Who Decides What Counts As Evidence?
In 109 studies in 2022 regarding the relationship between the Covid Vaccine and Autoimmune Disorders “Nearly 60% of the studies reported relapses or flares, and approximately one-quarter documented new-onset conditions in individuals with no prior history of autoimmunity.”
Claudia Chaufan, MD, PhD
School of Health Policy and Management
Faculty of Health, York University, Canada
“COVID-19 vaccines and autoimmune disorders: A scoping review,
AIMS Medical Science, 2025, 12(4): 325-349.“ 4/2026
Interview Summary – By Claudia Chaufan, MD, PhD
This interview presents the work of Claudia Chaufan, MD, PhD, a health policy scholar, professor, and non-practicing physician. Her research examines how medical evidence is produced, interpreted, and governed, and how issues of human significance come to be framed within medical jurisdiction, including the extension of medical and psychological labels to define and manage dissent in ways that shape policy compliance and institutional legitimacy. Her interest in the relationship between Covid-19 vaccination and autoimmune disorders emerged from a broader concern with how large-scale policy responses – including lockdowns, mandates, and mass vaccination – were justified and normalized, with limited space for critical scrutiny of their evidentiary basis.
To explore how potential harms were being assessed, Chaufan and her team conducted a scoping review of 109 studies published in 2022 on Covid-19 vaccination and six autoimmune conditions. The review identified three recurring patterns: relapses or flares in individuals with pre-existing autoimmune disease, new autoimmune conditions in those already affected, and new-onset autoimmune disorders in previously healthy individuals. Nearly 60% of studies reported relapses or flares, and approximately one-quarter documented new-onset conditions in individuals with no prior history of autoimmunity.Yet despite these findings, many studies continued to advance strong claims about vaccine benefit while treating signals of harm as tentative, incidental, or inconclusive. The interview argues that this reflects a broader epistemic imbalance: harms and benefits are not consistently evaluated according to the same evidentiary standards. Using Covid-19 and autoimmunity as a case study, Chaufan raises questions about epistemic consistency in medical research and the institutional processes that shape what counts as credible evidence.
Watch Video Overview of Interview by Kirk Hamilton PA
Kirk Hamilton: Can you please share your educational background and current position?
Claudia Chaufan: I earned my medical degree at the University of Buenos Aires in Argentina, where I practiced medicine for close to a decade, focusing primarily on clinical nutrition and diabetes care. That clinical experience remains foundational to how I approach questions of health and disease, even though my subsequent career has taken a more analytical and research-oriented direction.
I later pursued graduate studies at the University of California, Santa Cruz, where I completed first a Master’s and later a PhD in Sociology, along with graduate work in philosophy. This training allowed me to shift from clinical practice to a broader examination of health, not only as a biomedical phenomenon but as a social, political, and institutional one. My first academic appointment was at the University of California, San Francisco, where I worked as a researcher and professor of sociology and health policy.
I am currently a tenured Professor in the School of Health Policy and Management at York University in Toronto. My work sits at the intersection of health policy, sociology of health, and political economy, and over the past several years it has focused increasingly on the governance of Covid-19 policies, the organization of medical knowledge, and questions of epistemic integrity in biomedical research.
Kirk Hamilton: What got you interested in studying the role of autoimmune illness and its relationship to the Covid-19 vaccination?
Claudia Chaufan: Like many people, I was initially struck by the scale and global impact of the Covid event. My early work in 2020 was not focused on biomedical questions but rather on the geopolitical and policy dimensions of the response. What first captured my attention was the way in which the Covid event appeared to coincide with, and perhaps intensify, a broader geopolitical confrontation, particularly in relation to Western representations of China as an emerging competitor increasingly framed as a civilizational or existential threat—often through broad and loosely defined claims about risks to “our democracy” or “our way of life.” I spent many months following and trying to understand these developments.
At the same time, I became increasingly struck not only by the magnitude and character, but also by the duration, of unprecedented public health measures—including, though not limited to, lockdowns and medical mandates, especially vaccination—as they became normalized across Western countries. In other words, my initial engagement with Covid was primarily sociological and geopolitical rather than biomedical.
