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[ { "answer_id": 16690, "body": "<p>Erectile dysfunction (ED) can be caused by a wide variety of things <a href=\"https://health.stackexchange.com/a/7503\">covered in this answer</a>, but it cannot be caused by eating the kind of foods you are talking about.</p>\n", "score": 0 } ]

[ "sexual-arousal" ]

[ { "answer_id": 17705, "body": "<p>Hernia has a chance of recurring. That's why they use mesh to strengthen the wall and prevent recurrence of hernia. </p>\n\n<p>\"The incidence of recurrent hernia after primary repair of a groin hernia varies from 1% in specialized centers to 30% in general surveys. During the premesh era, it was estimated that primary inguinal hernia repairs had a 10%–30% recurrence rate and that the rate was 35% for recurrent hernia repairs\"</p>\n\n<p><strong>Source:</strong></p>\n\n<p>Recurrence after groin hernia repair-revisited</p>\n\n<p>Sri VengadeshGopal AchuthanWarrier </p>\n\n<p><a href=\"https://www.sciencedirect.com/science/article/pii/S1743919113000873\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/pii/S1743919113000873</a></p>\n", "score": 2 } ]

[ "exercise", "surgery", "hernia" ]

[ { "answer_id": 17762, "body": "<p>The problem here is the over-simplified (and inaccurate) idea that Thiomersal = mercury, it's <strong>not</strong>, rather it is a compound (chemical formula: C₉H₉HgNaO₂S) that has mercury atoms in it's molecules, the mercury vapors (Hg) are a different thing, chemically speaking.</p>\n\n<p>This means that mercury and Thiomersal will behave very differently in chemical terms, Thiomersal is metabolised by the body into <a href=\"https://en.wikipedia.org/wiki/Ethylmercury\" rel=\"noreferrer\">ethylmercury</a> (C₂H₅Hg+) which is eliminated from both the body and the brain <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1280342/\" rel=\"noreferrer\">relatively quickly</a> and does not bioaccumulate. Unlikle <a href=\"https://en.wikipedia.org/wiki/Methylmercury\" rel=\"noreferrer\">methylmercury</a> (CH₃Hg+) which is the organic mecury formed from inorganic mercury sources such as the aforementioned mercury vapors or ingesting liquid mercury) which stays in the body up to five times longer (offering significant opportunity for bioaccumulation in the food chain - most human exposure to methylmercury comes from eating fish such as swordfish, big-eye tuna and king mackerel).</p>\n\n<p>While Thiomersal itself can be quite toxic itself (which of course is exactly why it works so well as a preservative) as the old axiom states \"the dose maketh the poison\" and you need <em>much</em> higher doses that what is contained in vaccines to create adverse health effects in humans. And with the fact that it is eliminated completely from the body and doesn't bioaccumulate it's not a case that you need to worry about any cumulative effects.</p>\n\n<p>The removal of Thiomersal from childhood vaccines (it's still in single-vial forms of some flu vaccines) in the US/Europe (some other countries still use the variant of MMR that contains Thiomersal) was prompted (at least in part) by a mistaken presumption that ethylmercury would behave in the body in the same way that methylmercury does. Which we now know not to be the case.</p>\n\n<p>If you were to inject <em>elemental</em> mercury, then you'd be in the same situation as breathing in the vapors - even small doses can be dangerous because it metabolizes in to methylmercury and bioaccumulates.</p>\n\n<p><strong>NB:</strong> On a related note the distinction between ethyl- and methylmercury is what makes the chelation therapy some quacks/scam artists prescribe for autism to be doubly ineffective (not to mention it's potentially lethal effects!) because not only is autism not caused by mercury-poisoning but the mercury they are trying to chelate out is no longer even in the body in the first place!</p>\n", "score": 9 } ]

[ "brain", "injections", "mercury" ]

[ { "answer_id": 18054, "body": "<p><a href=\"https://www.mollersomega3.nl/mollers_en/fish-oil/omega-3?___store=mollers_en\" rel=\"nofollow noreferrer\">The omega-3 supplement provider</a> claims that omega-3 fatty acid supplements are important for proper functioning of the heart and brain, among other.</p>\n\n<p>This review <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483717/\" rel=\"nofollow noreferrer\">Reduction of heart rate by omega-3 fatty acids and the potential underlying mechanisms (PubMed, 2012)</a> concludes:</p>\n\n<blockquote>\n <p>Recent human and animal studies have shown that omega-3 fatty acids\n can reduce heart rate.</p>\n</blockquote>\n\n<p>In <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/16616012\" rel=\"nofollow noreferrer\">one small 2006 study in men with myocardial infarct</a>, omega-3 fatty acids decreased heart rate at rest from 73 +/- 13 to 68 +/- 13 beats/min. </p>\n\n<p>But this alone are just some dry statistical facts. For anyone with a high heart rate of an unknown origin, I strongly suggest to get a diagnosis from a heart specialist before starting any treatment, including omega-3 supplements. The treatment choice largely depends on the cause. </p>\n", "score": 3 } ]

[ "nutrition", "supplement" ]

[ { "answer_id": 19576, "body": "<p>On the <strong>chemical level,</strong> the toxicity of ethanol is mainly mediated by its breakdown product acetaldehyde. Alcohol is metabolized like this:</p>\n\n<p>ethanol &rightarrow; acetaldehyde &rightarrow; acetate &rightarrow; acetylCoA &rightarrow; CO₂ + water</p>\n\n<p>When alcohol is drunk in small amounts, acetaldehyde is quickly metabolized to CO₂ and water, but when drunk in large amounts, the greater amounts of acetaldehyde can damage the cells, mainly in the liver, pancreas, brain and heart.</p>\n\n<p>Alcohol breakdown also results in the creation of reactive oxygen species, such as hydrogen peroxide, which together with acetaldehyde attack certain parts of the cells. The damaged cells attract neutrophils, which, in the attempt to clean the mess, can cause further damage (more details in the <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3959903/\" rel=\"nofollow noreferrer\">Journal of Hepatology</a> and in <a href=\"https://www.youtube.com/watch?v=RudR2_VVoaw\" rel=\"nofollow noreferrer\">this nice video</a>).</p>\n\n<p>Alcohol breakdown also results in an increase of NADH and depletion of NAD, which stimulates fatty acid synthesis. </p>\n\n<p>On the <strong>tissue level,</strong> the stages of alcoholic liver damage are fat accumulation (steatosis), inflammation (hepatitis), cell death (necrosis) and conversion to fibrous tissue (fibrosis and cirrhosis). Chronic alcohol consumption also increases the risk for cancer of the mouth, throat, esophageus, colon, liver and breast (<a href=\"https://www.cdc.gov/cancer/alcohol/index.htm\" rel=\"nofollow noreferrer\">CDC. gov</a>).</p>\n\n<p>On the <strong>functional level,</strong> alcohol can kill you due to:</p>\n\n<ul>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532397/\" rel=\"nofollow noreferrer\">Brain impairment</a>:\n\n<ul>\n<li>Bleeding in the brain</li>\n<li>Depression of the cardiorespiratory centers in the brainstem</li>\n<li>Wernicke-Korsakoff syndrome due to alcohol-related vitamin B1 deficiency</li>\n<li>Hepatic encephalopathy caused by excessive amount of ammonia in the blood in advanced liver cirrhosis</li>\n</ul></li>\n<li>Heart failure:\n\n<ul>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/3711541\" rel=\"nofollow noreferrer\">Cardiomyopathy</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/9949788\" rel=\"nofollow noreferrer\">Irregular heart rhythm</a></li>\n<li><a href=\"https://www.journal-of-hepatology.eu/article/S0168-8278(15)00718-7/pdf\" rel=\"nofollow noreferrer\">Liver failure</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/books/NBK65575/\" rel=\"nofollow noreferrer\">Acute pancreatitis</a></li>\n</ul></li>\n</ul>\n\n<p><strong>How exactly alcohol is damaging?</strong> (See Table 1 in <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952076/\" rel=\"nofollow noreferrer\">this article</a>)</p>\n\n<ul>\n<li>Ethanol:\n\n<ul>\n<li>triggers triglyceride accumulation in the liver cells, which can result in cirrhosis</li>\n<li>causes DNA damage of the stem cells, which can result in cancer</li>\n</ul></li>\n<li>Acetaldehyde:\n\n<ul>\n<li>triggers inflammation, which can contribute to liver fibrosis</li>\n<li>damages DNA</li>\n<li>promotes oxidation of LDL cholesterol, which increases the risk of atherosclerosis</li>\n<li>inactivates clotting factors, which increases the risk of bleeding</li>\n</ul></li>\n</ul>\n\n<p>In conclusion, alcohol does not kill you by causing a chemical reaction with a certain molecule in the body (for example, like <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/3073059\" rel=\"nofollow noreferrer\">cyanide intoxication</a>) but by promoting or inhibiting certain processes that can result in tissue damage.</p>\n", "score": 5 } ]

[ "alcohol", "liver", "death", "alcoholism" ]

[ { "answer_id": 20567, "body": "<p>Firstly many of the radiations that screens produce are massively reduced from a decade ago. The greatest radiation is infra red in the form of heat, this can dry your skin but no more than being in an office that has heating in anyway or watching tv. \n<a href=\"https://www.radiationanswers.org/radiation-blog/is-that-a-laptop-on-your-lap.html\" rel=\"nofollow noreferrer\">https://www.radiationanswers.org/radiation-blog/is-that-a-laptop-on-your-lap.html</a></p>\n", "score": 0 }, { "answer_id": 20574, "body": "<p>The important thing is to distinguish between CRT monitors and other more modern technologies.</p>\n\n<p>CRT monitors do emit detectable amounts of X-rays and have an extremely strong EM field as a necessary part of their operation. They also have a \"degauss\" pulse on power-on which is very strong and can damage magnetic media nearby. One of those pages on EM radiation linked to a rat study that was using CRT monitors extremely close to rat cages.</p>\n\n<p>LCD/LED monitors do not have a \"standing\" field as part of their operation, but leak a small amount of EM from high-frequency signals. I do not believe there is any reliably documented harm from this level of EM.</p>\n", "score": 0 } ]

[ "computers", "radiation", "bioelectromagnetics" ]

[ { "answer_id": 21017, "body": "<p><a href=\"https://www.diabetes.org/diabetes/complications\" rel=\"nofollow noreferrer\">American Diabetes Association</a> has a comprehensive list of complications of diabetes type 1 and 2 (most complications can occur in both types). Here are some complications that are quite typical, but not all are specific for diabetes:</p>\n\n<ul>\n<li>Acanthosis nigricans</li>\n<li>Diabetic dermopathy</li>\n<li>Necrobiosis lipoidica diabeticorum</li>\n<li>Eruptive xanthomatosis</li>\n<li>Diabetic retinopathy</li>\n<li>Diabetic cataract</li>\n<li>Diabetic neuropathy with numbness and tingling</li>\n<li>Autonomic neuropathy with bladder and gastrointestinal issues</li>\n<li>\"Diabetic foot\" with skin color changes and ulcers</li>\n<li>Hyperglycemia hyperosmolar state</li>\n<li>Diabetic ketoacidosis</li>\n<li>Diabetic nephropathy</li>\n</ul>\n\n<p>Examples of complications that are common but not specific for diabetes: yeast skin infections, periodontitis, gingivitis, high blood pressure, high cholesterol levels, stroke, ischemic heart disease.</p>\n\n<p><a href=\"https://www.drugs.com/condition/diabetes-mellitus-type-ii.html\" rel=\"nofollow noreferrer\">Drugs.com</a> has a list of 164 drugs (a mixture of generic and brand names), and clicking to each quickly leads you to side effects. </p>\n\n<p><a href=\"https://www.diabetes.co.uk/features/diabetes-medication-side-effects.html\" rel=\"nofollow noreferrer\">Diabetes.co.uk</a> has a short list of side effects of various oral antidiabetic drugs (by groups of drugs):</p>\n\n<ul>\n<li>Sulfonylureas: low blood sugar, upset stomach, skin rash or itching, weight gain</li>\n<li>Biguanides/Metformin: sickness with alcohol, kidney complications, upset stomach, tiredness or dizziness, metal taste</li>\n<li>Alpha-glucosidase inhibitors: gas, bloating and diarrhoea</li>\n<li>Thiazolidinediones: weight gain, risk of liver disease, anaemia risk, swelling of legs or ankles,</li>\n<li>Meglitinides: weight gain, low blood sugar</li>\n</ul>\n\n<p>Here's another <a href=\"https://www.amboss.com/us/knowledge/Antidiabetic_drugs\" rel=\"nofollow noreferrer\">one-page list</a>.</p>\n\n<p>Most of these effects, except hypoglycemia, are quite general. Because diabetic patients often take drugs other than for diabetes, there is a great chance that the side effects of diabetic and nondiabetic drugs will overlap, so I'm not sure if you can associate the symptoms in your database with diabetic drugs with any certainty.</p>\n", "score": 1 } ]

[ "medications", "infection", "diabetes", "type-2-diabetes", "type-1-diabetes" ]

[ { "answer_id": 21297, "body": "<p><a href=\"https://www.arcgis.com/apps/opsdashboard/index.html#/bda7594740fd40299423467b48e9ecf6\" rel=\"nofollow noreferrer\">https://www.arcgis.com/apps/opsdashboard/index.html#/bda7594740fd40299423467b48e9ecf6</a></p>\n\n<blockquote>\n <p>We are tracking the COVID-19 spread in real-time on our interactive dashboard with data available for download. We are also modeling the spread of the virus. Preliminary study results are discussed on our blog.</p>\n</blockquote>\n\n<p>This is by the John Hopkins University.</p>\n", "score": 2 } ]

[ "covid-19", "covid-19-datasets" ]

[ { "answer_id": 21424, "body": "<p>You're missing two points:</p>\n\n<p>First, as of today, <a href=\"https://www.worldometers.info/coronavirus/\" rel=\"nofollow noreferrer\">the Netherlands had 1413 cases</a>.</p>\n\n<p>Second, the Netherlands is part of the <a href=\"https://en.wikipedia.org/wiki/Schengen_Area\" rel=\"nofollow noreferrer\">Schengen Area</a>. Because of the ease of movement within the area, the US government is treating the entire Area as as single unit for quarantine purposes. (Collectively, the area has about 60,000 cases.)</p>\n", "score": 4 }, { "answer_id": 21425, "body": "<p>At this time (17-March-2020) the state of New Hampshire has not found evidence of community transmission of the virus, and all 13 cases are associated with overseas travel.</p>\n\n<p>You have travelled in from overseas where there is community transmission so the possibility is much higher that you have been infected. The infected in the pre-symptomatic phase are still highly contagious spreading virus just by breathing based on small studies so far.</p>\n\n<p>Once community transmission is detected then it may be too late to start isolating people from out of state, and the whole state may need to go into self isolation as was done in China.</p>\n\n<p><a href=\"https://patch.com/new-hampshire/concord-nh/nh-officials-order-all-schools-be-shuttered-due-covid-19\" rel=\"nofollow noreferrer\">https://patch.com/new-hampshire/concord-nh/nh-officials-order-all-schools-be-shuttered-due-covid-19</a></p>\n", "score": 4 } ]

[ "epidemiology" ]

[ { "answer_id": 21690, "body": "<p>Rubella doesn't generally kill that's why they had those parties lacking a vaccine.</p>\n\n<p>Since we are now seeing many ICU beds being occupied by victims in their 30s etc， a different patient profile than in China, then it would be like using Russian roulette doing what you suggest.</p>\n", "score": 3 } ]

[ "covid-19", "immune-system", "weather" ]

[ { "answer_id": 23075, "body": "<p>No, because activity as a feature is too highly variant and there are probably a lot of other factors that would go into a formula like this.</p>\n\n<p>If you do a bit of research you will find that there are guidelines of fluid intake per day for certain groups of patients, e. g. in intensive care, dialysis patients,...: <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/?term=fluid+intake+per+day\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/?term=fluid+intake+per+day</a></p>\n\n<p>The first hit on \"formula fluid intake per day\" produces a hit from the Daily Mail (<a href=\"https://www.dailymail.co.uk/femail/food/article-4617270/How-water-REALLY-drink-day-revealed.html\" rel=\"nofollow noreferrer\">https://www.dailymail.co.uk/femail/food/article-4617270/How-water-REALLY-drink-day-revealed.html</a>), which does not have too high of an impact factor.</p>\n\n<p>The \"8 glasses of water per day\" rule is a one-size-fits-all rule that should not be used on people with e. g. organ damage such as heart failure, renal failure etc.</p>\n", "score": 1 } ]

[ "nutrition", "exercise", "water", "physiology", "hydration" ]

[ { "answer_id": 23634, "body": "<p>This is an emerging area of advice. It really depends on the pre-test probability of COVID-19 in your region, and the urgency of surgery.</p>\n<p>The Royal College of Surgeons, Edinburgh make the following recommendation</p>\n<p>9th April 2020</p>\n<blockquote>\n<p>Patients who present as abdominal emergencies who have an abdominal CT in their diagnostic investigations should also have a Chest CT scan (ref ––Updated General Surgery Guidance on Covid-19 – Intercollegiate / ASGBI 5th April 2020).</p>\n<p>Due to its low sensitivity and the low pre-test probability of disease (Scotland), computed tomography should only be deployed in very specific circumstances</p>\n</blockquote>\n<p>Your pre-test probability may be much higher which might justify CT chest if you don't have time to do rtPCR, and antibody studies.</p>\n<p><a href=\"https://www.rcsed.ac.uk/news-public-affairs/news/2020/april/intercollegiate-guidance-for-pre-operative-chest-ct-imaging-for-elective-cancer-surgery-during-the-covid-19-pandemic\" rel=\"nofollow noreferrer\">https://www.rcsed.ac.uk/news-public-affairs/news/2020/april/intercollegiate-guidance-for-pre-operative-chest-ct-imaging-for-elective-cancer-surgery-during-the-covid-19-pandemic</a></p>\n", "score": 1 } ]

[ "covid-19" ]

[ { "answer_id": 23678, "body": "<p><a href=\"https://www.cdc.gov/rabies/transmission/body.html\" rel=\"nofollow noreferrer\">The CDC points out</a> that:</p>\n\n<blockquote>\n <p>From numerous studies conducted on rabid dogs, cats, and ferrets, we know that when the rabies virus is introduced into a muscle through a bite from another animal, it travels from the site of the bite to the brain by moving within nerves. The animal does not appear ill during this time.</p>\n \n <p>The time between the bite and the appearance of symptoms is called the incubation period and it may last for weeks to months.</p>\n</blockquote>\n\n<p>Once the disease becomes established, it is 100% fatal (<a href=\"https://doi.org/10.1016/S0021-9975(08)80224-1\" rel=\"nofollow noreferrer\">King &amp; Turner, 1993</a>; <a href=\"https://www.researchgate.net/profile/Alan_Jackson6/publication/12229458_Rabies/links/56f9326708ae38d710a2fa53/Rabies.pdf\" rel=\"nofollow noreferrer\">Jackson, 2000</a>). However, if treated immediately after exposure it is possible to prevent the development of the disease in most cases (<a href=\"https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1026&amp;context=wolfrecovery\" rel=\"nofollow noreferrer\">Linnell et al. 2002</a>).</p>\n\n<p>The present treatment consists of a single injection of immunoglobulin (rabies antibodies grown in tissue culture) and multiple injections of rabies vaccine (<a href=\"https://www.researchgate.net/profile/Alan_Jackson6/publication/12229458_Rabies/links/56f9326708ae38d710a2fa53/Rabies.pdf\" rel=\"nofollow noreferrer\">Jackson, 2000</a>). Survival of patients treated is high except in some cases where bites have been inflicted directly on the head and neck (<a href=\"https://doi.org/10.1093/infdis/134.1.25\" rel=\"nofollow noreferrer\">Shah &amp; Jaswal, 1976</a>; <a href=\"https://doi.org/10.1093/clinids/10.Supplement_4.S766\" rel=\"nofollow noreferrer\">Fangtao et al. 1988</a>). This is because direct viral entry into the nerves without local replication results in very short incubation period, as occurs in cases with multiple bites in the head and neck region (<a href=\"https://doi.org/10.1007/s13311-016-0452-4\" rel=\"nofollow noreferrer\">Mahadevan et al. 2016</a>).</p>\n\n<h2>References</h2>\n\n<p>Fangtao, L., Shubeng, C., Yinzhon, W., Chenzhe, S., Fanzhen, Z., &amp; Guanfu, W. (1988). Use of serum and vaccine in combination for prophylaxis following exposure to rabies. <em>Reviews of infectious diseases, 10</em>(Supplement_4), S766-S770. <a href=\"https://doi.org/10.1093/clinids/10.Supplement_4.S766\" rel=\"nofollow noreferrer\">https://doi.org/10.1093/clinids/10.Supplement_4.S766</a></p>\n\n<p>Jackson, A. C. (2000). REVIEW ARTICLES-Rabies. <em>Canadian Journal of Neurological Sciences, 27</em>(4), 278-282. <a href=\"https://www.researchgate.net/profile/Alan_Jackson6/publication/12229458_Rabies/links/56f9326708ae38d710a2fa53/Rabies.pdf\" rel=\"nofollow noreferrer\">https://www.researchgate.net/profile/Alan_Jackson6/publication/12229458_Rabies/links/56f9326708ae38d710a2fa53/Rabies.pdf</a></p>\n\n<p>King, A. A., &amp; Turner, G. S. (1993). Rabies: a review. <em>Journal of Comparative Pathology, 108</em>(1), 1-39. <a href=\"https://doi.org/10.1016/S0021-9975(08)80224-1\" rel=\"nofollow noreferrer\">https://doi.org/10.1016/S0021-9975(08)80224-1</a></p>\n\n<p>Linnell, J., Andersen, R., Andersone, Z., Balciauskas, L., Blanco, J. C., Boitani, L., ... &amp; Loe, J. (2002). The fear of wolves: A review of wolf attacks on humans. <em>Norsk Institutt for Naturforskning</em> <a href=\"https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1026&amp;context=wolfrecovery\" rel=\"nofollow noreferrer\">https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1026&amp;context=wolfrecovery</a></p>\n\n<p>Mahadevan, A., Suja, M. S., Mani, R. S., &amp; Shankar, S. K. (2016). Perspectives in diagnosis and treatment of rabies viral encephalitis: insights from pathogenesis. <em>Neurotherapeutics, 13</em>(3), 477-492. <a href=\"https://doi.org/10.1007/s13311-016-0452-4\" rel=\"nofollow noreferrer\">https://doi.org/10.1007/s13311-016-0452-4</a></p>\n\n<p>Shah, U., &amp; Jaswal, G. S. (1976). Victims of a rabid wolf in India: effect of severity and location of bites on development of rabies. <em>Journal of Infectious Diseases, 134</em>(1), 25-29. <a href=\"https://doi.org/10.1093/infdis/134.1.25\" rel=\"nofollow noreferrer\">https://doi.org/10.1093/infdis/134.1.25</a></p>\n", "score": 1 }, { "answer_id": 23685, "body": "<p>It is thought you need to have completed the series of rabies vaccination <strong>for at least 7 days to be protected</strong>. If that is not the case, then you'll need rabies immunoglobulin as well.</p>\n<blockquote>\n<p>Pre-exposure rabies vaccination consists of three full intramuscular (i.m.) doses of cell-culture- or embryonated-egg-based vaccine given on days 0, 7 and 21 or 28 (a few days’ variation in the timing is not important). For adults, the vaccine should always be administered in the deltoid area of the arm; for young children (under 1 year of age), the anterolateral area of the thigh is recommended. Rabies vaccine should never be administered in the gluteal area: administration in this manner will result in lower neutralizing antibody titres.</p>\n</blockquote>\n<p>..</p>\n<blockquote>\n<p><strong>What is the difference between rabies vaccine and HRIG?</strong></p>\n<p>A course of rabies vaccines (given into the shoulder muscle) works to develop long term immunity, but this may take seven days to begin providing protection. For this reason, HRIG is usually given into the wound or site of injury to provide immediate short term protection while the rabies vaccines start to work. Long term protection is essential as rabies infection can take a long time to develop. Not everyone potentially exposed to rabies or ABLV will be advised to have HRIG. For example, HRIG is generally not required for people who have been previously vaccinated against rabies. When recommended, it is important to have the HRIG as well as the vaccine to ensure complete protection against rabies or ABLV.</p>\n</blockquote>\n<p><a href=\"http://conditions.health.qld.gov.au/HealthCondition/condition/14/119/117/Rabies-vaccine-human-rabies-immunoglobulin\" rel=\"nofollow noreferrer\">http://conditions.health.qld.gov.au/HealthCondition/condition/14/119/117/Rabies-vaccine-human-rabies-immunoglobulin</a></p>\n<p><a href=\"https://www.who.int/ith/vaccines/rabies/en/\" rel=\"nofollow noreferrer\">https://www.who.int/ith/vaccines/rabies/en/</a></p>\n", "score": 1 } ]

