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[ { "answer_id": 17006, "body": "<p>It was an assessment of your <a href=\"https://www.emsworld.com/article/10319034/assessing-mental-status\" rel=\"nofollow noreferrer\">mental status</a>. It's usually among the first questions an EMT will ask. The purpose is to determine if your are mentally alert and oriented. The reasons for this assessment are to look for possible brain injury (concussion or worse) and also other causes such as intoxication with alcohol or drugs, low blood sugar, and other conditions that can cause mental confusion. It also has legal ramifications. If they judge you to be mentally incompetent, your right to make medical decisions for yourself is extinguished, including the right to refuse care (I'm assuming US law here, but most developed countries are similar).</p>\n\n<p>This assessment has significant impact on the actions they take next. If you fail the test, they'll be wondering if your confusion is a result of injury from the crash or something else. Intoxication is always high on the list of possibilities, and so is low blood sugar. You would likely be asked if you are diabetic at that point, and they would probably do a finger stick to check blood sugar levels no matter what your answer. If your blood sugar is normal then they'll have to assume you've suffered head injury from the crash and expedite you accordingly. The smell of alcohol on your breath or signs of intoxication wouldn't change this course of events because drunks suffer head injuries too.</p>\n", "score": 5 } ]

[ "injury", "diagnosis" ]

[ { "answer_id": 17031, "body": "<p>Dysplasia describes abnormal cell morphology or differentiation without the proliferation rate being affected. Dysplasias can result in an increased number of one type of cell as a result of another type of cell being reduced in number (e.g. because the first type is failing to differentiate into the second, but not because any cell is proliferating more than usual).</p>\n\n<p>Hyperplasia describes increased cell proliferation which results from an adequate response to a growth signal. This includes for example red blood cell hyperplasia as a result of hypoxic environment or erythropoietin treatment.</p>\n\n<p>Neoplasia covers all forms of abnormal cell proliferation. Unlike a hyperplasia, neoplastic cells proliferate regardless of growth signal presence or absence. If the neoplastic cells are adhesive, they may stay together as a lump and form a tumour. If they invade other tissues, they are malignant and also called cancer.</p>\n\n<p>Polyps are abnormal \"growths\", i.e. appendages grown from a tissue that do not normally occur. Usually, the tissue that has grown itself is not abnormal; rather, there are abnormal amounts of a signal instructing the tissue to grow. In this case, the polyp is usually hyperplastic (increased cell number), and sometimes also hypertrophic (increased cell size). Polyps can progress to neoplasms, usually first benign, and at late stages malignant.</p>\n\n<p>The only term describing both hyper- and neoplasias is \"hyperproliferation\", which is not a medical term. This still doesn't include dysplasia, and I can't think of a term that would. Maybe \"non-nascent cell behaviours\"...</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Dysplasia\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Dysplasia</a> has a quick overview of -plasias and -trophies.</p>\n", "score": 4 }, { "answer_id": 17030, "body": "<p>The all-inclusive term for <strong>abnormal growths</strong> is <a href=\"https://library.med.utah.edu/WebPath/NEOHTML/NEOPL102.html\" rel=\"nofollow noreferrer\"><strong>neoplasm</strong></a> or, in Latin, neoplsia:</p>\n\n<blockquote>\n <p>Neoplasia is new, uncontrolled growth of cells that is not under\n physiologic control.</p>\n</blockquote>\n\n<p>Abnormal growths can be:</p>\n\n<ul>\n<li><strong>Benign:</strong> growing but not spreading or destroying nearby tissues</li>\n<li><strong>Malignant:</strong> invading nearby tissues or spreading to distant organs</li>\n</ul>\n\n<p>The term <a href=\"https://www.medicinenet.com/script/main/art.asp?articlekey=5863\" rel=\"nofollow noreferrer\"><strong>tumor</strong></a> refers to any abnormal localized mass of tissue, either benign or malignant.</p>\n\n<p>The term <a href=\"https://en.wikipedia.org/wiki/Polyp_(medicine)\" rel=\"nofollow noreferrer\"><strong>polyp</strong></a> covers all tumors that grow from the mucous membranes and project into the lumen of an organ.</p>\n", "score": 2 } ]

[ "hyperplasia" ]

[ { "answer_id": 17188, "body": "<p>The pathophysiology of how DELC (diagonal ear lobe creases) and CAD (coronary artery disease) could be related has not been proven, but most likely has to do with the fact that both the earlobe and the muscles of the heart are supplied by end arteries with few collateral arteries - so atherosclerosis could theoretically affect the phenotypes of both your ear and your heart.</p>\n\n<p>Frank's sign is neither sensitive (lots of false negatives) nor specific (lots of false positives), so it's clinical utility is low. That being said, there have been a mix of studies that found a statistically significant relationship between Diagonal Ear Lobe Creases (DELC) and Coronary Artery Disease (CAD) so, in my opinion, the relationship is worth investigating.</p>\n", "score": 1 } ]

[ "dermatology", "heart-disease", "diagnostics" ]

[ { "answer_id": 17293, "body": "<p>Cells of the blood are produced in the bone marrow by <a href=\"https://en.wikipedia.org/wiki/Haematopoiesis\" rel=\"noreferrer\">multiple steps of differentiation</a>, yielding intermediate precursor cells like metamyelocytes.</p>\n\n<p>Their presence in peripheral blood is abnormal. This is called myelocytosis or myelemia.</p>\n\n<p>Myelocytosis is very concerning if there is presence of morphologically abnormal cells (like blast), especially if <a href=\"https://en.wikipedia.org/wiki/Cytopenia\" rel=\"noreferrer\">other lineages are lowered</a>.</p>\n\n<p>However, an isolated report of up to 2% circulating metamyelocytes is not as concerning. As they are the last step before the <a href=\"https://en.wikipedia.org/wiki/Neutrophil\" rel=\"noreferrer\">normal circulating neutrophils</a>, the presence of metamyelocyte in the blood is indicative of high activity in the granulocytic lineage caused by :</p>\n\n<ul>\n<li>Compensating for a previously diminished number of neutrophils (for example, after chemotherapy)</li>\n<li>Active infection or inflammation, with <a href=\"https://en.wikipedia.org/wiki/Neutrophilia\" rel=\"noreferrer\">elevated neutrophils</a> (>7 giga/L)</li>\n<li>Use of granulocyte stimulating factor (G-CSF, <a href=\"https://en.wikipedia.org/wiki/Filgrastim\" rel=\"noreferrer\">filgrastim</a>) for stem cell donation or recovery from agranulocytosis</li>\n</ul>\n\n<p>If this finding persists across multiple blood draw, more severe causes may need to be considered :</p>\n\n<ul>\n<li><p><a href=\"https://www.nhs.uk/conditions/chronic-myeloid-leukaemia/\" rel=\"noreferrer\">Chronic Myeloid Leukemia</a></p></li>\n<li><p><a href=\"https://www.mayoclinic.org/diseases-conditions/myelodysplastic-syndrome/symptoms-causes/syc-20366977\" rel=\"noreferrer\">Myelodysplasia</a></p></li>\n<li>Cancer invading the bone marrow</li>\n</ul>\n", "score": 5 } ]

[ "blood-tests", "test-results", "white-blood-count", "morphology" ]

[ { "answer_id": 17329, "body": "<p>It is commonly known by plastic surgeons etc that the close association of skin and bone in the shin area leads to poor healing. Anatomical studies suggest that this is caused by the comparative lack of deep perforating vessels.</p>\n\n<p><a href=\"https://www.jprasurg.com/article/0007-1226(81)90061-8/pdf\" rel=\"noreferrer\">https://www.jprasurg.com/article/0007-1226(81)90061-8/pdf</a></p>\n", "score": 7 } ]

[ "coloration-discoloration", "blood-circulation", "self-healing-repairing", "bruising-bruise" ]

[ { "answer_id": 17330, "body": "<p>The severity of Tourette's varies from person to person and can range from mild, requiring no treatment, to severe, requiring medication and/or behavioral therapy. The tics that are the hallmark of Tourette's also change over time in frequency, type, and severity, so it is possible that someone with Tourette's might need medication at some times and not others. In fact, changes in the tics is a required component of a Tourette's diagnosis. For severe tics, there is also deep brain stimulation (DBS), which involves implanting a device in the brain to deliver targeted electrical stimulation to movement centers. However, DBS is still in early experimental stages so its safety and effectiveness aren't known at this time.</p>\n\n<p><a href=\"https://www.mayoclinic.org/diseases-conditions/tourette-syndrome/diagnosis-treatment/drc-20350470\" rel=\"noreferrer\">https://www.mayoclinic.org/diseases-conditions/tourette-syndrome/diagnosis-treatment/drc-20350470</a></p>\n", "score": 7 } ]

[ "mental-health", "treatment", "tourette-syndrome" ]

[ { "answer_id": 17370, "body": "<p>The Demodex mite is part of normal skin flora but is often implicated in conditions like rosacea, folliculitis and blepharitis (inflammation of the eyelids).</p>\n\n<p>Erythromycin is an effective treatment. Its <a href=\"http://chemistry.elmhurst.edu/vchembook/654antibiotic.html\" rel=\"noreferrer\">mechanism of action</a> is to bind to the 50s subunit of the ribosome (involved in manufacturing proteins in cells) and so inhibits the synthesis of proteins. While humans do not have this 50s ribosomal subunit, other species do, including many bacteria and parasites, so erythromycin can be effective.</p>\n\n<p>This goes for other antibiotics too. For example, <em>metronidazole</em> is used to treat the parasitic bowel infestation <a href=\"https://en.m.wikipedia.org/wiki/Giardiasis\" rel=\"noreferrer\">giardiasis</a>.</p>\n\n<hr>\n\n<p>Interestingly, macrolide antibiotics (of which erythromycin is one example), have also been shown to have anti-inflammatory effects and also have a pro-kinetic effect on the stomach; increasing its contractions and speed of emptying. It is sometimes used for this effect alone in conditions like gastric stasis and diabetic <a href=\"https://en.m.wikipedia.org/wiki/Gastroparesis\" rel=\"noreferrer\">gastroparesis</a>, where the stomach is slow to empty. <a href=\"https://gut.bmj.com/content/gutjnl/33/3/397.full.pdf\" rel=\"noreferrer\">This paper</a> has some more information.</p>\n\n<hr>\n\n<p>Antibiotics are drugs, and like many drugs can have multiple effects beside their most common use of combating bacterial infections.</p>\n\n<p>However, they still don’t work on viruses like cold and flu! :)</p>\n\n<p><a href=\"https://i.stack.imgur.com/EQhpf.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/EQhpf.jpg\" alt=\"Antibiotics don’t work for a cold or flu\"></a></p>\n\n<p><strong>Other sources</strong></p>\n\n<ul>\n<li><a href=\"https://bnf.nice.org.uk/drug/erythromycin.html\" rel=\"noreferrer\">British National Formulary - Erythromycin</a></li>\n<li><a href=\"https://www.reviewofoptometry.com/article/spotlight-on-demodex-eliminating-the-mitey-menace\" rel=\"noreferrer\">Review of Optometry - Demodex</a></li>\n<li><a href=\"http://www.microbiologynutsandbolts.co.uk/the-bug-blog/mighty-mini-mites\" rel=\"noreferrer\">Microbiology Nuts and Bolts - Mighty Mini Mites</a></li>\n<li><a href=\"https://en.m.wikipedia.org/wiki/Erythromycin\" rel=\"noreferrer\">Wikipedia - Erythromycin</a></li>\n</ul>\n", "score": 5 } ]

[ "antibiotics", "demodex", "mechanism-of-action" ]

[ { "answer_id": 17375, "body": "<p>This is known as antibiotic prophylaxis. It is to prevent infection in the bone (<a href=\"https://en.m.wikipedia.org/wiki/Osteomyelitis\" rel=\"nofollow noreferrer\">osteomyelitis</a>).</p>\n\n<p>If the bone surface is intact, pathogens like bacteria cannot penetrate it easily, but in the presence of an <a href=\"https://en.m.wikipedia.org/wiki/Open_fracture\" rel=\"nofollow noreferrer\">open fracture</a> (when the bony injury is exposed to the environment due to skin and subcutaneous tissue damage) antibiotics are used to prevent infection.</p>\n\n<p>In some countries, an open fracture may be known as a compound fracture.</p>\n\n<p>Source:</p>\n\n<ul>\n<li><a href=\"https://journals.lww.com/aenjournal/Abstract/2015/01000/Antibiotic_Prophylaxis_for_Open_Fractures_in_the.4.aspx\" rel=\"nofollow noreferrer\">Antibiotic Prophylaxis for Open Fractures in the Emergency Department</a></li>\n</ul>\n", "score": 3 } ]

[ "antibiotics", "bone-fractures" ]

[ { "answer_id": 17712, "body": "<p>\"The net daily synthesis of cholesterol is equal to the amount of cholesterol lost in the feces minus the dietary cholesterol\"</p>\n\n<p>The body synthesizes an amount approximately equal to the amount it absorbs</p>\n\n<p>Source:\nBalancing Cholesterol Synthesis and Absorption in the Gastrointestinal Tract\nDavid E. Cohen, M.D., Ph.D.</p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2390860/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2390860/</a></p>\n", "score": 3 } ]

[ "liver", "cholesterol" ]

[ { "answer_id": 17397, "body": "<p>According to a case report about a 24-year old woman (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3361850/\" rel=\"nofollow noreferrer\">PubMed Central</a>), in <strong>agoraphobia,</strong> during a panic attack, the sympathetic nervous system is activated, which results in adrenaline release, which causes symptoms, such as:</p>\n\n<blockquote>\n <p>...pounding heart, shortness of breath nervousness, dizziness, losing\n control on himself <strong>for few minutes.</strong></p>\n</blockquote>\n\n<p>So, from symptoms lasting few minutes, you can conclude that adrenaline is acting for few minutes and not all the time.</p>\n\n<p>According to one <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1464218/\" rel=\"nofollow noreferrer\">2005 study</a>, <strong>caffeine</strong> stimulates adrenaline release, but</p>\n\n<blockquote>\n <p><strong>adrenaline alone does not account for the effects of caffeine</strong> and\n additional mechanisms must be involved.</p>\n</blockquote>\n\n<p>From the above, one might think that caffeine could help you stay alert despite already being stimulated by adrenaline from anxiety.</p>\n\n<p>But, according to one <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4462044/\" rel=\"nofollow noreferrer\">2015 review article</a>:</p>\n\n<blockquote>\n <p>moderate-to-high consumers develop tolerance to caffeine and <strong>only low\n or nonconsumers can eventually benefit from an acute administration.</strong></p>\n</blockquote>\n\n<p><strong>In conclusion,</strong> one who drinks a lot of coffee on a daily basis, will probably develop tolerance to caffeine, in which case the wakening effect would be a placebo effect.</p>\n", "score": 3 } ]

[ "sleep", "caffeine", "physical-health", "adrenaline" ]

[ { "answer_id": 17449, "body": "<p>There is not enough evidence either in support or in rebuttal...</p>\n\n<blockquote>\n <p>EFFECTS OF CHRONIC OR REPEATED EXPOSURE:<br>\n Nicotine is a teratogen (capable of causing birth defects). Other developmental toxicity or reproductive toxicity risks are unknown. The information about nicotine as a carcinogen is inconclusive.</p>\n \n <p>^{<a href=\"https://www.cdc.gov/niosh/ershdb/emergencyresponsecard_29750028.html\" rel=\"nofollow noreferrer\">cdc.gov</a>}</p>\n \n <p>In summary, the findings of animal studies do not support the hypothesis that nicotine is a complete carcinogen. It is a tumor promoter in some experimental models, although not for tobacco-specific nitrosamines. Studies examining other classes of tobacco smoke carcinogens (e.g., polycyclic aromatic hydrocarbons) would need to be performed to better define the potential cancer risk inferred from animal studies. </p>\n \n <p><em>[...]</em></p>\n \n <p>There is insufficient data to conclude that nicotine causes or contributes to cancer in humans, but there is evidence showing possible oral, esophageal, or pancreatic cancer risks. Additionally, there is substantial experimental evidence indicating that nicotine is bioactive for a number of carcinogenic mechanisms in experimental systems. Although in vitro data are suggestive of relevant biological activity, this is not supported overall by the most recent experimental animal studies. In humans, there has been limited research and only one relatively short–term follow-up study on nicotine and cancer.</p>\n \n <p>_{Surgeongeneral.gov, <a href=\"https://www.surgeongeneral.gov/library/reports/50-years-of-progress/sgr50-chap-5.pdf\" rel=\"nofollow noreferrer\">Chapter 5 Nicotine</a> (PDF)}</p>\n</blockquote>\n", "score": 5 }, { "answer_id": 17456, "body": "<p>It is a common way to demonise substances in saying that they \"cause cancer\". In the case of recreational or habitual tobacco smoking there is no longer much debate over whether that is true or not. \"Smoking causes cancer\" is a commonly accepted fact now.</p>\n\n<p>But what exactly causes cancer within this model? Smoke from a cigarette is a mixture of evaporated plant material, pyrolised material, burnt paper etc. Quite a lot of substances in differing mixtures. An exact explanation of cause and effect for each \"ingredient\" of smoke is much more difficult than a relatively simple epidemiological correlation and conclusion or even a lab experiment with copious amounts of smoke.</p>\n\n<p>For nicotine ioslated and on itself it has recently been said that:</p>\n\n<blockquote>\n <ul>\n <li>In small doses, nicotine speeds up cell growth. In larger doses, it’s poisonous to cells.</li>\n <li>Nicotine kick-starts a process called epithelial-mesenchymal transition (EMT). EMT is one of the important steps in the path toward malignant cell growth.</li>\n <li>Nicotine decreases the tumor suppressor CHK2. This may allow nicotine to overcome one of the body’s natural defenses against cancer.</li>\n <li>Nicotine can abnormally speed up the growth of new cells. This has been shown in tumor cells in the breast, colon, and lung.</li>\n <li>Nicotine can lower the effectiveness of cancer treatment.</li>\n </ul>\n \n <p>via <a href=\"https://www.healthline.com/health/does-nicotine-cause-cancer#nicotine-and-cancer\" rel=\"nofollow noreferrer\">Healthline</a></p>\n</blockquote>\n\n<p>That can be criticised on numerous grounds. Whether a substance interferes with cancer treatments is wholly irrelevant to the question whether the substances causes it.<br>\nAssertions like these without the numbers, for example dose-response, effect sizes etc. I tend to either follow up to their sources or just ignore them altogether.</p>\n\n<p>In this case the source is </p>\n\n<blockquote>\n <p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4553893/\" rel=\"nofollow noreferrer\">Tore Sanner &amp; Tom K. Grimsrud: \"Nicotine: Carcinogenicity and Effects on Response to Cancer Treatment – A Review\", Frontiers in Oncology. 2015; 5: 196</a>. PMID 26380225 DOI 10.3389/fonc.2015.00196</p>\n</blockquote>\n\n<p>In there all of the points above quoted by healthline are present. Any yet they have to hide a caveat in the middle of the conclusion part:</p>\n\n<blockquote>\n <p>At present, it is not possible to draw a conclusion whether nicotine itself may act as a complete carcinogen.</p>\n</blockquote>\n\n<p>The demonisation of just nicotine seems to be mostly twofold, if we substract all the annoyances from smoking tobacco: habit or even addiction forming and limited amount of joy.</p>\n\n<p>If we look just at the substance alone, and exclude smoking or vaping or liquid-preparation inhalation, what is left?</p>\n\n<p>A practical outlook would be to examine nicotine replacement therapy.</p>\n\n<blockquote>\n <p><a href=\"https://link.springer.com/article/10.1007/s00204-016-1856-y\" rel=\"nofollow noreferrer\">Peter N. Lee &amp; Marc W. Fariss: \"A systematic review of possible serious adverse health effects of nicotine replacement therapy\", Archives of Toxicology (2017) 91:1565–1594</a>:</p>\n \n <p>We conducted a systematic literature review to identify and critically evaluate studies of serious adverse health effects (SAHEs) in humans using nicotine replacement therapy (NRT) products. Serious adverse health effects refer to adverse events, leading to substantial dis- ruption of the ability to conduct normal life functions. Strength of evidence evaluations and conclusions were also determined for the identified SAHEs. We evaluated 34 epidemiological studies and clinical trials, relating NRT use to cancer, reproduction/development, CVD, stroke and/or other SAHEs in patients, and four meta-analyses on effects in healthy populations. The overall evidence suffers from many limitations, the most significant being the short-term exposure (≤12 weeks) and follow-up to NRT product use in most of the studies, the common failure to account for changes in smoking behaviour following NRT use, and the sparse information on SAHEs by type of NRT product used. The only SAHE from NRT exposure we identified was an increase in respiratory congenital abnormalities reported in one study. Limited evidence indicated a lack of effect between NRT exposure and SAHEs for CVD and various reproduction/developmental endpoints. <strong>For cancer, stroke and other SAHEs, the evidence was inadequate to demonstrate any association with NRT use</strong>. Our conclusions agree with recent statements from authoritative bodies.</p>\n</blockquote>\n\n<p>Although we cannot categorically exclude the possibility that nicotine alone is a cancer causing or a cancer promoting agent with 100% certainty, we might conclude that the low level of serious adverse health effects from psychotropically effective doses in nicotine replacement therapy are a good indicator for the general safety of the <a href=\"https://medicalsciences.stackexchange.com/questions/10993/how-much-nicotine-is-in-tea-and-vegetables\">miniscule levels of nicotine</a> found in tomatoes, potatoes and even the egregious eggplant.</p>\n\n<p>Conflicts of interest:\nThis answer does not promote or advertise or justify the use of nicotine in any way. It does call for a sober evaluation of its properties. It also does promote and advertise the ingestion of vegetables disregarding the amount of nicotine in them completely.</p>\n", "score": 3 }, { "answer_id": 17454, "body": "<p>I'd want to add to Narusan's answer the following: While nicotine by itself doesn't seem to be a carcinogen, to some degree it <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2783463/\" rel=\"nofollow noreferrer\">may be converted</a> to carcinogenic N-nitrosonornicotine (a tobacco-specific nitrosamine) in the body, for example by bacterial activity. How much depends, among other things, on the route of administration.</p>\n\n<blockquote>\n <p>If Nicotine causes cancer, then as Potato or Tomatoes contain Nicotine according to the studies above, they would surely cause cancer as well.</p>\n</blockquote>\n\n<p>Even if that <em>were</em> (!) true, so what? In the probabilistic model of epidemiology “cause” is <strong>not</strong> like the ‘everyday’ conception of cause.</p>\n\n<p>For example, the classification is by the strength of evidence, not the degree of risk. That's why we hear something <a href=\"https://www.theguardian.com/society/2015/oct/26/bacon-ham-sausages-processed-meats-cancer-risk-smoking-says-who\" rel=\"nofollow noreferrer\">like this</a>:</p>\n\n<blockquote>\n <p>Bacon, ham and sausages rank alongside cigarettes as a major cause of cancer, the World Health Organisation has said, placing cured and processed meats in the same category as asbestos, alcohol, arsenic and tobacco.</p>\n</blockquote>\n\n<p>Therefore, I don't see a <em>reductio ad absurdum</em>.</p>\n\n<p>On a more serious note, even with eggplants you'd have to eat 10 kg to get to the level of a single cigarette.</p>\n\n<p>But that's not even why your reasoning is fallacious. It's wrong, like with the <a href=\"https://www.reuters.com/article/us-california-lawsuit-coffee/cancer-warnings-to-be-served-up-with-coffee-in-california-idUSKBN1I930H\" rel=\"nofollow noreferrer\">coffee cancer warnings</a> in California, to not consider the <em>whole</em> product (vegetable/fruit/…). <strong>You have to balance the carcinogens vs. the antioxidants and anticancer agents.</strong></p>\n", "score": 1 } ]

[ "cancer", "smoking", "nicotine", "tobacco", "e-cigarette-vape" ]

[ { "answer_id": 17600, "body": "<p>Question: How much vitamin C is actually present in a glass of orange juice, taking into account could have been passed months since <strong>harvesting-squeezing-bottling</strong> to drinking?</p>\n\n<p>The nutrition label of the bottled juice should tell what is in the bottled juice <strong>after</strong> harvesting-squeezing-bottling. <a href=\"https://ndb.nal.usda.gov/ndb/search/list?SYNCHRONIZER_TOKEN=0b300c79-bd31-4c63-8492-05f884a56e71&amp;SYNCHRONIZER_URI=%2Fndb%2Fsearch%2Flist&amp;qt=&amp;qlookup=orange%20juice&amp;ds=&amp;manu=\" rel=\"nofollow noreferrer\">USDA.gov has evaluated the amount of vitamin C in many <strong>brands</strong> of orange juices</a>, which can make you believe they evaluated the actual bottled orange juices from the shelves in stores.</p>\n\n<p><strong>After</strong> putting the orange juice on a shelf (According to <a href=\"https://www.sciencedirect.com/science/article/pii/088915759190050G\" rel=\"nofollow noreferrer\">ScienceDirect</a>):</p>\n\n<blockquote>\n <p>In general, degradation of vitamin C is a function of time.</p>\n</blockquote>\n\n<p><a href=\"http://www.vup.sk/en/download.php?start&amp;language=en&amp;bulID=9..\" rel=\"nofollow noreferrer\">In this study</a> they concluded it is <strong>time, room temperature, exposure to light and the addition of sugar</strong> that can affect the amount of vitamin C in fruit juices:</p>\n\n<blockquote>\n <p>...were stored for 28 days at 37 °C. After 14 days of storage,\n ascorbic acid was completely degraded...</p>\n \n <p>...retention of L-ascorbic acid is greatly affected by the storage\n temperature (4–50 °C).</p>\n</blockquote>\n\n<p>As a side note, here's a chart from <a href=\"https://nutritiondata.self.com/topics/processing\" rel=\"nofollow noreferrer\">NutritionData</a> that tells how freezing, drying, cooking and reheating affect the amount of vitamin C in a food.</p>\n\n<p>Here's <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/15738222\" rel=\"nofollow noreferrer\">one study about vitamin C degradation in milk</a>, just to show that you really need a lot of data to make final conclusions: </p>\n\n<blockquote>\n <p>The use of a 3-layered opaque bottle was associated with complete\n oxidation of vitamin C after 1 month of storage, whereas in the\n 6-layered opaque bottle, which has an oxygen barrier, the vitamin C\n content slowly decreased to reach 25% of the initial concentration\n after 4 months of storage.</p>\n</blockquote>\n", "score": 2 } ]

[ "micronutrients", "vitamin-c", "juice" ]

[ { "answer_id": 17760, "body": "<p>Like the left ventricle, the right ventricle goes through a contractile cycle: at diastole, the pressure is near zero (and must be &lt;0 relative to the right atrium, or it wouldn't fill with blood); at systole the pressure is maximal and drops quickly upon the end of contraction and closure of the pulmonary valve. <strong>Healthy right ventricular systolic pressure is typically less than 40 mmHg</strong> - far less than healthy peak left ventricular pressure which is normally stated as around 120 mmHg (like the right ventricle, the left ventricle is only briefly at such a high pressure; it decreases after the aortic valve closes).</p>\n\n<p><strong>Why is this so different from the left ventricle?</strong></p>\n\n<p>Similar to electricity, where <em>voltage</em> is a function of <em>current</em> and <em>resistance</em> (V=I*R), in a fluid system <em>pressure</em> is a function of <em>flow</em> and <em>resistance</em>.</p>\n\n<p>Peak systolic pressure in the right ventricle is most related to <em>resistance in the lungs</em>; peak systolic pressure in the left ventricle is most related to <em>resistance in the rest of the body</em>. Typically, resistance in the lungs is much much lower than resistance in the rest of the body, but medical conditions that cause increased resistance in the lungs can cause pulmonary hypertension (which will also mean hypertension in the right ventricle).</p>\n\n<p>Resistance in a vascular system is a function of both the total cross-sectional diameter of the vessels, and the length of the vessels. The path to the lungs from the heart is fairly short, and there is a very dense capillary bed.</p>\n\n<p><strong>But what about the lymphatic system and differences in flow?</strong></p>\n\n<p>The lymphatic system doesn't factor in much at all, the volume of blood pumped by the right and left ventricles (and therefore flow) is almost exactly the same: the only exception would be any amount of fluid lost in the lungs (your diagram shows this with fluid entering the lymph system in the pulmonary circulation), which would actually mean <em>less</em> fluid pumped by the left versus the right. The presence of the lymphatic system only reduces the amount of flow through the distal veins: as your diagram shows the fluid is returned to the bloodstream prior to arriving in the right ventricle. There is no place for \"extra\" fluid to enter only the left-side circulation without first passing through the right.</p>\n\n<hr>\n\n<p>Currie, P. J., Seward, J. B., Chan, K. L., Fyfe, D. A., Hagler, D. J., Mair, D. D., ... &amp; Tajik, A. J. (1985). Continuous wave Doppler determination of right ventricular pressure: a simultaneous Doppler-catheterization study in 127 patients. Journal of the American College of Cardiology, 6(4), 750-756.</p>\n\n<p>McLaughlin, V. V., Archer, S. L., Badesch, D. B., Barst, R. J., Farber, H. W., Lindner, J. R., ... &amp; Rubin, L. J. (2009). ACCF/AHA 2009 expert consensus document on pulmonary hypertension: a report of the American College of Cardiology Foundation Task Force on expert consensus documents and the American Heart Association developed in collaboration with the American College of Chest Physicians; American Thoracic Society, Inc.; and the Pulmonary Hypertension Association. Journal of the American College of Cardiology, 53(17), 1573-1619.</p>\n\n<p>Rudski, L. G., Lai, W. W., Afilalo, J., Hua, L., Handschumacher, M. D., Chandrasekaran, K., ... &amp; Schiller, N. B. (2010). Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography: endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. Journal of the American Society of Echocardiography, 23(7), 685-713.</p>\n", "score": 6 } ]

[ "blood-pressure" ]

[ { "answer_id": 17765, "body": "<blockquote>\n <p>Won't this (having a flu vaccine every year) put them in an uncharted territory as far as effects on the immune systems are concerned within a couple of decades?</p>\n</blockquote>\n\n<p>No</p>\n\n<p>You are exposed to and develop a memory response to many, many more pathogens than vaccines. Your collective immune memory from natural exposure to a pathogen is much, much larger than from vaccination.</p>\n\n<p>Effective vaccines reproduce the immune response of exposure to a pathogen (see the CDC pink book, <a href=\"https://www.cdc.gov/vaccines/pubs/pinkbook/prinvac.html\" rel=\"nofollow noreferrer\">Chapter 1</a>). Some use specific subgroups of antigens important for protective immunity, some use killed viruses that don't replicate in the host, and others use live attenuated viruses that replicate, but don't cause disease. The number of vaccines you get is much smaller than the number of different antigens you are exposed to. Considering the common cold alone, the incidence in the US is 6 per person year for children, 2 per person year for adults without exposure to children (see Cecil Medicine Ch. 369). Each of these exposures involves many different antigens. Vaccine related immune memory is a drop in the bucket.</p>\n\n<p>Beyond this, the basic premise (that you have a small amount of immune memory storage relative to the number of vaccines you receive) is wrong. There are over 3 billion B-cells in your body at any given time, with about 100 million different B cell receptors. This repertoire of antigen receptors is enough to match every single (or nearly every single, depending on who you ask) possible macromolecular antigen. For a protein, or protein conjugated antigen, the product of that match can produce long lived high affinity memory B cells, and long lived high affinity plasma cells. Your immune system has the memory capacity to deal with a great deal more antigens than the number of vaccines. You can read about these basic immunology details in Sompayrac's How the Immune System Works (Chapter 1 gives the numbers I've discussed here, and discusses how the repertoire of antigen receptors matches up with the number of possible antigens). Other basic immunology texts (e.g., Abbas, Janeway) cover the same, but can be a little more dense.</p>\n", "score": 9 } ]

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

[ { "answer_id": 17958, "body": "<p><strong>As suggested by one small human study and one study in mice, nicotine might improve Crohn's disease in the colon but aggravate Crohn's disease in the small intestine.</strong> </p>\n\n<p><a href=\"https://www.hindawi.com/journals/grp/2008/237185/\" rel=\"nofollow noreferrer\">Nicotine Enemas for Active Crohn's Colitis: An Open Pilot Study (Hindawi, 2008)</a></p>\n\n<blockquote>\n <p>Thirteen patients with active rectosigmoid Crohn's diseae...were given 6 mg\n nicotine enemas, each day for 4 weeks... Mean Crohn's disease activity\n index (CDAI) decreased from 202 to 153—the score was reduced in 6\n patients, unchanged in 3, and increased in one. Frequency of bowel\n movements decreased in 8 patients and the sigmoidoscopy grade was\n reduced in 7.</p>\n</blockquote>\n\n<p>In a study in mice (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/12072594/\" rel=\"nofollow noreferrer\">PubMed, 2002</a>) with chemically induced inflammatory bowel disease, nicotine (added into the drinking water) treatment improved inflammation of the colon but aggravated inflammation of the jejunum (a part of small intestine).</p>\n\n<p>This evidence if far too weak to make any conclusions/recommendations but suggests that differences in the nicotine effect might be due to disease location (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146835/\" rel=\"nofollow noreferrer\">Effect of smoking on inflammatory bowel disease: Is it disease or organ specific? - PubMed, 2007</a>).</p>\n", "score": 4 } ]

[ "smoking", "nicotine", "crohns", "ulcerative-colitis" ]

[ { "answer_id": 18010, "body": "<p><a href=\"https://teachmeanatomy.info/lower-limb/nerves/superficial-fibular-nerve/\" rel=\"nofollow noreferrer\">This anatomy site</a> doesn't provide reputable citations, but I don't see any obvious inaccuracies and it has a reasonable section on potential clinical presentations of superficial fibular nerve injuries:</p>\n<blockquote>\n<p>There are two relatively common pathologies involving the damage to the superficial fibular nerve; entrapment and direct damage (e.g from a comminuted fracture).</p>\n<h3>Superficial Fibular Nerve Entrapment</h3>\n<p>Superficial peroneal nerve entrapment (also known as nerve compression) can cause pain and paraesthesia over the lower leg and dorsum of the foot. Entrapment frequently results from ankle sprains or twisting of the ankle, as this causes the nerve to stretch in the lower leg.</p>\n<p>Another cause of nerve entrapment occurs at the point where the nerve exits the deep fascia of the leg, the nerve becoming compressed by this fascia. Surgical decompression of the nerve therefore is used to provide relief from the symptoms and pain.</p>\n<h3>Direct Damage to the Superficial Fibular Nerve</h3>\n<p>The superficial fibular nerve may be damaged by fracture of the fibula, or by a perforating wound to the lateral side of the leg.</p>\n<p>As the muscles that the superficial fibular nerve innervates are evertors, injury to the nerve may result in a loss of eversion. A loss of sensation over the majority of the dorsum of the foot and the anterolateral aspect of the lower leg could also result.</p>\n</blockquote>\n<p>ScienceDirect provides summary pages with excerpts from relevant publications on many topics, including the <a href=\"https://www.sciencedirect.com/topics/neuroscience/fibularis-muscles\" rel=\"nofollow noreferrer\">fibularis muscles</a>, which largely verifies the claims from the anatomy teaching site. I'll include two especially useful excerpts here.</p>\n<blockquote>\n<p><a href=\"https://www.sciencedirect.com/science/article/pii/B9781416024439500350\" rel=\"nofollow noreferrer\"><strong>Chapter 32 - Leg Injuries. Zetaruk &amp; Hyman. <em>Clinical Sports Medicine</em>. 2007.</strong></a></p>\n<h3>Presentation</h3>\n<p>Athletes with compression of this nerve present with pain, numbness or paraesthesias in the distribution of the superficial peroneal nerve (i.e. anterolateral lower leg and dorsum of foot, including second to fourth toes) during exercise and occasionally at rest.</p>\n<p><a href=\"https://i.stack.imgur.com/46TYb.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/46TYb.jpg\" alt=\"Superficial fibular nerve distribution\" /></a></p>\n<h3>Examination</h3>\n<p>Clinical examination reveals decreased sensation most consistently over the dorsum of the foot after exercise. Tinel's sign over the site of the compression or pain with passive ankle flexion/supination may be elicited. Pressure over the site of entrapment while the patient actively plantarflexes and inverts the ankle may reproduce symptoms. A fascial defect may be detected on palpation.</p>\n<h3>Treatment</h3>\n<p>Initial conservative treatment may include modification of aggravating activities and prevention of recurrent ankle inversions using bracing. Surgical decompression is the definitive treatment.</p>\n<p><a href=\"https://www.sciencedirect.com/science/article/pii/B9780444529022000199\" rel=\"nofollow noreferrer\"><strong>Chapter 19 - Compression and entrapment neuropathies. Bouche. <em>Handbook of Clinical Neurology</em>. 2013.</strong></a></p>\n<h3>Superficial Fibular Neuropathy</h3>\n<p>Superficial fibular nerve compression or entrapment is unusual. Peroneal compartment syndrome is an uncommon disorder in which the muscle swelling and necrosis are limited to the fibular muscles. It can be due to excessive exercise, blunt trauma, or rupture of the peroneus longus. Fracture of the fibula may damage only the superficial fibular nerve...Causes were varied: muscle herniation, varicose veins, anterior and/or lateral compartment syndrome, anterior fasciotomy, or contusion. There was decreased sensation and pain over the dorsum of the foot at rest or during exercise. Reduced nerve conduction velocity of the superficial fibular nerve below 44 m/s was considered abnormal.</p>\n</blockquote>\n<p>You'll notice that these articles make little mention of motor defects, including your hypothesized &quot;constant supination of the foot,&quot; like those motor deficiencies that occur with comparable <a href=\"https://en.wikipedia.org/wiki/Brachial_plexus_injury\" rel=\"nofollow noreferrer\">brachial plexus injuries</a>. This is because the eversion action of the muscles supplied by the superficial fibular nerve is supplemented by muscles innervated by the deep (profundus) fibular nerve (whereas brachial plexus injuries &quot;knock out&quot; entire muscle groups that work in opposition to a still-active group).</p>\n<p>With superficial fibular nerve pathologies, the supinating action of the muscles supplied by n. fibularis profundus isn't so strongly unopposed that a remarkable club foot presentation appears, but long-term superficial peroneal nerve dysfunction still limits function in the lower leg and can be treated non-invasively:</p>\n<blockquote>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684217/\" rel=\"nofollow noreferrer\"><strong>Evaluation and treatment of peroneal neuropathy. Baima &amp; Krivickas. <em>Curr Rev Musculoskelet Med</em>. 2008.</strong></a></p>\n<p>If the patient has isolated superficial peroneal nerve palsy, he may benefit from a shoe insert with a lateral wedge to prevent supination of the foot from weakness of the evertors.</p>\n</blockquote>\n", "score": 2 } ]

[ "anatomy" ]

[ { "answer_id": 18028, "body": "<p>There are apparently several reasons. I found an article (<a href=\"http://www.todayifoundout.com/index.php/2014/03/native-americans-didnt-wipe-europeans-diseases/\" rel=\"nofollow noreferrer\">http://www.todayifoundout.com/index.php/2014/03/native-americans-didnt-wipe-europeans-diseases/</a>) that basically calls out three specific reasons:</p>\n<ul>\n<li>Europeans had lived with and near domesticated animals for quite a while, and this helped boost their immune systems. Native Americans, for the most part, were hunter-gatherers who did not keep livestock.</li>\n<li>Europeans lived close together, and the interaction (and exchange of germs) that this caused helped to boost their immune systems.</li>\n<li>Europeans traveled a lot and interacted with citizens of other areas to a larger degree, and this helped boost their immune systems.</li>\n</ul>\n<p>Recurring theme? Several factors combined to help boost the immune systems of Europeans as compared to Native American tribes.</p>\n<p>However, if you read the article (recommended) you will find that it was a two-way street, at least to a degree. For example, one of the best-known diseases acquired in the New World and brought back to Europe was syphillis.</p>\n", "score": 4 } ]

[ "immune-system" ]

