standard\". </p>\n</blockquote>\n\n<p>which means that a competitor must perform better than the current gold standard over repeated and diverse tests.</p>\n\n<p>Single isolated cases like the examples you have given do contribute to the overall data, but are also to be treated as possible 'needles in haystacks'. Numerous tests are required to eliminate anomalies, and a variety of statistical methods can be used to determine if anomalies can be viewed as exceptions to the rule.</p>\n\n<p>In summary, no single test will suffice. It takes a multitude of tests over a variety of patients and conditions for a procedure to be validated.</p>\n" }, { "answer_id": 20222, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": true, "text": "<p>The accuracy of a new diagnostic test can be determined by comparing the test results with the results of a <strong>biopsy</strong> (taking a piece of tissue), which is done at some point <em>after</em> the test, and which should reliably confirm/exclude the pathology in question. </p>\n\n<p>For example, they tested <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/29679780\" rel=\"nofollow noreferrer\">the accuracy of \"multi-detector CT\" in differentiating between gallbladder inflammation and cancer</a>. They compared what the CT has shown and what the biopsy after gallbladder removal has shown. So, they did not compare the results of the new test with the \"gold standard test\" but with the cases of cancer they proved later by biopsy. </p>\n\n<p>They use the mentioned process not only to evaluate the accuracy of new tests but also to evaluate the results of the existing tests. For example, they try to determine if a certain \"shadow\" in the ultrasound image speaks for gallstones or cancer (which they can see after gallbladder removal).</p>\n" } ]
2019/10/05
[ "https://health.stackexchange.com/questions/20209", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16926/" ]
20,236
<p>When I said cold weather makes the blood not flow as well in the body, I would get the refutation that human body has a constant temperature in warm or cold weather, possibly at 36.7°C (or 37°C), because humans are warm blooded animals.</p> <p>But in the winter, more people have heart attack and studies have showed that the day after the first snowfall of the year, there are much more heart attacks happening.</p> <p>(Updated: I can't find the article any more. It said snow shoveling can cause heart attack, but in places where people don't need to shovel snow, the heart attack rate is also higher when it becomes cold.)</p> <p>How can this be explained with the refutation that "human body has a constant temperature in warm or cold weather" and therefore cold weather should not be the issue?</p> <p>If we do not consider the issue related to holiday stress or holiday social activities, it seems like <a href="https://www.thehealthy.com/heart-disease/heart-attack-risk-in-winter/" rel="noreferrer">some articles indicated it is due to blood vessel constricting in cold weather, causing blood more difficult to reach vital organs in the body</a>. There is also <a href="https://www.everydayhealth.com/heart-attack/living-with/heres-how-cold-weather-can-trigger-heart-attack/" rel="noreferrer">one article that is medically reviewed</a>. Is this the primary cause?</p>
[ { "answer_id": 20249, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 1, "selected": false, "text": "<p>The common consensus seems to be that in cold weather the heart must work harder to maintain the body temperature, and that the arteries contract to save energy, which leads to an increased rate of heart attacks.</p>\n<blockquote>\n<p>'In discussing the weather-heart attack connection, study leader David Erlinge, a professor of cardiology, said cold and windy weather “leads to a contraction of blood vessels in the skin to conserve energy,” which increases the workload of the heart.'</p>\n</blockquote>\n<p>From:</p>\n<blockquote>\n<p><a href=\"https://www.drweil.com/health-wellness/body-mind-spirit/heart/does-cold-weather-cause-heart-attacks/\" rel=\"nofollow noreferrer\">https://www.drweil.com/health-wellness/body-mind-spirit/heart/does-cold-weather-cause-heart-attacks/</a></p>\n</blockquote>\n<p>A comprehensive study has been conducted on the link between the weather and heart attacks:</p>\n<blockquote>\n<p>'We’ve long known that heart attacks are more likely to occur during cold weather. The latest news about this comes from a large study in Sweden that examined every one of the 274,029 heart attacks that occurred in that country between 1998 and 2013 and correlated each one with weather data. This was the most comprehensive study ever performed on weather and heart attacks. The researchers, from Lund University, reported that low temperatures were most strongly associated with the incidence of heart attacks, although they also looked at the effects of other weather factors including the atmospheric pressure, wind velocity, and duration of sunshine on each day of the 16-year study. They reported that heart attack rates were highest in the north of Sweden, which is colder, snowier and windier than other areas. The team also looked at air pollution as a possible risk factor, collecting data on it in Sweden’s three major cities for every day of the study’s duration. They found no evidence that pollution influenced the weather-related findings.'</p>\n</blockquote>\n<p>and the paper referenced:</p>\n<blockquote>\n<p><a href=\"https://jamanetwork.com/journals/jamacardiology/article-abstract/2706610\" rel=\"nofollow noreferrer\">David Erlinge et al, “Association of Weather with Day-to-Day Incidence of Myocardial Infarction A SWEDEHEART Nationwide Observational Study.” JAMA Cardiology, October 24, 2018, doi:10.1001/jamacardio.2018.3466</a></p>\n</blockquote>\n<p>A synopsis of the above paper is here:</p>\n<blockquote>\n<p><a href=\"https://www.hcpfeed.com/2018/10/31/association-of-weather-with-day-to-day-incidence-of-myocardial-infarction/\" rel=\"nofollow noreferrer\">https://www.hcpfeed.com/2018/10/31/association-of-weather-with-day-to-day-incidence-of-myocardial-infarction/</a></p>\n<p>In 274 029 patients, mean (SD) age was 71.7 (12) years. Incidence of MI increased with lower air temperature, lower atmospheric air pressure, higher wind velocity, and shorter sunshine duration. The most pronounced association was observed for air temperature, where a 1-SD increase in air temperature (7.4°C) was associated with a 2.8% reduction in risk of MI (unadjusted incidence ratio, 0.972; 95% CI, 0.967-0.977; P &lt;.001). Results were consistent for non–ST-elevation MI as well as ST-elevation MI and across a large range of subgroups and health care regions.</p>\n</blockquote>\n" }, { "answer_id": 20253, "author": "Steve Foutz", "author_id": 16991, "author_profile": "https://health.stackexchange.com/users/16991", "pm_score": 1, "selected": false, "text": "<p>Vascular resistance in the skin is very closely related to temperature of both outside and body core. Vascular resistance in other body organs is not related to outside temp and the body core temp (37C IS correct) does not change much in absence of disease. \n Studies mentioned above do not imply a cause, only a statistical relationship. Lots of things change when weather gets cold. People cut firewood. Shovel snow. Stay inside and get respiratory diseases. Drink more alcohol. So since these correlational studies don't explain or connect to a cause, you can make up whatever link you want. Maintaining body temperature being hard on the heart doesn't make sense, because core temp is not regulated by the heart, and generating heat is not particularly burdensome to the heart. </p>\n" }, { "answer_id": 20262, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 0, "selected": false, "text": "<p>This is how exposure to cold can result in heart attack:</p>\n\n<ul>\n<li>Cold triggers the release of norepinephrine (noradrenaline), which results in constriction of blood vessels in the skin and thus in an <strong>increase of blood pressure.</strong></li>\n<li>The heart needs to work harder to pump blood against the increased blood pressure, so it <strong>uses more oxygen.</strong></li>\n<li>In individuals with coronary atherosclerosis, the limited blood flow may not be able to deliver enough oxygen to meet increased heart oxygen demand, which results in pain (angina pectoris) or in <strong>ischemic damage of the heart muscle (myocardial infarction).</strong> </li>\n</ul>\n\n<p>The study below has shown that the described mechanism is harmful only for \"cold-intolerant\" patients with prolonged high blood pressure response, while in \"cold-tolerant\" patients, the heart rate can quickly decrease and thus normalize the blood pressure. </p>\n\n<p><a href=\"https://www.sciencedirect.com/science/article/pii/0735109794907471?via%3Dihub\" rel=\"nofollow noreferrer\">Mechanisms of cold intolerances in patients with angina (Journal of the American College of Cardiology, 1994)</a>:</p>\n\n<blockquote>\n <p>Seven cold-intolerant and seven cold-tolerant patients with angina\n underwent exercise treadmill testing at 6 and 25 °C with measurement\n of catecholamines. Baroreceptor function was assessed by the decrease\n in systolic blood pressure after patients stood up from the supine\n position.</p>\n \n <p><strong>Norepinephrine levels increased by 139% in the cold environment,</strong> but there were no differences between cold-intolerant and\n cold-tolerant patients. Consequently, <strong>blood pressure was higher in\n the cold environment</strong> in all patients, but the heart rate was\n similar. However, cold-intolerant patients had a steeper heart rate\n response in the cold and developed ischemia.</p>\n \n <p>Exposure to cold causes an increase in blood pressure with an\n associated increase in myocardial oxygen demand in all patients. In\n cold-tolerant patients, this increase may be offset by a reduction in\n heart rate if baroreceptor function is normal. If baroceptor function\n is abnormal, heart rate may not decrease in response to a cold-induced\n increased in pressure.</p>\n</blockquote>\n\n<p><strong>In conclusion,</strong> exposure to cold can cause heart attack because of increased blood pressure, not thermogenesis. It's unlikely that cold exposure, as expected in everyday environment, would cause heart attack in otherwise healthy individuals, and even in those with coronary atherosclerosis it would more likely cause pain (angina pectoris) rather than the actual heart attack (myocardial infarction). </p>\n" } ]
2019/10/10
[ "https://health.stackexchange.com/questions/20236", "https://health.stackexchange.com", "https://health.stackexchange.com/users/1464/" ]
20,248
<p>I have seen many non-scientific claims that cissus quadrangularis help heal a tendinopathy. For example:</p> <p><a href="https://www.resonatenutrition.com/cissus_quadrangulairs_joint_repair.html" rel="nofollow noreferrer">https://www.resonatenutrition.com/cissus_quadrangulairs_joint_repair.html</a> (<a href="https://web.archive.org/web/20191011162524/http://web.archive.org/screenshot/https://www.resonatenutrition.com/cissus_quadrangulairs_joint_repair.html" rel="nofollow noreferrer">mirror</a>):</p> <blockquote> <p>Today Cissus Quadrangularis is attracting a lot of attention and is used as a supplement in the fitness industry to aid bone recovery and improve body composition (i.e. reduce body fat). It has shown fantastic results for those suffering from joint pain including arthritis, inflammation and Osteoarthritis and many of our clients have found great imrovements in regards to accelerating tendon repair. </p> </blockquote> <p>Does cissus quadrangularis help prevent or heal a tendinopathy?</p>
[ { "answer_id": 20249, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 1, "selected": false, "text": "<p>The common consensus seems to be that in cold weather the heart must work harder to maintain the body temperature, and that the arteries contract to save energy, which leads to an increased rate of heart attacks.</p>\n<blockquote>\n<p>'In discussing the weather-heart attack connection, study leader David Erlinge, a professor of cardiology, said cold and windy weather “leads to a contraction of blood vessels in the skin to conserve energy,” which increases the workload of the heart.'</p>\n</blockquote>\n<p>From:</p>\n<blockquote>\n<p><a href=\"https://www.drweil.com/health-wellness/body-mind-spirit/heart/does-cold-weather-cause-heart-attacks/\" rel=\"nofollow noreferrer\">https://www.drweil.com/health-wellness/body-mind-spirit/heart/does-cold-weather-cause-heart-attacks/</a></p>\n</blockquote>\n<p>A comprehensive study has been conducted on the link between the weather and heart attacks:</p>\n<blockquote>\n<p>'We’ve long known that heart attacks are more likely to occur during cold weather. The latest news about this comes from a large study in Sweden that examined every one of the 274,029 heart attacks that occurred in that country between 1998 and 2013 and correlated each one with weather data. This was the most comprehensive study ever performed on weather and heart attacks. The researchers, from Lund University, reported that low temperatures were most strongly associated with the incidence of heart attacks, although they also looked at the effects of other weather factors including the atmospheric pressure, wind velocity, and duration of sunshine on each day of the 16-year study. They reported that heart attack rates were highest in the north of Sweden, which is colder, snowier and windier than other areas. The team also looked at air pollution as a possible risk factor, collecting data on it in Sweden’s three major cities for every day of the study’s duration. They found no evidence that pollution influenced the weather-related findings.'</p>\n</blockquote>\n<p>and the paper referenced:</p>\n<blockquote>\n<p><a href=\"https://jamanetwork.com/journals/jamacardiology/article-abstract/2706610\" rel=\"nofollow noreferrer\">David Erlinge et al, “Association of Weather with Day-to-Day Incidence of Myocardial Infarction A SWEDEHEART Nationwide Observational Study.” JAMA Cardiology, October 24, 2018, doi:10.1001/jamacardio.2018.3466</a></p>\n</blockquote>\n<p>A synopsis of the above paper is here:</p>\n<blockquote>\n<p><a href=\"https://www.hcpfeed.com/2018/10/31/association-of-weather-with-day-to-day-incidence-of-myocardial-infarction/\" rel=\"nofollow noreferrer\">https://www.hcpfeed.com/2018/10/31/association-of-weather-with-day-to-day-incidence-of-myocardial-infarction/</a></p>\n<p>In 274 029 patients, mean (SD) age was 71.7 (12) years. Incidence of MI increased with lower air temperature, lower atmospheric air pressure, higher wind velocity, and shorter sunshine duration. The most pronounced association was observed for air temperature, where a 1-SD increase in air temperature (7.4°C) was associated with a 2.8% reduction in risk of MI (unadjusted incidence ratio, 0.972; 95% CI, 0.967-0.977; P &lt;.001). Results were consistent for non–ST-elevation MI as well as ST-elevation MI and across a large range of subgroups and health care regions.</p>\n</blockquote>\n" }, { "answer_id": 20253, "author": "Steve Foutz", "author_id": 16991, "author_profile": "https://health.stackexchange.com/users/16991", "pm_score": 1, "selected": false, "text": "<p>Vascular resistance in the skin is very closely related to temperature of both outside and body core. Vascular resistance in other body organs is not related to outside temp and the body core temp (37C IS correct) does not change much in absence of disease. \n Studies mentioned above do not imply a cause, only a statistical relationship. Lots of things change when weather gets cold. People cut firewood. Shovel snow. Stay inside and get respiratory diseases. Drink more alcohol. So since these correlational studies don't explain or connect to a cause, you can make up whatever link you want. Maintaining body temperature being hard on the heart doesn't make sense, because core temp is not regulated by the heart, and generating heat is not particularly burdensome to the heart. </p>\n" }, { "answer_id": 20262, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 0, "selected": false, "text": "<p>This is how exposure to cold can result in heart attack:</p>\n\n<ul>\n<li>Cold triggers the release of norepinephrine (noradrenaline), which results in constriction of blood vessels in the skin and thus in an <strong>increase of blood pressure.</strong></li>\n<li>The heart needs to work harder to pump blood against the increased blood pressure, so it <strong>uses more oxygen.</strong></li>\n<li>In individuals with coronary atherosclerosis, the limited blood flow may not be able to deliver enough oxygen to meet increased heart oxygen demand, which results in pain (angina pectoris) or in <strong>ischemic damage of the heart muscle (myocardial infarction).</strong> </li>\n</ul>\n\n<p>The study below has shown that the described mechanism is harmful only for \"cold-intolerant\" patients with prolonged high blood pressure response, while in \"cold-tolerant\" patients, the heart rate can quickly decrease and thus normalize the blood pressure. </p>\n\n<p><a href=\"https://www.sciencedirect.com/science/article/pii/0735109794907471?via%3Dihub\" rel=\"nofollow noreferrer\">Mechanisms of cold intolerances in patients with angina (Journal of the American College of Cardiology, 1994)</a>:</p>\n\n<blockquote>\n <p>Seven cold-intolerant and seven cold-tolerant patients with angina\n underwent exercise treadmill testing at 6 and 25 °C with measurement\n of catecholamines. Baroreceptor function was assessed by the decrease\n in systolic blood pressure after patients stood up from the supine\n position.</p>\n \n <p><strong>Norepinephrine levels increased by 139% in the cold environment,</strong> but there were no differences between cold-intolerant and\n cold-tolerant patients. Consequently, <strong>blood pressure was higher in\n the cold environment</strong> in all patients, but the heart rate was\n similar. However, cold-intolerant patients had a steeper heart rate\n response in the cold and developed ischemia.</p>\n \n <p>Exposure to cold causes an increase in blood pressure with an\n associated increase in myocardial oxygen demand in all patients. In\n cold-tolerant patients, this increase may be offset by a reduction in\n heart rate if baroreceptor function is normal. If baroceptor function\n is abnormal, heart rate may not decrease in response to a cold-induced\n increased in pressure.</p>\n</blockquote>\n\n<p><strong>In conclusion,</strong> exposure to cold can cause heart attack because of increased blood pressure, not thermogenesis. It's unlikely that cold exposure, as expected in everyday environment, would cause heart attack in otherwise healthy individuals, and even in those with coronary atherosclerosis it would more likely cause pain (angina pectoris) rather than the actual heart attack (myocardial infarction). </p>\n" } ]
2019/10/11
[ "https://health.stackexchange.com/questions/20248", "https://health.stackexchange.com", "https://health.stackexchange.com/users/43/" ]
20,306
<p>Medicine is not my field, nor do I have mesothelioma. I'm also not seeking any clinical trials or experimental treatment. However, sometimes I find myself trying my read medical papers, either out of sheer interest or if I have a serious complication. I want to stress that I don't think self-diagnosis is a good idea, I just can't help myself sometimes.</p> <p>I find that quite a few papers I get from PubMed appear to be a "study of one". Consider this paper <a href="https://academic.oup.com/ejcts/article/41/6/1393/420831" rel="nofollow noreferrer">https://academic.oup.com/ejcts/article/41/6/1393/420831</a></p> <p>Or this: <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5728971/" rel="nofollow noreferrer">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5728971/</a></p> <p>I'm not saying this is a bad paper, I have no idea. However, I am curious as to how common and accepted this type of paper is within the field of medicine.</p> <p>On one hand, I can see that for pushing the limits of surgery, or any technique, it is interesting to see what people have had success with, even if it is just one patient. On the other hand, it is just one patient. How can anything be generalized from this?</p> <p>Is there a difference between treatment with medications and surgical technique? I can imagine that surgical techniques can be replicated with far more accuracy than results from medication, which are plagued by placebo and unclear method of operation (I'm making this stuff up, so please correct me).</p> <p>Again, I have no grounds of criticizing the work of either of the papers, they are just used as examples, and as mentioned, there are quite a few such papers. Indeed, if I do a search for "we present a case of", I get a ton of results for actual papers that lead with this. I'm sure there are many other, similar phrases that are also used for these single study cases.</p> <p>My question is simply, what does the academic medical field think of this type of paper? Can such a paper be a good paper? Is it usually considered a "bad paper", when compared to a paper that has, for example, many patients that received the same treatments, where variations and complications are discussed? Is this sort of paper simply part of the cutting edge of medical science, that all results are useful?</p>
[ { "answer_id": 20307, "author": "JohnP", "author_id": 64, "author_profile": "https://health.stackexchange.com/users/64", "pm_score": 2, "selected": false, "text": "<p>The difference is that you are looking at a case study, versus a scientific research study.</p>\n\n<p>The basic difference is that a case study is an in depth look at a single instance of something which may not be repeatable by others, and a scientific study is a broader examination of a group with results and experiments that can be repeated by others.</p>\n\n<p>As an example: Your second study is a specific surgical intervention in a case of a man that had a recurrent tumor in a specific spot with malignant pleural mesothelioma. This is not something that is likely to be repeatable over and over by others, but it still worth examining in case it happens again. So it's written up as a case study, and presented as such.</p>\n" }, { "answer_id": 20310, "author": "Nate", "author_id": 12678, "author_profile": "https://health.stackexchange.com/users/12678", "pm_score": 4, "selected": true, "text": "<p>To build off of what JohnP said, scientific evidence has a hierarchy of reliability. Some types of papers, by their very nature, are more academically rigorous and likely to lead you to the truth.</p>\n\n<p>Randomized controlled double-blind trials and meta-analyses are at the top of the hierarchy. These studies often have thousands of participants and are set up to produce statistically significant results. These studies form the backbone of evidence-based medicine.</p>\n\n<p>A case study, which looks at a finding or condition seen in one patient, is at the bottom of the hierarchy. It's impossible to draw true evidence-based conclusions off of this type of paper, since it essentially says \"here's what we saw, here's what we did, here's what happened\".</p>\n\n<p>However, case studies should not be written off as useless. There are two primary ways that these types of studies can be helpful. </p>\n\n<ul>\n<li>If you are treating a patient with an extremely rare condition or constellation of symptoms, a case study is the best guide you're going to get. If someone else did something which worked in a similar patient, that treatment may work in your patient. Many of those rare diseases will simply never have enough patients to fuel a randomized controlled trial.</li>\n<li>If there is an emerging phenomenon that has not yet been described in the literature. 2 notable examples are HIV/AIDS and the much more recent vaping pneumonitis. Both of these conditions were first identified by case reports (or case series, which is the same thing but with a handful of patients). This brought the issue to wider attention, and once this happened many other similar reports started pouring in. This can direct more academically rigorous research in that direction.</li>\n</ul>\n\n<p>References:</p>\n\n<p><a href=\"https://www.cdc.gov/mmwr/preview/mmwrhtml/june_5.htm\" rel=\"noreferrer\">First case series of patients with complications of AIDS</a></p>\n\n<p><a href=\"https://www.nejm.org/doi/10.1056/NEJMoa1911614\" rel=\"noreferrer\">First case series of vaping pneumonitis</a></p>\n" }, { "answer_id": 20317, "author": "Timur Shtatland", "author_id": 17046, "author_profile": "https://health.stackexchange.com/users/17046", "pm_score": 3, "selected": false, "text": "<p>\"Studies of one\" are also known as case studies, N-of-1 studies or case reports. I will refer to them below as <strong>case reports</strong>, for simplicity. They vary in quality just like any other type of studies. Case reports have a place in biomedical research and can often be very valuable, widely cited and/or otherwise influential. Double-blind randomized controlled clinical trials (RCTs), or, better, meta-analysis of multiple such trials, are the current gold standard. But they are obviously not always feasible for a variety of reasons.</p>\n\n<p>There are specific guidelines for writing case reports, for example:</p>\n\n<p>Riley D.S., et al (2017) J Clin Epidemiol. 89:218-235. doi: 10.1016/j.jclinepi.2017.04.026. CARE guidelines for case reports: explanation and elaboration document. <a href=\"https://www.sciencedirect.com/science/article/pii/S0895435617300379\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/pii/S0895435617300379</a></p>\n\n<p>This above article also lists a number of peer-reviewed journals that explicitly accept case reports (Table 1), important historical examples of case reports (section 1.1), and different types of case reports with specific examples (section 2).</p>\n\n<p><strong>Types of case reports:</strong></p>\n\n<ul>\n<li><p><strong>Research where the number of patients is limited for any reason.</strong> For example, research conducted the beginning of a potential disease outbreak, research on uniquely informative patients, reports of rare drug side effects, drug-drug and food-drug interactions. Others in this thread have also listed rare condition treatment and emerging phenomena.</p></li>\n<li><p><strong>Research that carries high cost</strong>. For example, whole genome or whole exome sequencing when those studies were still very expensive.</p></li>\n<li><p><strong>Research that cannot be applied in RCT for any reason, such as limitations of input, treatment scarcity, ethical considerations, etc.</strong></p></li>\n</ul>\n\n<p><strong>Specific examples and references:</strong></p>\n\n<ol>\n<li>Chen H., et al (2014) Lancet. 383(9918):714-21. doi: 10.1016/S0140-6736(14)60111-2. Clinical and epidemiological characteristics of a fatal case of avian influenza A H10N8 virus infection: a descriptive study. <a href=\"https://www.sciencedirect.com/science/article/pii/S0140673614601112\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/pii/S0140673614601112</a></li>\n</ol>\n\n<blockquote>\n <p>We report the first human infection with a novel reassortant avian\n influenza A H10N8 virus.</p>\n</blockquote>\n\n<ol start=\"2\">\n<li>Byun M., et al. (2010) J Exp Med. 207(11):2307-12. doi: 10.1084/jem.20101597. Whole-exome sequencing-based discovery of STIM1 deficiency in a child with fatal classic Kaposi sarcoma. <a href=\"http://jem.rupress.org/content/207/11/2307.long\" rel=\"nofollow noreferrer\">http://jem.rupress.org/content/207/11/2307.long</a></li>\n</ol>\n\n<blockquote>\n <p>Whole-exome sequencing-based discovery of STIM1 deficiency in a child\n with fatal classic Kaposi sarcoma.</p>\n</blockquote>\n\n<ol start=\"3\">\n<li>Garrett-Bakelman F.E., et al. (2019) Science. 364(6436). pii: eaau8650. doi: 10.1126/science.aau8650. The NASA Twins Study: A multidimensional analysis of a year-long human spaceflight. <a href=\"https://science.sciencemag.org/content/364/6436/eaau8650.long\" rel=\"nofollow noreferrer\">https://science.sciencemag.org/content/364/6436/eaau8650.long</a></li>\n</ol>\n\n<blockquote>\n <p>[...] significant changes in multiple data types were observed in\n association with the spaceflight period; the majority of these\n eventually returned to a preflight state within the time period of the\n study. These included changes in telomere length, gene regulation\n measured in both epigenetic and transcriptional data, gut microbiome\n composition, body weight, carotid artery dimensions, subfoveal\n choroidal thickness and peripapillary total retinal thickness, and\n serum metabolites.</p>\n</blockquote>\n\n<p><strong>Addressing your specific questions about \"studies of one\", N=1 studies, case studies, or case reports:</strong></p>\n\n<blockquote>\n <p>What does the academic medical field think of this type of paper?</p>\n</blockquote>\n\n<p>It depends on the field, and the quality of the specific study, and can vary a lot between respected, influential, etc, and irrelevant, not even acceptable for publication in high quality journal.</p>\n\n<blockquote>\n <p>Can such a paper be a good paper?</p>\n</blockquote>\n\n<p>Yes, again, depending on the field, and the quality of the specific study.</p>\n\n<blockquote>\n <p>Is it usually considered a \"bad paper\", when compared to a paper that\n has e.g. many patients that received the same treatments, where\n variations and complications are discussed?</p>\n</blockquote>\n\n<p><em>All other things being equal</em>, obviously a case study with N=1 would be inferior to a study with multiple independent patients. In cases like this, N=1 papers would have a hard time getting through peer review in high quality journals, because the reviewers are likely to be aware of the current standards in that specific field, such as RCTs, epidemiological or association studies. I doubt N=1 study on the effects of a well-known statin on cholesterol would be published, if multiple double-blind RCTs are already available on orders of magnitude more patients.</p>\n\n<blockquote>\n <p>Is this sort of paper simply part of the cutting edge of medical\n science, that all results are useful?</p>\n</blockquote>\n\n<p>In the context of this question, one can assume that a high quality case study is indeed \"cutting edge\", and there is a reason why N=1 was the best one could get at the time.</p>\n" } ]
2019/10/24
[ "https://health.stackexchange.com/questions/20306", "https://health.stackexchange.com", "https://health.stackexchange.com/users/12417/" ]
20,325
<p>Melatonin supplements are readily available over-the-counter. However, the dosage is not regulated and there are supplements available in a wide variety of doses.</p> <p>Information on how much melatonin the body is naturally producing is difficult to find, except to say that it varies by age. </p> <p>Being able to compare how much a supplement offers versus how much the body naturally produces could help people to have an informational conversation with their doctor about supplementation dosing. So, what is the range of naturally produced melatonin in the body per day?</p>
[ { "answer_id": 20332, "author": "Asad Iqbal", "author_id": 17068, "author_profile": "https://health.stackexchange.com/users/17068", "pm_score": 0, "selected": false, "text": "<p>EDIT:\nI misread before, so fixing with this edit. \nHere is more authentic resource: \n<a href=\"https://www.encyclopedia.com/science-and-technology/biochemistry/biochemistry/melatonin\" rel=\"nofollow noreferrer\">https://www.encyclopedia.com/science-and-technology/biochemistry/biochemistry/melatonin</a></p>\n\n<p>\"The typical adult male produces about 30 micrograms of melatonin during a typical day.\"</p>\n" }, { "answer_id": 20502, "author": "Bob Ortiz", "author_id": 16786, "author_profile": "https://health.stackexchange.com/users/16786", "pm_score": 1, "selected": false, "text": "<p>According to encyclopedia.com <sup>1</sup> the production of the hormone melatonin (5-methoxy-N-acetyltrypt-amine) varies over the course of a lifetime and over the course of a day.</p>\n<p>Newborn babies produce very little of this hormone but after the first few months of life the pineal gland <em>increases</em> its production of melatonin. The highest levels occur in children who are about four to seven years old. Older children and adults produce smaller amounts, as production <em>gradually decreases</em> during puberty. The typical <strong>adult male produces</strong> about <strong>30 micrograms</strong> of melatonin <strong>during a typical day</strong>.</p>\n<p>Also, the environment affects the production of melatonin. Darkness stimulates the pineal gland to produce melatonin, while the presence of light inhibits the release of this hormone. Exposure to (artificial) light during the night will inhibit melatonin production.</p>\n<p>Lastly, regarding melatonin supplementation in adults the standard dose used in studies ranges between 1 and 10 mg, although there isn’t currently a definitive “best” dosage. It’s believed supplements with a dosage in the 30-mg range may be harmful <sup>2</sup>. While the Canadian Paediatric Society recommends 1 mg of melatonin in infants, 2.5 to 3 mg in older children, and 5 mg in adolescents. <sup>3</sup></p>\n<hr />\n<p><sup> <em>1. <a href=\"https://www.encyclopedia.com/science-and-technology/biochemistry/biochemistry/melatonin\" rel=\"nofollow noreferrer\">https://www.encyclopedia.com/science-and-technology/biochemistry/biochemistry/melatonin</a></em></sup><br>\n<sup><em>2. <a href=\"https://bjanaesthesia.org/article/S0007-0912(17)31962-1/fulltext\" rel=\"nofollow noreferrer\">https://bjanaesthesia.org/article/S0007-0912(17)31962-1/fulltext</a></em></sup><br>\n<sup><em>3. Cummings C. Melatonin for the management of sleep disorders in children and adolescents. Paediatr Child Health. 2012;17(6):331–3 <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3380753/?report=reader\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3380753/?report=reader</a></em></sup></p>\n" } ]
2019/10/27
[ "https://health.stackexchange.com/questions/20325", "https://health.stackexchange.com", "https://health.stackexchange.com/users/9246/" ]
20,334
<p>Is it possible to physically simulate hypoxic training by doing periodic breath holds or breath regulation during aerobic activity? </p> <p>Ideally, it ought to be done in a hypobaric/hypoxic chamber whilst strapped to some monitors. But short of that, I can think of two ways - </p> <ol> <li>While running, every few minutes, I can try to hold my breath for a couple of steps initially and gradually increase it to 8-10 steps </li> <li>if I normally run say 6 steps per inhalation+exhalation cycle and I try to increase it to 7 and further on. </li> </ol> <p>What I would like to understand is </p> <ol> <li>if it will work?</li> <li>the risks involved, and how to mitigate them (e.g. a pulse oximeter on a finger to monitor?)</li> </ol> <p>I considered posting this question on the physical fitness SE, but did it here instead considering that I would prefer an answer by someone trained in the medical sciences. </p> <p>In general, based on past work (ref: <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0180380" rel="nofollow noreferrer">1</a>, <a href="https://www.researchgate.net/publication/280730398_Hypoxic_training_methods_for_improving_endurance_exercise_performance" rel="nofollow noreferrer">2</a>, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5721177/" rel="nofollow noreferrer">3</a>, and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6135973/" rel="nofollow noreferrer">4</a>) it seems that intermittent hypoxic training is indeed beneficial. But most "professional" work (both researchers and athletes) in the area uses hypoxic chambers - which is not practical for the average internet user. </p> <p>What is less clear is if breath control is an adequate method of simulating hypoxic training. The only reliable references (<a href="http://www.runbetternow.net/2016/03/01/breath-hold-exercise-better-for-hypoxic-training-than-elevation-training-mask/" rel="nofollow noreferrer">the runnbetternow website</a> and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3361916/" rel="nofollow noreferrer">an NIH publication by a yoga center</a>) I could find aren't exactly by medical professionals. FWIW, these references are in favor of the method. The question is if medical practitioners agree. </p> <p>The end goal here is to prepare for mountain activities. As it is not practical to move one's permanent base to a mountain top, one would like to be able to somehow simulate high altitude training whilst still living at sea level. Of course, this will be in addition to (not in lieu of) actually periodically training at altitude. </p>
[ { "answer_id": 20338, "author": "JohnP", "author_id": 64, "author_profile": "https://health.stackexchange.com/users/64", "pm_score": 3, "selected": true, "text": "<p>The approach you describe most likely will not work, and could be detrimental to your training.</p>\n\n<p>The main benefit of training at altitude is that the body will adapt to the lower concentration of oxygen by stimulating the production of erythropoietin which in turn causes the body to produce more red blood cells.</p>\n\n<p>What you are describing is a very limited version of intermittent hypoxic training (IHT). In subelite athletes, <a href=\"https://journals.humankinetics.com/view/journals/ijspp/4/1/article-p68.xml\" rel=\"nofollow noreferrer\">this has been shown</a> to have some effect, however it was 60 minutes of training using a protocol of 3-5 minutes of hypoxia followed by the same amount of time of normoxia (normal breathing). (Also <a href=\"https://www.sciencedirect.com/science/article/pii/S2095254615000836#bib0180\" rel=\"nofollow noreferrer\">cited here</a>.)</p>\n\n<blockquote>\n <p>In a study of male subelite competitive cyclists and triathletes, athletes were exposed to intermittent hypoxia (artificial brief intermittent LHTL) for 15 days over 3 weeks for 60 min per day with either 3 or 5 min periods of hypoxia followed by the same duration in normoxia. Cycling performance improved during incremental step exercise, including increases of 4.7% ± 3.1% in peak aerobic power, 4.4% ± 3.0% in lactate profile power, and 6.5% ± 5.3% in heart rate profile power compared to control measured 3 days post-intervention.35 Fourteen days after treatment, differences between the hypoxia groups were unclear, suggesting that intermittent hypoxia training should be timed for competitive events to take place within a few days following treatment. In a similar study, performance did not improve among elite athletes,36 suggesting that artificial brief intermittent LHTL should be considered mainly by subelite athletes.</p>\n</blockquote>\n\n<p>The most common method of attempting to achieve this is a training mask, which restricts air flow. Most studies (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4879455/\" rel=\"nofollow noreferrer\">like this one</a>) reject the claim that it helps by actually simulating altitude, but they do note that it helps train the respiratory muscles and may help improve lung usage.</p>\n\n<p>The short period that you describe really won't have enough of an impact on the body to stimulate altitude related changes in blood and plasma.</p>\n" }, { "answer_id": 20353, "author": "Michael Paul", "author_id": 8080, "author_profile": "https://health.stackexchange.com/users/8080", "pm_score": 1, "selected": false, "text": "<p>Since there is a good answer already I'll just add my two cents from my understanding of physiology: \nHypoventilation has two effects during exercise:</p>\n\n<ol>\n<li>Less available oxygen in your lungs and a somewhat less amount of oxygen in the blood that comes out of your lungs, which is not as big a difference as you might expect because hemoglobin is incredibly efficient at sucking up all available oxygen. Under stress conditions (heat, acid metabolites and CO2 all inhibit the binding of oxygen to hemoglobin) this sucking up is somewhat dampened but if the gradient is large enough large quantities of oxygen are still easily captured in the lungs.</li>\n<li>A large increase of CO2 in your blood, which in turn stimulates your breathing reflex, making it near impossible to force yourself to breathe less. This effect would be much larger.</li>\n</ol>\n\n<p>Furthermore, to be successful at high altitude survival there is one key aspect that needs to be there, and I'm not sure if it can be trained: Hyperventilation is essential to get enough oxygen into your blood under hypoxic conditions. Most people don't have a strong enough breathing reflex though to breath more when oxygen is low and CO2 is normal or low. It's not natural to hyperventilate, and not very healthy either. Maybe it can be trained at sea level to compensate for the stress that hyperventilation causes on your body? </p>\n\n<p>Interestingly, the people of Tibetan descent that lived in the Himalaya evolved a protecting mechanism <strong>against</strong> the increase of red blood cells during long stays at high altitudes. Other peoples that live at high altitude, for example those that live in the Andes lack this protection and their blood thickens up to a point where it causes serious health problems. </p>\n\n<p>Dehydration is another serious threat at high altitude: hyperventilation makes you lose plenty of water through your breath. And brain swelling is also a nasty complication of stays at very high altitudes...</p>\n" } ]
2019/10/29
[ "https://health.stackexchange.com/questions/20334", "https://health.stackexchange.com", "https://health.stackexchange.com/users/7299/" ]
20,406