[ "virus", "rabies", "saliva" ]

[ { "answer_id": 25030, "body": "<p>From the 2007 study {1}, imiquimod 5% cream successfully treated infiltrative BCCs for 60% of the 26 studied patients (outcome at 5-year follow-up)</p>\n<blockquote>\n<p>For the intent-to-treat data set, the long-term clearance rate for imiquimod was 65% for all BCCs (n = 36), 100% for superficial BCCs (n = 4), 75% for nodular BCCs (n = 6), <strong>60% for infiltrative BCCs (n = 26)</strong>, and 65% for both dosing regimens (n = 23 and n = 13). <strong>Multivariate analysis demonstrated that only baseline BCC size had a significant association with long-term clearance</strong> (P = .02) (odds ratio, 0.99; 95% confidence interval, 0.98-0.10): <strong>the smaller the tumor, the higher the chance to be cured with imiquimod</strong>.</p>\n</blockquote>\n<p>Limitations:</p>\n<ol>\n<li>Small sample size.</li>\n<li>Two authors of the study have disclosed a conflict of interest (paid by 3M Pharmaceuticals, which manufactures Imiquimod).</li>\n<li>The study was published in 2007. Hopefully larger, more objective studies have been published since then.</li>\n</ol>\n<p>In the 2018 study {2}, in table 1, 4 out of 5 infiltrative BCC were has retreated with imiquimod 5% cream (5 days/week during 6 weeks). Outcome at around 5-year follow-up.</p>\n<p>The 2013 letter {3} strongly advises against using imiquimod for a BCC that has not been confirmed to be superficial via biopsy:</p>\n<blockquote>\n<p>In any way there should be a clear consensus today that imiquimod treatment should only be applied to superficial BCC which have been biopsied before. Treatment of nodular or more aggressive BCC with imiquimod is obsolete. In case of recurrence after imiquimod treatment, surgery is always more damaging and more expensive because of the increased aggressivity as well as the poor clinical delimitation of these tumors.</p>\n</blockquote>\n<p>A similar concern is shared by the 2015 letter {4} for fluorouracil (but likely the same argument can be made for imiquimod):</p>\n<blockquote>\n<p>However, despite approval since the 1970’s, the Veterans Affairs Topical Tretinoin Chemoprevention trial noted that prior treatment with topical fluorouracil was associated with a higher risk of development of morpheaform BCCs. These authors concede that <strong>fluorouracil may have destroyed superficial cancer cells while leaving deeper pockets untouched</strong>. However, they open the door to a causal relationship between therapy and these tumors by stating that “fluorouracil treatment may predispose to development of morpheaform BCC.”</p>\n</blockquote>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} Fifty-five Basal Cell Carcinomas Treated With Topical Imiquimod: Outcome at 5-Year Follow-up. <a href=\"https://jamanetwork.com/searchresults?author=David+Vidal&amp;q=David+Vidal\" rel=\"nofollow noreferrer\">David Vidal, MD, PhD</a>; <a href=\"https://jamanetwork.com/searchresults?author=Xavier+Mat%c3%adas-Guiu&amp;q=Xavier+Mat%c3%adas-Guiu\" rel=\"nofollow noreferrer\">Xavier Matías-Guiu, MD, PhD</a>; <a href=\"https://jamanetwork.com/searchresults?author=Agust%c3%adn+Alomar&amp;q=Agust%c3%adn+Alomar\" rel=\"nofollow noreferrer\">Agustín Alomar, MD, PhD</a>. <em>Arch Dermatol.</em> 2007;143(2):264-276. <a href=\"https://doi.org/doi:10.1001/archderm.143.2.266\" rel=\"nofollow noreferrer\">https://doi.org/doi:10.1001/archderm.143.2.266</a></li>\n<li>{2} Bostanci, Seher, Pelin Kocyigit, Seçil Vural, Aylin Okcu Heper, and Aysenur Botsali. &quot;Long-term follow-up results of topical imiquimod treatment in basal cell carcinoma.&quot; Dermatologic Surgery 44, no. 1 (2018): 36-41. <a href=\"https://www.researchgate.net/profile/Secil_Vural/publication/320317367_Long-Term_Follow-Up_Results_of_Topical_Imiquimod_Treatment_in_Basal_Cell_Carcinoma/links/5b27ae41a6fdcc3cce9c2011/Long-Term-Follow-Up-Results-of-Topical-Imiquimod-Treatment-in-Basal-Cell-Carcinoma.pdf\" rel=\"nofollow noreferrer\">https://www.researchgate.net/profile/Secil_Vural/publication/320317367_Long-Term_Follow-Up_Results_of_Topical_Imiquimod_Treatment_in_Basal_Cell_Carcinoma/links/5b27ae41a6fdcc3cce9c2011/Long-Term-Follow-Up-Results-of-Topical-Imiquimod-Treatment-in-Basal-Cell-Carcinoma.pdf</a> (<a href=\"https://archive.vn/Nzt4K\" rel=\"nofollow noreferrer\">mirror</a>)</li>\n<li>{3} Skaria, A. M. &quot;Facial basal cell carcinomas recurring after imiquimod therapy.&quot; Dermatology 226, no. 1 (2013): 13. <a href=\"https://doi.org/10.1159/000345763\" rel=\"nofollow noreferrer\">https://doi.org/10.1159/000345763</a></li>\n<li>{4} Ruiz, Emily Stamell, Joel L. Cohen, and Adam Friedman. &quot;Before or after: is there a connection between the use of adjunctive nonmelanoma skin cancer treatments and subsequent invasive tumors?.&quot; J Drugs Dermatol 14 (2015): 3. <a href=\"https://jddonline.com/articles/dermatology/S1545961615P0450X/2\" rel=\"nofollow noreferrer\">https://jddonline.com/articles/dermatology/S1545961615P0450X/2</a></li>\n</ul>\n", "score": 0 } ]

[ "dermatology", "cancer", "treatment", "basal-cell-carcinoma" ]

[ { "answer_id": 25675, "body": "<p>I don't think there can be data on this, given how short the trials were. On the other hand, I don't think that scientists fear birth defects from COVID-19 vaccines (These vaccines' intended mechanism does not involve modifying <em>your</em> DNA, mind you)</p>\n<p>The only known mechanism I could find where a vaccine would cause birth defects was when the virus itself was causing birth defects, and the vaccine, rather than being useful, was enhancing the virus.\n(This is called <a href=\"https://en.wikipedia.org/wiki/Antibody-dependent_enhancement\" rel=\"noreferrer\">antibody-dependent enhancement</a>, and the virus in question was Zika, <a href=\"https://pubmed.ncbi.nlm.nih.gov/31130472/\" rel=\"noreferrer\">studied in mice</a>)</p>\n<p>That is not to say that birth defects from COVID-19 vaccination are known to be completely impossible. But one must weigh the rather theoretical (and likely non-existent) risk of COVID-19 vaccines causing birth defects vs the very real risk of dying from COVID-19.</p>\n", "score": 10 } ]

[ "covid-19", "vaccination", "side-effects", "coronavirus", "regulatory-agencies" ]

[ { "answer_id": 26160, "body": "<p>From <a href=\"https://en.wikipedia.org/wiki/Coronavirus\" rel=\"nofollow noreferrer\">Wikipedia</a>:</p>\n<blockquote>\n<p>The spikes are the most distinguishing feature of coronaviruses and are responsible for the corona- or halo-like surface. On average a coronavirus particle has 74 surface spikes.[54] Each spike is about 20 nm long and is composed of a trimer of the S protein. The S protein is in turn composed of an S1 and S2 subunit.</p>\n</blockquote>\n<p>So, a spike protein in its native conformation is a single protein consisting of a trimer of a 2-subunit dimer. <a href=\"https://en.wikipedia.org/wiki/Protein_quaternary_structure\" rel=\"nofollow noreferrer\">&quot;Quaternary structure&quot;</a> is a critical organizing feature of proteins, and it's typical to refer to a cluster of polypeptide chains as a single unit, and occasionally to refer to the individual components as separate proteins as well if they tend to function both together and separately. Anyone working in biology is familiar with this. Additionally, in case it isn't clear, a &quot;protein&quot; is not necessarily a covalently linked chain of atoms like a polypeptide chain is, but may instead be held together in part by hydrogen bonds or other intermolecular forces.</p>\n<p>&quot;Protein&quot; is often used as an <a href=\"https://en.wikipedia.org/wiki/Mass_noun\" rel=\"nofollow noreferrer\">uncountable noun</a>, for example when talking about protein in diet when someone says a meal has &quot;10 g protein&quot; you do not infer they mean a single polypeptide weighing 10 grams. Like &quot;fish&quot; and &quot;fishes&quot;, plural &quot;proteins&quot; often refers to &quot;multiple varieties of protein&quot; rather than &quot;multiple molecules&quot;. In other cases, when it makes sense to count individual molecules, protein can also be used as a countable noun.</p>\n<blockquote>\n<p>The injected spike protein was also found in the lung, spleen, kidney and liver of the mice</p>\n</blockquote>\n<p>This refers to multiple protein molecules (obviously), all of the same uncountable category (&quot;spike protein&quot;).</p>\n<blockquote>\n<p>The viral envelope of coronaviruses is typically made up of three proteins that include the membrane protein (M), the envelope protein (E), and the spike protein (S).</p>\n</blockquote>\n<p>This refers to three types of protein that &quot;make up&quot; the viral envelope; that is, the viral envelope is made up of constituent parts of these types. The number is not specified, but you can safely assume it's used in the uncountable noun sense.</p>\n<blockquote>\n<p>Members of the coronavirus family have sharp bumps that protrude from the surface of their outer envelopes. Those bumps are known as spike proteins</p>\n</blockquote>\n<p>Each bump is, like written above, an individual trimer. The author here is using protein as a countable noun which nonetheless makes sense here because they are not talking about spike protein contained in some soup, but rather the individual &quot;spikes&quot; visible under a microscope that each consist of a single fully assembled spike protein.</p>\n<blockquote>\n<p>The spike protein is composed of a linear chain of 1,273 amino acids, neatly folded into a structure, which is studded with up to 23 sugar molecules. Spike proteins like to stick together and three separate spike molecules bind to each other to form a functional &quot;trimeric&quot; unit</p>\n</blockquote>\n<p>Spike proteins are glycoproteins, so they aren't just an amino acid chain, they are modified with sugars. I infer from this sentence that there is some probability that the number of attached sugar molecules varies. It's still the same protein just like a boat is a boat no matter how many crew members you put on it. One can still assume that the function of the boat depends somewhat on the crew members yet it isn't a different boat if the crew is absent. This paragraph is clearly not written for an expert audience; someone is trying to describe the biology in terms for an interested but non-technical audience. That said, there's nothing wrong with them referring to both the individual polypeptide subunits as &quot;spike protein&quot; as well as the assembled trimer as &quot;spike protein&quot;.</p>\n<p>If you wanted to be specific about the S1 and S2 subunits or the individual component molecules you would use specific language to do that, but it gets incredibly clunky in descriptive language to refer to biological molecules by long, complicated, definitive names, as well as clunky and confusing to create new names for each to keep them separate. You're probably familiar with other proteins referred to this way, for example you may be familiar with <a href=\"https://en.wikipedia.org/wiki/Hemoglobin\" rel=\"nofollow noreferrer\">hemoglobin</a>, the protein that assists in carrying oxygen in blood. Hemoglobin is a heterotetramer made out of two alpha and two beta subunits. HBA1 is a protein. HBA2 is a protein. HBB is a protein. Two HBA1 proteins with two HBB proteins together makes one hemoglobin protein.</p>\n", "score": 2 } ]

[ "sars-cov-2", "proteins" ]

[ { "answer_id": 27394, "body": "<p>The American Academy of Pediatrics <a href=\"https://brightfutures.aap.org/Pages/default.aspx\" rel=\"nofollow noreferrer\">Bright Futures</a> public health initiative has developed a comprehensive assessment of approaches to <a href=\"https://brightfutures.aap.org/Bright%20Futures%20Documents/BF4_OralHealth.pdf\" rel=\"nofollow noreferrer\">Promoting Oral Health</a> in infants and children.</p>\n<p>The <a href=\"https://brightfutures.aap.org/Bright%20Futures%20Documents/BF4_OralHealth.pdf\" rel=\"nofollow noreferrer\">&quot;Promoting Oral Health&quot;</a> document describes in detail the reasoning and evidence for the recommendations.</p>\n<p>Of particular note is the section on 1-4 years:</p>\n<blockquote>\n<p>The key oral health priorities of this developmental\nstage are ...\npreventing caries and developing healthy oral\nhygiene habits. Early childhood also is a good\ntime for <strong>parents, caregivers, and health care professionals to build positive dietary habits</strong> as they\nintroduce new foods and the child establishes taste\npreferences [emphasis added].</p>\n</blockquote>\n<p>Thus, while a comprehensive dental exam and imaging studies may not be completed, the visit provides the opportunity to establish care with a Pediatric Dentist, review these positive habits, and answer any questions you may have.</p>\n<p>Dental caries are a major <a href=\"https://www.who.int/news-room/fact-sheets/detail/sugars-and-dental-caries\" rel=\"nofollow noreferrer\">public health problem</a> which disproportionally effect children with <a href=\"https://www.cdc.gov/oralhealth/oral_health_disparities/index.htm\" rel=\"nofollow noreferrer\">disadvantaged socioeconomic status</a>. These recommendations are one of many ways public health advocates are attempting to decrease these disparities.</p>\n", "score": 3 } ]

[ "dentistry", "pediatrics", "infant" ]

[ { "answer_id": 27452, "body": "<p>The chart says that 100 grams of chickpeas have 364 calories, and 6 grams of total fat. It also tells you that the 6 grams of total fat is 9% of the &quot;daily recommended value&quot; for fat: this is because the total daily recommended value is 65 grams of fat, so 6/65 grams is about 9%.</p>\n<p>These are fairly rough guidelines and there is no way for a universal rule to fit everyone. For a rough scaling you might base it on overall calorie needs, so if you only needed a 1200 calorie diet then the daily recommended fat would be about 65*1200/2000=39 grams, and 6 grams would be closer to 15% of the daily fat recommendation. There also may be more recent literature that suggests the guidelines should be updated, and I am not aware of any research that suggests these daily values should be met every day or that not meeting them exactly on average has any health impacts.</p>\n", "score": 4 } ]

[ "nutrition", "diet", "micronutrients", "macronutrient" ]

[ { "answer_id": 27543, "body": "<p>As described in <a href=\"https://radiopaedia.org/articles/ground-glass-opacification-3?lang=us\" rel=\"nofollow noreferrer\">this article</a> at radiopaedia.org , the meaning relevant to the question is likely:</p>\n<blockquote>\n<p>Ground glass opacification is also used in chest radiography to refer\nto a region of hazy lung radiopacity, often fairly diffuse, in which\nthe edges of the pulmonary vessels may be difficult to appreciate</p>\n<p>The use of the term ground glass derives from the industrial technique\nin glassmaking whereby the surface of normal glass is roughened by\ngrinding it.</p>\n</blockquote>\n", "score": 0 } ]

[ "terminology" ]

[ { "answer_id": 27589, "body": "<p>No vaccine in history has ever been 100% effective. It's not reasonable to expect it.</p>\n<p>All of the vaccines being distributed for which data are public are highly effective, though. This Q&amp;A over at Biology.SE explains how &quot;efficacy&quot; is calculated in the trials: <a href=\"https://biology.stackexchange.com/questions/96941/what-does-vaccine-efficacy-mean\">https://biology.stackexchange.com/questions/96941/what-does-vaccine-efficacy-mean</a></p>\n<p>Generally the higher efficacy numbers have been around 95% for symptomatic illness, and even more effective at preventing severe illness (hospitalization, death) than preventing symptomatic illness.</p>\n<p>Even if something is 99.9% effective, someone can write a news article about the cases in the 0.1%. These news reports are not a good basis to make decisions on. 95% efficacy means you are 95% less likely to get sick. That's a good thing.</p>\n", "score": 1 } ]

[ "covid-19", "vaccination" ]

[ { "answer_id": 29083, "body": "<p><strong>Clinical Trials</strong></p>\n<p>Initial safety data comes from the pre-approval clinical trials, as summarized by <a href=\"https://doi.org/10.1038/s41577-021-00525-y\" rel=\"nofollow noreferrer\">Male (2021)</a>:</p>\n<p><a href=\"https://i.stack.imgur.com/IEHXC.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/IEHXC.png\" alt=\"enter image description here\" /></a></p>\n<p>Note that pregnant women were not enrolled in the trials, and participants were asked to avoid conception, so these numbers are presumably of accidental pregnancies. Just eyeballing the results, there is no obvious difference in fertility or miscarriage between the control and experimental groups.</p>\n<p>Approval of mRNA vaccines for women of childbearing age was also influenced by the long safety track record of previous mRNA vaccines studied in humans <a href=\"https://en.wikipedia.org/wiki/MRNA_vaccine#Development\" rel=\"nofollow noreferrer\">since 2008</a>, animal studies demonstrating no reproduction-related safety concerns, and the high risk to pregnant women from infection.</p>\n<p>Several subsequent clinical trials demonstrated no difference in women's fertility pre and post vaccination (<a href=\"https://doi.org/10.1101/2021.05.30.21258079\" rel=\"nofollow noreferrer\">Safrai et al, 2021</a>; <a href=\"https://doi.org/10.1186/s12958-021-00757-6\" rel=\"nofollow noreferrer\">Orvieto et al, 2021</a>; <a href=\"https://doi.org/10.1016/j.xfre.2021.05.010\" rel=\"nofollow noreferrer\">Morris, 2021</a>).</p>\n<p><strong>Real-World Data</strong></p>\n<p>The pre-approval clinical trials are <a href=\"https://en.wikipedia.org/wiki/Placebo-controlled_study\" rel=\"nofollow noreferrer\">placebo-controlled</a> <a href=\"https://en.wikipedia.org/wiki/Randomized_controlled_trial\" rel=\"nofollow noreferrer\">RCTs</a>, meaning that participants were randomly injected with a vaccine or saline. We now have far more real-world data, but such data is no longer placebo-controlled, randomized, <a href=\"https://en.wikipedia.org/wiki/Blinded_experiment\" rel=\"nofollow noreferrer\">blinded</a>, or <a href=\"https://en.wikipedia.org/wiki/Matching_(statistics)\" rel=\"nofollow noreferrer\">matched</a>, so is in some ways lower quality, but this is substantially made up for by the much larger numbers and longer timeframe involved.</p>\n<p><a href=\"https://doi.org/10.1056/NEJMoa2104983\" rel=\"nofollow noreferrer\">Shimabukuro et al (2021)</a> first reported on 827 women in the US, vaccinated before or during pregnancy, who completed their pregnancy at follow-up:</p>\n<p><a href=\"https://i.stack.imgur.com/RYe2B.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/RYe2B.png\" alt=\"enter image description here\" /></a></p>\n<p>As an example of reading this table, congenital anomalies have a background (ie, unvaccinated) rate of about 3%; vaccinated women in the study had a rate of 2.2%. All the measures reported compare favourably against the background incidence rate. You may notice the missing data for spontaneous abortions - this was addressed in a <a href=\"https://doi.org/10.1056/NEJMc2113891\" rel=\"nofollow noreferrer\">separate note</a> confirming no difference (also see <a href=\"https://doi.org/10.1001/jama.2021.15494\" rel=\"nofollow noreferrer\">Kharbanda et al, 2021</a>).</p>\n<p>Unvaccinated women tend to be less educated, lower socioeconomic status, and may have predisposing health factors that compare unfavourably for reasons unrelated to the vaccine. A larger study by <a href=\"https://doi.org/10.1001/jama.2021.11035\" rel=\"nofollow noreferrer\">Goldshtein et al (2021)</a> of 1387 pregnant women in Israel attempts to compensate for some of the drawbacks of real-world data by comparing against 1427 unvaccinated pregnancies during the same period, matched for demographics:</p>\n<p><a href=\"https://i.stack.imgur.com/X1Skj.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/X1Skj.png\" alt=\"enter image description here\" /></a></p>\n<p>Again, vaccination does not appear to affect outcomes in any way for participants who completed pregnancy at follow-up.</p>\n<p>A more recent study by <a href=\"https://dx.doi.org/10.1016%2Fj.vaccine.2021.09.012\" rel=\"nofollow noreferrer\">Wainstock et al (2021)</a> of 913 vaccinated pregnant women matched with 3486 unvaccinated controls gives similar results:</p>\n<blockquote>\n<p>... no differences were found between the groups in pregnancy,\ndelivery and newborn complications, including gestational age at\ndelivery, incidence of small for gestational age and newborn\nrespiratory complications.</p>\n</blockquote>\n<p>The results are too many to include here, but check out <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8421099/table/t0015/?report=objectonly\" rel=\"nofollow noreferrer\">Table 3</a> for relative risk (odds ratios) of 15 outcome variables measured.</p>\n<p>The number of women enrolled in the above studies is relatively small compared with the hundreds of thousands who have been vaccinated prior to or during pregnancy around the world. Outcomes for these women are tracked more broadly by various health agencies as part of adverse event reporting. These agencies continue to report no difference in the rate of adverse events related to pregnancy and childbirth compared to background (<a href=\"https://health-infobase.canada.ca/covid-19/vaccine-safety/#specialInterest\" rel=\"nofollow noreferrer\">Canada</a>, <a href=\"https://www.gov.uk/government/publications/coronavirus-covid-19-vaccine-adverse-reactions/coronavirus-vaccine-summary-of-yellow-card-reporting#analysis-of-data\" rel=\"nofollow noreferrer\">UK</a>, <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/vaccines/safety/monitoring-pregnant-people.html\" rel=\"nofollow noreferrer\">USA</a>).</p>\n<p><strong>COVID-19 Infection</strong></p>\n<p>The real-world comparison data consists of unvaccinated uninfected pregnancies. Unvaccinated <em>infected</em> pregnancies have substantially worse outcomes, as summarized in a meta-analysis by <a href=\"https://doi.org/10.1136/bmj.m3320\" rel=\"nofollow noreferrer\">Allotey et al (2020)</a>:</p>\n<p><a href=\"https://i.stack.imgur.com/hVKN1.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/hVKN1.png\" alt=\"enter image description here\" /></a>\n<a href=\"https://i.stack.imgur.com/znCG3.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/znCG3.png\" alt=\"enter image description here\" /></a></p>\n<p>For example, the ICU admission rate for infected women is more than 18 times higher than uninfected women, and the neonatal death rate is more than twice as high. All the comparison rates (odds ratios) are substantially worse for unvaccinated pregnant women who become infected during their pregnancy (also see <a href=\"https://doi.org/10.1093/cid/ciab344\" rel=\"nofollow noreferrer\">Ko et al, 2021</a>; <a href=\"https://doi.org/10.1503/cmaj.202604\" rel=\"nofollow noreferrer\">Wei et al, 2021</a>; <a href=\"https://doi.org/10.1001/jamapediatrics.2021.1050\" rel=\"nofollow noreferrer\">Villar et al, 2021</a>).</p>\n<p><strong>Conclusion</strong></p>\n<p>Approximately 10% of the 67,271 women included (worldwide) in the above meta-analysis contracted COVID-19 during their pregnancy, and there is clearly a substantial risk associated with infection that led to the prioritization of pregnant women for vaccination as a particularly vulnerable group. On the other hand, women vaccinated prior to or during pregnancy do not evidence any difference from uninfected women. In other words, not vaccinating carries a substantial risk from infection, while vaccination does not appear to add any risk for women of childbearing age.</p>\n", "score": 3 } ]