[ { "answer_id": 18017, "body": "<p>It is extremely unlikely that common cold as such would kill you, but the complications could.</p>\n\n<p>The definition of a common cold is a <em>viral</em> infection of the <em>nose and throat</em> as reflected from its Latin names <a href=\"https://simple.wikipedia.org/wiki/Common_cold\" rel=\"nofollow noreferrer\">nasopharyngitis or rhinopharyngitis</a>.</p>\n\n<p>It is usually pneumonia as a complication of common cold (or <a href=\"https://www.cdc.gov/flu/consumer/symptoms.htm\" rel=\"nofollow noreferrer\">flu</a> or <a href=\"https://www.cdc.gov/measles/downloads/measlesdataandstatsslideset.pdf\" rel=\"nofollow noreferrer\">measles</a>...) that can be deadly. A young student recently died in the US from pneumonia as a complication of common cold caused by <em>Adenovirus</em> (<a href=\"http://www.sdailynews.com/2018/11/22/university-freshman-becomes-latest-casualty-of-adenovirus/\" rel=\"nofollow noreferrer\">S Daily News</a>).</p>\n\n<p>The risk factors for common cold complications can include impaired immunity (hereditary or acquired), anatomical abnormalities of the respiratory system, co-existent lung or other disease and old age.</p>\n\n<p>EDIT:</p>\n\n<p>To answer \"I have several times <a href=\"https://www.afp.com/en/news/15/us-missionarys-body-could-be-lost-battle-preserve-isolated-tribe-doc-1b203b1\" rel=\"nofollow noreferrer\">read</a> that common cold could kill this tribe\": The article does not claim that common cold can kill them, but they <em>believe</em> it could kill them:</p>\n\n<blockquote>\n <p><em>Fears</em> that 21st century diseases as mild as the common cold could kill off the tribe, or that experiencing electricity and the internet\n would devastate their lifestyle, has left them in a guarded bubble...</p>\n</blockquote>\n", "score": 5 }, { "answer_id": 18027, "body": "<p>Adding to Jan's answer, I found this, which was just published today. Emphasis is mine.</p>\n\n<p><a href=\"https://blogs.scientificamerican.com/observations/the-american-killed-by-asian-islanders-hoped-to-save-their-souls/\" rel=\"nofollow noreferrer\">https://blogs.scientificamerican.com/observations/the-american-killed-by-asian-islanders-hoped-to-save-their-souls/</a></p>\n\n<blockquote>\n <p>Last to succumb were the Jarawa, who live in dense forests on the\n western edge of South and Middle Andaman Islands and, until 1998, were\n defending their territory with their lives. They killed settlers who\n ventured into their territory to fish or hunt game, and got killed in\n return. That year however, they succumbed to decades of pacification\n efforts originally developed by Maurice V. Portman, a colonial\n administrator. Boatloads of Indian officials and anthropologists would\n land on Jarawa beaches, leave gifts of bananas, red cloth and other\n goodies from civilization, and retreat. The Jarawa were eventually\n seduced into laying down their arms and interacting with settlers in\n peace. <strong>Almost instantly, they were beset by epidemics of pneumonia,\n mumps, measles and other diseases; <em>even the common cold seemed to be\n lethal to them</em>.</strong> No one knows how many died.</p>\n</blockquote>\n\n<p>So there seems to be evidence that contact with long-isolated tribes can be lethal to them via the common cold.</p>\n", "score": 3 } ]

[ "immune-system", "common-cold" ]

[ { "answer_id": 18055, "body": "<p>I believe the procedure described is called either <a href=\"https://www.physio-pedia.com/Muscle_Energy_Technique\" rel=\"nofollow noreferrer\">muscle energy technique (MET)</a> or <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3588663/\" rel=\"nofollow noreferrer\">proprioceptive neuromuscular facilitation (PNT)</a>. More details are on <a href=\"http://www.leonchaitow.com/wp-content/uploads/2016/12/Naturopathic-Physical-Medicine.pdf\" rel=\"nofollow noreferrer\">Advantageceus.com (p. 229)</a>. Skin stimuli, like scratching or flicking, may be part of the mentioned techniques.</p>\n\n<p>This article on <a href=\"https://www.journalofosteopathicmedicine.com/article/S1746-0689(10)00030-1/fulltext\" rel=\"nofollow noreferrer\">International Journal of Osteopathic Medicine</a> says that \"MET application may reduce pro-inflammatory cytokines and desensitize peripheral nociceptors.\"</p>\n\n<p>According to one <a href=\"https://ir.dut.ac.za/bitstream/10321/272/1/Wilson_2002.pdf\" rel=\"nofollow noreferrer\">PhD dissertation published by Durban University of Technology</a> \"Both superficial and deep somatic mechanoreceptos, proprioceptors and nociceptors are stimulated by [chiropractic] manipulation, which sends strong afferent segmental impulses to the spinal cord resulting in central pain transmission inhibition.\"</p>\n\n<p>Studies:</p>\n\n<ul>\n<li><a href=\"https://www.researchgate.net/publication/265026184_Effect_of_Proprioceptive_Neuromuscular_Facilitation_Stretch_Techniques_on_Trained_and_Untrained_Older_Adults\" rel=\"nofollow noreferrer\">Effect of Proprioceptive Neuromuscular Facilitation Stretch Techniques on Trained and Untrained Older Adults (ResearchGate, 2002)</a>: \"PNF stretch techniques can be used to produce increases in knee-joint extension ROM in older adults.\"</li>\n<li><a href=\"https://www.sciencedirect.com/science/article/pii/S1443846103800151?via%3Dihub\" rel=\"nofollow noreferrer\">The effect of muscle energy technique on hamstring extensibility: the mechanism of altered flexibility (ScienceDirect, 2003)</a>: \"Muscle energy technique produced an immediate increase in passive knee extension.\"</li>\n<li><a href=\"https://www.researchgate.net/publication/325722511_The_Proprioceptive_Neuromuscular_Facilitation_Reduces_Isometric_Strength_in_Apparently_Health_Women_Short_Communication\" rel=\"nofollow noreferrer\">The Proprioceptive Neuromuscular Facilitation Reduces Isometric Strength in Apparently Health Women Short Communication (ResearchGate, 2018)</a>: \"30 seconds of stretching by PNF method is already enough to occasion sensibility decrease in muscular proprioceptors, tendinous and articular, as well as in nociceptors...\"</li>\n<li><a href=\"https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD009852.pub2/full\" rel=\"nofollow noreferrer\">Muscle energy technique for non‐specific low‐back pain (Cochrane, 2015)</a>: \"low‐quality evidence that MET is not effective for patients with lower back pain.\"</li>\n</ul>\n\n<p><strong>EDIT:</strong></p>\n\n<p>Christopher L (the OP) believes the procedure is called <strong>Proprioceptive Deep Tendon Reflex (P-DTR)</strong>.</p>\n\n<p>The inventor of the technique explains it in detail <a href=\"https://pdfs.semanticscholar.org/4c1f/543dab3cb4926c6a4f7d8ff6689c7e084ba2.pdf\" rel=\"nofollow noreferrer\">here</a>. Two other doctors describe it in <a href=\"https://pdtr-global.com/upload/pdf/PDTR_Smolensk_280417.pdf\" rel=\"nofollow noreferrer\">this document</a> found on the inventor's home page.</p>\n\n<p>The descriptions alone, even if they make sense, are not already an evidence. Scientific evidence about the effectiveness of treatment methods in neurology/orthopedy can come from placebo-controlled randomized clinical trials, but I haven't found even one. The search \"\"proprioceptive deep tendon reflex,\" using operators .gov or .edu, and the search in Google Scholar give no results. </p>\n", "score": 5 } ]

[ "muscle", "physiology", "neuroscience", "nociceptor" ]

[ { "answer_id": 18111, "body": "<p>The term \"knee damage\" can encompass many different conditions and injuries so let's just examine at some of the more common ones you might be looking at:</p>\n\n<h2>Osteoarthritis</h2>\n\n<p><a href=\"https://www.versusarthritis.org/about-arthritis/conditions/osteoarthritis-of-the-knee/?gclid=EAIaIQobChMIlYTf4KiG3wIVDrftCh3NCg62EAAYASAAEgKiQPD_BwE\" rel=\"noreferrer\">Osteoarthritis of the knee</a> is when the cartilage in the joint has become thin or worn and the body is unable to \"keep up\" with repairs. Walking generally isn't going to cause this unless you are severely overweight or you're walking in unsuitable footwear etc. Quite the reverse - after a period of rest to allow for some recuperation from a flare up walking is recommended as it is a low impact way of building strength in the knee and is good for losing weight etc. <em>Running</em> on the other hand is <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/11086751\" rel=\"noreferrer\">significantly higher impact</a> (walking means you experience ground reaction forces of ~ 1.2xBody weight, for running it's ~2.5xBody weight) and can aggravate the damage and you're also much more likely to experience various types of musculoskeletal injuries. Although offsetting that increased risk of injury is the potential for increased cardiovascular fitness from running vs walking.</p>\n\n<p>This is much more common in older people as the body's ability to repair itself decreases with age. </p>\n\n<h2>Tendonitis</h2>\n\n<p><a href=\"https://physioworks.com.au/injuries-conditions-1/patella-tendonitis-tendinopathy\" rel=\"noreferrer\">Patellla tendonitis</a> is an overuse injury where the patella tendon (which connects to the bottom of the knee cap) becomes inflamed or otherwise damaged such as a loss of collagen in the tendon. Similarly to osteoarthritis walking is rarely a cause of this - typically it requires much higher levels of impact than walking alone can produce unless severely overweight or excessive amounts of stair climbing. </p>\n\n<p>This can also happen in older people where it is the result of repetitive small amounts of damage over an extended period of time - and just like in osteoarthritis as the body's ability to heal falls away the rate of injury can exceed the rate of repair leading to chronic problems.</p>\n\n<p>Avoiding activities that cause pain and keeping up with low impact exercises to improve strength is recommended.</p>\n\n<h2>Summary</h2>\n\n<p>Basically if you take a sensible approach - walking on reasonably flat surfaces, keep weight low, use appropriate footwear, and apply a modicum of moderation walking generally doesn't do damage to knees unless something has compromised the body's ability to \"repair\" itself to a significant extent. The benefits however are many and can actually help <em>prevent</em> damage by improving both the strength of the joint and overall health and fitness. So that 30 mins brisk walking a day is doing you far more good than harm.</p>\n", "score": 4 }, { "answer_id": 20621, "body": "<p><strong>1) Walking can actually help, even in people who already have osteoarthritis.</strong></p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146701/\" rel=\"nofollow noreferrer\">Daily walking and the risk of incident functional limitation in knee OA: An observational study (Arthritis Care Research, 2014)</a>:</p>\n\n<blockquote>\n <p>Walking over 7 days was objectively measured as steps/day within a\n cohort of people with or at risk of knee OA from the Multicenter\n Osteoarthritis Study. </p>\n \n <p>Among 1788 participants (mean age 67, mean BMI 31 kg/m2, female 60%),\n each additional 1000 steps/day was associated with a 16% and 18%\n reduction in incident functional limitation by performance-based and\n self-report measures, respectively. </p>\n \n <p>More walking was associated with less risk of functional limitation\n over two years. Walking ≥ 6000 steps/day provides a preliminary\n estimate of the level of walking activity to protect against\n developing functional limitation in people with or at risk of knee OA.</p>\n</blockquote>\n\n<p><strong>2) Risk factors for osteoarthritis</strong></p>\n\n<p><a href=\"https://www.sciencedirect.com/science/article/pii/S1063458414013429?via%3Dihub\" rel=\"nofollow noreferrer\">Current evidence on risk factors for knee osteoarthritis in older adults: a systematic review and meta-analysis (Ostearthritis and Cartilage, 2015)</a>:</p>\n\n<ul>\n<li>Being overweight</li>\n<li>A job that requires a lot of knee bending, kneeling, squatting or lifting</li>\n<li>Walking disability</li>\n<li>Previous knee injury</li>\n<li>Female sex</li>\n<li>Increased age</li>\n<li>Repeated intense physical activity, for example, running >20 miles/week</li>\n</ul>\n", "score": 1 } ]

[ "walking", "strength-training" ]

[ { "answer_id": 18196, "body": "<p>Well, PEF (peak expiratory flow) varies thorough the day and it's at its lowest in the morning (which is when patients are usually instructed to take it x3, before their meds), so taking the highest value balances that out a little. </p>\n\n<p>Also, we <em>are</em> measuring PEF i.e. <em>maximum</em> speed of expiration, not <em>average</em> speed of expiration ;) And a patient's personal best (the highest PEF reading they've recorded for a span of 2-3 weeks) is useful for determining asthma zones (green for when a patient's PEF measures 80%-100% of their best value, yellow for 50%-80% &amp; red for &lt;50%), which in turn are needed to make an asthma action plan so that the patient knows when they can treat their symptoms without going to the hospital and when they should. Using the highest reading also gives a little leeway in such cases as ≤80% PEF is not as bad as it could be!</p>\n\n<p>Personal best PEF is also used to determine if a patient's meds need to be changed or the dose increased/reduced, etc.</p>\n\n<p>References:</p>\n\n<ol>\n<li><p><a href=\"https://thorax.bmj.com/content/59/11/922\" rel=\"nofollow noreferrer\">Reddel HK, Marks GB, Jenkins CR. When can personal best peak flow be determined for asthma action plans? Thorax 2004; 59: 922-4.</a></p></li>\n<li><p><a href=\"https://www.lung.org/lung-health-and-diseases/lung-disease-lookup/asthma/living-with-asthma/managing-asthma/create-an-asthma-action-plan.html\" rel=\"nofollow noreferrer\">Asthma action plan. American Lung Association.</a></p></li>\n<li><p><a href=\"https://ultra-medica.net/Uptodate21.6/contents/UTD.htm?0/53/854\" rel=\"nofollow noreferrer\">Bailey W, Gerald L. Peak expiratory flow rate monitoring in asthma.</a></p></li>\n</ol>\n", "score": 3 } ]

[ "asthma" ]

[ { "answer_id": 18290, "body": "<p>Not only in adults, even in children, if treated too late, the bone changes can be irreversible - they may not re-morph naturally.</p>\n\n<p>The article linked from your question: <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295456/\" rel=\"nofollow noreferrer\">Influence of Mouth Breathing on the Dentofacial Growth of Children: A Cephalometric Study (PubMed, 2014)</a> says:</p>\n\n<blockquote>\n <p>Because upper airway obstruction is an obstacle to normal dentofacial\n development, mouth breathing children deserve prompt attention before\n growth has proceeded irreversibly.</p>\n</blockquote>\n", "score": 4 } ]

[ "bones" ]

[ { "answer_id": 18301, "body": "<p>The Diagnostic and Statistical Manual of the American Psychiatric Association (APA), also known as the DSM, is the guide for any psychological disorders, and the <a href=\"https://www.appi.org/products/dsm-manual-of-mental-disorders\" rel=\"noreferrer\">DSM-5</a> which is the current version (APA, 2013) describes Social Anxiety Disorder as follows:</p>\n\n<blockquote>\n <p><strong>A.</strong> A persistent fear of one or more social or performance situations in which the person is exposed to unfamiliar people or to possible scrutiny by others. The individual fears that he or she will act in a way (or show anxiety symptoms) that will be embarrassing and humiliating.</p>\n \n <p><strong>B.</strong>  Exposure to the feared situation almost invariably provokes anxiety, which may take the form of a situationally bound or situationally pre-disposed Panic Attack.</p>\n \n <p><strong>C.</strong>  The person recognizes that this fear is unreasonable or excessive.</p>\n \n <p><strong>D.</strong>  The feared situations are avoided or else are endured with intense anxiety and distress.</p>\n \n <p><strong>E.</strong>  The avoidance, anxious anticipation, or distress in the feared social or performance situation(s) interferes significantly with the person's normal routine, occupational (academic) functioning, or social activities or relationships, or there is marked distress about having the phobia.</p>\n</blockquote>\n\n<p>A key point the DSM also points out is that in Social Anxiety Disorder, the fear, anxiety, or avoidance is:</p>\n\n<ul>\n<li>persistent</li>\n<li>typically lasting 6 or more months</li>\n<li>causes clinically significant distress or impairment in social, occupational or other important areas of functioning</li>\n<li>not due to direct physiological effects of a substance (e.g., drugs, medications)</li>\n<li>not due to a general medical condition not better accounted for by another mental disorder.</li>\n</ul>\n\n<h2>References</h2>\n\n<p>APA (2013). <em>Diagnostic and statistical manual of mental disorders (DSM-5®)</em>. American Psychiatric Publishing.</p>\n", "score": 8 } ]

[ "mental-health", "anxiety-disorders", "disorders" ]

[ { "answer_id": 18313, "body": "<p>Since I am assuming that you are obtaining generic drugs, the word after tab or cap is the brand that made the drug. Auro is Aurobindo, Shir is Shire, Sand is Sandoz, and Solc is Solco. Sunp/Sun is likely Sun and Sunovion, and Nort is likely Northwest biopharmaceuticals. As you stated earlier, cap is capsule and tab is tablet. There are also orally disintegrating tabs (ODT tabs or wafers), liquid (syrup), inhalers (puffs), nasal spray, eye drops... Honestly, there are so many methods of administration, that I would be here all day to go through all: rectal suppositories, ointments, gels, creams, extended release capsules, extended release tablets, all of which seem to be beyond the scope of the question you asked. </p>\n\n<p>All the brands in the US can be found here: \n<a href=\"https://en.wikipedia.org/wiki/Category:Pharmaceutical_companies_of_the_United_States\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Category:Pharmaceutical_companies_of_the_United_States</a></p>\n", "score": 8 } ]

[ "prescription", "labeling", "united-states" ]

[ { "answer_id": 18319, "body": "<p>Yes, is is possible to test for it, but with some very severe limitations for most classical tests, like Ishihara plates.</p>\n\n<p>If you go to the Wikipedia page for <a href=\"https://en.wikipedia.org/wiki/Ishihara_test\" rel=\"nofollow noreferrer\">Ishihara test</a> you may see a demonstration of effects that will or will not apply to your personal type of vision. This gets all the more striking if you show those pictures (preferably all the plates of this test) to a person with known one type of known <a href=\"https://en.wikipedia.org/wiki/Color_blindness\" rel=\"nofollow noreferrer\">Daltonism</a>.</p>\n\n<p>But this is exactly limited by what your initial thoughts indicate.\nGo for example to <a href=\"http://www.opticien-lentilles.com/daltonien_beta/new_test_daltonien.php\" rel=\"nofollow noreferrer\">Color vision test</a>, do the test with your standard screen, repeat the test with a known \"bad screen\". The test has a nice design but even people with some quite severe deficiencies can \"beat it\", all the more easier with bad screens, it they change the viewing angle (look from the side, tilt the screen).</p>\n\n<blockquote>\n <p><a href=\"http://www.color-blindness.com/2010/03/23/color-blindness-tests/\" rel=\"nofollow noreferrer\"><strong>The future of color vision testing</strong></a>\n Today in our digital world one might think, why don’t we have some simple computer based color blindness test. Unfortunately this is not as simple as it looks like. There are two main problems:</p>\n \n <ol>\n <li>Computers displays just make use of three main colors red, green and blue (RGB). Every other color gets mixed from those three colors. The anomaloscope and lantern tests use different light sources which can’t be simulated by a display.</li>\n <li>Every computer display has a different color range it covers, little differences in light sources, different brightness and more. This causes different test results. Only calibrated computers can be used to perform such computer based tests.</li>\n </ol>\n \n <p>The City University in London developed a computer based color vision test which is also based on the same principal as pseudoisochromatic plates and arrangement tests. The main difference is that the colors are constantly changing which gives some really good results. Just recently they used their <a href=\"http://www.color-blindness.com/2010/02/21/new-color-blindness-tests-sets-minimal-requirements-for-professional-flight-crew/\" rel=\"nofollow noreferrer\">test to check color vision in pilot candidates</a> and it looks like as the Color Assessment &amp; Diagnosis Test (CAD Test) could become a standard screening instrument for color vision testing. At least for certain professions, where color vision is critical but people with a mild form of color vision still perform perfectly.</p>\n \n <hr>\n \n <p><a href=\"https://www.city.ac.uk/health/research/centre-for-applied-vision-research/a-new-web-based-colour-vision-test\" rel=\"nofollow noreferrer\">City University of London: A new web-based colour vision test</a></p>\n \n <p>The web version of this test will run on a variety of monitors balanced for different phases of daylight. The movie was however prepared and will run best on a monitor balanced for ~9000K. This is usually the default factory setting for most colour monitors. The spectral characteristics of the pattern will be affected by ambient illumination and therefore this should be kept to a minimum (i.e., use the monitor in a dark room).</p>\n</blockquote>\n\n<hr>\n\n<p>Note that even though the above test was developed specifically \"for the web\" only gives you a rough indication of \"problems\" with colour vision.<br>\nAside from the problems mentioned in the quotes above, <em>accurate</em> colour is something very hard to <a href=\"https://www.eizo.com/library/basics/lcd_monitor_color_gamut/\" rel=\"nofollow noreferrer\">buy</a> hardware for. If they are even capable of displaying more than a compartively small subset of the full spectrum, most modern screens are tuned for <a href=\"http://www.displaymate.com/Color_Accuracy_ShootOut_1.htm\" rel=\"nofollow noreferrer\">'pop' and not realistic colour reproduction</a>:</p>\n\n<blockquote>\n <p>If you walk into a Walmart, Best Buy, or any major TV retailer, all of the TVs are showing identical videos, but their colors will be noticeably (to obnoxiously) different on every TV on the wall – even in Best Buy’s high-end Magnolia showrooms. Why is that? One reason is that the TV picture controls have been played with – but this would still be true even with factory fresh TVs right out of the box. It’s also true with Smartphones and Tablets that as a rule don’t provide any color controls, which is probably better because visual tweaking generally makes matters worse. And that is exactly the root cause of the problem that originates right at the factory – the displays are not individually fully adjusted and calibrated with instruments, and instead depend on visually tweaking at some point during manufacturing.</p>\n</blockquote>\n", "score": 6 } ]

[ "color-blindness" ]

[ { "answer_id": 18384, "body": "<p><strong>CAUSES and RISK FACTORS</strong> of skin tags</p>\n\n<p>In general, the exact cause and therefore prevention of skin tags is not known (<a href=\"https://emedicine.medscape.com/article/1060373-overview#showall\" rel=\"nofollow noreferrer\">Emedicine</a>). In some cases, skin tags could be associated with the following conditions:</p>\n\n<ul>\n<li>Skin aging and skin irritation due to obesity (<a href=\"https://emedicine.medscape.com/article/1060373-overview#showall\" rel=\"nofollow noreferrer\">Emedicine</a>)</li>\n<li>Diabetes type 2, especially if accompanied with metabolic syndrome (obesity, hyperglycemia, high blood pressure, high cholesterol levels) (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3991940/\" rel=\"nofollow noreferrer\">PubMed, 2014</a>)</li>\n<li>Human papillomavirus infection - a sexually transmitted disease (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/18583787\" rel=\"nofollow noreferrer\">PubMed, 2008</a>)</li>\n<li>Crohn's disease (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783618/\" rel=\"nofollow noreferrer\">PubMed, 2016</a>)</li>\n<li>Acromegaly or gigantism - increased growth due to increased levels of the growth hormone (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/16828406\" rel=\"nofollow noreferrer\">PubMed, 2006</a>)</li>\n<li>Genetic predisposition, Birt-Hogg-Dube syndrome and Nonne-Milroy-Meiges syndrome (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477464/\" rel=\"nofollow noreferrer\">PubMed, 2015</a>)</li>\n</ul>\n\n<p><strong>SKIN TAGS AS MARKERS OF COLONIC POLYPS</strong></p>\n\n<p>Studies and reviews that have found <em>no association</em> between skin tags and colonic polyps: <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/8410406\" rel=\"nofollow noreferrer\">PubMed, 1993</a>, <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/2754216\" rel=\"nofollow noreferrer\">PubMed, 1989</a> and <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783618/\" rel=\"nofollow noreferrer\">PubMed, 2016</a>.</p>\n\n<p>Some small studies have found <em>some association</em> between skin tags and colonic polyps: <a href=\"http://annals.org/aim/article-abstract/696614/skin-tags-cutaneous-marker-colonic-polyps?doi=10.7326%2F0003-4819-98-6-928\" rel=\"nofollow noreferrer\">Annals of Internal Medicine, 1983</a>, <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/3722480\" rel=\"nofollow noreferrer\">PubMed, 1986</a>. The association may be coincidental, since the prevalence of skin tags can be as high as 46% (<a href=\"https://emedicine.medscape.com/article/1060373-overview#showall\" rel=\"nofollow noreferrer\">Emedicine</a>).</p>\n\n<p><strong>PREVENTION</strong> of skin tags can include losing weight (if necessary), avoiding skin irritation, avoiding sexually transmitted diseases and treating eventual underlying disorders. </p>\n\n<p>Skin tags do not likely develop into skin cancers (<a href=\"https://www.ncbi.nlm.nih.gov/books/NBK448169/\" rel=\"nofollow noreferrer\">Stat Pearls</a>).</p>\n\n<p>A dermatologist can <strong>REMOVE</strong> skin tags if necessary; the growths usually do not recur (<a href=\"https://mospace.umsystem.edu/xmlui/bitstream/handle/10355/13999/ProceduresSkinTagRemoval.pdf?sequence=1&amp;isAllowed=y\" rel=\"nofollow noreferrer\">University of Missouri</a>).</p>\n\n<p><a href=\"https://www.dermnetnz.org/topics/skin-tag/\" rel=\"nofollow noreferrer\">Pictures</a></p>\n", "score": 5 }, { "answer_id": 18386, "body": "<p>Adding to @Jan's answer, to answer the part of the question regarding how skin tags are formed, I have found that <a href=\"https://www.aocd.org/page/SkinTags\" rel=\"nofollow noreferrer\">according to the American Orthopaedic College of Dermatology (AOCD)</a>, <strong>the actual cause of acrochordons is unknown, as it is not actually known how they are formed</strong>. There are <strong>several theories</strong> however:</p>\n\n<ul>\n<li>Irritation or friction to the skin, caused by skin rubbing on skin may play a role in their formation.</li>\n<li>Diabetes causing skin tags is thought to be through insulin resistance.</li>\n<li>The Human Papilloma Virus (HPV) was present in a high percentage of growths in a study of 49 patients with skin tags, suggesting the virus plays a role in development.</li>\n<li>It is also possible that skin tags are genetic or simply due to normal aging and loss of skin elasticity.</li>\n</ul>\n\n<p>Interestingly the AOCD also mentions that a rare genetic disorder called Birt-Hogg-Dube (BHD) Syndrome is characterised by numerous skin tags along with other symptoms, however looking at <a href=\"https://rarediseases.org/rare-diseases/birt-hogg-dube-syndrome\" rel=\"nofollow noreferrer\">the National Organisation for Rare Disorders (NORD) webpage for BHD syndrome</a>, these \"skin tags\" are known as <em>fibrofolliculomas</em> and appear to be different.</p>\n\n<blockquote>\n <p>The skin papules known as fibrofolliculomas that are associated with BHD syndrome commonly occur on the scalp, face and neck, but can also be found on the ear lobes and in the oral mucosa. They are generally 2-3mm in size, dome shaped, flesh-colored and are not associated with any pain or discomfort.</p>\n</blockquote>\n\n<p>Going by the theories mentioned by the AOCD, if skin tags are caused by skin friction, or aging and loss of skin elasticity, maintaining a healthy weight can reduce the numbers as there will be less skin folds to cause skin rubbing, but otherwise, there may be nothing really that can be done to prevent skin tags.</p>\n", "score": 2 } ]

[ "dermatology" ]

[ { "answer_id": 18458, "body": "<p>Cancer can be one of the most complicated concepts in medicine, not only because of the pathophysiology of cancer, but the complicated statistics involved in the epidemiology of the diseases and interpreting the results of studies on treatments.</p>\n\n<p>If your previous studies have been completely outside of the biological sciences, it will be very difficult to gain the degree of understanding that you seem to want. Even if you have some biology background, at best, you should definitely not expect to gain the expertise to confidently second-guess actual medical providers. </p>\n\n<p>However, I applaud you for your desire to understand as much as possible, and you certainly may be able to learn enough to follow along in conversations about risks and benefits of different treatment options, and to have educated discussions about what is going on with your loved one.</p>\n\n<p>You might FIRST START with patient education websites from the NIH or CDC on the basics of lung cancer, then fill in the gaps of details and background needed using textbooks on the underlying concepts. </p>\n\n<p>For that, these are some of the more popular texts used in medical school, if you are able to get your hands on them, which have good sections on lung cancer.</p>\n\n<ul>\n<li>Robbins and Cotran: Pathological Basis for Disease (or <a href=\"https://www.elsevier.com/books/robbins-basic-pathology/kumar/978-0-323-35317-5\" rel=\"noreferrer\">Robbins Basic Pathology</a>)</li>\n<li>West: Pulmonology <a href=\"https://books.google.com/books/about/West_s_Respiratory_Physiology.html?id=Wtj_oQEACAAJ&amp;source=kp_cover\" rel=\"noreferrer\">Physiology</a> and also <a href=\"https://rads.stackoverflow.com/amzn/click/1451107137\" rel=\"noreferrer\">Pathophysiology</a></li>\n<li>Harrison's Principles of Internal Medicine</li>\n</ul>\n\n<p>Advancing your understanding of the mechanisms underlying cancer development and progression:</p>\n\n<ul>\n<li>Pathoma (the sections on oncogenesis are fantastic)</li>\n</ul>\n\n<p>I would also do some reading on how to interpret the statistics pertinent to cancer, such as odds ratio, relative risk, number needed to treat, sensitivity/specificity, incidence, mortality rates, 5 year survival rates, etc. Statistics are not taught well in most schools these days and additional knowledge is important to being able to understand how decisions are made.</p>\n", "score": 6 } ]

[ "cancer", "lungs" ]

[ { "answer_id": 18455, "body": "<p>When a physician is studying someone for a suspected disorder related to the thyroid hormones, he/she should not only study the thyroid, but evaluate the hypothalamus-pituitary-thiroid endocrine axis and a frequent initial assumption is that the problem could be at any of these 3 levels instead of assuming the problem is in the thyroid gland.</p>\n\n<p>Thyroid serum profiles include TSH, because as you said, the problem might be at a pituitary level and also this allows for further evaluation of the feedback system of the axis. Another important note is that a healthy thyroid gland will produce thyroxine proportionally to the serum levels of TSH, that is it WILL work quickly enough in response to these high levels of TSH and produce high levels of thyroxine, however a healthy axis would also lower the TSH levels after this.</p>\n\n<p>To properly understand this we need to review that for this axis:</p>\n\n<ul>\n<li><p>The hypothalamus produces the Thyrotropin-releasing hormone (TRH) in an inversely proportional manner to thyroxine blood levels. TRH estimulates the production of Thyroid-stimulating hormone (TSH) in the pituitary.</p></li>\n<li><p>The pituitary produces TSH in a directly proportional manner to TRH levels and also in an inversely proportional manner to thyroxin blood levels (it has a negative feedback control independent of the hypothalamus and a positive one dependent on the hypothalamus). TSH estimulates the production of thyroxin by the thyroid.</p></li>\n<li><p>The thyroid produces thyroxin and this hormone then acts in several tissues across body regulating metabolism. Thyroxin production goes down if TSH levels go down.</p></li>\n</ul>\n\n<p>Now for some generic examples, if a patient has hypothiroidism signs and symptoms, and then we see a thiroid profile like this:</p>\n\n<ul>\n<li>Thyroxin levels: low</li>\n<li>TSH levels: high</li>\n</ul>\n\n<p>This suggests the problem is in the thyroid gland since the pituitary is doing its job by increasing TSH to demand more thyroxin, but the thyroid is not responding at all.</p>\n\n<p>Another example:</p>\n\n<ul>\n<li>Thyroxin levels: low</li>\n<li>TSH levels: low</li>\n</ul>\n\n<p>The problem could be in the pituitary this time since even though thyroxin is low the pituitary isn't asking for more thyroxin by producing more TSH.</p>\n\n<p>On the other hand if we suspect hyperthyroidism and we see:</p>\n\n<ul>\n<li>Thyroxin levels: high</li>\n<li>TSH levels: low</li>\n</ul>\n\n<p>We suspect of a thyroid-level problem again because the pituitary is trying to slow down the production by lowering TSH, but the thyroid is independently producing more and more thyroxin (one of the first things we would suspect is a thyroid hormone producing tumor).</p>\n\n<p>Another example:</p>\n\n<ul>\n<li>Thyroxin levels: high</li>\n<li>TSH levels: high</li>\n</ul>\n\n<p>We could suspect that there is something wrong in the pituitary (again it could be a tumor) since TSH levels are high regardless of high thyroxin levels, the pituitary is not slowing down in a situation in which it normally would.</p>\n\n<p>As you can see the disorders are produced when the feedback systems begin to be lost and the different levels of the axis become unresponsive or self-controlled.</p>\n\n<p>Other strange situations would include problems at hypothalamic level or production of thyroxin by tumors outside of the thyroid, but these are never suspected in first instance since they are very rare. </p>\n\n<p>A brief, but ok review of this axis can be read at <a href=\"https://en.wikipedia.org/wiki/Hypothalamic%E2%80%93pituitary%E2%80%93thyroid_axis\" rel=\"noreferrer\">Wikipedia</a> or if you want a more robust review you can consult <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3516896/\" rel=\"noreferrer\">Greenspan's endocrinology</a> which is what I read back in the day (:</p>\n", "score": 6 } ]

[ "endocrinology", "anatomy" ]

[ { "answer_id": 18464, "body": "<p>You are correct that carcinoma refers to types of cancer arising from epithelial tissue.</p>\n\n<blockquote>\n <p><a href=\"https://www.medicinenet.com/script/main/art.asp?articlekey=20677\" rel=\"noreferrer\">Definition of carcinoma</a>: Cancer that begins in the skin or in\n tissues that line or cover body organs.</p>\n</blockquote>\n\n<p>This includes tissues that line both the inner and outer surfaces of the body and that arise from cells originating in the endodermal, mesodermal or ectodermal germ layer during embryogenesis.\nSource: <a href=\"https://en.wikipedia.org/wiki/Carcinoma\" rel=\"noreferrer\">Wikipedia</a>.</p>\n\n<p>This also includes glandular tissue, even if this tissue is within an organ, as glands contain many ducts lined with secretory cells and this is also epithelium.</p>\n\n<p>However, in the specific case of epithelial ovarian cancer, it refers to cancers arising on the surface of the ovary (the <a href=\"https://en.m.wikipedia.org/wiki/Ovary\" rel=\"noreferrer\">germinal epithelium</a>), rather than the tissues within, as there is technically epithelial tissue inside as well. \nSource: <a href=\"https://www.cancerresearchuk.org/about-cancer/ovarian-cancer/types/epithelial\" rel=\"noreferrer\">Cancer Research UK</a>.</p>\n", "score": 6 } ]

[ "cancer", "terminology" ]

