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Thread: The science behind Covid-19 - All you need to know

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    With a German study showing that in one of the hardest hit areas in Germany the percentage of the population with antibodies is only approximately 15%, as was the case in the study in Lombardia, it's going to have to be a very staggered and different looking emergence, I think.


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    More contagious and faster spreading than anyone thought...

    https://wwwnc.cdc.gov/eid/article/26/7/20-0282_article

    "Severe acute respiratory syndrome coronavirus 2 is the causative agent of the 2019 novel coronavirus disease pandemic. Initial estimates of the early dynamics of the outbreak in Wuhan, China, suggested a doubling time of the number of infected persons of 6–7 days and a basic reproductive number (R0) of 2.2–2.7. We collected extensive individual case reports across China and estimated key epidemiologic parameters, including the incubation period. We then designed 2 mathematical modeling approaches to infer the outbreak dynamics in Wuhan by using high-resolution domestic travel and infection data. Results show that the doubling time early in the epidemic in Wuhan was 2.3–3.3 days. Assuming a serial interval of 6–9 days, we calculated a median R0 value of 5.7 (95% CI 3.8–8.9). We further show that active surveillance, contact tracing, quarantine, and early strong social distancing efforts are needed to stop transmission of the virus."

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    Quote Originally Posted by Maciamo View Post
    According to the French news website Futura-Sciences, 83% of Coronavirus patients in need of resuscitation in France are overweight or obese. The Guardian already announced 2 weeks ago that in the UK 70% of Corona patients in ICU were overweight or obese. So it would seem that excess weight is a major risk factor - possibly the most aggravating factor along with old age.
    Same data % of Obese with this Disease in the USA ...................but they avoid the word obese and use the outcomes of diseases/illnesses that obesity brings/creates, ie, diabetics etc

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    2 members found this post helpful.
    See:

    The Better Half: On the Genetic Superiority of Women review – bold study of chromosomal advantage

    "Sharon Moalem offers an intriguing theory on how two X chromosomes give women the edge in everything from colour vision to coronavirus"

    https://www.theguardian.com/books/20...omal-advantage

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    Quote Originally Posted by Regio X View Post
    See:

    The Better Half: On the Genetic Superiority of Women review – bold study of chromosomal advantage

    "Sharon Moalem offers an intriguing theory on how two X chromosomes give women the edge in everything from colour vision to coronavirus"

    https://www.theguardian.com/books/20...omal-advantage
    Did we need a study?

    Just kidding. :)

    Yes, it's been shown to be a factor for a lot of diseases.

    What people need to keep in mind is that for women, one of the X chromosomes comes from her father's mother, so she's getting alleles from the whole spectrum of her ancestry even on the X chromosomes.

    Also interesting from some recent studies is that there's some transference from the X as well.

    All of it makes tracing the "source" of the "good" alleles very challenging.

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    Quote Originally Posted by Angela View Post
    Did we need a study?

    Just kidding. :)

    Yes, it's been shown to be a factor for a lot of diseases.

    What people need to keep in mind is that for women, one of the X chromosomes comes from her father's mother, so she's getting alleles from the whole spectrum of her ancestry even on the X chromosomes.

    Also interesting from some recent studies is that there's some transference from the X as well.

    All of it makes tracing the "source" of the "good" alleles very challenging.
    Angela, I believe most of men would - and should - agree that it's indeed the better half. ;)

    I just didn't undestand the part in bold. Could you explain it, in short?

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    Quote Originally Posted by Regio X View Post
    Angela, I believe most of men would - and should - agree that it's indeed the better half. ;)

    I just didn't undestand the part in bold. Could you explain it, in short?
    I'm not at all sure about better, but stronger in terms of health, more long lived, as an average, yes. :)

    I don't know if the science on this has changed, but these are notes I made for myself a good while ago as to what goes on during the production of the egg and the sperm. I'm sure you know most if not all of it, but here it goes...

    The female body doesn't just pick one of its two X chromosomes to go into the egg. A unique X chromosome is made because the two X chromosomes swap some DNA or recombine. Damaged genes on the X are fixed in this way.

