Dr. Prasad reveals his "rethinking medical education" post was written by ChatGPT

And a look at his actual thoughts on the matter.

Shockingly (or maybe not so shockingly) Dr. Prasad just revealed that his recent post on rethinking medical education, which I wrote a response to, was actually written by ChatGPT.

My 'rethinking medical education' post was written 100% by ChatGPT

Apparently many of us were duped! Or at least partially (we’ll get to that in a bit).

I won’t deny that I did not pick up on subtle hints of AI tomfoolery, which would include the lack of grammatical mistakes as was pointed out in Prasad’s comments.

I guess I should feel solace in the fact that readers will be able to recognize that something is amiss if my posts began using fewer commas or consistent tense!

There’s not much denying that ChatGPT did a fairly decent job in forming a response based on the prompt Prasad provided, and I certainly won’t make any comments about recognizing the AI-like nature of the writing, as such remarks would be made in hindsight.

With the coming of AI it’s a reminder that it may become more difficult to determine whether what we read, see, or hear are real or constructions of AI made to present a simulacrum. In a world where everyone is online and personal interactions have been depleted, the biggest awareness that AI can bring to us as individuals is the resurgence of authenticity and originality. I don’t think AI is anywhere near being able to replicate authenticity, and being able to recognize one’s genuine nature will be far more critical in discerning the real thing from a fake imitation.

But nonetheless, what’s rather interesting is that the ideas put forth by ChatGPT did not come out of nowhere. This is, unsurprisingly, how ChatGPT and most AI similar to ChatGPT operate. But what this does tell us is that Prasad may have had similar ideas as the ones constructed by ChatGPT, which was also revealed by Prasad in the above post.

The relevant article published in Academic Medicine¹ appears to have actually been published in 2010 and not 2012:

The article is a rather interesting read. The premise seems to be in response to a 2008 comment Randolph Nesse made in The Lancet that the medical school curriculum should include evolutionary biology.

I’m sure Bret and Heather would be delighted by such remarks by Nesse, however with respect to Prasad that doesn’t appear to be the case.

Rather, the assertion that evolutionary biology become a part of the medical school curriculum didn’t appear to come to fruition. Prasad raises the question as to whether such a topic would prove relevant within a clinical setting in contrast to medical research. And, by extension, would such an argument of necessity extend to other science fields if one were to make an argument of consistency?

Prasad raises the following argument (emphasis mine):

We live in a new era of medicine. The Cardiac Arrhythmia Suppression Trial (CAST)³ and other major medical trials have highlighted ways in which reasoning from scientific principles, that is, storytelling, is not only insufficient for clinical decision making but also can be harmful. The CAST trial taught us that even drugs with sound pathophysiologic rationale could increase mortality. In light of the huge body of work in top-down, empiric research (which often falls under the heading of evidence-based medicine [EBM]), taking seriously suggestions such as Nesse's becomes harder. Nonetheless, Nesse is right to ask for consistency. Questioning the continued relevance of other sciences, including molecular biology and biochemistry, therefore seems reasonable. Ultimately, the pursuit of the basic sciences in medical education does make sense, but its primacy should be revoked. Medical educators should move toward a new model, one that declares the doctor–patient interaction as the most fundamental. This approach may serve as a new paradigm: encounter-based medical education.

Here, the idea is rather consistent to the ChatGPT-formulated prompt, in that Prasad is suggesting that basic science should take a backseat to empirical data provided from RCTs and a clinical setting.

The biggest issue I find in Prasad’s argument is that it frames scientific principles from the perspective of lacking curiosity and inquiry, while also taken results from RCTs as carte blanche ways of treating patients.

Suppose that the CAST² study provided in the excerpt above suggests increased mortality in those prescribed the medications outlined in the trial. The main question I would raise would be whether a clinical trial may provide a basis for why exactly those prescribed these medications would be at increased risk of mortality, whether through an examination of these drugs mechanisms or whether through genetic factors, or even with respect to comorbidities.

