Vaccines do NOT reduce dementia

#21

He calls 200 days too quick? While the pathologic markers take some time, 200 days seems like plenty to deteriorate. In fact, the protective effect of vaccines deteriorates over time - like even by 5 years. As we know, the pathologic markers aren’t completely predictive of symptoms.

200 days of reduced inflammation in the brain would seem like enough ttime to notice a difference.

The transcript is full of mistakes in just grammar and word choice. He mentions a paper in JAMA and we are supposed to guess which one? Gemini says that are 100s.

Not real science. Influencer trying to make coin. Doesn’t mean he doesn’t have some good points but the level of evidence he brings is very low.

#22

It’s the Australian cohort. I don’t think he’s right that it’s 100 days, it looks more like 250 days to me.

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#23

Looks like but doesn’t reach significance until later. Until significance is reached, it is noise.

And I’m sure you realize avoiding disease isn’t making you any smarter😄

The benefit would be there at first dose likely with just getting a bit stronger with the second. I don’t know the numbers but often, 50-70% of people might get protection from 1 dose of vaccine but we get a second to get to 90+%. So the effect for a majority probably starts with 1 dose and may not get any better with 20 doses.

At some point, this joker isn’t changing anything except lining his pocketbook with YouTube views. I am not sure of any rational person not getting a shingles vaccine in 2026 at age 50 - at least in the US where it is free. Shingles sucks so why even worry about it whether it helps dementia or not.

Personally, the anti-expert trend is unquestionably damaging to the public health of the US. Those who are smart and take advantage of this to make money are some of the most repugnant people in history. Being dogmatic about RCTs is not helpful. As a surgeon, we practice almost entirely without RCTs. Should we stop? Hmm - it seems like hemorrhage kills but we haven’t ever tried a RCT - so how do we know???

Full disclosure - my number one investment is in memory care facilities so I’ll make more money if people listen to this guy.

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#24

Both the Wales and the UK study were well powered and the analytic method (regression discontinuity) is the most appropriate tool for analyzing a time-shifted naturalistic experimental and control group. Several differences in the populations have been discussed as potential explanations for the disparate findings. One that caught my eye was the difference in classification criteria for dementia. The Wales study rested on the judgment of personal physicians who, by nature of the culture, were often close to the patient and might be among the “first to know,” The UK study rested on impersonal hospital admission classifications where we might expect to see a threshold requiring more advanced cases. This is not determinative but I think a good read of the two studies will not produce reasons to discount the Welsch study.

#25

Agreed on the “anti-expert, anti-science” subculture. We might see the immediate damage more in health but the problem is widespread. Climate. Oceanography. Air and water pollution.

#26

The point of all this is not to affirm or attack any participant in the discussion, but to look for ways to remove possibly faulty hypothesis in the Popperian sense. If we posit some alluring thesis, such as “vaccines reduce dementia”, we should first and foremost look for ways to falsify that thesis. The natural tendency we see, especially by influencers, but also many scientists, is to generate a thesis and then spend all one’s efforts in finding ways to support it, instead of pulling back and saying “let me first find good reasons why it might not be true, and only if I find none, to elevate the hypothesis status”. This is where critics come in. They can assist in the process you yourself should already be engaged in. Prasad is a skilled and trenchant critic of this thesis? Great! Fantastic! Because if I can withstand his critique, I am already a step closer to validating the thesis.

Nobody has a monopoly on truth and anybody can be wrong, including you, me or Vijay Prasad. But I for one appreciate the opportunity Prasad gives me to test my favored thesis and my possible hidden biases.

More discussion is better, but there is a caveat. The participants should bring arguments and evidence of sufficient rigor, otherwise endless low value flamewars of anti-vaxx flat earth type tussles are a pointless waste of time. I value Prasad not because I necessarily agree with him (I certainly don’t on some issues), but because he argues with a degree of rigor that rewards engagement, and that is both very valuable and in my experience relatively rare.

In that spirit - providing maximum opportunity for examining this complex issue - here’s a pop-sci article that’s actually pretty good, replete with studies mentioned which you can then chase down, including ones Prasad mentioned and including extensive quotes from researchers. More kindle for the fire - hopefully more light for all that heat!