[ "covid-19", "vaccination", "side-effects", "obstetrics", "data" ]

[ { "answer_id": 29208, "body": "<p>No, not really.</p>\n<p><a href=\"https://en.wikipedia.org/wiki/Cellular_senescence\" rel=\"nofollow noreferrer\">Cellular senecence</a> is defined as an cessation in division of the cell. Viruses viruses are obligate parasites which don't contain any metabolic pathways themselves and rely on cellular machinery to replicate themselve, so once they exit the cell, there is no metabolic activity attributable to the virus. Because of this there is no possibility of senescence or even of something similar to senesence.</p>\n<p>However, there are viruses that can integrate into the genome, such as the <a href=\"https://en.wikipedia.org/wiki/Endogenous_retrovirus\" rel=\"nofollow noreferrer\">endogenous retroviruses</a>, which are thought to be viruses that can no longer replicate, and have now become parts of our genome.</p>\n<p>There are also viruses like <a href=\"https://en.wikipedia.org/wiki/Varicella_zoster_virus\" rel=\"nofollow noreferrer\">Varicella virus</a> and <a href=\"https://en.wikipedia.org/wiki/Epstein%E2%80%93Barr_virus\" rel=\"nofollow noreferrer\">Epstein Barr virus</a> and other herpes viruses that can lie latent in the body, sometimes for many years, before reactivating and causing further disease. The mechanisms by which this latency occurs are virus specific, but it is thought that the host immune system plays a large role in much of both the establishment of latency and reactivation of the infection later in life. A review on Varicella infection can be found <a href=\"https://www.frontiersin.org/articles/10.3389/fmicb.2018.03170/full\" rel=\"nofollow noreferrer\">here</a>^*, which explains mechanisms etc.</p>\n<ul>\n<li>Sorel Front. Microbiol., 21 December 2018</li>\n</ul>\n", "score": 2 } ]

[ "virus", "cells" ]

[ { "answer_id": 29221, "body": "<h1>Vaccination is more about potential than current burden of disease.</h1>\n<p>Flu can spread rapidly in an unvaccinated population, and it can be deadly. The &quot;real&quot; average excess mortality from flu can be a bit controversial and is far enough from the topic that I don't want to dig through sources here, but if you go to the CDC or similar sites you can see some rather striking figures.</p>\n<p>Flu <em>has been</em> well controlled with masking and social distancing, but if COVID-19 ever truly declines, people will celebrate by abandoning many of these precautions. I have not seen much about fundamental reforms that would prevent future flu, such as guaranteed state-sponsored sick leave for all employees.</p>\n<p>When we look at current vaccination programs - China has vaccinated much more of its population against COVID-19 than most countries, even though it has had extremely few cases. People are vaccinated against polio in the U.S. even though it is extremely rare. The alternative for the country would be to await another massive outbreak of respiratory paralysis. At the individual level it is much less of a stretch to take a flu vaccine now against a virus that is quite likely to have an outbreak in the near future.</p>\n", "score": 1 } ]

[ "covid-19", "influenza" ]

[ { "answer_id": 29289, "body": "<p>No it won't stop mutating. Mutating is a feature of life with nucleic acids, no matter if you are a virus, bacterium, archaea, fungi, plant or animal.</p>\n<p>You can check on mutation rates in organisms with a simple google search for the terms &quot;mutation rate (species of interest)&quot;</p>\n", "score": 3 } ]

[ "covid-19", "vaccination", "virus", "coronavirus" ]

[ { "answer_id": 29385, "body": "<p><strong>Sagital abdominal diameter</strong> is <a href=\"https://diabetesjournals.org/care/article/27/8/2041/23397/Sagittal-Abdominal-Diameter-Is-a-Strong\" rel=\"nofollow noreferrer\">measured</a>:</p>\n<blockquote>\n<p>after a normal expiration while in the supine position with bent knees on a firm examination table and without clothes in the measurement area (Fig. 1)... at the level of iliac crest ... as the distance between the examination table up to the horizontal level, allowing the caliper arm to touch the abdomen slightly but without compression.</p>\n</blockquote>\n<p>Figure 1 from <a href=\"https://diabetesjournals.org/care/article/27/8/2041/23397/Sagittal-Abdominal-Diameter-Is-a-Strong\" rel=\"nofollow noreferrer\">Risérus <em>et al</em></a>:</p>\n<p><a href=\"https://i.stack.imgur.com/8hKW1.gif\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/8hKW1.gif\" alt=\"Image\" /></a></p>\n<p>This is different than the measurement you are proposing, but in general measures the front to back diameter of the abdomen. It has been previously used to estimate visceral fat content.</p>\n", "score": 5 } ]

[ "terminology", "measurement" ]

[ { "answer_id": 30503, "body": "<p>From <a href=\"https://www.worldometers.info/coronavirus/about/\" rel=\"nofollow noreferrer\">https://www.worldometers.info/coronavirus/about/</a></p>\n<blockquote>\n<p>Recoveries = this statistic is highly imperfect, because reporting can be missing, incomplete, incorrect, based on different definitions, or dated (or a combination of all of these) for many governments, both at the local and national level, sometimes with differences between states within the same country or counties within the same state. WHO recommends following the criteria of [symptoms resolve + 2 negative tests within 24 hours] or [symptoms resolve + additional 14 days], but this is only a recommendation. In some countries, when a patient is discharged from the hospital it is counted as &quot;recovered&quot; even if no test is performed. Some health officials now consider anyone who was diagnosed with COVID-19 three or more weeks ago and has not died to be recovered from the disease. In view of this, &quot;Active Cases&quot; and &quot;Closed Cases Outcome&quot; which both depend on the number of recoveries (in addition to an accurate death count and a satisfactory rate of case detection, both of which are lacking in the vast majority of countries) can be affected by this inherent flaw for many countries and for the total worldwide count</p>\n</blockquote>\n<p>In summary, the &quot;recoveries&quot; statistic is a bit messy because of different definitions of recovery. They do not require a record of a case being recovered to count as such, though, if a case is not a death it is considered a recovery in 2-3 weeks.</p>\n<p>It's best to interpret the graph of &quot;active cases&quot; as a moving average of infections; if &quot;active cases&quot; are at a high, that tells you that the number of infections over the past couple weeks is at a high. This is a pretty good measure of the recent virus activity.</p>\n<p>I'm not sure I follow your logic of why you expect cases to not be at a high; right now, the high case rates are probably most influenced by spread of <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/variants/about-variants.html\" rel=\"nofollow noreferrer\">variants like delta and omicron</a>. While there are in fact a couple &quot;new drugs&quot; out for treating COVID, they are not in widespread use, and while vaccination seems to be protecting people who are vaccinated compared to their unvaccinated neighbors, there are still a lot of unvaccinated people (both by stubborn choice and by poor access in developing countries) and still a lot of spread.</p>\n", "score": 1 } ]

[ "covid-19" ]

[ { "answer_id": 30815, "body": "<p>There is a bit of information around, and like @BryanKrause said, half-lives are a more useful measure of the life-time of the system rather than complete clearance, which can't be measured easily for something of this nature, due to the technologies we use to measure these sorts of things.</p>\n<p>As far as I can tell, there isn't any information that has been released specifically about the persistence of the spike mRNA from the vaccine, because this is hard to measure. Normally with these sorts of things we measure a proxy for the target. There have been several papers that looked at persistence of mRNA and protein production from the mRNA to see how long it lasted <em>in vivo</em> and <em>in vitro</em>.</p>\n<p>The easiest to understand is probably <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5523404/\" rel=\"nofollow noreferrer\">this paper</a>¹ (see fig 2C linked below), where they looked at luciferase (a light emitting protein) expression over time in mice injected with a mRNA. <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5523404/figure/F2/\" rel=\"nofollow noreferrer\">They show some production of light and hence luciferase expression to over 12 days</a>, though note that's a log-scale on the y-axis, so &lt;50% of maximal light (max of ~10⁷ relative luminescence units) is &lt;3 days, probably closer to 2 days. Conversely, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2775451/\" rel=\"nofollow noreferrer\">this paper</a>² (see Fig 4C linked -&gt;), found <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2775451/figure/F4/\" rel=\"nofollow noreferrer\">little expression 24 hours post-injection</a>. They also found no translocation in the body, which is similar to most, though I can also find information that there seems to be translocation of signal to the spleen and liver (as one might expect), as well as other sites, but I'll come to that.</p>\n<p>The best information isn't actually in the papers; it's in the Use Authorities from the medical governing bodies for various jurisdictions. I found one for the <a href=\"https://www.ema.europa.eu/en/documents/assessment-report/comirnaty-epar-public-assessment-report_en.pdf\" rel=\"nofollow noreferrer\">Pfizer/BioNTech vaccine</a>³ (BNT162b2 - beware that's ~140 pg PDF) from the European Union with some interesting information. They say that the excipients (lipid particles) have a half-life of 140 hours (p. 46) in the blood following intra-venous injection, and T_0.25 in the liver of 2 weeks, but also state that IM injection is similar.</p>\n<p>A proxy for the spike, luciferase again was also mentioned:</p>\n<blockquote>\n<p>Luciferase signals at the injection sites, most likely reflecting\ndistribution to the lymph nodes draining the injection sites, peaked 6h post injection with signals of approximately 10 000 times of buffer control animals. The signal decreased slowly during the first 72\nhours and after 6 and 9 days the signals were further weakened to approximately levels of 18 and 7\ntimes the signals obtained from animals injected with buffer control.</p>\n</blockquote>\n<p>They also looked at distribution by radioactive labeling of the mRNA and looking to see where it went. They used 50 micrograms of the RNA for this, which is more than a dose for a person, but put into a mouse! They probably used so much to get greater sensitivity from their measurements.</p>\n<blockquote>\n<p>Over 48 hours, distribution from the injection site to most tissues occurred, with the\nmajority of tissues exhibiting low levels of radioactivity.\nRadioactivity was detected in most tissues from the first time point (0.25 h) and results support that\ninjections site and the liver are the major sites of distribution. The greatest mean concentration was\nfound remaining in the injection site at each time point in both sexes. Low levels of radioactivity were\ndetected in most tissues, with the greatest levels in plasma observed 1-4 hours post-dose. Over 48\nhours, distribution was mainly observed to liver, adrenal glands, spleen and ovaries, with maximum\nconcentrations observed at 8-48 hours post-dose. Total recovery (% of injected dose) of radiolabeled\nLNP+modRNA outside the injection site was greatest in the liver (up to 21.5%) and was much less in\nspleen (≤1.1%), adrenal glands (≤0.1%) and ovaries (≤0.1%).</p>\n</blockquote>\n<p>So, it would seem that the mRNA itself is cleared fairly quickly; probably the majority is gone within 3-4 days. But some will persist for some time, perhaps as much as 6 weeks, and it will spread to many sites in the body, mainly the liver and spleen.</p>\n<p>References:</p>\n<ol>\n<li><p>Oberli, M. A., Reichmuth, A. M., Dorkin, J. R., Mitchell, M. J., Fenton, O. S., Jaklenec, A., Anderson, D. G., Langer, R., &amp; Blankschtein, D. (2017). Lipid Nanoparticle Assisted mRNA Delivery for Potent Cancer Immunotherapy. Nano letters, 17(3), 1326–1335. <a href=\"https://doi.org/10.1021/acs.nanolett.6b03329\" rel=\"nofollow noreferrer\">https://doi.org/10.1021/acs.nanolett.6b03329</a></p>\n</li>\n<li><p>Karikó, K., Muramatsu, H., Welsh, F. A., Ludwig, J., Kato, H., Akira, S., &amp; Weissman, D. (2008). Incorporation of pseudouridine into mRNA yields superior nonimmunogenic vector with increased translational capacity and biological stability. Molecular therapy : the journal of the American Society of Gene Therapy, 16(11), 1833–1840. <a href=\"https://doi.org/10.1038/mt.2008.200\" rel=\"nofollow noreferrer\">https://doi.org/10.1038/mt.2008.200</a></p>\n</li>\n<li><p>19 February 2021\nEMA/707383/2020 Corr.1*1\nCommittee for Medicinal Products for Human Use (CHMP)\nAssessment report\nComirnaty\nCommon name: COVID-19 mRNA vaccine (nucleoside-modified)\nProcedure No. EMEA/H/C/005735/0000</p>\n</li>\n</ol>\n", "score": 4 } ]

[ "covid-19", "vaccine", "mrna" ]

[]

[ "mri", "medical-imaging" ]

[ { "answer_id": 31562, "body": "<blockquote>\n<p>Apparently men can get pregnant now?</p>\n</blockquote>\n<p>Yes, in two very different cases:</p>\n<p>Trans men can have a uterus, can get pregnant and bear children.</p>\n<p>It is theoretically possible for an XY male to have an embryo implanted in their abdomen and it to develop as an ectopic pregnancy. This is discussed in <a href=\"https://en.wikipedia.org/wiki/Male_pregnancy#Ectopic_implant\" rel=\"nofollow noreferrer\">wikipedia</a>, and as they highlight that it is only a theoretical possibility, it would probably be fatal for both the parent and child:</p>\n<blockquote>\n<p>Robert Winston, a pioneer of in-vitro fertilization, told London's Sunday Times that &quot;male pregnancy would certainly be possible&quot; by having an embryo implanted in a man's abdomen – with the placenta attached to an internal organ such as the bowel – and later delivered surgically. Ectopic implantation of the embryo along the abdominal wall, and resulting placenta growth would, however, be very dangerous and potentially fatal for the host, and is therefore unlikely to be studied in humans</p>\n</blockquote>\n", "score": 1 } ]

[ "obstetrics", "male", "uterus" ]

[ { "answer_id": 31766, "body": "<p>While I suspect the wording is not intended to be problematic, given the <a href=\"https://www.unlv.edu/research/ORI-HSR/history-ethics\" rel=\"nofollow noreferrer\">long history of research abuse</a>, I believe it is important to mention that &quot;interesting patients&quot; are not &quot;kept&quot; for research. Participants are invited to volunteer for research studies while providing all of the necessary information about the benefits and risks of the study. They are free to end their participation at any time.</p>\n<p>That said, perhaps the prototypical research hospital is the US National Institutes of Health (NIH) Clinical Center:</p>\n<p><img src=\"https://upload.wikimedia.org/wikipedia/commons/thumb/1/16/NIH_Clinical_Center_South_Entrance.jpg/1080px-NIH_Clinical_Center_South_Entrance.jpg\" alt=\"Image of CRC\" />\n^{<a href=\"https://commons.wikimedia.org/w/index.php?title=User:Masm2016&amp;action=edit&amp;redlink=1\" rel=\"nofollow noreferrer\">Masm2016</a> via Wikipedia.}</p>\n<p>The <a href=\"https://clinicalcenter.nih.gov/about/welcome/faq.html\" rel=\"nofollow noreferrer\">NIH website</a> notes:</p>\n<blockquote>\n<p>The Clinical Center is where NIH conducts its intramural clinical research; and that research is done in a hospital setting with patient/participants who receive not only experimental treatments but also the best in hospital care.</p>\n</blockquote>\n<p>Expanding on the NIH's Clinical Center, <a href=\"https://en.wikipedia.org/wiki/Clinical_research_center\" rel=\"nofollow noreferrer\">Wikipedia also indicates</a> that:</p>\n<blockquote>\n<p>The term &quot;<strong>Clinical research center</strong>&quot; ... refers to any designated medical facility used to conduct clinical research, such as at a hospital or medical clinic.</p>\n</blockquote>\n<p>It goes on to list some high profile institutions with clinical research centers. In my experience, the exact name is slightly different at each institution and is referred to by its proper name and not a generic term.</p>\n", "score": 4 } ]

[ "terminology", "hospital" ]

[ { "answer_id": 31993, "body": "<blockquote>\n<p>what's the cause of multivitamins' ineffectiveness?</p>\n</blockquote>\n<p>Multivitamins are ineffective because in ordinary people with an ordinary diet, there isn't any deficiency to correct. The evidence for this is presented in your link in your question: taking a multivitamin is not associated with any significant health benefit.</p>\n<p>The contents of a multivitamin are things that you need &quot;enough&quot; of. Having more than enough is not better than having enough. If you have enough and take more, there is no benefit to gain. Having too much may even cause harm. The editorial linked in the question you reference titled <a href=\"https://www.acpjournals.org/doi/10.7326/0003-4819-159-12-201312170-00011?articleid=1789253\" rel=\"nofollow noreferrer\">&quot;Enough Is Enough&quot;</a>. This title is a play on words: &quot;enough is enough&quot; is an idiom used to emphasize an impatience with an ongoing situation - you might utter it when two of your friends are quarreling. However, in this case, it's true literally: enough of a vitamin is enough, and more is not better.</p>\n<p>There are exceptions, of course, and in those cases the typical medical approach would be to prescribe <strong>specific</strong> vitamins, not a generic &quot;for everyone&quot; multivitamin. <a href=\"https://www.cdc.gov/ncbddd/folicacid/index.html\" rel=\"nofollow noreferrer\">Folic acid</a> is one vitamin recommended for women who are or may become pregnant - most women likely get enough folic acid anyways, but public health authorities find that it's worth supplementing to prevent severe birth defects.</p>\n", "score": 5 } ]

[ "micronutrients", "multi-vitamin" ]

[ { "answer_id": 32197, "body": "<p>Consider this: you're a surgeon and you need to suture a layer of tissue that's beneath the skin. If you use sutures that don't dissolve, you'll have to reopen the wound weeks later, remove the lower layer(s) of sutures, and then re-suture the upper layer(s). That adds time, risk, cost, scarring, discomfort, and recovery time.</p>\n<p>That's why dissolvable sutures exist and it's no different with mesh. First, consider that a hernia isn't just a bulge. It's a gap that has opened in the abdominal muscles that allows intestines to protrude though the gap. These muscles aren't cut or injured, so just pulling them back together with an external device will do nothing. The muscles will not grow back together and once you remove the external device the hernia will still be there.</p>\n<p>So in a hernia repair operation the muscles aren't just pulled back together as is. The gap is surgically repaired, which basically means sutured back together.</p>\n<p><a href=\"https://www.upmc.com/services/general-surgery-trauma/services/hernia-surgery\" rel=\"nofollow noreferrer\">https://www.upmc.com/services/general-surgery-trauma/services/hernia-surgery</a></p>\n<blockquote>\n<p>To repair your hernia, your surgeon will:</p>\n<ul>\n<li>Push the bulging tissue or organ back where it belongs.</li>\n<li><strong>Repair the weak spot or opening in your muscle.</strong></li>\n<li>Use surgical mesh to strengthen and cover the hernia defect in some cases.</li>\n</ul>\n</blockquote>\n<p>Emphasis is mine, highlighting the point that answers your question.</p>\n<p>The mesh is there to strengthen the weak area of muscle without relying solely on the sutures. Once the repair is fully healed the mesh may no longer be needed so having it dissolve is desirable so that you don't have a permanent foreign object present.</p>\n<p>Although I hate using videos as supporting evidence, <a href=\"https://www.youtube.com/watch?v=pLw3AjZx3NQ\" rel=\"nofollow noreferrer\">this video</a> is barely a minute long and illustrates quite nicely what I explained above.</p>\n", "score": 1 } ]

[ "surgery", "hernia", "patches", "dissolve" ]

