Arete

Given the Gospel of John was written by an Alexandrian theologian, in Greek, 100 years after the death of Jesus - and I would assume you're quoting a subsequent English translation, how accurate do you think the direct quotes are?

Indeed. I also wasn't responding to you personally. Absolutely. I accepted a type iv pilus from a friendly giraffe earlier today, got a sweet new metabolic plasmid, and now I don't actually need to breathe air. I also ate a big lunch, but just replicated my circular genome and divided, and we felt great. It sure does. The Dean is sure going to be happy to hear that intro psych and microbiology are the same class. Gonna save the campus a bunch.

"I've been kicked out of every bar in the city for being too charming, witty and respectful."

Every human population has some form of religion extending back to the paleolithic and Neanderthals - which is an absurd level of coincidental convergence if there is no evolutionary explanation. So several hypotheses with varying levels of evidence exist. Most of them stem from the field of evolutionary psychology, which is... not my favorite field of evolutionary biology, to put it politely. In my opinion, the explanations provided tend to be high on the assumption that correlation indicates causation and light on direct hypothesis tests. That said, there is some meat on the bone in the sense that religion is a byproduct of adaptive cognitive systems (e.g. animacy detection, social cognition, precautionary reasoning) and there is some evidence that religious behavior correlates with evolutionary fitness via inclusive selection. In lay terms, being a member of a group can increase evolutionary fitness, leading to positive selection for group norms, even if those specific norms are not selectively advantageous in of themselves - e.g. participation in a religious ceremony allows access to the collective resources of the group, refusal leads to excommunication, and in many environments, death of self and/or one's offspring. Thus, positive selection for religious participation occurs. Why is this useful? Well, if done properly (see previous caveat) it allows for the generation of hypotheses and predictions of traits and evolutionary trajectories. Given that religious participation is less critical for fitness in modern societies, how labile are the psychological traits associated with religious participation? Are there specific genetic/epigenetic markers that predict propensity for religious belief - and is their presence/absence linked with other traits, such as risk of depression? etc. If you were to dismiss the entire body of evolutionary evidence as "irrational" or "a cult" for.... well... reasons I guess... you'd be rather myopically and ignorantly dismissing a body of potentially useful evolutionary anthropology and neurobiology.

I guess we will never know what dinosaurs ate since they didn't write it down either.

Realistically, in my house it's gonna be a Mossberg 500 loaded with Winchester #4, because that's what's in the safe. But if Andrzej Duda wants to give me a Mig 29 I'd do my best with it.

Well, if it were giving up a stool in a bar, there is virtually no cost beyond minor inconvenience and perceived loss of status. Given the cost of engaging the bully over something that has little value to me, I wouldn't consider it. On the other hand, if he barges through the front door of my house, declares that he's moving in and taking the master bedroom before smashing all the dishes and overturning the furniture, I might be a little more inclined to call the police/my friends and neighbors for help. If they sent me a Glock, a box of 9mm rounds and their thoughts and prayers in response, I'd probably be inclined to take matters into my own hands.

My wife loves it when I say that I'm ignoring her because I'm not listening to anything a rib says (disclaimer: she doesn't).

To elaborate, mitochondrial "Eve" and Y chromosome "Adam" aren't individuals, but hypothetical genetic alleles determined by the application of coalescent Bayesian statistics to observed human genetic diversity. These alleles were likely to be carried by multiple individuals, and they swept to fixation over generations - so were not the only genetic variants present at the time they arose. Take the following image. The purple allele at the base of the tree is the common ancestor of all extant individuals. However, other genetic lineages exist simultaneously alongside the presently fixed allele, and "Adam" and "Eve" are simply the genetic lineages that, through a combination of stochasticity and selection, give rise to the genetic diversity observed at present. Re skin color - the melanin content of skin is a highly labile trait, that evolutionarily trades off between skin cancer risk and vitamin D synthesis. Chimpanzees and Bonobos have light skin under dark hair, ancestral human populations had dark skin 1.2 million years ago, and there have been multiple independent lineages of humans that have subsequently evolved lighter pigmentation. Babies born to parents of different skin tones have variable skin pigmentation. The following photograph is of fraternal twins. As you might deduce, melanin content of skin is a poor indicator of genetic lineage in humans - and generally, no, the same individual does not have "multicolored" skin.

I am an associate editor for two journals in my field, and facilitate the peer review of a couple of papers per month. Generally, a prospective reviewer needs to have an active publication record in the field - which generally dictates they have a relevant PhD (though not always, sometimes grad students can review) and some kind of academic position. Generally, I would expect a reviewer for a virology paper to have worked/published on viruses, a reviewer for a bacteriology paper to have worked/published on bacteria, and also be familiar with the methodology e.g. I wouldn't send a genomics/bioinformatics paper to and old school physiologist and vice versa. Also, we always solicit the names of prospective reviewers from the authors of the paper themselves, although who I actually send it to is at my discretion. I usually have to solicit 6-12 reviewers to end up with 2 reviews.