Can Vaccines Really Help Prevent Dementia?

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#27

What should be done in the meanwhile as RCT’s are underway? The answer is in the middle. Shingles can be prevented, and there’s a chance that it will reduce the risk of dementia. There’s not enough evidence for Shingrix to be given as a prescription drug to prevent dementia. If that evidence is important, the research speed can be sped up so we don’t have to wait until 2037 for results. If there’s a will and money there’s a way.

Rejecting RCT’s as a necessary method in favor of observational studies is foolish, as all of the failed and even harmful vitamin trials have shown. Likewise rejecting some types of observational studies is on an equal footing, as it takes time and it’s expensive for them to be superseded, they aren’t a data request and some statistics.

Even in the best case scenario there’s a 1/5 reduction in risk of dementia, that’s still 4/5 risk on the table and shouldn’t cause complacency.

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#28
#29

Ok, the coincidence here is pretty interesting.

Dr. Simpson said exactly what I wanted to say just more succinctly and elegant.

The coincidence being that he is a bariatric surgeon like myself. The number of full time bariatric surgeons in the US is around 1000. It isn’t published but that is the typical number thrown around.

Which goes back to the point that we all our products of our professional backgrounds. Some more than others of course and I suspect surgeons are particularly impacted by their careers.

I appreciate the debate and the other point of view - as much as I can truly do that.

There is a big side issue here that probably gets me emotional and we know what that does to clear thinking. Only 35% of US adults over 50 have had the shingles vaccine. Only about 60% get the annual flu shot. The flu shot actually has RCTs with reduction in cardiac events and ACM. Yet the uptake is terrible.

The amount of needless suffering, probably dementia and death from the anti-science viewpoint is staggering. A quick back of the napkin number is 65,000 avoidable dementia cases diagnosed per year in the US for an intervention that is free and easy.

That is based on relatively short study follow ups with 18-20% reduction. The potential reduction for a population that starts fighting neuroinflammation at age 50 is likely much higher.

Measles is quick to notice and easily tracked. But there are far greater impacts from this attitude that are harder to see.

Little side anecdote, a flu vaccine RCT in 1999 showed reduced work absence by about 50%. More recently (2020) an observational study showed the exact same thing - 50%. Total biased observational group with no attempt to correct because they were looking at cost. Obvious bias does not always change the conclusion.

Prasad is not anti-science but he also profits by pandering to that viewpoint. Science is not advanced by youtube views. And the general public doesn’t have the skill set to interpret the studies. Look at the headline of this thread - no one here thinks that is correct. Having doubt is fine but saying there is no effect is not the same thing at all.

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#30

As someone who has spend a good portion of his life thinking about conceptualization, design, and methodology problems, I have a healthy respect for the value of the RCT in medicine. With this in mind, the RCT is a stage-appropriate design not suitable for early or even most mid-exploratory inquiries. Why? A full answer appeals to a lot of detail. A summary is that designing a workable RCT almost always entails gaining precision at the expense of verisimilitude or realism. Moreover, if you step back to look at the full corpus of scientific knowledge, you see that very little of it was derived from RCTs.

There being a possible causal relationship between the shingles vaccine and slowing or even preventing manifest dementia adds little to the rationale for taking the vaccine. The vaccine does a good job of preventing a disease that can be life threatening and is almost surely life shortening. What these investigations can and will likely do is expand our understanding of the nature and progression of dementias and how to prevent them. Much of this understanding is likely to come from research designs other than RCTs.

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#31

I strongly agree with this comment. I was saddened to see most of the arguments against either attacked the messenger (irrelevant to the truth of the message). I disagree with Vinay with a bunch of things but ideally these are not personality questions, they are scientific ones, and the data and evidence is what matters, not whether the guy who put forward a position is a saint or a devil.

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#32

Yes, the Wales natural experiment is hard to dismiss. The other natural experiments, such as Australia, less so, because the delta in vaccinations across the age cutoff is not as sharp. Your 25% chance of 20% relative reduction seems reasonable (in women only).
[Not All Observational Studies Are Worthless](https://purescience.substack.com/p/not-all-observational-studies-are?r=p3jgh)

#33

Your defense of Prasad is particularly amusing given your repeated lectures about intellectual humility, falsification, and the importance of engaging criticism.

