Ah, but there’s a big difference here between the Mpemba effect and your pre-print. You missed an important phrase at the end of your quote…i.e. that this phenom had been observed as far back as the time of Aristotle. So, as counterintuitive as it might be to someone stumbling across it for the first time, it’s been a long standing and consistent observation by multiple people.
As pointed out upstream, the counterintuitive nature of this not-yet-peer-reviewed-and-published pre-print, is a claim made by the study authors (and is presumably the hook that they hope will gain attention for this data trawl) and is being promoted without available supportive evidence.
Out of interest, how did you glom onto the article. It’s only a preprint…about as weak a form of data dissemination as it’s possible to get (anecdotes about family members nitwithstanding) … but it seems to have captured your imagination for some reason.
The second row shows unvaccinated with lower Covid infection rate than vaccinated, much like the preprint. However, here we have some demographic data that provides further insight. The unvaccinated group was significantly younger, was more likely to live in rural counties with lower Covid positivity rates, had fewer chronic conditions, and was significantly more likely to have previously had Covid than the vaccinated group. These factors would tend to reduce the risk of Covid infection independent of the vaccination status.
Bottom line is that the data in the reprint is not that unusual and reflects the complexity of trying to assess Covid resistance at this stage of the pandemic. IMO, those with occupation, age, or health factors that put them at high risk of Covid exposure should probably take the newest boosters. For those who are healthy and at average risk it is a judgement call, as for this group the benefits seem marginal.
Typically when people make this observation they don’t account for the molality of the solution, which affects freezing point.
As the article states, it is difficult to reproduce this effect in the lab. The reason for that is you can only observe this if you screw up the experiment in the first place.
But the data are not meaningless. They strongly suggest that at this point in time the impact of the Covid booster on the general population is marginal. Low enough that other factors can mask any beneficial effect.
That is worth knowing when deciding whether to get the newest booster.
That’s a sorry lookout for Balb/c mice (whatever they are…nothing resembling a mouse-as-we-know-it, I’ll wager) but how does it apply to actual people.
It is rare that I defend DrBob but c’mon. If a Balb/c mouse study showed evidence that “DrBob Miracle Wrinkle Remover” caused tumors, wouldn’t you want the matter to be further investigated before using?
A good question for all animal studies, be they for viruses or carcinogenicity.
Concerning people, the authors write in the abstract:
“Our findings demonstrate potential risks with the continuous use of SARS-CoV-2 vaccine boosters, providing immediate implications for the global COVID-19 vaccination enhancement strategies.”
Also:
“More information was needed to properly address relevant questions in the practical field of COVID-19 prophylaxis, such as the recommended condition for the use of additional booster vaccines, the suggested number of enhancement shots to be given and the potential adverse effects of continues administration of booster vaccines.”
“Presently, it is unclear whether extended administration of RBD vaccine boosters can re-establish protective immunity or is prone to induce immune tolerance.”
“Together, we provided crucial evidence that repetitive administration of RBD booster vaccines may negatively impact the immune response established by a conventional vaccination course and promote adaptive immune tolerance.”
“The evidenced immune tolerance from repetitive dosing with homologous boosters in our study suggests that caution should be exercised when optimizing the extended plan for SARS-CoV-2 booster vaccination.”
Here ya go. They have been widely used in research for almost a century. https://www.sciencedirect.com/topics/immunology-and-microbiology/bagg-albino-mouse
“BALB/c mice are distributed globally and among the five most widely used inbred strains in biomedical research, particularly in immunology and infectious disease research.”
I wouldn’t be remotely interested in anything inflicted on a mutant mouse…no matter how many reproducible studies a Gish Gallop vomits up.
First question to ask with any research study is “How closely do the study subjects resemble me?”. In that context, I’d want to see reproducible results on old white women.
Of course, they write that. All rodent research uses that sort of caveat. They wouldn’t get a single dollar in grant funding/look in with the lowest impact journal if they were honest and stated that, on balance of probabilities and past experience, our research only applies to Balb/c mice with little clinical application to human or veterinary medicine…but we got a publication (or preprint…to reiterate the original non publication)
The experiment as discussed in the research paper is not discussing how much of a viral load was administered. You can not assume an extreme viral load would not over power the booster while a lesser viral load NOT up against a vaccine booster would give the results a different outcomes.
Until the viral load is documented there is no proof that the research was accurate.
For instance if an un boosted mouse was testing positive with a minor viral load did a boosted mouse on average need more exposure to test positive for Covid?
That’s a pretty anti-science approach given the importance of animal models in science, particularly with respect to medical research. In most cases of drug development, one must first show no ill effects on mice (or some other poor critter) before even considering going to the expense of human trials, including that of old white women.
I take the opposite approach. If product A is bad for mice then I would not take product A unless human studies demonstrated it was safe for humans. In other words, I assume that mice and humans are related unless proven otherwise, while you assume the opposite. I think my approach is the more empirically supported as the vast majority of chemicals that are bad for mice are also bad for humans. That suggests similar physiologies.
Keep in mind that taking this many boosters for the same disease over such a short time period has never been done before. The effectiveness and risks of this approach is currently being tested in real time on the general population.
So you would want to see an old white woman in the coal mine before entering rather than accept that the young little yellow canary had died so you should probably not go inside?
I think it’s safe to say that some decision making doesn’t require testing to determine safety or otherwise. Prior plausibility will do. I cannot imagine a scenario whereby I’d be tempted to enter a coal mine…for heaps of reasons that a meta analysis using Old Ladies or canaries probably wouldn’t even show a problem.
Both my grandfathers were coal miners. My mum’s dad died before I was born of complications of “Miner’s Lung”. My dad’s dad was trapped for 4 days following a roof cave in. Although I’m reasonably sure conditions are a bit safer than they were a century plus ago (and canary technology rendered obsolete) , a coal mine visit is not on my bucket list.
Now, having said that, I’m not naive enough to imagine that the meds I’ve taken over the years arrived on the market without animal testing…but pretty much everything I can think of has had a track record of usage in humans…including post market testing. Not always in women, mind, as they’re historically underrepresented in clinical trials for many reasons…including women of childbearing age being specifically excluded for a time after the Thalidomide tragedy unraveled. Thalidomide was demonstrated to be very safe in animal studies and led to an overzealous roll out because of that.
Now that I think about it, my current regimen has probably not had a tremendous amount of testing on “people like me”…i.e. folk who have a track record of healthy lifestyle choices but still develop ASCVD because of a genetic predisposition. I think I’ll take my chances over sudden cardiac death (or worse)
The point being made is that having multiple boosters over a relatively short period of time has not been tested in humans. All we have is the animal data, in this case from mice. This particular mouse trial indicates that frequent booster vaccinations can suppress the immune response.
You’ve strongly implied that such data is irrelevant to deciding how frequently humans should get booster vaccinations. Don’t think that is a defensible position.