1. I'm a He. 2. You misquoted the abstract of Boehmer et. al. let alone actually read the paper itself. They used both inpatient and outpatient data, corrected their data for patient effects, and compared their data to other hospital patients rather than the population at large. 3. You provided no evidence whatsoever to support this being an overestimation of the myocarditis risk for COVID patients, no any actual evidence of anything but your own personal incredulity, which given you apparently didn't read the paper, indicates bad faith and little point engaging you. 4. Despite a statistic being openly reported in a publication, you demand I "show my working". My working is "actually reading the paper". 5. You provide no evidence of VAERS under-reporting vaccine side effects by your claimed 90-99%. Again, despite you repeatedly demanding others provide you with citations, you can seemingly pull numbers out of your posterior and we are all supposed take them as gospel, despite all indications that they are erroneous <- this underlined bit of text is a link to a peer reviewed publication. Ultimately, the "take down" was a a mix of logical fallacy, proof of bad faith argument, and mis-cited data because you apparently didn't actually read the papers you demanded. It clearly demonstrates you aren't worth engaging.

I did. You literally just quoted the links to the peer reviewed papers.

X-post with CharonY's edit Second edit just point out that that the Lancet study did not achieve a statistically significant result, primarily due to the fact they only observed 12 breakthrough transmission events. Even then, as CharonY points out - it demonstrates a 34% reduction in transmission. Also back to a more central point - if your concern is the prospect of acute myocarditis; acute myocarditis is observed in 0.146% COVID-19 cases in >16 year olds, and 0.0071% of vaccinated >16 year olds. COVID infection therefore has a 20 fold increase in the risk of acute myocarditis than BNT162b2 vaccine. So if the claim is that the long term effects of S protein induced myocarditis are unknown, you have a very succinct mathematical risk analysis between the risk of acquiring natural immunity vs vaccine immunity. If the claim is that administration of the BNT162b2 vaccine may cause acute myocarditis months/years after the fact, you should be able to demonstrate mechanism given the constant exposure to microbial mRNA that all humans experience.

The fact a phase III clinical trail MAY take a year =/= minimum requirement. The duration of clinical trials is, more often than not, dictated by finances - A company on the hook for the cost of clinical trial would never proceed to Phase 2 trials until the conclusion of successful Phase 1 trials due to the financial risk - massive public investment in these trials allowed for concurrent safety and efficacy trials, compressing the timeline by several years. Also, the COVID vaccine trials utilized unprecedented streamlining of regulatory processes - emergency scheduling of panels, skipping of lines for other approvals, etc. reducing the bureaucratic processing time from several months to days. Given the unprecedented manner in which these trials were conducted, the data is actually much denser than is typical for e.g. approval for the flu shot. Also, The vaccines all seem to reduce transmission by 40-60% https://www.nejm.org/doi/full/10.1056/NEJMoa2116597 https://www.nejm.org/doi/full/10.1056/nejmc2107717

Of course, my SFN rep points go on my CV right next to my H-index, Researchgate score and number of Twitter followers. This paper may be of interest - an analysis of toxic interactions on Reddit showed that less than 0.1% of subcommunities generate 38% of hostile interactions, and just under 1% generate over 74% of them.

Lorna Shore's And I Return to Nothingness EP was one of the best things to happen in 2021 and is currently getting me through making a phage lysate in the lab that was meant to be shipped out by close of business today.

Not to mention that the difference in biasing the data this way is that the vaccine vs COVID-19 risk analysis comes out in a favor of the vaccine by 5 orders of magnitude instead of 7.

R0 of the SARS COV 2 Omicron variant: 10 Risk of thromboembolism as a result of COVID infection: one in 5 Risk of thromboembolism as a result of AZ vaccine: one in 50,000 Uninformed/undereducated is one possibility. Phenomenally bad at math is another. To be blunt you're wrong and so are "they". Like not in a philosophical, "lesser evil. two sides of the coin" way - but more of a "mathematically defined to a near incalculable degree of probability" way. Vaccinating a human population for COVID19 will result in fewer deaths and loss of QALYs than not vaccinating the population, unequivocally.

OK, so the vast majority of mRNA vaccine components (i.e. lipids, PBS and sucrose) have been in use in various medications for decades. The only active component that could be considered novel is a strand of mRNA that encodes the SARS COV 2 S protein. Do you know what else mRNA is in? EVERY ORGANISMAL CELL ON THE PLANET. Every time you eat, breathe and drink you ingest mRNA. Your gut microbiome produces billions of strands of foreign mRNA inside your body every day, which can and do cross the gut epithelium into the bloodstream. Also, the mRNA from the vaccines is cleared from the body in around 72 hours, the spike proteins encoded by them in 21 days. So, given how ubiquitously and frequently your cells encounter foreign mRNA molecules, and that no component of the vaccine actually persists in the body long term, by what mechanism would the mRNA cause an adverse reaction years after the fact? I mean, no one knows if you sprout wings out your butt 30 years after drinking Monster Energy, but there's not really a mechanism that would lend itself to that being a realistic concern.