With respect to the medical aspects of Covid and vaccination—for the purposes of this interview, I will bracket the important question of what exactly these injections are and refer to them as “vaccines”—I had relatively little prior engagement with immunology or autoimmune disease.
As a clinician, I was aware of discussions linking viral infections to autoimmune conditions—type 1 diabetes, which I developed as a child, is one example—but I had never found that line of inquiry particularly compelling, nor had it played a central role in my work. In fact, an important part of my intellectual trajectory had moved in a different direction.
During my doctoral training in sociology and philosophy, I became deeply engaged with critical analyses of biomedical knowledge, particularly in relation to genetics. Influenced in part by the work of Richard Lewontin, I examined—over a series of papers—the conceptual and empirical limitations of genetic explanations for complex diseases such as diabetes (1–4). That work led me to question not only specific claims about causation, but more broadly how biomedical findings are framed, communicated, and sometimes overstated or misrepresented. It also contributed to a more general skepticism toward reductionist explanations and toward the ways in which medical knowledge is mobilized in policy and practice.
Against that background, what genuinely caught my attention during the Covid-19 period was not the possibility of infection-related autoimmunity, but rather the idea—entirely absent from my prior medical training—that vaccination itself might trigger autoimmune responses. As I began to investigate this more systematically, I encountered the work of Yehuda Shoenfeld, who had documented a range of autoimmune phenomena following vaccination over at least two decades (5). But as I kept reading, I realized the literature went back even further: I began to find isolated case reports and clinical observations from much earlier periods (6). What struck me the most about these findings, however, was that they were almost invariably accompanied by strong affirmations of the value of vaccines—not simply as background context, but as a way of anticipating and deflecting potential criticism, and of signaling adherence to what is expected or acceptable within the field.
More broadly, this led me to revisit a claim that is often taken for granted: that vaccination has been the primary driver of the dramatic decline in mortality from infectious diseases over the past century. That claim has in fact been challenged by a substantial body of epidemiological research, including the work of Thomas McKeown (7), John and Sonya McKinlay (8), among others, as well as historical public health data from countries such as the United States and the United Kingdom. These analyses document that mortality from many infectious diseases had already declined significantly prior to the introduction of mass vaccination. At minimum, this complicates straightforward causal claims and raises questions about how such narratives are constructed and sustained.
At any rate, this encounter was decisive. It shifted my attention from a general awareness of immune-related disease to a more focused and structured inquiry into vaccine-related autoimmunity. From there, I developed a formal research program, beginning with a published protocol (9), followed by a completed scoping review of the literature on Covid-19 vaccination and autoimmune disorders (10), and more recently an ongoing investigation—described in another published protocol (11)—into how standards of evidence are differentially applied depending on whether claims concern the benefits or harms of vaccination. At the same time, this line of work connected directly with my broader research concerns about epistemic integrity—specifically, how such findings are interpreted, qualified, or marginalized within biomedical research and policy discourse.
Kirk Hamilton: Can you tell us about your study and the basic results?
Claudia Chaufan: Initially, I conceived of a very broad project: to map the full range of autoimmune disorders reported in association with Covid-19 vaccination since the launch of the global campaign. However, the volume of emerging studies quickly made this approach unfeasible. My research time is limited given my substantial teaching load and graduate student supervision responsibilities, and so are the material resources available to support research assistants, many of whom are students or working adults with other obligations.
I therefore narrowed the scope of the review. Rather than attempting to map the entire field, I focused on six major autoimmune conditions of clear clinical significance: Graves’ disease, Hashimoto’s thyroiditis, multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, and type I diabetes mellitus. I further restricted the search to studies published in 2022, a period in which vaccination had become widespread and was, in many settings, reinforced through mandates tied to participation in professional and social life. By that time, key empirical and normative assumptions underlying these policies—such as the expectation that vaccination would prevent infection or transmission—had already come under sustained scrutiny.
The findings were nothing short of striking. Across the studies reviewed, there was consistent documentation of three patterns: exacerbation of pre-existing autoimmune conditions (often described as flares), the emergence of new autoimmune conditions in individuals with prior autoimmune disease, and new-onset autoimmune disorders in individuals with no documented history of such conditions. These findings were based largely on case reports and case series, which have well-known limitations. However, the consistency and breadth of reported phenomena across different conditions and settings made the overall pattern difficult to dismiss as incidental.