The biggest problem with such RCTs and clinical trials, is that they answer the what for a medication or treatment, as in whether people seem to benefit. However, they can never explain why some patients benefit or why some may experience worse outcomes. Such considerations are relegated to Discussion sections where clinicians provide suppositions with respect to their results. It then becomes the position of research-minded clinicians and scientists to dig deeper and find other explanations for the results seen in these trials.

In that regard, clinicians may just follow the results of such studies without investigating any further, and it becomes the job of scientists to figure it out.

I find this to be a rather hypocritical argument, as if to suggest that doctors have it all figured out when one can be just as likely to argue it is researchers who are piecing together the nuance.

This is why I find the following paragraph to be rather frustrating:

Thus far, I have suggested that the current method—two years of basic science presented as the foundation for clinical medicine—sanctions physicians' tendency to elevate storytelling over empiricism. In fact, direct evidence shows that some physicians do make this error. Tatsioni and colleagues¹⁸ selected theoretical benefits that were subsequently overturned by randomized controlled trial data and then tracked articles that persisted in supporting the original claim. One of these claims was that vitamin E provides cardiovascular benefit; the findings of the HOPE trial contradicted this supposed benefit. Tatsioni et al¹⁸ constructed a “qualitative list of counterarguments made to defend vitamin E effectiveness despite contradictory evidence.” Vitamin E defenders summoned the basic science rationale vociferously, passionately, and very nearly constantly. Tatsioni and colleagues¹⁸ specifically note that “diverse biological mechanisms were invoked in support.” This tendency to elevate storytelling, often overlooked by supporters of basic science, thus seems a very real concern.

These remarks, unfortunately, seem to provide a disservice to scientific principles, as it argues that explanations are unnecessary given that RCTs prove no benefit.

I was curious about this study in particular, and looked briefly into what exactly it stated with respect to the defenses provided.

When noting the biases in relation to vitamin E claims with respect to cardiovascular health, Tatsioni et al.³ noted the following rationale:

Box 1. Qualitative List of Counterarguments Made to Defend Vitamin E Effectiveness Despite Contradictory Evidence From Randomized Trials

Biases

Selection bias: meta-analysis did not put its results in perspective by reviewing the context of research on vitamin E including the many positive observational and interventional studies²⁸

Information bias: mortality estimates from CHAOS^a came from a research letter, not a peer-reviewed study, and included data after the study was officially ended, and thus subject to information bias²⁸

Genuine Diversity

Participant Characteristics

Genetic characteristics: genetic background of study subjects might have contributed to the differential results²⁹

Dietary habits: discrepancies may be explained by differences in the antioxidant content of the basal diet of the sample population under investigation³⁰

Stage of disease: some antioxidants, eg, vitamin E, might be more effective in the early phase of atherosclerosis, but much less so in the advanced clinically overt stage present in the majority of patients evaluated in clinical trials³¹

Oxidative stress status: studies that have included healthy subjects with decreased oxidative stress while vitamin E reduced oxidative stress in smokers (a condition of increased oxidative stress)³¹

Lifestyle characteristics: lifestyle of study subjects might have contributed to the differential results²⁹

Intervention: Vitamin E Form, Dose, Bioavailability

Vitamin E form: some trials utilized synthetic tocopherol, whose efficacy is not equivalent to the natural form³¹

Vitamin E dose: an adequate intake in the lowest intake category or a low interindividual variation intake may explain some of the negative findings³²

Vitamin E bioavailability: no control on how antioxidant vitamins were ingested: the bioavailability of vitamin E is higher when it is taken with lipid-rich meals. Antioxidant levels were not consistently measured in blood or tissues before and after supplementation: the same intake may produce different levels in distinct individuals³¹

Co-interventions

Beta-carotene (harmful co-intervention): most of the evidence for an elevated mortality risk came from two trials that administered vitamin E together with beta-carotene³³

Lack of appropriate cointervention: . . . single antioxidant supplementation might not be a good strategy, since antioxidant defenses normally behave as a network: therefore balanced intake is likely important³¹

Outcomes

Duration of follow-up: the possibility that antioxidants need to be taken more than five years to have a significant effect on atherosclerotic plaque formation cannot be dismissed³⁴

^aRefers to the mortality data of CHAOS, which, contrary to the main publication of the trial on cardiovascular events, had shown no benefit from vitamin E.