<p>I have asked here the question <a href="https://medicalsciences.stackexchange.com/questions/20389/">convention about best terms to take 5 htp</a>.<br> Questions like <em>convention about best terms to take X for humans</em>, might be too narrow, because, theoretically, as more possibly-therapeutic molecules are discovered, there could be an endless growth of questions like this. To me that's a problem and I didn't find the possible solution as described below.</p> <p>When I searched a knowledge base containing administration guidelines on all possibly-therapeutic molecules known in earth (as medicines and/or nutritional supplements) I found only printed books aimed for physicians, edited and published by a given country's health ministry; but nothing standardized globally and available for free read if Wikipedia is taken out of the picture.</p> <p>I thought; for example:<br> If there is the <em>International Statistical Classification of Diseases and Related Health Problems</em> (ICD) as fa form of standardization,<br> There should be a similarly designed drug standardization.</p> <p>There are sites like <a href="http://drugbank.com" rel="nofollow noreferrer">drugs.com</a> or <a href="https://drugbank.ca4" rel="nofollow noreferrer">drugbank.ca</a> but there is nothing globally standardized such as ICD for diseases.</p> <p>A globally standardized drug database could include the following variables, for example:</p> <ul> <li>The drug is recognized in at least 1 country as Dietary supplement / Medicine / both</li> <li>Priming tests for sensitivity</li> <li>Priming tests for allergy </li> <li>Ethnic groups that are likely to have sensitivity and/or allergy</li> <li>BMI adjustment</li> <li>On label usages (per global recommend)</li> <li>Off label usages (per local recommend)</li> <li>Therapeutic dosages</li> <li>Best to be taken before meal / in the middle of the meal / after meal</li> <li>foods and dietary supplements that might interact</li> <li>medicines that might interact</li> <li>The drug is best to be taken at which time of day (for example, in general Melatonin is best to be taken at night for some elderly and for some of those suffering from Free Running Sleep Disorder (FRSD) as well.</li> <li>chance for dependency/addiction</li> <li>Possible ways of admittance</li> <li>Communal recommendation for admittance (if there is one)</li> <li>and so forth</li> </ul> <p>Right now, the closest thing I found is individual sites as mentioned above or the drug categories in Wikipedia, but nothing standardized. </p> <p><strong>As ICD is a global standardization of diseases, is there a global standardization of drugs and if not, why?</strong></p>
[ { "answer_id": 20407, "author": "Chris Rogers", "author_id": 7951, "author_profile": "https://health.stackexchange.com/users/7951", "pm_score": 2, "selected": false, "text": "<p>The idea that the International Statistical Classification of Diseases and Related Health Problems (ICD) forms an international standard on health problems is contentious within some groups of people when there is the <a href=\"https://www.psychiatry.org/psychiatrists/practice/dsm\" rel=\"nofollow noreferrer\">Diagnostic and Statistical Manual of Mental Disorders (DSM)</a>, which cross-references the ICD and there can sometimes be conflicting criteria stated, (see <a href=\"https://journal.ahima.org/2016/08/10/dsm-5-vs-icd-10-cm/\" rel=\"nofollow noreferrer\">https://journal.ahima.org/2016/08/10/dsm-5-vs-icd-10-cm/</a> for more on that) but that is a separate issue.</p>\n\n<p>When it comes to an international standards for drugs, different countries have different regulations regarding drug use and drug licensing (see <a href=\"https://www.gov.uk/government/collections/drugs-licensing\" rel=\"nofollow noreferrer\">https://www.gov.uk/government/collections/drugs-licensing</a> for example on UK drug licensing) and therefore having an international control on drugs would not work.</p>\n\n<p>You mentioned drugs.com (US) and drugsbank.ca (Canada) and there is a go to for the UK medical profession called the <a href=\"https://bnf.nice.org.uk/\" rel=\"nofollow noreferrer\">British National Formulary (BNF)</a> which is part of the <a href=\"https://www.nice.org.uk/\" rel=\"nofollow noreferrer\">National Institute for Health and Care Excellence (NICE)</a>. I am pretty sure there are similar organisations in other countries controlling the use of drugs.</p>\n" }, { "answer_id": 20409, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 3, "selected": true, "text": "<p>I think the closest thing to a \"standardization of drugs\" are the pharmacopeia:</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/United_States_Pharmacopeia\" rel=\"nofollow noreferrer\">USP</a></p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/European_Pharmacopoeia\" rel=\"nofollow noreferrer\">European Pharmacopoeia</a></p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Japanese_Pharmacopoeia\" rel=\"nofollow noreferrer\">Japanese Pharmacopoeia</a></p>\n\n<p>(just some examples)</p>\n\n<p>As you will notice, these are not global standards, but each one defines the parameters by which a drug is of adequate quality and purity to be deemed that drug. To generate a global standard, it would be necessary to combine some truly massive documents into one, which would require agreement among everyone regarding which standards to use in the unified document.</p>\n\n<p>The WHO has an effort to make such a resource:</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/The_International_Pharmacopoeia\" rel=\"nofollow noreferrer\">The International Pharmacopoeia</a></p>\n\n<p>But as of now, it is more of a recommendation than a legally enforceable document in most locations (as far as I know). The WHO also has a great document talking about various pharmacopeia:</p>\n\n<p><a href=\"https://www.who.int/medicines/areas/quality_safety/quality_assurance/resources/InternationalMeetingWorldPharmacopoeias_QAS13-512Rev1_25032013.pdf\" rel=\"nofollow noreferrer\">https://www.who.int/medicines/areas/quality_safety/quality_assurance/resources/InternationalMeetingWorldPharmacopoeias_QAS13-512Rev1_25032013.pdf</a></p>\n\n<p>including their legal basis, origins, and a bit of history about attempts to develop international pharmacopeia.</p>\n\n<p>In that sense, it's somewhat more remarkable that there are internationally recognized diagnostic codes than that there isn't a (legally binding) internationally standardized pharmacopoeia.</p>\n\n<p>See also: <a href=\"https://xkcd.com/927/\" rel=\"nofollow noreferrer\">https://xkcd.com/927/</a></p>\n\n<p>The pharmacopeia are more interested in the manufacture and identity of drugs (and supplements), rather than indications or dosage recommendations. These are far too complex and depend on other variables to be collected in a single reference. That's partly why physicians and pharmacists exist, and why you should consult them for medical advice.</p>\n\n<p>Similarly, the ICD-10 is not something like a dichotomous key for diagnosis. It contains a list of diseases and their characteristics for standardization and billing purposes, but it is not a substitute for a physician's care.</p>\n" } ]
2019/11/14
[ "https://health.stackexchange.com/questions/20406", "https://health.stackexchange.com", "https://health.stackexchange.com/users/-1/" ]
20,442
<p>Are there ~simple means to reduce risk of GI (gastro-intestinal) bleeding associated with NSAIDs (non-steroidal anti-inflammatory drugs)(ie aspirin) - besides the common-sense answers?:</p> <ul> <li>Take with food</li> <li>Don't take NSAIDs ("and you'll have no risk")</li> <li>Etc.</li> </ul> <p>By 'simple means', I mean: specific foods, supplements, or over-the-counter drugs that make a difference?</p>
[ { "answer_id": 20446, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": true, "text": "<p>There is convincing evidence that measures, like crushing the tablets before use, taking them with food or water, lower doses and temporary discontinuation of use, are associated with the <strong>lower risk of gastrointestinal bleeding.</strong> </p>\n\n<p>DISCLAIMER: This information is not intended to interfere with any drug regime prescribed by a doctor.</p>\n\n<h2>How NSAIDs cause gastrointestinal bleeding?</h2>\n\n<p>According to <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/10749095\" rel=\"nofollow noreferrer\">Best Practice &amp; Research: Clinical Gastroenterology, 2000</a>:</p>\n\n<blockquote>\n <p>NSAIDs can cause damage to the gastroduodenal mucosa via several\n mechanisms, including the topical irritant effect of these drugs on\n the epithelium, impairment of the barrier properties of the mucosa,\n suppression of gastric prostaglandin synthesis, reduction of gastric\n mucosal blood flow and interference with the repair of superficial\n injury.</p>\n</blockquote>\n\n<h2>What can reduce the risk of bleeding?</h2>\n\n<p><strong>1) Chewing the tablet and taking it with food or water:</strong></p>\n\n<blockquote>\n <p>Don't swallow the aspirin pill; chew it, and then swallow it with a\n glass of water. Doing it that way gets the aspirin into your system\n rapidly, which is what you want. <em>(<a href=\"https://www.health.harvard.edu/heart-health/does-aspirin-stop-a-heart-attack\" rel=\"nofollow noreferrer\">Harvard Medical School</a>)</em></p>\n</blockquote>\n\n<p>Chewing will break the tablet, making it to go through the stomach faster thus decreasing its erosive effect. Water will stimulate gastric emptying thus reducing the contact time of aspirin with gastric mucosa. <em>Note, that milk or fruit juice will slow down gastric emptying.</em> You can still take aspirin with food or with food and water. Food will slow gastric emptying of aspirin, but will dilute it. I don't know which is better, food or water, but both make sense. </p>\n\n<p><strong>2) Smaller doses</strong> of NSAIDs will be likely less erosive that the greater ones.</p>\n\n<blockquote>\n <p>New formulations of NSAIDs may reduce risks of adverse events by using\n lower doses while providing effective analgesia.</p>\n \n <p>Lower-dose capsules that contain finely milled, rapidly absorbed NSAID\n particles may also provide analgesia at lower systemic doses. <em>(<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4310346/\" rel=\"nofollow noreferrer\">Drug, Healthcare and Patient Safety, 2015</a>)</em></p>\n</blockquote>\n\n<p><strong>3) Topical NSAIDs</strong> reduce the risk of side effects:</p>\n\n<blockquote>\n <p>Topical NSAIDs provided good levels of pain relief in acute conditions\n such as sprains, strains and overuse injuries, probably similar to\n that provided by oral NSAIDs. Gel formulations of diclofenac (as\n Emugel®), ibuprofen, and ketoprofen, and some diclofenac patches,\n provided the best effects. Adverse events were usually minimal. <em>(<a href=\"https://www.cochrane.org/CD007402/SYMPT_topical-non-steroidal-anti-inflammatory-drugs-acute-musculoskeletal-pain-adults\" rel=\"nofollow noreferrer\">Cochrane, 2015</a>)</em></p>\n</blockquote>\n\n<p><strong>4) Temporary discontinuation</strong> of NSAIDs reduces the risk of GI bleeding:</p>\n\n<blockquote>\n <p>All types and formulations of NSAIDs appear to increase the risk of\n UGIBs <em>[upper gastrointestinal bleedings]</em> but the effect appear not to be cumulative and diminish rapidly\n with discontinue of use. <em>(<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1874281/\" rel=\"nofollow noreferrer\">British Journal of Clinical Pharmacology, 2002</a>)</em></p>\n</blockquote>\n\n<p><strong>5) Vitamin C</strong></p>\n\n<blockquote>\n <p>Ascorbic acid supplementation has been associated with a decreased\n incidence of bleeding from peptic ulcer disease and with a reduction\n in NSAID-associated gastric mucosal damage. <em>(<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874117/\" rel=\"nofollow noreferrer\">Digestive Diseases and Sciences</a>)</em></p>\n</blockquote>\n\n<p>Aspirin + vitamin C tablets exist. </p>\n\n<p><strong>6 Foods to AVOID</strong></p>\n\n<ul>\n<li>Alcohol + NSAIDs can increase the risk of GI bleeding (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/10566713\" rel=\"nofollow noreferrer\">Am J Gatroenterol, 1999</a>)</li>\n</ul>\n\n<p><strong>7) Some NSAIDs are less often associated with GI bleeding than others:</strong></p>\n\n<p>According to the systematic review of studies <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714137/\" rel=\"nofollow noreferrer\">Individual NSAIDs and Upper Gastrointestinal Complications (Drugs Safety, 2012)</a>, NSAIDs with the lowest risk of GI bleeding are aceclofenac, celecoxib and ibuprofen, and the ones with the highest risk are piroxicam, ketorolac and azapropazone (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714137/figure/Fig2/\" rel=\"nofollow noreferrer\">Fig. 2</a>).</p>\n\n<hr>\n\n<p>Using OTC drugs, such as sucralfate and antacides, sounds promising but was disappointing in reducing the risk of GI bleeding:</p>\n\n<blockquote>\n <p>Despite promising results with <em>sucralfate</em> in smaller studies [30] or\n for short-term prophylaxis [26, 31], a randomized, controlled trial\n conduced by Agrawal and coworkers failed to show a significant benefit\n of sucralfate in the prevention of gastric ulcers in contrast to\n misoprostol [32].</p>\n \n <p>Data concerning <em>antacids</em> in the prevention of NSAID-related gastric\n mucosal injury are scarce, and also disappointing. Especially for\n long-term prophylaxis no clinical effect was observed with low-dose\n antacids [26]. <em>(<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1874281/\" rel=\"nofollow noreferrer\">British Journal of Clinical Pharmacology, 2002</a>)</em></p>\n</blockquote>\n" }, { "answer_id": 20497, "author": "practiZ", "author_id": 15382, "author_profile": "https://health.stackexchange.com/users/15382", "pm_score": 1, "selected": false, "text": "<p>Speaking from my humble experience, <strong>when prescribing NSAIDs</strong> (especially long-term, e.g. Aspirin as thrombosis prophylaxis) it is standard to <strong>combine those with PPIs</strong> (Proton Pump Inhibitors) as preventive medication against NSAID-associated GI-events. Clinical trials of this therapy generally show positive outcomes (you can find different articles on this subject, such as <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891010/\" rel=\"nofollow noreferrer\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3891010/</a>) which, of course, can be subject to discussion.</p>\n" } ]
2019/11/19
[ "https://health.stackexchange.com/questions/20442", "https://health.stackexchange.com", "https://health.stackexchange.com/users/13025/" ]
20,486
<p>I purchased a neti-pot, which came with salt packets: how is this salt different from table salt? Any reference or support is always appreciated</p> <p>UPDATE: My <a href="https://www.youtube.com/watch?v=wVkwHIH6NbA" rel="nofollow noreferrer">Bayer HyrdraSense Nasal Rinse Kit</a> salt packets contain MgCl NaCl, CaCl Na-Bicarbonate KCl. Instructions include boiling tap water and then cooling it to room temperature.</p> <p><a href="https://i.stack.imgur.com/sygoY.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/sygoY.jpg" alt="enter image description here"></a></p>
[ { "answer_id": 20495, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p>MgCl NaCl, CaCl, Na-Bicarbonate, and KCl can be all found in sea water and therefore in <a href=\"https://en.wikipedia.org/wiki/Sea_salt\" rel=\"nofollow noreferrer\">sea salt</a>, which means that this salt appears similar to sea salt, but it is obviously not natural sea salt because the description of <a href=\"https://www.hydrasense.ca/en/products/nasal-care/self-mix-nasal-care/netirinse/\" rel=\"nofollow noreferrer\">this HydraSense salt</a> says:</p>\n<blockquote>\n<p>The pre-measured and ready-to-mix salt packets contain: calcium\nchloride, magnesium chloride, potassium chloride, sodium bicarbonate\nand sodium chloride. <strong>Ingredients are not naturally sourced.</strong></p>\n</blockquote>\n<p>From this it's not clear if even NaCl itself is artificially produced or maybe they used sea or rock salt, purified it and added the mentioned ingredients.</p>\n<p>Other sources (<a href=\"https://info.umkc.edu/studenthealth/wp-content/uploads/2016/07/Neti-pot-07012014.pdf\" rel=\"nofollow noreferrer\">University of Missouri-Kansas City</a>, <a href=\"http://web.archive.org/web/20190126045544/https://www.brown.edu/campus-life/health/services/sites/brown.edu.campus-life.health.services/files/Sinus%20Irrigation%2016.pdf\" rel=\"nofollow noreferrer\">Brown University</a>) say that <strong>un-iodized salt (canning, kosher, pickling, or sea salt)</strong> can be used for Neti-Pot. This means salt without iodine, anti-caking agents (such as calcium silicate) or anything else added, which can be then mixed with baking soda (Na bicorbonate). So, &quot;table salt&quot; which typically contains iodine, anti-caking agents and other stuff should not be used. On <a href=\"https://fpnotebook.com/ent/pharm/nslsln.htm\" rel=\"nofollow noreferrer\">Family Practice Notebook</a> they say iodine can affect the function of small hair (cilia) in the respiratory tract. For the actual saline solution to be as little irritant to the nose as possible, it should be isotonic, that is 0.9% (9 g NaCl in 1 liter of water).</p>\n<p>I've found 4 reviews, all of which say that nasal irrigation with Neti-Pot may be useful for chronic sinusitis and some other conditions in the upper respiratory tract without any significant side effects:</p>\n<ul>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778074/\" rel=\"nofollow noreferrer\">American Family Physician, 2009</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6542345/\" rel=\"nofollow noreferrer\">PeerJ, 2019</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451967/\" rel=\"nofollow noreferrer\">International Journal of Environmental Research and Public Health, 2017</a></li>\n<li><a href=\"https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD011995.pub2/abstract\" rel=\"nofollow noreferrer\">Cochrane, 2016</a></li>\n</ul>\n<p>I have found no convincing evidence to say that certain &quot;special&quot; salt, which can be expensive, is better than table salt.</p>\n" }, { "answer_id": 20498, "author": "LаngLаngС", "author_id": 11231, "author_profile": "https://health.stackexchange.com/users/11231", "pm_score": 0, "selected": false, "text": "<p>Table salt contains additional unwanted ingredients. </p>\n\n<p><strong>What is neti-salt?</strong></p>\n\n<p>First link to vendor appearing in a websearch selling overpriced salt says:</p>\n\n<blockquote>\n <p>Ingredients: Pharmaceutical grade sodium chloride (99.99%) USP.<br>\n Directions: Place a heaping 1/4 teaspoon in your Neti Pot and add warm water.</p>\n</blockquote>\n\n<p>That is not to say that vendors opting for the name 'neti' aren't willing to also add 'exotic' stuff, that's then not beneficial either.</p>\n\n<p><strong>Regular kitchen table salt can be used but will cause problems because of all the additives.</strong></p>\n\n<p>Apart from possible unknown adulterations when using \"funny\" salts ('Himalaya' etc) just the usually <a href=\"https://en.wikipedia.org/wiki/Anticaking_agent\" rel=\"nofollow noreferrer\">allowed anti-caking agents for example are:</a></p>\n\n<p>341 tricalcium phosphate\n460(ii) powdered cellulose\n470b magnesium stearate\n500 sodium bicarbonate\n535 sodium ferrocyanide\n536 potassium ferrocyanide\n538 calcium ferrocyanide\n542 bone phosphate (i.e. Calcium phosphate)\n550 sodium silicate\n551 silicon dioxide\n552 calcium silicate\n553a magnesium trisilicate\n553b talcum powder\n554 sodium aluminosilicate\n555 potassium aluminium silicate\n556 calcium aluminosilicate\n558 bentonite\n559 aluminium silicate\n570 stearic acid\n900 polydimethylsiloxane </p>\n\n<p>Some of these are listed in the Eu as E170, E504, E535, E536, E551, E559…</p>\n\n<blockquote>\n <p><a href=\"https://sci-toys.com/ingredients/table_salt.html\" rel=\"nofollow noreferrer\">Table salt</a></p>\n \n <p>Table salt is sodium chloride combined with iodine sources (for nutrition), stabilizers for the iodine, and anti-caking compounds to make it pour by preventing it from absorbing water from the air.</p>\n</blockquote>\n\n<p>So supermarket bought regular table salt can be quite a bit too irritating for a nasal irrigation. Depending on jurisdiction not all ingredients have to be listed on table salt.</p>\n\n<blockquote>\n <p>Nasal irrigation is based on warm saline solution, i.e. salt dissolved in lukewarm tap water. ... However, chemical anti-caking (aka “free-flowing”) additives used in common table salt (e.g. sodium silicoaluminate) produce an unpleasant burning sensation in the nose and are not advised medically or by Yoga instructors.<br>\n <sub>–– <a href=\"https://www.erp4it.com/netinext/2011/04/the-focus-of-this-post-is-on-neti-as-a-regular-practice-in-the-american-bathroom-and-the-related-economic-and-usability-issu.html\" rel=\"nofollow noreferrer\">The problems of salt for neti - NetiNext</a></sub></p>\n \n <p>anti-caking agents or preservatives (these can be irritating to the nasal lining)<br>\n <sub>–– <a href=\"https://www.aaaai.org/conditions-and-treatments/library/allergy-library/saline-sinus-rinse-recipe\" rel=\"nofollow noreferrer\">SALINE SINUS RINSE RECIPE 2019 American Academy of Allergy, Asthma &amp; Immunology.</a></sub> </p>\n</blockquote>\n\n<p>With just a little chemistry knowledge anyone can conclude: among other things nasal irrigation is used for reducing mucus viscosity. This is clearly not an outcome achieved if adding bentonite into a solution for the nasal cavity. While listed as <a href=\"https://digitalfire.com/4sight/hazards/ceramic_hazard_bentonite_toxicity_31.html\" rel=\"nofollow noreferrer\">non-toxic non-irritating</a>, bentonite is used as cat litter, and hence it does in the nose what it does in the litter box: increases viscosity of mucus. This effect is there for all anti-caking agents. Some are directly irritating the membranes, all are doing the opposite of what one wants to achieve.</p>\n\n<p>For the US salt for use in organic products:</p>\n\n<p><strong>Common anti-caking/free-flow agents that are allowed in the US table salt include:</strong></p>\n\n<blockquote>\n <p>• Calcium silicate\n • Ferric ammonium citrate\n • Sodium ferrocyanide\n • Magnesium silicate\n • Magnesium carbonate\n • Propylene glycol\n • Aluminum calcium silicate\n • Sodium aluminosilicate</p>\n \n <p><a href=\"https://www.ams.usda.gov/sites/default/files/media/7%20Salt%20and%20Preservatives%20FINAL%20RGK%20V2.pdf\" rel=\"nofollow noreferrer\">USDA organic regulations (PDF)</a> </p>\n</blockquote>\n\n<p>Ordinary table salts may still contain (sodium and magnesium carbonate (E 500, E 504), sodium-, potassium- and calcium ferrocyanides (E 535, E 536, E 538), <a href=\"https://en.wikipedia.org/wiki/Silicon_dioxide\" rel=\"nofollow noreferrer\">silicon dioxide</a>, calcium- and magnesium silicates (E 551 – E 553), <a href=\"https://en.wikipedia.org/wiki/Ferrous_tartrate\" rel=\"nofollow noreferrer\">iron</a> <a href=\"https://en.wikipedia.org/wiki/Tartrate\" rel=\"nofollow noreferrer\">tartrate</a> (E 534). Aluminium salts are officially no longer allowed in Europe as an additive, but can be a <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782734/\" rel=\"nofollow noreferrer\">found</a> in <a href=\"https://www.nutritionmyths.com/aluminum-in-table-salt/\" rel=\"nofollow noreferrer\">some</a> <a href=\"https://timesofindia.indiatimes.com/life-style/health-fitness/photo-stories/table-salt-can-be-poisonous/photostory/64385362.cms\" rel=\"nofollow noreferrer\">salts</a>.</p>\n\n<p><a href=\"https://www.fsai.ie/faq/additives/list.html\" rel=\"nofollow noreferrer\">Additives List, E numbers in Numerical Order, Food Safety of Ireland, 2019.</a></p>\n\n<hr>\n\n<p>Main sources for bacterial contamination are neither the salts nor the water. Preparing a too large portion of solution in advance and letting it sit, and the pots used themselves are:</p>\n\n<blockquote>\n <p><strong>Although common and frequently based on potentially dangerous bacteria, contamination <em>is considered a false problem by some experts.</em> They think that the nasal cavity is naturally full of bacteria and the addition of new pathogens is not clinically relevant.</strong> </p>\n \n <p>The problem of sterility of the solutions and devices has been debated. </p>\n \n <p><strong>Solutions are at risk of contamination when large volumes of solution based on distilled water, bottled water, or boiled water are prepared at home, maintained in containers</strong> and used each time when NI is needed by withdrawing the required amount of liquid. Devices can be contaminated when they are continuously used without adequate cleaning. Lee et al. reported that <strong>after one and two weeks of use, irrigation bottles</strong> used by adults undergoing endoscopic sinus surgery that were washed with hot soapy water after each use <strong>were found to be contaminated by a large spectrum of bacteria, including Pseudomonas aeruginosa, Serratia marcescens, Proteus mirabilis, and Staphylococcus aureus</strong>. Similar findings were reported by other authors and, because in many cases contaminating bacteria were the same as those that could cause acute rhinosinusitis, it was suggested that the main source of device colonization was the sinonasal cavities. The risk of contamination seems independent of the type of device. Additionally, the use of a one-way valve irrigation bottle, theoretically capable of reducing the risk of reflux of contaminated solution in the device, was found to be practically ineffective. In contrast, contamination seems to be influenced by the composition of the solution. It was shown that acidic, isotonic saline solutions were more frequently associated with bacterial contamination probably because some of the most common contaminants grow optimally in similar environmental conditions. Finally, contamination was found more frequently with longer durations of NI use. With some exceptions, studies have reported that both bottles and bulb syringes were contaminated after one to two weeks of use in approximately 25% of the cases and in 45% after four weeks.</p>\n \n <p><sub>–– Nicola Principi &amp; Susanna Esposito: <a href=\"https://dx.doi.org/10.3390%2Fijerph14050516\" rel=\"nofollow noreferrer\">\"Nasal Irrigation: An Imprecisely Defined Medical Procedure\"</a>, Int J Environ Res Public Health. 2017 May; 14(5): 516. doi: 10.3390/ijerph14050516 PMCID: PMC5451967\n PMID: 28492494</sub></p>\n</blockquote>\n" } ]
2019/11/26
[ "https://health.stackexchange.com/questions/20486", "https://health.stackexchange.com", "https://health.stackexchange.com/users/7446/" ]
20,487
<p>Incubation periods are one of the many facts that we are expected to learn in medical school. However, I wonder how often they are used in diagnosing an infection because I do not think patients have the best memory of when their symptoms start.</p> <p>Patients may disregard earlier symptoms which are usually milder. Also, the incubation periods of several organisms are similar. Furthermore, invasion of of an infectious agent does not usually cause a symptom. Thus, it is difficult to even determine the incubation period of the infectious agent. </p> <p>My question is how often do you rely on the incubation period and what do you do to overcome these challenges?</p>
[ { "answer_id": 20493, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": true, "text": "<h2>Incubation periods of common infections</h2>\n\n<p>SKIN: </p>\n\n<ul>\n<li>Hand/foot/mouth disease..........3-6 days </li>\n<li><strong><a href=\"https://www.cdc.gov/vaccines/pubs/pinkbook/meas.html\" rel=\"nofollow noreferrer\">Measles</a>, <a href=\"https://www.kidshealth.org.nz/chickenpox\" rel=\"nofollow noreferrer\">chickenpox</a>..............7-21 days</strong> </li>\n<li><strong><a href=\"https://kidshealth.org/en/parents/german-measles.html\" rel=\"nofollow noreferrer\">Rubella</a>...................................14-23 days</strong></li>\n<li><strong><a href=\"https://wwwnc.cdc.gov/travel/yellowbook/2020/travel-related-infectious-diseases/lyme-disease\" rel=\"nofollow noreferrer\">Lyme disease(Borrelia)</a>..........3-30 days</strong> </li>\n<li>Scabies.....................................4-6 weeks </li>\n<li>Warts........................................4 weeks-6 months </li>\n</ul>\n\n<p>RESPIRATORY:</p>\n\n<ul>\n<li>Viral:\n\n<ul>\n<li><strong><a href=\"https://www.cdc.gov/vaccines/pubs/surv-manual/chpt06-influenza.html\" rel=\"nofollow noreferrer\">Influenza (Seasonal)</a>......1-4 days</strong> </li>\n<li>Colds, sore throat.............2-6 days</li>\n<li>Influenza (H1N1)...............4-6 days </li>\n<li>Cold sores (herpes).........2-12 days </li>\n</ul></li>\n<li>Bacterial: \n\n<ul>\n<li>Diphtheria, strep throat.....2-5 days </li>\n<li>Whooping cough..............7-10 days </li>\n<li>Tuberculosis.....................6-24 days</li>\n<li><strong><a href=\"https://www.cdc.gov/pneumonia/atypical/mycoplasma/about/causes-transmission.html\" rel=\"nofollow noreferrer\">Mycoplasma pneum.</a>......1-4 weeks</strong> </li>\n</ul></li>\n</ul>\n\n<p>GASTROINTESTINAL: </p>\n\n<ul>\n<li><strong><a href=\"https://www.cdc.gov/foodsafety/diseases/staphylococcal.html\" rel=\"nofollow noreferrer\">Staph</a> food poisoning..........30 min-8 hours</strong></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677557/\" rel=\"nofollow noreferrer\">Cholera</a>...................................12 hours-4.5 days</li>\n<li>Rotavirus..................................1-3 days</li>\n<li><strong><a href=\"https://www.cdc.gov/foodsafety/symptoms.html\" rel=\"nofollow noreferrer\">Salmonella/other bact</a>............6 hours-4 days</strong></li>\n<li><strong><a href=\"https://www.cdc.gov/dpdx/giardiasis/index.html\" rel=\"nofollow noreferrer\">Giardia food poisoning</a>..........1-14 days</strong> </li>\n<li><strong><a href=\"https://www.cdc.gov/parasites/pinworm/epi.html\" rel=\"nofollow noreferrer\">Pinworms</a>.................................1-2 months</strong> </li>\n<li><strong><a href=\"https://www.cdc.gov/vaccines/pubs/pinkbook/hepa.html\" rel=\"nofollow noreferrer\">Hepatitis A</a>...............................15-50 days</strong> </li>\n</ul>\n\n<p>TROPICAL FEVERS: </p>\n\n<ul>\n<li><a href=\"https://wwwnc.cdc.gov/travel/diseases/yellow-fever\" rel=\"nofollow noreferrer\">Yellow fever</a>............................3-6 days</li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88892/\" rel=\"nofollow noreferrer\">Dengue fever</a>..........................3-14 days</li>\n<li><a href=\"https://www.cdc.gov/parasites/cme/chagas/lesson_2/2.html\" rel=\"nofollow noreferrer\">Chagas disease</a>.....................1-2 weeks</li>\n<li><strong><a href=\"https://www.cdc.gov/malaria/about/disease.html\" rel=\"nofollow noreferrer\">Malaria</a>...................................7-30 days</strong></li>\n</ul>\n\n<p>SEXUALLY TRANSMITTED:</p>\n\n<ul>\n<li>Gonorrhea..............................2-5+ days </li>\n<li>Chlamydia..............................1-3 weeks</li>\n<li><strong><a href=\"https://www.cdc.gov/hiv/basics/whatishiv.html\" rel=\"nofollow noreferrer\">HIV/AIDS</a>................................2-4 weeks</strong></li>\n<li><strong><a href=\"https://wwwnc.cdc.gov/travel/yellowbook/2020/travel-related-infectious-diseases/hepatitis-b\" rel=\"nofollow noreferrer\">Hepatitis B</a>............................2-5 months</strong></li>\n</ul>\n\n<p>OTHER:</p>\n\n<ul>\n<li>Meningitis, bacterial...............2-10 days</li>\n<li><strong><a href=\"https://www.cdc.gov/vhf/tbe/symptoms/index.html\" rel=\"nofollow noreferrer\">Meningitis, viral</a>...................7-14 days</strong></li>\n<li><strong><a href=\"https://wwwnc.cdc.gov/travel/yellowbook/2020/travel-related-infectious-diseases/tetanus\" rel=\"nofollow noreferrer\">Tetanus</a>.................................3-21 days</strong></li>\n<li><strong><a href=\"https://kidshealth.org/en/teens/mono-long.html\" rel=\"nofollow noreferrer\">Infectious mononucleosis</a>..4-7 weeks</strong></li>\n</ul>\n\n<p><em>Sources (when not explicitly mentioned): <a href=\"https://www.summitmedicalgroup.com/library/pediatric_health/hhg_incubation/\" rel=\"nofollow noreferrer\">Summit Medical Group</a>, <a href=\"https://idph.iowa.gov/Portals/1/userfiles/79/Documents/Epi%20of%20Common%20Communicable%20Diseases%20June%202013%20-%20FINAL.pdf\" rel=\"nofollow noreferrer\">Iowa Department of Public Health</a></em></p>\n\n<hr>\n\n<h2>How can knowing incubation periods help?</h2>\n\n<p>Sometimes, you can get quite accurate information about the time of exposure and onset of symptoms. Knowing incubation periods may not help you make a diagnosis of exact infection but can help you estimate its possibility. Examples:</p>\n\n<p>1) A person with <strong>diarrhea</strong> eating out in other place than usual (restaurant/street fast food/open market/travel):</p>\n\n<ul>\n<li>6 hours to 4 days ago: likely bacterial food poisoning</li>\n<li>1-2 weeks ago, when travelling (India, South America...): possible parasitic infection (Giardia)</li>\n</ul>\n\n<p>2) A person being in a forest 2 weeks ago and remembering or not being bitten by a tick:</p>\n\n<ul>\n<li>Having a <strong>single big red \"bull's eye\" rash</strong>: possible Borrelia b. infection (Lyme disease)</li>\n<li>Having <strong>severe headache</strong>: possible viral meningoencephalitis</li>\n</ul>\n\n<p>3) A person with <strong>high fever</strong> travelling in Asia/Africa/South America:</p>\n\n<ul>\n<li>1 week ago: possible yellow or other tropical fever</li>\n<li>2-4 weeks ago: possible malaria</li>\n</ul>\n\n<p>4) A teacher with <strong>GI symptoms and jaundice</strong> camping with school children 1 month ago: possible hepatitis A.</p>\n" }, { "answer_id": 20494, "author": "chris", "author_id": 6512, "author_profile": "https://health.stackexchange.com/users/6512", "pm_score": 1, "selected": false, "text": "<p>I find incubation periods useful when trying to decide if some some symptom is, or is not, likely to be related to a suspected illness. For instance I recently had a patient whose child was diagnosed with Parvovirus B19 - slapped cheek disease. It was helpful to be able to tell her that most likely she was out of the window for infection. </p>\n" } ]
2019/11/26
[ "https://health.stackexchange.com/questions/20487", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17040/" ]
20,517
<p>Ever since the end of the <a href="https://en.wikipedia.org/wiki/Human_Genome_Project" rel="nofollow noreferrer">Human Genome project</a> we have been witnessing the steady advance of genome sequencing technology and the decline of the price required to perform it. This lead to the advent of commercial <a href="https://en.wikipedia.org/wiki/Personal_genomics" rel="nofollow noreferrer">personal genome sequencing</a> services with the appearance of a few companies about a decade ago, and the creation of a market which eventually spread to a few more companies and laboratories nowadays. For under €1000 or even under €500, it is possible today for an individual to contract a direct-to-consumer whole genome sequencing service and receive this information.</p> <p>However, for the informed citizen, suspicious about our current societal state of affairs regarding technology and privacy, some concerns come to mind about the guarantees of protection of a subject's genetic patrimony when pondering investing on one of these services.</p> <p>By extrapolating the past trend of the <a href="https://en.wikipedia.org/wiki/Personal_genomics#/media/File:Cost_per_Genome.png" rel="nofollow noreferrer">cost per genome sequenced</a>, one thought naturally comes to mind:</p> <blockquote> <p>Is it reasonable to expect the cost of sequencing an individual's genome to drop so much in the near future as to allow for a new kind of product to be developed and sold in the coming years with which one could perform personal genome sequencing at home?</p> </blockquote> <p>Additionally, let me also ask:</p> <blockquote> <p>What alternative options and safety mechanisms can we implement (or foresee to be implemented) at a personal and collective level to eliminate this privacy violation concern and protect the genome data on public and private servers?</p> </blockquote>
[ { "answer_id": 20525, "author": "Bob Ortiz", "author_id": 16786, "author_profile": "https://health.stackexchange.com/users/16786", "pm_score": 2, "selected": false, "text": "<p>I am working in the <a href=\"https://en.wikipedia.org/wiki/Information_security\" rel=\"nofollow noreferrer\" title=\"Information security\">information security</a> industry and personally following medical technology closely. Your first question kind of asks to <strong>predict the future</strong>, which nobody can. Yet, I will give you my <strong>personal opinion</strong> on the matter.</p>\n\n<blockquote>\n <p>Is it reasonable to expect the cost of sequencing an individual's genome to drop so much in the near future as to allow for a new kind of product to be developed and sold in the coming years with which one could perform personal genome sequencing at home?</p>\n</blockquote>\n\n<p>I would estimate that genome tech and genome research is still growing steadily and more practical uses and (medical) applications are yet to be found. Along with that, current productivity (see <a href=\"https://en.wikipedia.org/wiki/Genomics#/media/File:Number_of_prokaryotic_genomes_and_sequencing_costs.svg\" rel=\"nofollow noreferrer\" title=\"graph\">this graph</a>), effectiveness and accuracy can always be improved. </p>\n\n<p>That said, there is apparently a big need for this technology and as there is a need, there is inherently a need for innovation of that technology. Innovation often means increase productivity (doing more with less). The <a href=\"https://en.wikipedia.org/wiki/Moore%27s_law\" rel=\"nofollow noreferrer\" title=\"Moore&#39;s law\">Moore's law</a> <em>(although currently controversial)</em> is the observation that the number of transistors in dense integrated circuit doubles about every two years. That said, it applies directly to all technology that needs transistors (which is mostly all technology). <em>If you want another great example of technology where effectiveness has gone up and cost has gone down drastically, check out the development of solar technology in the last 60 years (see <a href=\"https://news.energysage.com/solar-panel-efficiency-cost-over-time/\" rel=\"nofollow noreferrer\" title=\"this article\">this article</a>). So in short, yes it is very likely that the cost will keep going down the coming decades.</em></p>\n\n<blockquote>\n <p>What alternative options and safety mechanisms can we implement (or foresee to be implemented) at a personal and collective level to eliminate this privacy violation concern and protect the genome data on public and private servers?</p>\n</blockquote>\n\n<p>Answering from an information security perspective this question can also only be answered in a very subjective way, meaning it is only an opinion. Data is data and humans are human. Sounds silly but I will explain. Ideally, you would want all sequencing devices to implement solid, future-proof and <a href=\"https://en.wikipedia.org/wiki/Post-quantum_cryptography\" rel=\"nofollow noreferrer\" title=\"quantum-safe encryption\">quantum-safe</a> encryption on the data processed, stored and exported by the machine. Yet, there are two problems here. </p>\n\n<p>First, data is data. Cheap tech means a consensus, when tech makers want to compete they could try to use weaker or no encryption at all. Also, how will this be enforced? By law? Then, who will enforce that law? What if people entirely make the device themself? What if the data is initially encrypted but later in the process handled or stored insecurely?</p>\n\n<p>Secondly, humans are human. As with all data protection and information security, the human is the weakest link in the chain. Data might be handled correctly at first but can you expect from an average user to deal with complicated technical processes and will it still be as secure when those processes are made extremely simple and user-friendly? By law, at least in the <a href=\"https://en.wikipedia.org/wiki/European_Union\" rel=\"nofollow noreferrer\" title=\"European Union\">European Union</a> with the <a href=\"https://en.wikipedia.org/wiki/General_Data_Protection_Regulation\" rel=\"nofollow noreferrer\" title=\"GDPR\">General Data Protection Regulation (GDPR)</a>, companies are responsible to protect your data. But, once they hand it over to you in a secure way and destroy it themself, it becomes entirely your own responsibility.</p>\n\n<hr>\n\n<p><em>Additionally, what if (some) people want to share this information for medical reasons. Imagine the massive amounts of data, where a great number of correlations can be found between diseases or where new unidentified diseases and currently unknown causes of diseases can be found. Imagine the information you'll get from the DNA of people with genetic immunity to certain diseases.</em></p>\n\n<p><em>I will exaggerate a bit now, my apology for entirely ignoring the privacy aspect here but: Would it be ethical to keep all this data private? Or is the only ethical thing to make it all part of one global scale medical research? Imagine the practical use cases of all this data. Should it be an acceptable risk? What is the actual risk of \"leaking\" your DNA data anyway? Using global research results for designer DNA with <a href=\"https://en.wikipedia.org/wiki/CRISPR\" rel=\"nofollow noreferrer\" title=\"CRISPR\">CRISPR</a>? You leave your physical DNA everywhere you go (see <a href=\"https://geneticliteracyproject.org/2015/05/12/you-leave-traces-of-your-microbiome-everywhere-you-go/\" rel=\"nofollow noreferrer\" title=\"this article\">this article</a>). Do we clean up all our hairs, skin cells, other bodily fluids that we left in all public places to prevent people from physically finding it? No! So, why would we do otherwise digitally in the <a href=\"https://en.wikipedia.org/wiki/Information_Age\" rel=\"nofollow noreferrer\" title=\"information age\">information age</a>?</em></p>\n" }, { "answer_id": 20655, "author": "Iron Pillow", "author_id": 332, "author_profile": "https://health.stackexchange.com/users/332", "pm_score": 1, "selected": false, "text": "<p>The first question relates to the retail price floor of genome sequencing hardware. As with any commercial product, price depends on demand. I don't envision much demand for home genome sequencing, for three reasons. </p>\n\n<ol>\n<li><p>The hardest part of genomic inquiries is not getting the data, but interpreting it. The demand for interpretation will grow, and I suspect that is where the competition will be. The interpretation products will require your data in order to operate, and it will always be easier to send them a cheek swab than to put a complicated piece of machinery in your home to get the data. </p></li>\n<li><p>If medical decisions are to be made on the basis of home genomic results, then they would have to yield very high quality results. You can probably build a jet engine at home, but you wouldn't fly in an airplane powered by your engine. So I don't see demand for home genomic medical testing matching even the demand for home blood pressure testing, upon which decisions are being made today, but always with a double-check obtained in the clinic.</p></li>\n<li><p>If the intended use is non-medical, there may be market overlap with portable research systems (e.g. Nanopore). The price points in that market will be higher than for consumer home uses, if for no other reason than researchers will get more value from portable testing than consumers. You might use the machine once on yourself and on your family, friends, and pets, and never again.</p></li>\n</ol>\n\n<p>The second question relates to protecting genomic information once it has left the confines of the home. It's impossible to do with certainty. If an attractive market for genomic information develops, then even trusted people and enterprises will violate that trust, despite whatever legal penalties may ensue, and despite whatever technological controls are in place. Information is information, and if it exists somewhere in readable form for any period of time, it can be copied. The only question is how many people need to be bribed or otherwise corrupted. Sysadmins are not incorruptible.</p>\n" } ]