    If this is still correct, the y chromosome also goes through a sort of recombination. It can do that because within itself it contains a second copy of its most important genes, and it can use these, which are a palindrome set, to try to correct any errors. In addition, there were papers which found that about 5% of the y matches pretty well with the X and recombine at those sites, also trying to repair errors.

    However, none of this is as good at getting rid of errors as having two whole X chromosomes for recombination.

    The way this was explained in the things that I read is that the lack of another whole chromosome with which to recombine when making sperm is the reason why the y has shrunk in size over time.

    Anyway, that's the way I understood it.

    When I first got interested in this discipline, one of the most difficult things for me was grasping how many female ancestors could be in my X chromosomes, not only from my mother's side, but from my father's side.

    To track inheritance through the X would be a mind boggling task.

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    Quote Originally Posted by Angela View Post
    I'm not at all sure about better, but stronger in terms of health, more long lived, as an average, yes. :)

    I don't know if the science on this has changed, but these are notes I made for myself a good while ago as to what goes on during the production of the egg and the sperm. I'm sure you know most if not all of it, but here it goes...

    The female body doesn't just pick one of its two X chromosomes to go into the egg. A unique X chromosome is made because the two X chromosomes swap some DNA or recombine. Damaged genes on the X are fixed in this way.

    If this is still correct, the y chromosome also goes through a sort of recombination. It can do that because within itself it contains a second copy of its most important genes, and it can use these, which are a palindrome set, to try to correct any errors. In addition, there were papers which found that about 5% of the y matches pretty well with the X and recombine at those sites, also trying to repair errors.

    However, none of this is as good at getting rid of errors as having two whole X chromosomes for recombination.

    The way this was explained in the things that I read is that the lack of another whole chromosome with which to recombine when making sperm is the reason why the y has shrunk in size over time.

    Anyway, that's the way I understood it.

    When I first got interested in this discipline, one of the most difficult things for me was grasping how many female ancestors could be in my X chromosomes, not only from my mother's side, but from my father's side.

    To track inheritance through the X would be a mind boggling task.
    Thanks. Got what you meant now. You were referring mainly to the limited recombination between Y and X, or more specifically between their pseudoautosomal regions (which have genes, btw).

    Yeah, X inheritance is interesting. Below two images that represent it nicely, shared by yourself time ago. :)

    Quote Originally Posted by Angela View Post
    X chromosome inheritance for a female:

    X chromosome inheritance for a male:

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    See:

    Alarmed as COVID patients' blood thickened, New York doctors try new treatments

    https://www.reuters.com/article/us-h...-idUSKCN22421Z

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    Quote Originally Posted by Regio X View Post
    See:
    Alarmed as COVID patients' blood thickened, New York doctors try new treatments
    https://www.reuters.com/article/us-h...-idUSKCN22421Z
    So, neurodegenerative diseases and MS (from a paper on the other thread), and now strokes and kidney disease. I'd rather have the stroke, personally.

    I'm struck by how they said the progression in the lung was almost as if the blood was too thick to move and circulate the air.

    This is most certainly not the flu.

    I don't know how this correlates with the preliminary testing in France showing nicotine (in patches or gum, not inhaled), is helpful. Nicotine increases heart rate, blood pressure, and breathing activity, so maybe it keeps the blood moving more, and more oxygen flowing, but I had always heard that it also leads to blood clots. Perhaps it isn't actually the nicotine which does that?

    When the heck are they going to figure this out?

    I started taking one baby aspirin a day a year or so ago on the doctor's orders. Maybe I'll take a regular one a day for a while.


    This is probably part of the reason why the year to year jump in deaths is so much higher virtually everywhere than the number of semi-official covid deaths. People are dropping dead of strokes, heart attacks, kidney failture etc. Every deceased person should be tested for the presence of Covid and if it could have contributed, i.e. a bunch of young or relatively young people with no known risks suddenly having strokes and heart attacks, for example.

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    SARS-CoV-2 is thought to use ACE2 (rs4646127) as a cell receptor for viral entry. The French paper proposes that nicotine down regulates the activity of ACE2 in lung tissues, which means that cell receptors used by the coronavirus are clogged or covered by nicotine, thus preventing it from infecting the lung.