Kirk Hamilton: What is the significance of a 60% flare-up in those with previous autoimmunity and 25% new-onset autoimmunity?
Claudia Chaufan: The significance of these figures requires careful interpretation, both in terms of what they show and what they do not show. These are not population-level estimates derived from large epidemiological datasets; rather, they emerge from the aggregation of clinical reports within the literature reviewed. As such, even if they do not provide precise estimates of incidence or risk, they identify recurring patterns that warrant attention.
That said, even as indicative figures, they are difficult to dismiss. A reported 60% rate of flare-ups among individuals with pre-existing autoimmune disease points to a consistent pattern of exacerbation following vaccination. Similarly, a 25% proportion of new-onset autoimmune conditions within the reviewed cases—many occurring in individuals with no prior history of autoimmune disease—cannot be readily explained away by invoking “susceptibility” as a default category.
The tendency to attribute such outcomes to pre-existing or latent individual predispositions raises a broader issue. In many areas of medicine, when a pattern of adverse events emerges following exposure to a given intervention, the primary question is whether the intervention itself may be contributing to harm, not how to identify which individuals are uniquely vulnerable. The fact that an adverse effect does not occur in all exposed individuals does not diminish its significance, nor does it justify shifting the burden of explanation onto those affected.
This is particularly important in the context of interventions administered to large populations of otherwise healthy individuals. Under such conditions, the threshold for safety and the standards of scrutiny should be correspondingly high. Observations of new-onset autoimmune disorders in previously healthy individuals therefore raise not only mechanistic questions but also questions of proportionality and responsibility in clinical and policy decision-making.
The broader issue, in my view, is not simply one of risk evaluation under uncertainty, but of how claims about risk were framed, communicated, and enforced. From early on, Covid-19 was presented by public health authorities and governments as posing a broadly uniform and severe threat, even as available data already indicated substantial variation in risk by age and health status. At the same time, potential adverse effects of vaccination were not merely treated as unproven; they were frequently dismissed, discounted, or categorized as misinformation, effectively placing them outside the bounds of legitimate inquiry.
This asymmetry has important implications. If the risk of severe Covid-19 outcomes is highly stratified, while an intervention is applied indiscriminately across entire populations—including healthy individuals with very low baseline risk—then the question is no longer simply one of balancing risks and benefits in the abstract. It becomes a question of proportionality, responsibility, and the standards of evidence deemed acceptable when medical interventions are extended to populations that may derive little or no direct benefit—or may even be seriously harmed.
Under such conditions, the expectation of rigorous scrutiny should increase, not decrease. Observations of adverse outcomes, including new-onset autoimmune disorders in previously healthy individuals, therefore raise not only clinical and mechanistic questions, but also more fundamental questions about the justification for broad, population-wide interventions—and the thresholds at which they should be considered, if at all.
Kirk Hamilton: Do you think these two findings are real in the sense of it the Covid 19 vaccine causing this versus some effect from most people having an episode (s) of Covid 19?
Claudia Chaufan: I do not mean to be blunt but am not entirely sure what you mean by “real.” What I can say is that the findings themselves are based on a substantial number of documented clinical observations. In our review, we identified over a hundred papers reporting associations between Covid-19 vaccination and autoimmune disorders, many of them describing individuals who developed symptoms shortly after receiving the injection, including individuals with no prior history of autoimmune disease. For the patients involved, these events are unquestionably real.
It is often pointed out—correctly—that case reports and case series are not designed to establish causality. However, what is striking is the asymmetry in how evidentiary standards are applied. Very demanding standards are invoked when considering whether vaccines might cause harm, yet far less stringent standards are often accepted when making claims about their benefits, including assertions that vaccines have saved “millions of lives.” This creates a situation in which causality is treated as both essential and effectively unattainable, depending on the direction of the claim.
In addition, there is a circularity in the way the evidence base has developed. Randomized controlled trials that might have helped clarify causal questions about adverse events were not pursued, in part because vaccination was assumed to be so beneficial that withholding it was considered unethical. But that assumption itself rests on causal claims that were never subjected to the same level of scrutiny. As a result, we are left in a position where causality is both presumed and rendered difficult to investigate—precisely the problem I am currently examining in my work on epistemic asymmetry in vaccination research (11).