2019/11/30
[ "https://health.stackexchange.com/questions/20517", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17199/" ]
20,543
<p>I've heard often <sup>1</sup> <sup>2</sup> that alternation between anti-dandruff shampoos containing ketoconazole, zinc pyrithione, coal tar, selenium disulfide or salicylic acid is needed for the treatment to stay effective.</p> <p>How come that after using the same anti-dandruff shampoo for a while it will be less effective? Also why is the same substance effective again after alternation between other shampoos? Does the dandruff itself changes and becomes (short-term) immune for a specific treatment or is there another reason?</p> <hr> <p><sup>1 Bhupinder Kaur MD, Jul 19, 2011. <a href="https://www.medhelp.org/posts/Dermatology/-Bhupinder-Kaur--MD/show/1554999" rel="noreferrer">https://www.medhelp.org/posts/Dermatology/-Bhupinder-Kaur--MD/show/1554999</a></sup><br> <sup>2 Abraham The Pharmacist, <a href="https://www.youtube.com/watch?v=DbV9bY4gD_Q&amp;feature=youtu.be&amp;t=149" rel="noreferrer">https://www.youtube.com/watch?v=DbV9bY4gD_Q&amp;feature=youtu.be&amp;t=149</a></sup></p>
[ { "answer_id": 20579, "author": "Rhyothemis princeps", "author_id": 17231, "author_profile": "https://health.stackexchange.com/users/17231", "pm_score": 2, "selected": false, "text": "<p>Malassezia overgrowth is thought be the cause of most cases of dandruff (1) and rotating treatments avoids the development of resistance. However, some have argued that overgrowth of Malassezia is a result rather than a cause of dandruff (2).</p>\n\n<p>1 - <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869</a></p>\n\n<p>2 - <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887514\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887514</a></p>\n" }, { "answer_id": 20594, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": true, "text": "<p>Currently, there seems to be no convincing evidence to say that alternating between shampoos prolongs their effectiveness in treating dandruff.</p>\n\n<p><strong>1)</strong> According to <a href=\"https://ec.europa.eu/health/archive/ph_risk/committees/sccp/documents/out181_en.pdf\" rel=\"nofollow noreferrer\">the Scientific Committee on Cosmetic Products and Non-food Products Intended for Consumers by European Commission, 2012</a>:</p>\n\n<blockquote>\n <p>There is at present no scientific evidence of development of\n resistance or cross-resistance of fungi to Ketoconazole, if\n Ketoconazole is used in cosmetic dandruff shampoo at concentrations up\n to 2 %.</p>\n</blockquote>\n\n<p><strong>2)</strong> <a href=\"https://www.drugs.com/monograph/nizoral-topical.html\" rel=\"nofollow noreferrer\">Drugs.com, 2019</a> and <a href=\"https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019927s031lbl.pdf\" rel=\"nofollow noreferrer\">FDA.gov, 2012</a> also do not mention any resistance to ketoconazole topical.</p>\n\n<p><strong>3)</strong> In <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5442545/\" rel=\"nofollow noreferrer\">this 2017 study</a>, (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5442545/figure/F2/?report=objectonly\" rel=\"nofollow noreferrer\">Fig 2</a>), they've observed that some strains of Malassezia fungi are resistant to ketoconazole, but this seems to be intrincis resistance, not the one that develops with repeated use, so alternating between shampoos would not work.</p>\n\n<p><strong>4)</strong> <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579488/\" rel=\"nofollow noreferrer\">One source</a> suggests that some people with seborrheic dermatitis can be resistant to topical treatments:</p>\n\n<blockquote>\n <p>For patients with persistent SD resistant to topical agents, oral\n antifungals may be an option. Oral itraconazole given in a dose of\n 200mg/day for one week, followed by a maintenance dose, resulted in\n clinical improvement of SD symptoms in two open-label trials.</p>\n</blockquote>\n\n<p>...but again, alternating shampoos here would not likely help.</p>\n\n<p><strong>5)</strong> Several comprehensive review articles about <strong>treatment of dandruff</strong> do not even mention \"resistance\" to anti-dandruff shampoos or the need for \"alternation\" of shampoos:</p>\n\n<ul>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887514/\" rel=\"nofollow noreferrer\">DANDRUFF: THE MOST COMMERCIALLY EXPLOITED SKIN DISEASE (Indian Journal of Dermatology, 2010)</a></li>\n<li><a href=\"https://www.aafp.org/afp/2000/0501/p2703.html\" rel=\"nofollow noreferrer\">Treatment of Seborrheic Dermatitis (American Family Physician, 2000)</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869/\" rel=\"nofollow noreferrer\">Seborrheic Dermatitis and Dandruff: A Comprehensive Review (Journal of Clinical and Investigative Dermatology, 2015)</a></li>\n<li><a href=\"https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/cfrsearch.cfm?cfrpart=358&amp;showfr=1&amp;subpartnode=21:5.0.1.1.30.8\" rel=\"nofollow noreferrer\">Drug Products for the Control of Dandruff, Seborrheic Dermatitis, and Psoriasis (U.S. Food and Drug Administration, 2019)</a></li>\n<li><a href=\"https://www.uspharmacist.com/article/is-it-dandruff-or-seborrheic-dermatitis\" rel=\"nofollow noreferrer\">Is It Dandruff or Seborrheic Dermatitis? (U.S. Pharmacist, 2013)</a></li>\n</ul>\n\n<p><strong>6)</strong> <a href=\"https://www.worldscientific.com/doi/abs/10.1142/9789814354868_0032\" rel=\"nofollow noreferrer\">Another source</a> claims that a combination, but not alternation, of substances could be used to circumverent resistance: </p>\n\n<blockquote>\n <p>Cosmetic and personal care products (anti-acne, anti-dandruff,\n anti-odorant, prickly heat talc, etc) use synthetic antimicrobials\n like Triclosan, Farnesol, Zinc Pyrithione etc or herbal extracts for\n the anti-microbial 'functional' benefit. The use of single\n anti-microbial agent would pave way for emergence of resistance in the\n cosmetically significant skin micro-organisms. To combat the\n development of resistance and deliver the anti-microbial benefit, a\n combination of synergistic antimicrobials can be used.</p>\n</blockquote>\n\n<hr>\n\n<p>A couple of sources recommend alternating shampoos, but without any argumentation:</p>\n\n<p><a href=\"https://www.mayoclinic.org/diseases-conditions/dandruff/diagnosis-treatment/drc-20353854\" rel=\"nofollow noreferrer\">Mayo Clinic</a>:</p>\n\n<blockquote>\n <p>If one type of shampoo works for a time and then seems to lose its\n effectiveness, try alternating between two types of dandruff shampoos.</p>\n</blockquote>\n\n<p><a href=\"https://health.students.vcu.edu/media/student-affairs/ushs/docs/SEBORRHEICDERMATITIS.pdf\" rel=\"nofollow noreferrer\">Virginia Commonwealth University</a>:</p>\n\n<blockquote>\n <p>Alternating medicated shampoos on a daily basis may also increase\n their effectiveness (eg, ketoconazole on Monday, zinc on Tuesday,\n selenium on Wednesday, tar on Thursday, etc).</p>\n</blockquote>\n" } ]
2019/12/04
[ "https://health.stackexchange.com/questions/20543", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16786/" ]
20,564
<p><em>Disclaimer: I am layman in the field, but I have a legit question to ask, so before closing, please note that I am showing enough "pre-research" and ask clarified question.</em></p> <hr> <p>I used an LCD monitor in the past and now an LED. As more as I have been sitting in front of monitor, my face becomes hotter and drier ( really feel it and after i get away, the "heating" feeling goes away in 1-2 hours), and every day I see the deterioration in my face skin as years go.</p> <p>I have two questions:</p> <ol> <li>Can someone get any harmful level of electromagnetic (or whatever measurement) radiation from monitor, if s/he sits in front of monitor (say, 17 inch) 8 hours a day, 365 days in year. (Some resources I've found are <a href="https://emfacademy.com/computer-monitor-radiation-everything-you-need-to-know/" rel="nofollow noreferrer">here</a>, and the demonstration of it like <a href="https://www.youtube.com/watch?v=1Squ8r7FFjk" rel="nofollow noreferrer">this</a> or <a href="https://youtu.be/N6VUOUd5XY4?t=34" rel="nofollow noreferrer">this</a> )?</li> <li>If the above answer is NO, then this 2nd question becomes pointless. But if answer is YES, then What measures can one take to protect himself/herself? I am not asking for a <em>specific</em> product recommendation - in general, what kind of "shields" (i.e. i've found something like <a href="https://youtu.be/N6VUOUd5XY4?t=34" rel="nofollow noreferrer">this</a>) can be used to get some level of protection?</li> </ol> <hr> <p>EDIT:</p> <p>I understand that in all external sources, we might find some products on sale ( neither my links or I am affiliated to any of them. I just found those sources and don't mind if they sell something or not. My topic has emphasized question, and i've included some sources I could find). To say frankly, I am not against to pay money in order to get health/protection. I am quite thanksfull to all sites that talk about problems (even so, if they sell stuff. That is quite normal event, including StackExchange, all business in the world has it's own financial interest. Even asking this question makes some monetary benefit to SE, probably you knew that.) So, instead, I need answers to the subject, however thanks for warning me about possible fraud. But this subject is life-critical to me and I really need all information about the subject.</p>
[ { "answer_id": 20579, "author": "Rhyothemis princeps", "author_id": 17231, "author_profile": "https://health.stackexchange.com/users/17231", "pm_score": 2, "selected": false, "text": "<p>Malassezia overgrowth is thought be the cause of most cases of dandruff (1) and rotating treatments avoids the development of resistance. However, some have argued that overgrowth of Malassezia is a result rather than a cause of dandruff (2).</p>\n\n<p>1 - <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869</a></p>\n\n<p>2 - <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887514\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887514</a></p>\n" }, { "answer_id": 20594, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": true, "text": "<p>Currently, there seems to be no convincing evidence to say that alternating between shampoos prolongs their effectiveness in treating dandruff.</p>\n\n<p><strong>1)</strong> According to <a href=\"https://ec.europa.eu/health/archive/ph_risk/committees/sccp/documents/out181_en.pdf\" rel=\"nofollow noreferrer\">the Scientific Committee on Cosmetic Products and Non-food Products Intended for Consumers by European Commission, 2012</a>:</p>\n\n<blockquote>\n <p>There is at present no scientific evidence of development of\n resistance or cross-resistance of fungi to Ketoconazole, if\n Ketoconazole is used in cosmetic dandruff shampoo at concentrations up\n to 2 %.</p>\n</blockquote>\n\n<p><strong>2)</strong> <a href=\"https://www.drugs.com/monograph/nizoral-topical.html\" rel=\"nofollow noreferrer\">Drugs.com, 2019</a> and <a href=\"https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019927s031lbl.pdf\" rel=\"nofollow noreferrer\">FDA.gov, 2012</a> also do not mention any resistance to ketoconazole topical.</p>\n\n<p><strong>3)</strong> In <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5442545/\" rel=\"nofollow noreferrer\">this 2017 study</a>, (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5442545/figure/F2/?report=objectonly\" rel=\"nofollow noreferrer\">Fig 2</a>), they've observed that some strains of Malassezia fungi are resistant to ketoconazole, but this seems to be intrincis resistance, not the one that develops with repeated use, so alternating between shampoos would not work.</p>\n\n<p><strong>4)</strong> <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579488/\" rel=\"nofollow noreferrer\">One source</a> suggests that some people with seborrheic dermatitis can be resistant to topical treatments:</p>\n\n<blockquote>\n <p>For patients with persistent SD resistant to topical agents, oral\n antifungals may be an option. Oral itraconazole given in a dose of\n 200mg/day for one week, followed by a maintenance dose, resulted in\n clinical improvement of SD symptoms in two open-label trials.</p>\n</blockquote>\n\n<p>...but again, alternating shampoos here would not likely help.</p>\n\n<p><strong>5)</strong> Several comprehensive review articles about <strong>treatment of dandruff</strong> do not even mention \"resistance\" to anti-dandruff shampoos or the need for \"alternation\" of shampoos:</p>\n\n<ul>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887514/\" rel=\"nofollow noreferrer\">DANDRUFF: THE MOST COMMERCIALLY EXPLOITED SKIN DISEASE (Indian Journal of Dermatology, 2010)</a></li>\n<li><a href=\"https://www.aafp.org/afp/2000/0501/p2703.html\" rel=\"nofollow noreferrer\">Treatment of Seborrheic Dermatitis (American Family Physician, 2000)</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869/\" rel=\"nofollow noreferrer\">Seborrheic Dermatitis and Dandruff: A Comprehensive Review (Journal of Clinical and Investigative Dermatology, 2015)</a></li>\n<li><a href=\"https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/cfrsearch.cfm?cfrpart=358&amp;showfr=1&amp;subpartnode=21:5.0.1.1.30.8\" rel=\"nofollow noreferrer\">Drug Products for the Control of Dandruff, Seborrheic Dermatitis, and Psoriasis (U.S. Food and Drug Administration, 2019)</a></li>\n<li><a href=\"https://www.uspharmacist.com/article/is-it-dandruff-or-seborrheic-dermatitis\" rel=\"nofollow noreferrer\">Is It Dandruff or Seborrheic Dermatitis? (U.S. Pharmacist, 2013)</a></li>\n</ul>\n\n<p><strong>6)</strong> <a href=\"https://www.worldscientific.com/doi/abs/10.1142/9789814354868_0032\" rel=\"nofollow noreferrer\">Another source</a> claims that a combination, but not alternation, of substances could be used to circumverent resistance: </p>\n\n<blockquote>\n <p>Cosmetic and personal care products (anti-acne, anti-dandruff,\n anti-odorant, prickly heat talc, etc) use synthetic antimicrobials\n like Triclosan, Farnesol, Zinc Pyrithione etc or herbal extracts for\n the anti-microbial 'functional' benefit. The use of single\n anti-microbial agent would pave way for emergence of resistance in the\n cosmetically significant skin micro-organisms. To combat the\n development of resistance and deliver the anti-microbial benefit, a\n combination of synergistic antimicrobials can be used.</p>\n</blockquote>\n\n<hr>\n\n<p>A couple of sources recommend alternating shampoos, but without any argumentation:</p>\n\n<p><a href=\"https://www.mayoclinic.org/diseases-conditions/dandruff/diagnosis-treatment/drc-20353854\" rel=\"nofollow noreferrer\">Mayo Clinic</a>:</p>\n\n<blockquote>\n <p>If one type of shampoo works for a time and then seems to lose its\n effectiveness, try alternating between two types of dandruff shampoos.</p>\n</blockquote>\n\n<p><a href=\"https://health.students.vcu.edu/media/student-affairs/ushs/docs/SEBORRHEICDERMATITIS.pdf\" rel=\"nofollow noreferrer\">Virginia Commonwealth University</a>:</p>\n\n<blockquote>\n <p>Alternating medicated shampoos on a daily basis may also increase\n their effectiveness (eg, ketoconazole on Monday, zinc on Tuesday,\n selenium on Wednesday, tar on Thursday, etc).</p>\n</blockquote>\n" } ]
2019/12/08
[ "https://health.stackexchange.com/questions/20564", "https://health.stackexchange.com", "https://health.stackexchange.com/users/7459/" ]
20,573
<p>For medical students and more generally for learning purposes, an open-source website with a 3D human body model, in which we can "navigate" (zoom and move/walk), a little bit like a "Google Streetview / Maps" user interface would be very useful.</p> <p>Where to find such a resource?</p> <p>Example of use case: I find it quite difficult to understand how pharynx/larynx/esophagus/mouth cavity/etc. are linked, and being able to "walk" in this zone in a 3D mode would be very insightful for learning purposes.</p>
[ { "answer_id": 20576, "author": "Basj", "author_id": 15931, "author_profile": "https://health.stackexchange.com/users/15931", "pm_score": 1, "selected": false, "text": "<p>I'll update this answer if I find new useful resources.</p>\n\n<p>I'm now trying this website: <a href=\"https://human.biodigital.com/view?id=production%2FmaleAdult%2Fmale_region_head_07&amp;lang=fr\" rel=\"nofollow noreferrer\">https://human.biodigital.com/view?id=production%2FmaleAdult%2Fmale_region_head_07&amp;lang=fr</a></p>\n\n<p>and it helped me a little bit to understand the laryngopharynx zone. The navigation is 3D (pan / zoom).</p>\n" }, { "answer_id": 30581, "author": "melvio", "author_id": 23654, "author_profile": "https://health.stackexchange.com/users/23654", "pm_score": 3, "selected": false, "text": "<p>I like the 3D atlases of <a href=\"https://www.openanatomy.org/atlas-pages/\" rel=\"noreferrer\">https://www.openanatomy.org/atlas-pages/</a>.</p>\n<p>You can remove anatomic structures and transact the body as if you're looking at CT-scanning images. They are great if you also want to understand the relation between the 3D-anatomy and CT-images. And best of all, it is completely open source.</p>\n<hr />\n<p>Here you can see an example of their thorax model. I removed the lungs such that observing the heart is easier.</p>\n<p><a href=\"https://i.stack.imgur.com/paiwh.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/paiwh.jpg\" alt=\"Heart example\" /></a></p>\n" } ]
2019/12/09
[ "https://health.stackexchange.com/questions/20573", "https://health.stackexchange.com", "https://health.stackexchange.com/users/15931/" ]
20,608
<p>When I look for ambulance and how fast it should come, I find information regarding allowed driving speed.</p> <p>However, for planning hospitals and roads, one should no how much time is on average required to reach a hospital. Depending on the region and the roads it can be quite different than approximating from the actual <em>distance</em> like in this <a href="http://goaspro.com/detect-optimal-location-for-hospitals-in-bangalore/" rel="nofollow noreferrer">contribution</a>.</p> <p>Are there any norms on that, or laws, or regulations? How does this compare internationally?</p>
[ { "answer_id": 20610, "author": "Chris Rogers", "author_id": 7951, "author_profile": "https://health.stackexchange.com/users/7951", "pm_score": 2, "selected": false, "text": "<p>The UK national standard sets out that all ambulance trusts must respond to:</p>\n\n<ul>\n<li><p>Category 1 calls (life-threatening injuries and illnesses) in 7 minutes <strong>on average</strong>.</p></li>\n<li><p>Category 2 calls (other emergency) in 18 minutes <strong>on average</strong>.</p></li>\n<li><p>Category 3 calls (urgent) in at least 9 out of 10 times before 120 minutes.</p></li>\n<li><p>Category 4 calls (less urgent) at least 9 out of 10 times before 180 minutes.<br><br>In some instances you may be given advice over the telephone or referred to another service such as a GP or pharmacist.</p></li>\n</ul>\n\n<p>For more on this and how calls are categorized, you can download a free PDF from <a href=\"https://www.england.nhs.uk/wp-content/uploads/2017/07/new-ambulance-standards-easy-read.pdf\" rel=\"nofollow noreferrer\">NHS England</a></p>\n" }, { "answer_id": 20616, "author": "Bob Ortiz", "author_id": 16786, "author_profile": "https://health.stackexchange.com/users/16786", "pm_score": 1, "selected": false, "text": "<p>In this report \"Ambulance Care Europe\" <sup>1</sup> in table 3.5 there is an emergency level and response times comparison between several EU countries. Showing a response time for emergencies in some countries at 5 minutes (Germany) in others 25 minutes (Norway, rural).</p>\n\n<p>For example, in The Netherlands regulations state that an ambulance in case of emergency has to be at the scene within 15 minutes after the phone call in 95% of the cases. However, in 2001 only 91,8% actually managed that. The Dutch government is trying to pass a law that requires arrival within 8 minutes. Also, 60% of Dutch citizens live within a 5-kilometer range from a hospital others on average 10 kilometers.</p>\n\n<p><em>In case of, (expected) CPR a private network of citizens in the area that can perform CPR and are volunteering in this network can also be alarmed by text to fetch a defibrillator in a specified public place near and bring it to the location, or go to a location directly and start CPR. Also, police or firefighters can be alarmed if the centralist thinks that the ambulance will be late. Out of experience, these volunteers often arrive faster because they are closer.</em></p>\n\n<hr>\n\n<p><sup>1 <a href=\"https://www.nivel.nl/sites/default/files/bestanden/Rapport_ambulance_care_europe.pdf\" rel=\"nofollow noreferrer\">https://www.nivel.nl/sites/default/files/bestanden/Rapport_ambulance_care_europe.pdf</a></sup></p>\n" } ]
2019/12/12
[ "https://health.stackexchange.com/questions/20608", "https://health.stackexchange.com", "https://health.stackexchange.com/users/9514/" ]
20,613
<p>My text book states that intravenous crystalloid infusion is a method of treating anaphylactic shock. </p> <p>I can't get why, as there is no fluid loss in case of anaphylactic shock, at least that is what I think.</p> <p>So why giving crystalloid solution? </p>
[ { "answer_id": 20614, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 1, "selected": false, "text": "<p>In anaphylaxic shock, vasodilation can result in severe hypotension. The aim of crystalloid infusion is to help correct hypotension. There are various treatment regimes possible, but most authors suggest (for adults):</p>\n\n<ol>\n<li>Epinephrine 0.5 mg i.m. (to reverse vasodilation)</li>\n<li>Oxygen, at least 70%, by mask, 15 liters/min</li>\n<li>Intravenous crystalloid infusion 500 -1,000 mL, initially (to help maintain normal blood pressure); colloid infusions are not better in increasing survival chance.</li>\n<li>A histamine (H1) antagonist, such as chlorpheniramine, 10 mg i.m. or i.v. (to relieve itch and urticaria; it takes >30 minutes to be effective)</li>\n<li>Hydrocortisone 200 mg i.m or i.v. (to inhibit inflammation; it takes several hours to be effective; no clear benefit)</li>\n</ol>\n\n<p>Sources:</p>\n\n<ul>\n<li><a href=\"https://patient.info/doctor/anaphylaxis-and-its-treatment\" rel=\"nofollow noreferrer\">Anaphylaxis and its treatment (Parient.info, 2015)</a></li>\n<li><a href=\"https://www.uptodate.com/contents/anaphylaxis-emergency-treatment\" rel=\"nofollow noreferrer\">Anaphylaxis: Emergency treatment (UpToDate, 2019)</a></li>\n</ul>\n" }, { "answer_id": 20615, "author": "Carey Gregory", "author_id": 805, "author_profile": "https://health.stackexchange.com/users/805", "pm_score": 2, "selected": false, "text": "<p>Your assumption that there is no fluid loss is wrong. In addition to the vasodilation Jan mentioned in his answer, there's significant fluid loss caused by increased permeability of the vasculature. The result is a massive fluid shift from the intravascular to extravascular space. This explains why swelling occurs in mucus membranes: fluid is leaking out of blood vessels into the surrounding tissue.</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4925788/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4925788/</a></p>\n\n<blockquote>\n <p>Anaphylactic shock is caused by vasodilation and vascular leakage\n resulting from enhanced permeability of the postcapillary venules in\n the vascular beds of visceral organs, skin, and mucous membranes.</p>\n</blockquote>\n\n<p>.</p>\n\n<blockquote>\n <p>The commonest cardiovascular manifestation is severe hypotension,\n <strong>usually caused by a massive shift of fluid from the intravascular to\n the extrayascular space</strong>. Arrhythmias are not uncommon. <strong>Profound losses\n of intravascular volume can occur quickly as a result of increased\n vascular permeability.</strong></p>\n</blockquote>\n" } ]
2019/12/12
[ "https://health.stackexchange.com/questions/20613", "https://health.stackexchange.com", "https://health.stackexchange.com/users/11984/" ]
20,712
<p>I'm making a character and trying to be biologically accurate. Said character has transfusion-dependent anemia (from Gunther disease/congenital erythropoietic porphyria) so I suppose exercising would be hard by default, but what are some other conditions that would make physical training unhealthy? Ideally, I'm trying to make it so even light exercising is bad, but severe would cause vomiting/fainting/etc.</p> <p>I posted this question on biology, but someone suggested I try asking here instead. I think that the question is less relevant there, so might as well ask here since I didn't get an answer anyway. I apologize for asking the same question twice.</p>
[ { "answer_id": 20722, "author": "De Novo", "author_id": 14173, "author_profile": "https://health.stackexchange.com/users/14173", "pm_score": 2, "selected": false, "text": "<p>If you're looking for a disease with childhood onset that requires exercise restriction, Long QT Syndrome (LQTS) may work, specifically LQT1. <a href=\"https://www.nhlbi.nih.gov/health-topics/long-qt-syndrome\" rel=\"nofollow noreferrer\">Here</a> is a lay overview. For more detail, see <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6785594/\" rel=\"nofollow noreferrer\">this review</a>. I'm not a cardiologist, and have never seen a patient with LQTS, so I'm honestly not sure how variable the presentation is. Generally, for LQT1, exercise or stress induced tachycardia can cause a life threatening arrhythmia called <a href=\"https://en.m.wikipedia.org/wiki/Torsades_de_pointes\" rel=\"nofollow noreferrer\">torsades de pointes</a> and sudden death. </p>\n\n<p>Treatment of LQT1 includes avoidance of stress, exercise restriction, and beta blockers. As discussed in the linked review above, certain extreme phenotypes may not be fully controlled with beta blockers. Pain, nausea, or perceived exercise intolerance (e.g., fatigue), the symptoms you mentioned in your comment, are not part of the described symptom complex. Rather elevated heart rate leads to the malignant arrhythmia. The symptom complex is that of the arrhythmia (palpitations, fainting, seizures, and death).</p>\n" }, { "answer_id": 20774, "author": "wisdom_seeker", "author_id": 17314, "author_profile": "https://health.stackexchange.com/users/17314", "pm_score": 2, "selected": false, "text": "<p>Here are medical conditions that come to mind, each with different symptoms:</p>\n\n<ol>\n<li>Severe exercise-induced asthma. Symptoms will be severe wheezing, O2 drop, potentially even death. Long-term anti-inflammatory medications can prevent exacerbations, though exacerbations can still be triggered in specific situations. Imagine a <em>deconditioned</em> character, in <em>fight-and-flight</em>, <em>running from danger</em> in <em>cold weather</em>, and especially with bronchi inflamed from <em>a respiratory infection</em>.</li>\n<li>POTS - postural orthostatic hypotension. A type of dysautonomia, a likely autoimmune condition that can trigger O2 drops, brain fog, nausea, fainting from minor exercise, or (in very severe cases) even from standing up and staying upright. It used to be thought that graduated exercise would help everyone. Not true.</li>\n<li>Chronic fatigue syndrome. Often infection-triggered, likely autoimmune, with antibodies to adrenergic receptors (adrenergic - think adrenalin). Causes <em>post-exercise malaise</em>, meaning dysproportionately severe symptoms for days/weeks after overdoing things, including much increased odds of fainting from POTS, overwhelming fatigue, GI symptoms (nausea, inability to digest..). Depending on the patient, the \"overdoing\" may be physical or cognitive, ranging from doing a college entrance exam, to cooking for a family visit, to walking around the block. </li>\n</ol>\n" } ]
2019/12/25
[ "https://health.stackexchange.com/questions/20712", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17325/" ]
20,733
<p>Kettlebell jugglers all have friction-made blisters on their palms. Gloves are forbidden by the rules. Well one juggler takes the handle of the kettlebell and throws it to the other. </p> <p>This is how juggling looks like <a href="https://www.youtube.com/watch?v=YKSK6agrUac" rel="nofollow noreferrer">https://www.youtube.com/watch?v=YKSK6agrUac</a></p> <p>What troubles me is that if blisters burst, can a desease be transmitted between jugglers?</p> <p>I asked my coach, he said to me not to worry. Well, he is not a doctor anyway.</p> <p>Could you help me understand whether there is any danger here?</p>
[ { "answer_id": 20740, "author": "Carey Gregory", "author_id": 805, "author_profile": "https://health.stackexchange.com/users/805", "pm_score": 0, "selected": false, "text": "<p>Yes, it's possible and a broken blister isn't even necessary. A number of diseases can be transferred from person to person by contact with intact skin or objects skin has touched such as doorknobs and... kettlebells. </p>\n\n<p>One of the most common modes of transmission is the fecal-oral route, which is explained below. </p>\n\n<p><a href=\"https://www.sahealth.sa.gov.au/wps/wcm/connect/public+content/sa+health+internet/health+topics/health+conditions+prevention+and+treatment/infectious+diseases/ways+infectious+diseases+spread\" rel=\"nofollow noreferrer\">Source</a></p>\n\n<blockquote>\n <p>Some infections are spread when microscopic amounts of faeces (poo)\n from an infected person with symptoms or an infected person without\n symptoms (a carrier) are taken in by another person by mouth. The\n faeces may be passed:</p>\n \n <p>directly from soiled hands to the mouth indirectly by way of objects,\n surfaces, food or water soiled with faeces. Examples of diseases\n spread from faeces:</p>\n \n <ul>\n <li>Campylobacter infection</li>\n <li>Cryptosporidium infection</li>\n <li>Giardia infection</li>\n <li>hand, foot and mouth disease</li>\n <li>hepatitis A</li>\n <li>meningitis (viral)</li>\n <li>rotavirus infection</li>\n <li>Salmonella infection</li>\n <li>Shigella infection</li>\n <li>thrush</li>\n <li>viral gastroenteritis</li>\n <li>worms</li>\n <li>Yersinia infection.</li>\n </ul>\n</blockquote>\n\n<p>So instead of worrying about the blisters on your teammates' hands, you should worry about how well they wash their hands after using the toilet.</p>\n\n<p>Other diseases can be spread by direct skin-to-skin contact or indirectly through a common object two people touch. Although there are only a few diseases that can be transmitted by direct skin-to-skin contact of intact skin, people are prone to touching their eyes, nose and mouth, so you have to include diseases that can be spread by contact with mucous membranes as well. </p>\n\n<blockquote>\n <p>Some infections are spread directly when skin or mucous membrane (the\n thin moist lining of many parts of the body such as the nose, mouth,\n throat and genitals) comes into contact with the skin or mucous\n membrane of another person. Infections are spread indirectly when skin\n or mucous membrane comes in contact with contaminated objects or\n surfaces.</p>\n \n <p>Examples of diseases spread by skin or mucous membrane contact:</p>\n \n <ul>\n <li>chickenpox</li>\n <li>cold sores (herpes simplex infection)</li>\n <li>conjunctivitis</li>\n <li>hand, foot and mouth disease</li>\n <li>head lice</li>\n <li>molluscum contagiosum</li>\n <li>ringworm</li>\n <li>scabies</li>\n <li>school sores (impetigo)</li>\n <li>Staphylococcus aureus infection</li>\n <li>warts.</li>\n </ul>\n</blockquote>\n\n<p>What can you do about this? Wash your hands frequently and develop a habit of never touching your eyes, nose, lips and mouth with your bare hands. This is why many gyms provide disinfectant wipes to wipe down exercise equipment after you've used it, but hand washing is more effective.</p>\n" }, { "answer_id": 20741, "author": "user1258361", "author_id": 9695, "author_profile": "https://health.stackexchange.com/users/9695", "pm_score": 2, "selected": true, "text": "<p>Absolutely - and burst blisters are the least of your concerns.</p>\n\n<p>Just take a look at this article:\n<a href=\"https://www.nytimes.com/2017/09/25/well/family/when-athletes-share-infections.html\" rel=\"nofollow noreferrer\">https://www.nytimes.com/2017/09/25/well/family/when-athletes-share-infections.html</a></p>\n\n<p>\"Wrestling and rugby are sufficiently well-known for skin-to-skin transfer that there are herpes virus skin infections actually named for them, Herpes gladiatorum and Herpes rugbiorum (also known as “scrum pox”). “Herpes can shut down a whole team,” Dr. Rice said; wrestlers need “regular skin checks before tournaments,” looking for herpes, impetigo and ringworm, and treating problems so the athletes can compete. Prophylactic medications can help prevent herpes recurrences.</p>\n\n<p>Among bacterial skin infections, community-acquired methicillin-resistant Staphylococcus aureus, or MRSA, has caused many infections among high school and college athletes. MRSA has been a major issue in professional sports as well, particularly football, with several N.F.L. teams having had to deal with outbreaks. These skin infections can be extremely serious, as can streptococcal skin infections, so identifying and treating the lesions is really important for the individual athlete’s health, as well as for containing possible spread.</p>\n\n<p>Athletes are also vulnerable to fungal skin infections, like Tinea corporis, or ringworm, not to mention athlete’s foot (Tinea pedis) and jock itch (Tinea cruris), two fungal infections whose popular names also reflect their tendency to hang around locker rooms. The fungal pathogens can be transmitted, skin to skin, but also by towels and contaminated surfaces.</p>\n" } ]
2019/12/30
[ "https://health.stackexchange.com/questions/20733", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17344/" ]
20,784
<p>Tobramycin <a href="https://www.merckmanuals.com/professional/ear,-nose,-and-throat-disorders/inner-ear-disorders/drug-induced-ototoxicity" rel="nofollow noreferrer">is ototoxic</a> and in some individuals with genetic predisposition Tobramycin can apparently cause rapid permanent balance and hearing loss.</p> <p>Yet, at least where I live, Tobramycin is prescribed for ear infections both as drops and as gels/creams (as eye drops but applied to ear under doctor recommendation). Why is this?</p>
[ { "answer_id": 20793, "author": "De Novo", "author_id": 14173, "author_profile": "https://health.stackexchange.com/users/14173", "pm_score": 3, "selected": true, "text": "<h3>Summary</h3>\n\n<p>Tobramycin is an aminoglycoside antibiotic. All aminoglycoside antibiotics carry a risk of irreversible ototoxicity. The risk is reduced when applied topically, but not eliminated. Even topical use should be avoided for middle ear infections (otitis media). For external ear infections (otitis externa), care should be taken, including ensuring an intact tympanic membrane. As <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284193/\" rel=\"nofollow noreferrer\">this Canadian review suggests</a>, it is important to discuss the risk of ototoxicity with patients when making a treatment decision.</p>\n\n<h3>Approval and use in the US, Canada, and the UK</h3>\n\n<p>There are no approved formulations of tobramycin for any ear infection in the US, but there is a <a href=\"https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/060613s013lbl.pdf\" rel=\"nofollow noreferrer\">suspension</a> containing neomycin that is approved for otitis externa. It contains a warning:</p>\n\n<blockquote>\n <p>WARNINGS: Neomycin can induce permanent sensorineural hearing loss due to cochlear\n damage, mainly destruction of hair cells in the organ of Corti. The risk is greater with prolonged\n use. Therapy should be limited to 10 consecutive days (see PRECAUTIONS-General). Patients\n being treated with eardrops containing neomycin should be under close clinical observation.\n CASPORYN HC Otic Suspension should not be used in any patient with a perforated tympanic\n membrane. </p>\n</blockquote>\n\n<p>To summarize the main points: <strong>Ototoxicity is a risk. Patients should be carefully observed. If the tympanic membrane is perforated, this drug is absolutely contraindicated.</strong></p>\n\n<p>Gentamicin drops are approved <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567906/\" rel=\"nofollow noreferrer\">in Canada for otitis externa</a>, and are <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/10401847/\" rel=\"nofollow noreferrer\">reported</a> to be used off label for otitis media.</p>\n\n<p>In <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/26584651\" rel=\"nofollow noreferrer\">this review</a>, aminoglycoside drops are described as first line therapy in the UK for chronic suppurative otitis media, much to the review authors' chagrin. </p>\n\n<h3>Background on aminoglycosides and ototoxicity</h3>\n\n<p>Aminoglycosides are generally reserved for severe infections (e.g., sepsis, pneumonia, endocarditis). This is, in part, due to the challenging side effect profile common to all members of this drug class, including irreversible ototoxicity, reported in up to 25% of patients in some series. Ototoxicity appears to depend on <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/8019890\" rel=\"nofollow noreferrer\">rapid uptake and slow elimination</a> by hair cells, which in turn depends on plasma concentration, but it is not predictable. Ototoxicity can occur after brief, low dose therapy, and may not manifest until after the drug has been withdrawn, with permanent disability resulting. As mentioned in the question, there are hereditary syndromes and certain genetic mutations that increase susceptibility, but ototoxicity can occur without them. </p>\n\n<p><strong>In summary, ototoxicity is a common, irreversible, unpredictable, and severe side effect of aminoglycoside use.</strong></p>\n\n<p>Goodman &amp; Gilman's The Pharmacologic Basis of Therapeutics provides a good overview of aminoglycosides, with a detailed section on ototoxicity.</p>\n\n<h3>Topical use doesn't eliminate systemic absorption</h3>\n\n<p>Topical preparations of aminoglycosides are approved in the U.S. for certain eye and skin infections. Topical use reduces, but does not eliminate absorption and systemic distribution these antibiotics (Goodman &amp; Gilman Ch. 54). This is not surprising, as infection and the associated inflammation compromise the barrier function of the skin. Absorption can be substantial in the presence of blistering or denuded skin. In the ear, specifically, while tympanic membrane perforation increases the risk of ototoxicity, <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/9425487\" rel=\"nofollow noreferrer\">there is detectable absorption</a> <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/10542926/\" rel=\"nofollow noreferrer\">without perforation</a>. </p>\n" }, { "answer_id": 20795, "author": "Rob", "author_id": 15969, "author_profile": "https://health.stackexchange.com/users/15969", "pm_score": 0, "selected": false, "text": "<blockquote>\n <p>Why is Tobramycin prescribed for ear infections?</p>\n</blockquote>\n\n<p>It doesn't seem to be recommended as eardrops for home use.</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Tobramycin#Spectrum_of_susceptibility\" rel=\"nofollow noreferrer\">Tobramycin</a> has spectrum of activity limited to gram negative bacilli and is <a href=\"https://www.merckmanuals.com/en-ca/professional/infectious-diseases/bacteria-and-antibacterial-drugs/aminoglycosides\" rel=\"nofollow noreferrer\">indicated</a> for <a href=\"https://en.wikipedia.org/wiki/Pseudomonas_aeruginosa#Antibiotic_resistance\" rel=\"nofollow noreferrer\">Pseudomonas aeruginosa</a>, a <a href=\"https://en.wikipedia.org/wiki/Hospital-acquired_infection#Organisms\" rel=\"nofollow noreferrer\">hospital-acquired infection</a>. <a href=\"https://en.wikipedia.org/wiki/Quinolone_antibiotic#History\" rel=\"nofollow noreferrer\">Fluoroquinolones</a> (for example), while also effective and not <a href=\"https://en.wikipedia.org/wiki/Ototoxicity#Antibiotics\" rel=\"nofollow noreferrer\">ototoxic</a>, have (in some cases) been <a href=\"https://www.merckmanuals.com/en-ca/professional/infectious-diseases/bacteria-and-antibacterial-drugs/fluoroquinolones\" rel=\"nofollow noreferrer\">withdrawn</a> from the US market.</p>\n\n<p>In a hospital setting, with patient monitoring, and the development of <a href=\"https://en.wikipedia.org/wiki/Multiple_drug_resistance#Bacterial_resistance_to_antibiotics\" rel=\"nofollow noreferrer\">multidrug resistance</a> by P. aeruginosa, it <strong>might be indicated</strong> after careful consideration of <a href=\"https://www.merckmanuals.com/en-ca/professional/infectious-diseases/bacteria-and-antibacterial-drugs/aminoglycosides\" rel=\"nofollow noreferrer\">risk factors</a>, other options, and patient examination. It can also be used for most staphylococci.</p>\n\n<p>An accurate <a href=\"https://en.wikipedia.org/wiki/Pseudomonas_aeruginosa#Biofilms_and_treatment_resistance\" rel=\"nofollow noreferrer\">diagnosis</a> to determine colonization versus infection might involve a <a href=\"http://www.microbiologynutsandbolts.co.uk/the-bug-blog/colonisation-vs-infection\" rel=\"nofollow noreferrer\">delay</a>. If the bacteria was contracted during bathing it may be expected to be gone once the ears are dry. <a href=\"https://en.wikipedia.org/wiki/Horizontal_gene_transfer\" rel=\"nofollow noreferrer\">Horizontal gene transfer</a> prevention from <a href=\"https://en.wikipedia.org/wiki/Pseudomonas_aeruginosa#Antibiotic_resistance\" rel=\"nofollow noreferrer\">P. aeruginosa</a> is another consideration. Topical <a href=\"https://en.wikipedia.org/wiki/Gentamicin\" rel=\"nofollow noreferrer\">Gentamicin</a> would normally only be used for a couple of days while awaiting bacterial cultures to determine what specific antibiotics the infection is sensitive to.</p>\n\n<p><a href=\"https://i.stack.imgur.com/OhNSV.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/OhNSV.jpg\" alt=\"Antibiotics Spectrum\"></a>\n<sup><sup>Source: Wikipedia: \"<a href=\"https://en.wikipedia.org/wiki/Broad-spectrum_antibiotic\" rel=\"nofollow noreferrer\">Broad-spectrum antibiotic</a>\".</sup></sup></p>\n" } ]