You write that “more discussion is better,” that we should actively seek criticism of our favored hypotheses, and that nobody—including Prasad—has a monopoly on truth.

And then you make the rather remarkable claim that you “will not find one critic of his who is the least credible themselves.”

That isn’t intellectual rigor. It’s fan-club logic dressed up in Popperian vocabulary.

There are, in fact, plenty of highly credentialed people who have substantively criticized Prasad, including physicians, cancer researchers, epidemiologists, and FDA scientists. David Kaslow, Jonathan Howard, David Gorski, Eliezer Van Allen, and others have raised specific substantive objections to his positions.

They can all be wrong, of course. That’s the point of scientific discourse.

But apparently your wonderfully sophisticated falsification framework has an interesting limitation: criticism is encouraged right up until it comes from someone who criticizes the person you admire. At that point, rather than examining the criticism, you simply announce that the critics aren’t credible.

How wonderfully convenient.

Perhaps before giving everyone else lessons in epistemology, you should try applying your own Popperian principles to your favored hypothesis about Prasad.

#35

I haven’t been following this thread as I already have my shingles vaccination and whether there are other benefits (or not) doesn’t make much difference to me at this point.

But - I see discussion is continuing, so I decided to run the video through my more rigorous analysis prompt in Gemini to see what the results are. Here is the analysis:

I. Executive Summary

This analysis critically evaluates the hypothesis that varicella-zoster virus (VZV) vaccination causally reduces the incidence of Alzheimer’s disease and related dementias (ADRD). The core thesis presented in the source video—and supported by recent large-scale epidemiology—is that widely publicized claims of a 20% relative reduction in 7-year dementia risk following shingles vaccination are artifacts of selection bias, residual confounding, and sample size limitations, rather than genuine neuroprotective biological effects.

Initial enthusiasm for this intervention originated from a high-profile Regression Discontinuity Design (RDD) study in Wales (Eyting et al., 2024), which exploited a strict birth-date eligibility cutoff (September 2, 1933) for live-attenuated zoster vaccine (Zostavax) rollout. However, a definitive replication analysis leveraging the primary English health system database expanded the RDD sample size by 18-fold to over 6.3 million individuals (Oxford/NDPCHS, 2025). While the English study confirmed the instrument’s validity by demonstrating a statistically significant reduction in acute herpes zoster incidence (absolute risk reduction of 0.12 percentage points; NNT ~833), the reported discontinuity for dementia incidence completely collapsed, yielding zero statistically significant risk reduction.

Furthermore, observational cohort studies alleging rapid dementia risk reduction within 100 to 200 days post-vaccination are biologically implausible. Alzheimer’s disease pathophysiology involves a 15-to-30-year preclinical phase of amyloid accumulation, tau hyperphosphorylation, and progressive neurodegeneration; acute therapeutic inversion over a 6-month window indicates selection bias and diagnostic capture artifacts. Systematic meta-analyses covering over 104 million participants (Age and Ageing, 2025) reveal that virtually all adult routine immunizations—including influenza, Tdap, pneumococcal, and hepatitis A vaccines—exhibit identical 20% to 35% observational reductions in dementia. This uniform non-specific association confirms the pervasive “Healthy Vaccinee Effect,” where vaccinated cohorts systematically display superior socioeconomic status, healthier lifestyle habits, lower BMI, and better vascular risk management.

Clinical recommendations for shingles vaccination must remain anchored strictly in its proven efficacy against herpes zoster and postherpetic neuralgia (Lal et al., 2015). Patients should not be advised to seek vaccination as a primary disease-modifying strategy for Alzheimer’s disease pending ongoing registry-based randomized controlled trials in Nordic cohorts.