    The relationship between nicotine and ACE2 has been explored in the framework of cardiovascular and pulmonary diseases [9]. Accordingly, in the ACE/ANG II/AT1R arm, nicotine increases the expression and/or activity of renin, ACE and AT1R, whereas in the compensatory ACE2/ANG-(1–7)/MasR arm, nicotine down regulates the expression and/or activity of ACE2 and AT2R, thus suggesting a possible contribution of acetylcholine receptors in ACE2 regulation. This possibility has not yet been explored in the framework of viral neuroinfections.

    In conclusion, we propose, and try to justify, the hypothesis that nAChRs play a critical role in the pathophysiology of SARS-CoV-2 infection and as a consequence propose nicotine and nicotinic orthosteric and/or allosteric agents as a possible therapy for SARS-CoV-2 infection. Interestingly, ivermectin, which has been recently shown to inhibit the replication of SARS-CoV-2 in cells in vitro [53], is a positive allosteric modulator of a7 nAChR [54]. The nicotinic hypothesis might be further challenged by additional clinical studies and by experimental observations determining whether SARS-CoV-2 physically interacts with the nAChR in vitro, for instance by electrophysiological recordings, high resolution EM and by animal model studies. Further work should also specify the still enigmatic relationships between ACE2 and nAChRs in the nervous system.

    https://www.qeios.com/read/article/571
    Давайте вместе снова сделаем мир великий!

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    Quote Originally Posted by ThirdTerm View Post
    SARS-CoV-2 is thought to use ACE2 (rs4646127) as a cell receptor for viral entry. The French paper proposes that nicotine down regulates the activity of ACE2 in lung tissues, which means that cell receptors used by the coronavirus are clogged or covered by nicotine, thus preventing it from infecting the lung.
    Thanks, Third Term.

    I'm not sure if this is right, but I think I remember they were giving it to some health care workers? What would be the effect of downregulating this activity in the lung?

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    See:

    "
    No case of a child passing coronavirus to an adult exists, evidence review shows

    There has not been a single instance of a child under 10 transmitting the virus, even in contact tracing carried out by WHO
    "

    https://www.telegraph.co.uk/news/202...idence-review/

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    Quote Originally Posted by Regio X View Post
    See:
    "
    No case of a child passing coronavirus to an adult exists, evidence review shows
    There has not been a single instance of a child under 10 transmitting the virus, even in contact tracing carried out by WHO
    "
    https://www.telegraph.co.uk/news/202...idence-review/
    Neither confirming or denying this, however the article and the report it is attempting to report on both state we need more evidence.

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    Very interesting article.

    "
    Do Your Genes Predispose You to COVID-19?

    Individual differences in genetic makeup may explain our susceptibility to the new coronavirus and the severity of the disease it causes
    "

    https://www.scientificamerican.com/a...u-to-covid-19/

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    1 members found this post helpful.
    Quote Originally Posted by Regio X View Post
    Very interesting article.
    "
    Do Your Genes Predispose You to COVID-19?
    Individual differences in genetic makeup may explain our susceptibility to the new coronavirus and the severity of the disease it causes
    "
    https://www.scientificamerican.com/a...u-to-covid-19/
    Two other studies have recently come out, posted on the other thread, one of which looks at it in terms of "continental" groups, which shows the highest susceptibility to severity of result in East Asians, followed by Africans, followed by Europeans.

    Another looks at it in terms of Europe and finds a higher susceptibility in Southern Europe versus Northern Europe.

    This all mirrors previously discovered higher susceptibilities to HIV infection, which shares some coding with CoV-2, and perhaps also to plague.

    Of course, this is all preliminary, and it would only be one factor, but if it turns out they're right, it would go some way to explaining differing outcomes in Europe, and also what is happening with black and Hispanic Americans, and what happened with the original SARS outbreak in Asia. At the slightest, earliest hint of a new virus in China East Asian countries rush to put on masks and isolate carriers. They've been down this road before.

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    I'm getting a bit skeptical of all the "miracle" claims for Vitamin D, but for what it's worth, this paper claims that low levels of Vitamin D correlate with more severe disease and death.