[ { "answer_id": 18546, "body": "<p>These are biologically plausible effects supported by moderate quality observational evidence. As a personal aside, I do not believe there is enough evidence for harm to recommend eliminating dairy products from a healthy person's diet. A full discussion of all the evidence for the impact of dairy in diet is beyond the scope of this answer, though, so lets move on to your specific question </p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Sex_steroid\" rel=\"nofollow noreferrer\">Sex steroids</a> are lipid soluble fused ring structures derived from cholesterol, and conserved across many species. They are not inactivated by pasteurization. In addition to being identified in dairy products and in the people who consume them, consumption of dairy products appears to be associated with some expected biological effects in humans, e.g., <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3712661/\" rel=\"nofollow noreferrer\">sperm quality</a>. That linked study as well as the other points are succinctly reviewed in the introduction to <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5699997/\" rel=\"nofollow noreferrer\">this article</a>. </p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Insulin-like_growth_factor_1\" rel=\"nofollow noreferrer\">Insulin like growth factor 1</a> (IGF-1) is a peptide hormone, but has been demonstrated to be active after pasteurization. It is also conserved across species. There is evidence (well summarized in both the narrative review and meta-analysis in <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5400803/\" rel=\"nofollow noreferrer\">this article</a>) for an association between consumption of dairy products, increased levels of circulating IGF-1, and downstream effects of that increased level (e.g., prostate cancer).</p>\n\n<p>You should note that it is not surprising that a hormone produced by another animal would be active in a human. See, <a href=\"https://www.nobelprize.org/prizes/medicine/1923/banting/facts/\" rel=\"nofollow noreferrer\">the 1923 Nobel Prize</a>.</p>\n\n<p>Just to be clear:\n<strong>This answer addresses the specific two questions posed in the OP: are hormones in milk and milk products active after pasteurization, and are cow hormones active in humans. This answer (and the evidence) does NOT provide support for the question, in balance is dairy good or bad for you, and does not address the claims in the linked article (a la a Skeptics.SE question)</strong></p>\n", "score": 5 }, { "answer_id": 18554, "body": "<p>If the main thrust of the question is indeed expressed in the title and tags of the question:</p>\n\n<blockquote>\n <p><strong>Q</strong> “There is a very strong correlation between consuming dairy products — such as milk — and acne, skin breakouts and aging.”</p>\n</blockquote>\n\n<p>Then the jury on that really isn't finished deciding:</p>\n\n<blockquote>\n <p>Is acne related to the ingestion of dairy products? It is not a new idea. It goes back to the early days of the last century and beyond. The counter-claim, that there is no relationship between diet and acne, has reached mythic proportions. It has never been substantiated, but it is repeated as gospel in all major dermatology textbooks. Epstein, commenting on contributions on the subject by Waisman, Bickers, and Rosenberg, trod the middle road. Inexplicably asserting that \"Controlled studies indicate that foods have no effect on acne,\" he nonetheless allowed, \"the patient should receive any assistance that dietary control may impart.\" <strong>In a review of 274 clinical trials of acne, the massive 2001 Evidence Report on the Management of Acne found <em>one</em> solitary paper that mentioned diet, but no trial reported specifically on patients’ diets.</strong></p>\n \n <p>Dairy products have been implicated as a possible factor in the etiology of prostate cancer in several large epidemiological studies, but not in all. The possible influences of dairy hormone in breast cancer are likewise unclear and in need of further definition.<br>\n The next few years will be fascinating for those of us interested in hormones and \"the blight of youth.\" One wonders what the impact will be upon our patients, our practices, and the industries that make milk, hormones, and acne products. Time alone will tell.</p>\n \n <p><a href=\"https://www.jaad.org/article/S0190-9622(04)02500-9/abstract\" rel=\"nofollow noreferrer\">F. William Danby: \"Acne and milk, the diet myth, and beyond\"</a>, J AM ACAD DERMATOL FEBRUARY 2005</p>\n</blockquote>\n\n<p>While it seems very much up for debate to either substantiate whether indeed industrialised milk production schemes result in increased hormone presence in milk sold, whether there is a difference between production methods and 'ingredients' in milk sold, whether this is then true for all dairy products.</p>\n\n<p>Case in point: water soluble pharmacologically active compounds will be greatly reduced in butter and ghee, molecules found in whey greatly reduced in most cheeses, and anything greatly processed is another game entirely. If yeasts, worms, insects bacteria ferment the milk-product, how much of the hormones is reduced by those organisms? –– or amplified?</p>\n\n<p>Milk as is not the main product consumed by most people and all dairy products are clearly not the same. Kefir is different from cheese, fresh or aged, with bacteria or fungi, from whey, from butter, from ghee, from protein-isolate and so on. Given the different profiles for all those products they either have to have something in common across the board or they have to be analysed separately.</p>\n\n<p>It is of course quite interesting to look for evidence that shows how much different modern milk and milk products are compared to just a few decades ago. Be it in nutritional or now even pharmacological profiles. </p>\n\n<p>But to start a comparison with dairy, hypothesising about hormones, then linking that all up to skin disorders seems very premature and theoretical. At least if there are not clear epidemiological indicators of indeed a possible link.</p>\n\n<p>Which suspects would there be to observe in the proposed link between acne and skin?</p>\n\n<p>Only the most prominent are:</p>\n\n<blockquote>\n <p>Prolactin, Somatostatin, Gonadotropin-releasing hormone, Luteinizing hormone, Thyroid-stimulating hormone, Thyreotropin-releasing hormone, Epidermal growth factor, Insulin-like growth factor 1, Insulin-like growth factor 2, Insulin, Vitamin D, Transferrin, Lactoferrin, Prostaglandins</p>\n</blockquote>\n\n<p>Now which of these are contained in fresh milk under which circumstances and therefore concentrations in the first place? How much of this is linked to milking pregnant cows?</p>\n\n<blockquote>\n <p><strong>Acne and milk</strong><br>\n Milk and other dairy products contain more than 60 molecules including prolactin, somatostatin, gonadotropin-releasing hormone, luteinizing hormone, thyroid-stimulating and thyreotropin-releasing hormones, insulin, epidermal growth factor, nerve growth factor, IGF-1 and 2, transforming growth factors, vitamin D, transferrin, lactoferrin and prostaglandins (Koldovsky, 1995). <strong>This makes it difficult to distinguish which of these factors could have an acneigenic effect, especially when this fact is combined with the broad range of dairy products</strong> (Table 25.2, Figure 25.4).<br>\n The most important factor of the ones mentioned above is the insulin-like growth factor. The IGFs are proteins with high sequence similarity to insulin. IGFs are part of a complex system that cells use to communicate with their physiologic environment. <strong>Cow milk contains IGF-1 and -2, even after pasteurization and homogenization, and bovine and human IGF-1 share exactly the same amino acid sequence</strong> (Melnik and Schmitz, 2009). High milk consumption increases IGF-1 levels 10%-20% in adults and 20%-30% in children (Hoppe et al., 2004 a, b) and milk and dairy products raise IGF-1 levels more than dietary proteins such as meat (Hoppe et al., 2005).<br>\n Milk also contains carbohydrates, including lactose, and therefore its consumption produces a glycemic response and an insulinemic response. The insulinemic response to ingested milk is actually three to six times what would be predicted from the carbohydrate load in the milk serving (Ostman et al., 2001). <strong>This happens for skimmed and full-fat milk, but not for cheese</strong> (Holt et al., 1997; Hoyt et al., 2005). <strong>The reasons are not yet understood, but they may</strong> relate to the insulinotropic effects of some of the other multiple hormones that are present in milk (Koldovsky, 1995).\n A glass of milk added to a low glycemic index meal can boost the insulin response up to 300% of the level produced by a high glycemic index meal and cow milk-formula does this even better than human breast milk (Liljeberg and Bjorck, 2001; Lucas et al., 1980). <strong>Different studies suggest that insulin rises in response to the whey component</strong> (20% of milk protein), <strong>whereas casein is responsible for the IGF-1 increase</strong> (Hoppe et al., 2006). Because whey and casein are both involved in stimulating androgen production, there is little point in further differentiating them in dietary restriction, since both should be avoided.</p>\n</blockquote>\n\n<p>If the result of the above is indeed true: \"whey and casein should both be avoided\" then this is still incomplete as to whether it is for example whey-protein itself (essentialist reading) or what's commonly in there (varying by methods of production) as well and surely not encompassing 'all dairy', as butter for example is largely free of both.</p>\n\n<p>Then it remains a stretch to conclude that \"stimulating androgen production\" is just \"all bad/causes acne\" on the one side and on the other side there are other types of causes that are \"stimulating androgen production\": hyperinsulinemia for example, which can also activate or upregulate IGF receptors. </p>\n\n<p>It is simply too simplistic to reduce the focus to just one or a few pathways and \"reason the rest\" from there.</p>\n\n<p>But take note that this is not the sole point of that article. The very next item was about 'glycemic index'. To give more context:</p>\n\n<blockquote>\n <p>Key facts</p>\n \n <ul>\n <li>Androgen excess, peroxisome proliferator-activated receptors and inflammation are the main pathogenetic mechanisms of acne.</li>\n <li>Nutrition seems to play an important role in skin biology and pathology, affecting the onset and clinical manifestation of several dermatologic disorders, including acne.</li>\n <li>The typical Western diet consists of numerous dairy sources and foods with high glycemic indices.</li>\n <li>A study performed by Adebamowo et al. (2005) demonstrated the association between dairy products and acne.</li>\n <li>A study provided by Smith et al. (2007) showed the link between high glycemic load intake of carbohydrates and acne.</li>\n <li>High glycemic carbohydrates and milk appear to raise serum insulin levels, free IGF-1 and insulin resistance, thus contributing to the pathogenesis of acne.</li>\n <li>IGF-1 seems to be the most important acneigenic factor contained in diet.</li>\n <li>At the genomic level, the effects of insulin and IGF-1 are mediated by the nuclear concentration of the transcription factor FoxO1.</li>\n <li>At the promoter level, SREBP-1c expression is suppressed by nuclear FoxO1, which is an important co-repressor of the retinoid X receptor and liver X receptor.</li>\n <li>Dermatologists should be able to include dietary restriction in acne therapy management.</li>\n </ul>\n \n <p>Summary points</p>\n \n <ul>\n <li>Skin reflects individual age, health and beauty.</li>\n <li>Nutritional customs affect several skin diseases including psoriasis, atopic dermatitis and acne. </li>\n <li>Epidemiological studies with milk and dairy products support the association of milk consumption with acne\n onset and clinical course.</li>\n <li>High glycemic load diets are also considered to be involved in acne pathogenesis because of the consequent\n hyperglycemia and hyperinsulinemia.</li>\n <li>Dermatologists should include restrictive dietary management in acne therapy in their daily clinical practice. </li>\n </ul>\n \n <p>A.I. Liakou, C.I. Liakou and C.C. Zouboulis: \"Acne and nutrition\", Victor R. Preedy (Ed): \"Handbook of diet, nutrition and the skin\", Wageningen Academic Publishers, Wageningen, 2012. </p>\n</blockquote>\n\n<p>Note especially that 'dairy' is not unique in containing these molecules, concentrationand consumption patterns have to be observed as well. Dosis facit venenum. But even if the same molecules are measured, the effect may not be same after all, as the milk vs meat example aboive illustrates. And how much of those are even present in milk 'now' compared to 'earlier times' is partly dependent on the alleged production methods of \"pregnant cows\". How much <a href=\"https://skeptics.stackexchange.com/questions/43363/is-the-majority-of-milk-in-industrialized-countries-obtained-from-pregnant-cows\">has that changed</a>? We can hardly know. </p>\n\n<p>One of the more prominent papers investigating a possible link comes sponsored from a food-giant:</p>\n\n<blockquote>\n <p>Bodo C. Melnik: \"Evidence for Acne-Promoting Effects of Milk and Other Insulinotropic Dairy Products\", Clemens RA, Hernell O, Michaelsen KF (eds): Milk and Milk Products in Human Nutrition. Nestlé Nutr Inst Workshop Ser Pediatr Program, vol 67, pp 131–145, Nestec Ltd., Vevey/S. Karger AG, Basel, © 2011. </p>\n</blockquote>\n\n<p>And that is quite a problem. The dairy side sponsoring research to show how \"good it is for you\", and from animal-rights over vegan to frankenfood-companies financing the other side of ideology. All sides looking for evidence that they <em>were</em> right, from the start. This is more like gnosis that science and it is extremely difficult to weed out all the chaff thrown in to the pool of knowledge.</p>\n\n<blockquote>\n <p>A meta-analysis can help inform the debate about the epidemiological evidence on dairy intake and development of acne. A systematic literature search of PubMed from inception to 11 December 2017 was performed to estimate the association of dairy intake and acne in children, adolescents, and young adults in observational studies. We estimated the pooled random effects odds ratio (OR) (95% CI), heterogeneity (I2-statistics, Q-statistics), and publication bias. We included 14 studies (n = 78,529; 23,046 acne-cases/55,483 controls) aged 7–30 years. ORs for acne were 1.25 (95% CI: 1.15–1.36; p = 6.13 × 10−8) for any dairy, 1.22 (1.08–1.38; p = 1.62 × 10−3) for full-fat dairy, 1.28 (1.13–1.44; p = 8.23 × 10−5) for any milk, 1.22 (1.06–1.41; p = 6.66 × 10−3) for whole milk, 1.32 (1.16–1.52; p = 4.33 × 10−5) for low-fat/skim milk, 1.22 (1.00–1.50; p = 5.21 × 10−2) for cheese, and 1.36 (1.05–1.77; p = 2.21 × 10−2) for yogurt compared to no intake. ORs per frequency of any milk intake were 1.24 (0.95–1.62) by 2–6 glasses per week, 1.41 (1.05–1.90) by 1 glass per day, and 1.43 (1.09–1.88) by ≥2 glasses per day compared to intake less than weekly. Adjusted results were attenuated and compared unadjusted. There was publication bias (p = 4.71 × 10−3), and heterogeneity in the meta-analyses were explained by dairy and study characteristics. In conclusion, any dairy, such as milk, yogurt, and cheese, was associated with an increased OR for acne in individuals aged 7–30 years. </p>\n \n <p><strong><em>However, results should be interpreted with caution due to heterogeneity and bias across studies.</em></strong> </p>\n \n <p>Christian R. Juhl et al: \"Dairy Intake and Acne Vulgaris: A Systematic Review and Meta-Analysis of 78,529 Children, Adolescents, and Young Adults\", Nutrients 2018, 10(8), 1049, <a href=\"https://doi.org/10.3390/nu10081049\" rel=\"nofollow noreferrer\">DOI</a></p>\n</blockquote>\n\n<p>So it remains currently at this:</p>\n\n<blockquote>\n <p><a href=\"https://www.webmd.com/skin-problems-and-treatments/acne/features/worst-foods-for-your-skin#1\" rel=\"nofollow noreferrer\">Dairy and Acne</a></p>\n \n <p>There's no definite link between dairy and acne, but there are theories about it.</p>\n</blockquote>\n", "score": 5 }, { "answer_id": 31001, "body": "<p>Milk is a specialised substance produced by mammals to support development during the infant growth phase. The nutritional content in milk represents a postnatal continuum of the support established during gestation between mother and child with particular emphasis on growth factors.</p>\n<p>Amongst the growth promoting signals in milk is the presence of IGF-1 and exosomes that contain various conserved microRNAs that persist following pasteurisation. The exosomes have evolved to survive digestion and enter the bloodstream. Their miRNA cargo directs pro-growth gene expression.</p>\n<p>Hence bovine milk is favoured amongst bodybuilders and power athletes for its anabolic effect. However, this growth state is mediated by activation of the mTor complex, a pro-aging and pro-oncogenic pathway.</p>\n<p>Unsurprisingly, there is a significant signal in the literature between cancer incidence (colonic, breast and prostate) and dairy consumption albeit with the usual confounding due to lack of distinction between dairy types. In contrast, we see no such ambiguity regarding quality plant based diets.</p>\n<p>In any case, dairy milk is a mTor activator and mTor activation is pro-aging and pro-acne.</p>\n<p>See</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8000710/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8000710/</a></p>\n<p><a href=\"https://www.bmj.com/content/367/bmj.l6204\" rel=\"nofollow noreferrer\">https://www.bmj.com/content/367/bmj.l6204</a></p>\n", "score": 1 } ]

[ "dermatology", "endocrinology", "acne", "milk", "dairy" ]

[ { "answer_id": 18548, "body": "<p>There are two broad types of prevalence statistics: point prevalence and period prevalence. In both cases, more details need to be specified in order to fully describe the statistic.</p>\n\n<p>Point prevalence is the proportion of people who have a disease at a given point in time. In other words, the total number of people in a given population who have a disease at a specific point in time divided by the number of people in that population. To be complete, it should include a case definition (how \"have a disease\" is defined), a population definition, and the particular point in time used.</p>\n\n<p>Period prevalence is the proportion of people who have or have at some point had a disease over a period of time. Here, instead of the total number with a disease at any one time, you include anyone who had the disease at any point during the period. Depending on the period you choose, the population may change, in which case, you would typically use the population at the midpoint of the period.</p>\n\n<p>A specific (and common) period to use for this statistic is \"lifetime\", which changes things slightly. Lifetime prevalence is typically reported as the proportion of people (alive now) who have had the disease at any point in their lifetime. The period in this case is not an absolute time period, but the lifetime of each person in the population. </p>\n\n<p>You can learn more about this in the CDC's online text <a href=\"https://www.cdc.gov/ophss/csels/dsepd/ss1978/\" rel=\"noreferrer\">Principles of Epidemiology in Public Health Practice</a>. Lesson 3 covers prevalence statistics.</p>\n", "score": 7 } ]

[ "statistics" ]

[ { "answer_id": 18682, "body": "<p>This answer would be for the Hygiene Hypothesis part of the question</p>\n\n<p><strong><em>Epidemiology studies in favour of Hypothesis</em></strong></p>\n\n<blockquote>\n <p>The geographical distribution of allergic and autoimmune diseases is a mirror image of the geographical distribution of various infectious diseases, including HAV, gastrointestinal infections and parasitic infections. <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n \n <p>migration studies have shown that offspring of immigrants coming from a country with a low incidence acquire the same incidence as the host country, as rapidly as the first generation for T1D and MS.  <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n</blockquote>\n\n<p>Eg. :</p>\n\n<ol>\n<li><p>This is well illustrated by the increasing frequency of diabetes in families of immigrants from Pakistan to the United Kingdom or the increased risk of MS in Asian immigrants moving to the United States </p></li>\n<li><p>The prevalence of systemic lupus erythematosus (SLE) is also much higher in African Americans compared to West Africans</p></li>\n</ol>\n\n<blockquote>\n <p>In countries where good health standards do not exist, people are chronically infected by those various pathogens. In those countries, the prevalence of allergic diseases remains low. Interestingly, several countries that have eradicated those common infections see the emergence of allergic and autoimmune diseases.  <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n</blockquote>\n\n<ul>\n<li><p>Proof of principle of the casual relationship between the decline of\ninfectious diseases and an increase of immunological disorders.</p></li>\n<li><p>The answer to this question comes from animal models of autoimmune and allergic diseases and, to a lesser degree, from clinical intervention studies.</p></li>\n<li><p>The incidence of spontaneous T1D is directly correlated with the sanitary conditions of the animal facilities, for both the non-obese diabetic (NOD) mouse and the bio-breeding diabetes-prone (BB-DP) rat : <strong>the lower the infectious burden, the higher the disease incidence</strong> <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a>\nOther examples -</p></li>\n<li><p>infection of NOD mice with a wide variety of bacteria, virus and parasites protects completely (‘clean’ NOD mice) from diabetes </p></li>\n<li><p>mycobacteria (e.g. complete Freund's adjuvant) prevent induction of experimental autoimmune encephalomyelitis and ovalbumin-induced allergic asthma.</p></li>\n</ul>\n\n<blockquote>\n <p>The decline is particularly clear for hepatitis A (HAV), childhood diarrhoea and perhaps even more spectacular for parasitic diseases such as filariasis, onchocercosis, schistosomiasis or other soil-transmitted helminthiasis. <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n \n <p>Epidemiological data of cross-sectional studies revealed that Schistosoma infections have a strong protective effect against atopy, as reviewed recently. Hookworms such as Necator americanus also seem to protect from asthma\n (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434398/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3434398/</a>)</p>\n</blockquote>\n\n<ul>\n<li><p>Interestingly, it's been thought that, if parasitic infections if decline, then eosinophils which are involved in allergic reactions and parasitic reactions, may in fact have a role in increased allergy.\n(Ref. Robbins and Cotran- Pathologic basis of diseases)</p></li>\n<li><blockquote>\n <p>It has been shown that helminth eradication increases atopic skin\n sensitization in Venezuela.\n  <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n</blockquote></li>\n</ul>\n\n<p><strong><em>Mechanism of Hygiene Hypothesis:</em></strong>\n <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828\" rel=\"nofollow noreferrer\">3</a></p>\n\n<ol>\n<li><p><em>Th1 to Th2 deviation</em> - </p>\n\n<ul>\n<li><p>Th1 T cells produce inflammatory cytokines such as IL-2, interferon\n(IFN)-γ and tumour necrosis factor (TNF)-α that are operational in\ncell-mediated immunity (including autoimmune diabetes).</p></li>\n<li><p>In contrast, Th2 T cells that produce IL-4, IL-5, IL-6 and IL-13\ncontribute to IgE production and allergic responses.</p></li>\n<li><p>IL - 5 most potent eosinophil activating cytokine known. Upon activation, eosinophils liberate proteolytic enzymes as well as two unique proteins called major basic protein and eosinophil cationic protein which damage tissue.It is now believed that the late phase reaction is a major cause of symptoms in some type 1 hypersensitivity reactions such as allergic asthma.\n(Ref. Robbins and Cotran- Pathologic basis of diseases)</p></li>\n<li><blockquote>\n <p>IL-4 enhances Th2 differentiation; also promote class switching of B cell to IgE. \n IL-13 enhances IgE production and acts on epithelial cells to stimulate mucus secretion.\n (Ref. Robbins and Cotran- Pathologic basis of diseases)</p>\n</blockquote></li>\n<li><p>IgE is involved in Type-1 Hypersensitivity, and hence it increases\nwill increase HST, like allergic asthma. (Ref. Robbins and Cotran- Pathologic basis of diseases)</p></li>\n<li><p>Given the reciprocal down-regulation of Th1 and Th2 cells, some authors suggested initially that in developed countries the lack of microbial burden in early childhood, which normally favours a strong Th1-biased immunity, redirects the immune response towards a Th2 phenotype and therefore predisposes the host to allergic disorders.</p></li>\n</ul></li>\n</ol>\n\n<p>2.<em>Antigen Competition</em></p>\n\n<ul>\n<li><blockquote>\n <p>The development of strong immune responses against antigens from infectious agents could inhibit responses to ‘weak’ antigens such as autoantigens and allergens. </p>\n</blockquote></li>\n</ul>\n\n<p>(<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828/</a>)</p>\n\n<ol start=\"3\">\n<li><p><em>Immunoregulation</em> </p>\n\n<ul>\n<li>Regulatory T cells which can suppress immune responses distinct from responses against the antigen in question, here antigens expressed by infectious agents (a phenomenon called bystander suppression)</li>\n</ul></li>\n</ol>\n\n<p>4.<em>Non Antigenic Ligand</em></p>\n\n<ul>\n<li><p>A number of experiments indicate that infectious agents can promote protection from allergic diseases through mechanisms independent of their constitutive antigens, leading to stimulation of non-antigen specific receptors. This concept is well illustrated by the example of Toll-like receptors (TLRs)</p></li>\n<li><p>It has also been observed that TLR stimulation could prevent the onset of spontaneous autoimmune diseases such as T1D in NOD.</p></li>\n<li><p>Another mechanism of TLR4 is studied,\nwhere a virus (RSV) which is linked with childhood asthma flips the 'switch' of TLR4. Now LPS a bacterial endotoxin also flips the switch but in a different way.</p>\n\n<ul>\n<li>When this education is lacking or weak, the response to RSV by some critical cells in the immune system’s defence against infections—called “T-cells”—might inadvertently trigger asthma instead of protecting the infant and clearing the infection. How this happens is a mystery that we are trying to solve.\n(Ref.- <a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm</a>)</li>\n</ul></li>\n<li><p>Gene-Environment Interaction\nEg. NOD2 - cytoplasmic sensor of bacteria expressed in Paneth and other intestinal epithelial cells; May control resistance to gut commensal bacteria.</p>\n\n<ul>\n<li>Correlation with Inflammatory Bowel Diseases. (Ref. Robbins and Cotran- Pathologic basis of diseases).</li>\n</ul></li>\n</ul>\n\n<p><em>Hygiene during early childhood/pre-natal</em></p>\n\n<blockquote>\n <p>Graham Rook and colleagues proposed a new explanation for the rise of immune disorders, which Rook called the “old friends” hypothesis. “We realized human beings coevolved with a whole host of organisms, and it was far more likely what was going on was that we were being deprived of organisms on which we are dependent.</p>\n \n <p>Maternal microbes colonize the human gut while babies are in utero, and again as they pass through the birth canal and start breastfeeding. Young children continue amassing microbiota in every contact with family members, while playing outside in the dirt, getting licked by dogs, and sharing toys with friends. The developing immune system takes cues from all of these encounters.</p>\n</blockquote>\n\n<p><strong><em>Recent Thoughts</em></strong></p>\n\n<ul>\n<li><p>To the public, “hygiene” is interpreted as personal cleanliness: washing hands, keeping food clean and fresh, sanitizing the home.<a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">2</a></p></li>\n<li><p>However, because the hypothesis has been largely uncoupled from infections, the idea that we need to be less hygienic is wrong.\n<a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">2</a></p></li>\n<li><p>Relaxing hygiene standards would not reverse the trend but only serve to increase the risks of infectious disease, says Bloomfield.\n<a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">2</a></p></li>\n<li><p>The second major concern among researchers is a lack of evidence demonstrating how to reduce rates of allergic and autoimmune diseases. <a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">2</a></p></li>\n<li><p><em>Although hygiene hypothesis proposes germ exposure but still diseases like Diabetes and Asthma are multifactorial in origin and hygiene may be playing only a part.</em><a href=\"https://www.mayoclinic.org/diseases-conditions/childhood-asthma/expert-answers/hygiene-hypothesis/faq-20058102\" rel=\"nofollow noreferrer\">1</a></p>\n\n<ul>\n<li>Eg. Asthma \n\n<blockquote>\n <p>But preventing asthma isn't as simple as avoiding antibacterial soap, having a big family or spending time on the farm. For one thing, a number of microbes — such as a respiratory syncytial virus (RSV) — may cause asthma rather than prevent it. In addition, infections that might help prevent asthma can cause a number of other health problems. The type of germ isn't the only factor that plays a role, either. The severity of infection and when the infection occurs during childhood also appear to matter.\n (Ref. <a href=\"https://www.mayoclinic.org/diseases-conditions/childhood-asthma/expert-answers/hygiene-hypothesis/faq-20058102\" rel=\"nofollow noreferrer\">https://www.mayoclinic.org/diseases-conditions/childhood-asthma/expert-answers/hygiene-hypothesis/faq-20058102</a>)</p>\n</blockquote></li>\n</ul></li>\n</ul>\n\n<p>More research is needed to understand exactly how childhood germ exposure might help prevent asthma. What we do know is that in children with asthma, exposure to germs is likely to do more harm than good.</p>\n\n<p><strong>Abbreviations</strong></p>\n\n<ul>\n<li><p>HAV - hepatitis A Virus</p></li>\n<li><p>T1D - type 1 diabetes</p></li>\n<li><p>MS- multiple sclerosis</p></li>\n<li><p>NOD - non-obese diabetic</p></li>\n<li><p>HST - hypersensitivity</p></li>\n<li><p>TLR - toll-like receptors</p></li>\n<li><p>LPS - lipopolysaccharide</p></li>\n</ul>\n\n<p><strong>References</strong>:</p>\n\n<ol>\n<li><a href=\"https://www.mayoclinic.org/diseases-conditions/childhood-asthma/expert-answers/hygiene-hypothesis/faq-20058102\" rel=\"nofollow noreferrer\">https://www.mayoclinic.org/diseases-conditions/childhood-asthma/expert-answers/hygiene-hypothesis/faq-20058102</a></li>\n<li><p><a href=\"https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm\" rel=\"nofollow noreferrer\">https://www.fda.gov/BiologicsBloodVaccines/ResourcesforYou/Consumers/ucm167471.htm</a></p></li>\n<li><p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841828/</a></p></li>\n<li><p>Robbins and Cotran- Pathologic basis of diseases</p></li>\n</ol>\n", "score": 5 }, { "answer_id": 18671, "body": "<p>In general, it seems that there has to be a slight distinction made between a diet during pregnancy and a mother's diet during breast feeding. Overall the available evidence is judged as 'not there' or 'too weak' to make any recommendation to avoid specific antigens.</p>\n<blockquote>\n<p>Evidence is inadequate to advise women to avoid specific foods during pregnancy or breastfeeding to protect their children from allergic diseases like eczema and asthma.</p>\n<p>We included five trials, involving 952 participants. Trials of mothers' avoidance of milk, eggs, and other potentially 'antigenic' foods during pregnancy or breastfeeding, or both, provide inadequate evidence about whether such avoidance helps prevent atopic eczema or asthma in the child. Women who avoided eating these foods gained significantly less weight during pregnancy in the one trial reporting on this outcome, raising the possibility of adverse nutritional effects on the mother or fetus. Finally, one small trial reported an inconclusive response of breastfed infants with atopic eczema when their mothers avoided consumption of cow milk and egg.</p>\n<p>Prescription of an antigen avoidance diet to a high-risk woman during pregnancy is unlikely to reduce substantially her child's risk of atopic diseases, and such a diet may adversely affect maternal or fetal nutrition, or both. Prescription of an antigen avoidance diet to a high-risk woman during lactation may reduce her child's risk of developing atopic eczema, but better trials are needed.</p>\n<p>Dietary antigen avoidance by lactating mothers of infants with atopic eczema may reduce the severity of the eczema, but larger trials are needed.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/22972039\" rel=\"nofollow noreferrer\">Kramer MS, Kakuma R.: &quot;Maternal dietary antigen avoidance during pregnancy or lactation, or both, for preventing or treating atopic disease in the child.&quot;</a> Cochrane Database of Systematic Reviews 2012, Issue 9. Art. No.: CD000133. DOI: 10.1002/14651858.CD000133.pub3</p>\n</blockquote>\n<p>To the contrary, a few studies highlight a possiblly protective effect revealed by correlational outcomes in a prospective study:</p>\n<blockquote>\n<p>Among mothers without P/TN (peanuts/tree nuts) allergy, <strong>higher</strong> peripregnancy <strong>consumption</strong> of P/TN was associated with <strong>lower risk</strong> of P/TN allergy in their offspring. Our study supports the hypothesis that early allergen exposure increases tolerance and lowers risk of childhood food allergy.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed?term=24366539\" rel=\"nofollow noreferrer\">Frazier AL, Camargo CA Jr, Malspeis S, Willett WC, Young MC: &quot;Prospective study of peripregnancy consumption of peanuts or tree nuts by mothers and the risk of peanut or tree nut allergy in their offspring.&quot;</a>, JAMA Pediatr. 2014;168(2):156.</p>\n</blockquote>\n<p>But that is not a universal:</p>\n<blockquote>\n<p>Maternal CM avoidance was associated with lower levels of mucosal-specific IgA levels and the development of CMA in infants.<br />\n(CM = cow's milk; CMA = cow milk allergy)\n<a href=\"https://www.ncbi.nlm.nih.gov/pubmed?term=24164317\" rel=\"nofollow noreferrer\">Järvinen KM1, Westfall JE, Seppo MS, James AK, Tsuang AJ, Feustel PJ, Sampson HA, Berin C.: &quot;Role of maternal elimination diets and human milk IgA in the development of cow's milk allergy in the infants.&quot;</a>, Clin Exp Allergy. 2014 Jan;44(1):69-78. doi: 10.1111/cea.12228.</p>\n</blockquote>\n<p>And if you then compare</p>\n<blockquote>\n<p>High maternal consumption of milk products during pregnancy may protect children from developing CMA, especially in offspring of non-allergic mothers.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed?term=26757832\" rel=\"nofollow noreferrer\">Tuokkola J et al.: &quot;Maternal diet during pregnancy and lactation and cow's milk allergy in offspring.&quot;</a>, Eur J Clin Nutr. 2016 May;70(5):554-9. doi: 10.1038/ejcn.2015.223. Epub 2016 Jan 13.</p>\n</blockquote>\n<p>Then I conclude that we do not know anything certain about this –– but any avoidance scheme seems quite unfounded.</p>\n<p>That is most unfortunate, as mothers were apparently quite shaken by 'scientific' and 'pseudo-scientific' in recent years:</p>\n<blockquote>\n<p>In conclusion, all mothers in the present study restricted at least one type of food without scientific rationale while breastfeeding and more than a third of nursing mothers experienced difficulties with diet restriction. Nursing mothers should be educated on proper diet practices while being warned about unscientific approaches to diet restriction. In recent systematic review, education and emotional support by healthcare providers could enhance breastfeeding). We expect this study will give scientific basis for dietary recommendation to breastfeeding mothers and could promote a breastfeeding.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5383635/\" rel=\"nofollow noreferrer\">Goun Jeong et al.: &quot;Maternal food restrictions during breastfeeding&quot;</a>, Korean J Pediatr. 2017 Mar; 60(3): 70–76.\nPublished online 2017 Mar 27. doi: 10.3345/kjp.2017.60.3.70\nPMCID: PMC5383635</p>\n</blockquote>\n", "score": 2 } ]

[ "immune-system", "allergy", "allergen" ]

[ { "answer_id": 18675, "body": "<p>Many well-done newer studies are supporting the theory that quality trumps quantity when it comes to sleep. <a href=\"https://www.lifehack.org/643556/quality-or-quantity-why-dont-you-sleep-on-it\" rel=\"nofollow noreferrer\">This excellent article at lifehack.org</a> lists 12 good sources, including “two studies (which) assessed how sleep quality and quantity affected college students’ health and well-being. The studies concluded that sleep quality was a better predictor for a healthy and happy life and improved well-being than sleep quantity.”</p>\n\n<p>For those who still want it boiled down to a number, here are the numbers the National Sleep Foundation updated in 2015:<a href=\"https://i.stack.imgur.com/lFdO0.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/lFdO0.jpg\" alt=\"https://www.sleepfoundation.org/press-release/national-sleep-foundation-recommends-new-sleep-times\"></a> link: <a href=\"https://www.sleepfoundation.org/press-release/national-sleep-foundation-recommends-new-sleep-times\" rel=\"nofollow noreferrer\">https://www.sleepfoundation.org/press-release/national-sleep-foundation-recommends-new-sleep-times</a></p>\n", "score": 4 }, { "answer_id": 19764, "body": "<p>If you are aged between <strong>26 to 64 year age</strong>, you need minimum <strong>7-9 hours of sleep</strong> (other factors like your physical work, stress plays extra role).</p>\n\n<p>If you are doing more physical hard work, you might need 8-9hrs of sleep, while with desk job, you are with 7hrs of sleep as well.</p>\n\n<p>You can check the National Sleep Foundation data as below for age wise sleeping hours required.\n<a href=\"https://i.stack.imgur.com/vrq6W.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/vrq6W.png\" alt=\"enter image description here\"></a></p>\n\n<p><a href=\"https://www.helpguide.org/articles/sleep/sleep-needs-get-the-sleep-you-need.htm\" rel=\"nofollow noreferrer\">source</a></p>\n", "score": 2 } ]

[ "sleep", "statistics", "reference-request" ]

[ { "answer_id": 18694, "body": "<p>In business school (MBA) we were taught to consumer test all permutations of a possible \"pitch.\" We would come up with permutations of the same label with different words and phrases on each. Then we would set up tables in public places and get feedback.</p>\n\n<p>Basically, these large public companies have huge marketing departments. They tested the heck out of various combinations of words. What you see on the shelf is the label that had the best response from consumers with regard to ultimately buying the product.</p>\n\n<p>My personal thoughts would be that anti-bacterial is a second order function that the average consumer would not understand. You are assuming that \"bacteria causes cavities\" is common knowledge. It isn't. The consumer understands \"cavity.\" Cavities are talked about from when we are very young; even in cartoons.</p>\n", "score": 1 } ]

[ "dentistry", "mouthwash" ]

[ { "answer_id": 18938, "body": "<p>Officially, I requested to Bayer who is innovator of Ciprofloxacin and received 1 in-vitro study article.</p>\n\n<p>The author of the in-vitro study concluded that there's possibility as strategic option for intestinal sterilization but clinical study with patients must be confirmed.</p>\n\n<p>Again, this is a in-vitro study but not human clinical study.</p>\n\n<p>In case you're interested with non-profit purpose, you can find the above-mentioned in-vitro study article at the bottom of below linked post or as attached.</p>\n\n<p>I don't mark this as an answer because this is not the direct clinical evidence I've been looking for.</p>\n\n<p>Link-</p>\n\n<p><a href=\"http://cafe.daum.net/greenmission/jUmJ/4\" rel=\"nofollow noreferrer\">Comparison of Antibacterial Activity of Fluoroquinolones with Their Sucralfate-complexes against Clinically-isolated Bacteria_Hitoshi et al_2009</a></p>\n", "score": 3 } ]

[ "absorption-absorb" ]

[ { "answer_id": 18734, "body": "<p>Per the <a href=\"https://www.cdc.gov/pertussis/about/faqs.html\" rel=\"noreferrer\">CDC</a>:</p>\n\n<blockquote>\n <p>A: Pertussis vaccines are effective, but not perfect. They typically\n offer good levels of protection within the first 2 years after getting\n the vaccine, but then protection decreases over time. Public health\n experts call this ‘waning immunity.’ Similarly, natural infection may\n also only protect you for a few years.</p>\n \n <p>In general, DTaP vaccines are 80% to 90% effective. Among kids who get\n all 5 doses of DTaP on schedule, effectiveness is very high within the\n year following the 5th dose – at least 9 out of 10 kids are fully\n protected. There is a modest decrease in effectiveness in each\n following year. About 7 out of 10 kids are fully protected 5 years\n after getting their last dose of DTaP and the other 3 out of 10 kids\n are partially protected – protecting against serious disease.</p>\n \n <p>CDC’s current estimate is that in the first year after getting\n vaccinated with Tdap, it protects about 7 out of 10 people who receive\n it. There is a decrease in effectiveness in each following year. About\n 3 or 4 out of 10 people are fully protected 4 years after getting\n Tdap.</p>\n \n <p>Keeping up-to-date with recommended pertussis vaccines is the best way\n to protect you and your loved ones.</p>\n</blockquote>\n\n<p>Given the size of the school and the effectiveness of the vaccine, it appears that ~30 infected kids is within what's expected.</p>\n", "score": 13 } ]

[ "vaccination" ]

[ { "answer_id": 18767, "body": "<p>Yes, or at least, that's what this article in a reputable medical journal says and there is no reason to be more skeptical of it than the normal skepticism that any isolated article deserves.</p>\n\n<p>The 10 year IRR they find is 0.04 (95% CI 0.01-0.36), after adjusting for age and BMI, which is a pretty strong effect. The article is not claiming this is the best or most predictive way to estimate risk, they are just pointing out that this might be a simple, no-cost method of assessing physical health (and note that they only tested men, and all of the men are firefighters).</p>\n\n<p>Note that the study does not claim nor should be interpreted as causal: that is, it is unlikely that training to do more push ups has a substantial cardiovascular benefit. Instead, people who can do a large number of push ups for their age are probably among the most physically fit in other ways, too.</p>\n\n<p>I think you can restate the claim to be \"physically fit men have lower risk of heart attack than non-physically fit men of the same age and weight, and # of push ups is a decent estimator of physical fitness\" and stated that way it doesn't sound all that controversial, and that's pretty much how the Science Alert article you linked to describes the results.</p>\n", "score": 5 }, { "answer_id": 18771, "body": "<p>Limitations of the study:<a href=\"https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778\" rel=\"nofollow noreferrer\">(3)</a></p>\n\n<ul>\n<li><p>First, the study assessed the association between push-ups and CVD events. The results do not support push-up capacity as an independent predictor of CVD risk. </p></li>\n<li><p>Second, because the study cohort consisted of middle-aged, occupationally active men, the study results may not be generalizable to women, older or nonactive persons, other occupational groups, or unemployed persons.</p></li>\n</ul>\n\n<p><strong>Previous studies and research</strong><a href=\"https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778\" rel=\"nofollow noreferrer\">(3)</a></p>\n\n<ul>\n<li><p>Cross-sectional studies have incorporated push-ups in the assessment of muscular fitness and its correlation with cardiometabolic risk markers.In those studies, the authors found that a higher level of muscular strength was associated with lower cardiometabolic risk independent of cardiorespiratory fitness in the cohorts observed.</p></li>\n<li><p>Muscular strength has been shown to have an independent protective effect for all-cause mortality and hypertension in healthy males and is inversely associated with metabolic syndrome incidence and prevalence.</p></li>\n</ul>\n\n<p>However, most of those studies were either cross-sectional or conducted with adolescent participants.</p>\n\n<p>Hands down, this article and the research conducted is exceptional and one of it's kind. \nBut one may fail to recognise that \n<strong><em>Heart attack itself is multifactorial disease and that's mentioned in the research paper-</em></strong> </p>\n\n<blockquote>\n <p>The results do not support push-up capacity as an <strong>independent predictor</strong> of CVD risk.\n <a href=\"https://ghr.nlm.nih.gov/primer/mutationsanddisorders/complexdisorders\" rel=\"nofollow noreferrer\">(1)</a>:</p>\n</blockquote>\n\n<ul>\n<li><p>Although complex disorders often cluster in families, they do not have a clear-cut pattern of inheritance. This makes it difficult to determine a person’s risk of inheriting or passing on these disorders.</p></li>\n<li><p>Secondly the other risk factors, just a few mentioned;</p>\n\n<ul>\n<li><p>Hemoglobin A1c</p></li>\n<li><p>Blood Pressure</p></li>\n<li><p>Low‐Density Lipoprotein</p></li>\n<li><p>Type 2 Diabetes Mellitus:</p></li>\n</ul></li>\n</ul>\n\n<p>Are quite well established(traditional risk factors) </p>\n\n<p>In 2016, the American Heart Association released a scientific statement concluding that “CRF should be measured in clinical practice… Indeed, decades of research have produced unequivocal evidence that CRF provides independent and additive morbidity and mortality data that when added to traditional risk factors significantly improves CVD risk prediction.<a href=\"https://www.ahajournals.org/doi/full/10.1161/01.CIR.102.14.1623\" rel=\"nofollow noreferrer\">(2)</a><a href=\"https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778\" rel=\"nofollow noreferrer\">(5)</a></p>\n\n<p>So alternatively <em>physical fitness will help to keep the traditional risk factors within the range or in control</em>,</p>\n\n<p>let's see an example: </p>\n\n<ul>\n<li><p>In men, Cardiorespiratory fitness was indirectly associated with all CHD risk factors among men without CHD. </p></li>\n<li><p>Triglycerides and HDL demonstrated significant higher-order associations with fitness<a href=\"https://www.ahajournals.org/doi/full/10.1161/01.CIR.102.14.1623\" rel=\"nofollow noreferrer\">(2)</a></p></li>\n</ul>\n\n<p><strong>Let's look at another example:</strong></p>\n\n<p>Let's say there's an athlete <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884475/\" rel=\"nofollow noreferrer\">(here)</a>with<a href=\"https://www.heart.org/en/health-topics/cholesterol/causes-of-high-cholesterol/familial-hypercholesterolemia-fh\" rel=\"nofollow noreferrer\"> familial hypercholesterolemia</a></p>\n\n<ul>\n<li><p>Now think, won't the athlete be able to do 40 or may be far more than that.</p></li>\n<li><p>Let's say there's another non-athlete with no history of hypercholesterolemia of same age and sex; he is not able to do even 5 pushups. </p></li>\n<li><p>But now it's quite tricky to think who will have a higher risk, but here it's also important to realize that <strong>this shows how and why multifactorial disease are difficult to screen and treat.</strong></p></li>\n</ul>\n\n<p>The example above may be <strong>rare</strong>, but they do form a part of medicine. In no way I want to prove that this article is far from truth, it's merely the part of a big big story.</p>\n\n<p><strong>This research,</strong></p>\n\n<ul>\n<li><p>Paves a way for new ways of screening just as- self examination of breast in breast cancer is.</p></li>\n<li><p>May also be used in assessing risk in clinics provided keeping in mind the other risk factors.</p></li>\n<li><p>The problem with typical CRF testing is that it’s typically expensive, time-consuming, and requires special personnel this research may help in this aspect. </p></li>\n<li><p>Lastly a greater data is needed and this has to compared to the well established risk factors.</p></li>\n</ul>\n\n<p><strong>Conclusion</strong>: As a risk factor this has strong association but this may be true for one individual (or patient) and may be not for other, as case may be that even a healthy and fit, able to do 40 pushups easily have an heart attack <a href=\"https://www.google.com/amp/s/tonic.vice.com/amp/en_us/article/jpnea7/how-does-someone-as-fit-as-bob-harper-have-a-heart-attack\" rel=\"nofollow noreferrer\">(here)</a></p>\n\n<p><strong>References</strong>:</p>\n\n<p>1:<a href=\"https://ghr.nlm.nih.gov/primer/mutationsanddisorders/complexdisorders\" rel=\"nofollow noreferrer\">https://ghr.nlm.nih.gov/primer/mutationsanddisorders/complexdisorders</a></p>\n\n<p>2:<a href=\"https://www.ahajournals.org/doi/full/10.1161/01.CIR.102.14.1623\" rel=\"nofollow noreferrer\">https://www.ahajournals.org/doi/full/10.1161/01.CIR.102.14.1623</a></p>\n\n<p>3:<a href=\"https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778\" rel=\"nofollow noreferrer\">https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2724778</a></p>\n\n<p>4:<a href=\"https://www.heart.org/en/health-topics/cholesterol/causes-of-high-cholesterol/familial-hypercholesterolemia-fh\" rel=\"nofollow noreferrer\">https://www.heart.org/en/health-topics/cholesterol/causes-of-high-cholesterol/familial-hypercholesterolemia-fh</a></p>\n\n<p>5:<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884475/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1884475/</a></p>\n\n<p>6:<a href=\"https://www.google.com/amp/s/tonic.vice.com/amp/en_us/article/jpnea7/how-does-someone-as-fit-as-bob-harper-have-a-heart-attack\" rel=\"nofollow noreferrer\">https://www.google.com/amp/s/tonic.vice.com/amp/en_us/article/jpnea7/how-does-someone-as-fit-as-bob-harper-have-a-heart-attack</a></p>\n", "score": 3 } ]