II. Insight Bullets

  1. Alzheimer’s disease (AD) represents a complex, multi-decade neurodegenerative pathology with an exceptionally low pre-test probability for single-agent preventive therapies.
  2. Billions of dollars in pharmacological research have yielded only marginal amyloid-clearing monoclonal antibodies (e.g., lecanemab, donanemab) with modest clinical efficacy and significant safety risks (ARIA).
  3. The prior probability that a single routine adult vaccine yields a ~20% relative reduction in overall dementia incidence is extremely low based on established neuropathological models.
  4. Observational comparisons between vaccinated and unvaccinated populations suffer from severe healthy user bias, making standard cohort studies scientifically invalid for causal inference.
  5. Individuals who elect to receive optional adult immunizations systematically differ from non-receivers across socioeconomic status, diet, exercise, smoking status, BMI, and medical adherence.
  6. Vaccinated cohorts demonstrate significantly tighter control of vascular risk factors—such as hypertension and glycated hemoglobin (HbA1c)—which are independent drivers of vascular dementia.
  7. To bypass healthy user bias, researchers utilized a Regression Discontinuity Design (RDD) in Wales based on a strict birth-date eligibility cutoff (September 2, 1933).
  8. The Wales RDD study reported a 3.5 percentage point (20% relative) reduction in 7-year incident dementia diagnoses among those eligible for the live-attenuated zoster vaccine (Zostavax).
  9. Critical anomalies in the Wales RDD data included a persistent effect in females but complete absence of effect in males, raising concerns regarding subgroup artifact.
  10. The effect size for dementia prevention reported in the Wales study exceeded the overall absolute risk reduction observed for herpes zoster prevention itself.
  11. A definitive replication study conducted in England expanded the RDD sample size by 18-fold, incorporating over 6.3 million individuals.
  12. The England RDD confirmed the primary instrumental variable validity: eligibility produced a sharp step-change in herpes zoster vaccination rates and reduced herpes zoster incidence.
  13. The England RDD revealed an absolute risk reduction for herpes zoster diagnosis of 0.12 percentage points, yielding a Number Needed to Treat (NNT) of ~833 to prevent one clinical zoster diagnosis over 8 years.
  14. When evaluating dementia outcomes across the 18-fold larger English population, the regression discontinuity completely collapsed, demonstrating zero statistically significant jump across the cutoff.
  15. Methodological sensitivity testing indicates that altering bandwidth or analytic parameters in the Wales dataset causes the confidence intervals to cross unity, confirming fragile statistical significance.
  16. Observational studies published in high-impact medical journals report separation in dementia risk curves as early as 100 to 200 days post-vaccination.
  17. A 100-to-200-day lag for dementia risk modification is biologically implausible given that Alzheimer’s neuropathology develops over 15 to 30 years prior to clinical symptom onset.
  18. Rapid separation of survival curves in vaccine observational studies is a classic hallmark of immortal time bias and differential medical diagnostic capture.
  19. Systematic reviews and meta-analyses of over 104 million participants demonstrate that influenza, Tdap, pneumococcal, and hepatitis vaccines all display ~20–35% reductions in incident dementia.
  20. The ubiquitous appearance of dementia risk reduction across non-related pathogen vaccines proves that the observed associations reflect non-specific healthy vaccinee confounding rather than target-specific viral neuroprotection.
  21. The varicella-zoster virus (VZV) latency hypothesis posits that viral reactivation in cranial ganglia triggers neuroinflammation, microglial activation, and amyloid/tau aggregation.
  22. Preventing subclinical VZV reactivation via vaccination was hypothesized to diminish chronic central nervous system (CNS) neuroinflammation.
  23. The lack of causal replication in large-scale English RDD data disproves the hypothesis that VZV reactivation is a major upstream driver of population-level dementia.
  24. Comparisons between recombinant adjuvanted vaccine (Shingrix / AS01) and live-attenuated vaccine (Zostavax) show lower observational dementia risk for Shingrix, attributed by some to AS01-mediated innate immune stimulation.
  25. Studies comparing AS01-adjuvanted Shingrix against AS01-adjuvanted RSV vaccines showed identical observational dementia reductions, suggesting the signal is driver-independent or artifactual.
  26. Transient innate immune activation via vaccine adjuvants (e.g., GM-CSF/sargramostim pathways) may transiently shift microglial clearance profiles without altering long-term neurodegenerative trajectory.
  27. Salami-slicing observational databases and reporting transient subgroup signals creates widespread false-positive literature in epidemiological research.
  28. Pragmatic randomized controlled trials (RCTs) in Nordic registry populations (Finland and Denmark) represent the true Level B gold standard required to evaluate vaccine-induced cognitive protection.
  29. High media coverage and academic enthusiasm for off-target vaccine benefits often reflect confirmation bias and narrative alignment rather than rigorous causal inference.
  30. Financial and policy decisions regarding adult immunization schedules should be made solely on proven primary endpoints (e.g., prevention of herpes zoster and postherpetic neuralgia).
  31. Relying on observational epidemiology to justify off-label or secondary vaccine mandates undermines institutional credibility when large-scale causal studies disprove the claims.
  32. Pre-test probability framing is essential in biomedical literature review: extraordinary causal claims require extraordinary, unconfounded evidence.
  33. Diagnostic coding in electronic health records (EHRs) contains substantial misclassification bias, requiring validated hospitalized or multi-source dementia criteria.
  34. Hospital-coded dementia definitions in large health databases provide higher specificity but may reflect acute medical events (e.g., delirium) rather than insidious Alzheimer’s progression.
  35. The absolute risk reduction (ARR) of public health interventions must be distinguished from relative risk reductions (RRR) to avoid overstating clinical utility.
  36. Shingles vaccination remains highly clinically indicated for older adults solely due to its robust efficacy against acute herpes zoster and debilitating postherpetic neuralgia.