[ { "answer_id": 32218, "body": "<p>The difference between the two concepts you are talking about is &quot;physiological&quot; <em>versus</em> &quot;pathological&quot; hypertrophy.</p>\n<p>Shimizu and Minamino note (2016. PMID <a href=\"https://pubmed.ncbi.nlm.nih.gov/27262674/\" rel=\"nofollow noreferrer\">27262674</a>:</p>\n<blockquote>\n<p>Cardiac hypertrophy is classified as physiological when it is associated with normal cardiac function or as pathological when associated with cardiac dysfunction.</p>\n</blockquote>\n<p>Kavazis wrote an excellent explaination (2015. PMID <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4575564/\" rel=\"nofollow noreferrer\">26331830</a>):</p>\n<blockquote>\n<p>‘Physiological’ cardiac hypertrophy can be provoked by exercise training and can lead to increase cardiac size that is characterized by normal cardiac morphology with a normal and/or enhanced cardiac function</p>\n</blockquote>\n<p>In contrast:</p>\n<blockquote>\n<p>‘Pathological’ cardiac hypertrophy is a condition that is characterized by the thickening of the heart muscle, a decrease in the size of the chambers of the heart, and a reduced capacity of the heart to pump blood to the tissues and organs around the body.</p>\n</blockquote>\n<p>The key difference between these types of hypertrophy is the stress (what Kavazis calls &quot;overloading stimulus&quot;) that causes the remodeling. In the case of pathological hypertrophy, the stimuli are often high blood pressure or heart valve dysfunction.</p>\n<p>For physiological hypertropy, Dornll notes (2007. PMID <a href=\"https://pubmed.ncbi.nlm.nih.gov/17389260/\" rel=\"nofollow noreferrer\">17389260</a>):</p>\n<blockquote>\n<p>The traditional view of exercised-induced cardiac adaptations is that they are favorable, or at least benign, and include increased cardiac mass (hypertrophy), enhanced aerobic capacity, and diastolic cardiac enlargement (remodeling), resulting in increased ventricular stroke volume and cardiac output. However, these are largely the consequences of endurance exercise training, such as long distance running or swimming, and are associated with eccentric remodeling of the heart. Physical conditioning that emphasizes strength training, such as weight lifting and wrestling, only modestly increases cardiac output but causes concentric cardiac hypertrophy without chamber dilation and an increase in peripheral vascular resistance.</p>\n</blockquote>\n<p>So pick your exercise regimen carefully if you're trying to maximize cardioprotection.</p>\n<p>Unfortunately, determining physiological exercise adaptations from pathological hypertrophy by electrocardiogram (ECG) is complex. It is also complicated by a history of trying to <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7682789/\" rel=\"nofollow noreferrer\">use race as a biological variable</a>.</p>\n<p>Augustine and Howard have some helpful hints which I have made some inline changes to (PMID <a href=\"https://pubmed.ncbi.nlm.nih.gov/30367318/\" rel=\"nofollow noreferrer\">30367318</a>):</p>\n<blockquote>\n<p>Physiological [T-wave inversions] in [athletes] can be normal in leads V1–[V4] and is more common in females. ...</p>\n<p>T wave inversion in lateral leads, ST segment depression and pathological Q waves warrant further investigation and are more likely to be associated with pathology.</p>\n</blockquote>\n", "score": 4 } ]

[ "heart-disease", "muscle", "heart", "electrocardiogram" ]

[ { "answer_id": 3143, "body": "<p>You didn't say which country you work in, so let's take the US as an example:</p>\n<blockquote>\n<ol start=\"2\">\n<li>Do I have a right to have my medical information kept private in the workplace?</li>\n</ol>\n<p>Your employer has a number of ways to obtain medical information about you, whether it's because you volunteer it when you call in sick or tell co-workers, or because you provide requested information on health insurance application or workers compensation claim forms. <strong>However, just because your employer has the information does not mean that it should be shared with everyone in the workplace, especially when you have not chosen to do so.</strong></p>\n<p>The basic legal principle that employers should follow is not to reveal medical information about you unless there is a legitimate business reason to do so. But because that standard is fairly vague, there are laws which more specifically protect the privacy of your medical records, such as the Americans with Disabilities Act, the law which makes it illegal to discriminate on the basis of an employee's disability. State laws may also provide additional protection.</p>\n</blockquote>\n<p>From: <a href=\"https://www.workplacefairness.org/medical-privacy-workplace\" rel=\"nofollow noreferrer\">Workplace Fairness</a> (emphasis mine)</p>\n<p>If you would like more reliable resources, I recommend the documents that WF refers to:</p>\n<ol>\n<li><a href=\"http://www.ada.gov/pubs/adastatute08.htm\" rel=\"nofollow noreferrer\">http://www.ada.gov/pubs/adastatute08.htm</a></li>\n<li><a href=\"http://www.hhs.gov/ocr/privacy/hipaa/understanding/index.html\" rel=\"nofollow noreferrer\">http://www.hhs.gov/ocr/privacy/hipaa/understanding/index.html</a></li>\n</ol>\n<p>Or if you would prefer the European approach:</p>\n<blockquote>\n<ol>\n<li><strong>Member States shall prohibit</strong> the processing of personal data revealing racial or ethnic origin, political opinions, religious or philosophical beliefs, trade-union membership, and <strong>the processing of data concerning health or sex life.</strong></li>\n</ol>\n</blockquote>\n<p>From: <a href=\"http://eur-lex.europa.eu/LexUriServ/LexUriServ.do?uri=CELEX:31995L0046:en:HTML\" rel=\"nofollow noreferrer\">Directive 95/46/EC of the European Parliament and of the Council of 24 October 1995 on the protection of individuals with regard to the processing of personal data and on the free movement of such data</a> (Article 8(1), emphasis mine)</p>\n<p>Hence, the bottom line is that it is utterly irrelevant whether your coworker does or does not have an underlying medical condition that you don't know about, because people have the right to health information privacy worldwide. In other words: <strong>your coworker's potential medical condition is none of your business</strong>.</p>\n<p>The right to privacy has been around for a while and as such should be understandable to any civilized human being. To be consistent with meeting health SE's reference requirements:</p>\n<blockquote>\n<p>Privacy addresses the question of who has access to personal information and under what conditions. [...]</p>\n<p>There are a variety of reasons for placing a high value on protecting the privacy, confidentiality, and security of health information (reviewed by Pritts, 2008). Some theorists depict privacy as a basic human good or right with intrinsic value (Fried, 1968; Moore, 2005; NRC, 2007a; Terry and Francis, 2007). They see privacy as being objectively valuable in itself, as an essential component of human well-being. They believe that respecting privacy (and autonomy) is a form of recognition of the attributes that give humans their moral uniqueness.</p>\n<p>The more common view is that privacy is valuable because it facilitates or promotes other fundamental values, including ideals of personhood (Bloustein, 1967; Gavison, 1980; Post, 2001; Solove, 2006; Taylor, 1989; Westin, 1966) such as:</p>\n<ul>\n<li>Personal autonomy (the ability to make personal decisions)</li>\n<li>Individuality</li>\n<li>Respect</li>\n<li>Dignity and worth as human beings</li>\n</ul>\n</blockquote>\n<p>From: <a href=\"http://www.ncbi.nlm.nih.gov/books/NBK9579/\" rel=\"nofollow noreferrer\">Beyond the HIPAA Privacy Rule: Enhancing Privacy, Improving Health Through Research.</a>.</p>\n<p>Although the linked text refers to privacy of information of health research participants, the introductory part (Definitions, Importance of Privacy) is about the general principle.</p>\n", "score": 2 } ]

[ "digestion", "disease" ]

[ { "answer_id": 3361, "body": "<p>Unless you are very short, your weight indicates that you are severely underweight, <a href=\"http://www.cdc.gov/healthyweight/assessing/\" rel=\"noreferrer\">see here for details</a>. If you are indeed underweight, then you should follow the advice given there:</p>\n\n<blockquote>\n <p>If you are concerned about being underweight, please seek a trained healthcare provider. </p>\n</blockquote>\n\n<p>The general advice that comes second to whatever your doctor's advice is, is given on <a href=\"http://www.eatright.org/resource/health/weight-loss/your-health-and-your-weight/healthy-weight-gain\" rel=\"noreferrer\">this page on healthy weight gain</a>. So, you'll need to increase your calorie intake, but make sure you get enough nutrients from all food groups.</p>\n", "score": 7 }, { "answer_id": 3359, "body": "<p>To increase weight and be healthy eat plenty of food rich in proteins (black beans, chickpeas, broccoli, potatoes, mushrooms), carbohydrates (Whole grain bread, pasta, cereals) and fat (avocado, olive oil, almonds, walnuts); include supplements and multivitamins in your diet, lift weights (don't do running or cardio) and plan your diet according to your activity level.</p>\n\n<p><a href=\"http://www.gainingweight101.com/gaining-weight-vegetarian-bodybuilding-diet-without-meat/\" rel=\"nofollow noreferrer\">http://www.gainingweight101.com/gaining-weight-vegetarian-bodybuilding-diet-without-meat/</a></p>\n\n<p><a href=\"http://www.peta.org/living/food/top-10-vegan-protein-sources/\" rel=\"nofollow noreferrer\">http://www.peta.org/living/food/top-10-vegan-protein-sources/</a></p>\n\n<p><a href=\"http://www.veggienumnum.com/nutrition/carbohydrates-dietary-fibre/\" rel=\"nofollow noreferrer\">http://www.veggienumnum.com/nutrition/carbohydrates-dietary-fibre/</a></p>\n\n<p><a href=\"http://www.helpguide.org/articles/healthy-eating/choosing-healthy-fats.htm\" rel=\"nofollow noreferrer\">http://www.helpguide.org/articles/healthy-eating/choosing-healthy-fats.htm</a></p>\n\n<p><a href=\"http://www.veganhealth.org/articles/fatstable\" rel=\"nofollow noreferrer\">http://www.veganhealth.org/articles/fatstable</a></p>\n", "score": 5 } ]

[ "nutrition", "diet", "micronutrients", "weight", "vegetarianism" ]

[ { "answer_id": 7334, "body": "<p>She had two periods afterwards so she is <strong>not</strong> pregnant. </p>\n\n<p>Who are you to demand that she take a test? You pretty much called her a liar when you did that. If you can't or won't accept her at her word about being on birth control, not being pregnant, etc, then I recommend you quit sleeping with women you have such a low opinion of.</p>\n", "score": 7 } ]

[ "obstetrics", "sex", "sexuality" ]

[ { "answer_id": 11195, "body": "<hr>\n\n<h2>Answer to the old question \"Can light-cheese cause ingrown toenails\":</h2>\n\n<p><strong>No</strong><br>\n<em>This Question might more be suited for Sceptic SE.</em><br>\nI suffered from an ingrown toenail, but all doctors agreed that it was caused by not cutting my nails properly (I.e. I cut too much of my nail) and so the skin started to grow into my nail bed.</p>\n\n<p>You will have to see a doctor about this, and the two options I know of <em>if there are infections caused by ingrown toenails</em> are surgery or to put brackets on your toe to pull it out of the nail bed.</p>\n\n<p>This has nothing to do with eating habits.</p>\n\n<p>EDIT:<br>\nIngrown toenails are caused by skin being in the way of the nail.<br>\nThere are two ways this can happen:<br>\n1. The skin is somewhere where it shouldn't be (i.e. growing into the nail bed if the nails has been cut too much)\nOr 2. The nail being somewhere where it shouldn't be (i.e. if you had strangely curved nails)</p>\n\n<p>Neither 1 nor 2 is related to eating habits or food consumption, hence the answer to your question is <strong>No</strong>.</p>\n\n<p>See <a href=\"http://www.mayoclinic.org/diseases-conditions/ingrown-toenails/symptoms-causes/dxc-20273047\" rel=\"nofollow noreferrer\" title=\"Mayo-Clinic\">Mayo-Clinic</a></p>\n", "score": 2 } ]

[ "contributing-factors", "nails", "sensitivity-intolerance" ]

[ { "answer_id": 13156, "body": "<p>Your question contains a number of over simplifications. Cancer isn't one disease. That's not an \"excuse\", it's a fact that was painfully learned by researchers who rolled up their sleeves to \"cure cancer\" and realized they had it wrong.</p>\n\n<p>Second, \"poisons\" (I presume you mean chemotherapy) are not the only treatment. You ignored not only surgery and radiation, which work for some people, but immunotherapy, which is producing some astonishing results for some particular cancers (not just where they started to grow, but their genetics, affect whether immunotherapy will work.) This <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038596/\" rel=\"nofollow noreferrer\">2014 article</a> talks about the research in that area and what has been learned. For melanoma, even stage 4 metastatic melanoma, projected survival time has gone from a small number of months to a decade or more, possibly to regaining the natural lifespan. One interesting sentence fragment:</p>\n\n<blockquote>\n <p>the availability of novel immunotherapies could potentially result in cancer turning into a controllable chronic disease in a considerable proportion of patients.</p>\n</blockquote>\n\n<p>And the field has moved dramatically even since that paper was published.</p>\n\n<p>I suggest reading <a href=\"https://www.scientificamerican.com/article/can-we-truly-cure-cancer/\" rel=\"nofollow noreferrer\">this Scientific American article</a> about what the phrase \"cure cancer\" involves. Yes, there are still a lot of people dying of cancer - I've been to my share of funerals - but there are plenty living with it and eventually dying of something else. </p>\n", "score": 2 } ]

[ "medications", "cancer", "research", "cure" ]

[ { "answer_id": 14516, "body": "<p>There are two main things to consider here:</p>\n\n<ol>\n<li>What kind of hairloss is there?</li>\n<li>What is in the product that is applied to the hair?</li>\n</ol>\n\n<p><strong>concerning 1:</strong> All humans loose their hair, constantly. That is part of the life cycle of hair und usually goes quite unnoticed when the hair is short and is progressively more obvious when the hair was allowed to grow longer. <br> </p>\n\n<blockquote>\n <p><a href=\"https://www.webmd.com/skin-problems-and-treatments/hair-loss/understanding-hair-loss-basics#1\" rel=\"noreferrer\">The average adult head has about 100,000 to 150,000 hairs and loses up to 100 of them a day; finding a few stray hairs on your hairbrush is not necessarily cause for alarm. <br> At any one time, about 90% of the hair on a person's scalp is growing. Each follicle has its own life cycle that can be influenced by age, disease, and a wide variety of other factors. This life cycle is divided into three phases: 1. Anagen -- active hair growth that lasts between two to six years 2. Catagen -- transitional hair growth that lasts two to three weeks\n 3. Telogen -- resting phase that lasts about two to three months; <strong>at the end of the resting phase the hair is shed</strong> and a new hair replaces it and the growing cycle starts again.</a></p>\n</blockquote>\n\n<p>Especially in males going <a href=\"https://en.wikipedia.org/wiki/Pattern_hair_loss\" rel=\"noreferrer\">bald with age</a> is very common. </p>\n\n<p>If it is this kind of genetic fate <em>or</em> because of underlying medical conditions (toxins, too much supplements…) asking questions on the web is no the best course of action. For that a medical examination is needed and prescriptions for <a href=\"https://www.webmd.com/skin-problems-and-treatments/hair-loss/men-hair-loss-17/slideshow-men-hair-loss-treatment\" rel=\"noreferrer\">finasterid or hair transplants</a> are equally unsuitable for 'the cloud'. Since hairloss <em>might</em> be just a cosmetic issue of aesthetics or an indication for serious issues a visit to a medical practitioner is strongly advised.</p>\n\n<p><strong>concerning 2.:</strong> <a href=\"https://www.codecheck.info/kosmetik_koerperpflege/haarstyling/gel/ean_4015000935722/id_1823963/Schwarzkopf_3_Wetter_Taft_Power_Styling_Gel_Mega_Stark.pro\" rel=\"noreferrer\">Checking for the ingredients of a specially preferred product mentioned in the qustion reveals that among other substances it contains some that are found to be of varying concern:</a> </p>\n\n<ul>\n<li>PEG-40, PEG-70: tensides, weakens the barrier function of skin </li>\n<li>Triethanolamine: immune system disruptor, potential allergen, irritant, nitrosamine producer</li>\n<li>Acrylates / Steareth-20 Methacrylate Copolymer: weakens barrier function of skin</li>\n<li>Disodium Edta: weakens cell membranes</li>\n<li>Polyester-5: the glue in the gel</li>\n<li>Phenoxyethanol: preservative, negative influence on immune system and nervous system, potential allergen</li>\n<li>Propylene Glycol: negative influence on immune system, potential allergen, suspected of being toxic or harmful to health </li>\n<li>Citral: potent allergen</li>\n</ul>\n\n<p>That means it is not an unrealistic assumption that indeed the product just causes trouble. It is a conglomerate of questionable ingredients. But that is far from certain! All of these substances are allowed in cosmetics after all. None of them is listed as directly causes premature hair loss. </p>\n\n<p>One explanation to consider is the perceptual issue of an aging man in panic finding these hairs: As stated earlier, hairs are constantly falling out. If some of them were glued together with gel before falling out that might just mean they did not increase in number; but that they only became much more noticeable that way.</p>\n\n<p>Using anything on hair is typically not necessary. If something is supicious: stop using it and watch if conditions improve.</p>\n", "score": 5 } ]

[ "side-effects", "hair" ]

[ { "answer_id": 14887, "body": "<p>Homeopathy remedies have no physiological effect (<a href=\"http://www.howdoeshomeopathywork.com\" rel=\"nofollow noreferrer\">http://www.howdoeshomeopathywork.com</a>). </p>\n\n<p>A homeopathic consultation along with the associated ritual of prescription etc may have a psychological or placebo effect. </p>\n\n<p>As far as the fish bone goes, chances are what you’re feeling is a scratch with associated inflammation which will go away in a few days (the perfect situation for a homeopathic remedy to “work”- a self limiting condition), but the only way to know for sure is to have someone competent have a look. </p>\n", "score": 2 } ]

[ "medications", "ear", "bones", "fish", "throat" ]

[ { "answer_id": 16722, "body": "<p>You do not need to make health-related conclusions from how the marketers behave or what they say.</p>\n\n<p>They give you the choice to buy either a fortified or non-fortified food, so they can earn from you in each case.</p>\n\n<p>Fortified foods are for those who believe they can benefit from an extra amount of a certain nutrient. People who believe that \"natural is the best\" might more likely chose non-fortified foods.</p>\n\n<p>There is an <a href=\"https://www.thyroid.org/iodine-deficiency/\" rel=\"nofollow noreferrer\">evidence</a>, for example, that iodized salt can decrease the incidence of goiter in areas with little iodine in the soil. Also, according to one <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/17344781\" rel=\"nofollow noreferrer\">2007 study from Bangladesh</a>:</p>\n\n<blockquote>\n <p>mandatory mass iodination of table salt consumption in a hyper-endemic\n iodine deficient area is safe and does not cause any side effect.</p>\n</blockquote>\n\n<p>To know if fortified foods have any side effects, you would need to search from nutrient to nutrient, consider different amounts and forms, etc.</p>\n", "score": 1 } ]

[ "supplement" ]

[ { "answer_id": 17309, "body": "<p>A definitive answer is unlikely because drug companies don't normally make it publicly known what drugs they're developing. </p>\n\n<p>There are a number of <a href=\"https://www.merckmanuals.com/professional/cardiovascular-disorders/arrhythmias-and-conduction-disorders/drugs-for-arrhythmias\" rel=\"nofollow noreferrer\">antiarrhythmic drugs</a> already available that could possibly treat palpitations, and there are also <a href=\"https://www.mayoclinic.org/tests-procedures/cardiac-ablation/about/pac-20384993\" rel=\"nofollow noreferrer\">ablation procedures</a>. Treatments exist now for arrhythmias. </p>\n", "score": 2 } ]

[ "cardiology", "cardiovascular-disease" ]

[ { "answer_id": 17496, "body": "<h2>No.</h2>\n<p>One is either infected or one isn't. There is no middle ground. Infection is defined as</p>\n<blockquote>\n<p><a href=\"http://medical-dictionary.thefreedictionary.com/infection\" rel=\"noreferrer\">invasion and multiplication of microorganisms in body tissues, as in an infectious disease.</a></p>\n</blockquote>\n<p>Also, biologically speaking, there aren't even viruses added because they remove them from their organism first (draw blood) and then re-insert them</p>\n", "score": 5 } ]

[ "blood", "infection", "hiv" ]

[ { "answer_id": 17820, "body": "<p>The problem is that dihydrotestosterone (DHT) does much more than contribute to hair loss. It also plays a crucial role in male sexual development and mood regulation. When DHT levels are reduced, either intentionally or unintentionally, it can impact these functions in unwanted ways and cause: </p>\n\n<p>Impotence,\nLower sex drive,\nDifficulty achieving orgasm,\nAbnormal ejaculation,\nGynecomastia (male breast development),\nDepression.</p>\n\n<p>However, these side effects only appear in a small minority of men. As with any medication, you should discuss with your hair loss physician whether DHT blockers or other pharmaceutical treatments offer a viable and effective option for addressing your hair loss issues.</p>\n\n<p>References:</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481923/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481923/</a></p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064044/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064044/</a></p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5023004/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5023004/</a></p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4339524/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4339524/</a></p>\n", "score": 5 } ]

[ "hairloss", "hormonal-imbalance" ]

[ { "answer_id": 18905, "body": "<p>The pathogenesis behind Aquagenic Urticaria isn't definitively known - and the extreme rarity of the condition makes studying it difficult (only ~100 cases published!)</p>\n\n<p>It does appear to be an allergic-type response - as shown in the linked article from your question the wheals are formed when histamine is released and AU appears to <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276800/#__sec2title\" rel=\"nofollow noreferrer\">respond to antihistamine treatment</a> in most cases. </p>\n\n<p>One theory (<a href=\"https://www.jaad.org/article/S0190-9622(86)70215-6/pdf\" rel=\"nofollow noreferrer\">Czarnetzki <em>et al</em></a> ) is that the patient isn't having an allergic reaction to the water itself but rather a water-soluble antigen present at the epidermal layer - and that when the antigen is dissolved in the water it then diffuses through the epidermal layer causing the mast cells to release histamine and produce the wheals. </p>\n\n<p>However that is probably not the full story - since there have been reported cases where there was no signs of a histamine response and treating with antihistamines proved ineffective (<a href=\"https://www.annallergy.org/article/S1081-1206(10)63071-2/pdf\" rel=\"nofollow noreferrer\">Luong <em>et al</em></a>)</p>\n\n<p>So to summarize - no definitive mechanism as been determined, but it's probably <em>not</em> a case of simply being allergic to H2O molecules.</p>\n", "score": 3 } ]

[ "allergy" ]