[ "exercise", "heart-disease", "heart-attack" ]

[ { "answer_id": 18976, "body": "<p>There seems to be <strong>no scientific evidence</strong> to support the claim that diabetes type 2 generally goes away on its own (without drugs, diet or weight loss) in the elderly.</p>\n\n<p>According to one analytical article in <a href=\"https://www.directclinicaltrial.org.uk/Pubfiles/Beating%20Diabetes%20McCombie%202017%20bmj.j4030.full.pdf\" rel=\"nofollow noreferrer\">BMJ, 2017</a>, remission of diabetes type 2 is \"currently very rarely achieved or recorded.\"</p>\n\n<p>In elderly, remission may be slightly more common. In a large cohort study (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237974/\" rel=\"nofollow noreferrer\">Diabetes Care, 2014</a>), \"<strong>1.5%</strong> of individuals with diabetes type 2 not treated with bariatric surgery or drugs (but treated with diet or weight loss) achieved at least partial remission over a 7-year period. Remission occured in <strong>2.2%</strong> of individuals 65 years or older (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237974/table/T4/\" rel=\"nofollow noreferrer\">table 4</a>).</p>\n\n<p>In one randomized clinical trial (<a href=\"https://www.ncbi.nlm.nih.gov/pubmed/23288372/\" rel=\"nofollow noreferrer\">PubMed, 2012</a>), intensive lifestyle intervention, including exercise, diet and weight loss, resulted in at least partial remission in 11.5% of individuals with diabetes type 2 within the 1st year of the intervention.</p>\n", "score": 3 } ]

[ "diet", "carbohydrates", "type-2-diabetes", "elderly-seniors-aged-old", "loss-of-appetite" ]

[ { "answer_id": 18818, "body": "<p>I have had a pain management course a couple of years ago - this was my research topic. As you pointed out the reasons are still unknown, also the treatment is basically aimed at treating symptoms an managing life with pain. This might be interesting to read if you are interested in this procedure called multimodal pain therapy [1]\nThe tender points are still the way of diagnosing FM.</p>\n\n<p>The best english Version I found is so far about FM is the NHS website [2] who have lined up all suspected contributing factors quite nicely (and was just recently updated):</p>\n\n<p>Abnormal pain messages\n-For unknown reason the receptors react differently to pain and the threshold of identifying pain and \"just\" normal sensations is going down</p>\n\n<p>Chemical imbalance\n-Serotonin, noradrenaline and dopamine are unusual low in fibromyalgia patients - please note, especially this is not something that can be assumed safely as a cause, it could very well also be a result from being constantly in pain.</p>\n\n<p>Sleep problems\n-That originally was assumed as a result of Fibromyalgia, but today we also see it as a possible risk factor. As mentioned above a clear cause and effect connection is not easy to establish</p>\n\n<p>Genetics\n-Some genetic prevalence is found, but since FM is very seldom, that also is not easy to prove. </p>\n\n<p>Trigger\n- As you mentioned psychical stress is one of the things that is quoted, but also Injuries, infections, surgery and even giving birth.</p>\n\n<p>I myself have seen around 10 FM patients, in my very limited personal experience most of them were post Injury/Surgery, some post viral infection and one was completely without any of the expected triggers and \"just\" had a depression\nThe studies often point also at other risk factors like smoking, unfortunately the same thing applies as before, due to small numbers and retrospective studies cause and effect are not clearly separable. </p>\n\n<p>[1] <a href=\"https://www.americannursetoday.com/multimodal-multidisciplinary-therapy-pain-management/\" rel=\"noreferrer\">https://www.americannursetoday.com/multimodal-multidisciplinary-therapy-pain-management/</a>\n[2]<a href=\"https://www.nhs.uk/conditions/fibromyalgia/causes/\" rel=\"noreferrer\">https://www.nhs.uk/conditions/fibromyalgia/causes/</a></p>\n", "score": 5 } ]

[ "pain", "fatigue", "fibromyalgia" ]

[ { "answer_id": 18869, "body": "<p>Yes, and that the recommended interval for dosage is twice daily.</p>\n\n<p>The convention for BID (twice daily) dosing is to write \"400 mg twice daily\" to indicate the dosage at each administration. Therefore it would be 400 mg + 400 mg = 800 mg total daily.</p>\n\n<p>With some medications, the dosage is listed as daily total, divided into BID or TID dosing. For example, \"1200 mg daily divided into BID or TID dosing\" would be 600 mg twice daily, or 400 mg three times daily.</p>\n\n<p><a href=\"https://www.drugs.com/dosage/amoxicillin.html\" rel=\"noreferrer\">This entry for amoxicillin</a> shows how it can be written both ways, though I have seen better wording in other references (like UpToDate or Epocrates but both require registration or paywall)</p>\n", "score": 5 } ]

[ "terminology", "prescription" ]

[ { "answer_id": 18984, "body": "<p>The following comprehensive scientific sources <strong>do not even mention any relationship between turmeric/curcumin and gynecomastia:</strong></p>\n\n<ul>\n<li><a href=\"https://ww5.komen.org/BreastCancer/Turmeric.html\" rel=\"nofollow noreferrer\">Turmeric, Natural Medicines Comprehensive Database, komen.org</a></li>\n<li><a href=\"https://nccih.nih.gov/health/turmeric/ataglance.htm#hed3\" rel=\"nofollow noreferrer\">Turmeric, National Center for Complementary and Integrative Health</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664031/\" rel=\"nofollow noreferrer\">Curcumin: A Review of Its’ Effects on Human Health, PubMed, 2017</a></li>\n<li><a href=\"https://examine.com/supplements/curcumin/#interactions-with-hormones_estrogen\" rel=\"nofollow noreferrer\">Curcumin, Examine.com, 2015</a></li>\n<li>Google .gov: or .edu: search for <em>turmeric</em> or <em>curcumin</em> + <em>gynecomastia</em></li>\n</ul>\n\n<hr>\n\n<p>The youtube videos and fixmanboobs.com.au site mentioned in the question are not backed up by any references.</p>\n\n<hr>\n\n<p>The <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354546/\" rel=\"nofollow noreferrer\">PubMed article</a> from the question mentions that curcumin can inhibit estrogen receptors and thus decrease estrogen activity but it does not say if this has any health effects.</p>\n\n<hr>\n\n<p><strong>In conclusion,</strong> there seems to be no scientific evidence to support the claim that turmeric/curcumin helps to reduce gynecomastia.</p>\n", "score": 3 }, { "answer_id": 18985, "body": "<p>There seems to be <em>no</em> clear and direct evidence for this.</p>\n<p>But a few angles might be worth exploring:</p>\n<blockquote>\n<p>Molecular Dynamics (MD) simulations found curcumin to be a stable inhibitor of aromatase (Singh et al 2016).</p>\n<p>The prepubertal gynecomastia in males and breast hypertrophy in females are conditions of aromatase excess syndrome (Metwalley and Farghaly 2013).</p>\n<p>Aromatase inhibitors are used as therapy for breast cancer, endometriosis, leiomyoma (fibroid tumors), idiopathic short stature, gynecomastia, and male hypogonadism, as they prevent estrogen formation (Le Ray et al 2012; Pavone and Bulun 2012; Singh 2013; Hero 2016; Blakemore and Naftolin 2016; Miller et al 2016).</p>\n<p>_{Singh S, Awasthi M, Pandey VP, Dwivedi UN (2016) Plant derived anti-cancerous secondary metabolites as multipronged inhibitor of COX, Topo and aromatase: Molecular modeling and dynamics simulation analyses. J Biomol Struct Dyn 1–65. doi: 10.1080/07391102.2016.1241720}</p>\n<p>_{Metwalley KA, Farghaly HS (2013) Aromatase excess syndrome presenting with prepubertal gynecomastia in an Egyptian child with type 1 neurofibromatosis. Indian J Hum Genet 19:472–4. doi: 10.4103/0971-6866.124379}</p>\n<p>_{Singh SK (2013) Aromatase inhibitors in male sex. Indian J Endocrinol Metab 17:S259-61. doi: 10.4103/2230-8210.119594}</p>\n<p>_{Blakemore J, Naftolin F (2016) Aromatase: Contributions to Physiology and Disease in Women and Men. Physiology (Bethesda) 31:258–69. doi: 10.1152/physiol.00054.2015}</p>\n<p>Seema Patel: &quot;Disruption of aromatase homeostasis as the cause of a multiplicity of ailments: A comprehensive review&quot;,The Journal of Steroid Biochemistry and Molecular Biology, Volume 168, April 2017, Pages 19-25 (DOI <a href=\"http://dx.doi.org/doi:10.1016/j.jsbmb.2017.01.009\" rel=\"nofollow noreferrer\">http://dx.doi.org/doi:10.1016/j.jsbmb.2017.01.009</a> <a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0960076017300092\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/abs/pii/S0960076017300092</a>)</p>\n</blockquote>\n<p>This is quite promising, but currently nothing more. Also in light of the multitude (<a href=\"https://www.mayoclinic.org/diseases-conditions/gynecomastia/symptoms-causes/syc-20351793\" rel=\"nofollow noreferrer\">https://www.mayoclinic.org/diseases-conditions/gynecomastia/symptoms-causes/syc-20351793</a>) of possible (<a href=\"https://my.clevelandclinic.org/health/diseases/16227-enlarged-male-breast-tissue-gynecomastia\" rel=\"nofollow noreferrer\">https://my.clevelandclinic.org/health/diseases/16227-enlarged-male-breast-tissue-gynecomastia</a>) causes for this one diagnosis.</p>\n", "score": 2 } ]

[ "natural-remedy", "testosterone", "estrogen", "gynecomastia-man-boobs" ]

[ { "answer_id": 18915, "body": "<p>Some recent estimated numbers recently were:</p>\n<p><strong>45% of all dental restorations world wide</strong> (Heintze 2012),<br />\n<strong>50% of all American fillings</strong></p>\n<p>But</p>\n<blockquote>\n<p>Many developed nations have virtually eliminated dental amalgam. Dental amalgam use is banned in Sweden and Norway; only used in 3% of all dental restorations in Japan and Finland; 5% in Denmark; 10% in the Netherlands, Switzerland, and Germany; and 20% in Singapore.</p>\n<p>Quoted from Chicago Declaration to End Dental Industry Mercury Use (<a href=\"https://mercuryfreedentistry.files.wordpress.com/2018/04/chicago-declaration-to-end-dental-industry-mercury-use-4-14-17.pdf\" rel=\"nofollow noreferrer\">PDF</a>)</p>\n</blockquote>\n<hr />\n<p>On amalgam use:</p>\n<p><a href=\"http://www.who.int/water_sanitation_health/medicalwaste/mercurypolpaper.pdf\" rel=\"nofollow noreferrer\">WHO Policy Paper (PDF)</a></p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/23082310\" rel=\"nofollow noreferrer\">SD Heintze &amp; V Rousson: &quot;Clinical effectiveness of direct Class II restorations—a meta-analysis&quot;</a> J Adhes Dent. 2012; 14(5):407-431.</p>\n<p>SK Makhija et al.: <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21628683/\" rel=\"nofollow noreferrer\">&quot;Practitioner, patient and carious lesion characteristics associated with type of restorative material: findings from The Dental Practice-Based Research Network&quot;</a>, J Am Dent Assoc. 2011; 142: 622-632.</p>\n<p>Simececk et al.: <a href=\"https://jada.ada.org/article/S0002-8177(14)64283-5/fulltext\" rel=\"nofollow noreferrer\">&quot;An evaluation of replacement rates for posterior resin-based composite and amalgam restorations in U.S. Navy and Marine recruits&quot;</a>, J Am Dent Assoc. 2009; 140 (2): 207. PMID: 19188417</p>\n<p>United States Food and Drug Administration: &quot;About dental fillings: potential risks. Last updated 2 February 2017. <a href=\"https://www.fda.gov/medicaldevices/productsandmedicalprocedures/dentalproducts/dentalamalgam/ucm171094.htm\" rel=\"nofollow noreferrer\">FDA Web site</a></p>\n<p>World Health Organization: &quot;Future Use of Materials for Dental Restoration&quot; (2011), <a href=\"http://www.who.int/oral_health/publications/dental_material_2011.pdf\" rel=\"nofollow noreferrer\">PDF</a> , p.21</p>\n<p>Bio Intelligence Service/European Commission: &quot;Review of the Community Strategy Concerning Mercury&quot; (p.213-14), 4 October 2010, (<a href=\"http://ec.europa.eu/environment/chemicals/mercury/pdf/review_mercury_strategy2010.pdf\" rel=\"nofollow noreferrer\">PDF</a>)</p>\n<p>BIO Intelligence Service (2012): &quot;Study on the potential for reducing mercury pollution from dental amalgam and batteries, Final report prepared for the European Commission-DG ENV&quot;, <a href=\"http://ec.europa.eu/environment/chemicals/mercury/pdf/Final_report_11.07.12.pdf\" rel=\"nofollow noreferrer\">PDF</a>, p.190–191.</p>\n<p>World Health Organization: &quot;Future Use of Materials for Dental Restoration&quot; (2011), (<a href=\"http://www.who.int/oral_health/publications/dental_material_2011.pdf\" rel=\"nofollow noreferrer\">PDF</a>, p.21.</p>\n<p>Letter, Federal Office for the Environment to Francesca Romana Orlando (8 August 2011), (<a href=\"http://www.toxicteeth.org/SVIZZERA.pdf\" rel=\"nofollow noreferrer\">PDF</a>).</p>\n<hr />\n<p>Commentary:</p>\n<p>Dental mercury amalgam is also an environmental and social justice problem:\n<a href=\"https://www.dentistrytoday.com/news/todays-dental-news/item/2843-berlin-declaration-shows-amalgam-has-entered-its-twilight-era\" rel=\"nofollow noreferrer\">Dentistry Today 2018: Berlin Declaration Shows Amalgam Has Entered Its Twilight Era</a></p>\n", "score": 4 } ]

[ "dentistry", "metal" ]

[ { "answer_id": 18925, "body": "<p>Since Melarsoprol is insoluble in water, dosage occurs via a 3.6% propylene glycol intravenous injection.</p>\n\n<blockquote>\n <p>As propylene glycol can dissolve plastic, the drug should preferably be administered using a glass syringe (only if sterilisation is reliable), otherwise inject immediately (but slowly) using a plastic syringe (<a href=\"https://medicalguidelines.msf.org/viewport/EssDr/english/melarsoprol-injectable-16682915.html\" rel=\"nofollow noreferrer\">Source</a>).</p>\n</blockquote>\n\n<p>Melarsoprol is sometimes colloquially referred to as \"arsenic in antifreeze\".</p>\n", "score": 4 }, { "answer_id": 18972, "body": "<p>The reason for it may not be the barrel of the syringe, but the rubber in the stopper which is of a different material. There was a <a href=\"https://www.ncbi.nlm.nih.gov/m/pubmed/6702838/\" rel=\"nofollow noreferrer\">study done on paraldehyde</a> and the affect it had on the plastic in syringes and needle hubs. The pertinent part (Note the time, there was no effect until after at least 3 hours immersion) is below (Emphasis mine).</p>\n\n<blockquote>\n <p>No measurable change in residue weight was noted in any syringes for up to three hours. Compared with the control, there was a significant increase in the average weight of residue in the Glaspak and in the Plastipak syringes at 6, 12, and 24 hours. There was no significant difference in the weight of residue between the Glaspak and Plastipak syringes at those times, however. The amount of residue for the plastic and metal needle hubs was not significantly different. <strong>The source of the extractive residue appeared to be the rubber plunger tip. Since the nature of the extractive material in the residue is not known, paraldehyde should be administered in all-glass syringes if possible; other syringe types can be used only if the drug is administered immediately.</strong></p>\n</blockquote>\n\n<p>So basically, it's possibly erring on the side of caution as they don't know how soon it might start dissolving stuff.</p>\n", "score": 2 } ]

[ "medications" ]

[ { "answer_id": 19423, "body": "<p><strong>Common cold,</strong> which is an acute viral infection of the nose, is <em>rarely</em> associated with fever in adults (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3928210/\" rel=\"nofollow noreferrer\">Canadian Medical Association Journal</a> ; <a href=\"https://dphhs.mt.gov/Portals/85/dsd/documents/DDP/MedicalDirector/CommonCold101713.pdf\" rel=\"nofollow noreferrer\">DPHHS Montana</a>).</p>\n\n<p><strong>Allergic rhinitis</strong> <em>does not usually cause fever;</em> it's not mentioned as a symptoms on major clinical websites (<a href=\"https://emedicine.medscape.com/article/134825-clinical#showall\" rel=\"nofollow noreferrer\">Emedicine</a> ; <a href=\"https://www.mayoclinic.org/departments-centers/allergic-diseases/minnesota/overview/specialty-groups/allergic-rhinitis\" rel=\"nofollow noreferrer\">Mayo Clinic</a> ; <a href=\"https://medlineplus.gov/ency/article/000813.htm\" rel=\"nofollow noreferrer\">MedlinePlus</a>). <a href=\"https://newsinhealth.nih.gov/2014/10/cold-flu-or-allergy\" rel=\"nofollow noreferrer\">News In Health</a> says allergic rhinitis \"never\" causes fever, while <a href=\"https://www.jacionline.org/article/S0091-6749(95)70211-3/fulltext\" rel=\"nofollow noreferrer\">The Journal Of Allergy and Clinical Immunology</a> says that fever \"is rarely found in patients with allergic rhinitis.\"</p>\n\n<p><strong>Non-allergic rhinitis</strong> (irritant, vasomotor, hormonal, medicamentous, gustatory, senile, etc.) is also not associated with fever according to various sources (<a href=\"https://emedicine.medscape.com/article/874171-overview\" rel=\"nofollow noreferrer\">Emedicine</a> ; <a href=\"https://www.mayoclinic.org/diseases-conditions/nonallergic-rhinitis/symptoms-causes/syc-20351229\" rel=\"nofollow noreferrer\">Mayo Clinic</a> ; <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3650992/\" rel=\"nofollow noreferrer\">World Allergy Organization</a> ; <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/28474799\" rel=\"nofollow noreferrer\">Allergy</a>). After some further research, there seems to be no evidence that non-allergic, non-infectious rhinitis would be associated with fever, but I can't exclude the possibility that sometimes could be.</p>\n\n<p><strong>In conclusion,</strong> the absence of fever does not help (much) in determining the type of rhinitis.</p>\n", "score": 4 } ]

[ "immune-system", "allergy", "nose", "fever", "runny-nose" ]

[ { "answer_id": 19926, "body": "<p>In short: It seems, there is not enough evidence to say that parathyroid-stimulating hormone secreted from the pituitary gland exists in humans. </p>\n\n<p><strong>A) Parathyroid Stimulating Hormone (PTH)</strong></p>\n\n<p>Some texts use the term <strong>parathyroid-stimulating hormone with the acronym PTH</strong> or in a way that suggests they actually meant parathyroid hormone.</p>\n\n<p><a href=\"https://jcs.biologists.org/content/joces/121/21/3581.full.pdf?with-ds=yes\" rel=\"nofollow noreferrer\">Journal of Cell Science (2008)</a>:</p>\n\n<blockquote>\n <p>...and parathyroid hormone-related peptide receptor (PTH1R), whose\n stimulation by <strong>parathyroid stimulating hormone (PTH)</strong> increases the\n intracellular levels of cAMP, IP3, DAG and Ca2+...</p>\n</blockquote>\n\n<p><a href=\"https://www.sciencedirect.com/science/article/pii/S0165032717323893?via%3Dihub\" rel=\"nofollow noreferrer\">Respiratory subtype of panic disorder: Can serum phosphate levels be a possible outcome to group cognitive-behavior therapy? (Journal of Affective Disorders, 2018)</a>:</p>\n\n<blockquote>\n <p>All patients underwent 12 structured sessions of group\n cognitive-behavioral therapy for PD (Otto and Deveney, 2005) and had\n their blood collected at baseline to assess fasting glucose, complete\n blood count, thyroid stimulating hormone, <strong>parathyroid stimulating\n hormone</strong>, ionized calcium, creatinine and phosphate levels.</p>\n</blockquote>\n\n<p><a href=\"https://emedicine.medscape.com/article/1091928-workup\" rel=\"nofollow noreferrer\">Chronic Mucocutaneous Candidiasis Workup (Emedicine, 2017)</a>:</p>\n\n<blockquote>\n <p>Other endocrine screening tests that may be considered include\n follicle-stimulating hormone, luteinizing hormone, prolactin,\n testosterone, <strong>parathyroid-stimulating hormone</strong>, calcium, phosphate,\n magnesium, and short synacthen test.</p>\n</blockquote>\n\n<p><a href=\"https://escholarship.org/content/qt4kq2z97b/qt4kq2z97b.pdf\" rel=\"nofollow noreferrer\">Dermatology Online Journal (2014)</a>:</p>\n\n<blockquote>\n <p>According to current guidelines for high risk patients (i.e. those\n that are genetically confirmed to have MEN-1), annual laboratory\n studies to include calcium, <strong>parathyroid stimulating hormone</strong>,\n prolactin, gastrin...</p>\n</blockquote>\n\n<p><em>^^From this <a href=\"https://www.niddk.nih.gov/health-information/endocrine-diseases/multiple-endocrine-neoplasia-type-1\" rel=\"nofollow noreferrer\">NIDDK article</a>, it is clear that parathyroid hormone is meant above.</em></p>\n\n<hr>\n\n<p><strong>B) Parathyroid Stimulating Hormone (PSH)</strong></p>\n\n<p>I've found a single text that mentions <strong>parathyroid stimulating hormone with the acronym PSH</strong>, in which they clearly suggest it is secreted from the pituitary gland and stimulates the release of parathyroid hormone.</p>\n\n<p><a href=\"https://www.sciencedirect.com/topics/medicine-and-dentistry/intertragic-notch\" rel=\"nofollow noreferrer\">Cranial Endocrine Glands Represented at Intertragic Notch (ScienceDirect, 2014)</a>:</p>\n\n<blockquote>\n <p>103.e Parathyrotrophin Hormones (PSH, Parathyroid-Stimulating Hormone) [IT 2] Location: Found on the most central part of wall of\n intertragic notch, below LM_9.</p>\n \n <p>Function: The parathyroid pituitary hormone PSH regulates parathormone\n release by the parathyroid gland. This point facilitates calcium\n metabolism and reduces muscle tetanus.</p>\n</blockquote>\n\n<p><strong>C)</strong> I haven't found any text in which <strong>parathyroid-stimulating hormone</strong> in <em>humans</em> would be mentioned with the acronym <strong>PTSH</strong> (like in <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/7420044\" rel=\"nofollow noreferrer\">this article</a> linked from the question, which mentions PTSH in <em>cows</em>).</p>\n", "score": 4 }, { "answer_id": 19925, "body": "<p>The pituitary does not have a direct effect on the parathyroid glands.</p>\n\n<blockquote>\n <p>The parathyroid gland and adrenal medulla are not controlled by the\n pituitary but play important roles in calcium metabolism and the\n adrenergic (sympathetic nervous system) function respectively. Source:\n <a href=\"https://www.sciencedirect.com/science/article/abs/pii/S0263931914001598\" rel=\"nofollow noreferrer\">Science Direct</a></p>\n</blockquote>\n\n<p>Although they are located close together, the thyroid and parathyroid glands work independently.</p>\n\n<p>The role of the parathyroid glands is to regulate blood calcium levels. They do this by secreting <a href=\"https://en.m.wikipedia.org/wiki/Parathyroid_hormone\" rel=\"nofollow noreferrer\">parathyroid hormone</a> (PTH) when calcium levels fall, in a negative feedback system.</p>\n\n<p>PTH has the following effects:</p>\n\n<ul>\n<li>Increases release of calcium from bone (by increasing osteoclasts activity)</li>\n<li>Reduces calcium losses in the kidneys</li>\n<li>Increase calcium absorption in the gut</li>\n</ul>\n\n<p>As a result, calcium levels in the blood will be corrected to normal levels.</p>\n\n<p>The hormone <a href=\"https://en.m.wikipedia.org/wiki/Calcitonin\" rel=\"nofollow noreferrer\">calcitonin</a> has the opposite effect of PTH. It is actually secreted by the thyroid gland itself in response to high calcium levels.</p>\n\n<p>Here is a diagram summarising the role of PTH (<a href=\"http://what-when-how.com/acp-medicine/diseases-of-calcium-metabolism-and-metabolic-bone-disease-part-1/\" rel=\"nofollow noreferrer\">source</a>):</p>\n\n<p><a href=\"https://i.stack.imgur.com/mTKfx.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/mTKfx.jpg\" alt=\"Effects of parathyroid hormone\"></a></p>\n\n<p>Here is a basic diagram showing interplaynof parathyroid hormone and calcitonin (<a href=\"http://biology.reachingfordreams.com/biology/endocrine-system/13-thyroid-and-parathyroid-gland-hormons\" rel=\"nofollow noreferrer\">source</a>):</p>\n\n<p><a href=\"https://i.stack.imgur.com/CiiHY.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/CiiHY.png\" alt=\"Parathyroid and calcitonin\"></a></p>\n\n<p>The study you mention relates to cattle and is almost 40 years old. There has been nothing that I can find in human research to suggest the presence of a clinically significant parathyroid-stimulating hormone.</p>\n", "score": 2 } ]

[ "endocrinology" ]

[ { "answer_id": 19853, "body": "<p>After internal bleeding, the blood serum from the blood can be reabsorbed back into the circulation (capillaries), and the blood cells can be phagocytosed by macrophages. The blood serum from the abdominal cavity can be resorbed by the peritoneal blood vessels and from the pleural space by the pleural lymphatic vessels. </p>\n\n<p>Some hematomas may not be reabsorbed and can form <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202869/\" rel=\"noreferrer\">encapsulated cysts</a> (in the brain) or <a href=\"https://www.endometriosis-uk.org/sites/default/files/files/Information/Understanding-endometriosis.pdf\" rel=\"noreferrer\">adhesions</a> (in the abdomen).</p>\n\n<p><strong>1) <a href=\"https://www.intechopen.com/books/muscle-injuries-in-sport-medicine/the-treatment-of-muscle-hematomas\" rel=\"noreferrer\">The Treatment of Muscle Hematomas (IntechOPen)</a></strong></p>\n\n<p>This source suggests that the serum from hematoma can be reabsorbed into the blood.</p>\n\n<blockquote>\n <p>The diathermy is based on application of electromagnetic waves; those\n oscillations induce a transfer of kinetic energy which is readily\n converted into heat. This effect of heat production in the tissues is\n called ”Joule effect”...The rational application of various forms of\n diathermy is based on accelerating the rate of <strong>absorption of the\n residual hematoma, due to increased blood circulation induced by the\n temperature.</strong></p>\n</blockquote>\n\n<p><strong>2) <a href=\"https://www.diagnosticimaging.com/articles/imaging-reveals-signs-intracranial-hemorrhage\" rel=\"noreferrer\">Imaging reveals signs of intracranial hemorrhage (Diagnostic imaging, 2005)</a></strong></p>\n\n<p>In the brain hematoma, macrophages phagocytize the red cells.</p>\n\n<blockquote>\n <p><strong>Macrophages and astroglial cells phagocytize the hematoma</strong> in the\n chronic stage. Extracellular methemoglobin is converted into\n hemosiderin and ferritin, which is stored within the macrophages.\n Intra-axial hematomas leave a cystic, fluid-filled, or collapsed brain\n defect.</p>\n</blockquote>\n\n<p><strong>3) <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/1308683\" rel=\"noreferrer\">Lymphatic versus nonlymphatic fluid absorption from the peritoneal cavity as related to the peritoneal ultrafiltration capacity and sieving properties (Blood Purification)</a></strong></p>\n\n<p>Concluding from this source, after abdominal bleeding the serum can be reabsorbed via peritoneum into the blood.</p>\n\n<blockquote>\n <p>Support for the contention that <strong>nonlymphatic fluid absorption\n directly into the capillaries is the major mode of fluid transport\n from the peritoneal cavity to the blood</strong> is given by measurements of\n the peritoneal-to-blood clearance of tracer albumin (or other\n proteins).</p>\n</blockquote>\n\n<p><strong>4) <a href=\"https://www.uptodate.com/contents/mechanisms-of-pleural-liquid-turnover-in-the-normal-state\" rel=\"noreferrer\">Mechanisms of pleural liquid turnover in the normal state (UpToDate)</a></strong></p>\n\n<p>Concluding from this source, after pleural bleeding, the serum can be resorbed by the lymphatic vessels in the parietal pleura. </p>\n\n<blockquote>\n <p>Available data indicate that pleural fluid is formed from the systemic\n vessels of the pleural membranes at an approximate rate of 0.6 mL/h\n and is <strong>absorbed at a similar rate by the parietal pleural lymphatic\n system.</strong></p>\n</blockquote>\n", "score": 5 } ]

[ "blood", "bleeding", "blood-vessels", "internal-bleeding" ]

[ { "answer_id": 21222, "body": "<p>No, you do <strong>not</strong> have to kill every single (targeted) germ. Often antibiotics are bacteriostatic which means they do not kill the germs but stop them from reproducing. Your immune system then does the job of killing them. If antibiotics are <strong>bacteriostatic or bacterizidal</strong> can but must not depend on their <strong>concentration</strong>. </p>\n\n<p>Please see <a href=\"https://en.wikipedia.org/wiki/Bacteriostatic_agent\" rel=\"nofollow noreferrer\">Wikipedia: Bacteriostatic agent</a> for more details.</p>\n", "score": 4 } ]

[ "bacteria", "antibiotics", "antibacterial-resistance" ]

[ { "answer_id": 20021, "body": "<p>I answered a similar question (<a href=\"https://psychology.stackexchange.com/a/17892\">Is autism caused by genetics?</a>) on Psychology &amp; Neuroscience where the following was found, plus I have added information regarding autoimmune responses concerning Autism.</p>\n\n<p>Autism spectrum disorder (ASD) now affects one in 68 births in the United States and is the fastest growing neurodevelopmental disability worldwide (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5373490/\" rel=\"nofollow noreferrer\">Edmiston, et al. 2017</a>) <em>[free access paper with links to cited papers]</em>. Alarmingly, for the majority of cases, the causes of ASD are largely unknown, but it is becoming increasingly accepted that ASD is no longer defined simply as a behavioral disorder, but rather as a highly complex and heterogeneous biological disorder (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5373490/\" rel=\"nofollow noreferrer\">Edmiston, et al. 2017</a>).</p>\n\n<p>With the information available, the genetic and environmental causes of Autism is open to speculation and interpretation.</p>\n\n<p>The paper you cited is referenced in Edmiston, et al. (2017) under citation number 28, and they stated (emphasis mine):</p>\n\n<blockquote>\n <p><strong>there are likely multiple, biologically defined subgroups within the ASD spectrum</strong>(3–7). Specifically, there is growing evidence that supports maternal immune dysfunction <strong>may</strong> underlie the behavioral abnormalities observed <strong>in a subset of children affected with the disorder</strong>(8). Several immunologic risk factors have been described including: genetic associations with immune-related genes(9–16), family history of autoimmune disease(15, 17–21), maternal inflammation and infection during pregnancy(22–27), and altered immune responses in the children, and are associated with increased impairments in core and associated features of ASD(28). More specific to this review, maternal anti-brain autoantibodies, which are thought to access the fetal compartment during gestation, have been identified as one risk factor for developing ASD and are proposed to contribute to early neurodevelopmental perturbations in the developing fetus(29–31).</p>\n \n <p>References</p>\n \n <ol start=\"3\">\n <li>Lord C, Risi S, Lambrecht L, Cook EH, Leventhal BL, DiLavore PC, et al. The autism diagnostic observation schedule-generic: a standard measure of social and communication deficits associated with the spectrum of autism. Journal of autism and developmental disorders. 2000;30:205–223.</li>\n <li>Newschaffer CJ, Croen La, Daniels J, Giarelli E, Grether JK, Levy SE, et al. The epidemiology of autism spectrum disorders. Annual review of public health. 2007;28:235–258.</li>\n <li>Snow AV, Lecavalier L, Houts C. The structure of the Autism Diagnostic Interview-Revised: diagnostic and phenotypic implications. Journal of child psychology and psychiatry, and allied disciplines. 2009;50:734–742.</li>\n <li>Ousley O, Cermak T. Autism spectrum disorder: Defining dimensions and subgroups. Current Developmental Disorders Reports. 2013;1:20–28.</li>\n <li>McDougle CJ, Landino SM, Vahabzadeh A, O’Rourke J, Zurcher NR, Finger BC, et al. Toward an immune-mediated subtype of autism spectrum disorder. Brain Research. 2015;1617:72–92.</li>\n <li>Onore C, Careaga M, Ashwood P. The role of immune dysfunction in the pathophysiology of autism. Brain, Behavior, and Immunity. 2012;26:383–392.</li>\n <li>Warren RP, Singh VK, Cole P, Odell JD, Pingree CB, Warren WL, et al. Increased frequency of the null allele at the complement C4b locus in autism. Clinical &amp; Experimental Immunology. 1991;83:438–440.</li>\n <li>Warren RP, Odell JD, Warren WL, Burger RA, Maciulis A, Daniels WW, et al. Strong association of the third hypervariable region of HLA-DRβ1 with autism. Journal of Neuroimmunology. 1996;67:97–102.</li>\n <li>Torres AR, Sweeten TL, Cutler A, Bedke BJ, Fillmore M, Stubbs EG, et al. The association and linkage of the HLA-A2 class I allele with autism. Human immunology. 2006;67:346–351.</li>\n <li>Campbell DB, Li C, Sutcliffe JS, Persico AM, Levitt P. Genetic evidence implicating multiple genes in the MET receptor tyrosine kinase pathway in autism spectrum disorder. Autism Research. 2008;1:159–168.</li>\n <li>Thanseem I, Nakamura K, Miyachi T, Toyota T, Yamada S, Tsujii M, et al. Further evidence for the role of MET in autism susceptibility. Neuroscience Research. 2010;68:137–141.</li>\n <li>Mostafa GA, Shehab AA. The link of C4B null allele to autism and to a family history of autoimmunity in Egyptian autistic children. Journal of Neuroimmunology. 2010;223:115–119.</li>\n <li>Jung JY, Kohane IS, Wall DP. Identification of autoimmune gene signatures in autism. Translational psychiatry. 2011;1:e63–e63.</li>\n <li>Torres AR, Westover JB, Gibbons C, Johnson RC, Ward DC. Activating killer-cell immunoglobulin-like receptors (KIR) and their cognate HLA ligands are significantly increased in autism. Brain, behavior, and immunity. 2012;26:1122–1127.</li>\n <li>Comi AM, Zimmerman AW, Frye VH, Law PA, Peeden JN. Familial Clustering of Autoimmune Disorders and Evaluation of Medical Risk Factors in Autism. Journal of Child Neurology. 1999;14:388–394.</li>\n <li>Atladóttir HO, Pedersen MG, Thorsen P, Mortensen PB, Deleuran B, Eaton WW, et al. Association of family history of autoimmune diseases and autism spectrum disorders. Pediatrics. 2009;124:687–694.</li>\n <li>Vinet É, Pineau CA, Clarke AE, Scott S, Fombonne É, Joseph L, et al. Increased Risk of Autism Spectrum Disorders in Children Born to Women With Systemic Lupus Erythematosus: Results From a Large Population-Based Cohort. Arthritis &amp; rheumatology (Hoboken, NJ) 2015;67:3201–3208.</li>\n <li>Wu S, Ding Y, Wu F, Li R, Xie G, Hou J, et al. Family history of autoimmune diseases is associated with an increased risk of autism in children: A systematic review and meta-analysis. Neuroscience and biobehavioral reviews. 2015;55:322–332.</li>\n <li>Chen S-W, Zhong X-S, Jiang L-N, Zheng X-Y, Xiong Y-Q, Ma S-J, et al. Maternal autoimmune diseases and the risk of autism spectrum disorders in offspring: A systematic review and meta-analysis. Behavioural brain research. 2016;296:61–69.</li>\n <li>Chess S. Autism in children with congenital rubella. Journal of autism and childhood schizophrenia. 1971;1:33–47.</li>\n <li>Meyer U, Nyffeler M, Engler A, Urwyler A, Schedlowski M, Knuesel I, et al. The time of prenatal immune challenge determines the specificity of inflammation-mediated brain and behavioral pathology. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2006;26:4752–4762.</li>\n <li>Smith SEP, Li J, Garbett K, Mirnics K, Patterson PH. Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2007;27:10695–10702.</li>\n <li>Atladóttir HÓ, Thorsen P, Østergaard L, Schendel DE, Lemcke S, Abdallah M, et al. Maternal Infection Requiring Hospitalization During Pregnancy and Autism Spectrum Disorders. Journal of Autism and Developmental Disorders. 2010;40:1423–1430.</li>\n <li>Patterson PH. Maternal infection and immune involvement in autism. Trends in Molecular Medicine. 2011;17:389–394.</li>\n <li>Garay PA, Hsiao EY, Patterson PH, McAllister AK. Brain, Behavior, and Immunity Maternal immune activation causes age- and region-specific changes in brain cytokines in offspring throughout development. 2012</li>\n <li>Ashwood P, Van de Water J. Is autism an autoimmune disease? Autoimmunity reviews. 2004;3:557–562.</li>\n <li>Braunschweig D, Van de Water J. Maternal autoantibodies in autism. Archives of neurology. 2012;69:693–699.</li>\n <li>Fox E, Amaral D, Van de Water J. Maternal and fetal antibrain antibodies in development and disease. Developmental Neurobiology. 2012;72:1327–1334.</li>\n <li>Fox-Edmiston E, Van De Water J. Maternal Anti-Fetal Brain IgG Autoantibodies and Autism Spectrum Disorder: Current Knowledge and its Implications for Potential Therapeutics. CNS Drugs. 2015;29:715–724.</li>\n </ol>\n</blockquote>\n\n<p>In conclusion, they pointed out that Maternal autoantibody related (MAR) ASD:</p>\n\n<blockquote>\n <p>has been noted by numerous researchers describing the presence of maternal autoantibodies reactive to fetal brain proteins in a subset of mothers of children with ASD. Further, there is now an abundance of evidence supporting their deleterious role in neurodevelopment. For the most part, these studies have described similar experimental outcomes and, given the clinical and biological heterogeneity of ASD, there likely exists a complex relationship between the presence of maternal anti-fetal brain antibodies and developmental trajectory of exposed offspring. It is still unclear how and when these maternal autoantibodies arise, but studies currently underway may provide increased insight into their ontogeny.</p>\n</blockquote>\n\n<h2>Genes causing ASD</h2>\n\n<p>The <a href=\"http://www.nhs.uk/Conditions/Autistic-spectrum-disorder/Pages/Causes.aspx\" rel=\"nofollow noreferrer\">NHS webpage on Autism</a> states (Emphasis mine)</p>\n\n<blockquote>\n <p><strong>Most researchers believe</strong> that certain genes a child inherits from their parents could make them more vulnerable to developing ASD.</p>\n \n <p><strong>Cases of ASD have been known to run in families</strong>. For example, younger siblings of children with ASD can also develop the condition, and it's common for identical twins to both develop ASD.</p>\n \n <p><strong>No specific genes linked to ASD have been identified</strong>, but it may be a presenting feature of some rare genetic syndromes, including Fragile X syndrome, Williams syndrome and <a href=\"http://www.nhs.uk/conditions/angelman-syndrome/Pages/Introduction.aspx\" rel=\"nofollow noreferrer\">Angelman syndrome</a>.</p>\n</blockquote>\n\n<h2>Environmental causes</h2>\n\n<p>The <a href=\"http://www.nhs.uk/Conditions/Autistic-spectrum-disorder/Pages/Causes.aspx\" rel=\"nofollow noreferrer\">NHS say</a> that</p>\n\n<blockquote>\n <p><strong>Some researchers believe</strong> that a person born with a genetic vulnerability to ASD only develops the condition if they're exposed to a specific environmental trigger.</p>\n \n <p><strong>Possible triggers</strong> include being born prematurely (before 35 weeks of pregnancy), or being exposed in the womb to alcohol or to certain medication, such as sodium valproate (sometimes used to treat epilepsy during pregnancy).</p>\n \n <p><strong>No conclusive evidence has been found</strong> linking pollution or maternal infections in pregnancy with an increased risk of ASD.</p>\n</blockquote>\n\n<p>Research Autism has some referenced information on <a href=\"http://researchautism.net/autism/causes-of-autism\" rel=\"nofollow noreferrer\">leading research into the causes of Autism</a> from the Medical Research Council, National Autistic Society and the Autism Society of America; and the crux of the matter from what is said here is that the causes are still being investigated and</p>\n\n<blockquote>\n <p>There is no known single cause for autism, but it is generally accepted that it is caused by abnormalities in brain structure or function</p>\n</blockquote>\n\n<p>The site also provides a <a href=\"http://researchautism.net/autism/causes-of-autism/publications-on-causes-of-autism\" rel=\"nofollow noreferrer\">list of publications on the <strong>possible</strong> causes of Autism</a></p>\n\n<h2>References</h2>\n\n<p>Edmiston, E., Ashwood, P., &amp; Van de Water, J. (2017). Autoimmunity, autoantibodies, and autism spectrum disorder. <em>Biological psychiatry, 81</em>(5), 383-390. doi: <a href=\"https://doi.org/10.1016/j.biopsych.2016.08.031\" rel=\"nofollow noreferrer\">10.1016/j.biopsych.2016.08.031</a> Pubmed Central: <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5373490/\" rel=\"nofollow noreferrer\">PMC5373490</a></p>\n", "score": 4 } ]