    See:
    http://www.irishhealth.com/article.h...OWwQ_g.twitter

    "Vitamin D may be an important factor in determining the severity of COVID-19 infections, new research from the Irish Longitudinal Study on Ageing (TILDA) at Trinity College Dublin has found.Vitamin D is known as the sunshine vitamin because it is produced in the skin by exposing the body to just 10-15 minutes per day of sunshine. Earlier this month, TILDA published a report which suggested that the vitamin plays an essential role in preventing respiratory infections, reducing antibiotic use, and boosting the immune system's response to infections.
    According to these latest TILDA findings, there are major discrepancies in mortality rates related to vitamin D levels at different latitudes worldwide. Countries in the southern hemisphere, such as Australia, are recording relatively low COVID-related mortality, which the TILDA researchers state can no longer feasibly be related to the later appearance and spread of the virus.
    They have pointed to the high prevalence of vitamin D deficiency in northern hemisphere countries, and the possible role of the vitamin in suppressing severe inflammatory responses seen in patients seriously ill with COVID-19.
    The researchers explained that vitamin D deficiency correlates with poor sunlight exposure, increasing age, high blood pressure, diabetes, obesity and ethnicity. These are all features associated with an increased risk of severe COVID-19.
    Currently, all countries that lie below a latitude of 35 degrees north have relatively low mortality from COVID-19. However, people in countries that lie 35 degrees north and above receive insufficient sunlight for adequate vitamin D levels in winter and spring. These include Italy and Spain, which have low population levels of vitamin D.
    The researchers pointed out that mortality rates from COVID-19 are higher at these latitudes, with the exception of Nordic countries, where vitamin D supplementation is widespread and deficiency is much less common."

    As a result of their findings, the researchers are recommending that all nursing home residents in Ireland take Vitamin D."

    My confidence in this is a little shaken given that you'd think they'd know that Vitamin D is present in cheese as well as milk ONLY if the milk, from which the cheese is made, of course, has been fortified with VItamin D supplements. It's not present in milk naturally, or only in tiny amounts. Maybe they're assuming all the cheese is made with fortified milk, but I don't think that's a valid assumption.

    On the other hand, black Americans have worse outcomes and numerous studies have shown they have chronically low Vitamin D levels, which makes sense given the color of their skin and the latitudes at which they currently live.

    I avoid the sun because I always get terribly burned, and I never drink milk, both because I don't like it or am used to it, and because I became slightly latose intolerant in my thirties, so I've been prescribed Vitamin D supplements in the past, but I'm not taking them now.

    I'm not convinced, but it can't hurt, so I guess I'll start again.

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    Very interesting article about re-using existing drugs to fight covid-19. Scientists identified 47 drugs with the potential to affect covid-19. Sent them to Pasteur Institute and Mount Sinai. Out of all of those these are the most promising:

    Disrupting Translation

    The two compounds are called ternatin-4 and zotatifin. Both of these are currently used to treat multiple myeloma and seem to fight COVID-19 by binding to and inhibiting proteins in the cell that are needed for translation.
    Plitidepsin is a similar molecule to ternatin-4 and is currently undergoing a clinical trial to treat COVID-19. The second drug, zotatifin, hits a different protein involved in translation. We are working with the CEO of the company that produces it to get it into clinical trials as soon as possible.

    Sigma receptors:


    Our original map identified two promising MV cell receptors for drug treatments, SigmaR1 and SigmaR2. Testing confirmed our suspicions.
    We identified seven drugs or molecules that interact with these receptors. Two antipsychotics, haloperidol and melperone, which are used to treat schizophrenia, showed antiviral activity against SARS-CoV-2. Two potent antihistamines, clemastineand cloperastine, also displayed antiviral activity, as did the compound PB28 and the female hormone progesterone.

    https://www.yahoo.com/news/found-tes...182645188.html





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    Clemastine is in Tavist, which I used to take and worded really well for me, but so far as I know it was taken off the market here. The only time I've seen Clemastine used is in medications for dogs. It's still on the market in Britain.

    I think clemastine would be contraindicated for people with certain blood disorders where they have too many red blood cells.