2020/01/07
[ "https://health.stackexchange.com/questions/20784", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17384/" ]
20,854
<p><strong>IMPORTANT NOTE:</strong> This question focuses on <em>scientific aspects</em> of gender dysphoria only. By no means I desire to disrespect anybody and will gladly have comments about any mistake I might have.</p> <p>My following question is specifically with the very basic idea of "mental illness" and nothing else --- Why WHO distinguishes between having a common mental illness (e.g. schizophrenia, depression, etc.) and being a transgender person, which by definition referred to people who <strong>* feel or think to*</strong> "have a gender identity that differs from their sex assigned at birth".</p> <p>Does being transgender a mental health condition? If no, why not?<br> That is to ask; why in some countries health agencies declassify transgender people as having "mental disorder" (in accordance with the world health organisation (WHO))?<br> <sub>In other words, what makes being transgender different than being mentally ill?</sub></p>
[ { "answer_id": 20793, "author": "De Novo", "author_id": 14173, "author_profile": "https://health.stackexchange.com/users/14173", "pm_score": 3, "selected": true, "text": "<h3>Summary</h3>\n\n<p>Tobramycin is an aminoglycoside antibiotic. All aminoglycoside antibiotics carry a risk of irreversible ototoxicity. The risk is reduced when applied topically, but not eliminated. Even topical use should be avoided for middle ear infections (otitis media). For external ear infections (otitis externa), care should be taken, including ensuring an intact tympanic membrane. As <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284193/\" rel=\"nofollow noreferrer\">this Canadian review suggests</a>, it is important to discuss the risk of ototoxicity with patients when making a treatment decision.</p>\n\n<h3>Approval and use in the US, Canada, and the UK</h3>\n\n<p>There are no approved formulations of tobramycin for any ear infection in the US, but there is a <a href=\"https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/060613s013lbl.pdf\" rel=\"nofollow noreferrer\">suspension</a> containing neomycin that is approved for otitis externa. It contains a warning:</p>\n\n<blockquote>\n <p>WARNINGS: Neomycin can induce permanent sensorineural hearing loss due to cochlear\n damage, mainly destruction of hair cells in the organ of Corti. The risk is greater with prolonged\n use. Therapy should be limited to 10 consecutive days (see PRECAUTIONS-General). Patients\n being treated with eardrops containing neomycin should be under close clinical observation.\n CASPORYN HC Otic Suspension should not be used in any patient with a perforated tympanic\n membrane. </p>\n</blockquote>\n\n<p>To summarize the main points: <strong>Ototoxicity is a risk. Patients should be carefully observed. If the tympanic membrane is perforated, this drug is absolutely contraindicated.</strong></p>\n\n<p>Gentamicin drops are approved <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567906/\" rel=\"nofollow noreferrer\">in Canada for otitis externa</a>, and are <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/10401847/\" rel=\"nofollow noreferrer\">reported</a> to be used off label for otitis media.</p>\n\n<p>In <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/26584651\" rel=\"nofollow noreferrer\">this review</a>, aminoglycoside drops are described as first line therapy in the UK for chronic suppurative otitis media, much to the review authors' chagrin. </p>\n\n<h3>Background on aminoglycosides and ototoxicity</h3>\n\n<p>Aminoglycosides are generally reserved for severe infections (e.g., sepsis, pneumonia, endocarditis). This is, in part, due to the challenging side effect profile common to all members of this drug class, including irreversible ototoxicity, reported in up to 25% of patients in some series. Ototoxicity appears to depend on <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/8019890\" rel=\"nofollow noreferrer\">rapid uptake and slow elimination</a> by hair cells, which in turn depends on plasma concentration, but it is not predictable. Ototoxicity can occur after brief, low dose therapy, and may not manifest until after the drug has been withdrawn, with permanent disability resulting. As mentioned in the question, there are hereditary syndromes and certain genetic mutations that increase susceptibility, but ototoxicity can occur without them. </p>\n\n<p><strong>In summary, ototoxicity is a common, irreversible, unpredictable, and severe side effect of aminoglycoside use.</strong></p>\n\n<p>Goodman &amp; Gilman's The Pharmacologic Basis of Therapeutics provides a good overview of aminoglycosides, with a detailed section on ototoxicity.</p>\n\n<h3>Topical use doesn't eliminate systemic absorption</h3>\n\n<p>Topical preparations of aminoglycosides are approved in the U.S. for certain eye and skin infections. Topical use reduces, but does not eliminate absorption and systemic distribution these antibiotics (Goodman &amp; Gilman Ch. 54). This is not surprising, as infection and the associated inflammation compromise the barrier function of the skin. Absorption can be substantial in the presence of blistering or denuded skin. In the ear, specifically, while tympanic membrane perforation increases the risk of ototoxicity, <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/9425487\" rel=\"nofollow noreferrer\">there is detectable absorption</a> <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/10542926/\" rel=\"nofollow noreferrer\">without perforation</a>. </p>\n" }, { "answer_id": 20795, "author": "Rob", "author_id": 15969, "author_profile": "https://health.stackexchange.com/users/15969", "pm_score": 0, "selected": false, "text": "<blockquote>\n <p>Why is Tobramycin prescribed for ear infections?</p>\n</blockquote>\n\n<p>It doesn't seem to be recommended as eardrops for home use.</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Tobramycin#Spectrum_of_susceptibility\" rel=\"nofollow noreferrer\">Tobramycin</a> has spectrum of activity limited to gram negative bacilli and is <a href=\"https://www.merckmanuals.com/en-ca/professional/infectious-diseases/bacteria-and-antibacterial-drugs/aminoglycosides\" rel=\"nofollow noreferrer\">indicated</a> for <a href=\"https://en.wikipedia.org/wiki/Pseudomonas_aeruginosa#Antibiotic_resistance\" rel=\"nofollow noreferrer\">Pseudomonas aeruginosa</a>, a <a href=\"https://en.wikipedia.org/wiki/Hospital-acquired_infection#Organisms\" rel=\"nofollow noreferrer\">hospital-acquired infection</a>. <a href=\"https://en.wikipedia.org/wiki/Quinolone_antibiotic#History\" rel=\"nofollow noreferrer\">Fluoroquinolones</a> (for example), while also effective and not <a href=\"https://en.wikipedia.org/wiki/Ototoxicity#Antibiotics\" rel=\"nofollow noreferrer\">ototoxic</a>, have (in some cases) been <a href=\"https://www.merckmanuals.com/en-ca/professional/infectious-diseases/bacteria-and-antibacterial-drugs/fluoroquinolones\" rel=\"nofollow noreferrer\">withdrawn</a> from the US market.</p>\n\n<p>In a hospital setting, with patient monitoring, and the development of <a href=\"https://en.wikipedia.org/wiki/Multiple_drug_resistance#Bacterial_resistance_to_antibiotics\" rel=\"nofollow noreferrer\">multidrug resistance</a> by P. aeruginosa, it <strong>might be indicated</strong> after careful consideration of <a href=\"https://www.merckmanuals.com/en-ca/professional/infectious-diseases/bacteria-and-antibacterial-drugs/aminoglycosides\" rel=\"nofollow noreferrer\">risk factors</a>, other options, and patient examination. It can also be used for most staphylococci.</p>\n\n<p>An accurate <a href=\"https://en.wikipedia.org/wiki/Pseudomonas_aeruginosa#Biofilms_and_treatment_resistance\" rel=\"nofollow noreferrer\">diagnosis</a> to determine colonization versus infection might involve a <a href=\"http://www.microbiologynutsandbolts.co.uk/the-bug-blog/colonisation-vs-infection\" rel=\"nofollow noreferrer\">delay</a>. If the bacteria was contracted during bathing it may be expected to be gone once the ears are dry. <a href=\"https://en.wikipedia.org/wiki/Horizontal_gene_transfer\" rel=\"nofollow noreferrer\">Horizontal gene transfer</a> prevention from <a href=\"https://en.wikipedia.org/wiki/Pseudomonas_aeruginosa#Antibiotic_resistance\" rel=\"nofollow noreferrer\">P. aeruginosa</a> is another consideration. Topical <a href=\"https://en.wikipedia.org/wiki/Gentamicin\" rel=\"nofollow noreferrer\">Gentamicin</a> would normally only be used for a couple of days while awaiting bacterial cultures to determine what specific antibiotics the infection is sensitive to.</p>\n\n<p><a href=\"https://i.stack.imgur.com/OhNSV.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/OhNSV.jpg\" alt=\"Antibiotics Spectrum\"></a>\n<sup><sup>Source: Wikipedia: \"<a href=\"https://en.wikipedia.org/wiki/Broad-spectrum_antibiotic\" rel=\"nofollow noreferrer\">Broad-spectrum antibiotic</a>\".</sup></sup></p>\n" } ]
2020/01/18
[ "https://health.stackexchange.com/questions/20854", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17445/" ]
20,859
<p>I googled and read about the kidneys, bladder, and urethra but no source explains the dynamic process.</p> <p>From my own personal experience, the process has four stages:</p> <ol> <li><p>The muscles are in normal mode. Then, a feeling comes that you need to empty the bladder.</p></li> <li><p>The muscles are relaxed so the flow starts.</p></li> <li><p>After the last drop, the muscles are contracted and this time a short flow happens (much fewer amount of urine comes out).</p></li> <li><p>Muscles go back to normal mode.</p></li> </ol> <p>I would like to ask specifically about stage <strong>3</strong>. Why does the last amount of urine come out this way? Why doesn't it simply go out with the rest of the urine? What's the responsible muscle?</p>
[ { "answer_id": 20860, "author": "JMP", "author_id": 97, "author_profile": "https://health.stackexchange.com/users/97", "pm_score": 1, "selected": false, "text": "<p>There's no extra muscle involved - it's like squeezing an almost-empty toothpaste tube to get the last bits of toothpaste out.</p>\n" }, { "answer_id": 20868, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": true, "text": "<p>The act of urination goes like this (<a href=\"https://www.visiblebody.com/learn/urinary/urine-storage-and-elimination\" rel=\"nofollow noreferrer\">Visible Body</a>):</p>\n\n<blockquote>\n <p>Micturition, or urination, is the act of emptying the bladder. When\n the bladder is full of urine, stretch receptors in the bladder wall\n trigger the micturition reflex. The <strong>detrusor muscle</strong> that surrounds\n the bladder <strong>contracts.</strong> <strong>The internal urethral sphincter\n relaxes,</strong> allowing for urine to pass out of the bladder into the\n urethra. Both of these reactions are involuntary. <strong>The external\n urethral sphincter</strong> is voluntary. It must be <strong>relaxed</strong> for urine to\n flow through the urethra and outside the body.</p>\n</blockquote>\n\n<p><a href=\"https://i.stack.imgur.com/TTbzi.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/TTbzi.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Picture: Bladder anatomy (source: <a href=\"https://commons.wikimedia.org/wiki/File:Illu_bladder.jpg\" rel=\"nofollow noreferrer\">Wikipedia</a>, creative commons license)</p>\n\n<p>So, to urinate, <em>normally,</em> all you need to do is to relax the external urethral sphincter. Sometimes, urination can spontaneously stop even if there is still some urine in the bladder; a common cause is <em><a href=\"https://www.webmd.com/men/prostate-enlargement-bph/features/enlarged-prostate-bph-complex-problem#1\" rel=\"nofollow noreferrer\">enlarged prostate</a></em> - it often enlarges with age. In this case, pressing on the prostate can remove the remaining urine. Also, it is possible to close the external urethral sphincter more consciously and thus prevent the leak of the remaining urine. The problem with the leak at the end may be relying on the external urethral sphincter to close by itself quickly, while it may need some time to do so if you don't think on it... </p>\n" } ]
2020/01/19
[ "https://health.stackexchange.com/questions/20859", "https://health.stackexchange.com", "https://health.stackexchange.com/users/3676/" ]
20,894
<p>I recently started using MyFitnessPal to try to lose weight and I noticed that a particular beer I had drunk has a tremendous number of calories relative to the number of grams of carbs it contains compared to something like rice or oatmeal. This ended up being a problem for me, because it made it harder for me to hit my macro goals for the day without going over my daily calorie limit.</p> <p>The nutritional information might be incorrect (this beer isn't from a country that I totally trust the nutritional labels for), or the person who put the nutritional information into MyFitnessPal might have done it incorrectly. I do remember hearing that beer has a lot of carbohydrates, which would seem to go against what I'm saying here.</p> <p>So: Can a calorie be neither protein, carbohydrate, nor fat?</p>
[ { "answer_id": 20895, "author": "De Novo", "author_id": 14173, "author_profile": "https://health.stackexchange.com/users/14173", "pm_score": 5, "selected": true, "text": "<p><a href=\"https://www.ncbi.nlm.nih.gov/m/pubmed/3015171/\" rel=\"noreferrer\">Ethanol is caloric</a> and is neither a carbohydrate, protein, or fat. </p>\n" }, { "answer_id": 23101, "author": "Dietitian Jenn", "author_id": 19256, "author_profile": "https://health.stackexchange.com/users/19256", "pm_score": 1, "selected": false, "text": "<p>This is probably a bit of both.</p>\n\n<p>By this, I mean that ethanol does contain calories, 7 kcal per gram of alcohol.</p>\n\n<p>Fat is 9 kcal/g, carbs and protein are 4 kcal/g.</p>\n\n<p>It is also possible that the nutrition label itself is calculated incorrectly, probably by mistake. If you're really bothered by the discrepancy, you could reach out to the company.</p>\n\n<p>Likewise, the info in My Fitness Pal could be incorrectly cited as well. These tools should be used as a guideline, not as concrete fact. If something seems off, you are absolutely correct in questioning it! I've found that in My Fitness Pal, scanning the bar code is typically more accurate than searching for the product. You could also look for a second entry for the product you are searching for and seeing if that one makes more sense.</p>\n" }, { "answer_id": 23106, "author": "bida.dari", "author_id": 17144, "author_profile": "https://health.stackexchange.com/users/17144", "pm_score": 2, "selected": false, "text": "<p>A calorie is a measure of heat given off by burning a substance.</p>\n\n<p>This article shows the origin of the term in the context of nutrition <a href=\"https://academic.oup.com/jn/article/136/12/2957/4663943\" rel=\"nofollow noreferrer\">https://academic.oup.com/jn/article/136/12/2957/4663943</a> </p>\n\n<p>One of the earlier uses of the term in a physiological metabolic context, as apposed to a physics context, was in a paper by a German scientist named J. R. Mayer. The Mayer quote shows an early use of the definition that comes up in nutrition classes. </p>\n\n<p>\"When substances endowed with considerable chemical affinity for each other combine chemically, much heat is developed during the process. We shall estimate the quantity of heat thus set free by the number of kilogrammes of water which it would heat 1°C. The quantity of heat necessary to raise 1 kilogramme of water 1 degree is called a unit of heat, Calorie. \"</p>\n\n<p>A calorie itself is not something you ingest, and there's no Dietary Reference Intake <a href=\"https://ods.od.nih.gov/Health_Information/Dietary_Reference_Intakes.aspx\" rel=\"nofollow noreferrer\">https://ods.od.nih.gov/Health_Information/Dietary_Reference_Intakes.aspx</a> for it, unlike everything else on the nutrition facts label (maybe that's why it's in separate box). </p>\n\n<p>It's a measure of energy generation, so it depends on the individual process of how it's generated, and I'm not sure if the FDA bases their label's numbers off of cellular metabolic data using digestive enzymes and gut flora, they might use something like a butane torch. It might be a good idea to take the calorie number as a reference point when considering your own metabolism, and not as an exact quantity. Many things can affect someone's metabolism, its efficiency and its rate, at cellular and molecular levels (and above and below probably).</p>\n\n<p>If you're thinking in terms of this definition, anything that causes metabolic reaction that generates heat could be measured as a calorie. Ethanol burns in a lab, but whether or not it generates heat in your body when it's metabolized depends on its metabolic processes <a href=\"https://en.wikipedia.org/wiki/Ethanol_metabolism\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Ethanol_metabolism</a> . </p>\n\n<p>If you wanted to know what substances generate heat in the body in general, the answer might be in the field of bioenergetics <a href=\"https://en.wikipedia.org/wiki/Bioenergetics\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Bioenergetics</a> , but that would include cellular respiration as well as enzymatic processes as the wiki article says, so breathing and processing anything (including your own dead cells thru apoptosis, or any drug you take or xenobiotic substance that enters your body <a href=\"https://www.sciencedirect.com/science/article/pii/S1359644612000359\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/pii/S1359644612000359</a>) could be shown to have a caloric value. Nutritionists and food producers are mostly focused on the calories from catabolic metabolism <a href=\"http://www.cte.sfasu.edu/wp-content/uploads/2012/01/2_Principles_of_Digestion_and_Metabolism.html\" rel=\"nofollow noreferrer\">http://www.cte.sfasu.edu/wp-content/uploads/2012/01/2_Principles_of_Digestion_and_Metabolism.html</a> by specifically liver enzymes, of something absorbed through the intestines (different parts of the intestines absorb different things, and not all gets processed catabolically). </p>\n\n<p>The food/nutrition industries' use of \"calories\" is a weirdly specific definition that presents a narrow view of bioenergetics -- bodies are way more complex and unique!</p>\n" } ]
2020/01/24
[ "https://health.stackexchange.com/questions/20894", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16397/" ]
20,967
<p>If I get infected once with the virus which causes a common cold, does that mean I will not get infected with the same strain of the virus ever in my lifetime? </p> <p>Is the immune system capable and smart enough to recognize the viruses that have infected me in the past, and kill them before it initiates its incubation within a cell? If so, why do I keep getting a common cold again and again? Do I keep exposing myself to a new different strain of the same virus?</p> <p>Based on the fact that there are over 200 different types of viruses that cause a common cold. To what extent do you think creating a universal vaccine for the common cold could be successful, and what are the challenges facing scientists in creating a successful universal vaccine?</p>
[ { "answer_id": 20968, "author": "anongoodnurse", "author_id": 169, "author_profile": "https://health.stackexchange.com/users/169", "pm_score": 4, "selected": true, "text": "<blockquote>\n <p>If I get infected once with the virus which causes a common cold, does that mean I will not get infected with the same strain of the virus ever in my lifetime? </p>\n</blockquote>\n\n<p>It depends on quirks of your immune system and the viral load you're exposed to, but in theory (based on vaccination and other studies), presence of the virus will trigger a suppressive response, not to nasal mucosal invasion but to viral replication and cell destruction/inflammation to the degree that you clinically manifest \"a cold\". </p>\n\n<p>Regarding your quirks,</p>\n\n<blockquote>\n <p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553670/\" rel=\"noreferrer\">The persistence of high-titer serotype-specific antibody is associated with protection from infection as well as reduced symptom severity following experimental challenge with the same serotype</a> (52). However, there is little cross-neutralization among serotypes, which presents a challenge to vaccine development, given that there are more than 100 different known HRV serotypes (53). Further support for the role of humoral immunity in the prevention and control of HRV infection was observed in a study of patients with primary hypogammaglobulinemia. These patients experienced more frequent and severe HRV infections than their healthy spouses despite the administration of replacement immunoglobulin therapy (54).</p>\n</blockquote>\n\n<p>That's only the beginning. Immunology is very complex.</p>\n\n<blockquote>\n <p>To what extent do you think creating a universal vaccine for the common cold could be successful...</p>\n</blockquote>\n\n<p>Close to, if not, zero.</p>\n\n<p>There are about 120 distinctly different serotypes of rhinovirus which cause the \"common cold\", which could require 120 separate vaccines. Also a significant percentage of \"colds\" are caused by other types of viruses (coronavirus - like tat in China right now, respiratory syncytial virus, influenza and parainfluenza viruses) as well as some bacteria.</p>\n\n<blockquote>\n <p>Human coronaviruses, members of the Coronaviridae family, were first identified in 1962 and have been <a href=\"https://academic.oup.com/cid/article/31/1/96/321510\" rel=\"noreferrer\">particularly difficult to isolate by use of standard cell culture techniques</a>.</p>\n</blockquote>\n\n<p>One needs to reliably grow a virus before making a vaccine.</p>\n\n<blockquote>\n <p>Efforts at vaccine development are hindered by the existence of more than <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553670/\" rel=\"noreferrer\">100 HRV serotypes with high-level sequence variability in the antigenic sites</a>.</p>\n</blockquote>\n\n<p>And</p>\n\n<blockquote>\n <p>Compared to patients with coronavirus-associated colds, there is no difference in respiratory symptom severity or duration.</p>\n</blockquote>\n\n<p>However, there is a light at the end of the tunnel: the older you get, the fewer new viruses you're exposed to (if you stay in one geograpical location), and the fewer colds you get. I haven't had a \"common cold\" in a few years now. If I move across the continent, I will have more colds.</p>\n" }, { "answer_id": 20969, "author": "Nicole C", "author_id": 17520, "author_profile": "https://health.stackexchange.com/users/17520", "pm_score": 0, "selected": false, "text": "<p>Edit: I'm new at this. In response to recommendations I received I've attempted to insert web citations. LMK if I did it wrong...</p>\n\n<p>Yes, your immune system can recognize and protect against viruses you've been infected with in the past. That's why folks typically only get the chickenpox once. But getting a cold does NOT protect you against future colds, largely for the same reasons that a vaccine is highly unlikely (read on...).</p>\n\n<p>There are multiple barriers to creating a successful vaccine against the common cold. First, as you noted, what we call 'the common cold' is really a constellation of symptoms that can be caused by over 200 different organisms <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5355621/\" rel=\"nofollow noreferrer\">1</a>, most of them viruses (including rhinovirus, respiratory syncytial virus, coronavirus, adenovirus) but also some bacteria (haemophilus influenzae, mycoplasma pneumoniae, and a couple others named ___ pneumoniae)<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC104573/\" rel=\"nofollow noreferrer\">2</a>. A successful vaccine would need to protect against at least the most common ones (similar to the yearly flu vaccine which typically covers 3 strains of influenza) - a more difficult task than creating a vaccine for, say, polio (which only has 3 strains <a href=\"https://www.cdc.gov/cpr/polioviruscontainment/diseaseandvirus.htm\" rel=\"nofollow noreferrer\">3</a>). Second, the reason you have to get the flu shot every year is because the virus mutates. The same goes for cold viruses - they mutate, and rather frequently <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5355621/\" rel=\"nofollow noreferrer\">1</a>, meaning a new vaccine would need to be developed at least annually.</p>\n\n<p>Additionally colds frankly just aren't a very high priority. While it is true that young babies, the very elderly, and those with certain health conditions can suffer serious complications from a cold, most of us just get an annoying cough &amp; nasal symptoms for a few days. Not a lot of investment is going to be made in preventing such a disease <a href=\"https://www.verywellhealth.com/why-there-will-never-be-a-vaccine-for-the-common-cold-770451#mild-illness\" rel=\"nofollow noreferrer\">4</a> (especially when there's so much money to be made in mitigating treatments).</p>\n\n<ul>\n<li>a pediatrician [all of the above is factual information except the $ made from cold treatments which represents my opinion ;) ]</li>\n</ul>\n" } ]
2020/02/03
[ "https://health.stackexchange.com/questions/20967", "https://health.stackexchange.com", "https://health.stackexchange.com/users/9074/" ]
20,970
<p>According to the data on the <a href="https://gisanddata.maps.arcgis.com/apps/opsdashboard/index.html#/bda7594740fd40299423467b48e9ecf6" rel="nofollow noreferrer">Johns Hopkins Coronavirus Tracker</a>, as of 3rd February 2020 there were 17491 confirmed cases of COVID-19 globally, 536 total recoveries and 362 deaths. From my non-expert calculation this implies a mortality rate of:</p> <p><code>(Nd / (Nd + Nr)) * 100 = 41%</code></p> <p>where:</p> <p>Nd is the total number of deaths, Nr is the total number of full recoveries.</p> <p>This leaves 16593 people still suffering from the disease who have neither recovered or died.</p> <p>This is in stark contrast to the publicly disseminated value of ~2% mortality, so have I made a mistake in my calculation or assumptions, or is COVID-19 much more dangerous than commonly claimed? </p> <p><strong>[After a helpful discussion in the comments, 'mortality rate' is not the correct term to use here, instead I should say '<a href="https://www.britannica.com/science/case-fatality-rate" rel="nofollow noreferrer">Case Fatality Ratio</a>'.]</strong></p>
[ { "answer_id": 20972, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 4, "selected": false, "text": "<p>The equation you use for mortality is only really useful in the very long term for a known disease, when most cases have resolved.</p>\n\n<p>It's not very informative in the short-term, when the vast majority of total cases are neither deaths nor recoveries.</p>\n\n<p>Right now, the vast majority of people diagnosed have a mild illness and are very unlikely to die, but it takes a long time for them to be considered in the \"recovered\" category. Additionally, many of those who have died are particularly vulnerable. From WHO:</p>\n\n<blockquote>\n <p>As with other respiratory illnesses, infection with 2019-nCoV can cause mild symptoms including a runny nose, sore throat, cough, and fever. It can be more severe for some persons and can lead to pneumonia or breathing difficulties. More rarely, the disease can be fatal. Older people, and people with pre-existing medical conditions (such as, diabetes and heart disease) appear to be more vulnerable to becoming severely ill with the virus.</p>\n</blockquote>\n\n<p>Estimates for mortality that you see in the news might instead be based on deaths/cases, or are based on expert comparisons to past epidemic coronavirus strains and knowledge of the typical course of the illness.</p>\n\n<p>Additionally, we don't know how accurate the numbers are, especially for cases. There may be many more mild cases that go unreported.</p>\n\n<p>There won't be good estimates of the actual mortality rate until more time has passed, and even in that case it is unlikely that a single number will be very informative. Instead, the risk will vary by age and other factors. Good sources for information, like the WHO, don't report mortality rates: they are only reporting cases and deaths at this time.</p>\n\n<p>Some good sources for further information:</p>\n\n<p><a href=\"https://www.who.int/emergencies/diseases/novel-coronavirus-2019\" rel=\"noreferrer\">https://www.who.int/emergencies/diseases/novel-coronavirus-2019</a></p>\n\n<p><a href=\"https://www.cdc.gov/coronavirus/2019-nCoV/summary.html\" rel=\"noreferrer\">https://www.cdc.gov/coronavirus/2019-nCoV/summary.html</a></p>\n\n<p><a href=\"https://www.nhs.uk/conditions/wuhan-novel-coronavirus/\" rel=\"noreferrer\">https://www.nhs.uk/conditions/wuhan-novel-coronavirus/</a></p>\n" }, { "answer_id": 20977, "author": "Igor G", "author_id": 17530, "author_profile": "https://health.stackexchange.com/users/17530", "pm_score": 4, "selected": false, "text": "<p>I'd like to chime in with an explanation of <em>what exactly</em> is wrong with the calculation offered in the question, rather than just saying \"it's a wrong formula\". Understanding the \"whys\" of the fallacy is important. So I'll try to answer your question from the math point of view.</p>\n\n<p><strong>TL;DR: The root cause of the fallacy is that recovery takes much longer that death.</strong></p>\n\n<blockquote>\n <p><code>(Nd / (Nd + Nr)) * 100 = 41%</code><br>\n where: Nd is the total number of deaths,<br>\n Nr is the total number of full recoveries.</p>\n</blockquote>\n\n<p>That formula (and the logic behind it) is correct as long as <code>Nd</code> and <code>Nr</code> both refer to <strong>the same fixed group of people</strong>. That is, if we had picked <code>N</code> infected people, waited for them <em>all</em> to reach the final state (recovery or death), and put those <code>Nr</code> and <code>Nd</code> to that formula above - then yes, it would give the statistical mortality rate in that group.</p>\n\n<p>However, the current counts of recovery/death outcomes do not refer to <em>the same group</em>. <code>Nd</code> in each WHO report refers to the group of all people infected thus far since the start of the outbreak. But the final outcome of <em>all</em> people in that group is yet unknown. Daily <code>Nr</code> refers only to a subgroup of all those infected (excluding those unknowns), see? So you can't take <code>Nd</code> and <code>Nr</code> from a WHO report and put those numbers to that formula - that would be apples and oranges...</p>\n\n<p>To illustrate this point, consider a grossly simplified imaginary situation:<br>\nthere's a disease which may lead to death on the 3rd day, while the rest of infected people will fully recover on the 15th day. In that case, <code>Nd</code> in the official report would encompass all people infected 3 days ago and before, while <code>Nr</code> would encompass all people infected 15 days ago and before. Given the high flow of new confirmed cases coming each day, the difference between those two groups is huge: it is all those people infected in 12 days!</p>\n\n<p>In our real case that difference is far greater than <code>Nr</code> and <code>Nd</code> combined, which means the error from ignoring that difference renders the calculation totally useless. (Well, it's useful as an absolute upper limit, but no more).</p>\n" }, { "answer_id": 20980, "author": "Ilmari Karonen", "author_id": 11944, "author_profile": "https://health.stackexchange.com/users/11944", "pm_score": 7, "selected": true, "text": "<p>The definition of mortality rate that you've given does not match any practical definition I'm familiar with.*</p>\n\n<p>When people talk about the mortality rate of a disease, what they <em>usually</em> mean is the <a href=\"https://en.wikipedia.org/wiki/Case_fatality_rate\" rel=\"noreferrer\">case fatality rate</a> or the <a href=\"https://www.cdc.gov/csels/dsepd/ss1978/lesson3/section3.html\" rel=\"noreferrer\">death-to-case ratio</a>, which is simply defined as <em>N</em><sub>d</sub> / <em>N</em><sub>i</sub>, where <em>N</em><sub>d</sub> is the number of deaths attributed to the disease over a given time period and <em>N</em><sub>i</sub> is the total number of new cases of the disease observed during the same time period. By this definition, the current case fatality rate of 2019-nCov according to your quoted figures is 362 / 17491 ≈ 2.07%.</p>\n\n<p>(The <a href=\"https://gisanddata.maps.arcgis.com/apps/opsdashboard/index.html#/bda7594740fd40299423467b48e9ecf6\" rel=\"noreferrer\">tracker</a> seems to have been updated since you asked your question, and now lists a total of 20679 confirmed cases and 427 deaths, for a CFR of 427 / 20679 ≈ 2.06%.)</p>\n\n<p><sup>*) As a theoretical definition of the mortality rate <em>in the long run</em>, when all infected patients have either died or recovered, it can sort of make sense. But then it becomes equivalent to the usual definition of the case fatality rate.</sup></p>\n\n<hr>\n\n<p>To compare this with your definition of \"mortality rate\" (as <em>N</em><sub>d</sub> / (<em>N</em><sub>d</sub> + <em>N</em><sub>r</sub>), where <em>N</em><sub>r</sub> is the number of individuals who have recovered from the disease), we need to start by observing that there's no single universal and unambiguous definition of what \"recovering from a disease\" means. Commonly used definitions tend to be something like \"no symptoms for <em>X</em> days\" and/or \"viral load below <em>N</em> particles per mL for <em>X</em> days\" or simply \"whenever a doctor declares that you're healthy again and lets you out of the hospital\".</p>\n\n<p>Now, let's say that we're using a (somewhat) objective definition of recovery like \"no detectable symptoms for two days\". The first observation is that any epidemic first observed less than two days ago would, according to your definition, inevitably have a mortality rate of 100% simply because none of the people infected so far would have had time to be considered definitely recovered yet. (That is assuming that at least one person had died from the infection; otherwise both the numerator and the denominator would be zero, and the rate thus undefined.)</p>\n\n<p>Further, even after some of the earliest cases have been symptom-free long enough to be counted as recovered, your definition would still yield a highly upwards biased estimate of the \"true\" long-term fatality rate during the early phase of the epidemic, when the number of new cases per day is still increasing. This is because, for most infectious diseases, any deaths typically occur when the disease is at its most severe state, whereas those who survive the disease will then experience a gradual decline in symptoms as their immune system succeeds in halting and reversing the progress of the infection.</p>\n\n<hr>\n\n<p>For an illustrative example, let's consider a hypothetical disease with a theoretical 1% long-term average CFR — that is to say, exactly 1% of all (recognizably) infected patients will die of the disease. Let's further assume that this disease typically takes two days to progress from the initial onset of recognizable symptoms to the state of maximum severity, which is when most of the deaths occur. After this, assuming that the patient survives, the symptoms gradually decline over the following three days. As remission is possible (but rare), doctors will generally consider a patient recovered only after showing no symptoms for at least two days. Thus, a typical case would progress as follows:</p>\n\n<blockquote>\n <p>onset of symptoms → increasing symptoms (2 days) → peak severity → declining symptoms (3 days) → no symptoms → observation (2 days) → officially recovered (total time: approx. 7 days from onset)</p>\n</blockquote>\n\n<p>or, for the 1% of patients for whom the disease is fatal:</p>\n\n<blockquote>\n <p>onset of symptoms → increasing symptoms (2 days) → death (total time: approx. 2 days from onset)</p>\n</blockquote>\n\n<p>Now, let's assume that, during the early period of an epidemic when the infection is still spreading exponentially, the number of new cases increases by a factor of 10 every three days. Thus, during this period, the number of new cases, recoveries and deaths per day might grow approximately as follows (assuming for the sake of the example that exactly 1%, rounded down, of the patients diagnosed on each day will die two days later):</p>\n\n<pre><code> | cases | recovered | deaths | | | \nday | new | total | new | total | new | total | Nd / Ni | Nd/(Nd+Nr) |\n----+-------+-------+-------+-------+-------+-------+---------+------------+\n 1 | 1 | 1 | 0 | 0 | 0 | 0 | 0.00% | N/A |\n 2 | 2 | 3 | 0 | 0 | 0 | 0 | 0.00% | N/A |\n 3 | 5 | 8 | 0 | 0 | 0 | 0 | 0.00% | N/A |\n 4 | 10 | 18 | 0 | 0 | 0 | 0 | 0.00% | N/A |\n 5 | 20 | 38 | 0 | 0 | 0 | 0 | 0.00% | N/A |\n 6 | 50 | 88 | 0 | 0 | 0 | 0 | 0.00% | N/A |\n 7 | 100 | 188 | 0 | 0 | 0 | 0 | 0.00% | N/A |\n 8 | 200 | 388 | 1 | 1 | 0 | 0 | 0.00% | 0.0% |\n 9 | 500 | 888 | 2 | 3 | 1 | 1 | 0.11% | 25.0% |\n 10 | 1000 | 1888 | 5 | 8 | 2 | 3 | 0.16% | 27.3% |\n 11 | 2000 | 3888 | 10 | 18 | 5 | 8 | 0.21% | 30.8% |\n 12 | 5000 | 8888 | 20 | 38 | 10 | 18 | 0.20% | 32.1% |\n</code></pre>\n\n<p>As you can see from the table above, naïvely calculating the case fatality rate as (total number of deaths) / (total number of cases) during this exponential growth period does underestimate the true long-term CFR by a factor of (in this case) about 5 due to the two-day lag time between infection and death. On the other hand, using your formula of (total deaths) / (total deaths + recovered) would <em>overestimate</em> the true CFR by a factor of about 30!</p>\n\n<p>Meanwhile, let's assume that, after the first 12 days, the growth of the epidemic saturates at 10,000 new cases per day. Now the total numbers will look like this:</p>\n\n<pre><code> | cases | recovered | deaths | | | \nday | new | total | new | total | new | total | Nd / Ni | Nd/(Nd+Nr) |\n----+-------+-------+-------+-------+-------+-------+---------+------------+\n 13 | 10000 | 18888 | 50 | 88 | 20 | 38 | 0.20% | 30.2% |\n 14 | 10000 | 28888 | 99 | 187 | 50 | 88 | 0.30% | 32.0% |\n 15 | 10000 | 38888 | 198 | 385 | 100 | 188 | 0.48% | 32.8% |\n 16 | 10000 | 48888 | 495 | 880 | 100 | 288 | 0.59% | 24.7% |\n 17 | 10000 | 58888 | 990 | 1870 | 100 | 388 | 0.66% | 17.2% |\n 18 | 10000 | 68888 | 1980 | 3850 | 100 | 488 | 0.71% | 11.2% |\n 19 | 10000 | 78888 | 4950 | 8800 | 100 | 588 | 0.74% | 6.3% |\n 20 | 10000 | 88888 | 9900 | 18700 | 100 | 688 | 0.77% | 3.5% |\n 21 | 10000 | 98888 | 9900 | 28600 | 100 | 788 | 0.80% | 2.7% |\n</code></pre>\n\n<p>As you can see, the two measures of mortality rate do eventually start converging as the growth of the epidemic slows down. In fact, in the long run, as the majority of patients either recover or die, they do both end up converging to the \"true\" long-term case fatality rate of 1%. But by then, the epidemic will be basically over.</p>\n\n<p>There are various ways to obtain a more accurate estimate of the long-term fatality rate even during the early exponential growth phase of an epidemic. One such method would be to look at the outcomes of a single cohort of patients diagnosed at the same time. For our hypothetical example epidemic, looking e.g. at just the 1000 patients diagnosed on day 10, we could get an accurate estimate of the CFR by day 12 simply by dividing the 10 deaths <em>within that cohort</em> by the total number of patients in the cohort. Furthermore, observing multiple cohorts would give us a pretty good idea of how long after diagnosis we would need to wait before the estimated case fatality rate for each cohort gets close to its final true value.</p>\n\n<p>Unfortunately carrying out this kind of cohort analysis for 2019-nCov would require more detailed information than the tracker you've linked to provides. Even the <a href=\"https://docs.google.com/spreadsheets/d/1UF2pSkFTURko2OvfHWWlFpDFAr1UxCBA4JLwlSP6KFo/edit?usp=sharing\" rel=\"noreferrer\">time series spreadsheet</a> the tracker links to doesn't directly provide such detailed cohort data, although it might be possible to obtain better estimates from it by making some more or less reasonable assumptions about the typical progress of the disease.</p>\n\n<hr>\n\n<p><strong>Addendum:</strong> A few preliminary cohort studies of the kind I describe above do appear to have already been published for 2019-nCoV.</p>\n\n<p>In particular, <a href=\"https://doi.org/10.1016/S0140-6736(20)30185-9\" rel=\"noreferrer\">\"A novel coronavirus outbreak of global health concern\"</a> by Wang <em>et al.</em> and <a href=\"https://doi.org/10.1016/S0140-6736(20)30183-5\" rel=\"noreferrer\">\"Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China\"</a> by Huang <em>et al.</em>, both published on January 24 in <em>The Lancet</em>, note that, out of the first 41 patients diagnosed with 2019-nCoV before Jan 2, 2020 in Wuhan, six had died (and 28 had been discharged, leaving seven hospitalized) by Jan 22, giving a case fatality rate of 14.6% in this cohort.</p>\n\n<p>However, they do advise treating this figure with due caution, noting a number of reasons (besides just the small number of cases examined) why it may not fully reflect the eventual long-term CFR:</p>\n\n<blockquote>\n <p>\"<em>However, both of these</em> [CFR] <em>estimates</em> [of 14.6% from the 41 patient cohort and of 2.9% from all 835 cases confirmed at the time of writing] <em>should be treated with great caution because not all patients have concluded their illness (ie, recovered or died) and the true number of infections and full disease spectrum are unknown. Importantly, in emerging viral infection outbreaks the case-fatality ratio is often overestimated in the early stages because case detection is highly biased towards the more severe cases. As further data on the spectrum of mild or asymptomatic infection becomes available, one case of which was documented by Chan and colleagues, the case-fatality ratio is likely to decrease.