III. Adversarial Claims & Evidence Table

[Export to Google Sheets]

Claim from Video Speaker’s Evidence Scientific Reality (Current Data) Evidence Grade (A-E) Verdict
Shingles vaccine (Zostavax) causally reduces 7-year dementia incidence by ~20% (3.5 percentage point drop). Eyting et al. Nature 2024/2025 Wales RDD study based on Sept 2, 1933 birth cutoff. Disproven by an 18-fold larger RDD study in England covering 6.3M people (Oxford/NDPCHS, 2025), where the dementia discontinuity completely collapsed (Eyting et al., 2024). Level C (Quasi-experimental RDD disproven by larger RDD) Unsupported
Shingles vaccination effectively reduces clinical herpes zoster diagnoses in real-world populations. England RDD step-change analysis (ARR 0.12 percentage points, NNT ~833 over 8 years) & drug label RCTs. Confirmed. Phase III RCTs for Zostavax (Oxman et al., 2005) and Shingrix (Lal et al., 2015) prove >50% and >90% efficacy against zoster, respectively. Level B (Phase III RCTs) Strong Support
Observational studies showing dementia reduction within 100–200 days post-vaccination reflect healthy vaccinee bias. Survival curve divergence in Annals of Internal Medicine, JAMA, and Nature Medicine papers occurring <1 year post-shot. Meta-analyses covering 104M subjects (Age and Ageing, 2025) confirm identical 20–35% reductions across flu, Tdap, pneumococcal, and hepatitis vaccines, proving non-specific selection bias. Level A (Meta-analyses of >104 million participants) Strong Support
AS01-adjuvanted recombinant vaccine (Shingrix) directly reduces dementia via innate immune stimulation. EHR propensity-score matched studies comparing Shingrix vs Zostavax and Shingrix vs RSV vaccine. Studies comparing Shingrix vs AS01-RSV vaccine (Taquet et al., 2025) showed no difference between adjuvanted vaccines. Disease-modifying effect on amyloid/tau remains unproven in RCTs. Level C (Observational EHR cohort study) Speculative
Ongoing randomized controlled trials in Denmark and Finland will confirm zero reduction in dementia. Empirical collapse in 6.3M English dataset and low biological pre-test probability. Registry-linked RCTs in Denmark and Finland are currently ongoing. Prospective double-blind trial results remain unblinded. Level E (Expert Projection / Hypothesis) Plausible

IV. Actionable Protocol (Prioritized)

High Confidence Tier (Backed by Level A/B Evidence)

  • Primary Herpes Zoster & Postherpetic Neuralgia Prevention:
    • Intervention: Administer the 2-dose recombinant zoster vaccine (Shingrix) for all adults aged ≥50 years (and adults aged ≥19 years who are immunocompromised), administered 2 to 6 months apart.
    • Evidence Base: Level B RCT evidence (Lal et al., 2015) demonstrating >90% efficacy in preventing herpes zoster and postherpetic neuralgia across all age brackets.
  • Vascular Dementia Risk Factor Optimization:
    • Intervention: Maintain strict glycemic control (HbA1c < 5.7%), blood pressure target (< 120/80 mmHg), lipid management, regular aerobic exercise (≥150 min/week), and complete smoking avoidance.
    • Evidence Base: Level A meta-analytic evidence confirming that mid-life cardiovascular risk optimization significantly reduces long-term vascular dementia and mixed dementia progression.