    I also don't know of any over the counter anti-histamines which contain cloperastine, but according to this, one of the antihistamines is pretty close in terms of the receptors.
    https://www.selleckchem.com/products...ochloride.html

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    Pretty good analysis of IFR from all over the world...ranges between .2-4%. So, they settled on .8%. From what I remember Dr. Fauci's estimate at the very beginning was about 1%.


    "Summary: Estimation of infectiousness and fatality of the SARS-CoV-2 virus in the COVID-19 global pandemic is complicated by ascertainment bias resulting from incomplete and non-representative samples of infected individuals. We developed a strategy for overcoming this bias to obtain more plausible estimates of the true values of key epidemiological variables. We fit mechanistic Bayesian latent-variable SIR models to confirmed COVID-19 cases, deaths, and recoveries, for all regions (countries and US states) independently. Bayesian averaging over models, we find that the raw infection incidence rate underestimates the true rate by a factor, the case ascertainment ratio CARt that depends upon region and time. At the regional onset of COVID-19, the predicted global median was 13 infections unreported for each case confirmed (CARt = 0.07 C.I. (0.02, 0.4)). As the infection spread, the median CARt rose to 9 unreported cases for every one diagnosed as of April 15, 2020 (CARt = 0.1 C.I. (0.02, 0.5)). We also estimate that the median global initial reproduction number R0 is 3.3 (C.I (1.5, 8.3)) and the total infection fatality rate near the onset is 0.17% (C.I. (0.05%, 0.9%)). However the time-dependent reproduction number Rt and infection fatality rate as of April 15 were 1.2 (C.I. (0.6, 2.5)) and 0.8% (C.I. (0.2%,4%)), respectively. We find that there is great variability between country- and state-level values. Our estimates are consistent with recent serological estimates of cumulative infections for the state of New York, but inconsistent with claims that very large fractions of the population have already been infected in most other regions. For most regions, our estimates imply a great deal of uncertainty about the current state and trajectory of the epidemic."
    https://sciencehouse.wordpress.com/2...ovid-19-paper/

    I saw an infection rate of 60% for Bergamo. That's approaching herd immunity.

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    1 members found this post helpful.
    Good news if true...

    Positive test results in recovered patients are false positives, not reinfection.
    http://www.koreaherald.com/view.php?ud=20200429000724

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    Quote Originally Posted by Maciamo View Post

    Another paper says that at lower temperatures, the virus could survive on a stainless steel surface from 5 to 28 days. It lasted longest in very cold and dry conditions: at 4°C and 20% humidity. So the environmental conditions play a role too.
    Here is another study, this one about this particular coronavirus, confirming the findings:
    Temperature significantly changes COVID-19 transmission in (sub)tropical cities of Brazil

    Cumulative data with the daily number of confirmed cases was collected from February 27 to April 1, 2020, for all 27 state capital cities of Brazil affected by COVID-19. A generalized additive model (GAM) was applied to explore the linear and nonlinear relationship between annual average temperature compensation and confirmed cases. Also, a polynomial linear regression model was proposed to represent the behavior of the growth curve of COVID-19 in the capital cities of Brazil.
    The GAM dose-response curve suggested a negative linear relationship between temperatures and daily cumulative confirmed cases of COVID-19 in the range from 16.8 °C to 27.4 °C. Each 1 °C rise of temperature was associated with a −4.8951% (t = −2.29, p = 0.0226) decrease in the number of daily cumulative confirmed cases of COVID-19. A sensitivity analysis assessed the robustness of the results of the model. The predicted R-squared of the polynomial linear regression model was 0.81053.
    In this study, which features the tropical temperatures of Brazil, the variation in annual average temperatures ranged from 16.8 °C to 27.4 °C. Results indicated that temperatures had a negative linear relationship with the number of confirmed cases. The curve flattened at a threshold of 25.8 °C. There is no evidence supporting that the curve declined for temperatures above 25.8 °C. The study had the goal of supporting governance for healthcare policymakers.