[ { "answer_id": 20855, "body": "<p><strong>Being transgendered is NOT a mental health condition</strong>.</p>\n<p>The American Psychiatric Association states that a mental health disorder requires distress or disability (<a href=\"https://www.apa.org/topics/lgbt/transgender\" rel=\"nofollow noreferrer\">APA, n.d.</a>).</p>\n<blockquote>\n<p>A psychological state is considered a mental disorder only if it causes significant distress or disability. Many transgender people do not experience their gender as distressing or disabling, which implies that identifying as transgender does not constitute a mental disorder.</p>\n</blockquote>\n<p>The WHO classified transgenderism as being a <em>gender identity disorder</em> in ICD-10 under the section entitled <em>mental and behavioural disorders</em>. However, in the latest version of the ICD, (<a href=\"http://www.who.int/classifications/icd/en/\" rel=\"nofollow noreferrer\">ICD-11</a>), gender incongruence is defined as <strong>a marked and persistent incongruence</strong> between a person's experienced gender and assigned sex and is under the section entitled <em>sexual health</em>.</p>\n<p>Dr. Lale Say, a reproductive health expert at the World Health Organization, said:</p>\n<blockquote>\n<p>It was taken out from mental health disorders because we had a better understanding that this was not actually a mental health condition (<a href=\"https://youtu.be/kyCgz0z05Ik\" rel=\"nofollow noreferrer\">Say, 2018</a>), and leaving it there was causing stigma.</p>\n</blockquote>\n<h3>References</h3>\n<p>APA, (n.d.). <em>Answers to Your Questions &amp; About transgender people, gender identity, and gender expression</em> Retrieved from: <a href=\"https://www.apa.org/topics/lgbt/transgender\" rel=\"nofollow noreferrer\">https://www.apa.org/topics/lgbt/transgender</a></p>\n<p>Say, (2018) *WHO: Revision of ICD-11 (gender incongruence/transgender) — questions and answers (Q&amp;A) Rterieved from: <a href=\"https://youtu.be/kyCgz0z05Ik\" rel=\"nofollow noreferrer\">https://youtu.be/kyCgz0z05Ik</a></p>\n", "score": 3 }, { "answer_id": 20861, "body": "<p>Transgender is a very broad and not a very well defined term, but a much more well defined term for which people most often mean is <em>feeling a persistent, consistent and insistent need for <a href=\"https://en.wikipedia.org/wiki/Transsexual\" rel=\"nofollow noreferrer\">transsexualism</a> since early as memory appeared in mind</em> (most often referred to as <a href=\"https://en.wikipedia.org/wiki/Gender_dysphoria\" rel=\"nofollow noreferrer\">gender dysphoria</a>) which as of itself is not a mental illness and generally isn't caused by a mental illness as I will further explain:</p>\n\n<p>Gender dysphoria can be caused by various <a href=\"https://en.wikipedia.org/wiki/Intersex\" rel=\"nofollow noreferrer\">intersexualism conditions</a> by which a human is somewhere between a female and a male at least by <em>brain anatomy and physiology</em> and of course, that effects <a href=\"https://en.wikipedia.org/wiki/Developmental_psychology\" rel=\"nofollow noreferrer\">developmental psychology</a> in the course of life (hence feeling, in a sense, somewhere between a female-woman and a male-man) but with a case-dependent <em>proper treatment</em>, if at all needed, a person can live functioning, constructing and possibly very happy life and do lots of good in this world.</p>\n\n<p>Further, gender dysphoria is a \"mental condition\" in the senses that:</p>\n\n<ul>\n<li>It requires tremendous amounts of time and energy to figure out how to deal with the dissonance between <em>gender sensation</em> or <em><a href=\"https://en.wikipedia.org/wiki/Gender_identity\" rel=\"nofollow noreferrer\">gender identity</a></em> and body appearance</li>\n<li><em>It requires tremendous amounts of time and energy to</em> chose how to deal with it and doing so in practice, which as of 2020 is going through a most likely (yet not necessary) vast change in body appearance, apparel, cosmetics, bureaucracy and so forth including taking hormonal treatment (and for some trans persons - different types of surgery)</li>\n<li>This is probably hardest (no pun intended): It requires dealing with ignorance and <a href=\"https://en.wikipedia.org/wiki/Transphobia\" rel=\"nofollow noreferrer\">transphobia</a> and often suffer from drug abuse, harsh violence and so forth (with many transgenders being, sadly, sexually abused, murdered or got suicide)</li>\n</ul>\n\n<p><strong>That said;</strong></p>\n\n<p>It should be noted that indeed there are some <strong>non general / extra ordinary / extremely rare</strong> cases in which some mental illness cause someone (as part of a <em>delusional</em> or <em>dissociative</em> phase) a gender dysphoria so she or he might actually transition based on wrong diagnosis in the end but these sad cases (which are barely seriously researched) will most likely end in <a href=\"https://en.wikipedia.org/wiki/Detransition\" rel=\"nofollow noreferrer\">detransition (permanent type)</a> and are different than generally all cases of transsexualism in <strong>etiology</strong>.<br>\nYet, these rare cases should be taken very seriously as people lost body parts and/or functions (such as gonads, genitals and female breast or hair or got a way softer voice and so forth) <code>or</code> got extra body parts and/or functions (such as female breast or more permanent hair or deeper voice and so forth) for which they are probably regret to this day.<br>\nI note that these <code>should-end-in-permanent-detransition</code> cases are neither the majority, nor the most of cases of gender dysphoria, per what I understand and explained.</p>\n\n<hr>\n\n<p>Update (comment notes that might get deleted):</p>\n\n<p>_{One has to differentiate between a <em>mental state</em> (or \"condition\"), a <em>mental disorder</em> (not being in order with the common mentality which isn't necessarily bad) and a <em>mental illness</em> (which at least harms or by proper consistent evidence, can consistently harm others and/or a person itself seriously);<br> As I have explained, transsexualism is a technical process that surly isn't a mental illness or disorder and gender dysphoria that usually cause it, generally isn't caused by a mental illness or disorder.}</p>\n\n<p>_{By my opinion, supporting both those who really need transsexualism and the tiny minority of detransitioners (permanent or not) and finding ways to prevent the extremely rare cases of <code>should-end-in-detransition</code> transsexualism (especially permanent type) is one way to make this world better.}</p>\n", "score": 3 } ]

[ "mental-health", "sexuality", "disorders", "gender-sex-identity", "gender-specific" ]

[ { "answer_id": 23297, "body": "<p>Sure, \"we\" are fighting the coronavirus. Or we are fighting the disease caused by coronavirus (COVID-19).</p>\n\n<p>I think it was quite clear what she meant.</p>\n\n<p>We could go into the semantics of whether one can \"fight\" a non-living thing, but it's probably not a particularly useful debate and is perhaps best left to linguists. </p>\n", "score": 1 } ]

[ "covid-19", "coronavirus" ]

[ { "answer_id": 25824, "body": "<blockquote>\n<p>I cannot easily find any research assessing the relationship between lockdowns and virus contagion/mortality.</p>\n</blockquote>\n<p>Try looking at it backwards: what encourages mutations (some of which will render an organism more <em>x</em> (and/or <em>y</em>, and/or <em>z</em>) and some of which will render it less <em>x</em> (and/or <em>y</em>, and/or <em>z</em>). To mutate, an organism must reproduce in order to pass on a mutation. Look at the <a href=\"https://blogs.biomedcentral.com/on-biology/2017/07/21/the-genesis-of-mrsa-resistance-emerged-years-before-the-introduction-of-methicillin-in-the-clinic/\" rel=\"nofollow noreferrer\">evolution of MRSA</a> as a good example: all that was needed was reproduction; environmental pressure selected the successful.</p>\n<p>Understanding this fundamental concept sheds light on the confusion you have.</p>\n<p>Simply stated, if lockdowns decrease the chances of viral replication (which they do very well), they will also decrease the chances of viral mutations, whether that be for a less contagious/lethal virus (not a good candidate for responding well to environmental pressure) or a more contagious/lethal one.</p>\n<blockquote>\n<p>Is this what is happening as a result of social distancing policy today and is it something epidemiologists weigh up against the risks to the healthcare system of a freer policies?</p>\n</blockquote>\n<p>Nope, not at all. Because that's not how viruses become more successful.</p>\n<p>Edited to add: Imagine a patient, J. Doe, early 60s, lives alone, leaves the house only to do monthly grocery shopping. During one of these outings, J. becomes infected with SARS-CoV 2. Early in the course of infection, a mutation occurs which increases the transmissibility of the virus by 50%. J., however, has mild symptoms only, and during a teleconference with a physician, J. is told to stay home and treat symptomatically. J. follows this advice, the infection runs its course, and the viruses die off. J. has avoided all contact with others and the newer, more transmissible virus had no where (else) to go.</p>\n<p>Now imagine J. Dope, early 60s, lives alone, doesn't like it, so goes out a lot despite warnings. During one of these outings, J. becomes infected with SARS-CoV 2. Early in the course of infection, a mutation occurs which increases the transmissibility of the virus by 50%. J., however, has mild symptoms only, so doesn't alter social behaviors. J. sheds the newer, more transmissible virus everywhere, and suddenly, a spike in cases is seen in the area J. lives.</p>\n<p>Which scenario is likely to increase the prevalence of the now more highly transmissible virus variant?</p>\n", "score": 3 } ]

[ "covid-19", "virus" ]

[ { "answer_id": 27470, "body": "<p>&quot;If a couple has no common defective gene, they can produce a big healthy population from just two people, right?&quot;</p>\n<p>No. As described in the review &quot;The genetic basis of disease&quot; Essays Biochem. 2018 Dec 3; 62(5): 643–723. Published online 2018 Dec 3. doi: 10.1042/EBC20170053\n&quot;we now know that, on average, each individual has several hundred variants that are either known, or predicted, to be damaging to gene function, including roughly 85 variants that lead to truncated (incomplete) protein products.&quot;</p>\n<p>Since a given 2nd generation offspring of a founding couple might have both their copies of a given gene be the exact same version from one grandparent, if that version is defective, both the offspring's copies will thus be defective. This is the consequence of inbreeding and is why for example conservation biologists try to preserve as many different individuals as possible as founders in a captive breeding program.</p>\n", "score": 2 } ]

[ "disease", "genetics", "reproduction" ]

[ { "answer_id": 28752, "body": "<p>As you note in your quote &quot;vaccination may reduce [data shows it does, substantially] an individual's overall risk of becoming infected&quot;. If an individual is not infected, they are not infectious and do not spread the virus. New mutations arise in proportion to the number of people infected, so if fewer people become infected (due to the vaccine), fewer new variants are generated.</p>\n<p>Here's one study that found &quot;CDC COVID-19 Study Shows mRNA Vaccines Reduce Risk of Infection by 91 Percent for Fully Vaccinated People&quot; CDC press release at <a href=\"https://www.cdc.gov/media/releases/2021/p0607-mrna-reduce-risks.html\" rel=\"nofollow noreferrer\">https://www.cdc.gov/media/releases/2021/p0607-mrna-reduce-risks.html</a></p>\n<p>Study is &quot;Prevention and Attenuation of COVID-19 by BNT162b2 and mRNA-1273 Vaccines&quot; doi: <a href=\"https://doi.org/10.1101/2021.06.01.21257987\" rel=\"nofollow noreferrer\">https://doi.org/10.1101/2021.06.01.21257987</a></p>\n<p>Exposure to COVID would be whatever mix of variants were circulating where and when they did the tests. The test population of health workers is described in the scientific paper as being from 8 locations (roughly half in Arizona). Data was collected from mid-December 2020 through mid-April 2021. &quot;Of 93 genetically sequenced viruses, 10 were variants of concern (8 B.1.429, 1 B.1.1.7, 1 B.1.427) and 1 was a variant of interest (P.2) (Table_S3)&quot;</p>\n<p>This is of course just one study, but illustrates the concept of protection against infection.</p>\n", "score": 5 } ]

[ "covid-19", "vaccination" ]

[ { "answer_id": 28851, "body": "<p>The way FDA approval works is that a manufacturer submits an application to the FDA for something they want to produce and market; FDA decides whether to approve or deny that application based on its contents.</p>\n<p>From <a href=\"https://investors.biontech.de/news-releases/news-release-details/pfizer-and-biontech-initiate-rolling-submission-biologics\" rel=\"noreferrer\">Pfizer and BioNTech's press release</a>, dated May 7th, 2021:</p>\n<blockquote>\n<p>Pfizer Inc. (NYSE: PFE) and BioNTech SE (Nasdaq: BNTX) today announced the initiation of a Biologics License Application (BLA) with the U.S. Food and Drug Administration (FDA) for approval of their mRNA vaccine to prevent COVID-19 in individuals 16 years of age and older</p>\n</blockquote>\n<p>From this we can infer that the application submitted for Comirnaty was for individuals 16+, so that's what FDA approved. We can infer that they did <strong>not</strong> ask for approval for anyone else, otherwise they would have announced it. They indicate this will happen once they have sufficient data:</p>\n<blockquote>\n<p>Pfizer and BioNTech also have submitted an application to expand the current EUA for their COVID-19 vaccine to include individuals 12 to 15 years of age. The Companies intend to submit a supplemental BLA to support licensure of the vaccine in this age group once the required data 6 months after the second vaccine dose are available.</p>\n</blockquote>\n<p>Presumably this is because trials started first in adults and older children so there were more data towards full approval in those groups, whereas data for younger children were collected more recently. The FDA only recently <a href=\"https://www.fda.gov/media/148542/download\" rel=\"noreferrer\">expanded the EUA to kids 12+ on May 10th</a>, just 3 days after they announced their application for full approval.</p>\n", "score": 5 } ]

[ "covid-19" ]

[ { "answer_id": 28958, "body": "<p>Unfortunately, there's no rule about viruses getting weaker. In fact the original SARS-CoV-2 was less deadly than some of the newer variants. In any case, SARS-CoV-2 has pretty much run rampant around the world even with the development of vaccines.</p>\n", "score": 4 } ]

[ "vaccination", "death" ]

[ { "answer_id": 29201, "body": "<blockquote>\n<p>we will never know that the vaccine have a probability to kill of ~0.1%</p>\n</blockquote>\n<p>Very unlikely given that randomized trials with thousands of participants have been conducted; <a href=\"https://doi.org/10.1016/j.vaccine.2017.03.092\" rel=\"nofollow noreferrer\">one meta-analysis</a> pooled 41,141 patients but &quot;None of the included trials reported any cases of vaccine-associated mortality&quot;.</p>\n", "score": 4 } ]

[ "vaccination", "statistics", "vaccine" ]

[ { "answer_id": 31299, "body": "<p>Vitamins A, D, E and K are fat-soluble.</p>\n<p>In solid food, you can trivially have both fat- and water-soluble molecules in a solid state.</p>\n<p>In purely liquid food, there needs to be an <a href=\"https://en.wikipedia.org/wiki/Emulsion\" rel=\"nofollow noreferrer\">emulsion</a> of a lipohibic and lipophilic phase to solute the fat- and water soluble vitamins. Milk would be one example of such an emulsion.</p>\n", "score": 2 } ]

[ "nutrition", "dermatology", "multi-vitamin" ]

[ { "answer_id": 11070, "body": "<p>You can get <a href=\"http://www.nhs.uk/Conditions/Genital-herpes/Pages/Introduction.aspx\" rel=\"nofollow noreferrer\">Genital Herpes</a> from someone licking your scrotum and there is no protection from Genital Herpes with condoms anyway as they don't cover the scrotum.</p>\n\n<p>With oral sex, the risk is only there for you if the person giving oral sex has a <a href=\"http://www.nhs.uk/conditions/Cold-sore/Pages/Introduction.aspx\" rel=\"nofollow noreferrer\">cold sore</a> and the risk is only there for your partner if you have Genital Herpes.</p>\n", "score": 4 } ]

[ "sti", "oral-sex", "condom", "genital-herpes" ]

[ { "answer_id": 20490, "body": "<p>The answer lies in the <a href=\"https://www.merriam-webster.com/dictionary/dietary%20supplement\" rel=\"nofollow noreferrer\">meaning of the word \"supplement\"</a>:</p>\n\n<blockquote>\n <p><strong>Definition of dietary supplement</strong></p>\n \n <p>: a product taken orally that contains one or more ingredients (such\n as vitamins or amino acids) that are intended to supplement one's diet\n and are not considered food</p>\n</blockquote>\n\n<p>The very meaning of the word means to \"add to\" so I don't think their disclaimer is unreasonable. Nobody can survive on supplements alone and even careful diets can be deficient in certain elements. </p>\n", "score": 1 } ]

[ "diet", "supplement", "pill" ]

[ { "answer_id": 21134, "body": "<blockquote>\n<p>why would natural selection stop at skin level?</p>\n</blockquote>\n<p>The division of humanity into &quot;races&quot; was not natural.\nYes, some (e.g. darker skin in sunnier locations) was natural,\nbut for the most part it was the result of human intelligence and racism.</p>\n<p>Genetic drift caused slight differences between isolated communities, but when those communities came into contact the interbreeding that would normally occur with non-intelligent species tended not to happen.</p>\n<p>People tend to favour those that look more like them and to fear those that look different, so it's natural to choose familiar looking mates.\nBeautiful people had more children than did ugly people.\nOver time, each group began to look more and more like its own ideal version.</p>\n<p>This deliberate, artificial, selection was based strictly on external features, so it was those features that eventually defined the races.</p>\n<p>There was no such process affecting internal features, so the &quot;evolution&quot; you are asking about simply didn't happen.</p>\n<p>EDIT:</p>\n<p>I hadn't realized that this process wasn't already well known.</p>\n<p>The idea certainly wasn't original to me. (I remember seeing, just within the last year, a quotation from a scientist (ethnologist?) at the beginning of a TV program that expressed the same idea, but of course I don't remember what it was.)</p>\n<p>I've searched for references for this process and can't find anything at the moment (I'll keep looking), other than something I wrote myself a few years ago:</p>\n<blockquote>\n<h2>Us versus Them</h2>\n<p>There is something in human nature that makes us want to identify with and to belong to groups of other human beings. We can see this grouping into &quot;us&quot; and &quot;them&quot; everywhere.</p>\n<p>Children separate themselves into girls and boys; high-school students separate into cliques of jocks, nerds, and preppies; adults separate into Masons, or Rotarians, or Kiwanis; sports lovers separate into Mets fans or Yankees fans; and so on.</p>\n<p>Two individuals can have extremely different backgrounds and interests, but if they meet as strangers and each is wearing a Yankees cap, they experience something that links them. There is no objective reason for this; unless they have bet money on the outcome of a game it really makes no difference to those individuals, much less the rest of the world, whether their team wins. But to them it <em>is</em> important; if the team wins they somehow feel that they personally have won, that they are personally better than they would have been had the team lost.</p>\n<p>This phenomenon happens at all levels. Many people are proud of their city, their state, or their country for no reason other than that they are part of those groups. If you think about it, it really doesn't make sense, but it <em>is</em> a fundamental part of what most humans are. (If Texas really were objectively better than Oklahoma, everyone would abandon the one state and move to the other. Texans might say that the reason this doesn't happen is because all Oklahomans are too stupid to see the truth, thereby further illustrating the &quot;us&quot; versus &quot;them&quot; phenomenon.)</p>\n<p>From a survival perspective, this attitude has had great benefits throughout history. If someone identifies more with you than with the person beside you, they are going to kill that person before they kill you. If you are in trouble, someone that identifies with you is much more likely to help you, even if only because they might hope the same of you someday. Having <em>other</em> people view the world in terms of &quot;us&quot; and &quot;them&quot; increases <em>your</em> chance of survival.</p>\n<h2>Selection</h2>\n<p>The earliest, most basic grouping was by family. We tend to look very much like our parents, our siblings, and our children, and we feel safest in their company. If we identify ourselves by that criterion, we will also have a slight tendency to identify with other people that look like us. We will naturally be more likely to work with, to be friends with, and to marry people that look like our family.</p>\n<p>Isolated groups will develop an ideal image of what they look like, and over time members of that group will come to look more and more like that ideal. Children whose appearance is outside the norm will be picked on, and as adults they will be outcasts. These funny-looking or ugly people will be far less likely to survive or to find mates, and over generations the genes that make them look different will be eliminated from the community.</p>\n<p>In a world of geographically isolated settlements, after dozens of generations, the inbreeding will greatly reduce each group's genetic variability. Each group will of course have its own unique selection of genes, different from that of all other groups. Where there is contact between groups, the &quot;us&quot; versus &quot;them&quot; nature will exaggerate those differences even more. It will be easy to see which members of the &quot;us&quot; community have &quot;them&quot; characteristics, and any such children will become outcasts.</p>\n<h2>Race</h2>\n<p>Over the centuries, this &quot;us&quot; versus &quot;them&quot; inspired inbreeding is what has created what we now call race. Racism isn't the natural consequence of the existence of race. The causal relationship is actually the exact opposite. Race is the inevitable outcome of human nature's &quot;us&quot; versus &quot;them&quot; mentality.</p>\n</blockquote>\n", "score": 1 } ]

[ "anatomy" ]

[ { "answer_id": 23056, "body": "<p>As @BryanKrause points out in a comment, there are many, many, <a href=\"https://en.wikipedia.org/wiki/Strain_(biology)\" rel=\"nofollow noreferrer\">strains</a> of Pneumococcus, many of which <strong>do not cause disease in otherwise healthy humans</strong>. The paper you referred to looked at 500 strains of Pneumococcus: \"They formed smooth colonies and were <strong>for the most part avirulent</strong> for mice.\" That is, most of the strains they looked were not disease causing! You may be more familiar with this phenomena with E. coli and food borne disease. All of us have guts full of E. coli which we live in a symbiotic relationship with. However, if you pick up the wrong strain from a contaminated salad bar, you can get very, very, sick. </p>\n\n<p>For bacteria, the species level is a fairly gross classification, and each strain may have subtle variations in the proteins presented at the surface of the bacterium. These surface proteins can play a key role in both the virulence of the bacteria, and our immune response to it. The <a href=\"https://www.cdc.gov/vaccines/hcp/adults/downloads/fs-pneumo-hcp.pdf\" rel=\"nofollow noreferrer\">CDC tracks 90 strains of Pneumococcus that are responsible for most serious human disease. The current pneumococcal polysaccharide vaccine is effective against 23 of those strains.</a>. Having been exposed to one of the non-disease causing strains does not necessarily confer immunity to a disease causing train. It depends on the details of the differences between the strains.</p>\n\n<p>In addition, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3582124/\" rel=\"nofollow noreferrer\">our immune systems tend to fail as we get older</a>. As we age our immune systems have a lessened ability to respond to new infections, and they can even \"forget\" how to respond to pathogens that have already been seen. That's why the CDC recommends this vaccine for adults over the age of 65, and younger adults with compromised immune systems. It isn't generally offered to healthy young people.</p>\n", "score": 2 }, { "answer_id": 23053, "body": "<p>There are two immune responses to an infection, primary and secondary. Vaccination makes it possible for the body to immediately switch to a secondary response. So that's why young adults are vaccinated again meningococcal disease so that they don't die from meningitis while the body is still mounting its primary immune response.</p>\n<blockquote>\n<p>The secondary immune responses can usually prevent disease, because the pathogen is detected, attacked and destroyed before symptoms appear. In general, adults respond more rapidly to infection than children. They are able to prevent disease or reduce the severity of the disease by mounting a rapid and strong immune response to antigens they have previously experienced. In contrast, children have not experienced as many antigens and are more likely to get sick.</p>\n<p>Memory of the infection is reinforced and long lived antibodies remain in circulation. Some infections, such as chickenpox, induce a life-long memory of infection. Other infections, such as influenza, vary from season to season to such an extent that even an adult is unable to adapt.</p>\n</blockquote>\n<p><a href=\"https://www.immune.org.nz/immunisation/immune-system-vaccination\" rel=\"nofollow noreferrer\">https://www.immune.org.nz/immunisation/immune-system-vaccination</a></p>\n", "score": 1 } ]

[ "vaccination", "bacteria" ]