Experimental Tier (Level C/D Evidence - High Safety Margins)

  • Adjuvanted Vaccine Utilization for Off-Target Innate Immunomodulation:
    • Intervention: Utilization of AS01-adjuvanted vaccines (Shingrix, AS01-RSV) in eligible older adults.
    • Evidence Base: Level C observational data (Taquet et al., 2025) and Level D preclinical animal models suggest transient myeloid/microglial activation. High safety margin when administered within standard ACIP guidelines for primary infectious indications, but unproven as a primary neuroprotective disease-modifying strategy.

Red Flag Zone (Debunked / Lacking Safety Data)

  • Seeking Vaccination Solely for Alzheimer’s / Dementia Prevention:
    • Debunked Claim: Administering shingles or other routine vaccines with the primary intent of preventing or treating dementia.
    • Evidence Status: Debunked by Level C national quasi-experimental RDD data (N=6.3M) showing complete absence of causal dementia reduction (Oxford/NDPCHS, 2025).
  • Relying on Rapid-Onset Anti-Dementia Claims:
    • Debunked Claim: Expecting cognitive protection or dementia delay within 100 to 365 days post-immunization.
    • Evidence Status: Methodologically invalid. Driven by healthy vaccinee bias, immortal time bias, and medical encounter capture frequency rather than neurodegenerative alteration.

V. Technical Mechanism Breakdown

[ Varicella-Zoster Virus (VZV) Reactivation ] │ ▼ [ Latency in Cranial Ganglia ] │ ▼ [ Neuroinflammation / Microglial Activation ] │ ▼ [ Hypothesized Amyloid/Tau Acceleration ] (Disproven at Population Level)

1. Varicella-Zoster Virus (VZV) Latency & Neuroinflammation Hypothesis

  • Pathophysiological Concept: Primary infection with VZV leads to lifelong viral latency in dorsal root, autonomic, and cranial ganglia (most notably the trigeminal ganglion). Subclinical or overt viral reactivation results in retrograde transport along neuronal axons, local neurovascular inflammation, double-stranded DNA sensing via the cGAS-STING pathway, and downstream microglial activation.
  • Proposed Linkage to Neurodegeneration: The infectious hypothesis of Alzheimer’s disease posits that chronic low-grade neuroinflammation triggered by herpesviruses accelerates central nervous system (CNS) proteinopathy—specifically amyloid-beta aggregation and hyperphosphorylated tau tangle propagation.
  • Translational Failure: While in vitro and preclinical models demonstrate that viral infection can seed protein aggregation, the 18-fold larger English RDD dataset (Oxford/NDPCHS, 2025) proves that suppressing population-level VZV reactivation via vaccination produces no measurable deviation in clinical dementia incidence.

2. Adjuvant-Mediated Innate Immune Activation (AS01 System)

  • Biochemical Components: The recombinant zoster vaccine (Shingrix) contains the AS01B adjuvant system, composed of monophosphoryl lipid A (MPL, a Toll-like receptor 4 [TLR4] agonist) and QS-21 (a natural triterpene saponin fraction from Quillaja saponaria).
  • Immunological Cascade: Local injection triggers co-activation of TLR4 and NLRP3 inflammasomes in antigen-presenting cells (dendritic cells and macrophages), producing rapid, transient secretion of interleukin-12 (IL-12) and interferon-gamma (IFN-g) in draining lymph nodes.
  • Microglial Clearing Hypothesis: Transmitted peripheral cytokine signals stimulate microglial morphological transitions into a transient phagocytic phenotype (analogous to GM-CSF/sargramostim pathways), theoretically enhancing clearance of soluble neurotoxic proteinaceous debris. However, comparison between Shingrix and AS01-adjuvanted RSV vaccines reveals identical observational hazard ratios, confirming that these signals represent non-specific epidemiological noise rather than target-specific disease modification.