</em>\"</p>\n</blockquote>\n\n<p>There's also a later paper titled <a href=\"https://doi.org/10.1016/S0140-6736(20)30211-7\" rel=\"noreferrer\">\"Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study\"</a> by Chen <em>et al.</em>, published on Jan 30, that examines a cohort of 99 patients diagnosed between Jan 1 to Jan 20 and reports a CFR of 11% within this cohort. However, the study only followed these patients up to Jan 25, by which time more than half of them (57 out of 99) still remained hospitalized.</p>\n" }, { "answer_id": 21002, "author": "Mick", "author_id": 17557, "author_profile": "https://health.stackexchange.com/users/17557", "pm_score": 2, "selected": false, "text": "<p>According to earlier answers, in this early phase of 2019-nCoV, Nd/(Nd+Nr) is an overestimator, and Nd/Nc is an underestimator. </p>\n\n<p>Since the currently bantered about rate matches the underwestimator Nd/Nc, you are correct that 2019-nCoV is more 'dangerous' than commonly claimed. I used quotes because dangerous a squirmy term.</p>\n\n<p>Noting that Nd/Nc equals Nd/(Nd+Nr) after the epidemic is over, a better estimate would be to track the two quotients over time, and extrapolate their curves to the point they meet. That would still be a biased estimator, but less so than either on it's own. I'm guessing there are more sophisticated estimators with less bias, and I've posted that question here:</p>\n\n<p><a href=\"https://medicalsciences.stackexchange.com/questions/21001/what-is-a-sophisticated-estimate-of-the-2019-ncov-fatality-rate\">What is a sophisticated estimate of the 2019-nCoV fatality rate?</a></p>\n" }, { "answer_id": 21771, "author": "Fizz", "author_id": 10980, "author_profile": "https://health.stackexchange.com/users/10980", "pm_score": 1, "selected": false, "text": "<p>I understand what you're trying/hoping to do here, but the correction method you try to apply is unsuitable. You need to explicitly account for the time delays to deaths <em>and</em> consider a confined population of cases <em>or</em> try to infer from a closed sample a correction factor to apply to the open-ended/ongoing epidemic. Such a study was recently <a href=\"https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.12.2000256\" rel=\"nofollow noreferrer\">published</a> <em>based</em> on the Diamond Princess (cruise ship) cases, using the information collected therein to correct (in this paper) the data on China.</p>\n\n<blockquote>\n <p>In real time, estimates of the case fatality ratio (CFR) and infection fatality ratio (IFR) can be biased upwards by under-reporting of cases and downwards by failure to account for the delay from confirmation to death. Collecting detailed epidemiological information from a closed population such as the quarantined Diamond Princess cruise ship in Japan can produce a more comprehensive description of asymptomatic and symptomatic cases and their subsequent outcomes. Our aim was to estimate the IFR and CFR of coronavirus disease (COVID-19) in China, using data from passengers of the Diamond Princess while correcting for delays between confirmation and death and for the age structure of the population.</p>\n</blockquote>\n\n<p><a href=\"https://i.stack.imgur.com/mOofi.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/mOofi.png\" alt=\"enter image description here\"></a></p>\n\n<blockquote>\n <p>During an outbreak, the so-called naive CFR (nCFR), i.e. the ratio of reported deaths date to reported cases to date, will underestimate the true CFR because the outcome (recovery or death) is not known for all cases, assuming all cases are detected. We can estimate the true denominator for the CFR (i.e. the number of cases with known outcomes) by accounting for the delay from confirmation to death. We assumed that the delay from confirmation to death followed the same distribution as the estimated time from hospitalisation to death, based on data from the COVID-19 outbreak in Wuhan, China, between 17 December 2019 and 22 January 2020, accounting for underestimation in the data as a result of as-yet-unknown disease outcomes [...]</p>\n \n <p>To adjust the CFR to account for delay to outcome, we use the method developed in <a href=\"https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0006852\" rel=\"nofollow noreferrer\">Nishiura et. al (2009)</a> where case and death incidence data are used to estimate the number of cases with known outcomes, i.e. cases where the resolution, death or recovery, is known to have occurred:</p>\n</blockquote>\n\n<p><a href=\"https://i.stack.imgur.com/fdGoq.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/fdGoq.png\" alt=\"enter image description here\"></a></p>\n\n<blockquote>\n <p>where <em>c<sub>t</sub></em> is the daily case incidence at time <em>t</em>, (with time measured in calendar days), <em>f<sub>t</sub></em> is the proportion of cases with delay <em>t</em> between onset or hospitalisation and death; <em>u<sub>t</sub></em> represents the underestimation of the known outcomes and is used to scale the value of the cumulative number of cases in the denominator in the calculation of the cCFR. Given that asymptomatic infections are typically not reported, especially during an ongoing outbreak of a novel infection, this correction is normally used to calculate the cCFR. However, because of the high level of testing on the cruise ship, we were able to use this correction to calculate the corrected IFR (cIFR). After that, we used the measured proportions of asymptomatic to symptomatic cases on the Diamond Princess to scale the cIFR to estimate the cCFR. [...]</p>\n \n <p><strong>We estimated that the all-age cIFR on the Diamond Princess was 1.3% (95% confidence interval (CI): 0.38–3.6) and the cCFR was 2.6% (95% CI: 0.89–6.7).</strong> However, as the age distribution on the ship was skewed towards older individuals (mean age: 58 years), we also report age-stratified estimates. Using the age distribution of cases and deaths on the ship to estimate for only individuals 70 years and older, the cIFR was 6.4% (95% CI: 2.6–13) and the cCFR was 13% (95% CI: 5.2–26). The 95% CI were calculated with an exact binomial test, with death count and either cases or known outcomes (depending on whether it was an interval for the naive or corrected estimate).</p>\n \n <p>Using an approach similar to <a href=\"https://projecteuclid.org/download/pdfview_1/euclid.ss/1421330546\" rel=\"nofollow noreferrer\">indirect standardisation</a>, we used the age-stratified nCFR estimates reported in a large study in China to calculate the expected number of deaths of people on board the ship in each age group, (assuming this nCFR estimate in the standard population was accurate). This produced a total of 15.15 expected deaths, which corresponds to a nCFR estimate of 5% (15.15/301) for the Diamond Princess, which falls within the top end of our 95% CI. As our cCFR for Diamond Princess was 2.6% (95% CI: 0.89–6.7), this suggests we need to multiply the nCFR estimates in China by a factor 52% (95% CI: 14–100) to obtain the correct value. <strong>As the raw overall nCFR reported in the data from China was 2.3%, this suggests the cCFR in China during that period was 1.2% (95% CI: 0.3–3.1) and the IFR was 0.6% (95% CI: 0.2–1.7)</strong>. Based on cases and deaths reported in China up to 4 March 2020, the nCFR calculation was considerably higher than the cCFR we estimate here (based on data taken from [8], nCFR = 2,984/80,422 = 3.71% (95% CI: 3.58–3.84)). The confidence intervals calculated for China using an indirect standardisation method reflect the uncertainty in the Diamond Princess estimates, as it is carried forward in the scaling.</p>\n</blockquote>\n\n<p>As you can see, if one does this correction properly, the \"death rate\" (cCFR) for Covid-19 is actually lower (than the nCFR).</p>\n\n<p>If the above is too dense/technical of an explanation, the <em>Nature</em> news <a href=\"https://www.nature.com/articles/d41586-020-00885-w\" rel=\"nofollow noreferrer\">coverage of it</a>:</p>\n\n<blockquote>\n <p>Another team used data from the ship to estimate that the proportion of deaths among confirmed cases in China, the case fatality rate (CFR), was around 1.1% — much lower than the 3.8% estimated by the World Health Organization (WHO).</p>\n \n <p><strong>The WHO simply divided China’s total number of deaths by the total number of confirmed infections</strong>, says Timothy Russell, a mathematical epidemiologist at the London School of Hygiene and Tropical Medicine. <strong>That method does not take into account that only a fraction of infected people are actually tested, and so it makes the disease seem more deadly than it is</strong>, he says.</p>\n \n <p>By contrast, Russell and his colleagues used data from the ship — where almost everyone was tested, and all seven deaths recorded — and combined it with more than 72,000 confirmed cases in China, making their CFR estimate more robust. [...]</p>\n \n <p>The group also estimates that the infection fatality rate (IFR) in China — the proportion of all infections, including asymptomatic ones, that result in death — is even lower, at roughly 0.5%. The IFR is especially tricky to calculate in the population, because some deaths go undetected if the person didn’t show symptoms or get tested.</p>\n</blockquote>\n\n<p>(Nature news says the [latter] paper had not been peer-reviewed/published, but in the meantime it has been published by <em>Eurosurveillance</em>, the same journal that had published the 1st Diamond Princess paper.)</p>\n\n<p>I should also noted that an 8th death was reported <a href=\"https://www.ship-technology.com/news/covid-19-diamond-princess-cruise-ship-eighth-death/\" rel=\"nofollow noreferrer\">much later</a> (March 20) in relation to the Diamond Princess. It probably doesn't substantially change the conclusions of that paper (which included only the 7 reported deaths you see in the graph.)</p>\n" } ]
2020/02/03
[ "https://health.stackexchange.com/questions/20970", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17521/" ]
21,014
<p>I am looking at the T2DM medications specified <a href="https://www.mayoclinic.org/diseases-conditions/type-2-diabetes/diagnosis-treatment/drc-20351199" rel="nofollow noreferrer">here</a> and have a few questions about them.</p> <p>1) Why don't I see drugs like <code>Troglitazone, Tolazamide, Acarbose, Acetohexamide, Chlorpropramide, Miglitol</code>? Aren't these drugs used to treat diabetes?</p> <p>2) I see in drug treatment, we have terms like monotherapy (single drug) and combination therapy (multiple drugs). But what is the combination window usually considered for calling a treatment combination therapy?</p> <p>By <em>combination window</em>, I mean the number of days both Drug 1 and Drug 2 should overlap. For example, let's say Jacky takes Drug A from Jan 1st till Jan 21st. He also takes Drug B from Jan 11th to Jan 21st. We see that there is an overlap of 10 days. Is there any minimum number of days that you look for to call a treatment combination therapy?</p>
[ { "answer_id": 21015, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 3, "selected": true, "text": "<p>The Mayo Clinic page shows only some antidiabetic drugs; they just didn't mentioned few more as you did. </p>\n\n<p>A <a href=\"https://www.uptodate.com/contents/management-of-persistent-hyperglycemia-in-type-2-diabetes-mellitus\" rel=\"nofollow noreferrer\">combination therapy for diabetes type 2 (UpToDate)</a> is a combination of at least 2 oral antidiabetic drugs, or a combination of one or more oral antidiabetic drugs with insulin. The term is used when the therapy is <em>planned as combined</em> and not when it occurs \"by chance,\" for example, when a doctor plans to discontinue one drug and introduce another drug before discontinuing the first one. I can't say what was the <em>intent</em> of the doctor who prescribed the drugs in your case, but if the first drug was discontinued and the second one continued after 21st, it was obviously not meant as a combination therapy. There is no official minimal time required to say it's a combination therapy, but it usually lasts at least few weeks, during which time its efficacy can be evaluated.</p>\n\n<p>Combinations of various drugs are possible, including the ones you've mentioned.</p>\n\n<p>A common side effect of antidiabetic drugs is hypoglycemia, which can be treated by temporary discontinuation of a drug or by other measures, including glucose injection, etc. Other side effects may need treatment with other drugs, but this is too broad to discuss here. </p>\n" }, { "answer_id": 21022, "author": "Chris", "author_id": 14056, "author_profile": "https://health.stackexchange.com/users/14056", "pm_score": 1, "selected": false, "text": "<p>I want to add a supplementary answer which provides a useful infographic produced by the British Medical Journal and based on the diabetes guideline issued by the UK National Institute for Health and Care Excellence (NICE).</p>\n\n<p>The guide shows the advisable combinations of oral medication in type 2 diabetes (there are a few possible combinations) and when to consider insulin therapy.</p>\n\n<p><a href=\"https://www.bmj.com/content/bmj/suppl/2016/04/06/bmj.i1575.DC1/diabetes-t2a-v19-web.pdf\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/PCpvP.jpg\" alt=\"BMJ infographic\"></a></p>\n\n<p>Click the image for a link to the PDF.</p>\n\n<p>Treatment usually starts with metformin, if it is tolerated and not contraindicated (e.g. rental impairment). Second and third-line agents are then added, usually with at least three months between initiation (this is because HbA1c values used for monitoring only change slowly, due to the long lifespan of a red blood cell).</p>\n\n<hr>\n\n<p>One point regarding side effects - hypoglycaemia is a common side effect of <em>some</em> oral diabetes drugs, but not all. Sulphonylureas (e.g. gliclazide) can definitely cause hypoglycaemia as they increase insulin production, but others, like l metformin, which reduces peripheral insulin resistance, will essentially never cause hypoglycaemia but very commonly cause gastrointestinal side effects.</p>\n\n<hr>\n\n<p><strong>N.B.</strong> This relates to the UK. Different drugs may or may not be licensed for use in other countries. Acarbose has been around a long time and is only used in a few situations and nowhere near first line, due to limited benefit and side effect profile.</p>\n\n<p>Additional reference: <a href=\"https://bnf.nice.org.uk/treatment-summary/diabetes.html\" rel=\"nofollow noreferrer\">BNF Diabetes Treatment Summary</a></p>\n" } ]
2020/02/07
[ "https://health.stackexchange.com/questions/21014", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17323/" ]
21,021
<p>I'm currently writing a book where one of my characters falls from about an 80-90 foot drop onto a solid stone surface onto her back. </p> <p>She's an average 32 female with a healthy diet and weight. She won't survive the fall but I don't quite know what the in-depth extent of the injuries she'd sustain and which one would ultimately kill her. </p> <p>I of course know she'd suffer broken bones and internal bleeding but I could do with specifics for the 'autopsy' later down the line.</p>
[ { "answer_id": 21026, "author": "Carey Gregory", "author_id": 805, "author_profile": "https://health.stackexchange.com/users/805", "pm_score": 4, "selected": true, "text": "<p>First off, she would be killed instantly. There wouldn't be any question of what might kill her \"ultimately\" because ultimately would be the moment she hit the ground. Yes, there have been <a href=\"https://en.wikipedia.org/wiki/Category:Fall_survivors\" rel=\"noreferrer\">people who survived falls</a> from much greater heights, with the record holder being <a href=\"https://en.wikipedia.org/wiki/Vesna_Vulovi%C4%87\" rel=\"noreferrer\">Vesna Vulović</a>, a Serbian flight attendant who fell 10,160 m (33,330 ft), but those are vanishingly rare incidents and most involved a great deal of luck (hitting things that slowed the fall such as trees and power lines, landing in snow drifts, etc). In general, an 80-90 foot fall onto a hard surface is certain instant death 99.99% of the time.</p>\n\n<p>Since she lands on her back, what will kill her most quickly is the massive head injury. Autopsy will find a crushed skull, massive brain injury, massive spinal cord injury, and possibly a detached brain stem, which would be instantly lethal.</p>\n\n<p>The second thing that will kill her is deceleration. When she hits the ground, her body stops its downward motion instantly, but <a href=\"https://www.physicsclassroom.com/class/newtlaws/Lesson-1/Newton-s-First-Law\" rel=\"noreferrer\">Newton's First Law of Motion</a> says her internal organs that are free to move will keep going. They'll keep traveling in the same downward direction at the same speed. The result of that will likely be the transection of her aorta, which will cause immediate exsanguination. This is because parts of the aorta are free to move and other parts are anchored in place:</p>\n\n<blockquote>\n <p><a href=\"https://www.ncbi.nlm.nih.gov/books/NBK459337/\" rel=\"noreferrer\">The aorta has some fixed regions, particularly the relatively fixed</a>\n aortic arch (to the thoracic inlet by the brachiocephalic vessels).\n The remaining portions of the aorta are relatively free. Ascending and\n descending aorta are relatively mobile. These can result in an unequal\n distribution of shear forces on the relatively fixed arch and mobile\n ascending and descending aorta and stress at the site of attachment of\n the aorta, particularly the aortic root and the aortic isthmus.</p>\n</blockquote>\n\n<p>As if the victim isn't dead enough by these two things, there will be a wide ranging assortment of other injuries, many of them lethal in and of themselves. The coroner will most likely find:</p>\n\n<ul>\n<li>Virtually every bone in her body will be fractured, including her skull, spine, ribs, pelvis, long bones of the arms and legs, scapulas, and clavicles.</li>\n<li>Her liver will be transected by the <a href=\"https://teachmeanatomy.info/abdomen/viscera/liver/\" rel=\"noreferrer\">falciform ligament</a> and the same deceleration forces that transected her aorta. This will also result in massive bleeding.</li>\n</ul>\n\n<p><a href=\"https://i.stack.imgur.com/ebEf9.png\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/ebEf9.png\" alt=\"Liver anatomy\"></a></p>\n\n<ul>\n<li>Deceleration injury will be widespread in almost all the other organ systems such as the lungs, spleen, intestines, and other blood vessels large and small.</li>\n</ul>\n\n<p>In general, even if a full team of trauma surgeons with a fully equipped OR was scrubbed in and ready right at the scene, she would still be dead on impact and nothing they could do would change that.</p>\n" }, { "answer_id": 21029, "author": "anongoodnurse", "author_id": 169, "author_profile": "https://health.stackexchange.com/users/169", "pm_score": 2, "selected": false, "text": "<p>I agree with @Carey Gregory's answer. I can tell you how a man falling only 30 feet landing on his back on concrete died.</p>\n\n<p>A 30 year old male working on the underside (?) of a bridge, unsecured, fell as above. There were no obvious external injuries. The skull was intact, etc.</p>\n\n<p>He arrived by ambulance unconscious and without a pulse. Advanced Trauma Life Support was carried out, but the injuries were too extensive.</p>\n\n<p>On Xray, he had comminuted fractures of both clavicles, multiple broken ribs, hemothorax on the right and left-sided hemopneumotorax. Otherwise there were no fractures.</p>\n\n<p>He died because the deceleration injuries to his chest caused both pulmonary arteries to shear off were they cross over the mainstem bronchi, and the left mainstem bronchus was shorn through as well. He basically died from massive blood loss into the thorax. He would have been rendered unconscious from the fall, and had he lived, might well ave had significant brain injury.</p>\n\n<p>A fall from almost 3 times that height would have smashed the back of his skull causing massive brain injuries as described above, likely broken his neck and back, broken the pelvis, maybe some long bones depending on the landing, and the internal injuries would be much more serious, although when death is the outcome, how much is <em>much more serious</em>? They would have been much more intensive.</p>\n" } ]
2020/02/07
[ "https://health.stackexchange.com/questions/21021", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17577/" ]
21,156
<p><strong>EDIT</strong>: After reading the comments and learning more about the current outbreak, I see that the premise of my question is incorrect. I mistakenly believed that the virus' mortality rate was around the same as that of the flu, when in fact it's much higher.</p> <hr> <p>My understanding is that the virus' mortality rate is around 2%, which is similar to the flu. It's less deadly than SARS.</p> <p>So why are people so worried, and why are governments going to such extreme measures to prevent it from spreading? My guesses are:</p> <ul> <li>We don't know enough about the long-term effects of the virus, so better safe than sorry</li> <li>The economic and social disruption caused by robust measures (e.g., quarantining) costs less than letting a new disease become pandemic, even if it isn't particularly deadly</li> <li>Mass hysteria fueled by the media and misinformation</li> <li>Governments feeling like they have to appear responsive to popular concern lest they seem lazy</li> <li>This virus affects more developed parts of the world, so it's more visible</li> <li>The Chinese government's over-the-top, authoritarian, "only in China"-style measures have left everyone in such awe that they think, "this must be really serious!" (When in fact the government's real intention is perhaps to cover up how badly they botched their initial handling of the outbreak.)</li> </ul> <p>As for one's chances of coming into contact with the virus, the total number of confirmed cases in the world as of writing is around 80k. Let's say that the true number is double that, or 160,000. That's still only ~1.5% of the population of Wuhan, the city where the initial outbreak occurred. Why should anyone be in the slightest bit concerned about going for a stroll down the main street?</p> <p>I'm not an expert in public health or medicine. It would be great to hear an expert's take on this question!</p>
[ { "answer_id": 21205, "author": "Count Iblis", "author_id": 856, "author_profile": "https://health.stackexchange.com/users/856", "pm_score": 3, "selected": false, "text": "<p>The danger posed to society from this disease doesn't come from the mortality rate, rather from the potential to make large fraction of the population ill. Unlike the flu virus, this virus is a new virus to which we have no immunity.</p>\n\n<p>About 10% of the infected people requires hospital treatment, which is a lot higher than in case of flu. The death rate of the order of 1% is achieved thanks to excellent hospital treatment. With a far larger fraction of the population infected with this virus compared to the flu and a far larger fraction of the infected people requiring hospital treatment compared to flu, the available hospital capacity to give everyone the treatment they need can be easily exhausted. The death rate due to the virus will then increase.</p>\n\n<p>Also, people who need treatment for other reasons can then also fail to get prompt medical attention. People suffering a heart attack who would have survived under normal circumstances thanks to getting prompt medical attention, may now end up dying too. </p>\n" }, { "answer_id": 21208, "author": "baradhili", "author_id": 17708, "author_profile": "https://health.stackexchange.com/users/17708", "pm_score": 1, "selected": false, "text": "<p>If we compare Covid19 to SARS or MERS - COVID19 seems to have a R0 slightly higher than SARS but lower than MERS. From various sources it appears that COVID-19 could be between 2 and 7, so compariable to diseases such as mumps and diphtheria in spread. Infection fatality rates vary wildly right now as the sample size is very small, but from 0.2% up to 18% (18% for early stage Hubei province infections). </p>\n\n<p>Comparisons to other diseases:-<a href=\"https://en.wikipedia.org/wiki/Herd_immunity\" rel=\"nofollow noreferrer\">Wiki-herd immunity</a> - I wanted to paste the table in here, but SE doesn't seem to support the MD table format</p>\n\n<p>refs:-</p>\n\n<ul>\n<li><a href=\"http://currents.plos.org/outbreaks/index.html%3Fp=40801.html\" rel=\"nofollow noreferrer\">http://currents.plos.org/outbreaks/index.html%3Fp=40801.html</a></li>\n<li><a href=\"https://wwwnc.cdc.gov/eid/article/26/2/19-0697_article\" rel=\"nofollow noreferrer\">https://wwwnc.cdc.gov/eid/article/26/2/19-0697_article</a></li>\n<li><a href=\"https://wwwnc.cdc.gov/eid/article/10/7/03-0647_article\" rel=\"nofollow noreferrer\">https://wwwnc.cdc.gov/eid/article/10/7/03-0647_article</a></li>\n<li><a href=\"https://www.who.int/news-room/detail/23-01-2020-statement-on-the-meeting-of-the-international-health-regulations-(2005)-emergency-committee-regarding-the-outbreak-of-novel-coronavirus-(2019-ncov)\" rel=\"nofollow noreferrer\">https://www.who.int/news-room/detail/23-01-2020-statement-on-the-meeting-of-the-international-health-regulations-(2005)-emergency-committee-regarding-the-outbreak-of-novel-coronavirus-(2019-ncov)</a></li>\n</ul>\n\n<p>But IMO the primary difference is that SARS and MERS occured before large-scale social-media monetization.. So there was little to gain by media/social media doing a major panic.. </p>\n" } ]
2020/02/26
[ "https://health.stackexchange.com/questions/21156", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17668/" ]
21,186
<p>Can a full-head helmet with the visor closed prevent getting infected by the Corona virus during a casual interaction with a carrier?</p> <p>For example, when buying something at a store or discussing something with someone for 10-15 minutes.</p> <p>How does it compare with the protection provided by a standard face mask (that can be purchased at a pharmacy)?</p>
[ { "answer_id": 21188, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 3, "selected": false, "text": "<p>It's better to use some guidelines from reputable sources rather than coming up with your own.</p>\n\n<p>The WHO does not recommend masks for healthy people in most circumstances, only <a href=\"https://www.who.int/emergencies/diseases/novel-coronavirus-2019/advice-for-public/when-and-how-to-use-masks\" rel=\"noreferrer\">when directly dealing with someone infected</a>, and in that case accompanied by careful hand washing.</p>\n\n<p>Their <a href=\"https://www.who.int/emergencies/diseases/novel-coronavirus-2019/advice-for-public\" rel=\"noreferrer\">advice for the general public</a> as of this posting (and this is good advice year-round anyways, not only when particular pathogens are present, because influenza and viruses that cause the common cold are always present) is to <strong>wash your hands</strong>, keep a distance from people who are sneezing/coughing, avoid touching your face, and cough or sneeze into a tissue or corner of the elbow rather than into the open or your hands.</p>\n" }, { "answer_id": 21663, "author": "Quinn Zacharias", "author_id": 17992, "author_profile": "https://health.stackexchange.com/users/17992", "pm_score": 3, "selected": true, "text": "<p>I think it's a great idea. It protects your eyes from respiratory droplets and keeps you from touching your face. I don't know how well it would work from keeping droplet from reaching your mouth, but probably pretty well, especially if you used it with an N95 respirator. It might be a little shocking/intimidating to people, so I would only use it in extremely infected areas. </p>\n" }, { "answer_id": 21664, "author": "Quinn Zacharias", "author_id": 17992, "author_profile": "https://health.stackexchange.com/users/17992", "pm_score": 2, "selected": false, "text": "<p>Now to address the whole debate about using respirators and masks. You absolutely want them. There has been a narrative throughout the western world that you don't need them, and they don't work. This is not the case. The CDC and WHO tell ordinary people to not wear respirators, but both organizations have political agendas and have frankly done a terrible job handling this public health crises. The truth is that there is a lack of respirators to go around when every single person should be wearing them. In Taiwan, their number one way to combat COVID19 is by having every single person in their population wear masks. Thus far, Tiawan has been one of the best countries in handling the COVID19 health crises. </p>\n\n<p>Now to address why N95/N99/N100/NIOSH respirators work. One of the leading pathways for transmitting this disease is through inhalation of respiratory droplets from other infected individuals. An immediate barrier that has been proven to be effective is having a mask/respirator to intercept these droplets before they reach your mucus membranes. The coronavirus is between 60 to 140 nm in diameter. Let's use the N95 mask for example. This mask captures all particulates at 300 nm at a rate of up to 95% or better. 300 nm is the particulate size that has the lowest capture efficiency. Anything smaller, including the coronavirus, will have an even higher capture efficiency. This virus is one of the most contagious pathogens we have had in recent human history. Any form of personal protection equipment is absolutely vital in keeping yourself from becoming infected. I would also recommend that when you are in a public areas you should wear eye protection, gloves and over coat that you leave outside your house. I do really think the motorcycle helmet is a very creative and potentially effective way to keep yourself protected. </p>\n" } ]
2020/02/28
[ "https://health.stackexchange.com/questions/21186", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17690/" ]
21,198
<p>In China, the largest number of reported COVID-19 infections was in Hubei province.</p> <p>Other countries are experiencing exponential increase in reported infections, while the remainder of China is reporting relatively small numbers of cases<sup><a href="https://github.com/CSSEGISandData/COVID-19/blob/master/csse_covid_19_data/csse_covid_19_time_series/time_series_19-covid-Confirmed.csv" rel="noreferrer">source_1</a></sup></p> <p>What protects Chinese provinces other than Hubei from COVID-19 outbreak?</p> <ul> <li>What is different about the remainder of China compared to the rest of the world?</li> <li>Is there anything we can learn from the provinces in China that so far were less affected by the virus than Hubei?</li> </ul>
[ { "answer_id": 21211, "author": "sme", "author_id": 17710, "author_profile": "https://health.stackexchange.com/users/17710", "pm_score": 4, "selected": true, "text": "<p>I live in Guangdong, and this is what I've been seeing &amp; reading about.</p>\n\n<p>Wuhan (city in Hubei) is where the outbreak supposedly began. And it went unnoticed for a while, which mean it was spreading locally more-so than it was spreading nationally/internationally. Near at the start of the Chinese New Year holiday, the government decided to quarantine all of Hubei province. So while other provinces already had infected people, they spread hadn't grown as significantly as it had in Hubei yet.</p>\n\n<p>The Chinese government then decided to take specific measures to control the epidemic. For starters, they required mask-wearing and encouraged staying indoors. They also began to set up body temperature checks all over the place (apartments, neighborhoods, roads leading into cities, and places of work once the holiday ended. Fever seems to be the first symptom, so this is why).</p>\n\n<p>If anyone in an apartment building was confirmed to have the virus, then the entire building and all residents were/are quarantined for 14 days (happened to a 30+ story apartment building next to mine). Elevators, doors, and other public spaces are often disinfected, particularly if a suspected case had been in the area. Again, I saw this at a temperature checkpoint, someone must've had a fever and a little bit later some folks came and sprayed down the area.</p>\n\n<p>Schools are also closed in all provinces across the country, and students are doing online schooling. Some companies are also allowing employees to work from home, or 'staggering' their work days (half come in into the office on Mon, Wed, Fri, the other half come in Tuesday and Thursday). This decreases the number of people a possible infected person can pass the virus to.</p>\n\n<p>On top of this, companies needed to 'apply' to be able to resume work. Here in Shenzhen, nobody could return to work within 14 days of returning from the city, assuming they left during the holiday. We also need to record down our body temp when coming to and leaving from work. According to an SMS I received from the local government, if 2 employees have a body temperature >= 37.3C, then it needs to be reported immediately, as it indicates a possible spread in that workplace.</p>\n\n<p>In short, the virus was able to take a foothold in Hubei, and it was noticed before it took a significant foothold in other provinces. Therefore other provinces had time to implement proactive and preventative measures, before the situation grew to Hubei-level of significance.</p>\n\n<p>The best way to prevent it from spreading is simple steps, such as not going outside unless its necessary, avoid close contact with others (defined as within 6 feet for an extended period of time), washing your hands, and disinfecting often-touched surfaces like door knobs, keyboards, cell phones, etc. It remains to be seen whether other countries will take the same rather drastic measures that are being taken in China, I suppose it all depends on how bad things get in other countries.</p>\n" }, { "answer_id": 21589, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 3, "selected": false, "text": "<blockquote>\n<p>“The biggest conclusion is that China has demonstrated that the course of the outbreak can be altered. Normally, an outbreak of this nature would have exponential growth, would reach a high peak, and would then decline naturally once all susceptible people have been infected, or developed the disease. This has not happened in China in a number of ways,” he said.</p>\n<p>“One: the shape of the course of the events - the graph, the epidemic curve, as we call it, of the numbers of cases over time - appears very unnatural. It is an epidemic that has been nipped as it was growing and stopped in its tracks. This is very clear from the data that we have, as well as the observations that we can see in society in general.</p>\n<p>&quot;So, that's a big lesson that the natural course of the outbreak does not need to be a very high peak that overrwhelms health services. This lesson in containment, therefore, is a lesson that other countries can learn from and adapt for their own circumstances&quot;.</p>\n</blockquote>\n<p>China acheived this feat in Hubei through the ruthless application of science and knowledge of infection control. In the absence of a known treatment, the standard measure from centuries of history is containment and isolation in the containment regions.</p>\n<p>They totally shut the borders to Wuhan, a city of 8 million people as well as other cities in the province of Hubei. This type of action has never been done in the history of mankind before. The border controls were put in place even before there was any stress on the health systems in Hubei Province. The onset of the pandemic was at the start of the Lunar Holidays which is the world's largest single yearly migration and this was shut down to stop the spread of virus.</p>\n<p>All the cities in China were basically shut down so that even in Urumqi in the far western border, people were not allowed on the streets without good cause. Any threat to the confined Muslim population was also eliminated in this way.</p>\n<p>This allowed medical staff all over China sufficient time to contact trace all infections, as well as gave them time to do case discovery as well as unprecedented actions ( random temperature checks, daily reporting of your temperature, tracing the movement of every citizen, separating every restaurant user from each other by barriers etc ) to stop the spread of the virus. There was mass movement of medical staff from Beijing and other centres to Wuhan to help control/treat the sick, and 1000 bed hospitals were built over the course of a week or so.</p>\n<p>This is how China protected the other provinces from the infection. The Chinese govt has called the citizens of Wuhan heroes for enduring such harsh measures which have protected the other billion citizens.</p>\n<p>Of course there is another story to all of this .. people left to die at home unable to access hospital care, a child with cerebral palsy who died at home as both parents had died and there was no one to care for him and other stories of immense human tragedy. And we must not forget our companions, the 10s of 1000s of pets left to starve as people were moved from apartments to isolation camps, and the efforts made to save them.</p>\n<p><a href=\"https://news.un.org/en/story/2020/03/1059502\" rel=\"nofollow noreferrer\">https://news.un.org/en/story/2020/03/1059502</a></p>\n<p><a href=\"https://www.nationalreview.com/news/coronavirus-wuhan-official-called-for-gratitude-education-to-teach-citizens-to-thank-xi-jinping-for-response/\" rel=\"nofollow noreferrer\">https://www.nationalreview.com/news/coronavirus-wuhan-official-called-for-gratitude-education-to-teach-citizens-to-thank-xi-jinping-for-response/</a></p>\n<p><a href=\"https://www.hongkongfp.com/2020/03/17/hero-coronavirus-crisis-china-according-state-propaganda/\" rel=\"nofollow noreferrer\">https://www.hongkongfp.com/2020/03/17/hero-coronavirus-crisis-china-according-state-propaganda/</a></p>\n" } ]
2020/03/01
[ "https://health.stackexchange.com/questions/21198", "https://health.stackexchange.com", "https://health.stackexchange.com/users/16873/" ]
21,206
<p>For this question, assume that the virus does not mutate.</p> <p>Can survivors be expected to develop immunity? Why or why not (what is the thought process)?</p> <p>The <a href="https://www.cdc.gov/coronavirus/2019-ncov/hcp/faq.html" rel="nofollow noreferrer">CDC FAQ indicates</a> that they do not know:</p> <blockquote> <p>Q: Can people who recover from COVID-19 be infected again?</p> <p>A: The immune response to COVID-19 is not yet understood. Patients with MERS-CoV infection are unlikely to be re-infected shortly after they recover, but it is not yet known whether similar immune protection will be observed for patients with COVID-19.</p> </blockquote> <p>As good as CDC is, I would expect that there are other excellent institutions and individuals that have insight.</p> <p><strong>CLARIFICATION:</strong> a survivor for this discussion is an COVID 19 infected patient that survives the infection. My understanding is that there is no reason to believe that the uninfected would develop immunity.</p> <p><strong>UPDATE:</strong> <a href="https://www.cnn.com/2020/12/20/uk/uk-coronavirus-variant-intl-gbr/index.html" rel="nofollow noreferrer">COVID 19 mutant strains have been detected in the UK</a>.</p>