What I find so strange is that some of the arguments made above seem rather sound- there are a multitude of reasons as to why a therapeutic intervention may, from a hypothetical standpoint, not actually work in practice.

But again, a curious mind would try to look for explanations, hypothesize, and investigate even further. From the perspective that Prasad reasons, such a position should not be taken because the clinical evidence isn’t there. There’s no statistical significance, so why bother looking deeper? Don’t bother trying to understand why some patients seem to benefit from a therapeutic while others don’t. Don’t bother trying to elucidate why some adverse reactions may arise, including years down the line when the clinical data may argue a beneficial use of a drug.

This was one of the issues I raised with respect to Molnupiravir. Sure, clinical trials may provide evidence of reduced hospitalization and mortality in the Molnupiravir group, but it doesn’t do anything to explain the concerns over the drugs mutagenicity and the effects this drug may have years down the line. As such, looking only at clinical trials will only focus on the symptoms and not wider concerns over a therapeutic.

This can be further emphasized by the following paragraph (emphasis mine):

The idea that knowledge can become dated may perhaps be more familiar to physicians as this educational proverb: “Half of what you are taught as medical students will in 10 years have been shown to be wrong. And the trouble is, none of your teachers know which half.”³² Fifty years of physicians have been educated with some variation of this maxim. And for most of the 20th century, it was likely fairly accurate. The progress of empiricism, however, puts it in question. Today, physicians often know which half will be proven wrong. Physicians know, for instance, that when they give the drug simvastatin to patients with angina or previous MI who have elevated total cholesterol, they can expect a 30% reduction in all-cause mortality compared with those taking placebo.³³ This fact was and will always be true, verified by multiple randomized controlled trials. However, its corollary, the basic science story that simvastatin (like all statins) acts through the inhibition of the enzyme HMG-CoA reductase lowering LDL cholesterol through its downstream effect, may very well not survive the test of time. In fact, it has already come under scrutiny: Statins likely have pleiotropic effects, and LDL levels may not solely guide their use.^34,35

This feels more like consensus medicine and an overemphasis on the infallible nature of RCTs, which is inherently incorrect. It’s rather arrogant to assume that RCTs will always be consistent, and it doesn’t get to answering why exactly mortality would be lower in those taking simvastatin relative to placebos.

In contrast, the piece that Prasad is critical of, which would be an example of science constantly changing and updating, actually leans more towards nuanced thinking.

Given that the prompt provided by Prasad was AI-generated, I think it would be fitting for people to read Prasad’s own words on the matter. My thoughts haven’t changed on the topic, and in fact has been strengthened based on the examples Prasad provided.

It’s clear that this approach to medicine is one that enforces narrow-minded viewpoints, and in a world where more critical thinking is needed we shouldn’t lean towards the model of medicine that Prasad is justifying.

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1. Prasad, Vinay MD. Perspective: Beyond Storytelling in Medicine: An Encounter-Based Curriculum. Academic Medicine 85(5):p 794-798, May 2010. | DOI: 10.1097/ACM.0b013e3181d6967f

2. Echt, D. S., Liebson, P. R., Mitchell, L. B., Peters, R. W., Obias-Manno, D., Barker, A. H., Arensberg, D., Baker, A., Friedman, L., & Greene, H. L. (1991). Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. The New England journal of medicine, 324(12), 781–788. https://doi.org/10.1056/NEJM199103213241201

3. Tatsioni, A., Bonitsis, N. G., & Ioannidis, J. P. (2007). Persistence of contradicted claims in the literature. JAMA, 298(21), 2517–2526. https://doi.org/10.1001/jama.298.21.2517