3. Methodological Failure: Healthy Vaccinee Effect & RDD Mechanics

  • Healthy Vaccinee Confounding: In observational electronic health record (EHR) studies, vaccinated cohorts exhibit systematically higher health literacy, greater income, lower baseline cardiovascular risk, reduced smoking prevalence, lower BMI, and increased adherence to preventive healthcare.
  • Immortal Time & Diagnostic Capture Bias: Observational cohorts require individuals to survive without a dementia diagnosis until vaccine administration date, introducing immortal time bias. Furthermore, vaccinated individuals interact with the healthcare system more frequently, leading to early differential diagnostic coding that distorts hazard ratio curves within the first 100–200 days post-vaccination.
  • Regression Discontinuity Design (RDD): RDD isolates causal local average treatment effects (LATE) by exploiting an arbitrary birth-date eligibility threshold (September 2, 1933). While small single-region cohorts (Wales, N=282,541) yielded a spurious local jump due to idiosyncratic noise, expanding the bandwidth to national populations (England, N=6.3 million) eliminated background variation, demonstrating a step-change for herpes zoster incidence but a flat, continuous line for dementia diagnosis.

Attribution: Produced by Gemini 1.5 Pro

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#36

Why are you so concerned with how I formulated the response rather than whether anything in it is wrong?

That seems remarkably consistent with the very behavior being discussed here: when you don’t have a substantive objection to the argument, change the subject to the person making it.

If you disagree with something I said, by all means, identify it and explain why it’s wrong. Otherwise, commenting on whether I used AI is about as intellectually substantive as commenting on the font.

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#37

Hey, I’m as open to being criticized as I know how to - so if there’s a critique, I welcome it! Apparently as you say I’m being overly a fanboy of Prasad and inconsistent with my own principles - ha, :smiling_face_with_tear:

Prominent and respected people, such as those critics of Prasad you mentioned, are not immune to the effects of social media. Prasad is deliberately provocative and courts controversy, which enrages his critics who fall for the bait. And sometimes this results in responses that are more driven by his personality than his actual argument, and as a result those critics don’t have credibility in that respect (they may be fine people in all other ways!). They allow themselves to be baited into such responses.

I guess it’s a personality quirk of mine, that I actually don’t mind provocateurs and “trash talkers”, as long as they can back up all that trash talking to an adequate degree that rewards discussion. In fact, it is often stating a position that’s deliberately exaggerated and done in a provocative manner that sparks genuinely interesting discussions. It’s the old bible verse Revelations 3:15-16 “So, because you are lukewarm, neither hot nor cold, I am about to spit you out of my mouth”. As a good atheist, I like citing bible verses :upside_down_face: - I like when people take strong positions, and don’t mind someone who dishes it out as long as they can also take it (and it’s at a high level, not merely nonsense, whether he’s right or wrong Prasad does). It makes for a stronger discussion. That’s why I like Prasad, not because I agree with him about everything (as I’ve said repeatedly, I don’t agree with him on many issues). And since I quoted the bible, I hasten to add a quote from a resolute atheist, the economist John Maynard Keynes “Words ought to be a little wild, for they are the assault of thoughts upon the unthinking.”

A vigorous discussion, sparked by a provocatuer like Prasad, I see as a positive. Do I overly praise Prasad? Possibly. But that doesn’t mean that I in any way hesitate to criticize his various claims or am upset by others criticizing his positions. Criticize away! And that applies to me as well - go ahead, critisize my positions, in fact, as I’ve stated many times, I prize criticism as an indispensable corrective to sitting in a bubble of self delusion… kind of the whole point of this thread, challenging ourselves and our firm convictions - OK, another quote that I’ve cited many times before, Richard Feynman “The first principle is that you must not fool yourself and you are the easiest person to fool.” So, I welcome any criticism you may have, and thank you for your words.

#38

I read the Neuropathy forum on Mayo Clinic website and there are several people who say they now have permenant neuropathy because they took the Shingles vaccine. I will PASS on that med. Also, I don’t know anyone that had shingles.

#39

Lol, you’re going to have a tough time if you do medical decisions based on anecdotes instead of clinical trials, and prospective cohort studies.

1 Like