[ { "answer_id": 21237, "author": "Alex Martian", "author_id": 5181, "author_profile": "https://health.stackexchange.com/users/5181", "pm_score": 1, "selected": false, "text": "<p>I would take a bold personal statement (AFAIK as of now there are no accepted scientific knowledge of that matter) that they will be immune from specific mutation, but there are already more than one, see my question I just asked: </p>\n\n<p><a href=\"https://medicalsciences.stackexchange.com/questions/21236/how-virus-is-distinguished-by-pcr-test-different-mutations-of-sars-cov-2\">How virus is distinguished by PCR test (different mutations of sars-cov-2)?</a>. </p>\n\n<p>Link to news article: </p>\n\n<p><a href=\"https://www.cnbc.com/2020/03/04/coronavirus-chinese-scientists-identify-two-types-covid-19.html\" rel=\"nofollow noreferrer\">https://www.cnbc.com/2020/03/04/coronavirus-chinese-scientists-identify-two-types-covid-19.html</a></p>\n\n<p>So these reported re-infections could be infections by other mutation of the virus.</p>\n" }, { "answer_id": 21539, "author": "brasscup", "author_id": 17877, "author_profile": "https://health.stackexchange.com/users/17877", "pm_score": 2, "selected": false, "text": "<p>This article from the UK Independent is a fair round-up of differing opinions on whether contracting the virus conveys immunity:\n<a href=\"https://www.independent.co.uk/life-style/health-and-families/coronavirus-immunity-reinfection-get-covid-19-twice-sick-spread-relapse-a9400691.html\" rel=\"nofollow noreferrer\">https://www.independent.co.uk/life-style/health-and-families/coronavirus-immunity-reinfection-get-covid-19-twice-sick-spread-relapse-a9400691.html</a>\nThere have been reports of patients getting reinfected following recovery. The most discussed occured this month. In Osaka, a tour bus operator in her 40s tested positive for COVID-19 for a second time. She was first diagnosed with coronavirus in late January and was discharged from hospital on February 1.\nBut there is disagreement as to whether it is an entirely new infection or a relapse.</p>\n" }, { "answer_id": 21640, "author": "Philipp Leitl", "author_id": 17885, "author_profile": "https://health.stackexchange.com/users/17885", "pm_score": 3, "selected": false, "text": "<p>There is a study from Chinese scientists from Bejing on this question:<br>\n<a href=\"https://www.biorxiv.org/content/10.1101/2020.03.13.990226v1.full.pdf\" rel=\"noreferrer\">Reinfection could not occur in SARS-CoV-2 infected rhesus macaques</a></p>\n\n<blockquote>\n <p>Combined with the follow-up virologic, radiological and pathological findings, the monkeys with re-exposure showed no recurrence of COVID-19, similarly to the infected monkey without rechallenge. Taken together, our results indicated that the primary SARS-CoV-2 infection could protect from subsequent exposures, which have the reference of prognosis of the disease and vital implications for vaccine design.</p>\n</blockquote>\n\n<p>One has to state that with four monkeys the statistics is very low, though.</p>\n\n<p>There is, however, also a risk for relapse and further mutations of the virus as already pointed out by brasscup and Alexei.</p>\n" }, { "answer_id": 23084, "author": "Albrecht Hügli", "author_id": 17790, "author_profile": "https://health.stackexchange.com/users/17790", "pm_score": 1, "selected": false, "text": "<p>Blood samples for antibodies against the novel corona virus are tested in several Swiss laboratories.</p>\n\n<p><em>The Inselspital Bern is currently not doing so because the quality of the results has not yet been adequately investigated, says the director of the University Clinic for Infectious Diseases.\nThe problem is that detection of antibodies in the blood does not necessarily mean that someone is also immune.</em></p>\n\n<p><em>Another problem in the use of blood tests as part of an exit strategy arises in terms of capacity: there is currently a shortage of test material in large quantities. This is confirmed by the Laboratory Medical Center Dr. Risch, where the first blood tests have recently been carried out in the laboratories in Buchs SG. The hospital staff, nursing staff and law enforcement officers have priority there, says Lorenz Risch, Chairman of the Board of Directors and Medical Director, towards SRF. Theoretically, you would have the capacity for around 1000 tests per day, but you can currently only make around a hundred in one or two days because the suppliers from Germany and the United States could no longer supply the so-called reagents.</em></p>\n\n<p><a href=\"https://www.srf.ch/news/schweiz/antikoerpertest-bei-corona-der-qualitaetsnachweis-ist-fuer-uns-noch-nicht-gegeben\" rel=\"nofollow noreferrer\">https://www.srf.ch/news/schweiz/antikoerpertest-bei-corona-der-qualitaetsnachweis-ist-fuer-uns-noch-nicht-gegeben</a></p>\n\n<p>The chief of the hospital says:</p>\n\n<p><strong>Antibody test at corona: the proof of quality is not yet given.</strong></p>\n" }, { "answer_id": 23531, "author": "meh", "author_id": 19564, "author_profile": "https://health.stackexchange.com/users/19564", "pm_score": 1, "selected": false, "text": "<p>There is one report i am aware of, this has not been entirely confirmed. Information changes rapidly in a situation like this. The best we can do is take precautions, and wait for the experts to speak on a position of authority. Weather its possible that a virus in general can do this? Yes. It is also possible for it to hide in reservoirs that the immune system cant get at easily. </p>\n\n<p><a href=\"https://qz.com/1837798/why-some-covid-19-patients-might-have-tested-positive-twice/\" rel=\"nofollow noreferrer\">https://qz.com/1837798/why-some-covid-19-patients-might-have-tested-positive-twice/</a></p>\n" }, { "answer_id": 23559, "author": "Henry Wei", "author_id": 17942, "author_profile": "https://health.stackexchange.com/users/17942", "pm_score": 2, "selected": false, "text": "<p>As of May 2020, data are very limited on whether infection confers immunity, let alone long term immunity. </p>\n\n<p>While COVID-19 related coronavirus is still being studied, a similar SARS coronavirus from 2003 has been studied.</p>\n\n<p>In a 2011 research study, scientists found that certain types of immunity called T cell memory did persist, while others (B cell related) did not. This immune memory response was more marked in severe infections as well. While this is promising that the human immune system can “remember” and potentially defend against repeat infection, the authors were careful to note that even T cell memory immunity did not necessarily mean the individuals were immune from reinfection.</p>\n\n<p>Source: <a href=\"https://www.jimmunol.org/content/jimmunol/186/12/7264.full.pdf\" rel=\"nofollow noreferrer\">https://www.jimmunol.org/content/jimmunol/186/12/7264.full.pdf</a></p>\n" } ]
2020/03/01
[ "https://health.stackexchange.com/questions/21206", "https://health.stackexchange.com", "https://health.stackexchange.com/users/7446/" ]
21,242
<p>Today the CDC released an <a href="https://www.epa.gov/sites/production/files/2020-03/documents/sars-cov-2-list_03-03-2020.pdf" rel="nofollow noreferrer">official list</a> of what kills the COVID-19 virus but the list does not mention 70% isopropyl alcohol.</p> <p>This is a fairly basic disinfectant and it seems it should have been on the list assuming it kills the virus and that is why I am asking. Thank you</p>
[ { "answer_id": 21249, "author": "Carey Gregory", "author_id": 805, "author_profile": "https://health.stackexchange.com/users/805", "pm_score": 4, "selected": true, "text": "<p>Yes, it does.</p>\n\n<p>According to the CDC, <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/community/home/cleaning-disinfection.html\" rel=\"noreferrer\">this</a> is how surfaces should be disinfected:</p>\n\n<blockquote>\n <h2>Surfaces</h2>\n \n <ul>\n <li><p>Wear disposable gloves when cleaning and disinfecting surfaces. Gloves should be discarded after each cleaning. If reusable gloves are\n used, those gloves should be dedicated for cleaning and disinfection\n of surfaces for COVID-19 and should not be used for other purposes.\n Consult the manufacturer’s instructions for cleaning and disinfection\n products used. Clean hands immediately after gloves are removed.</p></li>\n <li><p>If surfaces are dirty, they should be cleaned using a detergent or soap and water prior to disinfection.</p></li>\n <li><p>For disinfection, diluted household bleach solutions, <strong>alcohol solutions with at least 70% alcohol</strong>, and most common EPA-registered\n household disinfectants should be effective.</p>\n \n <ul>\n <li><p>Diluted household bleach solutions can be used if appropriate for the surface. Follow manufacturer’s instructions for application\n and proper ventilation. Check to ensure the product is not past its\n expiration date. Never mix household bleach with ammonia or any other\n cleanser. Unexpired household bleach will be effective against\n coronaviruses when properly diluted.</p>\n \n <ul>\n <li>Prepare a bleach solution by mixing:\n \n <ul>\n <li>5 tablespoons (1/3rd cup) bleach per gallon of water or</li>\n <li>4 teaspoons bleach per quart of water</li>\n </ul></li>\n </ul></li>\n <li><p>A list of products with EPA-approved emerging viral pathogens claims, maintained by the American Chemistry Council Center for\n Biocide Chemistries (CBC), is available at:\n <a href=\"https://www.americanchemistry.com/Novel-Coronavirus-Fighting-Products-List.pdf\" rel=\"noreferrer\">https://www.americanchemistry.com/Novel-Coronavirus-Fighting-Products-List.pdf</a>.\n Products with EPA-approved emerging viral pathogens claims are\n expected to be effective against COVID-19 based on data for harder to\n kill viruses. Follow the manufacturer’s instructions for all cleaning\n and disinfection products (e.g., concentration, application method and\n contact time, etc.).</p></li>\n </ul></li>\n <li><p>For soft (porous) surfaces such as carpeted floor, rugs, and drapes, remove visible contamination if present and clean with\n appropriate cleaners indicated for use on these surfaces. After\n cleaning: Launder items as appropriate in accordance with the\n manufacturer’s instructions. If possible, launder items using the\n warmest appropriate water setting for the items and dry items\n completely, or Use products with the EPA-approved emerging viral\n pathogens claims (examples at this linkpdf iconexternal icon) that are\n suitable for porous surfaces.</p></li>\n </ul>\n</blockquote>\n" }, { "answer_id": 21710, "author": "Nate", "author_id": 18012, "author_profile": "https://health.stackexchange.com/users/18012", "pm_score": 2, "selected": false, "text": "<p>The List does mention Isopropyl Alcohol. It's sixth on the list, and it's listed by its other name--Isopropanol. </p>\n\n<p>Isopropanol=Isopropyl Alcohol. Just like Ethanol=Ethyl Alcohol.</p>\n" } ]
2020/03/06
[ "https://health.stackexchange.com/questions/21242", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17681/" ]
21,279
<p>Is there any global database that enables the stochastic analysis of questions such as age distribution of fatalities, etc? </p> <p>A Google search produced only a WHO article database: <a href="https://www.who.int/emergencies/diseases/novel-coronavirus-2019/global-research-on-novel-coronavirus-2019-ncov" rel="nofollow noreferrer">https://www.who.int/emergencies/diseases/novel-coronavirus-2019/global-research-on-novel-coronavirus-2019-ncov</a></p> <p>Update: </p> <ul> <li><a href="https://www.kaggle.com/tags/covid19" rel="nofollow noreferrer">Kaggle</a> </li> <li><a href="https://gisanddata.maps.arcgis.com/apps/opsdashboard/index.html#/bda7594740fd40299423467b48e9ecf6" rel="nofollow noreferrer">ArcGIS Dashboard</a> </li> </ul>
[ { "answer_id": 21336, "author": "man zet", "author_id": 17804, "author_profile": "https://health.stackexchange.com/users/17804", "pm_score": 1, "selected": false, "text": "<p>You can find a collection of data that is updated on a daily basis on github. There is also included some code</p>\n\n<p><a href=\"https://github.com/globalcitizen/2019-wuhan-coronavirus-data\" rel=\"nofollow noreferrer\">https://github.com/globalcitizen/2019-wuhan-coronavirus-data</a></p>\n" }, { "answer_id": 21478, "author": "Philipp Leitl", "author_id": 17885, "author_profile": "https://health.stackexchange.com/users/17885", "pm_score": 2, "selected": false, "text": "<p>I recommend this github project from the <a href=\"https://systems.jhu.edu/\" rel=\"nofollow noreferrer\">Johns Hopkins University Center for Systems Science and Engineering (JHU CSSE)</a>:</p>\n\n<p><a href=\"https://github.com/CSSEGISandData/COVID-19\" rel=\"nofollow noreferrer\">https://github.com/CSSEGISandData/COVID-19</a></p>\n\n<p>They collect the official numbers from different organizations and ministries from all over the world and update their repository every day.<br>\nThey don't provide information about the age of patients though.</p>\n\n<p>There is a Japanese project, however, which provides also some age information:<br>\n<a href=\"https://covid19japan.com/\" rel=\"nofollow noreferrer\">https://covid19japan.com/</a><br>\nBut the Japanese people seem to be very disciplined and have a very low infection rate at the moment.</p>\n\n<p><strong>Update:</strong><br>\nI found a database with German Covid-19 cases including age information:<br>\n<a href=\"https://npgeo-corona-npgeo-de.hub.arcgis.com/datasets/dd4580c810204019a7b8eb3e0b329dd6_0\" rel=\"nofollow noreferrer\">https://npgeo-corona-npgeo-de.hub.arcgis.com/datasets/dd4580c810204019a7b8eb3e0b329dd6_0</a></p>\n\n<p>From the same company (ESRI) there are a lot more data sets online also for Covid-19. One might have to search for age information, though.<br>\n<a href=\"https://coronavirus-resources.esri.com/\" rel=\"nofollow noreferrer\">https://coronavirus-resources.esri.com/</a></p>\n" }, { "answer_id": 21666, "author": "DrMcCleod", "author_id": 17521, "author_profile": "https://health.stackexchange.com/users/17521", "pm_score": 1, "selected": false, "text": "<p>Kaggle has an ongoing <a href=\"https://www.kaggle.com/allen-institute-for-ai/CORD-19-research-challenge\" rel=\"nofollow noreferrer\">competition analysing COVID-19 related medical literature</a>.\nThis competition provides a large dataset, as well as already published analysis tools and other assistance to get you started.</p>\n" }, { "answer_id": 21770, "author": "Milla", "author_id": 14531, "author_profile": "https://health.stackexchange.com/users/14531", "pm_score": 0, "selected": false, "text": "<p><a href=\"http://go.usa.gov/xdbuc\" rel=\"nofollow noreferrer\">http://go.usa.gov/xdbuc</a>\nSelect a dataset and click Download button.\nYou can choose Fasta format</p>\n" }, { "answer_id": 21789, "author": "farud", "author_id": 18050, "author_profile": "https://health.stackexchange.com/users/18050", "pm_score": 1, "selected": false, "text": "<p>Additionaly to Philipp Leitl's answer:\nOverview of cases in Italy, provided by Instituto Superiore Di Sanita, updated on a daily basis (just change the date in the url) with death distribution by age:\n<a href=\"https://www.epicentro.iss.it/coronavirus/bollettino/Infografica_27marzo%20ENG.pdf\" rel=\"nofollow noreferrer\">https://www.epicentro.iss.it/coronavirus/bollettino/Infografica_27marzo%20ENG.pdf</a>\nThe korean Korea Centers for Disease Control and Prevention also publish some data on a daly basis, including case distribution by gender and age:\n<a href=\"https://www.cdc.go.kr/board/board.es?mid=a30402000000&amp;bid=0030\" rel=\"nofollow noreferrer\">https://www.cdc.go.kr/board/board.es?mid=a30402000000&amp;bid=0030</a>\nFor example, press release No 215, 26.3.2020:\n<a href=\"https://www.cdc.go.kr/board/board.es?mid=a30402000000&amp;bid=0030&amp;act=view&amp;list_no=366650&amp;tag=&amp;nPage=1\" rel=\"nofollow noreferrer\">https://www.cdc.go.kr/board/board.es?mid=a30402000000&amp;bid=0030&amp;act=view&amp;list_no=366650&amp;tag=&amp;nPage=1</a></p>\n" } ]
2020/03/10
[ "https://health.stackexchange.com/questions/21279", "https://health.stackexchange.com", "https://health.stackexchange.com/users/7446/" ]
21,285
<p>I would like to know if it has been proven or disproven that the Coronavirus/COVID-19 can be spread via public toilet seats?</p> <p>I am thinking that perhaps I should always carry around hand sanitizer with me and put some on each public toilet seat that I use. I would put it on some toilet paper and then rub down the toilet seat before sitting down.</p>
[ { "answer_id": 21287, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 4, "selected": true, "text": "<p>The virus causing COVID-19 infects the respiratory tract. It is spread in droplets of moisture when an infected person sneezes, coughs, and exhales. These droplets can be inhaled directly and can also end up on surfaces, where they can be picked up on your hands and then spread to your face.</p>\n\n<p>The WHO recommends <a href=\"https://www.who.int/emergencies/diseases/novel-coronavirus-2019/advice-for-public\" rel=\"noreferrer\">hand washing and avoiding touching your face with unwashed hands</a> as the primary ways to protect against infection.</p>\n\n<p>Could a toilet seat potentially transfer the virus? Perhaps, but there is nothing special about a toilet compared to other surfaces in a bathroom, and there are no recommendations to treat that surface in particular. The way that you would transfer virus from those surfaces would be by touching them with your hands and then touching your face. The WHO recommends hand washing to combat this.</p>\n" }, { "answer_id": 21447, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 1, "selected": false, "text": "<blockquote>\n<p>New research from China indicates that the novel coronavirus is also spread by fecal-oral transmission, not just by respiratory droplets or environmental contact.</p>\n<p>Hong Shan, MD, PhD, of Fifth Affiliated Hospital, Sun Yat-sen University, in Zhuhai, Guangdong Province, and colleagues noted that the gastrointestinal tract is a welcoming environment for the virus, also known as severe acute respiratory syndrome (SARS) CoV-2. &quot;Our immunofluorescent data showed that the ACE2 protein, which has been proved to be a cell receptor for SARS-CoV-2, is abundantly expressed in the glandular cells of gastric, duodenal, and rectal epithelia, supporting the entry of SARS-CoV-2 into the host cell,&quot; the team wrote.</p>\n</blockquote>\n<p>Among the key findings of the study, published online in Gastroenterology:</p>\n<p>A significant portion of coronavirus patients experience diarrhea, nausea, vomiting, and/or abdominal discomfort before the onset of respiratory symptoms</p>\n<p>Viral RNA is detectable in fecal samples from suspected cases, indicating that the virus sheds into the stool</p>\n<p>Viral gastrointestinal infection and potential fecal-oral transmission can last even after viral clearance from the respiratory tract</p>\n<p>The study looked at 73 patients hospitalized for possible COVID-19 and tested from February 1 to 14, 2020. Testing included serum, nasopharyngeal, and oropharyngeal swabs, as well as urine, stool, and tissue samples in accordance with China Disease Control and Prevention guidelines.</p>\n<p>A total of 39 patients (53.4%; 25 males and 14 females), tested positive for fecal SARS-CoV-2 RNA. The age of patients with positive RNA in stool ranged from 10 months to 78 years, and the duration of stool positivity ranged from 1 to 12 days. Furthermore, the stool of 17 patients (23.3%) remained positive even after respiratory samples tested negative.</p>\n<p>Intracellular staining of viral nucleocapsid protein in gastric, duodenal, and rectal epithelia showed that the virus infected glandular epithelial cells in these areas, the researchers reported. &quot;The continuous positive detection of the viral RNA from feces suggests that the infectious virions are secreted from the virus-infected gastrointestinal cells.&quot;</p>\n<p>&quot;Therefore, we strongly recommend that rRT-PCR [reverse transcriptase polymerase chain reaction] testing for SARS-CoV-2 from feces should be performed routinely in SARS-CoV-2 patients, and Transmission-Based Precautions for hospitalized SARS-CoV-2 patients should continue if feces tests positive by rRT-PCR testing,&quot; Shan and co-authors advised.</p>\n<p>Asked for his perspective, Douglas A. Corley, MD, PhD, of Kaiser Permanente San Francisco Medical Center and the University of California San Francisco, who was not involved with the research, told MedPage Today: &quot;A better understanding of how this virus is transmitted is key to preventing its spread. These observations may also help in improving how the disease is diagnosed through testing for the presence of virus in the stool of patients suspected of harboring this virus.&quot;</p>\n<p>Also commenting, Peter Hotez, MD, of the National School of Tropical Medicine at Baylor College of Medicine in Houston, said the study adds to scientific discussions about whether gastrointestinal transmissions are relevant to the novel coronavirus infections, &quot;especially in light of clinical descriptions of COVID-19 patients admitted to surgical wards in Wuhan who were thought to have abdominal emergencies.&quot;</p>\n<p>&quot;It is a potentially important finding of relevance to the emergence of COVID-19 globally, but the exact extent of gastrointestinal transmission of the virus remains unclear,&quot; Hotez told MedPage Today.</p>\n<p>He added that whether fecal oral transmission is common or uncommon therefore requires additional investigation: &quot;Also unclear is the significance of detection of viral RNA in the feces of patients with pulmonary disease, including those patients who were found to be PCR-negative in their respiratory secretions. The authors speculate that this might suggest that such patients may continue to transmit SARS-CoV-2, but this also requires further study,&quot; said Hotez, who was not involved in the study.</p>\n<p>In a second paper posted on the same day in the journal, Jinyang Gu, MD, of Xinhua Hospital of Jiao Tong University in Shanghai, and colleagues noted that evidence from the 2003 SARS epidemic also showed enteric involvement and the presence of virus in the stool of patients even after discharge from hospital. Interestingly, the team said, the first confirmed case of COVID-19 in the U.S., which occurred in Washington state, reported a 2-day history of nausea and vomiting on admission, followed by a loose bowel movement on the second day of hospitalization. The viral nucleic acids of loose stool and both respiratory specimens from this patient later tested positive.</p>\n<p>Gu's group also noted recent reports of mild to moderate liver injury in COVID-19 patients, including elevated aminotransferases, hypoproteinemia, and prothrombin time prolongation, while in the SARS epidemic of 2003, as many as 60% of patients had liver impairment.</p>\n<p>&quot;The presence of viral nucleic acids of SARS in liver tissue confirmed the coronavirus direct infection in liver, and percutaneous liver biopsies of SARS showed conspicuous mitoses and apoptosis along with atypical features such as acidophilic bodies, ballooning of hepatocytes, and lobular activities without fibrin deposition or fibrosis,&quot; Gu and co-authors wrote. &quot;Altogether, many efforts should be made to be alert [to] the initial digestive symptoms of COVID-19 for early detection, early diagnosis, early isolation, and early intervention.&quot;</p>\n<p>Disclosures</p>\n<p>The study was funded by the National Natural Science Foundation of China.</p>\n<p>Xiao and colleagues reported having no competing interests.</p>\n<p>Gu and co-authors disclosed no competing interests.</p>\n<p>Corley and Hotez reported having no competing interests in relation to their comments.</p>\n<p>Primary Source</p>\n<p>Gastroenterology</p>\n<p>Source Reference: Xiao F, et al &quot;Evidence for gastrointestinal infection of SARS-CoV-2&quot; Gastroenterol 2020; DOI: 10.1053/j.gastro.2020.02.055.</p>\n<p>Secondary Source</p>\n<p>Gastroenterology</p>\n<p>Source Reference: Gu J, et al &quot;COVID-19: Gastrointestinal manifestations and potential fecal-oral transmission&quot; Gastroenterol 2020; DOI: 10.1053/j.gastro.2020.02.054.</p>\n" } ]
2020/03/10
[ "https://health.stackexchange.com/questions/21285", "https://health.stackexchange.com", "https://health.stackexchange.com/users/-1/" ]
21,296
<p>I've read that the incubation period of the covid-19 virus ranges from 2 to 14 days with rare exceptions (e.g. <a href="https://www.worldometers.info/coronavirus/coronavirus-incubation-period/" rel="nofollow noreferrer">here</a>). However, a person carrying a virus could theoretically be contagious and transmit it without themselves having developed symptoms. My questions:</p> <ol> <li>Can carriers of covid-19 infect others before developing noticeable symptoms themselves?</li> <li>If so, what's known about the duration from the time of infection to the time the carrier becomes contagious?</li> </ol>
[ { "answer_id": 21304, "author": "Peter M. - stands for Monica", "author_id": 17787, "author_profile": "https://health.stackexchange.com/users/17787", "pm_score": 1, "selected": false, "text": "<p>re 1: <a href=\"https://medical.mit.edu/faqs/COVID-19#faq-7\" rel=\"nofollow noreferrer\">maybe</a></p>\n\n<p>re 2: Incubation period is <a href=\"https://annals.org/aim/fullarticle/2762808/incubation-period-coronavirus-disease-2019-covid-19-from-publicly-reported\" rel=\"nofollow noreferrer\">about 4.5 to 5.8 days</a></p>\n\n<p>but we don't know for sure, the virus is too new, and already there are possibly two strains (newer strain from Europe and USA is possibly more infectious), not sure if these possible two strains are handled differently, but some researchers are worried.</p>\n\n<p>One problem with so many infected people is that it gives the virus to chance mutate more.</p>\n" }, { "answer_id": 21432, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 1, "selected": false, "text": "<p>There's some computer modelling to suggest that 1:10 infections are caught from people with asymptomatic infection, and the virus is thought to be exhaled as the person breathes out. In fact a 9 patient study showed peak virus shedding is at about 5 days just before the patient becomes symptomatic when their immune system ramps up making antibodies to counter the virus, and reduce viral shedding.</p>\n<p>Uptodate ( not firewalled at present)</p>\n<blockquote>\n<p>Transmission of SARS-CoV-2 from asymptomatic individuals (or individuals within the incubation period) has also been described [17-21]. However, the extent to which this occurs remains unknown. Large-scale serologic screening may be able to provide a better sense of the scope of asymptomatic infections and inform epidemiologic analysis; several serologic tests for SARS-CoV-2 are under development [22].</p>\n</blockquote>\n<p><a href=\"https://www.uptodate.com/contents/coronavirus-disease-2019-covid-19\" rel=\"nofollow noreferrer\">https://www.uptodate.com/contents/coronavirus-disease-2019-covid-19</a></p>\n<blockquote>\n<p>Conclusions</p>\n<p>The clinical courses in subjects under study were mild, all being young- to middle-aged\nprofessionals without significant underlying disease. Apart from one patient, all cases were\nfirst tested when symptoms were still mild or in the prodromal stage, a period in which most\npatients would present once there is general awareness of a circulating pandemic disease5\n.\nDiagnostic testing suggests that simple throat swabs will provide sufficient sensitivity at this\nstage of infection. This is in stark contrast to SARS. For instance, only 38 of 98 nasal or\nnasopharyngeal swab samples tested positive by RT-PCR in SARS patients in Hong Kong15.\nAlso, viral load differed considerably. In SARS, it took 7 to 10 days after onset until peak\nRNA concentrations (of up to 5x105\ncopies per swab) were reached13,14. In the present study,\npeak concentrations were reached before day 5, and were more than 1000 times higher.\nSuccessful live virus isolation from throat swabs is another striking difference from SARS, for\nwhich such isolation was rarely successful16-18. Altogether, this suggests active virus\nreplication in upper respiratory tract tissues, where only minimal ACE-2 expression is found\nand SARS-CoV is therefore not thought to replicate19. At the same time, the concurrent use\nof ACE-2 as a receptor by SARS-CoV and SARS-CoV-2 corresponds to a highly similar\nexcretion kinetic in sputum, with active replication in the lung. SARS-CoV was found in\nsputum at mean concentrations of 1.2-2.8x106\ncopies per mL, which corresponds to\nobservations made here13.</p>\n</blockquote>\n<p><a href=\"https://www.medrxiv.org/content/10.1101/2020.03.05.20030502v1.full.pdf\" rel=\"nofollow noreferrer\">https://www.medrxiv.org/content/10.1101/2020.03.05.20030502v1.full.pdf</a></p>\n" }, { "answer_id": 21434, "author": "einpoklum", "author_id": 8418, "author_profile": "https://health.stackexchange.com/users/8418", "pm_score": 1, "selected": false, "text": "<p>Haaretz <a href=\"https://www.haaretz.co.il/news/world/europe/1.8680797\" rel=\"nofollow noreferrer\">reports</a> (Hebrew, possible paywall) about two studies, in Singapore and in Tianjin, China, on this matter:</p>\n\n<ul>\n<li>The average \"generation gap\" (i.e. the duration OP asked about - from contraction to becoming contagious) was established as 5.2 days (Singapore data) or 3.9 days (Tianjin data).</li>\n<li>The fraction of contractions due to infection by asymptomatic patients (whether they later become symptomatic or not) is 45%-84% (Singapore data) or 5%-87% (Tianjin data).</li>\n</ul>\n\n<p><strong>Bottom line answers (based on these studies):</strong></p>\n\n<ol>\n<li>Yes, they can and do infect others.</li>\n<li>Carriers become contagious a few days after contracting the virus (probably 4 or 5).</li>\n</ol>\n" }, { "answer_id": 23536, "author": "gotwo", "author_id": 17963, "author_profile": "https://health.stackexchange.com/users/17963", "pm_score": 3, "selected": true, "text": "<p><strong>To question 1, infection of others before symptoms of the carrier</strong></p>\n\n<p>Yes, carriers of Covid-19 can infect others before developing noticeable symptoms themselves.</p>\n\n<p>There is a study to a very traceable transmission chain in a company in Germany. <code>Person 1</code> was infected from a from China comming <code>person 0</code> after January 19, 2020. </p>\n\n<ul>\n<li><p>A <code>person 3</code> had contact only with <code>person 1</code> on January 20 and 21. However, <code>person 1</code> had first symptoms on the January 24th, so the infection occurred <strong>3 days before</strong> symptoms of the carrier. </p></li>\n<li><p>Another <code>person 4</code> had also contact only with <code>person 1</code> from January 21 to January 24. This infection occurred <strong>within 0 to 3 days</strong> before <code>person 1</code> first symptoms.</p></li>\n</ul>\n\n<p>This study can be read in detail here: <a href=\"https://www.nejm.org/doi/10.1056/NEJMc2001468\" rel=\"nofollow noreferrer\">https://www.nejm.org/doi/10.1056/NEJMc2001468</a>.</p>\n\n<p>There exist also an interview with <code>person 1</code>, which states that he met <code>person 0</code> on Monday (January 20).</p>\n\n<ul>\n<li><code>Person 0</code> doesn't show symptoms of illness during their presence. Symptoms were established on their return trip on January 22, so <code>person 1</code> was infected <strong>1 to 2 days</strong> before symptoms of <code>person 0</code>. </li>\n</ul>\n\n<p>The interview is readable here: <a href=\"https://www.br.de/radio/bayern1/coronavirus-in-bayern-100.html\" rel=\"nofollow noreferrer\">https://www.br.de/radio/bayern1/coronavirus-in-bayern-100.html</a>.</p>\n\n<p><strong>To question 2, duration until the carrier becomes contagious</strong></p>\n\n<ul>\n<li>The above study shows that <code>person 1</code> infected <code>person 3</code> already <strong>after 1 to 2 days</strong> after infection themselves.</li>\n</ul>\n\n<p>In addition, there is an study to 312 infections in Austria about the <a href=\"https://en.wikipedia.org/wiki/Serial_interval\" rel=\"nofollow noreferrer\">serial interval</a> which refers to the time between successive cases of transmission. </p>\n\n<ul>\n<li>According to this study, carriers of the virus contribute significantly to an infection already <strong>after day 1</strong>. The risk of transmission is <strong>highest on day 3</strong> and after 10 days the risk of transmission drops significantly, but is still present. </li>\n</ul>\n\n<p>You can see this study here: <a href=\"https://www.ages.at/en/wissen-aktuell/publikationen/schaetzung-des-seriellen-intervalles-von-covid19-oesterreich\" rel=\"nofollow noreferrer\">https://www.ages.at/en/wissen-aktuell/publikationen/schaetzung-des-seriellen-intervalles-von-covid19-oesterreich</a></p>\n" } ]
2020/03/11
[ "https://health.stackexchange.com/questions/21296", "https://health.stackexchange.com", "https://health.stackexchange.com/users/8418/" ]
21,298
<p>As the German chancellor said today, by the end of the year 60-70% of the population will have been through a COVID-19 infection. Where does that number come from?</p> <p>The basic mechanism is clear, and the magnitude is plausible: Let <code>n</code> be the average number of persons infected by one infected person. If <code>n</code> falls below 1, then the epidemy will run out. This will happen if an infected person mostly hits persons who are already immune.</p> <p>The question is: Why just 60-70%, not 40-50 or 80-90%? Does it come from historic precedence? Or from some formula that takes into account the value of <code>n</code> (the value before saturation has set in)? What citation classics could serve as reference?</p>
[ { "answer_id": 21307, "author": "WinEunuuchs2Unix", "author_id": 17751, "author_profile": "https://health.stackexchange.com/users/17751", "pm_score": 1, "selected": false, "text": "<p>Some Canadian experts said <a href=\"https://www.msn.com/en-ca/news/canada/coronavirus-could-infect-35-to-70-per-cent-of-canadians-experts-say/ar-BB10Z837?li=AAggNb9\" rel=\"nofollow noreferrer\">35% to 70%</a> will be infected:</p>\n\n<blockquote>\n <p>According to a disease-transmission model developed by University of\n Toronto researchers, the virus’ overall attack rate in Canada could\n exceed 70 per cent. That number drops sharply, by about half, “if we\n add modest control,” said epidemiologist Dr. David Fisman, one of the\n model’s creators, but it will take “aggressive social distancing and\n large scale quarantines” to reduce it further, he said.</p>\n \n <p>“That’s still a huge number of people ill, and critically ill people\n are a large fraction in this disease,” Fisman said in an email. “I’m\n not going to share more specific numbers because I think they will\n scare people to no particular end.”</p>\n</blockquote>\n\n<p>In reality no one knows. I can tell you if they contain the spread no more people will be infected. If they don't contain the spread more people will be infected. Steps like Italy took today where only essential work can occur and all business closed except transportation, grocery stores and pharmacies are a desperate attempt at containment that may be too late. That said given recent numbers it appears to have worked for China.</p>\n\n<p>The German Chancellor is wasting her time and ours spewing off meaningless numbers that will only serve to scare citizens of the nation she is supposed to lead. Something better would be her plan to make the homeless self-isolate for 14 days at home if they come into contact with someone who was positive or preemptively positive.</p>\n\n<p>Today the WHO leader said if American governments (Federal, State, County, City, etc) do not act it could be \"many, many millions\" dead in the USA. Today's US government talk to borrow 40 billion dollars to spend on the pandemic is not a plan.</p>\n" }, { "answer_id": 21429, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 1, "selected": false, "text": "<p>This is a rough estimate based on how contagious this virus is to provide a guess on when herd immunity can be reached.</p>\n\n<blockquote>\n <p>Rough estimates indicate that herd immunity to Covid-19 would be reached when approximately 60% of the population has had the disease</p>\n</blockquote>\n\n<p><a href=\"https://www.bbc.com/news/science-environment-51892402\" rel=\"nofollow noreferrer\">https://www.bbc.com/news/science-environment-51892402</a></p>\n\n<p>The percentage needed for herd immunity depends on the virus. So, for measles, it is required that about 95% of the community be immune before herd immunity is effective for your local population.</p>\n\n<p><a href=\"https://www.globalhealthnow.org/2019-12/myth-about-herd-immunity\" rel=\"nofollow noreferrer\">https://www.globalhealthnow.org/2019-12/myth-about-herd-immunity</a></p>\n" }, { "answer_id": 21433, "author": "DeltaIV", "author_id": 17859, "author_profile": "https://health.stackexchange.com/users/17859", "pm_score": 2, "selected": false, "text": "<p>Those are rough estimates coming from estimates of the <em>basic reproduction number</em> <em>R</em><sub>0</sub><sup>1</sup>, which for COVID-19 are between 2 and 3<sup>2</sup>. <em>R</em><sub>0</sub> is a measure of how transferable a disease is, and it measures on average how many people an infectious individual will pass the disease to. 1-1/<em>R</em><sub>0</sub> is the fraction of the total population which needs to develop immunity, either through a vaccine (which currently doesn't exist for COVID-19) or because they got infected and recovered, developing immunity. </p>\n\n<p>This can be intuitively understood in the following way: if 1 infectious individual infects on average 3 other susceptible individuals (<em>R</em><sub>0</sub>=3), then, if 1-1/3=2/3 of the total population develop immunity, then 2 out of the 3 persons which would normally be infected won't be. This means that on average one infectious individual infects another one, before recovering. Thus the size of the disease doesn't grow, but it ends up in a so-called \"endemic state\".</p>\n\n<p>Coming back to COVID-19 and considering the two extreme values for <em>R</em><sub>0</sub>:</p>\n\n<pre><code>&gt; R_0 &lt;- c(2,3)\n&gt; (1-1/R_0)*100\n[1] 50.00000 66.66667\n</code></pre>\n\n<p>we can see where the estimate you were referring to, comes from.</p>\n\n<p><em>R</em><sub>0</sub> is not to be confused with <em>R</em>, the <em>effective reproduction number</em>, which is the quantity we try to reduce through non-pharmacological interventions during an epidemic.</p>\n\n<hr>\n\n<h2>References</h2>\n\n<ol>\n<li>Milligan, Gregg N.; Barrett, Alan D. T. (2015). Vaccinology : an essential guide. Chichester, West Sussex: Wiley Blackwell. </li>\n<li><a href=\"https://www.imperial.ac.uk/media/imperial-college/medicine/sph/ide/gida-fellowships/Imperial-College-COVID19-NPI-modelling-16-03-2020.pdf\" rel=\"nofollow noreferrer\">https://www.imperial.ac.uk/media/imperial-college/medicine/sph/ide/gida-fellowships/Imperial-College-COVID19-NPI-modelling-16-03-2020.pdf</a></li>\n</ol>\n" } ]
2020/03/11
[ "https://health.stackexchange.com/questions/21298", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17785/" ]
21,314
<p>If a person gets COVID-19 and (hopefully) recovers at home without being hospitalized, how long should that person stay isolated before they can return to social interaction?</p>
[ { "answer_id": 21315, "author": "Pablo", "author_id": 7049, "author_profile": "https://health.stackexchange.com/users/7049", "pm_score": 0, "selected": false, "text": "<p>Doctors apply a test kit, if you no longer have the virus you are typically released. However, in China some people who gave negative results were released and later they found they still had the virus, because the tests were poor quality or other factors, so now doctors are suggested to combine epidemiological history, clinical and imaging manifestations with the test. But when the doctor releases you, that's when you can socially interact again. </p>\n\n<p><a href=\"https://www.scmp.com/news/china/society/article/3065022/coronavirus-why-do-recovered-patients-test-positive-again\" rel=\"nofollow noreferrer\">Coronavirus why do recovered patients test positive again</a></p>\n" }, { "answer_id": 23247, "author": "Carey Gregory", "author_id": 805, "author_profile": "https://health.stackexchange.com/users/805", "pm_score": 3, "selected": true, "text": "<p>The current <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/hcp/disposition-in-home-patients.html\" rel=\"nofollow noreferrer\">recommendations of the US Centers for Disease Control</a> (CDC) depend on whether testing is available and has been done. They offer two criteria, the first is non-test-based and the second is test-based.</p>\n\n<p>For persons who have not been tested, the recommended criteria are:</p>\n\n<blockquote>\n <p><strong>Persons with COVID-19 who have symptoms</strong> and were directed to care for\n themselves at home may discontinue isolation under the following\n conditions:</p>\n \n <ul>\n <li>At least 3 days (72 hours) have passed since recovery defined as resolution of fever without the use of fever-reducing medications and</li>\n <li>Improvement in respiratory symptoms (e.g., cough, shortness of breath); and,</li>\n <li>At least 7 days have passed since symptoms first appeared.</li>\n </ul>\n</blockquote>\n\n<p>For those who have been tested, the criteria are:</p>\n\n<blockquote>\n <p><strong>Persons who have COVID-19 who have symptoms</strong> and were directed to care\n for themselves at home may discontinue isolation under the following\n conditions:</p>\n \n <ul>\n <li>Resolution of fever without the use of fever-reducing medications and</li>\n <li>Improvement in respiratory symptoms (e.g., cough, shortness of breath) and</li>\n <li>Negative results of an FDA Emergency Use Authorized molecular assay for COVID-19 from at least two consecutive nasopharyngeal swab\n specimens collected ≥24 hours apart*** (total of two negative\n specimens). </li>\n </ul>\n \n <p>***All test results should be final before isolation is ended. Testing guidance is based upon limited information and is subject to change as\n more information becomes available.</p>\n</blockquote>\n\n<p>Keep in mind that COVID-19 is a new disease with many unknowns and therefore the recommendations above can and probably will change as more is learned, so anyone using this answer to make a decision should visit the CDC link I provided at the beginning of this answer before making that decision.</p>\n" } ]
2020/03/12
[ "https://health.stackexchange.com/questions/21314", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17796/" ]
21,316
<p>Coronavirus death rates are higher for people in the range of 80+ (14,8%) and 70-79 years old (3,6%). However, there are countries, specially in Africa, where life expectancies are in the 50-60 and 60-70 years old range. Some people (like Bill Gates) warned about possible catastrophes if the virus massively reachs Africa. Could it happen than the lower life expectancy of those countries prevents more people from dying? Is people who lives 60 years old in countries with lower life expectancy, expected to have the mortality rates for Coronavirus of the people of the same age in countries with higher life expectancy, or a person of 60 years old in countries like those is in a physical state of an older person in a more developed country and as such have a higher mortality rate? </p>