Healthcare worker =/= clinician. Hospitals employ people in custodial, dining, maintenance, shipping and receiving, grounds keeping, payroll, mailrooms, etc. A CharonY points out, vaccine compliance in actual physicians is significantly higher than the general population. So as per the OP - 80,000 represents 6% of the 1.4 million NHS workforce, of which a smaller proportion would actually be medical staff, of which an even smaller proportion would actually have expertise in infectious disease. So the "LoOk aT AlL ThE eXpeRtS WhO wOn'T TaKe ThE ExPeRiMeNtAl VaCcINe!??!" is disingenuous and requires considerable torturing of the data, reminiscent of the "LoOk aT AlL ThE eXpeRtS WhO DoNt BeLieVE ThE EvOluTiOn LiE!!?!" intellectual fallacy.

My lab routinely works on wastewater, clinical enteric and mucosal samples. If someone isn't willing to get COVID, influenza, hepatitis vaccinations and wear appropriate PPE, they need to look for a different line of work. I'm not accepting liability for someone being a moron, nor am I trusting the work of a microbiologist who doesn't understand how vaccines work. If you are immunocompromised to the point where getting a vaccine is an unacceptable risk to your health, a BSL2+ is not a place you should be. I imagine if I was in charge of a clinic, I'd feel pretty much the same.

Except you said this: We we now seem to agree is patently false. Individual health decisions have population level consequences, especially when it comes to infectious disease and vaccines. We know that cohorts where all individuals have two doses of either BNT162b2 or ChAdOx1 vaccine display approximately half the R0 of unvaccinated cohorts. Given the stratified risk of hospitalization and mortality, vaccination rate has a significant correlation with morbidity and mortality for even relatively small populations. The relative individual risk of adverse vaccine side effects, along with the overall public health burden of vaccine side effects is several orders of magnitude lower than that of Covid19. So you can't really argue from a logical or mathematical perspective that the the relative impact of Covid19 vaccination refusal is lower than the risk of the vast majority of other freedoms that are legislatively curtailed for the public good, nor that the individual burden of being vaccinated is unprecedentedly high. Given the above relative risk model, I don't think Djokovic's right to be phenomenally bad at math trumps the right of others to travel internationally without unnecessary exposure to an unprecedentedly deadly infectious disease. Djokovic has right to not get vaccinated, but it comes with the consequence of restricted travel to foreign countries, and other curtailments on his full participation in society, because his decision does effect others. Also, I think over the last 250 years or so, most societies have determined that vaccination against infectious diseases falls within that realm of obligation should one wish to fully participate in said societies, which led to a subsequent doubling of average life expectancy in said societies.

That's not how vaccines work. Smallpox, rinderpest and polio were not eradicated with vaccination campaigns because the vaccines were 100% effective. They were eradicated because a high enough proportion of the population were inoculated in order to lower the transmission rate below the level of replacement. If a large enough proportion of the population do not vaccinate, R0 remains above 1 and the pathogen continues to spread. As there is no such thing as vaccine that is 100% effective 100% of the time, this puts those who cannot mount an immune response to the vaccine (e.g. chemotherapy patients, organ donor recipients, autoimmune disorder patients, etc) at risk. The main reason for otherwise healthy individuals to get vaccinated against infectious diseases is to lower the risk of infection for vulnerable individuals in the population. Personal freedom is never absolute. You still need to pass a driver's test to operate a car. You can't poop in the street. You can't build a pillow fort in the middle of the freeway, and you can't send your kid to public school without being vaccinated against infectious diseases.

There's a few non-mutually exclusive hypotheses regarding the evolutionary origins of viruses. The "virus-first" hypothesis posits that virus evolution occurred on parallel with cellular life. If that were the case then yes, virus origins, or at least some virus origins may well be separate from cellular life. Also note, many viruses are not terrestrial. If all humans are descended from Adam and Eve, how come a French woman has never given birth to a Singaporean? If you're related to your cousins, how come one of them has never given birth to your child? Common ancestry doesn't infer that organisms will spontaneously change into fundamentally different organisms. In fact if a bacterium woke up one day and discovered it had divided into a bacteria and an elephant, it would completely contradict contemporary evolutionary theory. I often wonder what would happen if fundamentalists ever gained the self awareness to realize how counterproductive and hypocritical being petulant and condescending on the internet is.

The vaccines all seem to reduce transmission by 40-60% https://www.nejm.org/doi/full/10.1056/NEJMoa2116597 https://www.nejm.org/doi/full/10.1056/nejmc2107717