From a clinical and ethical standpoint, this matters. As I mentioned earlier, when a medical intervention is administered to healthy individuals—particularly younger populations—the threshold for safety should be extraordinarily high. One may be attempting to “fix” a problem that does not exist for large segments of the population, at potentially significant cost. Yet in many of the studies reviewed, even when authors documented autoimmune phenomena following vaccination, the conclusions often emphasized reassurance and continued vaccination, with limited discussion of precautionary approaches.
More broadly, this raises a question about how such interventions are framed within public health. There is a tendency to group mass vaccination campaigns alongside classic public health measures such as access to clean water, adequate nutrition, improved housing, and sanitation—interventions that address fundamental conditions of health and are not themselves sources of biological risk in the way a foreign substance injected into the body is. In other words, vaccines are not obviously equivalent to clean, drinkable water; the analogy is not only imperfect but potentially misleading. Even when vaccines are framed as a “social determinant of health,” they are pharmaceutical products—interventions that act within the body and carry risks—and therefore belong to a different analytical category. Treating them so (vaccines), lowers the level of scrutiny applied to their widespread use. This, in my view, warrants care and critical examination.
Kirk Hamilton: Do you have any idea what is the triggering component in the Covid vaccine? i.e. the synthetic made spike protein?
Claudia Chaufan: Actually, we did not chart this issue so I cannot give you an answer based on a systematic observation. However, there are plausible hypotheses grounded in immunology. The spike protein is one candidate that has received attention, particularly in relation to mechanisms such as molecular mimicry, where immune responses directed at a viral protein may cross-react with host tissues. This is not a novel concept, but its relevance in the context of Covid-19 vaccines is still being investigated.
At the same time, it is important to recognize that the vaccine is not only the spike protein. The mRNA platform and the lipid nanoparticles used for delivery are also biologically active components. These are designed to stimulate an immune response, which is their intended function, but that also means they can have effects beyond the narrowly defined target.
The key point, however, is that framing the issue in terms of a specific “triggering component” is conceptually misleading. It shifts attention toward identifying individual susceptibility or isolating a particular mechanism, rather than asking a more fundamental question: what are the implications of administering a biologically active substance, at scale, to large populations of otherwise healthy individuals? In most areas of medicine, the burden of proof rests on demonstrating that an intervention is effective, safe, necessary, and better than known alternatives—including the alternative of doing nothing—before it is widely deployed, rather than on identifying which individuals may be uniquely vulnerable after the fact.
Focusing on “triggers” can therefore function as a way of redistributing responsibility, from the intervention itself to the individuals affected by it. Yet biological outcomes are often contingent, shaped by complex and context-dependent interactions rather than a single identifiable cause. The fact that not all individuals experience adverse effects does not diminish the need for scrutiny; if anything, it underscores the importance of evaluating the intervention itself, rather than attributing outcomes primarily to presumed variations in susceptibility. Under conditions of mass administration, that distinction becomes critical.
Kirk Hamilton: Did any of the studies reviewed check for IGG antibody levels to the spike protein?
Claudia Chaufan: This was not a central or consistently reported focus in the studies included in the scoping review. The literature I examined was primarily composed of case reports and case series documenting clinical presentations of autoimmune conditions, and these studies varied considerably in the level of immunological detail they provided.
Some studies did include laboratory data, including antibody measurements, but there was no systematic or standardized assessment of IgG antibody levels—let alone specific subclasses such as IgG4—across the body of literature. As a result, it is difficult to draw general conclusions about antibody profiles from the studies reviewed.
This points to a broader limitation in the existing evidence base. If questions about immune response—including antibody dynamics—are to be addressed more rigorously, they require study designs that go beyond descriptive clinical reporting and incorporate more detailed and standardized immunological measurements.
Kirk Hamilton: Is there any other comment you would like to make on this subject?
Claudia Chaufan: I would emphasize that the central issue here is not only the identification of possible adverse events, but how such findings are interpreted within biomedical and policy contexts. A recurring observation in my work is that studies often document events that may be significant yet frame them in ways that minimize their implications or disconnect them from broader questions of causation and risk.