[ "autoimmune-disease", "autism" ]

[ { "answer_id": 20093, "body": "<p>Generally, based on pharmacokinetics and safety or efficacy.</p>\n\n<p>Drugs are metabolized and eliminated from the body at some rate, with the rate and mechanism depending on the specific drug. Both <a href=\"https://en.wikipedia.org/wiki/Paracetamol\" rel=\"nofollow noreferrer\">acetaminophen</a> (Tylenol) and <a href=\"https://en.wikipedia.org/wiki/Ibuprofen\" rel=\"nofollow noreferrer\">ibuprofen</a> have a half-life of around 2-4 hours, for example, and take about 1 hour after oral administration to reach peak serum levels.</p>\n\n<p>Many drugs have side effects that get worse at higher doses. The key is not just the acute dose but how much of the drug is circulating at any given time.</p>\n\n<p>Looking for repeat dose PK measurements, the first study I came across happened to involve IV administration of acetaminophen in neonates every 6 hours:</p>\n\n<p><a href=\"https://i.stack.imgur.com/zQCTo.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/zQCTo.png\" alt=\"enter image description here\"></a></p>\n\n<p>(from Palmer, G. M., Atkins, M., Anderson, B. J., Smith, K. R., Culnane, T. J., McNally, C. M., ... &amp; Hunt, R. W. (2008). IV acetaminophen pharmacokinetics in neonates after multiple doses. British journal of anaesthesia, 101(4), 523-530.)</p>\n\n<p>You will see that at this frequency, the peak concentration levels off after a few doses and doesn't continue increasing.</p>\n\n<p>Other drugs are meant to deliver a roughly constant therapeutic effect (this is more relevant for long-term prescription medications, such as drugs to regulate blood pressure, hormonal birth control, etc), and the frequency of dosing is meant to keep the therapeutic effect within an appropriate range (with some balance for convenience). Missing a dose might even lead to a rebound effect and make a symptom worse.</p>\n\n<p>You are right, however, that the exact numbers are a bit fuzzy, both because different people metabolize a given drug at different rates and because there isn't some magic danger time: if a bottle of ibuprofen says every 4-6 hours, realistically there is not much difference if someone took a pill at 3 hours and 58 minutes after their last dose. The numbers printed on a label for an OTC drug are going to be safe for most people and indicate a dosing scheme that has been tested in clinical trials.</p>\n", "score": 4 } ]

[ "medications", "dosage" ]

[ { "answer_id": 20122, "body": "<p>Yes</p>\n\n<p>It’s zero.</p>\n\n<p>See: Doll, R., &amp; Hill, A. B. (1950). Smoking and carcinoma of the lung; preliminary report. <em>British medical journal</em>, 2(4682), 739–748. doi: <a href=\"https://doi.org/10.1136/bmj.2.4682.739\" rel=\"noreferrer\">10.1136/bmj.2.4682.739</a> pubmed central: <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2038856/\" rel=\"noreferrer\">PMC2038856</a></p>\n\n<p>And their follow up papers. And pretty much the entire medical literature on smoking. </p>\n", "score": 10 } ]

[ "alcohol", "smoking", "nicotine" ]

[ { "answer_id": 20128, "body": "<p>Urgent care is for things that your normal physician could treat, but you are outside their hours or unable to get an appointment within a reasonable time for the condition.</p>\n\n<p>Emergency rooms are for medical emergencies.</p>\n\n<hr>\n\n<p><strong>Examples of things that can be treated in Urgent Care (via the <a href=\"https://healthblog.uofmhealth.org/health-management/urgent-care-vs-emergency-room-whats-difference\" rel=\"nofollow noreferrer\">University of Michigan</a>)</strong>:</p>\n\n<p>Cold/flu, sprained ankle, broken bones in wrist/hand/ankle/foot without severe displacement or skin punctured, sore throat, nausea, minor cuts, eye/ear infection, minor burns</p>\n\n<hr>\n\n<p><strong>Things for which you should go to the ER (or better, call 911/emergency services)</strong>:</p>\n\n<p>Extremely high fever, severe trauma, broken bones severely displaced or puncturing skin, difficulty breathing, heart attack/stroke, uncontrolled bleeding, poisoning, major burns</p>\n\n<hr>\n\n<p>In summary, if you could die, go to the ER. If you have a non-life threatening acute medical issue, urgent care. If in question or unsure, go to the ER.</p>\n", "score": 5 }, { "answer_id": 25703, "body": "<p>Nice visual summary from the practice <a href=\"https://urgentcarelajolla.com/services/\" rel=\"nofollow noreferrer\">https://urgentcarelajolla.com/services/</a> (ER = Emergency Room):</p>\n<p><a href=\"https://i.stack.imgur.com/RmlJR.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/RmlJR.png\" alt=\"enter image description here\" /></a></p>\n", "score": 0 } ]

[ "emergency-room" ]

[ { "answer_id": 20253, "body": "<p>Vascular resistance in the skin is very closely related to temperature of both outside and body core. Vascular resistance in other body organs is not related to outside temp and the body core temp (37C IS correct) does not change much in absence of disease. \n Studies mentioned above do not imply a cause, only a statistical relationship. Lots of things change when weather gets cold. People cut firewood. Shovel snow. Stay inside and get respiratory diseases. Drink more alcohol. So since these correlational studies don't explain or connect to a cause, you can make up whatever link you want. Maintaining body temperature being hard on the heart doesn't make sense, because core temp is not regulated by the heart, and generating heat is not particularly burdensome to the heart. </p>\n", "score": 2 }, { "answer_id": 20249, "body": "<p>The common consensus seems to be that in cold weather the heart must work harder to maintain the body temperature, and that the arteries contract to save energy, which leads to an increased rate of heart attacks.</p>\n<blockquote>\n<p>'In discussing the weather-heart attack connection, study leader David Erlinge, a professor of cardiology, said cold and windy weather “leads to a contraction of blood vessels in the skin to conserve energy,” which increases the workload of the heart.'</p>\n</blockquote>\n<p>From:</p>\n<blockquote>\n<p><a href=\"https://www.drweil.com/health-wellness/body-mind-spirit/heart/does-cold-weather-cause-heart-attacks/\" rel=\"nofollow noreferrer\">https://www.drweil.com/health-wellness/body-mind-spirit/heart/does-cold-weather-cause-heart-attacks/</a></p>\n</blockquote>\n<p>A comprehensive study has been conducted on the link between the weather and heart attacks:</p>\n<blockquote>\n<p>'We’ve long known that heart attacks are more likely to occur during cold weather. The latest news about this comes from a large study in Sweden that examined every one of the 274,029 heart attacks that occurred in that country between 1998 and 2013 and correlated each one with weather data. This was the most comprehensive study ever performed on weather and heart attacks. The researchers, from Lund University, reported that low temperatures were most strongly associated with the incidence of heart attacks, although they also looked at the effects of other weather factors including the atmospheric pressure, wind velocity, and duration of sunshine on each day of the 16-year study. They reported that heart attack rates were highest in the north of Sweden, which is colder, snowier and windier than other areas. The team also looked at air pollution as a possible risk factor, collecting data on it in Sweden’s three major cities for every day of the study’s duration. They found no evidence that pollution influenced the weather-related findings.'</p>\n</blockquote>\n<p>and the paper referenced:</p>\n<blockquote>\n<p><a href=\"https://jamanetwork.com/journals/jamacardiology/article-abstract/2706610\" rel=\"nofollow noreferrer\">David Erlinge et al, “Association of Weather with Day-to-Day Incidence of Myocardial Infarction A SWEDEHEART Nationwide Observational Study.” JAMA Cardiology, October 24, 2018, doi:10.1001/jamacardio.2018.3466</a></p>\n</blockquote>\n<p>A synopsis of the above paper is here:</p>\n<blockquote>\n<p><a href=\"https://www.hcpfeed.com/2018/10/31/association-of-weather-with-day-to-day-incidence-of-myocardial-infarction/\" rel=\"nofollow noreferrer\">https://www.hcpfeed.com/2018/10/31/association-of-weather-with-day-to-day-incidence-of-myocardial-infarction/</a></p>\n<p>In 274 029 patients, mean (SD) age was 71.7 (12) years. Incidence of MI increased with lower air temperature, lower atmospheric air pressure, higher wind velocity, and shorter sunshine duration. The most pronounced association was observed for air temperature, where a 1-SD increase in air temperature (7.4°C) was associated with a 2.8% reduction in risk of MI (unadjusted incidence ratio, 0.972; 95% CI, 0.967-0.977; P &lt;.001). Results were consistent for non–ST-elevation MI as well as ST-elevation MI and across a large range of subgroups and health care regions.</p>\n</blockquote>\n", "score": 1 }, { "answer_id": 20262, "body": "<p>This is how exposure to cold can result in heart attack:</p>\n\n<ul>\n<li>Cold triggers the release of norepinephrine (noradrenaline), which results in constriction of blood vessels in the skin and thus in an <strong>increase of blood pressure.</strong></li>\n<li>The heart needs to work harder to pump blood against the increased blood pressure, so it <strong>uses more oxygen.</strong></li>\n<li>In individuals with coronary atherosclerosis, the limited blood flow may not be able to deliver enough oxygen to meet increased heart oxygen demand, which results in pain (angina pectoris) or in <strong>ischemic damage of the heart muscle (myocardial infarction).</strong> </li>\n</ul>\n\n<p>The study below has shown that the described mechanism is harmful only for \"cold-intolerant\" patients with prolonged high blood pressure response, while in \"cold-tolerant\" patients, the heart rate can quickly decrease and thus normalize the blood pressure. </p>\n\n<p><a href=\"https://www.sciencedirect.com/science/article/pii/0735109794907471?via%3Dihub\" rel=\"nofollow noreferrer\">Mechanisms of cold intolerances in patients with angina (Journal of the American College of Cardiology, 1994)</a>:</p>\n\n<blockquote>\n <p>Seven cold-intolerant and seven cold-tolerant patients with angina\n underwent exercise treadmill testing at 6 and 25 °C with measurement\n of catecholamines. Baroreceptor function was assessed by the decrease\n in systolic blood pressure after patients stood up from the supine\n position.</p>\n \n <p><strong>Norepinephrine levels increased by 139% in the cold environment,</strong> but there were no differences between cold-intolerant and\n cold-tolerant patients. Consequently, <strong>blood pressure was higher in\n the cold environment</strong> in all patients, but the heart rate was\n similar. However, cold-intolerant patients had a steeper heart rate\n response in the cold and developed ischemia.</p>\n \n <p>Exposure to cold causes an increase in blood pressure with an\n associated increase in myocardial oxygen demand in all patients. In\n cold-tolerant patients, this increase may be offset by a reduction in\n heart rate if baroreceptor function is normal. If baroceptor function\n is abnormal, heart rate may not decrease in response to a cold-induced\n increased in pressure.</p>\n</blockquote>\n\n<p><strong>In conclusion,</strong> exposure to cold can cause heart attack because of increased blood pressure, not thermogenesis. It's unlikely that cold exposure, as expected in everyday environment, would cause heart attack in otherwise healthy individuals, and even in those with coronary atherosclerosis it would more likely cause pain (angina pectoris) rather than the actual heart attack (myocardial infarction). </p>\n", "score": 0 } ]

[ "heart-attack" ]

[ { "answer_id": 20265, "body": "<p>Telemedicine is still health care; health care is highly regulated, and regulations and licensing vary on a country-by-country and state-by-state basis (and perhaps to more local levels, as well). A doctor licensed to practice in, say, the UK, can't practice medicine in the US without getting a license to do so.</p>\n<p>Some of the restrictions may be bypassed in the future by legislation that accounts for the potential of long-distance care, but on the other hand there may be significant safety concerns that are good reason to maintain the status quo.</p>\n<p>I'm not sure what the best sources are to explain this, so I'll just quote <a href=\"https://en.wikipedia.org/wiki/Telehealth#In_policy\" rel=\"noreferrer\">Wikipedia</a>:</p>\n<blockquote>\n<p>Restrictive licensure laws in the United States require a practitioner to obtain a full license to deliver telemedicine care across state lines. Typically, states with restrictive licensure laws also have several exceptions (varying from state to state) that may release an out-of-state practitioner from the additional burden of obtaining such a license. A number of states require practitioners who seek compensation to frequently deliver interstate care to acquire a full license.</p>\n<p>...</p>\n<p>More specific and widely reaching laws, legislations and regulations will have to evolve with the technology. They will have to be fully agreed upon, for example, will all clinicians need full licensing in every community they provide telehealth services too, or could there be a limited use telehealth licence? Would the limited use licence cover all potential telehealth interventions, or only some? Who would be responsible if an emergency was occurring and the practitioner could not provide immediate help – would someone else have to be in the room with the patient at all consult times? Which state, city or country would the law apply in when a breach or malpractice occurred? [99][122]</p>\n<p>A major legal action prompt in telehealth thus far has been issues surrounding online prescribing and whether an appropriate clinician-patient relationship can be established online to make prescribing safe, making this an area that requires particular scrutiny.[98] It may be required that the practitioner and patient involved must meet in person at least once before online prescribing can occur, or that at least a live-video conference must occur, not just impersonal questionnaires or surveys to determine need.[123]</p>\n</blockquote>\n", "score": 6 } ]

[ "health-policy" ]

[ { "answer_id": 20579, "body": "<p>Malassezia overgrowth is thought be the cause of most cases of dandruff (1) and rotating treatments avoids the development of resistance. However, some have argued that overgrowth of Malassezia is a result rather than a cause of dandruff (2).</p>\n\n<p>1 - <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869</a></p>\n\n<p>2 - <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887514\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887514</a></p>\n", "score": 3 }, { "answer_id": 20594, "body": "<p>Currently, there seems to be no convincing evidence to say that alternating between shampoos prolongs their effectiveness in treating dandruff.</p>\n\n<p><strong>1)</strong> According to <a href=\"https://ec.europa.eu/health/archive/ph_risk/committees/sccp/documents/out181_en.pdf\" rel=\"nofollow noreferrer\">the Scientific Committee on Cosmetic Products and Non-food Products Intended for Consumers by European Commission, 2012</a>:</p>\n\n<blockquote>\n <p>There is at present no scientific evidence of development of\n resistance or cross-resistance of fungi to Ketoconazole, if\n Ketoconazole is used in cosmetic dandruff shampoo at concentrations up\n to 2 %.</p>\n</blockquote>\n\n<p><strong>2)</strong> <a href=\"https://www.drugs.com/monograph/nizoral-topical.html\" rel=\"nofollow noreferrer\">Drugs.com, 2019</a> and <a href=\"https://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019927s031lbl.pdf\" rel=\"nofollow noreferrer\">FDA.gov, 2012</a> also do not mention any resistance to ketoconazole topical.</p>\n\n<p><strong>3)</strong> In <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5442545/\" rel=\"nofollow noreferrer\">this 2017 study</a>, (<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5442545/figure/F2/?report=objectonly\" rel=\"nofollow noreferrer\">Fig 2</a>), they've observed that some strains of Malassezia fungi are resistant to ketoconazole, but this seems to be intrincis resistance, not the one that develops with repeated use, so alternating between shampoos would not work.</p>\n\n<p><strong>4)</strong> <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579488/\" rel=\"nofollow noreferrer\">One source</a> suggests that some people with seborrheic dermatitis can be resistant to topical treatments:</p>\n\n<blockquote>\n <p>For patients with persistent SD resistant to topical agents, oral\n antifungals may be an option. Oral itraconazole given in a dose of\n 200mg/day for one week, followed by a maintenance dose, resulted in\n clinical improvement of SD symptoms in two open-label trials.</p>\n</blockquote>\n\n<p>...but again, alternating shampoos here would not likely help.</p>\n\n<p><strong>5)</strong> Several comprehensive review articles about <strong>treatment of dandruff</strong> do not even mention \"resistance\" to anti-dandruff shampoos or the need for \"alternation\" of shampoos:</p>\n\n<ul>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887514/\" rel=\"nofollow noreferrer\">DANDRUFF: THE MOST COMMERCIALLY EXPLOITED SKIN DISEASE (Indian Journal of Dermatology, 2010)</a></li>\n<li><a href=\"https://www.aafp.org/afp/2000/0501/p2703.html\" rel=\"nofollow noreferrer\">Treatment of Seborrheic Dermatitis (American Family Physician, 2000)</a></li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4852869/\" rel=\"nofollow noreferrer\">Seborrheic Dermatitis and Dandruff: A Comprehensive Review (Journal of Clinical and Investigative Dermatology, 2015)</a></li>\n<li><a href=\"https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/cfrsearch.cfm?cfrpart=358&amp;showfr=1&amp;subpartnode=21:5.0.1.1.30.8\" rel=\"nofollow noreferrer\">Drug Products for the Control of Dandruff, Seborrheic Dermatitis, and Psoriasis (U.S. Food and Drug Administration, 2019)</a></li>\n<li><a href=\"https://www.uspharmacist.com/article/is-it-dandruff-or-seborrheic-dermatitis\" rel=\"nofollow noreferrer\">Is It Dandruff or Seborrheic Dermatitis? (U.S. Pharmacist, 2013)</a></li>\n</ul>\n\n<p><strong>6)</strong> <a href=\"https://www.worldscientific.com/doi/abs/10.1142/9789814354868_0032\" rel=\"nofollow noreferrer\">Another source</a> claims that a combination, but not alternation, of substances could be used to circumverent resistance: </p>\n\n<blockquote>\n <p>Cosmetic and personal care products (anti-acne, anti-dandruff,\n anti-odorant, prickly heat talc, etc) use synthetic antimicrobials\n like Triclosan, Farnesol, Zinc Pyrithione etc or herbal extracts for\n the anti-microbial 'functional' benefit. The use of single\n anti-microbial agent would pave way for emergence of resistance in the\n cosmetically significant skin micro-organisms. To combat the\n development of resistance and deliver the anti-microbial benefit, a\n combination of synergistic antimicrobials can be used.</p>\n</blockquote>\n\n<hr>\n\n<p>A couple of sources recommend alternating shampoos, but without any argumentation:</p>\n\n<p><a href=\"https://www.mayoclinic.org/diseases-conditions/dandruff/diagnosis-treatment/drc-20353854\" rel=\"nofollow noreferrer\">Mayo Clinic</a>:</p>\n\n<blockquote>\n <p>If one type of shampoo works for a time and then seems to lose its\n effectiveness, try alternating between two types of dandruff shampoos.</p>\n</blockquote>\n\n<p><a href=\"https://health.students.vcu.edu/media/student-affairs/ushs/docs/SEBORRHEICDERMATITIS.pdf\" rel=\"nofollow noreferrer\">Virginia Commonwealth University</a>:</p>\n\n<blockquote>\n <p>Alternating medicated shampoos on a daily basis may also increase\n their effectiveness (eg, ketoconazole on Monday, zinc on Tuesday,\n selenium on Wednesday, tar on Thursday, etc).</p>\n</blockquote>\n", "score": 2 } ]

[ "dermatology", "hair", "scalp", "dandruff", "shampoo" ]

[ { "answer_id": 20709, "body": "<p>\"Chronic inflammatory response syndrome\" (CIRS) is a new term for what was (and still is) known as sick building syndrome or building-related illness. Hypersensitivity pneumonitis seems to be a similar condition.</p>\n\n<p><strong>Chronic Inflammatory Response Syndrome (CIRS)</strong></p>\n\n<p>According to how <a href=\"https://www.nihadc.com/health-programs/chronic-inflammatory-response-syndrome-cirs.html\" rel=\"nofollow noreferrer\">National Integrated Health Associates (NIHA)</a> describes symptoms of CIRS, the condition seems to be very similar to sick building syndrome.</p>\n\n<p>Shoemaker et al in this paper <a href=\"https://www.survivingmold.com/docs/POA_MOLD_7_27_10_final.pdf\" rel=\"nofollow noreferrer\">Research Committee Report on Diagnosis and Treatment of Chronic Inflammatory Response Syndrome Caused by Exposure to the Interior Environment of Water-Damaged Buildings</a>, refer to sick building syndrome several times. All the references about the treatment lead only to Shoemaker and the co-authors. CIRS is not mentioned in the <a href=\"https://www.icd10data.com/search?s=%22chronic%20inflammatory%20response%20syndrome%22\" rel=\"nofollow noreferrer\">International Classification of Diseases (ICD-10)</a>.</p>\n\n<p><strong>Sick building syndrome</strong></p>\n\n<p>Sick building syndrome is still an officially recognized health condition by several health-related authorities:</p>\n\n<ul>\n<li><a href=\"https://www.cdc.gov/niosh/nioshtic-2/20031618.html\" rel=\"nofollow noreferrer\">The National Institute for Occupational Safety and Health (NIOSH), 2006</a></li>\n<li><a href=\"https://www.osti.gov/biblio/962711-quantification-association-ventilation-rates-sick-building-syndrome-symptoms\" rel=\"nofollow noreferrer\">U.S. Department of Energy Office of Scientific and Technical Information (OSTI), 2009</a></li>\n<li><a href=\"https://www.epa.gov/sites/production/files/2014-08/documents/base_3c2o2.pdf\" rel=\"nofollow noreferrer\">Environmental Protection Agency (EPA), 2002</a></li>\n<li>In the 2020 version of International Classification of Diseases (ICD-10), it is mentioned under the code <a href=\"https://icdlist.com/icd-10/Z57.39\" rel=\"nofollow noreferrer\">Z57.39 (Occupational exposure to other air contaminants)</a></li>\n</ul>\n\n<p>Articles:</p>\n\n<ul>\n<li><a href=\"https://www.sciencedirect.com/science/article/pii/S0140673696072200?via%3Dihub\" rel=\"nofollow noreferrer\">Sick Building Syndrome (The Lancet, 1997)</a> (On Science Direct)</li>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796751/\" rel=\"nofollow noreferrer\">The sick building syndrome (Indian Journal Of Occupational &amp; Environmental Medicine, 2009)</a></li>\n</ul>\n\n<p>The term is used when the <em>cause in a specific case is not known;</em> contaminants may include molds, other microbes, pollens, motor vehicle and building exhausts, etc. <strong>Symptoms</strong> may include headache, irritation of the eyes, nose or throat, dry cough, dry or itchy skin, dizziness, nausea, difficulty in concentrating, fatigue and sensitivity to odors (<a href=\"https://www.epa.gov/sites/production/files/2014-08/documents/sick_building_factsheet.pdf\" rel=\"nofollow noreferrer\">EPA.gov, 1991</a>).</p>\n\n<p>In most articles about sick building syndrome, there is no specific diagnostic or treatment protocol mentioned, but preventative measures, such as the removal from exposure and renovating the building, are suggested.</p>\n\n<p><strong>Building-related illness</strong></p>\n\n<p>According to <a href=\"https://www.msdmanuals.com/professional/pulmonary-disorders/environmental-pulmonary-diseases/building-related-illnesses?query=Building-Related%20Illnesses\" rel=\"nofollow noreferrer\">MSD Manual, 2018</a>, building-related illness is the term that is replacing the term sick building syndrome; symptoms listed are about the same. <a href=\"https://www.uptodate.com/contents/building-related-illness-and-building-related-symptoms\" rel=\"nofollow noreferrer\">UpToDate</a> suggests that the term should be used when it is associated with a <em>specific</em> illness.</p>\n\n<p><strong>Hypersensitivity Pneumonitis (Extrinsic Allergic Alveolitis)</strong></p>\n\n<p>According to <a href=\"https://www.msdmanuals.com/professional/pulmonary-disorders/interstitial-lung-diseases/hypersensitivity-pneumonitis\" rel=\"nofollow noreferrer\">MSD Manual</a>:</p>\n\n<blockquote>\n <p>Hypersensitivity pneumonitis is a syndrome of cough, dyspnea, and\n fatigue caused by sensitization and subsequent hypersensitivity to\n environmental (frequently occupational) antigens.</p>\n</blockquote>\n\n<p>..which may be similar to conditions described above, but with causes including outdoor contaminants (molds, industrial gases, etc.) and with inflammation limited to the lungs. A clear diagnosis can be made with the help of imaging tests, bronchoalveolar lavage, etc, and treatment is with corticosteroids.</p>\n\n<p>In <strong>summary,</strong> indoor molds could cause inflammation in the body, but except in hypersensitivity pneumonitis, there seems to be no well referenced diagnostic or treatment protocols. Symptoms seem to be reversible and may resolve spontaneously after removal from exposure. </p>\n", "score": 3 } ]

[ "research", "toxins", "mold" ]

[ { "answer_id": 20868, "body": "<p>The act of urination goes like this (<a href=\"https://www.visiblebody.com/learn/urinary/urine-storage-and-elimination\" rel=\"nofollow noreferrer\">Visible Body</a>):</p>\n\n<blockquote>\n <p>Micturition, or urination, is the act of emptying the bladder. When\n the bladder is full of urine, stretch receptors in the bladder wall\n trigger the micturition reflex. The <strong>detrusor muscle</strong> that surrounds\n the bladder <strong>contracts.</strong> <strong>The internal urethral sphincter\n relaxes,</strong> allowing for urine to pass out of the bladder into the\n urethra. Both of these reactions are involuntary. <strong>The external\n urethral sphincter</strong> is voluntary. It must be <strong>relaxed</strong> for urine to\n flow through the urethra and outside the body.</p>\n</blockquote>\n\n<p><a href=\"https://i.stack.imgur.com/TTbzi.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/TTbzi.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Picture: Bladder anatomy (source: <a href=\"https://commons.wikimedia.org/wiki/File:Illu_bladder.jpg\" rel=\"nofollow noreferrer\">Wikipedia</a>, creative commons license)</p>\n\n<p>So, to urinate, <em>normally,</em> all you need to do is to relax the external urethral sphincter. Sometimes, urination can spontaneously stop even if there is still some urine in the bladder; a common cause is <em><a href=\"https://www.webmd.com/men/prostate-enlargement-bph/features/enlarged-prostate-bph-complex-problem#1\" rel=\"nofollow noreferrer\">enlarged prostate</a></em> - it often enlarges with age. In this case, pressing on the prostate can remove the remaining urine. Also, it is possible to close the external urethral sphincter more consciously and thus prevent the leak of the remaining urine. The problem with the leak at the end may be relying on the external urethral sphincter to close by itself quickly, while it may need some time to do so if you don't think on it... </p>\n", "score": 4 }, { "answer_id": 20860, "body": "<p>There's no extra muscle involved - it's like squeezing an almost-empty toothpaste tube to get the last bits of toothpaste out.</p>\n", "score": 1 } ]

[ "urine" ]

[ { "answer_id": 20895, "body": "<p><a href=\"https://www.ncbi.nlm.nih.gov/m/pubmed/3015171/\" rel=\"noreferrer\">Ethanol is caloric</a> and is neither a carbohydrate, protein, or fat. </p>\n", "score": 11 }, { "answer_id": 23106, "body": "<p>A calorie is a measure of heat given off by burning a substance.</p>\n\n<p>This article shows the origin of the term in the context of nutrition <a href=\"https://academic.oup.com/jn/article/136/12/2957/4663943\" rel=\"nofollow noreferrer\">https://academic.oup.com/jn/article/136/12/2957/4663943</a> </p>\n\n<p>One of the earlier uses of the term in a physiological metabolic context, as apposed to a physics context, was in a paper by a German scientist named J. R. Mayer. The Mayer quote shows an early use of the definition that comes up in nutrition classes. </p>\n\n<p>\"When substances endowed with considerable chemical affinity for each other combine chemically, much heat is developed during the process. We shall estimate the quantity of heat thus set free by the number of kilogrammes of water which it would heat 1°C. The quantity of heat necessary to raise 1 kilogramme of water 1 degree is called a unit of heat, Calorie. \"</p>\n\n<p>A calorie itself is not something you ingest, and there's no Dietary Reference Intake <a href=\"https://ods.od.nih.gov/Health_Information/Dietary_Reference_Intakes.aspx\" rel=\"nofollow noreferrer\">https://ods.od.nih.gov/Health_Information/Dietary_Reference_Intakes.aspx</a> for it, unlike everything else on the nutrition facts label (maybe that's why it's in separate box). </p>\n\n<p>It's a measure of energy generation, so it depends on the individual process of how it's generated, and I'm not sure if the FDA bases their label's numbers off of cellular metabolic data using digestive enzymes and gut flora, they might use something like a butane torch. It might be a good idea to take the calorie number as a reference point when considering your own metabolism, and not as an exact quantity. Many things can affect someone's metabolism, its efficiency and its rate, at cellular and molecular levels (and above and below probably).</p>\n\n<p>If you're thinking in terms of this definition, anything that causes metabolic reaction that generates heat could be measured as a calorie. Ethanol burns in a lab, but whether or not it generates heat in your body when it's metabolized depends on its metabolic processes <a href=\"https://en.wikipedia.org/wiki/Ethanol_metabolism\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Ethanol_metabolism</a> . </p>\n\n<p>If you wanted to know what substances generate heat in the body in general, the answer might be in the field of bioenergetics <a href=\"https://en.wikipedia.org/wiki/Bioenergetics\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Bioenergetics</a> , but that would include cellular respiration as well as enzymatic processes as the wiki article says, so breathing and processing anything (including your own dead cells thru apoptosis, or any drug you take or xenobiotic substance that enters your body <a href=\"https://www.sciencedirect.com/science/article/pii/S1359644612000359\" rel=\"nofollow noreferrer\">https://www.sciencedirect.com/science/article/pii/S1359644612000359</a>) could be shown to have a caloric value. Nutritionists and food producers are mostly focused on the calories from catabolic metabolism <a href=\"http://www.cte.sfasu.edu/wp-content/uploads/2012/01/2_Principles_of_Digestion_and_Metabolism.html\" rel=\"nofollow noreferrer\">http://www.cte.sfasu.edu/wp-content/uploads/2012/01/2_Principles_of_Digestion_and_Metabolism.html</a> by specifically liver enzymes, of something absorbed through the intestines (different parts of the intestines absorb different things, and not all gets processed catabolically). </p>\n\n<p>The food/nutrition industries' use of \"calories\" is a weirdly specific definition that presents a narrow view of bioenergetics -- bodies are way more complex and unique!</p>\n", "score": 3 }, { "answer_id": 23101, "body": "<p>This is probably a bit of both.</p>\n\n<p>By this, I mean that ethanol does contain calories, 7 kcal per gram of alcohol.</p>\n\n<p>Fat is 9 kcal/g, carbs and protein are 4 kcal/g.</p>\n\n<p>It is also possible that the nutrition label itself is calculated incorrectly, probably by mistake. If you're really bothered by the discrepancy, you could reach out to the company.</p>\n\n<p>Likewise, the info in My Fitness Pal could be incorrectly cited as well. These tools should be used as a guideline, not as concrete fact. If something seems off, you are absolutely correct in questioning it! I've found that in My Fitness Pal, scanning the bar code is typically more accurate than searching for the product. You could also look for a second entry for the product you are searching for and seeing if that one makes more sense.</p>\n", "score": 1 } ]

[ "nutrition", "calories" ]

[ { "answer_id": 21048, "body": "<p>TL:DR: The job of the lymphatic system is to remove excess fluid generated during the course of normal blood circulation from extravascular tissue, and to fight infection. Anything that might increase this burden on the lymph nodes remaining post mastectomy (e.g. venipuncture, IVs, finger sticks, etc.) is discouraged.</p>\n<hr />\n<p>As most breast cancers (75%) occur in the upper outer quadrant of the breast, lymphatic drainage - and metastatic cancer cells - goes to the axillary nodes. Some, all, or none of the nodes are removed with the breast tissue, depending on the cancer and the surgeon. All lymph passes through lymph nodes, so when some are removed, the remaining nodes filter more fluid than normally.</p>\n<p>The arm on the mastectomy side is <strong>permanently</strong> off limits to any procedures (technically even blood pressure measurements) if any lymph nodes were removed during the mastectomy (they do not grow back), or if there as been radiation (which damages lymph nodes) to that side. That's because there are a reduced number of lymph nodes in the underarm area to handle the work of the lymphatic system for that arm, and doing anything which might stress the remaining nodes can cause permanent swelling of the arm (lymphedema.)</p>\n<blockquote>\n<p><a href=\"https://www.oncolink.org/frequently-asked-questions/cancers/blood-pressures-and-ivs-after-mastectomy\" rel=\"nofollow noreferrer\">The goal is to reduce your risk of developing lymphedema.</a> Having a mastectomy alone does not put you at risk for lymphedema. The risk comes when you have lymph nodes removed or damaged. If you had any of the following, you should take precautions to reduce your risk of lymphedema:</p>\n<p>-Removal of all lymph nodes in the underarm area, which is called an axillary node dissection<br />\n-Removal of a limited number of “key” lymph nodes from the underarm area, which is called sentinel lymph node biopsy<br />\n-Having radiation to the chest wall and armpit after surgery</p>\n</blockquote>\n<p>During routine admission to the hospital for something unrelated, if the patient has had a mastectomy or radiation, a brightly colored band is placed on the affected wrist to alert all staff to use the other side if there is a chance you may not be able to voice an opinion (e.g. in the OR or under sedation from pain meds).</p>\n<p>Lymphedema can occur any time after mastectomy, often in the first 5 years, but has occurred even up to 20 years later. Because lymphedema is such a problematic condition, anything to reduce the possibility of it developing is recommended, even if the probability is low.</p>\n<blockquote>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652571/\" rel=\"nofollow noreferrer\">Patients with lymphedema have chronic, progressive swelling, pain, recurrent infections, and significantly decreased quality of life.</a> The swelling can progress to gigantic proportions causing gross disfigurement with severe detrimental effects. In addition, lymphedema is a significant source of biomedical expenditures with one recent study demonstrating a more than $10,000 increase in the annual treatment costs of cancer survivors with lymphedema as compared with those without lymphedema6.</p>\n<p>Treatment for lymphedema remains suboptimal and is, in most cases palliative with a goal of preventing disease progression rather than a cure. Medical and surgical treatments have been reported but in general these therapies have been disappointing...</p>\n</blockquote>\n<p>There is no way to know who will develop lymphedema and who will not. The greater the number of axillary lymph nodes removed, the greater the chance of lympedema, but even people with as few as 2 nodes removed have developed it. Therefore, with or without strong supporting evidence, an abundance of caution is advised, as lymphedema is such a terrible post-operative complication.</p>\n", "score": 5 } ]

[ "blood-tests" ]

[ { "answer_id": 24280, "body": "<p>According to <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1115047/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1115047/</a> a hymen appears to be absent in &lt; 0.03% patients (citation of a much older paper: <a href=\"https://pubmed.ncbi.nlm.nih.gov/3627892/\" rel=\"nofollow noreferrer\">https://pubmed.ncbi.nlm.nih.gov/3627892/</a>).</p>\n", "score": 2 } ]

[ "health-education", "physiology", "reference-request" ]

[ { "answer_id": 21202, "body": "<p>Although the latter term is less publicized in the mass media, <a href=\"https://www.who.int/emergencies/diseases/novel-coronavirus-2019/technical-guidance/naming-the-coronavirus-disease-(covid-2019)-and-the-virus-that-causes-it\" rel=\"nofollow noreferrer\">a WHO page</a> basically calls it official too, although it was the <a href=\"https://en.wikipedia.org/wiki/International_Committee_on_Taxonomy_of_Viruses\" rel=\"nofollow noreferrer\">ICTV</a> that came up with it:</p>\n<blockquote>\n<p>Viruses are named based on their genetic structure to facilitate the development of diagnostic tests, vaccines and medicines. Virologists and the wider scientific community do this work, so viruses are named by the International Committee on Taxonomy of Viruses (ICTV).</p>\n<p>Diseases are named to enable discussion on disease prevention, spread, transmissibility, severity and treatment. Human disease preparedness and response is WHO’s role, so diseases are officially named by WHO in the International Classification of Diseases (ICD).</p>\n<p>ICTV announced “severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)” as the name of the new virus on 11 February 2020. This name was chosen because the virus is genetically related to the coronavirus responsible for the SARS outbreak of 2003. While related, the two viruses are different.</p>\n<p>WHO announced “COVID-19” as the name of this new disease on 11 February 2020, following guidelines previously developed with the World Organisation for Animal Health (OIE) and the Food and Agriculture Organization of the United Nations (FAO).</p>\n<p>WHO and ICTV were in communication about the naming of both the virus and the disease.</p>\n</blockquote>\n<p>So yeah, the two names originate from different organizations (as far as I can tell the ICTV is not subordinated to the WHO in any way), but they apparently held some talks on the matter. Nonetheless, the WHO does seem a little displeased with including &quot;SARS&quot; in the virus name...</p>\n<blockquote>\n<p>From a risk communications perspective, using the name SARS can have unintended consequences in terms of creating unnecessary fear for some populations, especially in Asia which was worst affected by the SARS outbreak in 2003.</p>\n<p>For that reason and others, WHO has begun referring to the virus as “the virus responsible for COVID-19” or “the COVID-19 virus” when communicating with the public. Neither of these designations are intended as replacements for the official name of the virus as agreed by the ICTV.</p>\n</blockquote>\n<p>Likewise, some virologists <a href=\"https://www.sciencemag.org/news/2020/02/bit-chaotic-christening-new-coronavirus-and-its-disease-name-create-confusion\" rel=\"nofollow noreferrer\">were displeased</a> with the WHO name. In the later published SARS-CoV-2 <a href=\"https://www.nature.com/articles/s41564-020-0695-z\" rel=\"nofollow noreferrer\">(naming) paper</a> of ICTV's CSG (<em>Coronaviridae</em> Study Group) they do &quot;mend fences&quot; however, saying that:</p>\n<blockquote>\n<p>By uncoupling the naming conventions used for coronaviruses and the diseases that some of them cause in humans and animals, we wish to support the WHO in its efforts to establish disease names in the most appropriate way. [...] The further advancement of naming conventions is also important because the ongoing discovery of new human and animal viruses by next-generation sequencing technologies can be expected to produce an increasing number of viruses that do not (easily) fit the virus–disease model that was widely used in the pre-genomic era [...]. Having now established different names for the causative virus (SARS-CoV-2) and the disease (COVID-19), the CSG hopes that this will raise awareness in both the general public and public health authorities regarding the difference between these two entities. The CSG promotes this clear distinction because it will help improve the outbreak management and also reduces the risk of confusing virus and disease, as has been the case over many years with SARS-CoV (the virus) and SARS (the disease).</p>\n</blockquote>\n", "score": 3 } ]

[ "terminology", "virus" ]