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7182516/



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    1 members found this post helpful.
    See:

    "
    Blood Clots Are Mysteriously Tied to Many Coronavirus Problems

    Research begins to pick apart the mechanisms behind a deadly COVID-19 complication
    "

    https://www.scientificamerican.com/a...irus-problems/

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    Prediction of mortality in COVID 19 patients ten days in advance.

    https://www.nature.com/articles/s422..._GL_NRJournals

    "The sudden increase in COVID-19 cases is putting high pressure on healthcare services worldwide. At this stage, fast, accurate and early clinical assessment of the disease severity is vital. To support decision making and logistical planning in healthcare systems, this study leverages a database of blood samples from 485 infected patients in the region of Wuhan, China, to identify crucial predictive biomarkers of disease mortality. For this purpose, machine learning tools selected three biomarkers that predict the mortality of individual patients more than 10 days in advance with more than 90% accuracy: lactic dehydrogenase (LDH), lymphocyte and high-sensitivity C-reactive protein (hs-CRP). In particular, relatively high levels of LDH alone seem to play a crucial role in distinguishing the vast majority of cases that require immediate medical attention. This finding is consistent with current medical knowledge that high LDH levels are associated with tissue breakdown occurring in various diseases, including pulmonary disorders such as pneumonia. Overall, this Article suggests a simple and operable decision rule to quickly predict patients at the highest risk, allowing them to be prioritized and potentially reducing the mortality rate."

    Anyone know the snps for these so they could be checked in raw data?

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    1 members found this post helpful.
    APOE e4 genotype predicts severe COVID-19 in the UK Biobank community cohort

    Not one I would have predicted, that's for sure...

    https://www.medrxiv.org/content/10.1....07.20094409v2

    The apolipoprotein E (ApoE) gene makes a protein which, when combined with fat, becomes a lipoprotein. The lipoprotein ApoE is a very low-density lipoprotein, responsible in part for removing cholesterol from the bloodstream. Variations in ApoE affect cholesterol metabolism, which in turn alter your chances of having heart disease and in particular a heart attack or a stroke. Variations in ApoE are also associated with altered odds of having Alzheimer's disease and other diseases.
    There are three relatively common allelic variants of ApoE, as defined by two SNPs, rs429358 and rs7412 known as ApoE-ε2, ApoE-ε3, and ApoE-ε4. The proteins produced by these genes are called ApoE2, ApoE3, and ApoE4. The most common variant overall is the "standard" ApoE-ε3, and therefore more people inherited one ApoE-ε3 from each parent than any other of the possible pairs of variants. Note that each of these types can actually have additional changes too, so there are different subtypes as well.
    Common name Genoset Magnitude rs429358 rs7412 Comment
    Apo-ε1/ε1 gs267 6 (C;C) (T;T) the rare missing allele
    Apo-ε1/ε2 gs271 2.5 (C;T) (T;T)
    Apo-ε1/ε3 gs270 2.6 (C;T) (C;T) ambiguous ε2/ε4 or ε1/ε3
    Apo-ε2/ε4 gs270 2.6 (C;T) (C;T) ambiguous ε2/ε4 or ε1/ε3
    Apo-ε1/ε4 gs272 2.5 (C;C) (C;T)
    Apo-ε2/ε2 gs268 4 (T;T) (T;T) good; lowest risk
    Apo-ε2/ε3 gs269 2 (T;T) (C;T)
    Apo-ε3/ε3 gs246 2 (T;T) (C;C) the most common
    Apo-ε3/ε4 gs141 3 (C;T) (C;C)
    Apo-ε4/ε4 gs216 6 (C;C) (C;C) ~11x increased Alzheimer's risk


    A rare form of the ApoE3 allele, rs121918393, also known as the Christchurch (R136S) mutation, appears to convey a significant amount of resistance to PSEN1-based form of autosomal dominant Alzheimer’s, according to a 2019 study.[1]

    There's more. Ancestry apparently does a lousy job with this and the results might be inaccurate.

    For me:

    rs429358:TT

    rs7412:CT

    Well, I guess I'm E2/E3.

    Not the worst.

    Another bad one:rs4420638
    I'm AA. GG is trouble.

    I wonder if this is about whether it affects your heart or just gives you pneumonia.

    At any rate, take it all with a grain of salt. This is not yet exact science.

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