This raises questions about epistemic standards. If similar patterns of evidence were observed in other contexts, would they be interpreted in the same way? Are the thresholds for considering a causal relationship applied consistently across domains, or do they shift depending on prior ideological commitments, institutional incentives, or policy implications that may disrupt entrenched interests?
ore broadly, this connects to issues of governance and the production of knowledge—questions that also inform my teaching. Decisions about what counts as sufficient evidence, which questions are prioritized, and how uncertainty is communicated are not purely technical matters; they are shaped by institutional settings and policy objectives. In the classroom, I try to encourage students to examine these processes critically and to distinguish between empirical claims, normative assumptions, and the frameworks through which both are interpreted.
My concern is less about advancing a definitive claim in one direction or another, and more about ensuring that the evaluation of evidence remains open as new data emerge—and, importantly, that it is conducted in a manner that is transparent, ethically grounded, and open to democratic scrutiny.
References
1. Chaufan C. How much can a large population study on genes, environments, their interactions and common diseases contribute to the health of the American people? Social Science & Medicine. 2007;65(8):1730–41.
2. Chaufan C. Unpacking the heritability of diabetes: The problem of attempting to quantify the relative contributions of nature and nurture. DataCrítica: International Journal of Critical Statistics. 2009;2(2):23–38.
3. Chaufan C. What Can the Slim Initiative in Genomic Medicine for the Americas (SIGMA) Contribute to Preventing, Treating, or Decreasing the Impact of Diabetes among Mexicans and Latin Americans? Kalfou: A Journal of Comparative and Relational Ethnic Studies. 2018;5(1):24–35.
4. Chaufan C, Joseph J. The ‘missing heritability’ of common disorders: Should health researchers care? International Journal of Health Services. 2013;43(2):281–303.
5. Shoenfeld Y, Aron-Maor A. Vaccination and Autoimmunity—‘vaccinosis’: A Dangerous Liaison? Journal of Autoimmunity. 2000 Feb 1;14(1):1–10. doi:10.1006/jaut.1999.0346
6. Oski FA, Naiman JL. Effect of Live Measles Vaccine on the Platelet Count. New England Journal of Medicine. 1966 Aug 18;275(7):352–6. doi:10.1056/NEJM196608182750703
7. McKeown T, Record RG. Reasons for the Decline of Mortality in England and Wales during the Nineteenth Century. Population Studies. 1962;16(2):94–122. doi:10.2307/2173119
8. McKinlay JB, McKinlay SM. The Questionable Contribution of Medical Measures to the Decline of Mortality in the United States in the Twentieth Century. The Milbank Memorial Fund Quarterly Health and Society. 1977;55(3):405–28. doi:10.2307/3349539
9. Chaufan C, Manwell L, Heredia C, McDonald J, Chaufan C, Manwell L, et al. COVID-19 vaccines and autoimmune disorders: A scoping review protocol. AIMSMEDS. 2023;10(4):medsci-10-04-025. doi:10.3934/medsci.2023025
10. Chaufan C, Manwell L, Heredia C, McDonald J, Chaufan C, Manwell L, et al. COVID-19 vaccines and autoimmune disorders: A scoping review. AIMSMEDS. 2025;12(4):325–49. doi:10.3934/medsci.2025023
11. Chaufan C. Interpreting autoimmune risks in the COVID-19 vaccine literature: A two-phase qualitative coding protocol on biological mechanisms and epistemic integrity. ALLERGY. 2025;9(3):190–204. doi:10.3934/Allergy.2025015
Staying Healthy Today is a reader-supported publication.
To receive new posts and support my work, consider becoming a free or paid subscriber.
($5.00/month or $50/year would be appreciated for this weekly publication)
Kirk Hamilton PA-C
Prescription 2000, Inc.
Health Associates Medical Group
3301 Alta Arden, Suite 3
Sacramento, CA 95825
(916) 489-4400 (w)
krhammer@surewest.net
StayingHealthyToday.Substack.com
www.StayingHealthyToday.com
www.KwikerMedical.com
www.HealthyLivingforBusypeople.com