[ { "answer_id": 22928, "body": "<p>If you want clear scientific evidence on this (effectiveness of masks use in the general public), I think there's <a href=\"https://medicalsciences.stackexchange.com/a/21698/10980\">no such study</a> out, although there is some data pointing toward a combination of masks and hand hygiene being sometimes effective (the effect size might no be large though given the lack of uniform results even on this \"combo\").</p>\n\n<p>As far guidelines go, the Lancet has a <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/32203710\" rel=\"nofollow noreferrer\">mini survey</a> of the varying stance of various government and health authorities as of March 20.</p>\n\n<p>There are also some <a href=\"https://www.bbc.com/news/world-us-canada-52126183\" rel=\"nofollow noreferrer\">recent developments</a> regarding the stance of the US gov't and CDC:</p>\n\n<blockquote>\n <p>One internal memo for the Centers for Disease Control and Prevention says that even simple cloth masks could help reduce the risk of virus transmission, the Washington Post reports.</p>\n</blockquote>\n\n<p>It's also clear the prior CDC stance was substantially influenced by the shortage affecting medical professionals:</p>\n\n<blockquote>\n <p>Dr Fauci told CNN he would \"lean towards\" recommending a \"much more broad, community-wide use of masks outside of the health care setting\" once there was a sufficient supply of masks for healthcare workers.</p>\n</blockquote>\n\n<p>Prior CDC (2009) [pandemic] recommendations, do/did include respirators for vulnerable populations, <em>when no alternatives exist</em>, like simply them avoiding a \"crowded setting\" (see table/image below). I'll also emphasize from there that with respect to inhalation, a distinction (of degree of protection) can made between masks and respirators:</p>\n\n<blockquote>\n <p>The optimal use of respirators requires fit testing, training and medical clearance. Proper use is recommended to maximize effectiveness. The use of facemasks may be considered as an alternative to respirators, although they are not as effective as respirators in preventing inhalation of small particles, which is one potential route of influenza transmission. There is limited evidence available to suggest that use of a respirator without fit-testing may still provide better protection than a facemask against inhalation of small particles. Respirators are not recommended for children or persons who have facial hair.</p>\n</blockquote>\n\n<p><a href=\"https://i.stack.imgur.com/UxGl4.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/UxGl4.png\" alt=\"enter image description here\"></a></p>\n", "score": 1 } ]

[ "covid-19", "epidemiology", "face-mask-respirator", "guidelines", "prophylaxis" ]

[ { "answer_id": 21403, "body": "<p>I doubt we have data to answer this question but since flu like illnesses keep recurring year after year as the virus mutates then it seems unlikely that exposure to something which most people get has had any benefit to those being exposed to the novel coronavirus SARS-CoV-2.</p>\n<blockquote>\n<p>In general, estimates suggest that 2% of the population are healthy carriers of a CoV and that these viruses are responsible for about 5% to 10% of acute respiratory infections.[3]</p>\n<p>Common human CoVs: HCoV-OC43, and HCoV-HKU1 (betaCoVs of the A lineage); HCoV-229E, and HCoV-NL63 (alphaCoVs). They can cause common colds and self-limiting upper respiratory infections in immunocompetent individuals. In immunocompromised subjects and the elderly, lower respiratory tract infections can occur.</p>\n<p>Other human CoVs: SARS-CoV, SARS-CoV-2, and MERS-CoV (betaCoVs of the B and C lineage, respectively). These cause epidemics with variable clinical severity featuring respiratory and extra-respiratory manifestations. Concerning SARS-CoV, MERS-CoV, the mortality rates are up to 10% and 35%, respectively.</p>\n</blockquote>\n<p>Furthermore, the fact that there have been no or near no deaths amongst children raises the speculative possibility that previous exposure might make the illness worse since children have fewer years of exposure to seasonal coronaviruses.</p>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/books/NBK554776/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/books/NBK554776/</a></p>\n", "score": 2 } ]

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

[ { "answer_id": 23247, "body": "<p>The current <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/hcp/disposition-in-home-patients.html\" rel=\"nofollow noreferrer\">recommendations of the US Centers for Disease Control</a> (CDC) depend on whether testing is available and has been done. They offer two criteria, the first is non-test-based and the second is test-based.</p>\n\n<p>For persons who have not been tested, the recommended criteria are:</p>\n\n<blockquote>\n <p><strong>Persons with COVID-19 who have symptoms</strong> and were directed to care for\n themselves at home may discontinue isolation under the following\n conditions:</p>\n \n <ul>\n <li>At least 3 days (72 hours) have passed since recovery defined as resolution of fever without the use of fever-reducing medications and</li>\n <li>Improvement in respiratory symptoms (e.g., cough, shortness of breath); and,</li>\n <li>At least 7 days have passed since symptoms first appeared.</li>\n </ul>\n</blockquote>\n\n<p>For those who have been tested, the criteria are:</p>\n\n<blockquote>\n <p><strong>Persons who have COVID-19 who have symptoms</strong> and were directed to care\n for themselves at home may discontinue isolation under the following\n conditions:</p>\n \n <ul>\n <li>Resolution of fever without the use of fever-reducing medications and</li>\n <li>Improvement in respiratory symptoms (e.g., cough, shortness of breath) and</li>\n <li>Negative results of an FDA Emergency Use Authorized molecular assay for COVID-19 from at least two consecutive nasopharyngeal swab\n specimens collected ≥24 hours apart*** (total of two negative\n specimens). </li>\n </ul>\n \n <p>***All test results should be final before isolation is ended. Testing guidance is based upon limited information and is subject to change as\n more information becomes available.</p>\n</blockquote>\n\n<p>Keep in mind that COVID-19 is a new disease with many unknowns and therefore the recommendations above can and probably will change as more is learned, so anyone using this answer to make a decision should visit the CDC link I provided at the beginning of this answer before making that decision.</p>\n", "score": 3 }, { "answer_id": 21315, "body": "<p>Doctors apply a test kit, if you no longer have the virus you are typically released. However, in China some people who gave negative results were released and later they found they still had the virus, because the tests were poor quality or other factors, so now doctors are suggested to combine epidemiological history, clinical and imaging manifestations with the test. But when the doctor releases you, that's when you can socially interact again. </p>\n\n<p><a href=\"https://www.scmp.com/news/china/society/article/3065022/coronavirus-why-do-recovered-patients-test-positive-again\" rel=\"nofollow noreferrer\">Coronavirus why do recovered patients test positive again</a></p>\n", "score": 0 } ]

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

[ { "answer_id": 21399, "body": "<p>There's yet another reason: a test can provide only a certain amount of information gain. If the probability to have contracted Covid-19 before the test is too low, even though we know more after the test we may not be able to draw practical conclusions that are any different from the recommendations without test. In other words, if the recommendation goes from \"stay at home and avoid contact to others\" to \"stay at home and avoid contact to others\" the test would be wasted.</p>\n\n<p>The Covid-19 tests are not suitable for screening purposes (i.e. searching for infections among a population where infections are [still] very rare). They are to sort out who is infected and who isn't among high-risk populations where 1 in 10 (or more) are actually infected. </p>\n\n<hr>\n\n<p>You may want to look at <a href=\"https://medicalsciences.stackexchange.com/a/21379/11479\">my longish answer</a> to <a href=\"https://medicalsciences.stackexchange.com/q/21337/11479\">How accurate are coronavirus tests?</a> for relevant background.</p>\n\n<hr>\n\n<p>E.g., with the newly emergency approved Roche test, we may say that a positive test result increases the odds of having Covid-19 by factor of somewhere around 30 - 100, a negative result decreases the odds by a factor of 1/50 - 1/17. </p>\n\n<p>If you are in a risk group with a prevalence of 8 %, the pre-test odds of 8 : 92 </p>\n\n<ul>\n<li>increase to (240 to 800) : 92 or a post-test probability of having Covid-19 of 70 to 90 % with a positive test result, and</li>\n<li>decrease to 8 : (4600 to 1564), i.e. the post-test probability of having Covid-19 is somewhere around 0.5 to 0.2 %</li>\n</ul>\n\n<p>These post-test probabilities allow practical conclusions: if you're negative, you're fine and can be let to meet the public, if you're positive you need to go to quarantine and/or treatment. </p>\n\n<p>8 % prevalence is my guesstimate for those who are currently (Mar 15th) tested in the US (and incidentally, also in Germany).</p>\n\n<p>Now consider the overall US population. With currently <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/cases-in-us.html\" rel=\"nofollow noreferrer\">1629 cases</a> and a population of 328 mio., we'd get pre-test odds of 1629 : 328 mio*. </p>\n\n<p>The test results change this to </p>\n\n<ul>\n<li>positive result: (27700 to 162900) : 328 mio or a post-test probability of having Covid-19 of 0.008 to 0.005 %</li>\n<li>negative result: we don't even need to calculate this, because the pre-test probability was only 0.0005 %, post-test probability is lower.</li>\n</ul>\n\n<p>Even if we assume that there's a dark number of yet unknown Covid-19 cases, say, a factor 20 over the known cases, the post-test probabiliy after a positive test is about 0.2 % to 1%. </p>\n\n<p>What would be the practical conclusion? Well, probably that the positive case should stay at home as much as possible and avoid contacts. Certainly not that they can rely on acquiring immunity against SARS-CoV-2.</p>\n\n<p>Even for low risk groups who have flu-like symptoms but no known contact to Covid infected people (or other high-risk situations) the pre-test probability of having Covid is too low to allow the test to make a meaningful difference: after all, even if it is \"only a common flu\", they should stay at home, get well and not infect others meanwhile. \nWhile the pre-test probability is likely to increase (because more people get infected), in order to keep the health system/hospitals working the recommendation will probably not change: stay at home in self-quarantine as long as the symptoms are mild, so that the health system is not burdened by cases that get well on their own.</p>\n\n<p>We may also say that were the whole US population to be tested in that situation, the 32500 true cases of Covid would be drowned in 3 - 10 mio. false positve cases.</p>\n\n<hr>\n\n<p>*328 mio - 1629 ≈ 328 mio</p>\n", "score": 5 }, { "answer_id": 21326, "body": "<p>CDC guidelines for when patients should be tested have changed since the ones you list. <a href=\"https://emergency.cdc.gov/han/2020/han00429.asp?deliveryName=USCDC_511-DM22106\" rel=\"nofollow noreferrer\">CDC now says</a>:</p>\n<blockquote>\n<p>Clinicians should use their judgment to determine if a patient has signs and symptoms compatible with COVID-19 and whether the patient should be tested. Most patients with confirmed COVID-19 have developed fever1 and/or symptoms of acute respiratory illness (e.g., cough, difficulty breathing). Priorities for testing may include:</p>\n<p>Hospitalized patients who have signs and symptoms compatible with COVID-19 in order to inform decisions related to infection control.</p>\n<p>Other symptomatic individuals such as, older adults (age ≥ 65 years) and individuals with chronic medical conditions and/or an immunocompromised state that may put them at higher risk for poor outcomes (e.g., diabetes, heart disease, receiving immunosuppressive medications, chronic lung disease, chronic kidney disease).</p>\n<p>Any persons including healthcare personnel, who within 14 days of symptom onset had close contact with a suspect or laboratory-confirmed COVID-19 patient, or who have a history of travel from affected geographic areas (see below) within 14 days of their symptom onset.</p>\n</blockquote>\n<p>This is a broad definition that gives clinicians the freedom to judge, though it still emphasizes priority for cases similar to the older guidelines.</p>\n<p>However, guidelines and reality may not match. Via <a href=\"https://www.npr.org/sections/health-shots/2020/03/11/814189027/no-guarantee-youll-get-tested-for-covid-19-even-if-your-doctor-requests-it\" rel=\"nofollow noreferrer\">NPR</a>:</p>\n<blockquote>\n<p>There's still a big gap between what the federal government is promising and what state and local labs can deliver.</p>\n<p>...</p>\n<p>...those labs have a limited capacity to test, so some have been turning down doctors' requests.</p>\n<p>The novel coronavirus test isn't simple, like the ones for the flu, strep or pregnancy. The kits detecting the coronavirus are configured more for a research lab than a hospital — and certainly can't be run in a doctor's office. It takes four to six hours to perform the tests on patient samples.</p>\n</blockquote>\n<p>Therefore, at this point the main reason that people with symptoms are being denied tests seems to involve a shortage of the tests, and possibly prioritization of tests for other patients. Hopefully these problems will be resolved going forward.</p>\n", "score": 4 }, { "answer_id": 21402, "body": "<p>Because the USA has been extremely poorly prepared for this pandemic there has been a severe shortage of test kits. A number of other egregious errors were made including declining to accept the German test offered to them, or using the South Korean test kits. South Korea have been testing 10,000 people a day which is more than the USA has since the outbreak developed.</p>\n\n<p>In this situation the clinicians have triaged as much as they could to decide who to test developing an evolving set of clinical and epidemiological criteria which have loosened. But what they didn't know was that the virus been likely been circulating in the community for some weeks as community transmission was detected in late February.</p>\n\n<p>At this time the most appropriate response is to self isolate if one develops any respiratory symptoms, and advise close contacts. Because testing has been very limited it is nearly impossible to satisfy the epidemiological criterion of knowing about a contact with the disease. </p>\n\n<p><a href=\"https://www.nytimes.com/2020/03/10/us/coronavirus-testing-delays.html\" rel=\"nofollow noreferrer\">https://www.nytimes.com/2020/03/10/us/coronavirus-testing-delays.html</a></p>\n", "score": 1 }, { "answer_id": 21330, "body": "<p>If everyone would like to be tested who shows some symptoms of this infection you could test probably 50% of the population: <em>\"me too!\"</em> As the capacity of tests is limited it is really necessary that these test kits are reserved for persons that are diagnosed by a doctor. In case of a pandemia - and if this is one - people should keep distance to others, wash their hands and shouldn't go to work if they think they are infected. People with severe symptoms should stay at home and call the doctor and get information by phone. </p>\n\n<p>And save the disinfection solutions and masks for the doctors and medical staff and the ill people.</p>\n", "score": 0 }, { "answer_id": 21334, "body": "<p>Because the CDC won't let them test them. Understand that hospitals can't perform tests for Covid-19--originally only the CDC could. Now, some state laboratories can test. Either way, hospitals can't test people whom the labs don't allow testing for. It's not entirely the hospital's decision.</p>\n\n<p>Keep in mind that some of these restrictions are pretty common sense. For instance, some of these requirements restrict that if you have these symptoms, but we know you have the Flu (which has similar symptoms), then there's no reason to test you for Covid-19. It's pretty reasonable to assume that these symptoms are because of the Flu.</p>\n", "score": 0 } ]

[ "covid-19", "test" ]

[ { "answer_id": 21384, "body": "<p>Here's an <a href=\"https://www.theguardian.com/commentisfree/2020/mar/12/science-soap-kills-coronavirus-alcohol-based-disinfectants\" rel=\"noreferrer\">article</a> that I found helpful, to understand why washing hands with soap is so helpful, and how it helps (Pall Thordarson is a professor of chemistry at the University of New South Wales, Sydney):</p>\n\n<blockquote>\n <p>Why does soap work so well on the Sars-CoV-2, the coronavirus and\n indeed most viruses? The short story: because the virus is a\n self-assembled nanoparticle in which the weakest link is the lipid\n (fatty) bilayer. Soap dissolves the fat membrane and the virus falls\n apart like a house of cards and dies – or rather, we should say it\n becomes inactive as viruses aren’t really alive.</p>\n \n <p>The slightly longer story is that most viruses consist of three key\n building blocks: ribonucleic acid (RNA), proteins and lipids. A\n virus-infected cell makes lots of these building blocks, which then\n spontaneously self-assemble to form the virus. Critically, there are\n no strong covalent bonds holding these units together, which means you\n do not necessarily need harsh chemicals to split those units apart.\n When an infected cell dies, all these new viruses escape and go on to\n infect other cells. Some end up also in the airways of lungs.</p>\n \n <p>When you cough, or especially when you sneeze, tiny droplets from the\n airways can fly up to 10 metres. The larger ones are thought to be the\n main coronavirus carriers and they can go at least two metres.</p>\n \n <p>These tiny droplets end on surfaces and often dry out quickly. But the\n viruses remain active. Human skin is an ideal surface for a virus. It\n is “organic” and the proteins and fatty acids in the dead cells on the\n surface interact with the virus.</p>\n \n <p>When you touch, say, a steel surface with a virus particle on it, it\n will stick to your skin and hence get transferred on to your hands. If\n you then touch your face, especially your eyes, nostrils or mouth, you\n can get infected. And it turns out that most people touch their face\n once every two to five minutes.</p>\n \n <p>Washing the virus off with water alone might work. But water is not\n good at competing with the strong, glue-like interactions between the\n skin and the virus. Water isn’t enough.</p>\n \n <p>Soapy water is totally different. Soap contains fat-like substances\n known as amphiphiles, some of which are structurally very similar to\n the lipids in the virus membrane. The soap molecules “compete” with\n the lipids in the virus membrane. This is more or less how soap also\n removes normal dirt from the skin.</p>\n \n <p>The soap not only loosens the “glue” between the virus and the skin\n but also the Velcro-like interactions that hold the proteins, lipids\n and RNA in the virus together.</p>\n \n <p>Alcohol-based products, which pretty much includes all “disinfectant”\n products, contain a high-percentage alcohol solution (typically 60-80%\n ethanol) and kill viruses in a similar fashion. But soap is better\n because you only need a fairly small amount of soapy water, which,\n with rubbing, covers your entire hand easily. Whereas you need to\n literally soak the virus in ethanol for a brief moment, and wipes or\n rubbing a gel on the hands does not guarantee that you soak every\n corner of the skin on your hands effectively enough.</p>\n \n <p>So, soap is the best, but do please use alcohol-based sanitiser when\n soap is not handy or practical.</p>\n</blockquote>\n", "score": 7 }, { "answer_id": 21358, "body": "<p>Yes, the virus can be made un-harmful by soap and water. From the Economist:</p>\n\n<blockquote>\n <p>The outer proteins sit athwart a membrane provided by the cell in\n which the virion was created. This membrane, made of lipids, breaks up\n when it encounters soap and water, which is why hand-washing is such a\n valuable barrier to infection.</p>\n</blockquote>\n\n<p>This should give you enough key terms to read further about why this is effective.</p>\n", "score": 5 }, { "answer_id": 21345, "body": "<p>There are obvious sufficient data and enough evidence that all virus are transmitted by droplet infection (body contact) and shake hands. Washing hand makes sense as the infection is happening mostly yourself if you have contact with your hands in your face, mouth, nose, eyes.</p>\n\n<p>So don't shake hands, clean your hands by washing or desinfecting after touching the cars and bags in a supermarket or any other objects, as you can transport a virus with your hands in body openings - as everybody touches his face may be 100's of times a day unconsciously. </p>\n\n<p><a href=\"https://www.healthline.com/health-news/how-to-not-touch-your-face\" rel=\"nofollow noreferrer\">https://www.healthline.com/health-news/how-to-not-touch-your-face</a></p>\n\n<p>In normal times we can be overprotective to ourselves. \"More dirt\" could be an option or devise in education, but not in times when schools and kinder gardens have to be closed because of an epidemia or a pandemia. </p>\n\n<p><a href=\"https://www.medscape.com/viewarticle/926373\" rel=\"nofollow noreferrer\">https://www.medscape.com/viewarticle/926373</a></p>\n", "score": 4 }, { "answer_id": 21535, "body": "<p>\"Situations Leading to Reduced Effectiveness of Current Hand Hygiene against Infectious Mucus from Influenza Virus-Infected Patients\", a study published in \"MSphere\", compared using \"antiseptic hand rubbing\" (hand sanitizer) against \"antiseptic hand washing\" (washing hands with antiseptic or antimicrobial soap), and found that washing hands is effective at killing the Influenza A virus.</p>\n\n<p>\"Reducing viral contamination from finger pads: handwashing is more effective than alcohol-based hand disinfectants\", a study published in the \"Journal of Hospital Infection\", found that hand washing for 30 seconds is effective against MNV1 and noroviruses.</p>\n\n<p>\"Epidemiologic Background of Hand Hygiene and Evaluation of the Most Important Agents for Scrubs and Rubs\", a study published in \"Clinical Microbiology Reviews\", found that \"simple hand wash reveals the best results compared with other possible hand treatments\".</p>\n\n<p>I believe that these findings, plus other research, have been generalized to all viruses, including COVID-19.</p>\n", "score": 2 }, { "answer_id": 21581, "body": "<p>There is a report from Taiwan where it was described that installing hand wash stations in the emergency department was the only infection control measure which was significantly associated with the protection from healthcare workers from acquiring the SARS-CoV, indicating that hand hygiene can have a protective effect</p>\n<blockquote>\n<p>Healthcare workers are at risk of acquiring a SARS infection while caring for SARS patients. Many rational ICMs were implemented to protect HCWs during the panic of the SARS epidemic. For example, NPIR, PPE, and hand washing were all implemented by each hospital as required by the health department. However, nosocomial transmission still occurred despite the above-mentioned measures [1,5,6,14]. Yen et al. formulated the concept of traffic control, an integrated infection control strategy involving triaging patients (using barriers and zones of risk) and checkpoint spots for hand washing [7]. Traffic control was shown to significantly reduce the rate of SARs in HCWs (0.03 cases/bed vs HCWs in other hospitals 0.13 cases/bed) during the 3-week study period [7]. However, there were limitations in the study; the authors were unable to demonstrate that traffic control was the key factor in reducing the number of HCWs acquiring the SARS infection. Understanding the causal relationship is important to validate the effectiveness of each ICM among so many integrated measures.</p>\n<p>Our analysis showed that the timing of the ICM implementation was critically important. Hospitals in which HCW SARS transmission did not occur implemented ICM B earlier than those experiencing SARS transmission to HCWs (Figure 1). The hypothetical causal relationship model between the ICMs and the HCWs acquiring SARS was supported by our SEM analysis in which the following ICMs were the causes of preventing SARS transmission: traffic control in the ED (including triage on patients with fever of unknown aetiology, increasing installation of hand washing facilities in the ED, bleach disinfection performed after cross-contact in patient transfer, and mandatory body temperature surveillance), installation of a fever screening station outside the ED, availability of an outbreak standard operation protocol, mandatory body temperature surveillance in hospital, hand washing setup at each checkpoint in the hospital, standardized patient transfer procedure, availability of a simplified isolation room. It appears that successful control of SARS infection is not based on an individual measure, but on the integration of several measures.</p>\n<p>Installation of a fever screening station outside the ED was the most important factor, and contributed 51% of the effectiveness towards the prevention of SARs in HCWs. During the SARS epidemic, as patients overwhelmingly flooded into hospitals and caused chaos within the ED [6,18] it was rational for each hospital to screen the patients outside the hospital. The outside fever screening station was first developed by the Singaporeans [19]; this was done in accordance with the ancient concept of quarantine against the black plague during the 14th century. Our finding quantitatively validated this approach. The fever screening station acted as the security guard in the front line of protection.</p>\n<p>The second most important factor was the traffic control measures in the ED (19%). HCWs in the ED are at the front line of contact with SARS patients and the most likely to be infected [6,18,20]. The environmental survey also found a high sample positive rate for SARS coronavirus RNA in the ED [6]. Our finding validated the need to protect HCWs in the ED using traffic control, as this is an important factor for protecting all HCWs from hospital-acquired SARS. The retrospective observation also confirmed our finding that the nosocomial transmission of SARS in Taiwan declined significantly after the implementation of traffic control in the ED of hospitals as mandated by the Department of Health. By implementing traffic control in the ED, direct contact of SARS patients and contamination of the environment can be minimized by screening patients with fever, transferring and isolating patients, and disinfecting the environment.</p>\n<p>Hospital management is important since it affects the other factors associated with protecting HCWs from SARS, including availability of outbreak standard operation protocols (12%), mandatory body temperature surveillance in hospital (9%), hand washing setups at each checkpoint in hospital (3%), availability of a simplified isolation room (3%), and standardized patient transfer protocols (3%). During the SARS epidemic, body temperature measurement and hand washing were encouraged spontaneously, and the compliance rate was higher during the non-epidemic period. Standardized outbreak control and patient transfer procedures were part of the hospital standard operation protocols. Hospitals with better management are less likely to have HCWs acquiring SARS or any other nosocomial infections. The Six Sigma process may be implemented into the hospital infection control procedures to prevent further unknown infections [21–23].</p>\n</blockquote>\n<p><a href=\"https://www.journalofhospitalinfection.com/article/S0195-6701(20)30046-3/fulltext\" rel=\"nofollow noreferrer\">https://www.journalofhospitalinfection.com/article/S0195-6701(20)30046-3/fulltext</a></p>\n<p>Quantitative evaluation of infection control models in the prevention of nosocomial transmission of SARS virus to healthcare workers: Implication to nosocomial viral infection control for healthcare workers\n<a href=\"https://www.tandfonline.com/doi/full/10.3109/00365540903582400\" rel=\"nofollow noreferrer\">https://www.tandfonline.com/doi/full/10.3109/00365540903582400</a></p>\n", "score": 1 } ]

[ "virus", "disease-transmission", "covid-19", "hand", "hand-sanitizers" ]

[ { "answer_id": 21446, "body": "<p>\"data to date suggest that 80% of infections are mild or asymptomatic, 15% are severe infection, requiring oxygen and 5% are critical infections, requiring ventilation.\"</p>\n\n<p><img src=\"https://i.stack.imgur.com/h7Jp6.jpg\" alt=\"\"></p>\n\n<p><a href=\"https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200306-sitrep-46-covid-19.pdf?sfvrsn=96b04adf_2\" rel=\"nofollow noreferrer\">https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200306-sitrep-46-covid-19.pdf?sfvrsn=96b04adf_2</a></p>\n", "score": 3 } ]

[ "covid-19" ]

[ { "answer_id": 21656, "body": "<p>An early release paper dated 23 March 2020 is now staying that SARS-CoV-2 RNA has been recovered 17 days after both infected and asymptomatic presumed infected passengers left the cabins of the Diamond Pricess cruise ship.</p>\n\n<p>The discovery of virus on surfaces of asymptomatic passengers again demonstrates that viral shedding occurs in this phase in amounts sufficient to contaminate the environment.</p>\n\n<blockquote>\n <p>SARS-CoV-2 RNA was identified on a variety of surfaces in cabins of both symptomatic and asymptomatic infected passengers up to 17 days after cabins were vacated on the Diamond Princess but before disinfection procedures had been conducted (Takuya Yamagishi, National Institute of Infectious Diseases, personal communication, 2020). Although these data cannot be used to determine whether transmission occurred from contaminated surfaces, further study of fomite transmission of SARS-CoV-2 aboard cruise ships is warranted.</p>\n</blockquote>\n\n<p><a href=\"https://www.cdc.gov/mmwr/volumes/69/wr/mm6912e3.htm\" rel=\"nofollow noreferrer\">https://www.cdc.gov/mmwr/volumes/69/wr/mm6912e3.htm</a> \nPublic Health Responses to COVID-19 Outbreaks on Cruise Ships — Worldwide, February–March 2020 \nEarly Release / March 23, 2020 / 69</p>\n", "score": 2 } ]

[ "sars-cov-2" ]

[ { "answer_id": 21701, "body": "<p>Italy has 60 million people and around 70 thousand (known) cases. That's barely more than 1 in 1000 <a href=\"https://en.wikipedia.org/wiki/Prevalence\" rel=\"noreferrer\">prevalence</a>. For most countries it's less than this. So, you'd need a huge sample for a good estimate. And those tests/resources are better deployed where suspected cases are, for the time being.</p>\n<p>And sensible or not, I've heard this from a colleague, and it's <a href=\"https://www.nineoclock.ro/2020/03/26/pilot-project-for-testing-10500-people-in-bucharest-for-the-novel-coronavirus/\" rel=\"noreferrer\">confirmed</a> by the news that Romania's capital Bucharest plans to randomly test a sample of 10,500 people to determine the extent of the virus spread over there.</p>\n<blockquote>\n<p>Manager of the “Matei Bals” Infectious Diseases Institute Adrian Streinu-Cercel has announced that a pilot project for testing 10,500 persons for the novel coronavirus will start in Bucharest within a scientific study to detect those infected with SARS CoV-2 virus, from the desire to thus prevent the severe forms of illness.</p>\n<p>Streinu-Cercel mentioned that, for a population of approximately 2 million inhabitants, the testing of 9,558 persons is necessary, with a correction of 10% being applied to this number. He also stated that the sample can be resized along the way. In this regard, Streinu-Cercel referred to the recommendations of the World Health Organization, which asked that testing be conducted to detect COVID 19. The manager of the “Matei Bals” Institute showed that it is necessary to test the medical staff and patients, but also the population, in order to know if “it’s healthy, if it is currently infected or went through the infection” with this virus, these three pieces of information completely changing how this pandemic is approached in the near future. [...]</p>\n<p>Streinu-Cercel underscored that, in lack of screening, the mild forms can go undetected, generating subsequent forms of severe infections. He also mentioned that the Minister of Health approved this project and stressed that this is a study with “scientific value,” not a simple testing. At the same time, he mentioned that in Bucharest there are 188 people diagnosed positively.</p>\n</blockquote>\n<p>Note that ~200 cases in 2M is 1:10,000.</p>\n<p>Ha, ha, the more amusing part is that this <a href=\"https://www.romaniajournal.ro/society-people/pm-about-testing-10000-in-bucharest-for-covid-19-just-stories-testing-algorithm-updated-what-categories-take-priority/\" rel=\"noreferrer\">turned out</a> to be &quot;fake news!&quot; But it's actually informative to read the &quot;retraction/information&quot; as to why they are not actually doing such a study [obviously: insufficient testing capacity for the proposed sample.]</p>\n<blockquote>\n<p>After the manager of the “Matei Bals” Institute for Infectious Diseases, Adrian Streinu-Cercel and Bucharest mayor Gabriela Firea had announced on Thursday that 10,514 people from 5 different age groups in Bucharest will be tested for the novel Coronavirus, PM Ludovic Orban reacted and said this is not possible.</p>\n<p>“We cannot establish the people to be tested randomly. Selecting 10,000 are just stories, there is a priority list for testing, it depends on how the situation and the testing capacity are developing,” the PM told a conference at the Health Ministry’s HQs.</p>\n<p>Orban said that the medical staff and those targeted by the epidemiological inquiries are qualifying for testing first, adding that “Romania has not been ready and the testing capacity has been limited”.</p>\n<p>The premier said that “the testing capacity in Romania will increase up to 2,000 next week” and will gradually rise, but to select 10,000 people “are just stories”, the more the death toll has been low in Romania.</p>\n</blockquote>\n<p>In <a href=\"https://www.thehindubusinessline.com/news/icmr-500-random-tests-for-covid-19-come-up-negative/article31092901.ece\" rel=\"noreferrer\">older news</a> I see that India conducted a random test on 500 of their citizens. Rather predictably, they all came out negative.</p>\n<p>And for some more official objections of the same kind <a href=\"https://www.dw.com/en/germanys-coronavirus-response-separating-fact-from-fiction/a-53053822\" rel=\"noreferrer\">DW reported on Apr 7</a>...</p>\n<blockquote>\n<p>Germany's center for disease control, the Robert Koch Institute, has criticized Germany's methods of testing, complaining for example that too many asymptomatic individuals were being tested. The RKI called for an end to this practice on the grounds that <strong>Germany could risk running out of tests</strong>. Therefore, asymptomatic people are currently not being recommended for testing.</p>\n</blockquote>\n<p>By the way, if what you want to find out are the proportion of asymptomatic cases, there are some studies (albeit on fairly contained populations) that may have an answer to that, <a href=\"https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.10.2000180\" rel=\"noreferrer\">e.g. one</a> on the Diamond Princess (the cruise ship quarantined off Japan):</p>\n<blockquote>\n<p>[Overall:] Our estimated asymptomatic proportion is at 17.9% (95%CrI: 15.5–20.2%), which overlaps with a recently derived estimate of 33.3% (95% confidence interval: 8.3–58.3%) from data of Japanese citizens evacuated from Wuhan.</p>\n<p>[Caveat:] Considering that most of the passengers were 60 years and older, the nature of the age distribution may lead to underestimation if older individuals tend to experience more symptoms.</p>\n</blockquote>\n<p>From a <a href=\"https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.12.2000256\" rel=\"noreferrer\">2nd study</a> on the Diamond Princess, it's informative to read the testing strategy/order:</p>\n<blockquote>\n<p>Overall 3,063 PCR tests were performed among [the 3,711] passengers and crew members. Testing started among the elderly passengers, descending by age.</p>\n</blockquote>\n<p>An interesting counterpoint to the healthcare providers' perspective is that economists seem to <a href=\"http://www.igmchicago.org/surveys/testing-for-coronavirus-infections-and-antibodies/\" rel=\"noreferrer\">strongly agree</a> on the need for random testing (or better said, per some comments which corrected the question, population-representative testing) in order to calibrate the length of the lockdown from their perspective, of limiting &quot;economic damage&quot; caused by the lockdowns themselves.</p>\n", "score": 8 }, { "answer_id": 21714, "body": "<blockquote>\n <p>Would that not give us a picture of the proportion of people who have the virus?</p>\n</blockquote>\n\n<p>Yes, but: at the moment, this is probably not worth while in most countries. </p>\n\n<ul>\n<li>As Fizz explained, tests are scarce, so we need to use them where the outcome of the test does make a difference in treatment and/or for containing the disease/slowing down the spread.</li>\n<li>Right now, the development of Covid-19 case numbers is quite dynamic in many countries. The percentage we find by testing today will be outdated if not tomorrow then by the end of the week. </li>\n<li><p>In order to get good estimates of a <em>low</em> prevalence, we need to test large numbers of people and we need tests that have both high sensitivity and specificity. Right now, the tests that are used have not undergone a full validation procedure (in order to have them available asap). </p>\n\n<p>One consequence of that is that while we can know that they work sufficiently well to be useful for testing high risk patients, e.g. for some test we may know that sensitivity is better than 94% and specificity is better than 97%. If we test a general population with a prevalence of 1 in 1000 using a test with 97% specificity, we'll get around 30 false positives and 1 true positive (with 94% sensitivity). In other words, rather than measuring the prevalence of SARS-CoV-2 infections in the general population, we measured 1 - specificity of the test. Unfortunately, we wouldn't know this. </p></li>\n</ul>\n\n<p>As a rule of thumb, we can measure prevalences that are >> 1 - specificity of the test. So if we expect a prevalence of 1 : 1000, we'd ask for a test that has specificity at least 99.95 % (with that, we'd observe 1.5 positive in 1000). In order to know that a test has a specificity > 99.95 %, we'd need to validate it with at least 10000 truly negative patients all of which would need to be recognized correctly. Right now, the test may have been validated with 100 negative samples. If you want to read more background about this, I have long answers to <a href=\"https://medicalsciences.stackexchange.com/q/21337/11479\">How accurate are coronavirus tests?</a> and <a href=\"https://medicalsciences.stackexchange.com/q/21318/11479\">Why are people with COVID-19 symptoms being denied tests in the US?</a></p>\n\n<hr>\n\n<p><strong>Sentinel Samples</strong></p>\n\n<p>While we do not have such a random sampling scheme from the population right now, we have something that goes into this direction here in Germany: samples from so-called sentinel practices. Sentinel practices are medical practices throughout the country that send patient samples to a central lab where they are analyzed for a number of viruses as part of influenza surveillance. The tested viruses now include also SARS-CoV-2. </p>\n\n<p>These samples are not a random sample of the population you ask for: </p>\n\n<ul>\n<li>they are taken of patients that show up at the doctor's with acute respiratory disease, </li>\n<li>and right now with the further systematic restriction that these are patients that were not thought to be at a particularly high risk of having Covid-19 (those are sent to the SARS-CoV-2 testing).</li>\n</ul>\n\n<p>In week 12 (Mar 16 - 22), 3 of the 193 sentinel samples that were tested for SARS-CoV-2 were positive. That's a prevalence of 1,6 %, 95 % confidence interval roughly being 0.4 - 4 % (in other words, we have an order of magnitude). </p>\n\n<p>I don't have information on the specificity of the SARS-CoV-2 test used for the sentinel samples, but the published data reports two weeks with 0 positive among 191 + 229 = 420 samples, and if we take those as true negatives, specificity would be better than 99 %.</p>\n\n<hr>\n\n<p>I expect that studies will be done once the first wave of Covid-19 is over and once properly validated antibody tests are available. In contrast to the RNA tests now (which test an active infection), antibody tests can say whether someone had such an infection recently (possibly as recent as right now) or a while ago. </p>\n\n<p>The specificity requirements are the same regardless of whether RNA or antibodies are tested.</p>\n", "score": 5 }, { "answer_id": 21729, "body": "<blockquote>\n<p>why not take a random sample of a few thousand people people, and test all of them to see how many of them have the virus?</p>\n</blockquote>\n<p>Iceland did it, see <a href=\"https://english.alarabiya.net/en/features/2020/03/25/Coronavirus-Iceland-s-mass-testing-finds-half-of-carriers-show-no-symptoms\" rel=\"nofollow noreferrer\">https://english.alarabiya.net/en/features/2020/03/25/Coronavirus-Iceland-s-mass-testing-finds-half-of-carriers-show-no-symptoms</a>:</p>\n<blockquote>\n<p>As of Sunday night, the country’s health authorities and the biotechnology firm deCode Genetics have tested more than 10,300 people. That might not sound like a large number, compared to the around 350,000 Americans who have been tested for coronavirus according to the COVID Tracking Project, but it is a far higher percentage of tests per capita - a ratio Icelandic authorities have claimed is the highest in the world.</p>\n<p>But it is not just the numbers of people being tested that is unusual about Iceland’s approach.</p>\n<p>Unlike other countries, where people are only tested if they exhibit symptons of coronavirus or have come into contact with known spreaders, the country is testing thousands of people from the general population who don’t exhibit any symptoms of the virus whatsoever – helping to reveal information about the nature of the pathogen and its symptoms.</p>\n</blockquote>\n<p>This was also done in a city in Italy:</p>\n<blockquote>\n<p>In COVID-19, The University of Padua, Veneto Region and the Red Cross tested the populationof Vò, Italy, 3300 people, to establish the natural history of the virus, the transmission dynamicsand categories of risk. &quot; they found &gt;50 of those who tested positive to be asymptomatic” according to Professor Sergio Romagnani.</p>\n</blockquote>\n<p>The same question was asked on politics.SE:\n<a href=\"https://politics.stackexchange.com/q/50897/2231\">Has there been a random survey of a population for COVID-19?</a></p>\n<p>Update (2020-11-01): <a href=\"https://www.theguardian.com/world/2020/nov/01/half-slovakia-population-covid-tested-covid-one-day\" rel=\"nofollow noreferrer\">More than 2.5 million Slovaks took swab tests on Saturday, with 25,850 testing positive</a></p>\n<hr />\n<p>References:</p>\n<ul>\n<li>{1} 2020-03-25 - Stanford COVID-19 Evidence Service - Addressing COVID-19 Face Mask Shortages [v1.2] <a href=\"https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2\" rel=\"nofollow noreferrer\">https://archive.org/details/20200325stanfordcovid19evidenceserviceaddressingcovid19facemaskshortagesv1.2</a></li>\n</ul>\n", "score": 2 }, { "answer_id": 23065, "body": "<p>Denmark did this recently and found that <a href=\"https://www.dr.dk/nyheder/indland/blodbanker-tester-om-donorer-har-haft-coronavirus\" rel=\"nofollow noreferrer\">2.7% of Danes living in the Capital region already have antibodies for the disease</a>. This isn't randomized per se as these samples are from people donating blood, but so far it's as good as it gets.</p>\n", "score": 1 }, { "answer_id": 24375, "body": "<p>One technique that is also being trialled is <a href=\"https://www.csiro.au/en/News/News-releases/2020/Australian-researchers-trace-sewage-for-early-warning-COVID-19-spread\" rel=\"nofollow noreferrer\">testing wastewater/sewerage</a> for RNA from the SARS-CoV2 virus. This won't help you identify who has the virus, but it could inform a city that had previously eliminated the virus that someone has brought the virus back again.</p>\n", "score": 1 }, { "answer_id": 23237, "body": "<p>It is being done. The Czech Republic is currently preparing such a study }to begin on the 20th April) to find out the number of asymptomatic patients to better predict the future evolution of the number of infected people. A bit older source in English <a href=\"https://news.expats.cz/coronavirus-in-the-czech-republic/czech-covid-19-central-control-team-plans-blanket-testing-in-sample-of-prague-population/\" rel=\"nofollow noreferrer\">https://news.expats.cz/coronavirus-in-the-czech-republic/czech-covid-19-central-control-team-plans-blanket-testing-in-sample-of-prague-population/</a> Much more updated information exists in Czech <a href=\"https://www.seznamzpravy.cz/clanek/prazdniny-podle-prymuly-v-ceskem-hotelu-s-vylety-po-hradech-a-bez-festivalu-99893\" rel=\"nofollow noreferrer\">https://www.seznamzpravy.cz/clanek/prazdniny-podle-prymuly-v-ceskem-hotelu-s-vylety-po-hradech-a-bez-festivalu-99893</a></p>\n\n<p>\"Testování vzorku 17 tisíc lidí v České republice na protilátky proti koronaviru začne v pondělí 20. dubna, do dalšího pondělí budeme znát výsledky.\" \"Testing of the sample of 17 thousand people in the Czech Republic for antigens against coronavirus will begin on Monday 20th April. By the next Monday we will know the results.\"</p>\n", "score": 0 } ]