[ { "answer_id": 25191, "body": "<p><strong>You seem to have misunderstood efficacy.</strong></p>\n<p>The 95% efficacy figure is a derived from a ratio of the number of cases in the control group (no vaccine) to the number of cases in the vaccine group. So, if both groups have 1000 people, perhaps 100 people in the control group become infected, while only 5 people in the vaccine group become infected. The vaccine efficacy is 95%, since the number of cases in the vaccine group is 95% lower than what you saw in the no-vaccine group (note that these numbers are illustrative and not actual figures).</p>\n<p>A 95% efficacy does not mean that 5% of people will die from the disease. It doesn't even mean that 5% of people will become infected. It means that 95% of people <em>who would have otherwise been infected</em> will not be. If everyone was magically vaccinated today, you would expect the number of cases to drop by 95%, and the number of deaths from the disease to drop by a similar amount. Instead of 2.5% of the population dying, it might be more like 0.13%.</p>\n<p>Note that there will be major downstream effects since viruses spread in an exponential manner - an important number you may have heard of is called R0, which represents the average number of new people an infected person will infect. A vaccine can cause R0 to drop below 1, meaning that the number of cases will dwindle over time. It's not just the case that a vaccine will prevent infection in 95% of people who would have otherwise gotten the disease, it also drastically lowers the number of people who &quot;would have otherwise gotten the disease&quot;, since 95% of vaccinated individuals won't spread the disease.</p>\n", "score": 5 }, { "answer_id": 25189, "body": "<p>Two major reasons and one minor:</p>\n<ul>\n<li><p><strong><a href=\"https://en.wikipedia.org/wiki/Herd_immunity\" rel=\"nofollow noreferrer\">Herd immunity</a></strong>: The 95% for which the vaccine works are not only spared from the disease, but they also do not infect others and thus do not contribute to spreading the virus. In absence of hygienic countermeasures, an average person infected with Covid-19 infects about 3 others on average (<a href=\"https://en.wikipedia.org/wiki/Basic_reproduction_number\" rel=\"nofollow noreferrer\">basic reproductive rate</a>). As this number is bigger than 1, the virus can spread; otherwise it would die out. Now, if 95% of those 3 would be immune thanks to the vaccine, only 0.15 people would get infected on average, which is far less than 1 (and it gets even better with hygiene). If the entire population were vaccinated instantly (with 95% success rate), Covid-19 would die out in a few weeks, simply because it could not spread anymore.</p>\n</li>\n<li><p><strong>Independence of probabilities:</strong> There is no reason to expect that the vaccine works exclusively for people who would also survive an infection. For a simple calculation, let’s assume that the vaccine is equally likely to work for everybody, i.e., independent of their chances to survive an infection¹. In that case the vaccine saves 95% of the 2.5% that would be killed by the virus and only 0.125% would die (0.05·0.025 = 0.00125).</p>\n</li>\n<li><p><strong>It’s not only about deaths</strong>. Survivors of Covid-19 can still suffer from severe long-lasting or permanent damage. This is also something you want to avoid.</p>\n</li>\n</ul>\n<hr />\n^{\n¹ This is a simplifying assumption, because whether the vaccine works for you depends on your immune system, which also influences whether you survive corona. However, probably nobody knows yet how strong this correlation is and what its direction is, i.e., whether the vaccine works better or worse for corona-sensitive people (this would also depend on the individual vaccine). The assumption is certainly closer to the truth than that the vaccine only works for those who would survive anyway.\n}\n", "score": 4 } ]

[ "covid-19" ]

[ { "answer_id": 27493, "body": "<p>This question is like saying that a log cabin is almost identical to a skyscraper - they’re just buildings, and many of the parts used in one are also used in the other - they’re just arranged differently. For example, water (H2O) is only one atom different to Hydrogen Peroxide (H2O2) - and you certainly wouldn’t want to be drinking that.</p>\n", "score": 5 }, { "answer_id": 32174, "body": "<p>I'm just assuming, but my guess is because Methamphetamine is able to cross the blood brain barrier unlike Pseudoephedrine, which cannot. But that's not the only possibility why one drug is so much stronger than the other. The way molecules rotate polarized light also seems to have an effect on how the body reacts to it. Such as L-Methamphetamine (levomethamphetamine) was or is sold out right in Vick inhalers, but does nothing to the central nervous system. Unlike D-Methamphetamine (dextromethamphetamine).\nThis part is just a total guess... but since the only difference is an oxygen molecular, I'd guess that would have something to do with how the body consumes the molecular. So jumble all that together and you're a lot closer to your answer. I know it's impossible to do a simple search for this information, because web results contradict each other and most just label it all just bad and is utterly useless for gaining an understanding. Hydrochloric acid isn't something you'd want to consume, but most pills are the HCl salt form of a drug. Such as pseudoephedrine medications.\nCause clearly your question is comparing a log cabin with a chimney to a log cabin without a chimney.</p>\n", "score": 0 } ]

[ "side-effects" ]

[ { "answer_id": 27632, "body": "<p>First up Coleman's, well, he's a crank. There's no other word for it - he's an AIDS denialist, a COVID-denialist, and the lion's share of his career has been spent writing lurid tabloid &quot;advice&quot; columns in such bastions of facts and integrity as <em>The People</em> and <em>The Sun</em>, running premium-rate sex advice phone lines and writing (mostly) self-published books. He hasn't been a licensed doctor for some five years and he hasn't been actively practicing medicine for longer.</p>\n<p>None of this means he's necessarily <em>wrong</em>, mind you. Although it would suggest approaching any of his, er, proclamations with a substantial dose of skepticism.</p>\n<p>The book you refer to, and in particular it's pivotal claim was so sketchy and poorly evidenced as to attract an <a href=\"http://news.bbc.co.uk/1/hi/england/devon/4117064.stm\" rel=\"nofollow noreferrer\">advertising ban</a> from the Advertising Standards Authority.</p>\n<p>But it's not only Coleman's book that's making this sort of claim, if it were then I doubt anyone who didn't buy their headgear in the baking supplies aisle would give it a second thought. As you mention there's actual papers, published in serious medical journals making some pretty scary-sounding claims about the levels of medical error.</p>\n<p>The Johns Hopkins paper you mention is perhaps the most often touted (and IIRC the highest figure that doesn't come from someone like Gary Null or Mike Adams) at ~250,000 but before that there was the Institute of Medicine's report <em>&quot;To Err Is Human&quot;</em> in 1999 which had a lower-but-still-alarming estimate of 44,000 to 96,000 per year.</p>\n<p>But these analyses aren't without issues, the IoM report was perhaps a little too keen to mark things as &quot;errors&quot; when there wasn't really anything to back that up and scaling up from two studies that looked at specific areas of the US to the whole country has a bit of a &quot;finger in the air&quot; feel to it.</p>\n<p>The Makary and Daniel paper takes a couple of relatively small studies (<em>Landrigan et al</em> and <em><a href=\"https://www.healthaffairs.org/doi/full/10.1377/hlthaff.2011.0190\" rel=\"nofollow noreferrer\">Classen et al</a></em>) which looked at adverse events and then performs some pretty sweeping up-scaling. <em>Classen</em> is structured around <em>every</em> adverse event being &quot;preventable&quot;, and this is what Markary and Daniel scale up from the 1,000 hospital admissions in the study (vs. ~37million a year total in the US) to produce their upper estimate of 400,000 deaths per year.</p>\n<p>The biggest study included was the 2004 <a href=\"https://www.healthgrades.com/media/english/pdf/HG_Patient_Safety_Study_Final.pdf\" rel=\"nofollow noreferrer\">HealthGrades Quality Study</a> which looked at &quot;Patient Safety Incidents&quot; which include:</p>\n<ul>\n<li>Complications of anesthesia</li>\n<li>Death in low mortality Diagnostic Related Groupings (DRGs)</li>\n<li>Decubitus ulcer (bed sores)</li>\n<li>Death among surgical inpatients with serious treatable complications</li>\n<li>Iatrogenic pneumothorax</li>\n<li>Selected infections due to medical care</li>\n<li>Post-operative hip fracture</li>\n<li>Post-operative hemorrhage or hematoma</li>\n<li>Post-operative physiologic and metabolic derangements</li>\n<li>Post-operative respiratory failure</li>\n<li>Post-operative pulmonary embolism or deep vein thrombosis</li>\n<li>Post-operative sepsis</li>\n<li>Post-operative abdominal wound dehiscence</li>\n<li>Accidental puncture or laceration</li>\n<li>Transfusion reaction</li>\n</ul>\n<p>Some of those you can clearly see <em>could be</em> but not necessarily <em>are</em> the result of medical errors. And as the authors of the report point out the numbers of fatalities resulting from some of these are heavily skewed by the fact that this is coming from Medicare data - which means it's predominantly the over 65's (Is the notion that the elderly are more frail and consequently more likely to die after surgery <strong>really</strong> news to anyone?) Which makes Markary and Daniel's scaling of this to the whole US population to get their ~250,000 figure, shaky at best.</p>\n<p>A recurring problem for studies trying to examine this is that there's an awful lot of estimating going on, a great deal of use of indirect measures to signal an &quot;error&quot; may have occurred and a veritable cornucopia of differing methods for determining what truly counts as a &quot;medical error&quot;.</p>\n<p>A recent (2020) systemic review from Yale - <em><a href=\"https://link.springer.com/article/10.1007/s11606-019-05592-5\" rel=\"nofollow noreferrer\">Rodwin et al</a></em> was published in the Journal of Internal Medicine and attempts to address this indirectness. They did so by examining studies of in-patient deaths rather than admissions and then looking to see if they were preventable. To quote:</p>\n<blockquote>\n<p>Studies that review series of admissions and determine whether adverse events occurred, whether the events were preventable, and what harms resulted have been criticized for indirectness when used to estimate the number of deaths due to medical error.5, 6 In contrast, studies of inpatient deaths offer a more direct way of estimating the rate of preventable deaths.</p>\n</blockquote>\n<p>They attempted to address some of the scaling issues of previous efforts thusly:</p>\n<blockquote>\n<p>Studies limited to specific populations such as pediatric, trauma, or maternity patients were excluded because our primary research question was to determine the overall rate of preventable mortality in hospitalized patients and these populations are less generalizable.</p>\n</blockquote>\n<p>This review went on to establish that the likely figure is far lower than suggested by the Johns Hopkins paper, estimating it to be around 22,000 per annum and this would also place it far, far lower on the &quot;cause of death&quot; leaderboard:</p>\n<blockquote>\n<p>While the rate of preventable mortality in hospitalized patients is lower than is often reported, it still represents what would be the 15th leading cause of death in the USA and deserves the continued attention of clinicians, hospital administrators, and policy makers.</p>\n</blockquote>\n<p>There's still some pretty big limitations to the Yale study - The determination of whether a death was preventable or not is still essentially subjective - determined by physician review. And there was a dearth of suitable studies from the US for example so you're trying to metric the rate of errors in the US from data in other countries, and the US medical system has some pretty significant differences to the ones in use in places like Canada and Europe.</p>\n<p>Another US-aimed study attempting to determine the role of medical errors in deaths is <em><a href=\"https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2720915\" rel=\"nofollow noreferrer\">Sunshine et al</a></em> from 2016 suggests that the numbers of deaths where an &quot;Adverse Effect of Medical Treatment&quot; (AEMT) as they call it was the underlying cause of death is low (~5,200) and higher where the AEMT was in the cause of death &quot;chain&quot; (~108,780) that the estimated proportion of these that is classed as &quot;misadventure&quot; (i.e. medical error) is only about 8.5% so the figures are pretty low (about 9,572). The data underlying the study isn't going to capture everything, as they authors point out:</p>\n<blockquote>\n<p>The GBD approach for estimating mortality associated with AEMT also has limitations. First, ICD-coded death certificates have been shown to have varying degrees of reliability in identifying medical harm. They may have limited ability to distinguish between variation in completeness of death certificate reporting and variation in the occurrence of AEMT events. It is also probable that many deaths involving AEMT are not captured either because of motivated misreporting or unintentional omission.</p>\n</blockquote>\n<p>So it's probably a lower-bound at best - but still interesting when compared with the Yale findings.</p>\n<p><em>If</em> the Yale figure is accurate is this still too high? Probably. Does this mean there should be continuing efforts to reduce this figure as much as possible? Absolutely. Eliminating errors entirely is..unrealistic. But physicians and other medical professionals are human and humans do make mistakes, it doesn't make them monsters and it doesn't mean that seeking medical treatment is more dangerous than not.</p>\n<p>Sure if you go into hospital with appendicitis there's a non-zero chance the surgeon is going to slip, slice something they shouldn't and you might die, but I think it's a fairly safe bet that your chances are a hell of a lot worse if you stay home.</p>\n", "score": 4 } ]

[ "medications", "practice-of-medicine", "death", "medical-records" ]

[ { "answer_id": 28830, "body": "<p>There is no &quot;authoritative document&quot; like you ask for. The FDA doesn't set concrete standards for efficacy and safety; rather, they review applications for vaccines and other drugs on a case-by-case basis according to safety, efficacy, other available treatments, and severity of the condition.</p>\n<p>The FDA has issued <a href=\"https://www.fda.gov/media/139638/download\" rel=\"nofollow noreferrer\">guidance to industry</a> about how they expect to review vaccines and consider data (they issue these sorts of guidance documents for all sorts of things), but none of it is binding. Most of it is pretty vague, for example on efficacy:</p>\n<blockquote>\n<p>To generate sufficient data to meet the BLA approval standard, late phase clinical\ntrials to demonstrate vaccine efficacy with formal hypothesis testing will likely\nneed to enroll many thousands of participants, including many with medical\ncomorbidities for trials seeking to assess protection against severe COVID-19</p>\n</blockquote>\n<p>And for safety:</p>\n<blockquote>\n<p>The pre-licensure safety database for preventive vaccines for infectious diseases\ntypically consists of at least 3,000 study participants vaccinated with the dosing\nregimen intended for licensure. FDA anticipates that adequately powered efficacy\ntrials for COVID-19 vaccines will be of sufficient size to provide an acceptable\nsafety database for each of younger adult and elderly populations, provided that no\nsignificant safety concerns arise during clinical development that would warrant\nfurther pre-licensure evaluation.</p>\n</blockquote>\n<p>This isn't saying anything about <em>requirements</em>, it's saying &quot;hey, here's what people usually do to convince us, so you know what the rough expectations are&quot;.</p>\n<p>Other guidance seems to be more specific:</p>\n<blockquote>\n<p>To ensure that a widely deployed COVID-19 vaccine is effective, the primary\nefficacy endpoint point estimate for a placebo-controlled efficacy trial should be at\nleast 50%, and the statistical success criterion should be that the lower bound of\nthe appropriately alpha-adjusted confidence interval around the primary efficacy\nendpoint point estimate is &gt;30%.</p>\n<p>The same statistical success criterion should be used for any interim analysis\ndesigned for early detection of efficacy.</p>\n<p>A lower bound ≤30% but &gt;0% may be acceptable as a statistical success\ncriterion for a secondary efficacy endpoint, provided that secondary endpoint\nhypothesis testing is dependent on success on the primary endpoint.</p>\n</blockquote>\n<p>but note this is about <em>trial design</em>, not bounds for acceptance.</p>\n", "score": 3 } ]

[ "united-states", "regulatory-agencies", "vaccine" ]

[ { "answer_id": 28930, "body": "<p><strong>TL;DR: No, there is no medical reason to feed ice cream to surgery patients.</strong></p>\n<p>Although it's just a fictional movie, the premise is probably sound. He was recovering from surgery for a gunshot wound to the buttocks, and he kept asking for ice cream, which a young soldier freshly back from a tropical war zone would likely relish. Ice cream is high in protein, which a surgery patient needs, plus it has plenty of calories and fat, so it will clearly sustain him. So why would the nurses deny him if that's what he wants to eat? After all, he's a young, fit, otherwise healthy young man with no reason not to eat ice cream for a few days if he wants.</p>\n<p>Are general surgery patients today routinely encouraged to eat ice cream? I can find no indication whatsoever in the medical literature (or popular press or anywhere else) that they are, and I can't imagine any reason why they would be.</p>\n<p>But what about kids being fed ice cream after tonsillectomies?</p>\n<p>Yes, that's common practice for the simple reason that soft foods are required following tonsillectomy, cold foods are soothing to a sore throat, and ice cream is both. It's even been referred to as a form of cryotherapy in <a href=\"https://clinicaltrials.gov/ct2/show/NCT04164511\" rel=\"nofollow noreferrer\">one ongoing clinical trial</a>, and Cleveland Clinic includes it in their <a href=\"https://my.clevelandclinic.org/health/treatments/17562-tonsillectomy-postop-care\" rel=\"nofollow noreferrer\">list of post-op food options</a>.</p>\n<p>But being shot in the butt isn't throat surgery, and neither are the vast majority of other surgeries.</p>\n<p>So, no. There's nothing medically important about ice cream following surgery.</p>\n", "score": 2 } ]

[ "nutrition", "surgery", "post-surgical" ]

[ { "answer_id": 30577, "body": "<p>Your first source does not appear to support the idea that boosters are now ineffective, only that they are possibly less effective.</p>\n<blockquote>\n<p>We next examined the impact of a Pfizer booster dose, administrated 7 months after Pfizer vaccination. The sera were collected one month after the third dose. The booster dose enhanced\nneutralization titers against D614G and Delta by 39 and 49 fold... It was also associated with strong increase of the neutralization activity against Omicron 100% of the tested sera displayed a neutralizing activity at this time point.</p>\n</blockquote>\n<p>We can only speculate but I would guess the reason why there hasn't been a major change in public health policy is likely that this is still preliminary research and it would be unwise to hastily halt a very large programme that has up to now been quite effective.</p>\n", "score": 5 }, { "answer_id": 30611, "body": "<p>As OP doesn't like the data presented in the other answers I will add the data recently published in <a href=\"https://www.nejm.org/doi/full/10.1056/NEJMc2119641?query=RP\" rel=\"nofollow noreferrer\">New England Journal of Medicine</a> article titled &quot;<em>Plasma Neutralization of the SARS-CoV-2 Omicron Variant</em>&quot;¹</p>\n<p>In this article the authors compare vaccine with and without booster to infection with booster. The findings are that vaccination with booster (6 months post initial vaccination course) results in higher neutralization titres by as much as 38x. Infection followed by vaccination results in greater neutralization titres, providing up to 154x higher. It is not discussed how this relates to protection from disease, but generally increased neutralizing titres will relate to greater protection.</p>\n<p>(only) Fig from article:</p>\n<p><a href=\"https://i.stack.imgur.com/jmvQM.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/jmvQM.jpg\" alt=\"NEJM neutralization titres omicron\" /></a></p>\n<p>There is also <a href=\"https://www.nejm.org/doi/full/10.1056/NEJMc2119358\" rel=\"nofollow noreferrer\">this article</a> (also from NEJM) showing the neutralization titres of 2 vs 3 Pfizer vaccines in a very small (20 people/group) study in Israel, which shows that with the regular course of vaccination, there is some neutralization of the Omicron, but not much, but when boosted that value increases².</p>\n<p><a href=\"https://i.stack.imgur.com/EEMWW.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/EEMWW.png\" alt=\"NEJM Omi neutralization\" /></a></p>\n<p>In addition, there is a <a href=\"https://www.medrxiv.org/content/10.1101/2021.12.27.21268278v1.full\" rel=\"nofollow noreferrer\">pre-print from a Danish study</a> that found that the odds-ratio risk of infection is 0.54 for booster vaccinated compared to fully vaccinated³. An odds-ratio of 1.00 would be the same as the reference value, so a lower value is less risk of infection.</p>\n<p><a href=\"https://i.stack.imgur.com/RuMYv.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/RuMYv.png\" alt=\"Archive\" /></a></p>\n<p>Edited to add a paper from <a href=\"https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(21)00267-6/fulltext\" rel=\"nofollow noreferrer\">Lancet Microbe</a> linked by OP in the comments which looked at the efficacy of the several vaccines against some of the variants, not Omicron, but covering Delta. In this paper⁴ they found, as others have done that there is a reduction in the efficacy of the vaccine against variants, and attempted to model what would happen if boosted or not. The figures are fairly complex, but show that protection from vaccination without booster is lower than if boosted for all of the vaccines studied:</p>\n<p>Figure 3 from Lancet:\n<a href=\"https://i.stack.imgur.com/BYNh1.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/BYNh1.png\" alt=\"Lancet 1\" /></a></p>\n<p>Figure 4 from Lancet:\n<a href=\"https://i.stack.imgur.com/cceeN.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/cceeN.png\" alt=\"Lancet 2\" /></a></p>\n<p>In conclusion, with the data presented in other answers, it seems that booster vaccination provides protection against the omicron variant that the regular vaccination course does not, and also provides protection against the other variants too.</p>\n<p>1: Schmidt <em>et al</em>., NEJM. Dec 30 2021.</p>\n<p>2: Nemet <em>et al</em>., NEJM. Dec 29 2021.</p>\n<p>3: Lyngse <em>et al</em>., MedArchive. Dec 17 2021.</p>\n<p>4: Cromer <em>et al</em>., Lancet Microbe 3(1), e52-e61, Jan 01 2022.</p>\n", "score": 5 }, { "answer_id": 30586, "body": "<p>The discussion section in the <a href=\"https://media.nature.com/original/magazine-assets/d41586-021-03827-2/d41586-021-03827-2.pdf\" rel=\"nofollow noreferrer\">paper</a> in your first link makes the case for the booster programs:</p>\n<blockquote>\n<p>A booster dose significantly improves the quality and the level of the humoral immune response and is associated with a strong protection against severe forms of disease. An accelerated deployment of vaccines and boosters throughout the world is necessary to counteract viral spread.</p>\n</blockquote>\n<p>This was consistent with the reduced neutralization levels they saw of the booster vs Omicron compared with booster vs Delta, and they cited an Israeli study <a href=\"https://www.thelancet.com/action/showPdf?pii=S0140-6736%2821%2902249-2\" rel=\"nofollow noreferrer\"><em>Barda et al</em></a> to support that this does indeed translate into clinical outcomes.</p>\n<blockquote>\n<p>Could you please clarify this: &quot;Altogether, these results indicate that Omicron is poorly or not neutralized by vaccinees’ sera sampled 5 months after vaccination. The booster dose triggered a detectable cross-neutralization activity against Omicron. However, even after the booster dose the variant displayed a reduction of ED50 of 18 and 6 fold, when compared to D614G and Delta, respectively.&quot;</p>\n</blockquote>\n<p>Pretty much what it says - at ~5 months after the previous vaccination the performance against Omicron was poor, it was already reduced vs Delta at that interval as well, and since the vaccination isn't <em>quite</em> as effective against the Omicron variant as it is against Delta the end result was that at that point in the cycle it was barely doing anything against Omicron.</p>\n<p>When you add the booster dose in it's more effective against Omicron (albeit still not <em>as</em> effective as it is against Delta),</p>\n<p>At two doses + 5 months less than 12% of individuals were producing neutralizing antibodies sufficient for an effect against Omicron but at <em>three</em> doses 100% of the individuals they tested contained neutralizing antibodies:</p>\n<p><a href=\"https://i.stack.imgur.com/xnGWn.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/xnGWn.png\" alt=\"Extended Data Fig.5 ('a' and 'b')\" /></a></p>\n<p>Yes the antigenic differences between Delta and Omicron means the <em>levels</em> of these antibodies capable of neutralizing it is lower vs Omicron than the other variants but it's still sufficient to have a significant benefit in reducing the severity of the disease in those that get it, i.e. fewer people in hospital, fewer &quot;severe&quot; cases, and of course fewer deaths:</p>\n<p><a href=\"https://i.stack.imgur.com/4jHkj.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/4jHkj.png\" alt=\"Barda et al Fig.1\" /></a></p>\n<p>It might sound callous but frankly those who aren't sick enough to need hospital treatment aren't in much danger, and the &quot;treatment&quot; for them is to stay at home for 7-10 days and try not to cough on too many people in the meantime.</p>\n<p>The paper on the use of therapeutic mAbs that a better &quot;targeted&quot; to Omicron than those produced by the immune response of vaccinated/convalescent individuals looks interesting, although as seen in the <em>Schwartz</em> article the performance against Omicron varies considerably among the different mAbs, arguably falling victim to the same differences in the new variant that have affected the vaccine performance. I'm not saying it's not worth pursuing - and certainly in the UK the NHS is using sotrovimab treatments (which seems to work against Omicron) for those in certain <a href=\"https://www.nhs.uk/medicines/sotrovimab/who-can-and-cannot-have-sotrovimab/\" rel=\"nofollow noreferrer\">high-risk categories</a> who have tested positive.</p>\n<p>But there's some scaling issues to consider - sotrovimab is given on an IV over a 30 minute period plus a 30 minute monitoring period. So that's an <em>hour</em> per patient, plus any booking in and admin overhead, at a time when clinical resources are already at premium. A vaccine booster takes seconds to administer (certainly my whole appointment from walking in the door of the building to back out was less than 5 minutes including all the admin!), and can be administered by staff with a comparatively low level of clinical training and also be done pretty much <em>anywhere</em> (pharmacy, shopping center, gazebo in a carpark etc).</p>\n<p>So the vaccines are already here, already tested, already mass-produced and already have a logistical infrastructure in place to give them to people on a massive scale. So, with the waning immunity offered by the previous two doses in the populations of places like Great Britain and France coupled with the highly infectious nature of Omicron a quickly spun-up booster program that provides not perfect but still pretty good protection to the general population seems to be a rather sensible route to take.</p>\n", "score": 3 } ]