[ { "answer_id": 21320, "author": "Ray Butterworth", "author_id": 17364, "author_profile": "https://health.stackexchange.com/users/17364", "pm_score": 3, "selected": true, "text": "<p>Age is a red herring, only a secondary characteristic correlating to death rates.</p>\n\n<p>It's people that are already seriously ill or already have weak immune systems that are most likely to die soon after contracting Covid-19. And it's when people are clustered in a close community that they are most likely to contract the disease.</p>\n\n<p>In our society, the people in those circumstances tend to be old and in health-care facilities.\nAs a result, most of our deaths so far have involved people over 80 years old.</p>\n\n<p>In other societies, a lack of old people doesn't necessarily mean a lack people living in close quarters, that are weak or sick.</p>\n\n<p>There's certainly no shortage of such conditions in many parts of Africa.</p>\n\n<p>From <a href=\"https://ourworldindata.org/coronavirus\" rel=\"nofollow noreferrer\">Coronavirus Disease (COVID-19) - Our World in Data</a>:</p>\n\n<p><a href=\"https://i.stack.imgur.com/JUM5S.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/JUM5S.png\" alt=\"enter image description here\"></a></p>\n" }, { "answer_id": 21324, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": false, "text": "<p>Death risk from COVID-19 increases greatly with underlying diseases:</p>\n\n<blockquote>\n <p>Patients who reported no pre-existing (\"comorbid\") medical conditions\n had a case fatality rate of 0.9% <em>(<a href=\"https://www.worldometers.info/coronavirus/coronavirus-age-sex-demographics/\" rel=\"nofollow noreferrer\">Worldometer, Feb 29, 2020</a>).</em></p>\n</blockquote>\n\n<p>The most common underlying diseases in those who died from COVID-19 were: cardiovascular disease, diabetes, chronic respiratory disease, hypertension and cancer. So, it's not really age, but an underlying disease that increases the risk of death in COVID-19. </p>\n\n<p>The median age of those who died so far from COVID-19 in <strong>Italy</strong> with life expectancy 83.4 years was <strong>81 years:</strong></p>\n\n<blockquote>\n <p>Borrelli said the median age of the people who have died from the\n virus in Italy is 81 years of age <em>(<a href=\"https://edition.cnn.com/world/live-news/coronavirus-outbreak-03-06-20-intl-hnk/h_9ba4751542191c2e9408c3181ff6fbf1\" rel=\"nofollow noreferrer\">CNN, March 6, 2020</a>)</em>.</p>\n</blockquote>\n\n<p>and in <strong>China</strong> with life expectancy 74.6 years, it was <strong>75 years:</strong></p>\n\n<blockquote>\n <p>On 23 February 2020, the number of people diagnosed with COVID‐19 in\n China was 1879 times of that on 10 January 2020. They estimated the\n case fatality rate of COVID‐19 to be 2.84% based on their patient\n pool. The authors also found that the ratio of male to female deaths\n was 3.25:1, the median age of death was 75 years <em>(<a href=\"https://onlinelibrary.wiley.com/doi/10.1002/jmv.25722\" rel=\"nofollow noreferrer\">Journal of\n Medical Virology, Feb 25, 2020</a>).</em></p>\n</blockquote>\n\n<p>In the <a href=\"https://www.worldometers.info/coronavirus/\" rel=\"nofollow noreferrer\">US</a> with life expectancy 78.9 years, it was <strong>80 years</strong>.</p>\n\n<p>The risk of death from COVID-19 increases with chronic diseases and therefore with age. Moth deaths so far have been on Northern hemisphere in countries with life expectancy above 74 years. Moth countries with life expectancy lower than 65 years are on Southern hemisphere or around equator, where it is warm now, which is a likely reason for much fewer cases of infection there.</p>\n\n<p>In countries with low life expectancy, mainly in Africa, there are other potential risk factors for COVID-19: widespread parasitic diseases (malaria, intestinal parasites, etc.), malnutrition and less available health care, which are not associated with age. </p>\n\n<p><strong>In conclusion,</strong> even if in the countries with low <a href=\"https://en.wikipedia.org/wiki/List_of_countries_by_life_expectancy\" rel=\"nofollow noreferrer\">life expectancy</a>, lower average age (and hence less chronic diseases) can be a protective factor against COVID-19 <a href=\"https://www.worldometers.info/coronavirus/\" rel=\"nofollow noreferrer\">deaths</a> (Worldometer), we do not yet know the effects of other risk factors in these countries.</p>\n" }, { "answer_id": 25658, "author": "ttulinsky", "author_id": 21337, "author_profile": "https://health.stackexchange.com/users/21337", "pm_score": 0, "selected": false, "text": "<p>The Accepted Answer by Ray Butterworth, while reasonable when it was written (March 2020), now appears to be <strong>wrong</strong>. Hardest hit countries have mainly been those with longest life expectancies (Europe, N. America) while Africa has had very low death rates from Covid (Europe 964 per million, Africa 70 per million, <a href=\"https://ourworldindata.org/coronavirus-data-explorer?zoomToSelection=true&amp;minPopulationFilter=1000000&amp;country=USA%7EAfrica%7EEurope&amp;region=World&amp;deathsMetric=true&amp;interval=total&amp;hideControls=true&amp;perCapita=true&amp;smoothing=0&amp;pickerMetric=location&amp;pickerSort=asc\" rel=\"nofollow noreferrer\">Our World In Data</a>, 2021 Feb 5). Multiple studies have found a high correlation between life expectancy and covid deaths, e.g. <a href=\"https://www.frontiersin.org/articles/10.3389/fpubh.2020.604339/full#SM6\" rel=\"nofollow noreferrer\">Frontiers | Covid-19 Mortality: A Matter of Vulnerability Among Nations Facing Limited Margins of Adaptation</a>,</p>\n<p><a href=\"https://bmjopen.bmj.com/content/10/11/e042750\" rel=\"nofollow noreferrer\">Factors associated with COVID-19 infections and mortality in Africa: a cross-sectional study using publicly available data | BMJ Open</a></p>\n" } ]
2020/03/12
[ "https://health.stackexchange.com/questions/21316", "https://health.stackexchange.com", "https://health.stackexchange.com/users/7049/" ]
21,318
<p>I have heard several times now, from both people I personally know and from others who have posted their stories online that they do not qualify for COVID-19 testing.</p> <p>From the stories I have heard, to qualify you have to: 1. Had contact with a known case of COVID-19 2. Been to a country heavily infected with COVID-19 3. Have symptoms that have progressed to the point where hospitalization is required</p> <p>We now have a reported 1339 cases in the US with likely many more undiagnosed by medical professionals or the CDC.</p> <p>Why, when we are in a state of pandemic and all countries scrambling to get a handle on the virus, are clinics, primary cares, and even hospitals not administering tests to those who exhibit symptoms unless one of these other criteria are met?</p> <p>With an incubation period of 2-14 days, it is entirely possible to have contact with someone who has it and not know you got it from them.</p>
[ { "answer_id": 21326, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 2, "selected": false, "text": "<p>CDC guidelines for when patients should be tested have changed since the ones you list. <a href=\"https://emergency.cdc.gov/han/2020/han00429.asp?deliveryName=USCDC_511-DM22106\" rel=\"nofollow noreferrer\">CDC now says</a>:</p>\n<blockquote>\n<p>Clinicians should use their judgment to determine if a patient has signs and symptoms compatible with COVID-19 and whether the patient should be tested. Most patients with confirmed COVID-19 have developed fever1 and/or symptoms of acute respiratory illness (e.g., cough, difficulty breathing). Priorities for testing may include:</p>\n<p>Hospitalized patients who have signs and symptoms compatible with COVID-19 in order to inform decisions related to infection control.</p>\n<p>Other symptomatic individuals such as, older adults (age ≥ 65 years) and individuals with chronic medical conditions and/or an immunocompromised state that may put them at higher risk for poor outcomes (e.g., diabetes, heart disease, receiving immunosuppressive medications, chronic lung disease, chronic kidney disease).</p>\n<p>Any persons including healthcare personnel, who within 14 days of symptom onset had close contact with a suspect or laboratory-confirmed COVID-19 patient, or who have a history of travel from affected geographic areas (see below) within 14 days of their symptom onset.</p>\n</blockquote>\n<p>This is a broad definition that gives clinicians the freedom to judge, though it still emphasizes priority for cases similar to the older guidelines.</p>\n<p>However, guidelines and reality may not match. Via <a href=\"https://www.npr.org/sections/health-shots/2020/03/11/814189027/no-guarantee-youll-get-tested-for-covid-19-even-if-your-doctor-requests-it\" rel=\"nofollow noreferrer\">NPR</a>:</p>\n<blockquote>\n<p>There's still a big gap between what the federal government is promising and what state and local labs can deliver.</p>\n<p>...</p>\n<p>...those labs have a limited capacity to test, so some have been turning down doctors' requests.</p>\n<p>The novel coronavirus test isn't simple, like the ones for the flu, strep or pregnancy. The kits detecting the coronavirus are configured more for a research lab than a hospital — and certainly can't be run in a doctor's office. It takes four to six hours to perform the tests on patient samples.</p>\n</blockquote>\n<p>Therefore, at this point the main reason that people with symptoms are being denied tests seems to involve a shortage of the tests, and possibly prioritization of tests for other patients. Hopefully these problems will be resolved going forward.</p>\n" }, { "answer_id": 21330, "author": "Albrecht Hügli", "author_id": 17790, "author_profile": "https://health.stackexchange.com/users/17790", "pm_score": 0, "selected": false, "text": "<p>If everyone would like to be tested who shows some symptoms of this infection you could test probably 50% of the population: <em>\"me too!\"</em> As the capacity of tests is limited it is really necessary that these test kits are reserved for persons that are diagnosed by a doctor. In case of a pandemia - and if this is one - people should keep distance to others, wash their hands and shouldn't go to work if they think they are infected. People with severe symptoms should stay at home and call the doctor and get information by phone. </p>\n\n<p>And save the disinfection solutions and masks for the doctors and medical staff and the ill people.</p>\n" }, { "answer_id": 21334, "author": "Chipster", "author_id": 17726, "author_profile": "https://health.stackexchange.com/users/17726", "pm_score": 0, "selected": false, "text": "<p>Because the CDC won't let them test them. Understand that hospitals can't perform tests for Covid-19--originally only the CDC could. Now, some state laboratories can test. Either way, hospitals can't test people whom the labs don't allow testing for. It's not entirely the hospital's decision.</p>\n\n<p>Keep in mind that some of these restrictions are pretty common sense. For instance, some of these requirements restrict that if you have these symptoms, but we know you have the Flu (which has similar symptoms), then there's no reason to test you for Covid-19. It's pretty reasonable to assume that these symptoms are because of the Flu.</p>\n" }, { "answer_id": 21399, "author": "cbeleites unhappy with SX", "author_id": 11479, "author_profile": "https://health.stackexchange.com/users/11479", "pm_score": 3, "selected": false, "text": "<p>There's yet another reason: a test can provide only a certain amount of information gain. If the probability to have contracted Covid-19 before the test is too low, even though we know more after the test we may not be able to draw practical conclusions that are any different from the recommendations without test. In other words, if the recommendation goes from \"stay at home and avoid contact to others\" to \"stay at home and avoid contact to others\" the test would be wasted.</p>\n\n<p>The Covid-19 tests are not suitable for screening purposes (i.e. searching for infections among a population where infections are [still] very rare). They are to sort out who is infected and who isn't among high-risk populations where 1 in 10 (or more) are actually infected. </p>\n\n<hr>\n\n<p>You may want to look at <a href=\"https://medicalsciences.stackexchange.com/a/21379/11479\">my longish answer</a> to <a href=\"https://medicalsciences.stackexchange.com/q/21337/11479\">How accurate are coronavirus tests?</a> for relevant background.</p>\n\n<hr>\n\n<p>E.g., with the newly emergency approved Roche test, we may say that a positive test result increases the odds of having Covid-19 by factor of somewhere around 30 - 100, a negative result decreases the odds by a factor of 1/50 - 1/17. </p>\n\n<p>If you are in a risk group with a prevalence of 8 %, the pre-test odds of 8 : 92 </p>\n\n<ul>\n<li>increase to (240 to 800) : 92 or a post-test probability of having Covid-19 of 70 to 90 % with a positive test result, and</li>\n<li>decrease to 8 : (4600 to 1564), i.e. the post-test probability of having Covid-19 is somewhere around 0.5 to 0.2 %</li>\n</ul>\n\n<p>These post-test probabilities allow practical conclusions: if you're negative, you're fine and can be let to meet the public, if you're positive you need to go to quarantine and/or treatment. </p>\n\n<p>8 % prevalence is my guesstimate for those who are currently (Mar 15th) tested in the US (and incidentally, also in Germany).</p>\n\n<p>Now consider the overall US population. With currently <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/cases-in-us.html\" rel=\"nofollow noreferrer\">1629 cases</a> and a population of 328 mio., we'd get pre-test odds of 1629 : 328 mio*. </p>\n\n<p>The test results change this to </p>\n\n<ul>\n<li>positive result: (27700 to 162900) : 328 mio or a post-test probability of having Covid-19 of 0.008 to 0.005 %</li>\n<li>negative result: we don't even need to calculate this, because the pre-test probability was only 0.0005 %, post-test probability is lower.</li>\n</ul>\n\n<p>Even if we assume that there's a dark number of yet unknown Covid-19 cases, say, a factor 20 over the known cases, the post-test probabiliy after a positive test is about 0.2 % to 1%. </p>\n\n<p>What would be the practical conclusion? Well, probably that the positive case should stay at home as much as possible and avoid contacts. Certainly not that they can rely on acquiring immunity against SARS-CoV-2.</p>\n\n<p>Even for low risk groups who have flu-like symptoms but no known contact to Covid infected people (or other high-risk situations) the pre-test probability of having Covid is too low to allow the test to make a meaningful difference: after all, even if it is \"only a common flu\", they should stay at home, get well and not infect others meanwhile. \nWhile the pre-test probability is likely to increase (because more people get infected), in order to keep the health system/hospitals working the recommendation will probably not change: stay at home in self-quarantine as long as the symptoms are mild, so that the health system is not burdened by cases that get well on their own.</p>\n\n<p>We may also say that were the whole US population to be tested in that situation, the 32500 true cases of Covid would be drowned in 3 - 10 mio. false positve cases.</p>\n\n<hr>\n\n<p>*328 mio - 1629 ≈ 328 mio</p>\n" }, { "answer_id": 21402, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 1, "selected": false, "text": "<p>Because the USA has been extremely poorly prepared for this pandemic there has been a severe shortage of test kits. A number of other egregious errors were made including declining to accept the German test offered to them, or using the South Korean test kits. South Korea have been testing 10,000 people a day which is more than the USA has since the outbreak developed.</p>\n\n<p>In this situation the clinicians have triaged as much as they could to decide who to test developing an evolving set of clinical and epidemiological criteria which have loosened. But what they didn't know was that the virus been likely been circulating in the community for some weeks as community transmission was detected in late February.</p>\n\n<p>At this time the most appropriate response is to self isolate if one develops any respiratory symptoms, and advise close contacts. Because testing has been very limited it is nearly impossible to satisfy the epidemiological criterion of knowing about a contact with the disease. </p>\n\n<p><a href=\"https://www.nytimes.com/2020/03/10/us/coronavirus-testing-delays.html\" rel=\"nofollow noreferrer\">https://www.nytimes.com/2020/03/10/us/coronavirus-testing-delays.html</a></p>\n" } ]
2020/03/12
[ "https://health.stackexchange.com/questions/21318", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17798/" ]
21,332
<p>Recently, German Chancellor Angela Merkel gave a speech about the importance of slowing down Covid-19. Among her remarks <a href="https://www.nytimes.com/2020/03/11/world/europe/coronavirus-merkel-germany.html" rel="nofollow noreferrer">were</a></p> <blockquote> <p>The most important thing, the chancellor said, is to slow down the spread of the coronavirus to win time for people to develop immunity</p> </blockquote> <p>How does that work? Can immunity be developed without actually catching the disease or via a vaccine?</p>
[ { "answer_id": 21333, "author": "Bryan Krause", "author_id": 8728, "author_profile": "https://health.stackexchange.com/users/8728", "pm_score": 4, "selected": true, "text": "<p>It's hard to know exactly what another person is thinking, but Merkel is probably referencing <a href=\"https://en.wikipedia.org/wiki/Herd_immunity\" rel=\"noreferrer\">herd immunity</a>.</p>\n\n<p>Assuming that people who are infected and recover will be less susceptible to infection in the future (the extent to which is currently unknown), those people have effectively been naturally vaccinated, which can help slow down future spread.</p>\n" }, { "answer_id": 21335, "author": "Albrecht Hügli", "author_id": 17790, "author_profile": "https://health.stackexchange.com/users/17790", "pm_score": 0, "selected": false, "text": "<p>Immunity can be built by a bigger group of people that has been infected and healed from the sickness. This immunity of the group gives the virus no chance to spread again.</p>\n\n<p><em>no chance</em> is too strict. <em>It will be harder</em> to spread is more appropriate. </p>\n" }, { "answer_id": 21452, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 1, "selected": false, "text": "<p>Merkel and other world leaders were likely talking about herd immunity (they may have walked that back now) but we don't know if the immunity from the infection is long-lasting or not. For instance, it is said seasonal coronavirus immunity lasts less than a year so they're not particularly immunogenic.</p>\n\n<p>Furthermore, the virus has several mutations and we don't know if exposure to one mutation is sufficient to produce immunity against another. Given that's it's not particularly immunogenic it seems it won't.</p>\n\n<blockquote>\n <p>When people are infected with OC43 and HKU1—two other coronaviruses that regularly circulate among humans and cause common colds—they stay immune for less than a year. By contrast, immunity against the first SARS virus (from 2003) holds for much longer. No one knows whether SARS-CoV-2 will hew to either of these extremes, and according to one recent study, its behavior could mean anything from annual outbreaks to a decades-long quiet spell.</p>\n</blockquote>\n\n<p><a href=\"https://www.theatlantic.com/health/archive/2020/03/coronavirus-pandemic-herd-immunity-uk-boris-johnson/608065/\" rel=\"nofollow noreferrer\">https://www.theatlantic.com/health/archive/2020/03/coronavirus-pandemic-herd-immunity-uk-boris-johnson/608065/</a></p>\n" } ]
2020/03/12
[ "https://health.stackexchange.com/questions/21332", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17801/" ]
21,337
<p>As of time of writing it's quite common to see headlines about so-and-so who have tested positive for Covid-19, e.g. <a href="https://www.foxnews.com/world/canadian-pm-justin-trudeaus-wife-sophie-tests-positive-for-coronavirus-officials-say" rel="noreferrer">Canadian PM Justin Trudeau's wife, Sophie, tests positive for coronavirus, officials say</a></p> <p>However, these articles don't usually say how reliable the testing is. I couldn't find any recent information on it via Google, either (there are some results, e.g. <a href="https://www.medicinenet.com/script/main/art.asp?articlekey=228250" rel="noreferrer">this</a>, but they are old).</p> <p>How accurate are the tests? What are the odds that Sophie Trudeau's results are a false positive, or that Justin Trudeau's negative result is a false negative?</p>
[ { "answer_id": 21379, "author": "cbeleites unhappy with SX", "author_id": 11479, "author_profile": "https://health.stackexchange.com/users/11479", "pm_score": 5, "selected": true, "text": "<p>Short answer: Sophie Trudeau's positive test <em>may</em> still mean 3 : 1 odds of <em>not</em> having contracted Covid-19, but the odds could also be far more towards having Covid-19.<br>\nJustin Trudeau's negative test almost certainly means he was negative when tested. Of course, should Sophie be positive, that may have changed by now.</p>\n\n<hr>\n\n<p><strong>Update:</strong> I found a web page of the <a href=\"https://www.fda.gov/medical-devices/emergency-situations-medical-devices/emergency-use-authorizations#covid19ivd\" rel=\"nofollow noreferrer\">FDA listing tests that have this Emergency Use Approval</a>. Each of them has manufacturer instuctions that list their test results towards the end. Some of the submitted test results use ≈100 negative samples in the clinical evaluation. But there is also one that has only 13 positive cases (all of which were correctly found) in their test - but that one got the emergency approval already early in February.<br>\nThe latest 2 (by Thermo and Roche) used 60/60 and 50/100 cases for their clinical evaluation (all results correct). That gets the lower end of the confidence intervals for sensitivity and specificity to 94 - 97 % (with the lower end of the c.i. we'd thus have LR+ >≈ 20 or 17, expected values would be 61 or 51, respectively. For LR- &lt;≈ 1/20 or 1/32 (expected 1/61 or 1/100). </p>\n\n<hr>\n\n<p>Long version: Let's do some number juggling and see whether we can extract something useful. The following calculations are based on a somewhat worst-case scenario: the FDA emergency validation guidelines specify outcomes that such a new test in the current emergency situation must meet, and I calculate from the low end of performance that could be expected meet these criteria under somewhat unlucky circumstances.</p>\n\n<p>So we know minimum performance requirements, but I do not know [yet] how good (= how much better than minimum performance) the tests are.</p>\n\n<h3>Sensitivity and Specificity</h3>\n\n<p>The starting point would be <a href=\"https://en.wikipedia.org/wiki/Sensitivity_and_specificity\" rel=\"nofollow noreferrer\">sensitivity and specificity</a> of the respective test. I haven't found any published data on these, but the FDA has a <a href=\"https://www.fda.gov/media/135659/download\" rel=\"nofollow noreferrer\">Policy for Diagnostics Testing for Coronavirus Disease-2019</a> that says how labs that develop a test should do an \"emergency validation\". They can then get Emergency Use Approval. </p>\n\n<ul>\n<li><strong>Sensitivity</strong> tells us: of all truly Covid-19-positive specimen, which percentage is correctly recognized as positive by the test; I'm going to use <strong>87.5 %</strong> (see below)</li>\n<li><strong>Specificity</strong> tells us: of all specimen that are truly negative for Covid-19, which percentage is correctly recognized by the test.</li>\n</ul>\n\n<p>Sensitivity and specificity can be measured by standardized protocols, and they characterize the performance of the test. </p>\n\n<p>From a patient's or doctor's point of view, however, they are not very useful numbers as they (we) need the answer to the inverse questions:</p>\n\n<h3>Predictive values</h3>\n\n<ul>\n<li><strong>positive predictive value PPV:</strong> given that the test yielded <em>positive</em>, what is the probability that the patient truly has the virus?</li>\n<li><strong>negative predictive value NPV:</strong> given that the test yielded <em>negative</em>, what is the probability that the patient truly does not have the virus?</li>\n</ul>\n\n<p>Predictive values can be calculated from sensitivity and specificity together with the <a href=\"https://en.wikipedia.org/wiki/Prevalence\" rel=\"nofollow noreferrer\">prevalence</a> (or, as we are talking about newly infected patients, the <a href=\"https://en.wikipedia.org/wiki/Incidence_(epidemiology)\" rel=\"nofollow noreferrer\">incidence</a>) of virus among the tested population. Here's how they go for the assumed sensitivity and specificity:</p>\n\n<p><a href=\"https://i.stack.imgur.com/p75G6.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/p75G6.png\" alt=\"predictive values\"></a><br>\nred for positive test outcomes, dark green for negative test outcomes. posterior probability = <em>after</em> the test said something, what is the probability that the test result is correct = NPV for negative test result, PPV for positive test result.</p>\n\n<p>Good estimates of prevalence are often difficult to obtain, because we need the prevalence among those who are tested and that is (and should be) quite different from the prevalence of the disease in the general population. </p>\n\n<p>For some countries such as <a href=\"https://github.com/pcm-dpc/COVID-19/blob/master/schede-riepilogative/regioni/dpc-covid19-ita-scheda-regioni-20200314.pdf\" rel=\"nofollow noreferrer\">Italy, we have numbers of performed tests</a> (<a href=\"https://en.wikipedia.org/wiki/COVID-19_testing\" rel=\"nofollow noreferrer\">Wiki page giving numbers for more countries</a>): as of today (March 14th), they ran 109170 tests and have a total of 21157 cases. Not all tests are for initial diagnosis (AFAIK, a patient is considered cured only after a bunch of tests are negative), but as most cases are still \"fresh\", we may the ratio positive cases : tests run as one surrogate for the prevalence in the tested population. This would be around 20 % for Italy. </p>\n\n<p>From the diagram we can then read for a new patient being tested the first time:</p>\n\n<ul>\n<li>if the test outcome is <em>positive</em>, chances are ≈ 75 % (or greater as I'm calcluating with the lower end of the possible range from the emergency validation) that the patient really has Covid-19.<br>\nSo, up to 25 % false positives. </li>\n<li>if the test outcome is <em>negative</em>, chances are ≈ 95 % (or greater...) that the patient really does not have Covid-19.<br>\nSo, up to 5 % false negatives. </li>\n</ul>\n\n<p><a href=\"https://www.canada.ca/en/public-health/services/diseases/2019-novel-coronavirus-infection.html\" rel=\"nofollow noreferrer\">Canada</a> currently reports 25 positive out of a total of 796 tests, so about 3 % prevalence in the tested population.</p>\n\n<p>For the USA, the CDC reports <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/cases-in-us.html\" rel=\"nofollow noreferrer\">case numbers</a> and <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/cases-updates/testing-in-us.html\" rel=\"nofollow noreferrer\">test numbers</a>, currently 1629 cases with (3995 + 15749) tests - but it is not entirely clear to me whether the populations completely coincide. Anyways, I'll use 8 % as guesstimate for prevalence.</p>\n\n<pre><code>| prevalence | PPV | NPV | Country/Population | \n+------------+------+--------+--------------------+\n| 3 % | 26 % | 99.6 % | Canada |\n| 8-9 % (?) | 50 % | 98.8 % | USA, Germany |\n| 20 % | 75 % | 95 % | Italy |\n\n</code></pre>\n\n<p>Now that is the population of \"everyone who is tested\". At least for Germany (March 14th) but probably also for Canada and the US, tests are done on people who show symptoms and on people that are known to have had contact with Corona virus cases: if they are found to be positive, they are sent home to quarantine and wait whether they did acutally catch the disease. But we may still say that the \"people who are tested\" population has subpopulations with and without symptoms.<br>\nSo if there are further point of suspicion, say, the patient does cough, we'd say they belong to a high risk subpopulation with higher prevalence of Covid-19 compared to the overall prevalence among tested, so the chance of a false positive would be lower for them. </p>\n\n<p>This will change as tests are performed only on people who show symptoms (by now, March 16th, everyone is already told to stay at home in Germany and self-isolate as well as possible - the test result will not change this in any way). </p>\n\n<h3>Handy for quick calculation: <a href=\"https://en.wikipedia.org/wiki/Likelihood_ratios_in_diagnostic_testing\" rel=\"nofollow noreferrer\">likelihood ratio positive (LR+) and negative (LR-)</a></h3>\n\n<p>If we express the prevalence as odds (1 : 99 instead of 1 %), LR+ and LR- allow easy back-of-the envelope calculations. </p>\n\n<p>LR+ = sensitivity / (1 - specificity) ≈ 11 or better for our test and \nLR- = (1 - sensitivity) / specificity ≈ 0.05 = 1/20 or better for our test.</p>\n\n<p>so they are indpendent of the prevalence and they tell us how the odds change due to the test: the posterior probability (predictive values) are the the pre-test odds multiplied with the likelihood ratio. In that sense, they tell us how much information we gain due to test (for positive and negative outcomes).</p>\n\n<p>So, Canada reported odds of 25 positive : 771 negative tests. So for Sophie Trudeau, the odds went from 25 : 771 (or 3 %) to 25 : 771 * 11 = 273 : 771 ≈ 1 : 3 or 25 %. For Justin Trudeau 25 : 771 / 20 = 25 : 15420 ≈ 1 : 617 or 0.16 % of being Covid-19 positive (slight discrepancy to above due to rounding).</p>\n\n<p>On the other hand, if we start testing more and more people for whom the risk of actcually having contracted the virus is lower and lower, we soon won't be able to draw meaningful conclusions from the test results any more: I'm in Germany, currently the <a href=\"https://www.rki.de/DE/Content/InfAZ/N/Neuartiges_Coronavirus/Fallzahlen.html\" rel=\"nofollow noreferrer\">federal info page</a> lists 3800 confirmed cases. Even if we assume that there is a huge dark figure and in reality 20 x as many people are infected* that would be a prevalence in the general population of 0.1 %, the odds are 1 infected : 1.5 mio non-infected. If someone who does not belong to any particular risk group were tested positive, their odds would increase by factor 11, i.e. roughly 1 : 140000. A negative test result would decrease the odds by a factor of 1/20 to 1 : 31 mio. However, both results are of no practical use as they don't change the situation: pre-test situation is \"very unlikely to be Covid-19 case\", post-test situation is still \"very unlikely to be Covid-19 case\".</p>\n\n<p><strong>This is why, even if there were testing capacities for the whole population, tests don't make sense unless we know there are some risk factors such as some kind of respiratory disease or contact to someone who is known to have the virus.</strong> And why it is sensible to say that on slightly suspicious circumstances (= low, but not extremely low prevalence), one should self-quarantine/avoid contact but there's no point in testing [yet].</p>\n\n<hr>\n\n<h3>Detais on how I estimate sensitivity and specificity</h3>\n\n<ul>\n<li>The lab first determines the limit of detection (LoD) for virus RNA. The LoD here is the lowest concentration at which 19 out of 20 replicate tests are positive (that would be 95 % sensitivity, but for samples spiked in the lab, but with a relevant and as difficult as possible matrix such as sputum). </li>\n<li><p>Next, [leftover] clinical samples are used: </p>\n\n<ul>\n<li><p>As there may not be any positive samples available, the lab can spike negative samples with virus RNA; a minimum of 20 samples are spiked within a range of 1 - 2 LoD plus 10 samples to cover the remaining clinical range.<br>\nOf these, at most 1 is allowed to have negative outcome (and that must be one in the lower concentration range). Thus, 29 positive out of 30 true positive. </p></li>\n<li><p>Also 30 non-reactive specimens are tested. The policy doesn't say a number of false positives that is permissible, so I'm going to assume that must be zero. </p></li>\n</ul></li>\n<li><p>The lab can then start with real patient samples. The first 5 positive and the first 5 negative cases must be confirmed by an approved test (and must all match). </p></li>\n</ul>\n\n<p>Pooling the 2 \"rounds\" of testing clinical samples, we have:</p>\n\n<ul>\n<li>34 (or 35) positive tests out of 35 truly positive specimen -> sensitivity at least 97 % with 95% credible interval 87.5 - 100 %,</li>\n<li><p>specficity 100 % with 95% credible interval 92 - 100 %</p></li>\n<li><p>There are additional checks required but they don't help us here.</p></li>\n<li><p>Sampling errors are not included in this validation.<br>\nI'm <em>not</em> a clinical chemist, but I'm analytical chemist and in general analytical chemistry, that can easily be the dominating source of error. In that case, the above numbers would be useless.</p></li>\n<li><p>Particularly the sensitivity may drop over time as the virus mutates. </p></li>\n<li><p>To deal with this, in some cases multiple tests are done (read that in some newspaper article which I don't find at the moment).<br>\nWhen doing multiple tests, tests by different providers are used if possible: as they are developed from different virus samples, this gives a better coverage for mutations in the virus than doing the same test in replicate.</p></li>\n</ul>\n\n<hr>\n\n<p>* Very handwavy scenario I derived from the <a href=\"https://en.wikipedia.org/wiki/2019%E2%80%9320_coronavirus_pandemic#/media/File:2020_coronavirus_patients_in_China.svg\" rel=\"nofollow noreferrer\">development of case numbers in China after their quarantine/shutdown on Jan 26</a>, assuming an incubation period of 2 weeks and that noone got infected after quarantine started.</p>\n\n<hr>\n\n<p>Update Jun 3rd, 2020:</p>\n\n<ul>\n<li><p><a href=\"https://www.instand-ev.de/System/rv-files/340%20EN%20SARS-CoV-2%20Genome%20EQAS%20April%202020%2020200502j.pdf\" rel=\"nofollow noreferrer\">Results of a round robin test/ring trial in April in Germany on detection of SARS-CoV2 RNA</a> (retrieved from <a href=\"https://www.instand-ev.de/en/eqas-online/service-for-eqa-tests.html#rvp//340/2003/\" rel=\"nofollow noreferrer\">https://www.instand-ev.de/en/eqas-online/service-for-eqa-tests.html#rvp//340/2003/</a>)</p>\n\n<ul>\n<li>7 samples: 4 positive for SARS-CoV2 covering a factor of 1000 in concentration of virus RNA; 3 negative for SARS-CoV: 1 negative for any coronavirus, 1 positive for HCoV OC43 but not SARS-CoV2 and 1 positive for HCoV 229E but not SARS-CoV2.</li>\n<li><p>463 laboratories participated, submitting a total of 983 results per sample (1 lab can submit results for several methods)</p></li>\n<li><p>The final evaluation comprises only 4 out of the 7 samples: while the ring trial was still ongoing, the ground truth and a preliminary evaluation was published for 3 samples in order to allow labs to use the results to adjust their procedure.</p></li>\n<li><p>There was a problem with 24 labs (59 lab×methods) where results for two samples (the positive 1:100000 dilution and the negative with HCoV 22E) were interchanged. </p></li>\n</ul>\n\n<p><em>I'll disregard these two samples for now.</em></p>\n\n<ul>\n<li><p><strong>Specificity</strong> was 969/983 = 98.6 % for the negative and 961/983 = 97.8% for the negative with HCoV OC43 (sample was unblinded).<br>\nThe report notes that it is not clear whether the false positives are a result of the specificity of the method itself or whether they stem from contamination of the test samples with SARS-CoV2 in the labs. </p></li>\n<li><p><strong>Sensitivity</strong> was 980/983 = 99.7 % for the highest (sample was unblinded) and 914/983 = 93.0% for the lowest virus RNA concentration.</p></li>\n</ul>\n\n<p>Such a ring trial measures the performance of diagnostic method and lab handling of the samples together. </p></li>\n<li><p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066521/\" rel=\"nofollow noreferrer\">Wenling Wang <em>et al.</em>: Detection of SARS-CoV-2 in Different Types of Clinical Specimens, JAMA, 2020 May 12; 323(18): 1843–1844.</a> reports on sensitivity of RT-PCR tests for various sampling procedure/locations. 1070 specimen collected from 205 confirmed Covid-19 patients.<br>\nThey report 5 of 8 nasal swabs (95%c.i. 30 - 90%) to be positive and 126 of 398 pharyngeal swabs (95% c.i. 27 - 36%). <a href=\"https://pubs.rsna.org/doi/10.1148/radiol.2020200642\" rel=\"nofollow noreferrer\">This other study, while not primarily about PCR sensitivity reports about 60 %</a></p>\n\n<p><em>The paper has very few details, e.g. on the point in time when samples were taken.</em></p>\n\n<p>This study measures the sensitivity of method, lab handling and sampling procedure together. </p>\n\n<p>Experts in radion interviews I heard over the last months were talking about sensitivity in the order of magnitude of 70 - 80 % due to difficult sampling (requiring trained staff, preferrably taking 2 swabs [but swabs were scarce at some point], the correct procedure for nasopharyngeal sampling being painful, the correct point in time wrt. the course of the disease)</p>\n\n<p>In any case, the overall sensitivity seems to be dominated by sampling error rather than lab handling or the sensitivity of the RT-PCR.</p></li>\n</ul>\n\n<p>So my initial guesstimates were too optimistic for overall sensitivity, but specificity looks better than the initial worst-case scenario: we have an LR⁺ of around 50, but LR⁻ is only about 1/4.</p>\n\n<p>Important Note: all this is about the <strong>real time PCR tests for virus RNA</strong>. <a href=\"https://medicalsciences.stackexchange.com/questions/23192/why-are-novel-coronavirus-anitbody-tests-disparaged/23469#23469\">Antibody tests have their own and actually quite different characteristics.</a></p>\n" }, { "answer_id": 21554, "author": "Rob", "author_id": 15969, "author_profile": "https://health.stackexchange.com/users/15969", "pm_score": 2, "selected": false, "text": "<blockquote>\n <p>Is there any figure about the accuracy of COVID-19 tests?</p>\n</blockquote>\n\n<p>A thorough review of prior research found: Using \"<a href=\"https://en.wikipedia.org/wiki/Reverse_transcription_polymerase_chain_reaction\" rel=\"nofollow noreferrer\">rRT-PCR</a>; First-line screening tool: E gene assay; Confirmatory testing: RdRp gene assay.\" one can obtain \"95% detection probability, 100% specificity\".</p>\n\n<p>Reference:</p>\n\n<p>The Journal of Clinical Medicine review: \"<a href=\"https://doi.org/10.3390/jcm9030623\" rel=\"nofollow noreferrer\">Potential Rapid Diagnostics, Vaccine and Therapeutics for 2019 Novel Coronavirus (2019-nCoV): A Systematic Review</a>\", J. Clin. Med. 2020, 9(3), 623 explains:</p>\n\n<blockquote>\n <p>\"A systematic search was carried out in three major electronic databases (PubMed, Embase and Cochrane Library) to identify published studies examining the diagnosis, therapeutic drugs and vaccines for Severe Acute Respiratory Syndrome (SARS), Middle East Respiratory Syndrome (MERS) and the 2019 novel coronavirus (2019-nCoV), in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.</p>\n \n <p>...</p>\n \n <p>An initial search identified a total <strong>of 1,065 articles</strong> from PubMed, Embase and Cochrane Library. There were 236, 236 and 593 articles related to diagnostics, therapeutics and vaccines, respectively. After reviewing for inclusion and exclusion and the removal of duplications, <strong>a total of 27 studies were used for the full review</strong>.</p>\n \n <p>...</p>\n \n <p>The first <strong>validated</strong> diagnostic test was designed in Germany. Corman et al. had initially designed a candidate diagnostic RT-PCR assay based on the SARS or SARS-related coronavirus as it was suggested that circulating virus was SARS-like. Upon the release of the sequence, assays were selected based on the match against 2019-nCoV upon inspection of the sequence alignment. Two assays were used for the RNA dependent RNA polymerase (RdRP) gene and E gene where E gene assay acts as the first-line screening tool and RdRp gene assay as the confirmatory testing. All assays were highly sensitive and specific in that they did not cross-react with other coronavirus and also human clinical samples that contained respiratory viruses.\"</p>\n</blockquote>\n\n<p>Sources:</p>\n\n<ul>\n<li><p><a href=\"https://dx.doi.org/10.2807%2F1560-7917.ES.2020.25.3.2000045\" rel=\"nofollow noreferrer\">Detection of 2019 novel coronavirus (2019-nCoV) by real-time RT-PCR</a>, Euro Surveill. 2020 Jan 23; 25(3): 2000045.</p>\n\n<blockquote>\n <p>\"All assays were highly sensitive, with best results obtained for the E gene and RdRp gene assays (5.2 and 3.8 copies per reaction at <strong>95% detection probability</strong>, respectively). These two assays were chosen for further evaluation. One of the laboratories participating in the external evaluation used other basic RT-PCR reagents (TaqMan Fast Virus 1-Step Master Mix) and repeated the sensitivity study, with equivalent results (E gene: 3.2 RNA copies/reaction (95% CI: 2.2–6.8); RdRP: 3.7 RNA copies/reaction (95% CI: 2.8–8.0).</p>\n \n <p>...</p>\n \n <p>In total, this testing yielded <strong>no false positive outcomes</strong>. In four individual test reactions, weak initial reactivity was seen but they were negative upon retesting with the same assay. These signals were not associated with any particular virus, and for each virus with which initial positive reactivity occurred, there were other samples that contained the same virus at a higher concentration but did not test positive. Given the results from the extensive technical qualification described above, it was concluded that this initial reactivity was not due to chemical instability of real-time PCR probes but most probably to handling issues caused by the rapid introduction of new diagnostic tests and controls during this evaluation study.\".</p>\n</blockquote></li>\n<li><p><a href=\"https://en.wikipedia.org/wiki/COVID-19_testing\" rel=\"nofollow noreferrer\">COVID-19 testing</a>:</p>\n\n<blockquote>\n <p>\"Testing for the <a href=\"https://en.wikipedia.org/wiki/Severe_acute_respiratory_syndrome_coronavirus_2\" rel=\"nofollow noreferrer\">respiratory illness</a> named <a href=\"https://en.wikipedia.org/wiki/Coronavirus_disease_2019\" rel=\"nofollow noreferrer\">coronavirus disease 2019</a> (COVID-19) and the associated <a href=\"https://en.wikipedia.org/wiki/SARS-CoV-2\" rel=\"nofollow noreferrer\">SARS-CoV-2 virus</a> is possible with two main methods: <a href=\"https://en.wikipedia.org/wiki/Molecular_recognition\" rel=\"nofollow noreferrer\">molecular recognition</a> and <a href=\"https://en.wikipedia.org/wiki/Serology\" rel=\"nofollow noreferrer\">serology</a> testing.</p>\n \n <p>Molecular methods leverage <a href=\"https://en.wikipedia.org/wiki/Polymerase_chain_reaction\" rel=\"nofollow noreferrer\">polymerase chain reaction</a> (PCR) along with <a href=\"https://en.wikipedia.org/wiki/Nucleic_acid_tests\" rel=\"nofollow noreferrer\">nucleic acid tests</a>, and other advanced analytical techniques, to detect the genetic material of the virus using real-time <a href=\"https://en.wikipedia.org/wiki/Reverse_transcription_polymerase_chain_reaction\" rel=\"nofollow noreferrer\">reverse transcription polymerase chain reaction</a> for diagnostic purposes.</p>\n \n <p>Serology testing, leverages <a href=\"https://en.wikipedia.org/wiki/ELISA\" rel=\"nofollow noreferrer\">ELISA</a> antibody test kits to detect the presence of antibodies produced by the host <a href=\"https://en.wikipedia.org/wiki/Immune_system\" rel=\"nofollow noreferrer\">immune system</a> against the virus. </p>\n \n <p>...</p>\n \n <p>Serology antibody testing is being used both for surveillance and investigational purposes including, in China, confirmation of recovery only, while the molecular test methodologies are used to diagnosis active infections.\".</p>\n \n <p>\"There are several serology techniques that can be used depending on the antibodies being studied. These include: ELISA, agglutination, precipitation, complement-fixation, and fluorescent antibodies and more recently chemiluminescence.\".</p>\n</blockquote></li>\n</ul>\n" }, { "answer_id": 24246, "author": "Dan Dascalescu", "author_id": 811, "author_profile": "https://health.stackexchange.com/users/811", "pm_score": 2, "selected": false, "text": "<p>First off, it depends on which test - blood draw for antibodies (past infection), or saliva/nasal swab for current infection.</p>\n<p>Here is an easy-to-understand answer from <a href=\"https://www.health.harvard.edu/diseases-and-conditions/if-youve-been-exposed-to-the-coronavirus\" rel=\"nofollow noreferrer\">Harvard Heath</a>:</p>\n<blockquote>\n<p>&quot;If you get the nasal/throat swab or saliva test, you will get a false negative test result:</p>\n<ul>\n<li>100% of the time on the day you are exposed to the virus. (There are so few viral particles in your nose or saliva so soon after infection that the test cannot detect them.)</li>\n<li>About 40% of the time if you are tested four days after exposure to the virus.</li>\n<li>About 20% of the time if you develop symptoms and are tested three days after those symptoms started.\nThis possibility of a false negative test result is why anyone who has symptoms that could be due to COVID-19, or has been exposed to someone known to be infected, must isolate even if they test negative for coronavirus.&quot;</li>\n</ul>\n</blockquote>\n" } ]