[ "covid-19" ]

[ { "answer_id": 21753, "body": "<p>This question can't be answered with any certainty due to the lack of published full data, or the conflicting data when it is being published.</p>\n\n<p>When blanket testing was done of the isolated town of Vo’Eugeano, they reported a high percentage of those tested were asymptomatic. They gave no figures. And this contrasted with the original reports from the WHO in China (<a href=\"https://www.bmj.com/content/368/bmj.m1165\" rel=\"nofollow noreferrer\">https://www.bmj.com/content/368/bmj.m1165</a>)</p>\n\n<blockquote>\n <p>“the proportion of truly asymptomatic infections is unclear but appears to be relatively rare and does not appear to be a major driver of transmission.”</p>\n</blockquote>\n\n<p>So, for instance, did the Italians follow the <em>asymptomatic</em> until they cleared the virus? Did they check for emerging symptoms such as anosmia? Diarrhoea?</p>\n\n<p>Our best guess is that the people who are going to be minimally symptomatic are those who are least affected with the disease, and this includes, older children ( but not the very young ), female, non-smokers/non-vaping, blood group O, and no existing medical co-morbidities such as hypertension, diabetes, cardiopulmonary disease.</p>\n\n<p>This paper says 86% of Chinese had undocumented infection with a high probability of many of them being not very symptomatic.</p>\n\n<blockquote>\n <p>We estimate 86% of all infections were undocumented (95% CI: [82%–90%]) prior to 23 January 2020\n travel restrictions. Per person, the transmission rate of undocumented infections was 55% of documented\n infections ([46%–62%]), yet, due to their greater numbers, undocumented infections were the infection\n source for 79% of documented cases. These findings explain the rapid geographic spread of SARS-CoV2\n and indicate containment of this virus will be particularly challenging.</p>\n</blockquote>\n\n<p>Substantial undocumented infection facilitates the rapid\ndissemination of novel coronavirus (SARS-CoV2)\nRuiyun Li1\n<em>, Sen Pei2</em>†, Bin Chen3*, Yimeng Song4, Tao Zhang5, Wan Yang6, Jeffrey Shaman2†\n1\nMRC Centre for Global Infectious Disease Analysis, Department of Infectious Disease Epidemiology, School of Public Health, Faculty of Medicine, Imperial College London,\nLondon W2 1PG, UK. 2\nDepartment of Environmental Health Sciences, Mailman School of Public Health, Columbia University, New York, NY 10032, USA. 3\nDepartment of\nLand, Air and Water Resources, University of California, Davis, Davis, CA 95616, USA. 4Department of Urban Planning and Design, The University of Hong Kong, Hong Kong. 5\nMinistry of Education Key Laboratory for Earth System Modeling, Department of Earth System Science, Tsinghua University, Beijing 10084, P. R. China. 6Department of\nEpidemiology, Mailman School of Public Health, Columbia University, New York, NY 10032, USA.\n<a href=\"https://science.sciencemag.org/content/early/2020/03/24/science.abb3221/tab-pdf\" rel=\"nofollow noreferrer\">https://science.sciencemag.org/content/early/2020/03/24/science.abb3221/tab-pdf</a></p>\n", "score": 2 } ]

[ "covid-19" ]

[ { "answer_id": 22792, "body": "<blockquote>\n <p>Like everything else, we're instructed by past experiences. Although there weren't a lot of data on neurologic aspects of MERS and SARS, there were some papers describing neurologic complications in those patients. In rare cases, complications including ADEM (acute disseminated encephalomyelitis)-like demyelination, encephalitis, and brainstem encephalitis were reported. They also saw some peripheral and non–central nervous system stuff, including things that looked like Guillain-Barré syndrome or what they would sometimes call critical illness polyneuropathy</p>\n</blockquote>\n\n<p><a href=\"https://www.medscape.com/viewarticle/927562\" rel=\"nofollow noreferrer\">https://www.medscape.com/viewarticle/927562</a></p>\n\n<p>So, yes, severely affected covid-19 patients may develop something that looks like GBS.</p>\n", "score": 2 } ]

[ "covid-19", "autoimmune-disease", "coronavirus", "sars-cov-2" ]

[ { "answer_id": 22853, "body": "<p><a href=\"https://www.kaggle.com/allen-institute-for-ai/CORD-19-research-challenge/tasks\" rel=\"nofollow noreferrer\">https://www.kaggle.com/allen-institute-for-ai/CORD-19-research-challenge/tasks</a> is hosting such a \"competition\" based on scientific papers related to covid-19. You can find many notebooks showing what people have tried.</p>\n\n<p>However, to be useful, <a href=\"https://www.kaggle.com/allen-institute-for-ai/CORD-19-research-challenge/discussion/138761\" rel=\"nofollow noreferrer\">I think</a> patient data would be very valuable as well. Scientific text mining is in some ways currently quite limited for covid-19.</p>\n", "score": 2 }, { "answer_id": 22856, "body": "<p>Yes, they can, see e. g. <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/30905159\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/30905159</a> (field of cheminformatics) re the possiblity of drug discovery in general via machine learning. Generally, a vaccine is a specific applicative field of drug discovery that might benefit from machine learning as well, e. g. <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4395155/\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4395155/</a>.</p>\n", "score": 2 } ]

[ "covid-19", "vaccination" ]

[ { "answer_id": 23032, "body": "<p>It's true that we do not have strong evidence that people who have been infected by SARS-COV-2 are immune to re-infection. However, there are a couple of reasons that it is very likely that people will not be reinfected:</p>\n\n<p>1) Though coronaviruses and RNA viruses in general mutate rapidly, making it difficult for the immune system to develop a lasting response, <a href=\"https://www.washingtonpost.com/health/the-coronavirus-isnt-mutating-quickly-suggesting-a-vaccine-would-offer-lasting-protection/2020/03/24/406522d6-6dfd-11ea-b148-e4ce3fbd85b5_story.html\" rel=\"nofollow noreferrer\">the SARS-COV-2 virus is showing relative stability</a>. This means that our immune system, once it makes antibodies, can use those antibodies in future responses to the virus.</p>\n\n<p>2) <a href=\"https://www.biorxiv.org/content/biorxiv/early/2020/03/14/2020.03.13.990226.full.pdf\" rel=\"nofollow noreferrer\">This study in macaques</a> showed that monkeys who had recovered from viral infection did not show any signs of reinfection when exposed to the virus again. </p>\n", "score": 4 } ]

[ "covid-19" ]

[ { "answer_id": 23158, "body": "<p>Cardiovascular disease is known to worsen during infections such as influenza through two proposed mechanisms:</p>\n<ul>\n<li>cytokines from the resulting inflammation cause weaken atherosclerotic plaques and cause plaque rupture/thrombosis</li>\n<li>stress from illness can precipitate decompensated heart failure in predisposed patients</li>\n</ul>\n<p>Two studies from Wuhan have looked into this so far. One cohort study of 416 patients found that 19.7% of COVID-19 patients developed myocardial infarction during their hospitalization and had higher rates of mortality (51.2% MI vs 4.5% no MI)[2]. Another cohort study of 187 patients found that 27.8% of their patients developed MI with a similar mortality rate (59.6% MI vs 8.9% no MI). Patients from both studies who developed MIs seem to be older and have preexisting hypertension, diabetes and coronary artery disease.</p>\n<p>From these studies, the current data support the idea that getting COVID-19 increases the risk of having an MI, especially in those with risk factors.</p>\n<p>Update: The <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-guidance-management-patients.html\" rel=\"nofollow noreferrer\">CDC</a> states that patients with COVID-19 can also develop a hypercoagulable state, leading to thrombotic complications such as an MI. Unfortunately, the pathogenesis of COVID-19-related hypercoagulability is unknown.</p>\n<p>Source:</p>\n<ol>\n<li><p><a href=\"https://jamanetwork.com/journals/jamacardiology/fullarticle/2763844\" rel=\"nofollow noreferrer\">JAMA Cardiology: Association of Coronavirus Disease 2019 (COVID-19) With Myocardial Injury and Mortality</a></p>\n</li>\n<li><p><a href=\"https://jamanetwork.com/journals/jamacardiology/fullarticle/2763524\" rel=\"nofollow noreferrer\">JAMA Cardiology: Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China</a></p>\n</li>\n<li><p><a href=\"https://jamanetwork.com/journals/jamacardiology/fullarticle/2763845\" rel=\"nofollow noreferrer\">JAMA Cardiology: Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)</a></p>\n</li>\n</ol>\n", "score": 6 }, { "answer_id": 23190, "body": "<p>A <a href=\"https://jamanetwork.com/journals/jama/fullarticle/2763485\" rel=\"nofollow noreferrer\">case series in Seattle published in JAMA on March 17, 2020</a> describes a potential cardiomyopathy associated with coronavirus in critically-ill patients. Current thinking includes a potential direct cardiac effect of the COVID-19 viral infection, rather than atherosclerotic or ischemic disease per se.</p>\n\n<p>The authors noted:</p>\n\n<blockquote>\n <p>It is unclear whether the high rate of cardiomyopathy in this case\n series reflects a direct cardiac complication of SARS-CoV-2 infection\n or resulted from overwhelming critical illness. Others have described\n cardiomyopathy in COVID-19, and further research may better\n characterize this risk</p>\n</blockquote>\n\n<p>They go on to cite two other reports on potential COVID-19 related cardiomyopathy and cardiac impacts.</p>\n\n<p>Mullen  B. COVID-19 clinical guidance for the cardiovascular care team. Published online March 6, 2020. Accessed March 16, 2020. <a href=\"https://www.acc.org/~/media/665AFA1E710B4B3293138D14BE8D1213.pdf\" rel=\"nofollow noreferrer\">https://www.acc.org/~/media/665AFA1E710B4B3293138D14BE8D1213.pdf</a></p>\n\n<p>Zheng  YY, Ma  YT, Zhang  JY, Xie  X.  COVID-19 and the cardiovascular system.  Nat Rev Cardiol. 2020. doi:10.1038/s41569-020-0360-5PubMedGoogle Scholar</p>\n", "score": 3 } ]

[ "covid-19", "cardiology", "cardiovascular-disease" ]

[ { "answer_id": 23578, "body": "<p>Seasonal and cyclical effects have been studied prior to COVID-19, including day-of-week influences on Emergency Department visit volume.</p>\n\n<p>For example, in a study of emergency departments in Western New York:</p>\n\n<blockquote>\n <p>“The final ARMA (2,0) model indicated an autoregressive structure with\n up to a 2-day lag. ED volume is lower on weekends than on weekdays,\n and the highest volumes are on Mondays. Summer and fall seasons\n demonstrated higher volumes, whereas lower volume outliers were\n associated with holidays.”</p>\n</blockquote>\n\n<p>Source:\n<a href=\"https://www.researchgate.net/publication/297746060_Medical_Mondays_ED_Utilization_for_Medicaid_Recipients_Depends_on_the_Day_of_the_Week_Season_and_Holidays\" rel=\"nofollow noreferrer\">https://www.researchgate.net/publication/297746060_Medical_Mondays_ED_Utilization_for_Medicaid_Recipients_Depends_on_the_Day_of_the_Week_Season_and_Holidays</a></p>\n\n<p>Factoring this effect is likely important to understanding the baseline expected volume, and its cyclicity. Other methods include looking at visit volume for plausibly UN-related reasons, eg diarrheal illness, to understand a baseline cycle in ER visits even during a pandemic when care-seeking behavior may change from original cycles.</p>\n", "score": 3 }, { "answer_id": 23579, "body": "<p>I haven't seen a lot of research on these intra-weekly (reporting) trends on anything health-related, but there is <a href=\"https://academic.oup.com/milmed/article/181/4/364/4158510\" rel=\"nofollow noreferrer\">one paper</a> on such trend on ILI reporting, alas just in the military:</p>\n<blockquote>\n<p>In this report, we describe and analyze a periodic pattern in influenza-like illness within active military populations, derived from the Defense Medical Surveillance System data set. <strong>We find that there is a well-defined pattern with peak incidence on Monday, decaying to Friday, and remaining roughly constant over the weekend. Moreover, we find that the pattern systematically changes in response to public holidays.</strong> We quantitatively describe the effect of this modulation, and show how these results may be used to detrend military and, by extension, civilian data sets. As medical data streams become more timely, these results may be used to infer near-real-time daily estimates of influenza-like illness incidence, which may form the basis of a forecasting tool for imminent outbreaks.</p>\n</blockquote>\n<p>Note that this is a very large data set (n &gt; 1 million observations.)</p>\n<blockquote>\n<p>A power spectrum of incidence measurements quantifies how the variance in the data is distributed over the frequency components into which that data can be decomposed. In other words, it is a measure of the energy per unit time falling within different frequency bins. For our purposes, it indicates where periodicities in the data may be found. The Nyquist frequency corresponds to 1/2 t, which because the data are daily averages, corresponds to 0.5 day⁻¹. The four major peaks, which are marked by the dashed lines, correspond to periods of 1 year, 7 days, 3.5 days, and 2.33 days. The latter two frequencies are merely harmonics of the fundamental 7-day period.</p>\n<p><a href=\"https://i.stack.imgur.com/kcdQv.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/kcdQv.png\" alt=\"enter image description here\" /></a></p>\n</blockquote>\n<p>So a weekly [reporting] pattern (for Covid-19) doesn't seem so unusual in this perspective.</p>\n<p>The paper is a bit more complicated than this as they looked at the intra-week patterns for two different definitions of ILI. For the more strict definition, the was less intra-week variation.</p>\n<p>They have some conclusions based on that:</p>\n<blockquote>\n<p>It is also important to acknowledge that these data reflect attendance at the clinic and not onset of symptoms. It is unlikely that onset data would display any strong intra-weekly variations, although a modest modulation may be possible because of behavioral changes during a typical week. [...]</p>\n<p>Our results illustrate that the renormalization kernel is data set specific. [...] because of the notable difference in the kernels on Sundays, we suggest that the disease too plays a role. The subset of ILI-large cases that we also identified as ILI-small represents a group who were displaying more severe respiratory problems. Therefore, it is likely that these individuals could not wait until Monday before seeing a medical professional. Moreover, with an average latency period of approximately 1.6 days, patients with influenza who became infected on Thursday or Friday would not recognize their symptoms as severe for another day, forcing them to seek treatment on Sunday.</p>\n</blockquote>\n", "score": 3 } ]

[ "covid-19", "statistics", "healthcare-data", "covid-19-datasets" ]

[ { "answer_id": 23632, "body": "<blockquote>\n <p>Outbreaks and pseudo-outbreaks related to contaminated germicides have most commonly been reported with contaminated antiseptics. Outbreaks from contaminated high-level disinfectants have rarely, if ever, been reported. Outbreaks from contaminated intermediate- and low-level disinfectants have occasionally been reported. All outbreaks associated with contaminated germicides have occurred due to gram-negative bacilli or mycobacteria.</p>\n</blockquote>\n\n<ul>\n<li>Weber, D. J., Rutala, W. A., &amp; Sickbert-Bennett, E. E. (2007). Outbreaks associated with contaminated antiseptics and disinfectants. Antimicrobial agents and chemotherapy, 51(12), 4217-4224.</li>\n</ul>\n\n<p>Weber et al suggest that the most common issues are with <em>antiseptics</em> rather than disinfectants, per se, where the distinction is that antiseptics are those applied to tissue and disinfectants are those applied to surfaces/inanimate objects. Indeed, your original source also refers to <em>antiseptics</em> rather than disinfectants.</p>\n\n<p>The same chemicals can be used as either in different formulations, so that might lead to some confusion. The citation mentioned contains references to several particular incidents and tables detailing the likely cause; for several of the issues with antiseptics, it seems the contamination was traced to water used to dilute a disinfectant, improper storage, and contaminated bottles or tubing.</p>\n", "score": 2 } ]

[ "disease-transmission", "disinfection", "fda" ]

[ { "answer_id": 23723, "body": "<p>While hospitals, clinics, long term care homes and such are of course <strong>open and working</strong> seven days a week, administrative staff typically only work 5 days a week. So someone comes to work Monday and reports 3 deaths (that may actually have occurred on Saturday or Sunday.) They may not do that first thing Monday, they may have other things going on. </p>\n\n<p>Meanwhile whoever they report to has some cut off for when \"things you tell me today\" go into \"today's number.\" Maybe it's noon, I have no idea, it could be 5pm, whatever. So some of the things that are reported to that person on Monday get reported to the big country-wide reporting mechanisms Tuesday. </p>\n\n<p>As a result you will see two days with less deaths reported, and those two days are more likely to be Sunday and Monday than Saturday and Sunday. Sure, if the graphs were \"deaths that happened on day X\" and not \"deaths we were told about on day X\" this wouldn't happen. However in normal times, not all deaths are observed (never mind reported) on the day they happen: people who die alone at home and are discovered later, for example, or people who are suspected of having died in a house fire but it takes several days to find some remains, that sort of thing. The norm has been to count them on the day they are reported.</p>\n", "score": 3 }, { "answer_id": 23732, "body": "<p>While people don't usually have a preference for dying on particular days determining how they died is subjected to delays. A medical examiner or other expert had to determine whether the death is from covid-19 or one of the many comorbid conditions that the person suffered from. Furthermore, there are deaths in the community that need to be examined. You can see that actual numbers change over time with hindsight, and the weekend factor introduces a delay in reporting.</p>\n<blockquote>\n<p>One of the most pernicious ways has to do with the time it takes to tabulate deaths due to Covid-19, especially in jurisdictions where hospitals are overworked. In New York City, for example, some deaths are reported to the city’s health department within hours, but others take days — sometimes a week or more — to get tabulated. This delay means that on any given date, when officials announce the daily death toll, they do so having received only a fraction of the death reports that will eventually come in.</p>\n<p>On the afternoon of April 1, for example, New York City officials declared that 1,374 people had died of the virus to date. But the accounts of deaths kept coming in. Two days later, the tally of people who had died on or before April 1 had climbed to more than 1,700. By April 5 it stood at 1,878. As of April 9, the official count was 2,253, a roughly 60 percent increase over the initial tally. This number will likely continue to rise, slowly, for several more days.</p>\n</blockquote>\n<p><a href=\"https://undark.org/2020/04/11/covid-19-data-lag-deaths-new-york\" rel=\"nofollow noreferrer\">https://undark.org/2020/04/11/covid-19-data-lag-deaths-new-york</a></p>\n<p><a href=\"https://www.livescience.com/how-covid-19-deaths-are-counted.html\" rel=\"nofollow noreferrer\">https://www.livescience.com/how-covid-19-deaths-are-counted.html</a></p>\n", "score": 3 } ]

[ "covid-19", "coronavirus", "statistics", "death", "covid-19-datasets" ]

[ { "answer_id": 23726, "body": "<p>The results are probably in the Chinese press, but are being reported elsewhere</p>\n\n<blockquote>\n <p>China has reported 51 new coronavirus cases including 40 asymptomatic infections, majority of them in the contagion’s first epicentre Wuhan, where over six million tests have been conducted in the last 10 days, health officials said on Monday.</p>\n</blockquote>\n\n<p>So, looks like large scale testing has detected 40 cases which were asymptomatic. It looks like because they didn't have capacity in their 60 testing stations that they have been batch testing, and then going back to test a batch if positive.</p>\n\n<p><strong>Update 1-June-2020</strong></p>\n\n<p>Forbes reports that 200 asymptomatic individuals were detected with the testing so far of 6.68M people</p>\n\n<blockquote>\n <p>Over the last two weeks, 6.68 million have been newly tested for the new SARS coronavirus, first discovered in the city back in December. They discovered that out of all those people, only 200 had contracted the virus but had no symptoms, meaning that just 0.002% of those newly tested this month had it and not one required hospitalization.</p>\n</blockquote>\n\n<p><a href=\"https://www.thehindu.com/news/international/china-reports-over-50-new-coronavirus-cases-mostly-in-wuhan/article31667737.ece\" rel=\"nofollow noreferrer\">https://www.thehindu.com/news/international/china-reports-over-50-new-coronavirus-cases-mostly-in-wuhan/article31667737.ece</a></p>\n\n<p><a href=\"https://www.forbes.com/sites/kenrapoza/2020/05/27/wuhan-chinas-coronavirus-testing-shows-a-0002-infection-rate/#71cfac991093\" rel=\"nofollow noreferrer\">https://www.forbes.com/sites/kenrapoza/2020/05/27/wuhan-chinas-coronavirus-testing-shows-a-0002-infection-rate/#71cfac991093</a></p>\n", "score": 2 }, { "answer_id": 23824, "body": "<p>From <a href=\"https://time.com/5847226/wuhan-10-million-coronavirus-tests/\" rel=\"nofollow noreferrer\">Time: June 3, 2020</a></p>\n\n<blockquote>\n <p><strong>Wuhan Tests Nearly 10 Million People in 19 Days, Finding Just 300 Coronavirus Infections</strong></p>\n \n <p>(BEIJING) — The Chinese city of Wuhan, where the coronavirus was first detected late last year, has tested nearly 10 million people in an unprecedented 19-day campaign to check an entire city.</p>\n \n <p>It identified just 300 positive cases, all of whom had no symptoms. The city found no infections among 1,174 close contacts of the people who tested positive, suggesting they were not spreading it easily to others.</p>\n \n <p><strong>...</strong></p>\n</blockquote>\n\n<p><em>Given what's happening in the US and other places in the world, I personally don't believe this number. But, this is what Time says, I just report it.</em></p>\n", "score": 2 } ]

[ "covid-19", "test", "pcr" ]

[ { "answer_id": 23772, "body": "<p><a href=\"https://www.nature.com/articles/ncomms5212\" rel=\"nofollow noreferrer\">Nature Communications</a> have such a database.</p>\n<blockquote>\n<p><strong>Human symptoms–disease network</strong></p>\n<p><em>XueZhong Zhou, Jörg Menche, Albert-László Barabási &amp; Amitabh Sharma</em></p>\n<p>Published: 26 June 2014</p>\n</blockquote>\n<p>They count the number of times a disease and a symptom keywords both appear on the same <a href=\"https://pubmed.ncbi.nlm.nih.gov/\" rel=\"nofollow noreferrer\">PudMed</a> article, and assign a <a href=\"https://en.wikipedia.org/wiki/Tf%E2%80%93idf\" rel=\"nofollow noreferrer\">TF-IDF</a> value to each pair.</p>\n<p>In their words:</p>\n<blockquote>\n<p><strong>Acquisition of symptom and disease relationships</strong></p>\n<p>The association between symptoms and diseases were then quantified using term co-occurrence (number of PubMed identifiers in which two terms appear together;</p>\n</blockquote>\n<p>Link to the database:</p>\n<blockquote>\n<p><a href=\"https://static-content.springer.com/esm/art%3A10.1038%2Fncomms5212/MediaObjects/41467_2014_BFncomms5212_MOESM1045_ESM.txt\" rel=\"nofollow noreferrer\">https://static-content.springer.com/esm/art%3A10.1038%2Fncomms5212/MediaObjects/41467_2014_BFncomms5212_MOESM1045_ESM.txt</a></p>\n</blockquote>\n<p>(<a href=\"https://www.nature.com/articles/ncomms5212#Sec18\" rel=\"nofollow noreferrer\">Supplementary Data 3</a> from the article)</p>\n", "score": 6 }, { "answer_id": 23855, "body": "<p>What you're looking for is used by AI or Bayesian networks for online diagnosis. These databases are commercially sensitive and likely only accessible by API rather than raw data. For example, ISABEL, has been around for 20 years </p>\n\n<p><a href=\"https://www.isabelhealthcare.com/products/integration\" rel=\"nofollow noreferrer\">https://www.isabelhealthcare.com/products/integration</a></p>\n", "score": 2 } ]

[ "disease", "symptoms", "database" ]

[ { "answer_id": 23962, "body": "<p>Yes, there are.</p>\n<p><a href=\"https://www.devoteam.com/newsroom/covid-19-ai-model-confirms-at-98-5-there-will-be-no-second-wave-this-summer-or-this-winter-according-to-devoteams-data-scientists/\" rel=\"nofollow noreferrer\">This study</a> for France says there is a 1.5% chance of a second wave. <a href=\"https://www.redanalysis.org/2020/05/11/second-wave-for-covid-19/\" rel=\"nofollow noreferrer\">This article</a> discusses three different papers modelling successive waves of covid (not only two). As usual, conclusions depend on modelling assumptions and different scenarios. For instance, <a href=\"https://theconversation.com/coronavirus-what-a-second-wave-might-look-like-138980\" rel=\"nofollow noreferrer\">this article</a> states the outcome depends on how R and other factors (whether the virus mutate or not) behave.</p>\n<p>A personal reflection, if I may. The modelling answer has two sides. One is the epidemiological dynamics, and the other is the behavioural one. As an economist, I am particularly concerned with the latter, which I think is particularly difficult to predict and <strong>the models above do not consider</strong>. Covid-19 was a new thing four months ago and uncertainty led to panic (remember toilet paper buying spree?), significant willingness and openness to testing and, in the end, lockdowns. A second wave will for sure be different. Since the virus is evidently less dangerous as originally imagined (particularly for the population not at-risk, the majority), and most normal people do not want lockdowns again (as it can be seen from the reaction to their easing), there could be less willingness to cooperate with public health authorities. For instance, <strong>it might well be that individuals with probably mild cases won't report them.</strong> Why bother? This behavioural change could have devastating consequences for the development of a second wave. I would expect any reasonable analysis to incorporate this and other behavioural responses in the analysis. As said, the above do not consider them.</p>\n", "score": 1 } ]

[ "covid-19", "disease-transmission", "epidemiology", "infectious-diseases", "who-world-health-org" ]

[ { "answer_id": 24022, "body": "<p>I don't know if it's <strong>just</strong> handwashing, but <a href=\"https://www1.health.gov.au/internet/main/publishing.nsf/Content/cda-surveil-ozflu-flucurr.htm\" rel=\"nofollow noreferrer\">Australia is reporting</a> a significant decrease in flu this season:</p>\n<blockquote>\n<p>Following a high start to the 2020 interseasonal period, currently, influenza and influenza-like illness (ILI) activity are lower than average across all systems for this time of year. At the national level, notifications of laboratory-confirmed influenza have substantially decreased since mid-March and remain low.</p>\n</blockquote>\n<p>In the detailed PDF for May, which was linked from the first link above but is now gone, they say:</p>\n<blockquote>\n<p>Interpretation of 2020 influenza activity data should take into account, but are not limited to, the impact of social distancing measures, likely changes in health seeking behaviour of the community including access to alternative streams of acute respiratory infection specific health services, and focussed testing for COVID-19 response activities. Current COVID-19 related public health measures and the community’s adherence to public health messages are also likely having an effect on transmission of acute respiratory infections, including influenza. </p>\n</blockquote>\n<p>And provide a lot of graphs. I think this one is the most impressive:</p>\n<p><a href=\"https://i.stack.imgur.com/joNNo.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/joNNo.png\" alt=\"enter image description here\" /></a></p>\n<p>The &quot;second half of June&quot; detailed PDF is <a href=\"https://www1.health.gov.au/internet/main/publishing.nsf/Content/cda-surveil-ozflu-flucurr.htm/$File/flu-06-2020.pdf\" rel=\"nofollow noreferrer\">here</a>, but may go away. Future readers should go to the first link and look for links under the Full Report heading.</p>\n", "score": 2 } ]

[ "covid-19", "prevention", "common-cold" ]

[ { "answer_id": 24171, "body": "<p>I like your curiosity and logical thinking - you're just missing a few pieces of the puzzle.</p>\n<p>The sun emits ultraviolet light radiation which is the component of sunlight that is able to damage skin.</p>\n<p>Ultraviolet (UV) is a form of electromagnetic radiation with wavelengths between 10 to 400 nanometers, shorter than that of visible light but longer than X-rays. To put nanometers into perspective - A human hair is around 75,000 nanometers in diameter. There are sub-types of UV which define the wavelength size:</p>\n<ol>\n<li>Ultraviolet A - UVA - 400–315 nanometers</li>\n<li>Ultraviolet B - UVB - 315–280 nanometers</li>\n<li>Ultraviolet C - UVC - 280–100 nanometers</li>\n</ol>\n<p>Interestingly UVB is essential synthesize Vitamin D.</p>\n<p>UV light is able to damage DNA. This results with humans cells (typically skin cells) to attempt to repair themselves. As a result sometimes genetic mutations arise - some of which give the cell the ability to divide more frequently (cancer). The process of UV damage is shown in the image below.</p>\n<p><a href=\"https://i.stack.imgur.com/oAXyM.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/oAXyM.png\" alt=\"UV damaging DNA\" /></a></p>\n<p>Although advertises I'm sure would love you to believe that Vitamin D should always be gained from their supplement, the world health organisation states the following &quot;<a href=\"https://www.who.int/uv/resources/FAQ/uvhealtfac/en/index1.html\" rel=\"nofollow noreferrer\">...5 to 15 minutes of casual sun exposure of hands, face and arms two to three times a week during the summer months is sufficient to keep your vitamin D levels high.</a>&quot;. Yes I understand - <em>supplements avoid aforementioned damage to DNA</em> - but you will be safe if you follow the above directive (it's free) and learn more information on other methods to prevent damage when in situations of long-term exposure.</p>\n<p>In terms of further scientific reading I would like to direct you toward higher quality literature. <a href=\"https://www.angelo.edu/services/library/handouts/peerrev.php\" rel=\"nofollow noreferrer\">This web-page explains the difference between and the best information resource out of: News articles, Journal articles and, Peer-reviewed scientific articles.</a> In saying this, I also think Wikipedia in the 21st century has gained a highly respected and excellent reputation for free high quality information.</p>\n<p><a href=\"https://www.who.int/gho/phe/ultraviolet_radiation/exposure/en/\" rel=\"nofollow noreferrer\">Attached is a Chloropleth map displaying the total average daily ambient ultraviolet radiation (UVR) level across the world.</a></p>\n", "score": 5 } ]

[ "dermatology", "vitamin-d", "uv-rays", "sun-exposure" ]

[ { "answer_id": 24211, "body": "<p>The transmission of a disease from an animal to humans is called zoonosis.\nAnd researchers have found out that COVID 19 was transmitted to humans via bats.\nThese viruses enter into the human system via various ways:-</p>\n<ol>\n<li>When an infected animal bites the human</li>\n<li>When a human has cracked skin and comes in contact with potentially infectious fluids of animals such as blood, saliva, etc.</li>\n</ol>\n<p>There maybe a role of an intermediate animal too in the transmission.</p>\n<p>The two main questions, the answers to which show us how the virus transmits from bats to humans are:-</p>\n<ol>\n<li>Can the virus reach the host cell?</li>\n</ol>\n<p>A) In case of COVID 19, the fact that bats and even the predicted intermediate animal (pangolin) were being sold at the market in Wuhan shows that contact was present between the suspected animal and humans.</p>\n<ol start=\"2\">\n<li>Can the virus bind to the receptors(gates) and enter the host cell in order to replicate?</li>\n</ol>\n<p>A) Researches have found evidence that SARS CoV 2 virus binds to ACE 2(Angiotensin converting enzyme 2) receptors on the host cell. And this capability of the virus develops through mutations(changes in the genes) when they are in animals which are called reservoirs because they store these viruses.</p>\n<p>And while it can be assumed that someone might have created this virus to make it harmful to humans, evidence suggests otherwise. I have added reference regarding the evidence about this point(ref 1). The explanation to this is very technical and goes to the molecular level. To explain it in simple terms, if you want to make a new virus, you need to take an old virus and the make changes in it to make it new. But evidence shows that the novel corona virus do not have a lot of similarity to the known existing viruses at the molecular level.</p>\n<p>I hope this satisfies your curiosity .</p>\n<p>References:-</p>\n<p>1.\n<a href=\"https://www.sciencedaily.com/releases/2020/03/200317175442.htm\" rel=\"nofollow noreferrer\">https://www.sciencedaily.com/releases/2020/03/200317175442.htm</a></p>\n<p>2.\n<a href=\"https://www.vox.com/science-and-health/2020/2/12/21133560/coronavirus-china-bats-pangolin-zoonotic-disease\" rel=\"nofollow noreferrer\">https://www.vox.com/science-and-health/2020/2/12/21133560/coronavirus-china-bats-pangolin-zoonotic-disease</a></p>\n", "score": 2 } ]

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

[ { "answer_id": 25752, "body": "<p>I wouldn't be surprised if dogs could detect COVID-19, as they can help detect <a href=\"https://www.sciencedaily.com/releases/2019/01/190115144053.htm\" rel=\"nofollow noreferrer\">hypoglycaemia in diabetics</a>, warn people who are about to have an <a href=\"https://epilepsyfoundation.org.au/understanding-epilepsy/epilepsy-and-seizure-management-tools/seizure-alert-dogs/\" rel=\"nofollow noreferrer\">epileptic seizure</a> and have been used to <a href=\"https://www.medicalnewstoday.com/articles/323620\" rel=\"nofollow noreferrer\">sniff out some cancers</a>.</p>\n<p><a href=\"https://www.nature.com/articles/d41586-020-03149-9\" rel=\"nofollow noreferrer\">This article on Nature's website</a> (23 November 2020) has the following</p>\n<blockquote>\n<p>Canines seem to detect coronavirus infections with remarkable\naccuracy, but researchers say large-scale studies are needed before\nthe approach is scaled up.</p>\n</blockquote>\n", "score": 2 } ]

[ "covid-19", "coronavirus", "diagnosis", "smell", "body-odor" ]

[ { "answer_id": 24394, "body": "<p>In the US, in order for a mask to be labeled &quot;medical&quot;, that mask must be approved by the FDA as a medical device. With so many new people manufacturing masks coupled with the public demand for masks, it is likely not profitable to delay to seek FDA approval. The FDA also is unlikely to approve a new manufacturer's mask without ASTM testing.</p>\n<p>Thus, it is possible that these KN95 masks are a functional equivalent to N95 masks approved for medical use, but have not yet been approved by FDA.</p>\n<p>Keep in mind that that coronavirus particles (fancy scientific name “virions”) are spheres with diameters of approximately 0.125 microns (125 nm). The smallest particles are 0.06 microns, and the largest are 0.14 microns. (Lancet)</p>\n<p>The <a href=\"https://smartairfilters.com/en/blog/can-masks-capture-coronavirus/\" rel=\"nofollow noreferrer\">article here</a> may be useful to help you sort through the efficiency of masks.</p>\n", "score": 9 }, { "answer_id": 24397, "body": "<p>Typically for an N95 mask to be considered &quot;medical grade&quot; it must be compatible with a sterile environment, such as by filtering both inhaled and exhaled air.</p>\n<p>Surgical masks provide some filtration of exhaled air, which is why they're useful in surgury (e.g. keep saliva off an operating region).\nI have an N95 mask advertised for environments with dust and smoke (e.g. to wear while working with soil to <a href=\"https://worksafe.govt.nz/topic-and-industry/legionnaires-disease/legionnaires-disease-and-legionellosis/\" rel=\"nofollow noreferrer\">prevent Legionnaires' disease</a>). In these environments there's no need to filter air on the exhale; such filter would add to cost and increase the effort to exhale. For this reason &quot;medical grade&quot; N95 masks may be more expensive and more humid than those with a valve for exhaling air.</p>\n<p>Unless there's a significant difference in how the filters are manufactured, then these masks are effectively the same for filtration of inhaled air. If medical grade masks were able to filter 99% of particles within a given size range then they would be N99 masks, not N95 masks.</p>\n<p>However as @BobE mentioned &quot;medical grade&quot; likely must pass further tests and conform to other regulations (and perhaps requiring more expensive quality control measures) which would drive up the prices and could delay a product from reaching market.</p>\n", "score": 3 }, { "answer_id": 24399, "body": "<p>The mask protects people from <strong>the person wearing the mask</strong>. In surgery, my colleagues and I wear a mask to protect the patient's open wound from me. Do not make the mistake of thinking that you, as the mask wearer, are conferring a degree of protection that provides safety.</p>\n", "score": 1 } ]

[ "covid-19", "face-mask-respirator", "personal-protective-equipment", "protection", "regulatory-agencies" ]

[ { "answer_id": 24429, "body": "<p>Parenchyma is functional tissue, i. e. tissue that has a specific function. Organs are built from functional tissue and connective/structural tissue (stroma). In the kidney this is e. g. Gerota's fascia (stroma) vs. the tissue producing urine (glomerula etc.).</p>\n<p>You can look up more combinations of what parts of organs are parenchyma and which are stroma at e. g. Wikipedia: <a href=\"https://en.m.wikipedia.org/wiki/Parenchyma\" rel=\"noreferrer\">https://en.m.wikipedia.org/wiki/Parenchyma</a></p>\n<p>The NIH definition reads: &quot;Solid organ which consists of parenchyma and connective tissue stroma; the stroma subdivides the parenchyma into lobes, segments, lobules, acini, or cortex and medulla. Examples: lung, liver, spleen, kidney, parathyroid gland.&quot; (<a href=\"https://www.semanticscholar.org/topic/Parenchymatous-organ/1409347\" rel=\"noreferrer\">https://www.semanticscholar.org/topic/Parenchymatous-organ/1409347</a>)</p>\n<p>So in short parenchymatous organs are those that have parenchyma and are solid versus those that have a lumen or pouch or similar.</p>\n", "score": 5 } ]

[ "anatomy", "internal-organs" ]

[ { "answer_id": 24438, "body": "<p>Liver donation - <em>an act of great honor</em> - should only be done once.</p>\n<p>Liver regeneration occurs via compensatory hyperplasia.</p>\n<blockquote>\n<p>Regeneration of the liver can be more correctly defined as <em>compensatory hyperplasia</em> where in the remaining liver tissue expands to meet the metabolic needs of the organism. Unlike anatomic true regeneration, the expanding liver does not regain its original gross anatomical structure.</p>\n</blockquote>\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3976740/\" rel=\"nofollow noreferrer\">Source</a></p>\n<p>Thus, the structure is very different and not ideal for another surgery recipient.</p>\n", "score": 2 } ]

[ "liver", "organ-donation", "internal-organs", "organ-transplant", "organ-damage" ]

[ { "answer_id": 24878, "body": "<p><a href=\"https://www.zorinaq.com/\" rel=\"nofollow noreferrer\">Marc Bevand</a> presents this graph of IFR versus age for both COVID-19 and flu:</p>\n<p><img src=\"https://i.stack.imgur.com/Fzj7r.png\" alt=\"[https://raw.githubusercontent.com/mbevand/covid19-age-stratified-ifr/master/covid_vs_flu.png]\" /></p>\n<p>The sources of data are documented on this <a href=\"https://github.com/mbevand/covid19-age-stratified-ifr\" rel=\"nofollow noreferrer\">github page</a>. There is a summary of the sources in the <a href=\"https://github.com/mbevand/covid19-age-stratified-ifr/blob/master/README.md\" rel=\"nofollow noreferrer\">README file</a>.</p>\n<p>Unfortunately, the IFR data in the graph does not come with error bars.\nHowever, most of the underlying sources do include error bars.\nFor instance, Table 1 of <a href=\"https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30243-7/fulltext\" rel=\"nofollow noreferrer\">&quot;Estimates of the severity of coronavirus disease 2019: a model-based analysis&quot;, by Verity, et. al.</a> states:</p>\n<pre><code>| age group | IFR | confidence interval |\n|-----------+----------+---------------------|\n| 0–9 | 0.00161% | (0.000185–0.0249) |\n| 10–19 | 0.00695% | (0.00149–0.0502) |\n| 20–29 | 0.0309% | (0.0138–0.0923) |\n| 30–39 | 0.0844% | (0.0408–0.185) |\n| 40–49 | 0.161% | (0.0764–0.323) |\n| 50–59 | 0.595% | (0.344–1.28) |\n| 60–69 | 1.93% | (1.11–3.89) |\n| 70–79 | 4.28% | (2.45–8.44) |\n| ≥80 | 7.80% | (3.80–13.3) |\n</code></pre>\n<p>In contrast, the <a href=\"https://www.cdc.gov/coronavirus/2019-ncov/hcp/planning-scenarios.html\" rel=\"nofollow noreferrer\">&quot;US CDC&quot; COVID-19 IFR data</a> are presented as &quot;current best estimates&quot; which do not state confidence intervals.</p>\n<p>I found the graph by google searching for &quot;ifr flu by age&quot;, and clicking the &quot;Images&quot; link. Sifting through the graphs led to <a href=\"https://twitter.com/zorinaq/status/1311025455655301120\" rel=\"nofollow noreferrer\">tweets</a> which reference the github page.</p>\n", "score": 4 } ]