[ "covid-19", "covid", "omicron" ]

[ { "answer_id": 30652, "body": "<p>To my knowledge no, nobody has specifically studied this in relation to COVID-19. I can't really prove the negative but I tried a few combinations of search terms in to PubMed and came up with nothing.</p>\n<p>The &quot;Hot Toddy&quot; (with varying exact recipes) does however have a long history as a folk remedy for cold and flu symptoms and you'll often find many people willing to provide subjective anecdotes about how it always makes them feel better.</p>\n<p>So is there anything to it?</p>\n<p>A <a href=\"https://www.rhinologyjournal.com/Rhinology_issues/719.pdf\" rel=\"noreferrer\">paper</a> in <em>Rhinology Journal</em> describing a pilot study published in 2008 looked at whether drinking a <em>hot</em> beverage versus a cold one had any effect. They looked at both objective measurements of nasal conductance and subjects' subjective evaluations of the severity of their symptoms (runny nose, cough, sneezing,\nsore throat, chilliness and tiredness).</p>\n<p>While there doesn't appear to have been any measurable improvement in the nasal conductance - the subjective results were more promising:</p>\n<blockquote>\n<p>The results demonstrate that a hot fruit drink can provide subjective relief from all the six symptoms of common cold that\nwere scored in this study. Ingestion of the same drink at room\ntemperature only provided relief for three of the symptoms.\nThis demonstrates the extra benefit provided by the increase\nin drink temperature and supports the traditional use of hot\ndrinks to relieve common cold symptoms.</p>\n</blockquote>\n<p>The exact mechanism behind that relief is undetermined although there is speculation in the paper including placebo effect and some interaction with the major palatine nerve.</p>\n<p>But heat is only <em>one</em> aspect of a hot toddy! What about the others? Well the lemon is going to give you some vitamin C - which is certainly good for you in general terms it's been a matter of consternation about it's usefulness when it comes to colds and similar illnesses. I'm not even going to <em>begin</em> to try and settle <em>that</em> particular argument. <a href=\"https://www.nature.com/articles/1602261.pdf\" rel=\"noreferrer\">Here's</a> a modestly-sized study in <em>Nature</em> that says vit-C helps reduce the frequency of colds (but not the severity or duration) and <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8078152/\" rel=\"noreferrer\">here's</a> a large systemic review from Cochrane says <em>no</em> reduction in incidence but some reduction in severity and duration with regular supplementation (but questionable benefit <em>therapeutically</em>).</p>\n<p>The evidence for honey is clearer - a systemic review published in the <a href=\"https://www.phc.ox.ac.uk/news/honey-better-than-usual-care-for-easing-respiratory-symptoms-especially-cough\" rel=\"noreferrer\">BMJ</a> suggests that honey is good - especially for cough-related symptoms:</p>\n<blockquote>\n<p>The researchers analysed studies that compared the effect of taking honey, in forms such as teas, neat, or mixed with other ingredients, to either usual care – such as antibiotics, or over-the-counter cough syrups and medications – or medically inert placebos. Studies compared symptoms such as cough severity, cough frequency and symptom length.</p>\n<p>They found that, compared to usual care, honey was associated with a significantly greater reduction in symptoms, specifically cough severity and frequency.</p>\n</blockquote>\n<p>Finally.. the whiskey. The alcohol is potentially going to have a small dehydrative effect and can suppress immune activity. So the whiskey is unlikely to be doing you an <em>actual</em> good - but I suppose it might cheer you up if you're a little buzzed.</p>\n<p>Now, all of this has been about the various illnesses that all get grouped together under the umbrella of &quot;the common cold&quot;. COVID-19 is caused by a coronavirus called SARS-CoV-2, some &quot;common colds&quot; are caused by other coronaviruses but most are caused by rhinovirus, so same symptoms: different cause (hilariously getting a rhinovirus might actually <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8083659/\" rel=\"noreferrer\">protect</a> the host from SARS-CoV-2). So does any of this prior research matter for the Hot Toddy going up against COVID-19?</p>\n<p>Only in so much as if the subjective relief of &quot;cold&quot; symptoms holds for their analogs in mild COVID-19 infection - the honey might help with the cough etc. Not even the most wildly enthusiastic claims about the medicinal properties of the hot toddy have ever suggested it can do anything about the more serious symptoms of a severe COVID-19 case - pneumonia and so on.</p>\n<p>And there's just nothing there to suggest that it would prevent COVID-19 or that it would actually <em>treat</em> the infection so I'd have to say that's why you haven't seen any &quot;Hot Toddy as treatment for COVID-19&quot; studies and you're not likely to either.</p>\n<p>You might see some studies on the effectiveness of home-care treatments for mild cases later on - as academic curiosity if nothing else. But in the current situation - where you've got a serious disease doing serious harm to many people globally the focus us rightly on treatments for severe cases, and there's just no real reason for the scientists and doctors doing that to say <em>&quot;You know what Jim - my gran always swore by a Hot Toddy when she had a cold, shall we give that a go?&quot;</em></p>\n", "score": 9 } ]

[ "covid-19", "medications", "virus", "home-remedies" ]

[ { "answer_id": 31379, "body": "<p>You are quite wrong that no-one has looked at efficacy of ClO₂.</p>\n<p>There have been numerous studies on this topic as listed in <a href=\"https://pubmed.ncbi.nlm.nih.gov/?term=Chlorine%20dioxide%20OR%2010049-04-4%20%5Brn%5D\" rel=\"nofollow noreferrer\">PubMed</a> (1552 according to them, though lots of these will be about disinfection of surfaces etc or activity in non-human species), with everything from COVID-19 (e.g. <a href=\"https://pubmed.ncbi.nlm.nih.gov/35841377/\" rel=\"nofollow noreferrer\">this one</a>¹), to bacterial infections and fungal infections being examined.</p>\n<p>Generally the uses examined have been as a surface cleaner, such as a mouthwash or a sanitizing wipe. There is limited use for it in situations other than these because of the nature of the chemical.</p>\n<p>So far, no-one has found any efficacy for ingestion of these compounds because, and it's not a surprising conclusion... they don't work. Basically what happens once ingested is that the chemical acts as an oxidizer, reacting with whatever is available to be oxidized, be it lipids, proteins, etc. In the case of a viral infection while there are high loads of virus in the body, these are still vastly dwarfed by the biological compounds from the body, so the molecules of ClO₂ are much much more likely to hit a cell, mucus, etc from the body than they are an infecting organism.</p>\n<p>As <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8522852/\" rel=\"nofollow noreferrer\">this</a>² article states:</p>\n<blockquote>\n<p>It is necessary to understand the mechanism of action of oxidizing agents, such as chlorine dioxide and sodium chlorite. As mentioned previously, these substances serve as disinfectants due to their oxidizing properties. This means they can oxidize other compounds via an oxidation–reduction reaction [24]. Ultimately, chemical reactions will induce disruption of protein synthesis and outer membrane permeability due to rapid efflux of potassium ion, leading to the destruction of the transmembrane ionic gradient [25, 26]. This effect is not specific to a particular organism; human cells, like other microorganisms, are also affected [27].</p>\n</blockquote>\n<p>To put it into some perspective, I've added the below.</p>\n<p>The webcomic XKCD gave a reasonable explanation of how abundant viruses are in their <a href=\"https://what-if.xkcd.com/80/\" rel=\"nofollow noreferrer\">What-if</a>? series. Basically what it boils down to is that <em>in the natural state</em> you have about 10¹² (a thousand billion) virions in you all the time. These are mostly <a href=\"https://en.wikipedia.org/wiki/Bacteriophage\" rel=\"nofollow noreferrer\">bacteriophages</a>, so only infect bacteria. However, if you gathered these 10¹² virions <em>from all the people on the planet</em>, they would still only make up about 10 40-gallon (10 x 150 litre) barrels in volume. That's the equivalent of a box 1 metre width x 1 m height x 1.5 m (3.3 x 3.3 x 5 feet) long in total.</p>\n<p>I did a back-of-the-envelope calculation on how much that would be in volume per person. Assuming 1500 l (10 x 150 l) and 8 billion (7.96 billion actually) people on the planet, it works out to be about 0.2 <strong><a href=\"https://www.cancer.gov/publications/dictionaries/cancer-terms/def/microliter\" rel=\"nofollow noreferrer\">microlitres</a></strong> (actually 0.1875) per person. That's a drop so small that it is hard to measure, but because I work in a lab I can, so I did and took a photo (excuse the blurriness, it's hard to focus at that range/scale with a cell-phone camera):</p>\n<p><a href=\"https://i.stack.imgur.com/KZ2sA.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/KZ2sA.png\" alt=\"enter image description here\" /></a></p>\n<p>That's a centimetre ruler, each small division is 1 millimetre. The blue drop is 0.2 microlitres. So, if you compare that volume (~0.2 ul) to the volume of a human body, you can see why the ClO₂ molecules would be massively more likely to interact with a human tissue component than the virus itself, and hence why ingestion certainly doesn't work.</p>\n<p>Now, you might be thinking, &quot;But what about COVID infection, that's not a normal state&quot; - well, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7685332/\" rel=\"nofollow noreferrer\">this paper</a>³ estimates about 10¹¹ RNA copies per person per infection - lets assume that's the number of virions (it's not - many more RNA produced than virions, but for calculation's sake...) that's still only one tenth of the 10¹² virions normally present i.e. 1.1 x10¹² instead of 1.0 x10¹² particles, so it doesn't change the amount/volume meaningfully!</p>\n<p>References:</p>\n<ol>\n<li><p>Travis BJ, Elste J, Gao F, Joo BY, Cuevas-Nunez M, Kohlmeir E, Tiwari V, Mitchell JC. Significance of chlorine dioxide-based oral rinses in preventing SARS-CoV-2 cell entry. Oral Dis. 2022 Jul 16. doi: 10.1111/odi.14319. Epub ahead of print. PMID: 35841377.</p>\n</li>\n<li><p>Arellano-Gutiérrez G, Aldana-Zaragoza EH, Pérez-Fabián A. Intestinal perforation associated with chlorine dioxide ingestion: an adult chronic consumer during COVID-19 pandemic. Clin J Gastroenterol. 2021 Dec;14(6):1655-1660. doi: 10.1007/s12328-021-01527-y. Epub 2021 Oct 18. PMID: 34664196; PMCID: PMC8522852.</p>\n</li>\n<li><p>Sender R, Bar-On YM, Gleizer S, Bernsthein B, Flamholz A, Phillips R, Milo R. The total number and mass of SARS-CoV-2 virions. medRxiv [Preprint]. 2021 Apr 5:2020.11.16.20232009. doi: 10.1101/2020.11.16.20232009. Update in: Proc Natl Acad Sci U S A. 2021 Jun 22;118(25): PMID: 33236021; PMCID: PMC7685332.</p>\n</li>\n</ol>\n", "score": 5 } ]

[ "medications" ]

[ { "answer_id": 9239, "body": "<p>The average bowel transit time - the time needed for a food to travel from mouth to stool - in a healthy person is probably around 12-14 hours. Source: <a href=\"https://medlineplus.gov/ency/article/003887.htm\" rel=\"nofollow\">MedlinePlus</a></p>\n\n<p>When a certain food or nutrient (lactose, fructose) irritates the bowel, the bowel transit time can be much shorter and it could very well be just 2-3 hours. But abdominal pain, gas or loose stools in IBS can appear even faster than that concluded from the bowel transit time, for example as soon as 15 minutes after a meal. This is because the stool and gas you excrete does not come from your last meal but more likely from your previous meals.</p>\n\n<p>It is gastrocolic reflex that causes the movements of your large intestine, when the food reaches your stomach. This is why breakfast helps to have a bowel movement in the morning.</p>\n\n<p><strong>EDIT:</strong></p>\n\n<p>Apples and mangoes are high in \"net fructose,\" which means they contain more fructose than glucose. When a person has less symptoms after removing foods high in net fructose from the diet, it means he can have fructose malabsorption (FM), which is described in detail here <a href=\"http://www.nutrientsreview.com/carbs/monosaccharides-fructose.html\" rel=\"nofollow\">here</a>.</p>\n\n<p>Foods high in <strong>net fructose</strong> (to avoid in FM): apples, pears, mangoes, agave, watermelon, honey, beverages sweetened by high fructose corn syrup (HFCS), carambola, feijoa, nance, guava, grapes (for more detailed list see the link above).</p>\n\n<p>Additionally, a person with FM can have gas and loose stools after eating foods high in <strong>sorbitol</strong> and other sugar alcohols (polyols), such as <strong>xylitol, maltitol or mannitol,</strong> which can be found in \"sugar-free\" chewing gum, certain low-calorie drinks, prunes, grapes, sweet cherries, apricots and peaches.</p>\n\n<p>Additionally, a person with FM can get gas after eating foods high in <strong>fructooligosaccharides (FOS):</strong> Jerusalem artichokes, red onions and bananas.</p>\n\n<p>NOTE, that not all foods high in fructose should be avoided, but only foods high in \"net fructose\" (described in the above link).</p>\n\n<p>If a person who has fructose malabsorption as the only or main gastrointestinal problem, eliminates foods with nutrients marked in bold above, he should see an obvious improvement within <strong>48 hours</strong> and more improvement within a week. After improvement, a person can try to introduce certain less suspicious foods back (but only one food in 48 hours to be able to identify eventual symptoms).</p>\n\n<p>A person who has FM, often has a slight problem in absorbing lactose due to <em>temporary</em> lactose intolerance, so it can help if he avoids milk, curd, yogurt, ice cream (cheese and butter should be fine).</p>\n\n<p>Elimination of all nutrients mentioned above at once is called a <a href=\"http://www.nutrientsreview.com/carbs/fodmaps.html\" rel=\"nofollow\">low-FODMAP diet</a>.</p>\n\n<p>So, when someone thinks he has FM, he can start with a low-fructose diet or a bit more thorough low-FODMAP diet.</p>\n\n<p>People who have FM often think they have IBS. If one wants to be officially diagnosed, he can ask a gastroenterologist to perform a \"hydrogen breath test with fructose.\" The condition is usually life-long.</p>\n\n<p>Fructose malabsorption should not be confused with a rare hereditary fructose intolerance (HFI), which can cause much more severe symptoms after consumption of even minute amounts of fructose.</p>\n\n<p>Disclaimer: I did not diagnosed anyone here with FM, but this post can help people who have IBS-like symptoms (gas, loose stools, vague abdominal pains).</p>\n\n<p>Similar conditions:</p>\n\n<ul>\n<li>Food allergies usually cause <em>itching and tingling around the mouth</em> within few minutes of ingestion. An allergologist can make a diagnosis on the basis of the skin test.</li>\n<li>Intestinal parasites can cause various abdominal symptoms. A gastroenterologist can make a diagnosis from a stool test.</li>\n</ul>\n", "score": 1 } ]

[ "nutrition", "diet", "digestion", "gastroenterology" ]