2020/03/13
[ "https://health.stackexchange.com/questions/21337", "https://health.stackexchange.com", "https://health.stackexchange.com/users/12423/" ]
21,342
<p>I have been hearing a lot of people say that it is recommended to wash your hands thoroughly in order to maximise protection against COVID-19 infection. I also heard that the washing hands rumours are just a way to make people believe that they are protecting themselves and that the washing hands thing is actually not backed up by real data. </p> <p><strong>Question:</strong> </p> <blockquote> <p>Is washing hands really that useful? And if yes, is there any data backed up to defend this?</p> </blockquote> <p>The reason i'm asking this is because an expert in this field said that the "data is very week behind this" and "it's not going to have a big impact on preventing infection" (<a href="https://www.youtube.com/watch?v=E3URhJx0NSw" rel="noreferrer">https://www.youtube.com/watch?v=E3URhJx0NSw</a>) 43:32 and that the data behind the virus being infected through the eyes is very sparse (<a href="https://www.youtube.com/watch?v=E3URhJx0NSw" rel="noreferrer">https://www.youtube.com/watch?v=E3URhJx0NSw</a>) 44:00</p>
[ { "answer_id": 21345, "author": "Albrecht Hügli", "author_id": 17790, "author_profile": "https://health.stackexchange.com/users/17790", "pm_score": 2, "selected": false, "text": "<p>There are obvious sufficient data and enough evidence that all virus are transmitted by droplet infection (body contact) and shake hands. Washing hand makes sense as the infection is happening mostly yourself if you have contact with your hands in your face, mouth, nose, eyes.</p>\n\n<p>So don't shake hands, clean your hands by washing or desinfecting after touching the cars and bags in a supermarket or any other objects, as you can transport a virus with your hands in body openings - as everybody touches his face may be 100's of times a day unconsciously. </p>\n\n<p><a href=\"https://www.healthline.com/health-news/how-to-not-touch-your-face\" rel=\"nofollow noreferrer\">https://www.healthline.com/health-news/how-to-not-touch-your-face</a></p>\n\n<p>In normal times we can be overprotective to ourselves. \"More dirt\" could be an option or devise in education, but not in times when schools and kinder gardens have to be closed because of an epidemia or a pandemia. </p>\n\n<p><a href=\"https://www.medscape.com/viewarticle/926373\" rel=\"nofollow noreferrer\">https://www.medscape.com/viewarticle/926373</a></p>\n" }, { "answer_id": 21358, "author": "Mariah", "author_id": 17341, "author_profile": "https://health.stackexchange.com/users/17341", "pm_score": 3, "selected": false, "text": "<p>Yes, the virus can be made un-harmful by soap and water. From the Economist:</p>\n\n<blockquote>\n <p>The outer proteins sit athwart a membrane provided by the cell in\n which the virion was created. This membrane, made of lipids, breaks up\n when it encounters soap and water, which is why hand-washing is such a\n valuable barrier to infection.</p>\n</blockquote>\n\n<p>This should give you enough key terms to read further about why this is effective.</p>\n" }, { "answer_id": 21384, "author": "aparente001", "author_id": 402, "author_profile": "https://health.stackexchange.com/users/402", "pm_score": 4, "selected": true, "text": "<p>Here's an <a href=\"https://www.theguardian.com/commentisfree/2020/mar/12/science-soap-kills-coronavirus-alcohol-based-disinfectants\" rel=\"noreferrer\">article</a> that I found helpful, to understand why washing hands with soap is so helpful, and how it helps (Pall Thordarson is a professor of chemistry at the University of New South Wales, Sydney):</p>\n\n<blockquote>\n <p>Why does soap work so well on the Sars-CoV-2, the coronavirus and\n indeed most viruses? The short story: because the virus is a\n self-assembled nanoparticle in which the weakest link is the lipid\n (fatty) bilayer. Soap dissolves the fat membrane and the virus falls\n apart like a house of cards and dies – or rather, we should say it\n becomes inactive as viruses aren’t really alive.</p>\n \n <p>The slightly longer story is that most viruses consist of three key\n building blocks: ribonucleic acid (RNA), proteins and lipids. A\n virus-infected cell makes lots of these building blocks, which then\n spontaneously self-assemble to form the virus. Critically, there are\n no strong covalent bonds holding these units together, which means you\n do not necessarily need harsh chemicals to split those units apart.\n When an infected cell dies, all these new viruses escape and go on to\n infect other cells. Some end up also in the airways of lungs.</p>\n \n <p>When you cough, or especially when you sneeze, tiny droplets from the\n airways can fly up to 10 metres. The larger ones are thought to be the\n main coronavirus carriers and they can go at least two metres.</p>\n \n <p>These tiny droplets end on surfaces and often dry out quickly. But the\n viruses remain active. Human skin is an ideal surface for a virus. It\n is “organic” and the proteins and fatty acids in the dead cells on the\n surface interact with the virus.</p>\n \n <p>When you touch, say, a steel surface with a virus particle on it, it\n will stick to your skin and hence get transferred on to your hands. If\n you then touch your face, especially your eyes, nostrils or mouth, you\n can get infected. And it turns out that most people touch their face\n once every two to five minutes.</p>\n \n <p>Washing the virus off with water alone might work. But water is not\n good at competing with the strong, glue-like interactions between the\n skin and the virus. Water isn’t enough.</p>\n \n <p>Soapy water is totally different. Soap contains fat-like substances\n known as amphiphiles, some of which are structurally very similar to\n the lipids in the virus membrane. The soap molecules “compete” with\n the lipids in the virus membrane. This is more or less how soap also\n removes normal dirt from the skin.</p>\n \n <p>The soap not only loosens the “glue” between the virus and the skin\n but also the Velcro-like interactions that hold the proteins, lipids\n and RNA in the virus together.</p>\n \n <p>Alcohol-based products, which pretty much includes all “disinfectant”\n products, contain a high-percentage alcohol solution (typically 60-80%\n ethanol) and kill viruses in a similar fashion. But soap is better\n because you only need a fairly small amount of soapy water, which,\n with rubbing, covers your entire hand easily. Whereas you need to\n literally soak the virus in ethanol for a brief moment, and wipes or\n rubbing a gel on the hands does not guarantee that you soak every\n corner of the skin on your hands effectively enough.</p>\n \n <p>So, soap is the best, but do please use alcohol-based sanitiser when\n soap is not handy or practical.</p>\n</blockquote>\n" }, { "answer_id": 21535, "author": "cowlinator", "author_id": 17909, "author_profile": "https://health.stackexchange.com/users/17909", "pm_score": 2, "selected": false, "text": "<p>\"Situations Leading to Reduced Effectiveness of Current Hand Hygiene against Infectious Mucus from Influenza Virus-Infected Patients\", a study published in \"MSphere\", compared using \"antiseptic hand rubbing\" (hand sanitizer) against \"antiseptic hand washing\" (washing hands with antiseptic or antimicrobial soap), and found that washing hands is effective at killing the Influenza A virus.</p>\n\n<p>\"Reducing viral contamination from finger pads: handwashing is more effective than alcohol-based hand disinfectants\", a study published in the \"Journal of Hospital Infection\", found that hand washing for 30 seconds is effective against MNV1 and noroviruses.</p>\n\n<p>\"Epidemiologic Background of Hand Hygiene and Evaluation of the Most Important Agents for Scrubs and Rubs\", a study published in \"Clinical Microbiology Reviews\", found that \"simple hand wash reveals the best results compared with other possible hand treatments\".</p>\n\n<p>I believe that these findings, plus other research, have been generalized to all viruses, including COVID-19.</p>\n" }, { "answer_id": 21581, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 1, "selected": false, "text": "<p>There is a report from Taiwan where it was described that installing hand wash stations in the emergency department was the only infection control measure which was significantly associated with the protection from healthcare workers from acquiring the SARS-CoV, indicating that hand hygiene can have a protective effect</p>\n<blockquote>\n<p>Healthcare workers are at risk of acquiring a SARS infection while caring for SARS patients. Many rational ICMs were implemented to protect HCWs during the panic of the SARS epidemic. For example, NPIR, PPE, and hand washing were all implemented by each hospital as required by the health department. However, nosocomial transmission still occurred despite the above-mentioned measures [1,5,6,14]. Yen et al. formulated the concept of traffic control, an integrated infection control strategy involving triaging patients (using barriers and zones of risk) and checkpoint spots for hand washing [7]. Traffic control was shown to significantly reduce the rate of SARs in HCWs (0.03 cases/bed vs HCWs in other hospitals 0.13 cases/bed) during the 3-week study period [7]. However, there were limitations in the study; the authors were unable to demonstrate that traffic control was the key factor in reducing the number of HCWs acquiring the SARS infection. Understanding the causal relationship is important to validate the effectiveness of each ICM among so many integrated measures.</p>\n<p>Our analysis showed that the timing of the ICM implementation was critically important. Hospitals in which HCW SARS transmission did not occur implemented ICM B earlier than those experiencing SARS transmission to HCWs (Figure 1). The hypothetical causal relationship model between the ICMs and the HCWs acquiring SARS was supported by our SEM analysis in which the following ICMs were the causes of preventing SARS transmission: traffic control in the ED (including triage on patients with fever of unknown aetiology, increasing installation of hand washing facilities in the ED, bleach disinfection performed after cross-contact in patient transfer, and mandatory body temperature surveillance), installation of a fever screening station outside the ED, availability of an outbreak standard operation protocol, mandatory body temperature surveillance in hospital, hand washing setup at each checkpoint in the hospital, standardized patient transfer procedure, availability of a simplified isolation room. It appears that successful control of SARS infection is not based on an individual measure, but on the integration of several measures.</p>\n<p>Installation of a fever screening station outside the ED was the most important factor, and contributed 51% of the effectiveness towards the prevention of SARs in HCWs. During the SARS epidemic, as patients overwhelmingly flooded into hospitals and caused chaos within the ED [6,18] it was rational for each hospital to screen the patients outside the hospital. The outside fever screening station was first developed by the Singaporeans [19]; this was done in accordance with the ancient concept of quarantine against the black plague during the 14th century. Our finding quantitatively validated this approach. The fever screening station acted as the security guard in the front line of protection.</p>\n<p>The second most important factor was the traffic control measures in the ED (19%). HCWs in the ED are at the front line of contact with SARS patients and the most likely to be infected [6,18,20]. The environmental survey also found a high sample positive rate for SARS coronavirus RNA in the ED [6]. Our finding validated the need to protect HCWs in the ED using traffic control, as this is an important factor for protecting all HCWs from hospital-acquired SARS. The retrospective observation also confirmed our finding that the nosocomial transmission of SARS in Taiwan declined significantly after the implementation of traffic control in the ED of hospitals as mandated by the Department of Health. By implementing traffic control in the ED, direct contact of SARS patients and contamination of the environment can be minimized by screening patients with fever, transferring and isolating patients, and disinfecting the environment.</p>\n<p>Hospital management is important since it affects the other factors associated with protecting HCWs from SARS, including availability of outbreak standard operation protocols (12%), mandatory body temperature surveillance in hospital (9%), hand washing setups at each checkpoint in hospital (3%), availability of a simplified isolation room (3%), and standardized patient transfer protocols (3%). During the SARS epidemic, body temperature measurement and hand washing were encouraged spontaneously, and the compliance rate was higher during the non-epidemic period. Standardized outbreak control and patient transfer procedures were part of the hospital standard operation protocols. Hospitals with better management are less likely to have HCWs acquiring SARS or any other nosocomial infections. The Six Sigma process may be implemented into the hospital infection control procedures to prevent further unknown infections [21–23].</p>\n</blockquote>\n<p><a href=\"https://www.journalofhospitalinfection.com/article/S0195-6701(20)30046-3/fulltext\" rel=\"nofollow noreferrer\">https://www.journalofhospitalinfection.com/article/S0195-6701(20)30046-3/fulltext</a></p>\n<p>Quantitative evaluation of infection control models in the prevention of nosocomial transmission of SARS virus to healthcare workers: Implication to nosocomial viral infection control for healthcare workers\n<a href=\"https://www.tandfonline.com/doi/full/10.3109/00365540903582400\" rel=\"nofollow noreferrer\">https://www.tandfonline.com/doi/full/10.3109/00365540903582400</a></p>\n" } ]
2020/03/13
[ "https://health.stackexchange.com/questions/21342", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17807/" ]
21,353
<p>According to the World Health Organization's <a href="https://www.who.int/docs/default-source/coronaviruse/20200312-sitrep-52-covid-19.pdf" rel="nofollow noreferrer">situation report</a> for March 12th, the African region has only recorded 51 cases of the Covid-19 virus, and only one of these cases has been fatal. The disease has so far only been recorded in 9 of the 54 African countries, with only three of these countries reporting more than a couple of cases.</p> <p>Given the wider spread of the disease in practically every other region, and that the African population is around 1.3 billion, this appears to be a clear anomaly.</p> <p>What reasons are there for this apparent inconsistency with expectations?</p>
[ { "answer_id": 21378, "author": "DrMcCleod", "author_id": 17521, "author_profile": "https://health.stackexchange.com/users/17521", "pm_score": 3, "selected": false, "text": "<p>Health care in many sub-Saharan African countries is extremely sparse. As an example, Sierra Leone has <a href=\"https://www.pbs.org/wgbh/nova/article/ebola-doctors/\" rel=\"noreferrer\">less than 250 doctors for the entire country</a>.\nAs a result, it is likely that cases in that and similar countries are grossly under-reported.</p>\n" }, { "answer_id": 22978, "author": "Fizz", "author_id": 10980, "author_profile": "https://health.stackexchange.com/users/10980", "pm_score": 1, "selected": false, "text": "<p>Additional reason(s): a part of Africa is in the southern hemisphere. The flu season <a href=\"https://www.bbc.com/news/world-africa-52125713\" rel=\"nofollow noreferrer\">starts there next month</a>. South Africa has imposed heavy handed measures in the hope of preventing an outbreak, e.g.:</p>\n<blockquote>\n<p>Of course, there have been mistakes, and worse. The police and army have, at times, acted with thuggish abandon in their attempts to enforce the three-week-long lockdown, humiliating, beating, and even shooting civilians on the streets of the commercial capital, Johannesburg, and elsewhere. [...]</p>\n<p>But overall, as South Africans mark their first week under one of the strictest lockdowns introduced anywhere in the world - no jogging outside, no sales of alcohol or cigarettes, no dog-walking, no leaving home except for essential trips and prison or heavy fines for law-breaking - there is an argument to be made that a government so often attacked as corrupt and inefficient, and a private sector so often seen as aloof and greedy, are rising to meet what is widely anticipated to be the greatest challenge this young democracy has ever seen.</p>\n</blockquote>\n" } ]
2020/03/13
[ "https://health.stackexchange.com/questions/21353", "https://health.stackexchange.com", "https://health.stackexchange.com/users/20998/" ]
21,355
<p>As of March 13, <a href="https://www.nbcmiami.com/news/local/15-new-cases-of-coronavirus-announced-in-florida/2204960/" rel="nofollow noreferrer">45/301 people have tested positive/negative for COVID-19 in Florida</a>. What is the expected false positives/negatives here?</p> <p>UPDATE (March 14): 71/478 from what I consider <a href="http://www.floridahealth.gov/diseases-and-conditions/COVID-19" rel="nofollow noreferrer">the best source</a>.</p>
[ { "answer_id": 21380, "author": "cbeleites unhappy with SX", "author_id": 11479, "author_profile": "https://health.stackexchange.com/users/11479", "pm_score": 1, "selected": false, "text": "<p>See long answer for <a href=\"https://medicalsciences.stackexchange.com/q/21337/7951\">How accurate are coronavirus tests?</a></p>\n\n<p>With the \"worst-case numbers\" from there which I take from the minimum performance requirements the FDA currently uses with an emergency validation to allow labs to quickly implement Covid-19 tests without undergoing the full validation procedure they normally take, we have LR+ ≈ 11 and LR- ≈ 1/20.</p>\n\n<p>The tests may be (and probably are) actually much better.</p>\n\n<p>If we take 71 positive : 478 negative tests as a surrogate for the prevalence of Covid-19 infected among the tested population (14.5 %), the post-test probabilities of having Covid-19 are</p>\n\n<ul>\n<li><p>71 : 478 * 11 = 781 : 478 ≈ 5 : 3 for those who tested positive, i.e. ≈ 62 % PPV or post-test probability of having Covid-19.<br>\nThus, as many as 38 % of the 71 or 27 <em>could</em> be false positives.</p></li>\n<li><p>71 : 478 * 1/20 = 71 : 9560 ≈ 1 : 135 or 0.7 % post-test probability of nevertheless really having Covid-19.<br>\nI.e. up to maybe 1 false negative case.</p></li>\n</ul>\n\n<hr>\n\n<p>Update: I've updated the linked answer since I've meanwhile found more detailed data on the actual validation performed for several tests. \nMost of them used more than the minimum required sample size, but it's not that 1000s of validation samples were run. (The infamous CDC test got emergency approval after only 13 positive validation cases, though, so even less. But that was beginning of Feb, and they may not have had more test samples available at that time)</p>\n\n<p>If we want to calculate with expected instead of worst-possible performance for e.g. the Thermo Fisher test, LR+ and LR- would be 61 and 1/61, respectively. </p>\n\n<p>PPV would then have been 90 % (7 false positives) and NPV 0.25 % (0 false negatives). </p>\n" }, { "answer_id": 23722, "author": "gotwo", "author_id": 17963, "author_profile": "https://health.stackexchange.com/users/17963", "pm_score": 0, "selected": false, "text": "<p>The published numbers probably based on the <a href=\"https://en.wikipedia.org/wiki/Reverse_transcription_polymerase_chain_reaction\" rel=\"nofollow noreferrer\">PCR</a> test. About the PCR I has found some information few time ago.</p>\n\n<p>At first it is to consider that there is only a certain period in which a sample from a certain area shows results in the PCR. For throat swab samples <a href=\"https://pubs.rsna.org/doi/10.1148/radiol.2020200642\" rel=\"nofollow noreferrer\">was found</a> that it can take <strong>4 to 8 days</strong> for an existing infection to be displayed with PCR. The time period in which the test remains positive is limited to <strong>4 to 15 days</strong>, although the disease continued to develop. <a href=\"https://www.medrxiv.org/content/10.1101/2020.02.11.20021493v2.full.pdf\" rel=\"nofollow noreferrer\">Now</a> nasal samples are recommended before taking a throat swab, but there will also be a suitable period for sampling.</p>\n\n<p>In expansion, how accurate are the PCR tests in the period in which the tests should reliable be positive. There is a <a href=\"https://link.springer.com/content/pdf/10.1007/s11427-020-1661-4.pdf\" rel=\"nofollow noreferrer\">study</a> in which PCR tests were carried out daily. There is shown that inside of period with positive results, some tests produced a negative result.\nThe days only from first day with a positive result to the last day with a positive result gives a total period of 84 days over all patients. During this time, also 11 tests with negative results were produced. This gives a value of <strong>13.7%</strong> negative test results, even though the patient was infected with COVID-19.</p>\n\n<p>It must be noted that PCR testing is not a simple yes/no test. The result first depends whether a sufficient number of viruses is obtained.</p>\n\n<ul>\n<li>As written above, it is important to choose the correct region of body.</li>\n<li>It must be the relevant time at which the viruses are in the selected region.</li>\n<li>The sample must be obtained in the correct manner.</li>\n<li>The viral load in the patient himself has to be suffice (<a href=\"https://www.medrxiv.org/content/10.1101/2020.03.24.20042689v1\" rel=\"nofollow noreferrer\">medrxiv.org</a>)</li>\n</ul>\n\n<p><a href=\"https://academic.oup.com/clinchem/advance-article/doi/10.1093/clinchem/hvaa099/5819547\" rel=\"nofollow noreferrer\">Here</a> is described that for a number of 484 copies of SARS-CoV-2 RNA per milliliter some PCR test products detect SARS-CoV-2 with <strong>100%</strong> but one other of the approved products detects <strong>0%</strong> of virus.</p>\n\n<p>So there is not the one accuracy. It is to be asked which type of test kit was used by which manufacturer, who took how the sample, etc. Every single item can significantly impact the accuracy of a test.</p>\n" } ]
2020/03/13
[ "https://health.stackexchange.com/questions/21355", "https://health.stackexchange.com", "https://health.stackexchange.com/users/9517/" ]
21,357
<p>The COVID-19 R0 factor is 2-3, while SARS had an R0 factor of 2-5. However, COVID-19 has infected around 130,000 people and growing, while SARS totalled just under 9000 people infected.</p> <p>Why is COVID-19 spreading faster and wider than SARS? What other factors have let COVID-19 reach pandemic levels, while SARS was contained and eradicated? Could the R0 factor be higher than believed? Was it initially slower to be contained?</p> <p>Full disclosure, I'm not in medicine or a medical scientist. I'm a software developer and data scientist, and this has piqued my interested in the spread of infectious disease.</p>
[ { "answer_id": 21359, "author": "Mariah", "author_id": 17341, "author_profile": "https://health.stackexchange.com/users/17341", "pm_score": 2, "selected": false, "text": "<p>It is possible that with SARS fewer people were transmitting the virus, but those who were were \"super-spreaders\". R_0 is an average of those transmitting.</p>\n\n<p>Source:</p>\n\n<p><a href=\"http://www.cidrap.umn.edu/news-perspective/2020/01/data-suggest-ncov-more-infectious-1918-flu-what-does-mean\" rel=\"nofollow noreferrer\">http://www.cidrap.umn.edu/news-perspective/2020/01/data-suggest-ncov-more-infectious-1918-flu-what-does-mean</a></p>\n\n<p>Another possibility is that the high mortality rate in SARS actually prevented it from spreading widely.</p>\n\n<p>Source:</p>\n\n<p><a href=\"http://nautil.us/issue/83/intelligence/the-man-who-saw-the-pandemic-coming\" rel=\"nofollow noreferrer\">http://nautil.us/issue/83/intelligence/the-man-who-saw-the-pandemic-coming</a></p>\n" }, { "answer_id": 21422, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 3, "selected": false, "text": "<p>The viruses are acting differently. SARS-CoV-2 virus is much more infectious with a much higher viral replication rate, and with people exhaling the virus in the pre-symptomatic phase whereas SARS this was not happening. Once the infected individual becomes symptomatic their bodies are producing antibodies which helps shut down viral particle shedding though virus is still being transmitted by cough which aerolizes the virus at a further distance then just by exhalation.</p>\n<blockquote>\n<p>The nine patients, who were admitted to the same Munich hospital, were studied because they had had close contact with an index case. Cell cultures and real-time polymerase chain reaction (RT-PCR) were done on throat swabs and samples of sputum, stool, blood, and urine. Throat swabs showed very high viral shedding during the first week of symptoms.</p>\n<p>The findings contrasted starkly with those from the 2003 outbreak of SARS in terms of viral load. &quot;In SARS, it took 7 to 10 days after onset until peak RNA concentrations (of up to 5x105 copies per swab) were reached,&quot; the researchers wrote. &quot;In the present study, peak concentrations were reached before day 5, and were more than 1,000 times higher.&quot;</p>\n</blockquote>\n<p>but the mean incubation period is 5 days.</p>\n<p><a href=\"http://www.cidrap.umn.edu/news-perspective/2020/03/study-highlights-ease-spread-covid-19-viruses\" rel=\"noreferrer\">http://www.cidrap.umn.edu/news-perspective/2020/03/study-highlights-ease-spread-covid-19-viruses</a></p>\n" } ]
2020/03/13
[ "https://health.stackexchange.com/questions/21357", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17812/" ]
21,364
<p>It is recommended to regularly wash hands with soap to slow the spread of COVID-19. However regularly washing with soap can be harmful to the skin. Soap-free cleansers such as QV Wash are frequently used in place of soap by those with dermatological conditions.</p> <p>How effective are soap-free cleansers are at slowing the spread of COVID-19?</p>
[ { "answer_id": 21455, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 2, "selected": false, "text": "<p>You need a molecule that disrupts the lipid layer of the virus to expose its RNA, and deactivate it.</p>\n<p>Until the manufacturer of QV Wash can confirm that it is capable of inactivating viruses, in particular the sars2-ncov-19 virus, then you should assume it won't work.</p>\n<blockquote>\n<p>When you wash your hands with soap and water, you surround any microorganisms on your skin with soap molecules. The hydrophobic tails of the free-floating soap molecules attempt to evade water; in the process, they wedge themselves into the lipid envelopes of certain microbes and viruses, prying them apart.</p>\n<p>“They act like crowbars and destabilize the whole system,” said Prof. Pall Thordarson, acting head of chemistry at the University of New South Wales. Essential proteins spill from the ruptured membranes into the surrounding water, killing the bacteria and rendering the viruses useless.</p>\n</blockquote>\n<p><a href=\"https://www.nytimes.com/2020/03/13/health/soap-coronavirus-handwashing-germs.html\" rel=\"nofollow noreferrer\">https://www.nytimes.com/2020/03/13/health/soap-coronavirus-handwashing-germs.html</a></p>\n" }, { "answer_id": 22999, "author": "gmatht", "author_id": 17819, "author_profile": "https://health.stackexchange.com/users/17819", "pm_score": 0, "selected": false, "text": "<p>According to my local pharmacy anything that foams up (as QV Wash does) should work.</p>\n\n<p>When queried as to the effectiveness of QV Wash in preventing COVID-19 the manufacturers responded:</p>\n\n<blockquote>\n <p>Our QV cleansers are pH balanced, soap-free products designed for use on sensitive skin. As such, they are as effective as 'soap' for hand hygiene, but gentler on the skin.</p>\n</blockquote>\n" } ]
2020/03/14
[ "https://health.stackexchange.com/questions/21364", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17819/" ]
21,368
<p>An early measure to avoid the spread of COVID-19 has been the cancellations of flights from infected zones, e.g.: <a href="https://www.reuters.com/article/health-coronavirus-spain-flights/corrected-spain-cancels-flights-from-italy-for-two-weeks-in-a-bid-to-stop-coronavirus-idUSE8N29W006" rel="nofollow noreferrer">https://www.reuters.com/article/health-coronavirus-spain-flights/corrected-spain-cancels-flights-from-italy-for-two-weeks-in-a-bid-to-stop-coronavirus-idUSE8N29W006</a></p> <p>(I wonder about the effectiveness, specificity, and sensibility of such measures, for instance, if I am a tourist that has been barely in contact with locals, it should be better to go back home, in isolation if necessary. But that is a different question)</p> <p>However, surface connection has not been cancelled, and I could go back from Italy to Spain driving or by train. Also ships continue travelling, although maybe moving from Europe to US would not be that practical...</p> <p>Is there a purely epidemiological reason why air transport is inherently more prone to contagions, or otherwise more dangerous? Or is it just that it is easier for a government to close airports than roads?</p>
[ { "answer_id": 21373, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 0, "selected": false, "text": "<p>Air transport has been cancelled in different countries differently. In the US, they cancelled all air transport from EU. In several EU countries only air transport from China, Iran and Italy (countries with moth infections and deaths) has been cancelled. In Europe, initially most infections were spread from Italy.</p>\n\n<p>Countries that border to Italy have severely restricted land transport from Italy. Austria has completely closed the border. Some countries do not accept trucks that come from Italy.</p>\n" }, { "answer_id": 25276, "author": "Allure", "author_id": 12423, "author_profile": "https://health.stackexchange.com/users/12423", "pm_score": 1, "selected": false, "text": "<p>Flights are much faster than cars/trains/boats. In turn, that means COVID spreads slower if cars/trains/boats are the only viable means of transport. It also means that COVID spreads in a connected way: if there was no air travel for example, you would not expect to see COVID in Europe before it hits Western Asia. With it, Europe can be affected first.</p>\n<p>Compare e.g. what happened with the Black Death. During that time when the fastest means of travel was by horse, it took several years for the disease to spread around Europe, and it never actually reached China. These days, it only took a few weeks for the disease to get from China to Europe, and then around the world.</p>\n" } ]
2020/03/14
[ "https://health.stackexchange.com/questions/21368", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17823/" ]
21,372
<p>There is a public figure/writer on the Internet which plays a sort of "informal journalist", who stated in a tweet (without a source), that "Italy is hit hard, experts say, because they have the oldest population in Europe."</p> <p>Now this can be interpreted in two ways. That death rates are higher because of this (it makes sense), or that the disease is spread faster because of this. Could this last idea be true?</p> <p>Is an old population a contributing factor for the spread of the disease, or does the disease infect younger and older populations in the same way?</p>
[ { "answer_id": 21375, "author": "Jan", "author_id": 3002, "author_profile": "https://health.stackexchange.com/users/3002", "pm_score": 2, "selected": true, "text": "<p>There are some theories that the COVID-19 outbreak started in hospitals (<a href=\"https://www.vox.com/2020/3/10/21171217/coronavirus-covid-19-italy-hospitals\" rel=\"nofollow noreferrer\">VOX, March 13, 2020</a>):</p>\n\n<blockquote>\n <p>Another theory is that intense spread of the virus in the hospital\n system, before doctors realized there was a problem, may have\n amplified the outbreak. Some 10 percent of medical workers in Lombardy\n have been infected, according to a March 3 Washington Post report, and\n health workers account for 5 percent of those infected in the country.</p>\n</blockquote>\n\n<p>In hospitals, in general, there are more older people.</p>\n\n<p>There were also several cases of quick spread of infection in nursing homes.</p>\n\n<p>Hospitals and nursing homes are environments where people live close together, so this is why infection can spread quickly among older people.</p>\n\n<p>Younger people get infected in schools, when they travel to areas with lot of infected people and when they engage in contact sports, for example.</p>\n\n<p>One of the reasons for a lot of cases in Italy is that they didn't act quickly when the inefction started.</p>\n" }, { "answer_id": 21405, "author": "y.s lee", "author_id": 17759, "author_profile": "https://health.stackexchange.com/users/17759", "pm_score": 0, "selected": false, "text": "<p>Although COVID-19 spreads among young people with active social activities, the mortality rate of young people is extremely small. However, the elderly who have relatively little social activity have a high mortality rate.</p>\n\n<p>Italy is the world's second-largest country with the highest proportion of elderly people, so it has a relatively large number of deaths compared to the number of infected people.</p>\n" }, { "answer_id": 21426, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 0, "selected": false, "text": "<p>The issue is as you state that Italy has a very high elderly population, something like 23% whereas in China it is only 12%. Death rates have been high amongst the elderly.</p>\n\n<blockquote>\n <p>Italy has had 12 462 confirmed cases according to the Istituto Superiore di Sanità as of March 11, and 827 deaths. Only China has recorded more deaths due to this COVID-19 outbreak. The mean age of those who died in Italy was 81 years and more than two-thirds of these patients had diabetes, cardiovascular diseases, or cancer, or were former smokers. It is therefore true that these patients had underlying health conditions, but it is also worth noting that they had acute respiratory distress syndrome (ARDS) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia, needed respiratory support, and would not have died otherwise. Of the patients who died, 42·2% were aged 80–89 years, 32·4% were aged 70–79 years, 8·4% were aged 60–69 years, and 2·8% were aged 50–59 years (those aged >90 years made up 14·1%). The male to female ratio is 80% to 20% with an older median age for women (83·4 years for women vs 79·9 years for men).</p>\n</blockquote>\n\n<p><a href=\"https://www.wsj.com/articles/italy-with-elderly-population-has-worlds-highest-death-rate-from-virus-11583785086\" rel=\"nofollow noreferrer\">https://www.wsj.com/articles/italy-with-elderly-population-has-worlds-highest-death-rate-from-virus-11583785086</a></p>\n\n<p><a href=\"https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30627-9/fulltext\" rel=\"nofollow noreferrer\">https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30627-9/fulltext</a></p>\n" } ]
2020/03/14
[ "https://health.stackexchange.com/questions/21372", "https://health.stackexchange.com", "https://health.stackexchange.com/users/7049/" ]
21,374
<p>For example: during the current covid 19 outbreak the reported numbers are number of infections after various measures like social distancing or quarantine have been used - so it doesn't make much sense to compare it to the r0 if a disease like flu, where similar measures aren't used.</p> <p>Is there an objective measurement? Something like what are the chances of getting infected in some controlled conditions</p>
[ { "answer_id": 21408, "author": "y.s lee", "author_id": 17759, "author_profile": "https://health.stackexchange.com/users/17759", "pm_score": -1, "selected": false, "text": "<p>I don't think it makes any sense to discuss such a part now. Although there have been sars and mers, covid-19 is the first virus it encounters, and it takes a long time for the data to be properly cleaned up. That is why it is most accurate to interpret it based on what is currently being presented. The power that covid-19 spreads is the most powerful when compared to the infectious diseases we have encountered so far. In general, it can be spread by talking about 5 minutes in or around 1m, but there are reports that have been spread even less than the circumstances.</p>\n" }, { "answer_id": 21449, "author": "Mark", "author_id": 333, "author_profile": "https://health.stackexchange.com/users/333", "pm_score": 2, "selected": false, "text": "<p><a href=\"https://en.wikipedia.org/wiki/Basic_reproduction_number\" rel=\"nofollow noreferrer\">R0 <em>is</em> the objective measure you're looking for</a>.</p>\n\n<p>The \"basic reproduction number\", R0, is the rate of rate of spread independent of any external factors such as quarantine or social distancing. You appear to be confusing it with R, the \"effective reproduction number\", which measures the rate of spread after countermeasures and population immunity have been applied.</p>\n" }, { "answer_id": 21609, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 2, "selected": true, "text": "<p>R0 is the basic reproduction number describing how many cases are expected to be infected by a single case. This value is not a biological constant.</p>\n<blockquote>\n<p>With an R0 (reproduction number) estimated at 2.5 (based on China), many experts predict that between 20 and 60% of the world population could get infected (which means at least 0.5M deaths).</p>\n<p>However, the R0 varies during the course of an epidemic as a result of a series of determinants and interventions</p>\n</blockquote>\n<p>such as containment and mitigation factors, and eventually herd immunity and vaccination.</p>\n<p><a href=\"https://www.isglobal.org/en/coronavirus-lecciones-y-recomendaciones\" rel=\"nofollow noreferrer\">https://www.isglobal.org/en/coronavirus-lecciones-y-recomendaciones</a></p>\n" } ]
2020/03/14
[ "https://health.stackexchange.com/questions/21374", "https://health.stackexchange.com", "https://health.stackexchange.com/users/17827/" ]
21,401
<p>I just got back from the Netherlands and read a notice on the CDC web site that says I "must" self quarantine for 14 days.</p> <p>I guess I don't understand. I think the Netherlands has 2 cases and my home state of New Hampshire has 6. So, the logic is what? I am potentially infected and the rest of New Hampshire is not. I mean if New Hampshire has more cases than the Netherlands, doesn't that mean every one of the 1.4 million people in New Hampshire should "self quarantine"?</p> <p>What is the logic here?</p> <p><a href="https://i.stack.imgur.com/0WZVy.png" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/0WZVy.png" alt="enter image description here"></a></p>
[ { "answer_id": 21408, "author": "y.s lee", "author_id": 17759, "author_profile": "https://health.stackexchange.com/users/17759", "pm_score": -1, "selected": false, "text": "<p>I don't think it makes any sense to discuss such a part now. Although there have been sars and mers, covid-19 is the first virus it encounters, and it takes a long time for the data to be properly cleaned up. That is why it is most accurate to interpret it based on what is currently being presented. The power that covid-19 spreads is the most powerful when compared to the infectious diseases we have encountered so far. In general, it can be spread by talking about 5 minutes in or around 1m, but there are reports that have been spread even less than the circumstances.</p>\n" }, { "answer_id": 21449, "author": "Mark", "author_id": 333, "author_profile": "https://health.stackexchange.com/users/333", "pm_score": 2, "selected": false, "text": "<p><a href=\"https://en.wikipedia.org/wiki/Basic_reproduction_number\" rel=\"nofollow noreferrer\">R0 <em>is</em> the objective measure you're looking for</a>.</p>\n\n<p>The \"basic reproduction number\", R0, is the rate of rate of spread independent of any external factors such as quarantine or social distancing. You appear to be confusing it with R, the \"effective reproduction number\", which measures the rate of spread after countermeasures and population immunity have been applied.</p>\n" }, { "answer_id": 21609, "author": "Graham Chiu", "author_id": 3414, "author_profile": "https://health.stackexchange.com/users/3414", "pm_score": 2, "selected": true, "text": "<p>R0 is the basic reproduction number describing how many cases are expected to be infected by a single case. This value is not a biological constant.</p>\n<blockquote>\n<p>With an R0 (reproduction number) estimated at 2.5 (based on China), many experts predict that between 20 and 60% of the world population could get infected (which means at least 0.5M deaths).</p>\n<p>However, the R0 varies during the course of an epidemic as a result of a series of determinants and interventions</p>\n</blockquote>\n<p>such as containment and mitigation factors, and eventually herd immunity and vaccination.</p>\n<p><a href=\"https://www.isglobal.org/en/coronavirus-lecciones-y-recomendaciones\" rel=\"nofollow noreferrer\">https://www.isglobal.org/en/coronavirus-lecciones-y-recomendaciones</a></p>\n" } ]
2020/03/16
[ "https://health.stackexchange.com/questions/21401", "https://health.stackexchange.com", "https://health.stackexchange.com/users/5371/" ]