[ "covid-19", "epidemiology", "influenza" ]

[ { "answer_id": 25357, "body": "<p>From another <a href=\"https://www.pnas.org/content/117/41/25897\" rel=\"nofollow noreferrer\">2020 paper</a> which makes this distinction (in those terms) but cites an older <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7158572/\" rel=\"nofollow noreferrer\">2020 paper</a> that never mentions &quot;suppression&quot; but e.g. refers to China's strategy as &quot;containment&quot;... it's easy to search for the (right) terms in the 6th ed. of the <em>Dictionary of Epidemiology</em>, which again doesn't mention &quot;suppression&quot; but...</p>\n<blockquote>\n<p>containment: The concept of regional eradication of a communicable disease, first proposed\nby Soper in 1949 for the elimination of smallpox. Containment of a worldwide\ncommunicable disease demands a globally coordinated effort, so that countries that\nhave effected an interruption of transmission do not become reinfected following\nimportation from neighboring endemic areas.</p>\n</blockquote>\n<p>Mitigation is a less obscure term, but only defined rather broadly in that dictionary as</p>\n<blockquote>\n<p>mitigation: Reduction of the risk of disaster. Actions taken to avoid or minimize negative\nenvironmental, medical, or social impacts</p>\n</blockquote>\n<p>The [re]definition in sharper terms of R is pretty new, I conclude, and in line with the UK government's focus on R (at the time anyway), which has itself received <a href=\"https://www.nature.com/articles/d41586-020-02009-w\" rel=\"nofollow noreferrer\">some flak</a>.</p>\n<p>One could argue that &quot;containment&quot; is a somewhat bad term for &quot;regional eradication&quot;, and that &quot;suppression&quot; is a better one, but I haven't quite seen someone make this word argument explicit.</p>\n<p>A March 2020 <a href=\"http://www.oecd.org/coronavirus/policy-responses/flattening-the-covid-19-peak-containment-and-mitigation-policies-e96a4226/\" rel=\"nofollow noreferrer\">OECD paper</a>, while making the same rough dichotomy uses &quot;containment&quot;:</p>\n<blockquote>\n<p>In the absence of effective drugs and vaccines, containment and mitigation measures are the key public health interventions currently available to minimise the dramatic health consequences caused by COVID‑19. More specifically:</p>\n<p>Containment strategies aim to minimise the risk of transmission from infected to non-infected individuals in order to stop the outbreak. This may include actions to detect cases early on and trace an infected individual’s contacts, or the confinement of affected persons;</p>\n<p>Mitigation strategies aim to slow the disease, and to reduce the peak in health care demand. This may include policy actions such as social distancing, including a full society ‘lock-down’, and improved personal and environmental hygiene.</p>\n</blockquote>\n<p>It's not too clear who wrote that, as they only give some OECD secretariat contacts, and they might not be the actual authors...</p>\n<p>As far putting containment in opposition to mitigation... it's hard to say when such a contrast started to be made. A quick search finds at least one <a href=\"https://journals.sagepub.com/doi/pdf/10.1177/0037549715581637\" rel=\"nofollow noreferrer\">2015 paper </a> from China on their response to the 2009 H1N1 outbreak that speaks of containment <em>and</em> mitigation, and looking a bit through the paper I don't see a place where they make a sharp contraposition. So it may be a bit hard to find when the distinction was turned into a clear contrast.</p>\n", "score": 1 } ]

[ "epidemiology" ]

[ { "answer_id": 24925, "body": "<p>&quot;Effective dose&quot; is not a physical quantity, but a calculated summary value meant to evaluate the risk of some radiation exposure to other sources and to set occupational limits.</p>\n<p>From Fisher &amp; Fahey 2017:</p>\n<blockquote>\n<p>Effective dose is a mathematical construct, concept, or surrogate of risk, used in radiation protection as the basis for calculating annual radiation limits to workers and members of the public from exposure to radiation and intakes of radionuclides.</p>\n</blockquote>\n<p>The <a href=\"https://en.wikipedia.org/wiki/International_Commission_on_Radiological_Protection\" rel=\"nofollow noreferrer\">International Commission on Radiological Protection</a> is the body that determines how to make these calculations. They weight the absorbed dose targeted to different organs by the risk of radiation exposure to those organs.</p>\n<p>So yes, radiation exposure to the head has a higher risk to tissues in the head than elsewhere in the body, but the effective dose is a measure that allows for equivalent comparisons to be made when radiation is targeted elsewhere or received by the whole body.</p>\n<p>The Fisher &amp; Fahey paper goes into more depth on the appropriate and inappropriate uses for this measure and related measures, so I recommend it for further reading if you are interested.</p>\n<p>Fisher, D. R., &amp; Fahey, F. H. (2017). Appropriate use of effective dose in radiation protection and risk assessment. Health physics, 113(2), 102.</p>\n", "score": 2 } ]

[ "radiology" ]

[ { "answer_id": 25439, "body": "<p>The &quot;-meran&quot; suffix was selected by the World Health Organisation (WHO) as a common stem suffix for mRNA drug products in 2016 (though the technology originated in the early 1990s). Curevac were involved in pioneering this technology and they made the application. See <a href=\"https://www.prnewswire.com/news-releases/curevac-announces-meran-has-been-approved-by-the-world-health-organization-as-suffix-for-mrna-drug-substances-300222034.html\" rel=\"nofollow noreferrer\">this article</a> announcing the news.</p>\n<p>From the WHO <a href=\"https://www.who.int/medicines/services/inn/innquidance/en/\" rel=\"nofollow noreferrer\">guidance on International Nonproprietary Name (INN)</a>:</p>\n<blockquote>\n<p>Another important feature of the INN system is that the names of pharmacologically-related substances demonstrate their relationship by using a common &quot;stem&quot;. By the use of common stems the medical practitioner, the pharmacist, or anyone dealing with pharmaceutical products can recognize that the substance belongs to a group of substances having similar pharmacological activity.</p>\n</blockquote>\n<blockquote>\n<p>The extent of INN utilization is expanding with the increase in the number of names. Its wide application and global recognition are also due to close collaboration in the process of INN selection with numerous national drug nomenclature bodies. The increasing coverage of the drug-name area by INN has led to the situation whereby the majority of pharmaceutical substances used today in medical practice are designated by an INN. The use of INN is already common in research and clinical documentation, while their importance is growing further due to expanding use of generic names for pharmaceutical products.</p>\n</blockquote>\n<p>While INN use is widespread, it is not complete, nor is it a requirement for drug approval at local or national level.</p>\n<blockquote>\n<p>The process of INN selection follows three main steps:</p>\n<ol>\n<li><p>A request/application is made by the manufacturer or inventor;</p>\n</li>\n<li><p>After a review of the request a proposed INN is selected and published for comments;</p>\n</li>\n<li><p>After a time-period for objections has lapsed, the name will obtain the status of a recommended INN and will be published as such if no objection has been raised.</p>\n</li>\n</ol>\n</blockquote>\n<p>The process is entirely separate from drug approval through national agencies (like the FDA in the USA, EMA in the EU and MHRA in the UK). It may take some time to complete as it includes time for objections to be registered. Commonly, drugs are referred to by a code name during trials, before being assigned an INN and of course a proprietary name later.</p>\n<p>For example, the <a href=\"https://en.m.wikipedia.org/wiki/Tozinameran\" rel=\"nofollow noreferrer\">Pfizer-BioNTech COVID-19 vaccine</a> has an INN of &quot;Tozinameran&quot; but was code-named &quot;BNT162b2&quot; during development and trials.</p>\n<p><a href=\"https://www.who.int/medicines/services/inn/20_480_Annex_INN_Form_nucleic_20200518.pdf?ua=1\" rel=\"nofollow noreferrer\">Specific guidance</a> is available on the application process for nucleus acid drugs (like mRNA).</p>\n<hr />\n<blockquote>\n<p>INN are selected in principle only for single, well-defined substances that can be unequivocally characterized by a chemical name (or formula). It is the policy of the INN programme not to select names for mixtures of substances, while substances that are not fully characterized are included in the INN system in exceptional cases only.</p>\n</blockquote>\n<p>Not every substance can or should have an INN. However, as you rightly state, mRNA vaccines are getting INNs ending in the &quot;-meran&quot; suffix.</p>\n<hr />\n<p>In summary, I suspect that the Moderna vaccine will get a INN with a &quot;-meran&quot; suffix, but as these vaccines are only just being approved for emergency use, the process has not completed yet. I could not find any information on the status (if any) of an INN application for Moderna’s mRNA-1273 vaccine, but I did find an <a href=\"https://www.ema.europa.eu/en/news/update-assessment-marketing-authorisation-application-modernas-mrna-1273-covid-19-vaccine\" rel=\"nofollow noreferrer\">update</a> from the EMA about the approval process.</p>\n<hr />\n<p><strong>Other sources</strong></p>\n<p>Wikipedia: <a href=\"https://en.m.wikipedia.org/wiki/International_nonproprietary_name\" rel=\"nofollow noreferrer\">INN</a>, <a href=\"https://en.m.wikipedia.org/wiki/RNA_vaccine\" rel=\"nofollow noreferrer\">RNA Vaccines</a></p>\n", "score": 4 } ]

[ "covid-19", "vaccination", "who-world-health-org" ]

[ { "answer_id": 25483, "body": "<p>You say:</p>\n<blockquote>\n<p>I can't find any evidence or articles that specifically confirm that our immune system won't start targeting healthy ligands, such as hormones, other proteins, or even pharmaceutical drugs assuming they may have a similar enough structure to the mRNA-manufactured spike protein.</p>\n</blockquote>\n<p>&quot;mRNA-manufactured&quot; is a red herring here. If the spike protein could cause such an auto-immune response you'd see it from any vaccine that uses the SARS-CoV-2 spike in any shape or form (e.g the classic protein-subunit vaccines that are in phase III trials), as well as from the SARS-CoV-2 virus itself.</p>\n<p>Now it's true that the virus itself does cause an immune overreaction in some people but this actually <a href=\"https://www.sciencedirect.com/science/article/abs/pii/S1568997220300926\" rel=\"noreferrer\">leads</a> to ARDS often leading to death--something that would be hard to miss in clinical trials of the vaccine.</p>\n<p>Speaking of such auto-immune reactions, some have been observed from the vaccines, <a href=\"https://www.nbcsandiego.com/news/local/fda-modernas-covid-19-vaccine-may-cause-side-effects-in-people-with-facial-fillers/2485434/\" rel=\"noreferrer\">involving</a> cosmetic facial fillers. You can't compare these to ARDS.</p>\n<p>It is a more reasonable question if <a href=\"https://www.bmj.com/content/370/bmj.m3026\" rel=\"noreferrer\">&quot;long Covid&quot;</a> reactions could be caused by administration of the vaccine alone, but again &quot;long Covid&quot; symptoms from the actual virus don't take months to <em>emerge</em>, even though various symptoms do persist that long. (I'm actually not sure how quickly the reactions observed in those with cosmetic facial fillers actually subside--maybe you can ask a more focused q on that.)</p>\n<p>Furthermore, consider that phase II or III trials for the vaccines have been done for roughly 6-9 months now... (Actually, the FDA advisory on facial fillers is <a href=\"https://www.nbc12.com/2020/12/30/moderna-covid-vaccine-may-cause-side-effects-people-with-facial-fillers/\" rel=\"noreferrer\">based</a> on the two or so people who had them among the tens of thousands in the phase III trials. Those reactions were actually in line with the reactogenicity more generally observed in the trials--see another <a href=\"https://medicalsciences.stackexchange.com/a/25382/10980\">answer</a> of mine here which touched on that. Note that that might not actually be from the spike protein though.)</p>\n", "score": 6 } ]

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

[ { "answer_id": 25707, "body": "<p>They both <a href=\"https://www.nature.com/articles/d41587-020-00022-y\" rel=\"nofollow noreferrer\">encode</a> the full spike.</p>\n<blockquote>\n<p>The two mRNA front-runners share many commonalities. Both take advantage of modified RNA chemistry to encode the SARS-CoV-2 spike protein with stabilizing mutations added to lock the shape-shifting surface protein into a form easily recognizable to the immune system. Both also use lipid nanoparticle (LNP) delivery systems.</p>\n</blockquote>\n<p>In slightly more (comparative) <a href=\"https://www.nature.com/articles/s41577-020-00480-0\" rel=\"nofollow noreferrer\">detail</a> it's also known they both use the same proline substitions, which stabilize the protein:</p>\n<blockquote>\n<p>The S protein is metastable when produced as a recombinant protein and prone to transform from its pre-fusion to a post-fusion conformation, shedding the S1 subunit. However, the S1 subunit is the immunodominant antigen during CoV infections due to its accessibility for immune recognition and it contains neutralizing epitopes mainly on its RBD. Strategies to stabilize the S protein in its pre-fusion conformation and enhance pre-fusion S protein expression are thought to increase the quality and quantity of vaccine-induced antibodies targeting the functionally relevant epitopes on the S1 subunit. Pallesen et al. reported two proline substitutions (2P) at the apex of the central helix and HR1 that can retain the S proteins of MERS-CoV, SARS-CoV and HKU1 in the antigenically optimal pre-fusion conformation. The resulting antigen, S-2P, induced much greater nAb titres than wild-type S protein in mice. Learning from the previous experience with these CoVs, the S-2P design is now being used in several vaccine strategies against COVID-19.</p>\n<p><strong>SARS-CoV-2 S-2P (comprising proline substitutions at residues K986 and V987) is used as the target antigen in three gene-based vaccine candidates (mRNA vaccines by Moderna/National Institute of Allergy and Infectious Diseases (NIAID) and BioNTech/Pfizer</strong> and a recombinant Ad26 vaccine by Janssen Pharmaceutical Companies) and a protein-based candidate (by Novavax) (Table 1). Moreover, mutation at the cleavage sites in the S protein is also believed to stabilize the pre-fusion conformation of the S protein. S-2P in the Janssen Ad26-vectored vaccine (Ad26.COV2.S) and in the Novavax protein-based vaccine (NVX-CoV2373) contains additional mutations at the S1–S2 polybasic cleavage site from RRAR to SRAG or QQAQ to render it protease resistant, which helps to further stabilize the S protein in its pre-fusion conformation.</p>\n</blockquote>\n<p>As you can see, some other vaccines have additional tweaks to the proteins, but it's not known/said if Pfizer and Moderna's differ in any way in that regrad.\nPfizer has released more data on the exact sequence they used (<a href=\"https://berthub.eu/articles/11889.doc\" rel=\"nofollow noreferrer\">through the WHO</a>); the published sequence includes the untranscribed stabilizing elements. I don't know if Moderna has publicly released the same level of information (i.e. exact sequence) for a meaningful, detailed comparison.</p>\n", "score": 6 } ]

[ "covid-19", "mrna" ]

[ { "answer_id": 29344, "body": "<p>With medicine, no single person is omniscient to all the necessary facts, and physiological differences between individuals complicate this. That said, here are a few general points that would address your question from my perspective.</p>\n<p><strong>Allergies</strong></p>\n<p>Allergies come in multiple forms, ranging from severe, anaphylactic reactions to mild sensitivities. The severest forms are in the minority, and most allergic responses are not immediate nor life-threatening.</p>\n<p><strong>Testing</strong></p>\n<p>Doctors most often test for the severe allergic reactions. This can be done via an IgE RAST test. But there is another important test which should be done to check for the less immediate allergic reactions, which are the majority of allergies: IgG. The IgG test will show results for allergic responses that are not so immediate.</p>\n<p><strong>Alternative</strong></p>\n<p>An individual can actually test for allergies without the help of a blood test by carefully controlling the diet and recording any allergic response. With foods, owing to the length of time for them to transit the GI tract, they can be &quot;in the system&quot; for about three days. To test for an allergy, one may start with a food that is least likely to be an allergen, e.g. rice, and consume only plain rice for three days. Then, assuming the allergic responses have not occurred, add one more food to the diet and watch to see if any signs of a reaction occur within about the next 8 hours. Absent any reaction, add another food, and so on. Keep a careful record of the foods, times, and reactions, and follow this record to determine which food(s) are problematic.</p>\n<p>Allergies are induced by proteins since the immune system response is toward proteins. But even an oil, such as soybean oil, may induce an allergic response if the processing of that oil left traces of proteins. It takes very little exposure to induce an allergic response. In most cases, a minute amount of the allergen will have the same effect as a large quantity of it. If you are allergic to milk, you may as well have a whole glass of it as to have a little non-dairy creamer with calcium caseinate (milk protein) as one of its minor ingredients.</p>\n<p><strong>Lifetime of an Allergy</strong></p>\n<p>Allergies can have a limited lifespan, depending on how the individual handles them. If one has zero exposure to a specific allergen for a considerable length of time--say 18 months or more, the immune response may weaken to the point of &quot;forgetting&quot; the allergy. I know of a beekeeper who developed an anaphylactic reaction to the bee stings and had to quit working with bees. He carried an &quot;anakit&quot; (shot of epinephrine) with him for several years, just in case he were to be stung. After ten years had passed, he received an accidental sting, but had no reaction. His body had forgotten the allergy.</p>\n<p><strong>Why Some Foods Banned for Life?</strong></p>\n<p>Any food to be avoided for life implies a non-allergy-based rationale. Chocolate, for example, has some phytochemicals that are similar to our hormones and which have an effect on skin, and many people have experienced increased symptoms of acne or eczema after consuming chocolate. This is not, however, due to an allergic reaction per se.</p>\n<p>Another possibility is that one has consumed too much of something like zinc, and the skin condition is triggered as a result of the body's elevated levels. Zinc is ordinarily considered an essential nutrient, and many people experience zinc deficiency; but zinc can also become toxic if one is overexposed to it. A mineral test, such as a hair-mineral analysis (HMA) test, may be indicated to determine if this might be a factor.</p>\n<p><strong>Conclusion</strong></p>\n<p>With so many possible variables, answers may be hard to find. I would suggest looking more at minerals, vitamins, and longer-term allergic reactions such as those identified by an IgG test.</p>\n<hr />\n<p><strong>References to Some Scientific Publications on Benefits to IgG Testing</strong></p>\n<p>Alpay K, Ertas M, Orhan EK, Üstay DK, Lieners C, Baykan B. Diet restriction in migraine, based on IgG against foods: a clinical double-blind, randomized, crossover trial. Cephalalgia. 2010;30(7):829-837. doi: <a href=\"https://doi.org/10.1177/0333102410361404\" rel=\"nofollow noreferrer\">10.1177/0333102410361404</a>.</p>\n<p>Atkinson W, Sheldon TA, Shaath N, Whorwell PJ. Food elimination based on IgG antibodies in irritable bowel syndrome: a randomized controlled trial. Gut. 2004;51(10):1459-1464. doi: <a href=\"https://doi.org/10.1136/gut.2003.037697\" rel=\"nofollow noreferrer\">10.1136/gut.2003.037697</a>.</p>\n<p>Aydinlar EI, Dikmen PY, Tiftikci A, Saruc M, Aksu M, et al. IgG-based elimination diet in migraine plus irritable bowel syndrome. Headache. 2013;53(3):514-525. doi: <a href=\"https://doi.org/10.1111/j.1526-4610.2012.02296.x\" rel=\"nofollow noreferrer\">10.1111/j.1526-4610.2012.02296.x</a>.</p>\n<p>Bentz S, Hausmann M, Piberger H, Kellermeier S, Paul S, et al. Clinical relevance of IgG antibodies against food antigens in Crohn’s disease: a double-blind crossover diet intervention study. Digestion. 2010;81(4):252-264. doi: <a href=\"https://doi.org/10.1159/000264649\" rel=\"nofollow noreferrer\">10.1159/000264649</a>.</p>\n<p>Bernardi D, Borghesan F, Faggian D, Bianchi FC, Favero E, et al. Time to reconsider the clinical value of immunoglobulin G4 to foods. Clin Chem Lab Med. 2008;46(5):687-690. doi: <a href=\"https://doi.org/10.1515/CCLM.2008.131\" rel=\"nofollow noreferrer\">10.1515/CCLM.2008.131</a>.</p>\n<p>Cai C, Shen J, Zhao D, Qiao Y, Xu A, et al. Serological investigation of food specific immunoglobulin G antibodies in patients with inflammatory bowel diseases. PLoS ONE. 2014;9(11):1-8. doi: <a href=\"https://doi.org/10.1371/journal.pone.0112154\" rel=\"nofollow noreferrer\">10.1371/journal.pone.0112154</a>. [includes Crohn’s and Ulcerative colitis]</p>\n<p>Drisko J, Bischoff B, Hall M, McCallum R. Treating Irritable Bowel Syndrome with a food elimination diet followed by food challenge and probiotics. J Am Coll Nutr. 2006;25(6):514-522. doi: <a href=\"https://doi.org/10.1080/07315724.2006.10719567\" rel=\"nofollow noreferrer\">10.1080/07315724.2006.10719567</a>.</p>\n<p>Fritscher-Ravens A, Pflaum T, Mösinger M, et al. Many Patients With Irritable Bowel Syndrome Have Atypical Food Allergies Not Associated With Immunoglobulin E. Gastroenterology. 2019;157(1):109-118 doi: <a href=\"https://doi.org/10.1053/j.gastro.2019.03.046\" rel=\"nofollow noreferrer\">10.1053/j.gastro.2019.03.046</a>.</p>\n<p>Gunasekeera V, Mendall MA, Chan D, Kumar D. Treatment of Crohn’s Disease with an IgG4-Guided Exclusion Diet: A Randomized Control Trial. Dig Dis Sci. 2016;61(4):1148-1157. doi: <a href=\"https://doi.org/10.1007/s10620-015-3987-z\" rel=\"nofollow noreferrer\">10.1007/s10620-015-3987-z</a>.</p>\n<p>Jian L, Anqi H, Gang L, Litian W, Yanyan X, et al. Food exclusion based on IgG antibodies alleviates symptoms in ulcerative colitis. Inflammatory Bowel Diseases. 2018; 24(9):1918-1925. doi: <a href=\"https://doi.org/10.1093/ibd/izy110\" rel=\"nofollow noreferrer\">10.1093/ibd/izy110</a>.</p>\n<p>Mitchell N, Hewitt CE, Jayakody S, Islam M, Adamson J, Watt I, et al. Randomised controlled trial of food elimination diet based on IgG antibodies for the prevention of migraine like headaches. Nutr J. 2011;10:85. doi: <a href=\"https://doi.org/10.1186/1475-2891-10-85\" rel=\"nofollow noreferrer\">10.1186/1475-2891-10-85</a>.</p>\n<p>Rajendran N, Kumar D. Food-specific IgG4-guided exclusion diets improve symptoms in Crohn’s disease: a pilot study. Colorectal disease. 2011;13(9):1009-1013 doi: <a href=\"https://doi.org/10.1111/j.1463-1318.2010.02373.x\" rel=\"nofollow noreferrer\">10.1111/j.1463-1318.2010.02373.x</a>.</p>\n<p>Sub Lee H, Jae Lee K. Alterations of food-specific serum IgG4 titers to common food antigens in patients with Irritable Bowel Syndrome. J Neurogastroenterol Motility. 2017;23(4):578-584. doi: <a href=\"https://doi.org/10.5056/jnm17054\" rel=\"nofollow noreferrer\">10.5056/jnm17054</a>.</p>\n<p>Uhde M, Caio G, De Giorgio R, Green PH, Volta U, Alaedini A. Subclass Profile of IgG Antibody Response to Gluten Differentiates Non-Celiac Gluten Sensitivity from Celiac Disease. Gastroenterology. 2020; S0016-5085(20)34992-1. doi: <a href=\"https://doi.org/10.1053/j.gastro.2020.07.032\" rel=\"nofollow noreferrer\">10.1053/j.gastro.2020.07.032</a>.</p>\n<p>Wang G, Ren J, Li G, Hu Q, Gu G, Ren H. The utility of food antigen test in the diagnosis of Crohn’s disease and remission maintenance after exclusive enteral nutrition. Clinics and Research in Hepatology and Gastroenterology. 2018;42(2):145-152. doi: <a href=\"https://doi.org/10.1016/j.clinre.2017.09.002\" rel=\"nofollow noreferrer\">10.1016/j.clinre.2017.09.002</a>.</p>\n<p>Xie Y, Zhou G, Xu Y, He B, Wang Y, Ma R, et al. Effects of Diet Based on IgG Elimination Combined with Probiotics on Migraine Plus Irritable Bowel Syndrome. J Pain Res. 2019;7890461. doi: <a href=\"https://doi.org/10.1155/2019/7890461\" rel=\"nofollow noreferrer\">10.1155/2019/7890461</a>.</p>\n<p>Zar S, Benson M, Kumar D. Food-specific Serum IgG4 and IgE titers to common food antigens in Irritable Bowel Syndrome. Am J Gastroenterol. 2005;100(7):1550-1557. doi: <a href=\"https://doi.org/10.1111/j.1572-0241.2005.41348.x\" rel=\"nofollow noreferrer\">10.1111/j.1572-0241.2005.41348.x</a>.</p>\n<p>Zuo XL, Li YQ, Li WJ, Guo YT, Lu XF, et al. Alterations of food antigen-specific serum immunoglobulins G and E antibodies in patients with irritable bowel syndrome and functional dyspepsia. Clin Exper Allergy. 2007;37:823-830. doi: <a href=\"https://doi.org/10.1111/j.1365-2222.2007.02727.x\" rel=\"nofollow noreferrer\">10.1111/j.1365-2222.2007.02727.x</a>.</p>\n", "score": 2 } ]

[ "diet", "dermatology", "allergy" ]

[ { "answer_id": 25758, "body": "<p>Apparently, yes fluoridated mouthwash seems beneficial against carries, at least in children. ADA <a href=\"https://www.ada.org/en/member-center/oral-health-topics/mouthrinse\" rel=\"noreferrer\">says</a>:</p>\n<blockquote>\n<p>Fluoride ions, which promote remineralization, may be provided by certain mouthwashes. A Cochrane systematic review found that regular use of fluoride mouthwash reduced tooth decay in children, regardless of exposure to other sources of fluoride (i.e., fluoridated water or toothpaste containing fluoride).</p>\n<p>[citing:] Marinho VC, Higgins JP, Logan S, Sheiham A. <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6999805/\" rel=\"noreferrer\">Topical fluoride (toothpastes, mouthrinses, gels or varnishes) for preventing dental caries in children and adolescents.</a> Cochrane Database Syst Rev 2003(4):CD002782.</p>\n</blockquote>\n<p>Mouthwashes also seem to help with gingivitis, although which active ingredient is best/responsible for that seems less clear:</p>\n<blockquote>\n<p>When used in mouthwashes, antimicrobial ingredients like cetylpyridinium, chlorhexidine, and essential oils have been shown to reduce plaque and gingivitis when combined with daily brushing and flossing. While some studies have found that chlorhexidine achieved better plaque control than essential oils, no difference was observed with respect to gingivitis control.</p>\n</blockquote>\n<p>Frankly that seems more controversial, as the meta-analyses <a href=\"https://pubmed.ncbi.nlm.nih.gov/26227646/\" rel=\"noreferrer\">cited</a> (by ADA) for the latter seems to have had some comments/correspondence. I didn't follow the exchange.</p>\n<p>The NHS <a href=\"https://www.nhs.uk/conditions/gum-disease/treatment/\" rel=\"noreferrer\">recommends</a> against using a mouthwash with chlorhexidine for longer than 4 weeks because of the staining it can cause.</p>\n", "score": 5 } ]

[ "dentistry", "oral-health", "brushing-teeth", "mouthwash", "mouth" ]

[ { "answer_id": 26224, "body": "<p>Literally translating the terms would say that bradycardia is a &quot;slow heart&quot; and a bradyarrhythmia is a &quot;slow abnormal/irregular (heartbeat)&quot;. In many cases they will substantially overlap, and I think you will find that different writers make different levels of distinction between them, so you'll have to use surrounding context to infer the intended meaning.</p>\n<p>Consider the opinion statement at the beginning of this article:</p>\n<p>Dresing, T. J., &amp; Wilkoff, B. L. (2001). Bradyarrhythmias. Current treatment options in cardiovascular medicine, 3(4), 291-298.</p>\n<p>in which the authors argue:</p>\n<blockquote>\n<p>In our opinion, the term bradyarrhythmia should be reserved for bradycardias (heart rates less than 60) that are associated with symptoms such as syncope or near-syncope, congestive heart failure, exercise intolerance, fatigue, or a confusional state that improves with resolution of the bradycardia.</p>\n</blockquote>\n<p>They're suggesting that &quot;bradycardia&quot; should be reserved for the simple meaning of a &quot;slower than normal resting heart rate&quot; &lt;60 beats per minute, and &quot;bradyarrhythmia&quot; should be used only when some evidence of pathology is present. An athlete with a naturally slow heart rate due to their level of physical fitness could then be said to have &quot;bradycardia&quot; but not a &quot;bradyarrhythmia&quot;.</p>\n<p>Why mention this opinion at the beginning of their paper? I think the best explanation is that the authors see the terms used interchangeably (especially implied assumptions that slow heart rate == pathology) and are looking to separate them better.</p>\n", "score": 3 } ]

[ "cardiology", "blood-circulation", "electrocardiogram", "cardiac-physiology" ]

[ { "answer_id": 27604, "body": "<p>Trivial in concept, sure, but not necessarily trivial in practice. It's not about just producing a handful of doses in a proof-of-concept; if you want to produce a different version of a vaccine at scale it means either building a bunch of new equipment or retooling a previous production line to make the whole vaccine. Since only a minority of people are vaccinated world-wide, it makes sense that the original vaccines continue to be manufactured since these are still effective against the variants that are being transmitted (maybe not as effective as they can be, of course). Right now, it's almost certainly more important to get <em>any</em> vaccine into arms rather than the ideal vaccine.</p>\n<p>That said, it would be false to state that vaccines to target variants are not in the pipeline. Pfizer <a href=\"https://www.cnbc.com/2021/07/08/pfizer-says-it-is-developing-a-covid-booster-shot-to-target-the-highly-transmissible-delta-variant.html\" rel=\"noreferrer\">announced today</a>, for example, that they are developing a booster to target the delta variant. Presumably other vaccine manufacturers are doing so as well - not everything in pharmaceutical research labs gets reported. Manufacturers have to make cost-benefit analyses about what variants to target. Had they prepared a variant booster a few months ago it might have targeted the alpha variant rather than delta variant, for example; today, it seems targeting the delta variant is more pressing.</p>\n<p>I'd also add that, as far as I know, no regulatory agency has declared that <em>no</em> clinical trials of an &quot;updated&quot; mRNA vaccine is necessary, or publicly specified what data are required, so I think that's just speculation so far, although well-informed. If descendants of COVID-19 become endemic like influenza, then it seems likely that a regulatory framework similar to that for the annual influenza vaccine would allow new formulations to be distributed without large-scale testing (like in this Q&amp;A: <a href=\"https://medicalsciences.stackexchange.com/questions/24637/\">Flu vaccine paradox</a>), but we aren't there yet.</p>\n", "score": 7 } ]

[ "covid-19", "vaccination" ]

[ { "answer_id": 29367, "body": "<p>The <a href=\"https://www.rxlist.com/adderall_vs_ritalin/drugs-condition.htm\" rel=\"noreferrer\">Adderall vs. Ritalin page on Rx List</a> gives the answer.</p>\n<blockquote>\n<p>Both Adderall (amphetamine and dextroamphetamine) and Ritalin (methylphenidate) are central nervous system stimulants used to treat attention deficit hyperactivity disorder [ADHD].</p>\n<p>Methylphenidate (also sold as Concerta) isn't an amphetamine and its effects tend to be milder than those of Adderall. Patients also report a more pronounced effect on cognitive function and thought processes when taking Ritalin as opposed to Adderall, which comes with a number of effects on the body such as increased heart rate and others.</p>\n</blockquote>\n<p>I would imagine that the reason for it to be banned in chess is that</p>\n<blockquote>\n<p>Ritalin may help increase attention and decrease impulsiveness.</p>\n</blockquote>\n<p>Therefore, it could potentially create an unfair advantage to those who are under the influence.</p>\n<p>However, the World Anti Doping Agency (WADA) do have <a href=\"https://www.wada-ama.org/en/what-we-do/science-medical/therapeutic-use-exemptions\" rel=\"noreferrer\">Therapeutic Use Exemptions (TUEs)</a>. This allows those suffering from ADHD for example, to continue their medication therapy as long as they satisfy strict criteria. (See <a href=\"https://www.usada.org/spirit-of-sport/education/athletes-adhd-know-about-tues/\" rel=\"noreferrer\">the USADA webpage</a> for more)</p>\n<blockquote>\n<p>Athletes with ADHD can continue using necessary prohibited stimulant medications while competing in sanctioned sports as long as they receive a Therapeutic Use Exemption (TUE), which requires them to demonstrate that they can satisfy strict criteria for TUE approval.</p>\n</blockquote>\n", "score": 7 }, { "answer_id": 30518, "body": "<p>I agree that the regulation is worded inappropriately, and that methylphenidate is not an amphetamine. However, I would like to provide a more thorough answer than &quot;rxlist.com says so&quot;. We'll have to borrow a few ideas from organic chemistry.</p>\n<p><em>Amphetamine</em> is a substance with a specific molecular structure, shown below (under the title &quot;Adderall&quot;), and <em>an amphetamine</em> is any of many substances with molecular structures based on that of amphetamine (examples in the second image). You can think of amphetamine as the parent structure of a class of substances which are called <em>substituted amphetamines</em> or simply <em>amphetamines</em>. For instance, if the group of atoms circled in blue on the methylphenidate structure was placed on the amphetamine structure, you would have a substituted amphetamine (&quot;an amphetamine&quot;).</p>\n<p><a href=\"https://i.stack.imgur.com/hRYSs.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/hRYSs.jpg\" alt=\"enter image description here\" /></a></p>\n<p>Methamphetamine, MDMA, ephedrine, methylephedrine and pseudoephedrine are also amphetamines in this sense. I've highlighted in green groups that are added to <em>amphetamine</em> to produce some of these <em>amphetamines</em>.</p>\n<p><a href=\"https://i.stack.imgur.com/1U4iu.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/1U4iu.jpg\" alt=\"enter image description here\" /></a></p>\n<p>So, why isn't methylphenidate an amphetamine? The blue group doesn't make a difference, because adding it to amphetamine would just produce a substituted amphetamine. It is the group of atoms circled in red that matter. You see, <em>amphetamine</em> is a portmanteau of <em><strong>a</strong>lpha-<strong>m</strong>ethyl<strong>ph</strong>en<strong>et</strong>hyl<strong>amine</strong></em>, which signifies that amphetamine is a <em>phenethylamine</em> molecule with a <em>methyl group</em> (CH3) in the <em>alpha</em> location, as depicted below. (Phenethylamines are an interesting class of molecules in their own right, including many drugs and neurotransmitters such as dopamine, norepinephrine and adrenaline.)</p>\n<p><a href=\"https://i.stack.imgur.com/rK8w5.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/rK8w5.jpg\" alt=\"enter image description here\" /></a></p>\n<p>The group in the alpha position is crucial to our question. If the group at the alpha position is not CH3, then the molecule is not an amphetamine. In methylphenidate, the group in the alpha position (circled in red) is a chain of four carbon atoms (and their associated hydrogens) which may be represented as CH2-CH2-CH2-CH2 (and happens to connect to the N atom at the far end, though this doesn't matter for our purposes). Since methylphenidate has a 4-carbon chain in the alpha position of its molecular structure, it cannot be called an <strong>am</strong>phetamine, because as mentioned in the previous paragraph the <strong>am</strong> implies there is a 1-carbon (<strong>m</strong>ethyl) group in the <strong>a</strong>lpha position.</p>\n<p><a href=\"https://i.stack.imgur.com/hRYSs.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/hRYSs.jpg\" alt=\"enter image description here\" /></a></p>\n<p>Despite this, methylphenidate and amphetamine do have a lot in common. They both belong to the <em>functional</em> class of CNS stimulants, as the OP and the other answerer are aware. In addition, methylphenidate and amphetamine do both belong to a common <em>structural</em> class, which is the phenethylamine class. That is to say, both methylphenidate and amphetamine are (substituted) phenethylamines.</p>\n<p>Therefore, one way in which the chess WADA policy could be reworded is:</p>\n<blockquote>\n<p><strong>Phenethylamine Stimulants</strong> - Ritalin or amphetamines such as\nAdderall, ephedrine, pseudoephedrine or methylephedrine, when\nexceeding the urine concentrations listed below.</p>\n</blockquote>\n<p>Using the category <em>phenethylamine stimulants</em> would be scientifically correct and provide a useful contrast to the category of non-prohibited stimulants, i.e. caffeine.</p>\n", "score": 4 } ]

[ "medications", "mental-health", "biochemistry", "stimulants", "adhd" ]

[ { "answer_id": 30572, "body": "<p>Interesting question. According to [1]:</p>\n<blockquote>\n<p>Postural hypotension has been estimated to occur in some 15% of patients who take plain levodopa during the first year of treatment</p>\n</blockquote>\n<p>So the hypotension side effect is <em>postural</em> (orthostatic) in nature, not general.\nThis makes sense. Dopamine activates the sympathetic nervous system.</p>\n<p>So let's say that dopamine already increased heart rate, vasoconstriction, and blood pressure. If someone on L-dopa stands up, they don't have a lot of homeostatic control mechanisms left to counteract the orthostatic pooling of blood in the legs. The result is a decrease in blood pressure of the brain. This could result in orthostatic hypotension, lightheadedness, and even collapse.</p>\n<p>On the other hand, [1] also states:</p>\n<blockquote>\n<p>it is doubtful whether the difference is significant.</p>\n</blockquote>\n<p>In other words, patients that require L-dopa probably already have a high risk of postural hypotension. This is not an unreasonable statement because L-dopa is typically used in the treatment of Parkinson disease. And autonomic dysfunction is common in Parkinson disease.</p>\n<p>[1] Aronson JK, et al. Meyler's side effects of drugs. 16th ed. Amsterdam. Page 4:545. Elsevier, 2016.</p>\n", "score": 2 } ]

[ "central-nervous-system" ]

[ { "answer_id": 30674, "body": "<p>As you stipulated no trauma and it has been lifelong, <a href=\"https://www.nationwidechildrens.org/conditions/hoarse-voice-dysphonia\" rel=\"nofollow noreferrer\">the first link you provided</a> says that it could be down to</p>\n<blockquote>\n<p>Vocal cord paralysis</p>\n<ul>\n<li>Patients can be born with a weak vocal cord or develop weakness with movement of the vocal cords from a nerve injury. The patient will often have a raspy voice that is weak or breathy.</li>\n</ul>\n</blockquote>\n", "score": 3 } ]

[ "pediatrics", "voice" ]

[ { "answer_id": 30736, "body": "<p>A virus isolated from rare blood samples was believed to be able to cause hepatitis, and this virus was designated as the hepatitis F virus. (Source: <a href=\"https://www.medicinenet.com/hepatitis_f/definition.htm\" rel=\"noreferrer\">MedicineNet</a>)</p>\n<blockquote>\n<p>Further investigation has failed to confirm the existence of this virus. There is no known hepatitis F virus.</p>\n</blockquote>\n<p>For more information on the candidate Hepatitis F virus, see <a href=\"https://doi.org/10.1007/978-4-431-68255-4_19\" rel=\"noreferrer\">Fagan &amp; Harrison (1994)</a>.</p>\n<h2>References</h2>\n<p>Fagan, E. A., &amp; Harrison, T. J. (1994). Candidate hepatitis F virus in sporadic non-A, non-B acute liver failure: exclusion in liver of hepatitis viruses A, E, C and B by polymerase chain reaction. In <em>Viral Hepatitis and Liver Disease</em> (pp. 73-76). Springer, Tokyo. <a href=\"https://doi.org/10.1007/978-4-431-68255-4_19\" rel=\"noreferrer\">https://doi.org/10.1007/978-4-431-68255-4_19</a></p>\n", "score": 10 } ]

[ "hepatitis" ]