[ { "answer_id": 25531, "body": "<p>Summary:</p>\n<p>To answer the bounty question</p>\n<blockquote>\n<p>I am looking for a simple and straightforward answer which describes in a few sentences the mechanism by which the adaptive immune system, informed by a vaccine, would prevent infection of the epithelia of the respiratory system by a virus.</p>\n</blockquote>\n<p><em>a</em> (not <em>the</em>) mechanism by which the adaptive immune system affects respiratory viruses before cell entry is antibodies presence in mucus, which does seem to have a noticeable [counter]effect on <em>viral particle mobility</em> in mucus <em>for the specific viruses against which the host has antibodies</em>. (See last section of this answer for details.)</p>\n<p>However, I'll also that (adaptive) humoral immune system response in the mucus is hardly the end of the adaptive immune system relevance to the epithelium, as avoiding cellular infection <em>altogether</em> cannot be <em>guaranteed</em> by mucus (even with antibodies in it). The epithelium is also &quot;guarded&quot; by adaptive cellular mechanisms (e.g. T cells) that preferentially attack [epithelium] cells infected with specific viruses, as &quot;bits&quot; of these viruses are exposed on infected cells' surface via MHC I.</p>\n<hr />\n<p>Basically, the immune system <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197993/\" rel=\"nofollow noreferrer\">does function in the respiratory epithelium</a> contra to your theory, and the usual cascade of innate mechanisms triggering the adaptive ones also works in the epithelium:</p>\n<blockquote>\n<p>Several immune cell populations are resident in epithelium including CD103+ CD8+ T cells and CD103+ conventional dendritic cell populations which act as sentinel cells. Other immune cell populations including innate lymphoid cells (ILCs), mucosal associated invariant T cell (MAIT), natural killer cells (NKT) and γδ T cells are in close proximity to the epithelium. [...]</p>\n<p>The airway epithelium utilizes structural and barrier defence provided by the mucociliary escalator and their incumbent anti-microbial proteins, and intra- or epithelial-associated immune cells like resident dendritic cells, invariant natural killer T (iNKT) cells, γδ T cells and intra-epithelial lymphocytes.</p>\n</blockquote>\n<p>You're correct that respiratory viruses often have the epithelium as their preferred/evolved target, but this is also where they are usually &quot;defeated&quot; (in fact if they're not defeated there, the host is usually in big trouble). Furthermore, experimentally interfering with this signalling cascade results in much worse outcomes--see emphasized part on dendritic cells further below.</p>\n<blockquote>\n<p>Upon binding sialic acid receptors on the epithelial cell surface, IAV are internalised via receptor-mediated endocytosis [...] The host cell begins sensing IAV as soon as it is internalised, utilising pathogen recognition receptors (PRRs), primarily the Toll-like receptors (TLRs) and RNA-sensing RIG-I–like receptors (RLRs), such as retinoic acid–inducible gene I (RIG-I) and melanoma differentiation-associated protein 5 (MDA-5) [...]</p>\n</blockquote>\n<p>Those (TLRs, RLRs etc.) are indeed part of the innate immune system, but that's not the end of the story:</p>\n<blockquote>\n<p>Activation of type I interferons is the key consequence of intracellular recognition of IAV infection by TLRs and RLRs. These cytokines bind to the IFN-α/β receptor (IFNAR) on infected as well as neighbouring cells and induces the transcription of a large group of genes (interferon stimulated genes or ISG) whose main task is to limit spread of infection. [...] In epithelial cells, type I IFN has the additional task of acting as an early warning system, communicating viral threat between infected and uninfected cells. [...]</p>\n</blockquote>\n<p>But epithelial cells also signal &quot;the invasion&quot; through a more specific mechanism: type III interferons (IFN-λ). In any case:</p>\n<blockquote>\n<p>Activation of both type I and III IFN results in induction of hundreds of ISGs. ISGs trigger apoptosis, shut down protein synthesis and activate key components of the innate and adaptive immune systems, including antigen presentation and production of cytokines involved in activation of T, B, and natural killer (NK) cells.</p>\n</blockquote>\n<p>So, thanks to interferons the adaptive immune system does get triggered, even in the epithelium. Furthermore</p>\n<blockquote>\n<p>There is substantial cross-talk between epithelial and immune cells sequestered in the epithelium. CD103+cDCs continuously sample the airway via extended dendrites and respond to chemokines and cytokines (including type I and III IFNs) and DAMPs secreted by IAV- infected epithelial cells</p>\n<p><strong>Intra-epithelial dendritic cells are essential to generate protective IAV-specific CD8+ T cells; mice lacking this DC subset succumb to severe disease and impaired viral clearance.</strong></p>\n</blockquote>\n<p>Basically, not having the adaptive immune system active/functional in the epithelium is usually fatal for the host, even in relation to &quot;mere&quot; influenza infection. <a href=\"https://en.wikipedia.org/wiki/Dendritic_cell\" rel=\"nofollow noreferrer\">DCs</a> &quot;act as messengers between the innate and the adaptive immune systems.&quot;</p>\n<p>Also, at least the epithelium of the lungs has additional defenses (iNKT cells). If you look at <a href=\"https://en.wikipedia.org/wiki/Natural_killer_T_cell\" rel=\"nofollow noreferrer\">their Wikipedia page</a>, the NKT cells are somewhat of a hybrid of adaptive (T cells) and innate (NK cells) immune system; they in turn release a plethora of signalling molecules &quot;large quantities of interferon gamma, IL-4, and granulocyte-macrophage colony-stimulating factor, as well as multiple other cytokines and chemokines (such as IL-2, IL-13, IL-17, IL-21, and TNF-alpha)&quot; that activate the adaptive immune system, although I think NKTs mostly respond to bacterial rather than viral infections. (I could be wrong though on this.) But if they do &quot;get triggered&quot;, e.g. in a co-infection scenario (not uncommon in pneumonias), NKTs seem to help with the viral [part of the] infection as well (going back to quoting from the review paper [1st link]):</p>\n<blockquote>\n<p>In the mouse, presence, and exogenous activation, of lung iNKT cells by α-GalCer, protects against lethal H1N1 and H3N2 influenza in prophylactic settings.</p>\n</blockquote>\n<p>But to reiterate again the more common mechanisms:</p>\n<blockquote>\n<p>The epithelial cells’ attempt to clear IAV results in inevitable tissue injury, in part because of collateral damage from the accompanying innate immune response and direct induction of apoptosis by IAV, <strong>but also because cytotoxic T cells will eventually kill cells with IAV peptides presented on their MHC class I molecules</strong>. If epithelial cells are not killed they undergo apoptosis or de-differentiation. If IAV reaches the alveolar epithelium, various injurious events can occur. [...]</p>\n</blockquote>\n<p>Speaking of that last (emphasized) issue, the influenza viruses <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6548845/\" rel=\"nofollow noreferrer\">&quot;try pretty hard&quot;</a> to make themselves invisible to the MHC I pathway.</p>\n<blockquote>\n<p>we showed that infection of several cell types, including epithelial A549 cells, with a panel of IAV and IBV viruses downregulated the surface MHC-I expression on IAV/IBV-infected cells during the late stages of influenza virus infection in vitro. [...] Importantly, the two viruses utilized two distinct mechanisms for MHC-I downregulation.</p>\n</blockquote>\n<p>If MHC I (triggering T cells) wasn't a problem for them, why would they have evolved these camouflage/countermeasures?</p>\n<hr />\n<p>Since you confusion (or argument) seems to be whether Cytotoxic CD8+ T cells are or aren't part of the adaptive immune system (they are), let's side-step such categorization discussion and simply <a href=\"https://www.nature.com/articles/s41586-020-2814-7\" rel=\"nofollow noreferrer\">observe</a> that a Covid-19 mRNA vaccine trains them so that significant fraction recognize the virus bits:</p>\n<blockquote>\n<p>Fractions of RBD-specific IFNγ+ CD8+ T cells reached up to several per cent of total peripheral blood CD8+ T cells in immunized individuals</p>\n</blockquote>\n<p>RBD here means the receptor binding domain (protein) of the specific virus (SARS-CoV-2 in this case).</p>\n<p>(The same is true for vaccines that target the full spike protein, which are the ones actually approved by regulators, although the corresponding <a href=\"https://www.medrxiv.org/content/10.1101/2020.12.09.20245175v1.full\" rel=\"nofollow noreferrer\">paper(s)</a> still seem to be in the preprint stage. The latter paper speaks of &quot;S-specific CD8+&quot;, meaning SARS-CoV-2 spike-specific.)</p>\n<hr />\n<p>Now, if you want to focus/ask only what happens <em>before any cell entry</em>, the humoral immune system is present in mucus. It (also) has innate (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4752725/\" rel=\"nofollow noreferrer\">e.g.</a> mucins, lactoferrin) and adaptive components; antibodies <em>are</em> present in the mucus.</p>\n<p>Antibodies importance (relative to innate mechanism) in mucus has been less studied, but their presence in mucus has surely been (commonly) observed, and some studies comparing viral movement speeds in mucus do suggest that specific antibodies slow down the corresponding viruses in mucus <a href=\"https://erj.ersjournals.com/content/49/1/1601709\" rel=\"nofollow noreferrer\">e.g.</a>:</p>\n<blockquote>\n<p>To investigate whether trapping of influenza in airway mucus can be attributed primarily to haemagglutinin binding to mucin-associated sialic acid, we prepared VLPs fluorescently labelled internally using HIV-1 GAG-mCherry capsid proteins in the core, and expressing both neuraminidase and haemagglutinin from H1N1 (influenza A/PR/8/34) (WT-Inf), or the same neuraminidase and haemagglutinin that has the sialic acid-binding domain deleted (ΔSAB-Inf) and hence cannot bind directly to mucins. Interestingly, both WT-Inf and ΔSAB-Inf were trapped in airway mucus to a similar extent as H1N1 and H3N2, with roughly 98% of WT-Inf and 97% of ΔSAB-Inf immobilised in airway mucus and average diffusivities ∼1700- and ∼1100-fold lower than expected speeds in buffer, respectively (figure 1b, online supplementary movies S4 and S5). [...]</p>\n<p>Using whole-virus ELISA assays, we detected substantial quantities of endogenous IgG and IgA against influenza in airway mucus (data not shown), as well as against both WT-Inf and ΔSAB-Inf VLPs. [...] This leaves open the possibility that influenza-specific antibodies in airway mucus may immobilise virions by cross-linking the antibody–virus complex to mucus constituents, such as mucins. We sought to measure virus and VLP mobility in airway mucus devoid of antibodies; however, we were not able to adequately remove Ig by dialysis, possibly due to membrane clogging, and mucus secretions isolated from air–liquid interface cultures of bronchial epithelial cells did not produce a sufficiently rigid matrix to immobilise mucoadhesive latex nanoparticles. We also attempted to “saturate” the mucus–antibody barrier by mixing &gt;20-fold more unlabelled than labelled influenza viruses into airway mucus prior to adding labelled viruses, and still observed no discernible difference in the trapping of the labelled influenza viruses. Therefore, <strong>we investigated whether the lack of binding antibodies in mucus correlates to greater virus mobility by tracking HIV VLPs that were prepared similarly to the influenza VLP, but expressing HIV YU2 gp160. We found no detectable HIV-binding IgG or IgA in airway mucus (figure 1d, e), and HIV VLPs exhibited markedly greater diffusivity in airway mucus (figure 1b, online supplementary movie S6; p&lt;0.05), with &gt;45% of HIV VLPs classified as mobile and ∼10-fold higher ensemble effective diffusity than WT-Inf and ΔSAB-Inf. HIV VLP mobility was similar to that of PS-PEG in the same airway mucus samples (data not shown).</strong></p>\n<p>Together, these results demonstrate that influenza virus can be trapped in human airway mucus without binding to sialic acids on mucins, in good agreement with the evidence that human influenza viruses possess haemagglutinin that preferentially binds α2,6-linked sialic acids on the airway epithelium rather than α2,3-linked sialic acids on mucins. Trapping of influenza in human airway mucus can probably be attributed to the presence of influenza-binding antibodies that can cross-link individual virions to the mucus mesh network. <strong>Importantly, adhesive interactions between the array of pathogen-bound antibodies and mucus gel provide a universal strategy that enables the otherwise relatively nonadaptive and nonspecific biochemistry and microstructure of mucus secretions across different mucosal surfaces to be fortified with adaptive antibodies against an ever-changing spectrum of pathogens.</strong></p>\n<p><a href=\"https://i.stack.imgur.com/fIgYe.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/fIgYe.png\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n<p>But before you get too excited about this finding, remember that the immune systems is &quot;defense in depth&quot;, some virus particles will make it through the mucus, even if you do have specific antibodies against them there; this is when\nthe cellular mechanisms kick in. There's no one mechanism that is going to be 100% foolproof.</p>\n", "score": 4 }, { "answer_id": 30768, "body": "<p>Trying to understand your question:</p>\n<p>a. Can vaccination, by inducing antibodies, prevent infection, i.e. shield off the virus before it enters any cell, in locations that seem to be inaccessible for antibodies and lymphocytes?</p>\n<p>b. If innate immunity successfully hinders infection and renders vaccination superfluous and redundant can the latter be considered effective?</p>\n<p>c. Considering vaccination being able to prevent symptomatic or severe illness but not infectivity and epidemic spread what is the role of innate versus adaptive immunity in both, prevention of disease and epidemic spread?</p>\n<p>If c. were correct understanding one prospective answer might be: Whereas, indeed, innate immunity prevents the spread of the virus, adaptive immunity prevents symptomatic disease. Another intricacy: In case innate immunity cannot prevent infection and epidemic spread, why doesn't vaccine/adaptive immunity come in stopping the spread - if it successfully prevents symptomatic disease? I see that point to your question and that's why I am out to publish my personal view, see inverted text at the end.</p>\n<p>Answering:</p>\n<p>According to not very basic textbook knowledge antibodies/immunoglobulins are able to cross the blood tissue barrier. Immunoglobulins' sizes permit the evasion from blood and the invasion of interstitium/tissue/epithelia. IgE is a known example of specialized immunoglobulins that take care of outer epithelia. There do exist local lymphocytes, <a href=\"https://en.wikipedia.org/wiki/Langerhans_cell\" rel=\"nofollow noreferrer\">Langerhans cells</a>, that make it across the vessel wall under regular circumstances, no inflammation or infection needed beforehand; they are in place.</p>\n<p>In fact, not IgE, but IgA seems tailored for mucosa.</p>\n<p>&quot;IgA is the 2nd most common serum Ig. IgA is the major class of Ig in secretions - tears, saliva, colostrum, mucus. Since it is found in secretions secretory IgA is important in local (mucosal) immunity. Normally IgA does not fix complement, unless aggregated. IgA can bind(...) to some cells - PMN's and some lymphocytes.&quot;\n<a href=\"http://www.microbiologybook.org/mayer/IgStruct2000.htm\" rel=\"nofollow noreferrer\">http://www.microbiologybook.org/mayer/IgStruct2000.htm</a></p>\n<p>While the question whether antibodies not only cross the blood-epithelial barrier but the blood-air-barrier as well is to be answered to the affirmative, there is a debate about the extent to which this holds for the fencing off of respiratory at the blood-air-barrier (not blood-tissue barrier), which makes your question non-trivial:</p>\n<p>&quot;...Translocation of large serum proteins (e.g., albumin, IgG) via paracellular routes by restricted passive diffusion does not appear to be the primary route, although under pathological conditions such passive diffusion may become the main route of protein leak.&quot; <a href=\"https://journals.physiology.org/doi/pdf/10.1152/ajplung.00235.2002\" rel=\"nofollow noreferrer\">Protein transport across the lung epithelial barrier\nKim/Malik, 2003</a></p>\n<p>As the quote above might suggstest the response of the adaptive immune system might seem late or reluctant, in accordance with the intention of your question I assume. Adaptive immunity might set in when infective spread has already happened. Even if antibodies have not waned they do not seem to be very willing to fit in where or when needed, in the mucosa.</p>\n<p>On the other hand, imagine just one single epithelial cell the infection of which adaptive immunity could not prevent. If any shedding of virions from that one cell will encounter antibodies, and any lysis of that one cell will immunize local lymphocytes in between infected single cells of the epithelial you may consider vaccination/adaptive immunity effective.</p>\n<p>Effectiveness of adaptive immunity may not being perturbed if it allows the transfection of one single cell as this signal of invasion is needed to trigger defence cascade.</p>\n<p>Antibodies in between cells of epithelia and local lymphocytes, &quot;Langerhans cells&quot;, may not be able to &quot;prevent infection&quot;, however in principle, these elements of the adaptive immune response are able to prevent any further spreading.</p>\n<p>Regarding the argument that there are no antibodies in the mucus, on the outside to prevent any &quot;one cell&quot; being invaded by virus one must admit that, in principle, this goes for the innate immune system as well as far as it is based on cell signaling, too.\nIn other words: adaptive immunity needs initiating infection to start a signaling cascade and does not prevent such infection; it would logically stop itself from starting. However, same applies to the interferon system of innate immune system that needs infection to start the interferon cascade.</p>\n<p>*The following is my personal opinion that tries to answer your question &quot;in deep&quot;.\n&quot;How can vaccines be effective against respiratory viruses when it is the innate immune system that is the primary response to such pathogens?&quot;</p>\n<p>Yes, you are right in some way. Indeed, there seem to be many variants or even species of respiratory viruses where vaccines are able to prevent symptomatic disease, however are not able to restrict viruses in replication sufficiently in order to prevent epidemic spread and non-symptomatic infection.</p>\n<p>For instance, he Omicron variant of the Corona virus CoV-19, arguably a new serotype, may well illustrate a yet non-accepted principle of mutational viral evolution that pertains to balancing the innate and the adaptive immune system, assuming that the virus renders itself, paradoxically, more vulnerable to the innate system or other factors of the non-adaptive innate immunity, thereby not contacting the adaptive immune system and circumventing it, not even causing &quot;much&quot; immunity. This principle of escape from immunitiy is different from the strategy of hiding away by turning silent, especially by integrating, as retro viridae do, into the genome. My point is that from a single cell, compare the above, there might leak out into the air, lung a very large amount for infectious virus particle, so there is no latency at all. There is only a restriction by the innate immunity, that, in the intention of your question, is &quot;just&quot; not strong enough to stop infectivity and shedding of infectious virus by isolated cells.</p>\n<p>Counterintuitively mutations turn out to be successful that render the virus less pathogenic and/or less infectious because the virus refrains from defending itself against the innate response as it is rewarded by non-immunizing and non-coping with existing adaptive immunity. It is the price the adaptive defence pays out to the virus for the virus weakening itself to a point of being beaten in first line by the innate immune system. In that mutational to and fro there are limits: for the virus there is a minimum of infectivity that must be &quot;left over&quot;. Otherwise there will be some remake of the weakened.</p>\n<p>Thus, vaccines may tend not to prevent the infectious spread. This is no trivial posting: the adaptive immune systeme accepts infectivity that is not pathogenic, not intrusive enough for to be bothered. The being late and the ineffectiveness is the price mutations certain respiratory viruses are being awarded if they let themselves be restricted to no invasiveness of the body, thus, in principle, harmlessness, paired with high incidental rates and epidemic spread. If there is hiding away of retro viruses, there is retreat of certain respiratory viruses.</p>\n<p>The principle of evolution I hereby postulate thus pertains to the selective advantage for the virus that lies in not inducing immunity by not encountering antibodies and/or antigen presenting cells. Stated principle is that adaptive immunity, hence vaccination, by evolutionary art, does not fill the gap of infectiousness, epidemic infectivity, that innate immunity may or may not open.</p>\n<p>It is the selective advantage viral evolution must have: the spread. Let me explain the spread. To spread is the reward adaptive immunity does not take away. Only then viral mutations find succes in letting the viruses being dampened, at the verge of extinction, by the interferon system of innate immnity. Thus vaccination, by principle, in many cases can only prevent disease, not infection.</p>\n<p>Known mechanisms of adaptive immunity seen anew show that adaptive immunity &quot;comes late&quot;:</p>\n<ol>\n<li><p>Antigen presenting cells take up antigens that are derived from already infected, then succumbed, lysed cells.</p>\n</li>\n<li><p>T-cytotoxic cells await the apoptotic signal of already infected cells - most important, as an argument: specific T-Killer cells are known to become &quot;anergic&quot; when encountering their target, they have to wait until they get primed in lymph nodes, they come very late</p>\n</li>\n<li><p>The only defense of the adaptive system seems to be &quot;neutralizing&quot; antibodies that throw themselve in between the virus and the cell, theoretically. But then: they wane very quickly, and in my opinion, this regular waning fast of antibodies is coherent with the stated principle of reluctancy of the adaptive response.</p>\n</li>\n</ol>\n<p>What regards the viral turning itself either more or less exposed to the innate system of immunity I name two mechanisms, there may be more:</p>\n<ol>\n<li><p>Syncytialization</p>\n</li>\n<li><p>Interferon signalling</p>\n</li>\n</ol>\n<p>Respiratory Syncytial Virus by its name exemplifies: like Corona-Viridae this respiratory virus induces syncytialisation, i.e. fusion of one infected cell with others that surround it. While this is considered circumventing the adaptive immune system as far as more and more cells are infected without virus entering the interstitial or humoural space in between cells it is - in terms of my arguing - a mechanism of balancing and modulation: known are viral mutations that change binding of viral factors to syncytialization promoters of the host cell thus changing the degree of pushing back the entry of adaptive immune response.</p>\n<p>As far as respiratory virus mentioned in your question use the way of syncytialization of infection one can say vaccines will be dampened. Vaccination sets in only as soon as there is lysis of syncytia (for the APS to uptake antigen, after &quot;persistence ended&quot; and/or MHC-presentation by syncytia with preexisting immunity).</p>\n<p>Very intriguing in the context of your question is the barely popular fact of the placenta more or less being a syncytia that prevents the adaptive system of immunity from working, as it is said to block contacting the father's foreign antigens. Viral genes in the humane genome are held responsible. Analogy permitted, the pneumocytes type II, target cells of CoV, are very extended in form and appear as large extended shields. It is rare knowledge that CoV induces their syncytialisation, and if the latter is considered &quot;infection&quot;, it is hidden and cannot be coped with by adaptive response nor vaccination. Thus, if induced by viral infection, syncytia of the lung cells can not only be seen as hideaways from the adaptive immune system but also as,in principle, fencing off a separate room - the mucosal room - which antibodies and lymphocytes cannot enter, which refers to your question.</p>\n<p>Some references:</p>\n<p>[Liangyu Lin et al. 2021],1<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8114657/\" rel=\"nofollow noreferrer\">4</a>Syncytia formation during SARS-CoV-2 lung infection: a disastrous unity to eliminate lymphocytes</p>\n<p><a href=\"https://medicalsciences.stackexchange.com/posts/30768/edit\">Cattin-Ortolá et al.</a><a href=\"https://pubmed.ncbi.nlm.nih.gov/34504087/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/34504087/</a>\nSequences in the cytoplasmic tail of SARS-CoV-2 Spike facilitate expression at the cell surface and syncytia formation*</p>\n<p>&quot;Placental transfer - IgG is the only class of Ig that crosses the placenta. Transfer is mediated by a receptor on placental cells for the Fc region of IgG.&quot;</p>\n<p>The Omikron variant of Cov might be an example of a presumably highly infectious, (in many cases) but non-symptomatic disease that still manages to cause the formation of antibodies. According to my reasoning and in the intention of your question I assume their building up might be weak, which, in result, has already be confirmed by re-infection with Omicron - within same season - being reported in Great Britan. Even if there were adapted vaccination against a respiratory virus variant, according to my reasoning, it should &quot;not work well&quot; against infectivity, non-pathgenicity only following suit the non-contacting of the realms of adaptive immunity, to affirmatively answer your question and putting my reasoning up for test in the near future, hopefully.</p>\n<p>I will reference all this by tomorrow if allowed to.</p>\n", "score": 1 } ]

[ "virus", "immune-system", "vaccination" ]

[ { "answer_id": 31982, "body": "<p>OK, I'll bite...</p>\n<p>I'm assuming you are from the USA, based on your post about sporting people collapsing (note - not dying AFAIK, not being an American I don't follow their sports), one of which made news headlines. I don't know how many people got the vaccines in the USA, but you can see some data on this at <a href=\"https://coronavirus.jhu.edu/vaccines/us-states#vaccination-rollout-us\" rel=\"nofollow noreferrer\">John's Hopkins</a>, which indicates at least 50% of people in all states got a full course of the vaccine.</p>\n<p>Now, note that 50% means 1 in every 2 people - if people were dropping dead, wouldn't you expect to be hearing of massive surges of death right now (at the time of writing; Feb 2023) - like half the people at your work/school/church?</p>\n<p>I found a paper published by a big group of people known as the <a href=\"https://en.wikipedia.org/wiki/Cochrane_(organisation)\" rel=\"nofollow noreferrer\">Cochrane Group</a>, which is a British organization dedicated to helping people make evidence based health decisions. They are now international, and the study is authored by a range of people, mostly from Europe, but also South Africa and Chile.</p>\n<p>In this study (read for free at <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9726273/\" rel=\"nofollow noreferrer\">PubMed Central</a>) they looked at vaccine effectiveness and safety for the COVID vaccines - looking at 12 vaccines, mixed vaccine schedules (i.e. people taking different types/makes of vaccines), different exposure times, ages etc as explained in the technical parts of the paper, but for those who aren't scientists, it has non-technical summaries:</p>\n<blockquote>\n<p>We found 41 worldwide studies involving 433,838 people assessing 12 different vaccines. Thirty‐five studies included only healthy people who had never had COVID‐19. Thirty‐six studies included only adults, two only adolescents, two children and adolescents, and one included adolescents and adults. Three studied people with weakened immune systems, and none studied pregnant women.</p>\n<p>Most cases assessed results less than six months after the primary vaccination. Most received co‐funding from academic institutions and pharmaceutical companies. Most studies compared a COVID‐19 vaccine with placebo. Five evaluated the addition of a 'mix and match' booster dose.</p>\n</blockquote>\n<p>Anyway... on to answer the question. In the words of the study:</p>\n<blockquote>\n<p>For the Pfizer, CoronaVac, Sinopharm‐Beijing, and Novavax vaccines, there is insufficient evidence to determine whether there was a difference between the vaccine and placebo mainly because the number of serious adverse events was low.</p>\n<p>Moderna, AstraZeneca, Janssen, and Bharat vaccines probably result in no or little difference in the number of serious adverse events.</p>\n</blockquote>\n<p>This indicates that out of the 400,000 odd people they looked at (admittedly over less than 6 months in most cases, but we'd only had the vaccines for a 18 months or so at the time of writing), there were no effects that they could see that indicated problems over and above giving a fake vaccination. For the Pfizer, all cause mortality was 68 per 100,000, but placebo was 64/100,000. This indicates that for every 100,000 people between 60 and 70 people will die <strong>from any cause</strong> after the administration of the working vaccine <strong>OR</strong> a fake (placebo) vaccine. Similarish numbers are seen for the other types of vaccines, though typically lower deaths (&lt;50/100,000) for more traditional types (inactivated virus, protein subunit, etc.).</p>\n<p>Now, there is one significant adverse event associated with the mRNA vaccines (the new type - Pfizer/BioNTech and Moderna), which is myocarditis. This is a heart problem which can occur with some infections, such as influenza virus, common cold viruses, bacteria and fungal infection. It can also be caused by the SARS-COV-2 (Covid) virus itself too, and is a result of the spike protein interacting with the tissues of the heart. This is the one that athletes are concerned about, because strenuous exercise puts a strain on the heart itself. However, if you refer to the figures in my answer <a href=\"https://medicalsciences.stackexchange.com/questions/29184/does-this-covid-19-vaccine-study-suggests-a-1-to-718-rate-of-adverse-effects/29207#29207\">here</a> about vaccine adverse effects, you will see that the virus causes these effects at a higher or equal rate to the vaccine, but the vaccine reduces your overall risk of adverse events and death significantly compared to SARS-CoV-2 infection.</p>\n<p><a href=\"https://medicalsciences.stackexchange.com/questions/29184/does-this-covid-19-vaccine-study-suggests-a-1-to-718-rate-of-adverse-effects\">Based on the table given</a> in the question I am answering in the linked post in the paragraph above, we would expect to see myocarditis in 1-5 people per 100,000 vaccinated with the BioNTech vaccine. This is a pretty small number, certainly not the millions you should be seeing if the vaccine were really affecting/killing lots of people...</p>\n<p>TLDR: no evidence to support the claims.</p>\n<p>Source information:</p>\n<p>Graña C, Ghosn L, Evrenoglou T, Jarde A, Minozzi S, Bergman H, Buckley BS, Probyn K, Villanueva G, Henschke N, Bonnet H, Assi R, Menon S, Marti M, Devane D, Mallon P, Lelievre JD, Askie LM, Kredo T, Ferrand G, Davidson M, Riveros C, Tovey D, Meerpohl JJ, Grasselli G, Rada G, Hróbjartsson A, Ravaud P, Chaimani A, Boutron I. Efficacy and safety of COVID-19 vaccines. Cochrane Database Syst Rev. 2022 Dec 7;12(12):CD015477. doi: 10.1002/14651858.CD015477. PMID: 36473651; PMCID: PMC9726273.</p>\n", "score": 4 } ]

[ "covid-19", "vaccination", "side-effects" ]