Johns Hopkins Continues to Mislead the Public on the State of the Science on Vaccines and Autism

Major medical institutions just are not getting the message. The science is not only not settled: The question is the most important neglected question in medical science - ever.

“The science is settled” is a phrase invoked not to convey certainty but to halt inquiry. This rhetorical flourish has been used repeatedly in public health communications, particularly regarding the long-standing controversy over a potential link between vaccines and autism spectrum disorders (ASD). A recent example of this can be found in the March 19, 2025 article from Johns Hopkins Public Health, titled “Vaccines Don’t Cause Autism. Why Do Some People Think They Do?”

In the article, Dr. Daniel Salmon, a vaccinologist and director of the Johns Hopkins Institute for Vaccine Safety, discusses the origins of the vaccine-autism debate, attributing it mainly to the 1998 case series published by Dr. Andrew Wakefield and colleagues. The article, which claims that 16 studies exist that definitively answer the question of vaccines and autism, argues that Wakefield's now-retracted paper initiated a cascade of misinformation that public health authorities have spent decades refuting. It claims that a wealth of rigorous studies has “settled the science” and that the persistence of public doubt stems from cognitive biases and unfortunate timing rather than legitimate scientific controversy.

This narrative is both misleading and incomplete. It fails to acknowledge a substantial body of peer-reviewed evidence across disciplines—epidemiology, immunology, toxicology, molecular biology, and clinical medicine—that supports concern over vaccine-related neurodevelopmental outcomes. It omits biological plausibility, disregards whistleblower disclosures and court-admitted vaccine injuries, and relies on an artificially narrow scope of reference. It also ignores the history of the CDC sharing 27 studies, 22 of which where rejected by the National Academy of Science’s Institutes of Medicine, leaving 5; four of these were underpowered, leaving one study. That history will be part of future article.

The purpose of this rebuttal is not to assert that vaccines do cause autism in all cases, but to make the case—based on published literature and verifiable findings—that the issue remains scientifically unresolved, and prematurely declaring it “settled” is a disservice to science, to public trust, and to families seeking answers, and that the Johns Hopkins article blissfully ignores peer-reviewed studies worth considering that show their conclusion is recklessly irresponsible.

Beyond Wakefield: The Ignored Landscape of Peer-Reviewed Evidence

The Johns Hopkins article frames the entire vaccine-autism controversy as a consequence of a single discredited case series—Andrew Wakefield’s 1998 paper in The Lancet. While that paper did draw international attention, it was a pilot study that never concluded that vaccines cause autism. It was also not the first nor the most substantial source of information on the topic raising concerns about vaccine safety. Reducing decades of inquiry to one retracted article is both historically and scientifically false.

CDC’s Own Early Findings: The Verstraeten Signal

In 1999, CDC epidemiologist Thomas Verstraeten presented findings at the CDC’s Epidemic Intelligence Service (EIS) conference based on internal analyses of the Vaccine Safety Datalink (VSD). The results showed a relative risk (RR) of 7.6 (95% CI: 1.8–31.5) for autism in children receiving more than 25 μg of mercury from thimerosal-containing vaccines (TCVs) in the first month of life compared to those with no exposure (Verstraeten et al., Simpsonwood VSD communication). The degree of institutional suppression found in the minutes of the meeting is massive. Notably, this finding was never published in its original form. Instead, subsequent iterations of the dataset were revised over four years, after discussion by participants:

"The number of dose related relationships [between mercury and autism] are linear and statistically significant. You can play with this all you want. They are linear. They are statistically significant." - Dr. William Weil, American Academy of Pediatrics. Simpsonwood, GA, June 7, 2000

"The issue is that it is impossible, unethical to leave kids unimmunized, so you will never, ever resolve that issue [regarding the impact of mercury]." - Dr. Robert Chen, Chief of Vaccine Safety and Development, Centers For Disease Control, Simpsonwood, GA, June 7, 2000

"Forgive this personal comment, but I got called out at eight o'clock for an emergency call and my daughter-in-law delivered a son by c-section. Our first male in the line of the next generation and I do not want that grandson to get a Thimerosal containing vaccine until we know better what is going on. It will probably take a long time. In the meantime, and I know there are probably implications for this internationally, but in the meanwhile I think I want that grandson to only be given Thimerosal-free vaccines." - Dr. Robert Johnson, Immunologist, University of Colorado, Simpsonwood, GA, June 7, 2000

Whistleblower Testimony: Dr. William Thompson and Data Removal

In 2014, CDC senior scientist Dr. William Thompson disclosed that he and other co-authors omitted statistically significant data from a 2004 study on MMR timing and autism risk in African-American boys. According to Thompson, removing subjects without “valid Georgia birth certificates” - certainly NOT a justifiable confounding variable - reduced the odds ratio from 3.36 to a non-significant result (Hooker et al., 2014). These statements were corroborated with internal documents and audio recordings, yet have never been addressed in CDC policy or mainstream narratives.

Independent VSD Analyses: Increased Risk Across Multiple Disorders

Several independent studies have re-analyzed VSD data and confirmed increased risks:

• Young, Geier, & Geier (2008): This study found significantly increased rate ratios for autism, tics, ADHD, and emotional disturbances among children exposed to mercury from TCVs. Control outcomes (e.g., head injury, fractures) showed no increase, strengthening causal plausibility.

• Geier et al. (2013) conducted a two-phase study. Phase I found a higher risk of ASD following thimerosal-containing DTaP compared to thimerosal-free versions. Phase II confirmed increased odds of ASD for infants who received thimerosal-containing hepatitis B vaccines in the first six months of life.

These studies were based on the same CDC-linked datasets previously used to deny any vaccine-autism connection, yet reached very different conclusions when analyzed without institutional filtering.

Mercury Metabolism and ASD Susceptibility: Holmes et al. (2003)

In a novel analysis, Holmes, Blaxill, and Haley (2003) measured mercury levels in first baby haircuts of autistic children and matched neurotypical controls. Autistic children had an 8-fold lower mean mercury level (0.47 ppm vs. 3.63 ppm), suggesting impaired excretion and a possible susceptibility to mercury retention. Among children with severe autism, levels were even lower (0.21 ppm), reinforcing the idea that differential detoxification mechanisms may play a critical role in ASD vulnerability.

Molecular and Genetic Factors: Geier & Geier (2007)

In a case series of 11 children with ASD and confirmed mercury toxic encephalopathy, the authors reported elevated porphyrins and neurological findings consistent with mercury poisoning. These children also exhibited a regressive pattern consistent with what has been observed in thousands of parental reports and clinical observations (Geier & Geier, 2007).

---

These findings were available long before the public was told that the “science was settled.” They were not produced by Wakefield. They came from the CDC, whistleblowers, and independent researchers analyzing government-linked data. By erasing this rich and troubling landscape of evidence, the Johns Hopkins article does not promote scientific clarity—it enforces a sanitized and politically convenient narrative.

Thimerosal and Mercury: Evidence from Epidemiology, Mechanisms, and Models

Thimerosal, an ethylmercury-containing preservative, was widely used in childhood vaccines until the early 2000s and remains in flu vaccines today. Despite longstanding claims that ethylmercury is rapidly cleared and thus biologically insignificant, multiple lines of evidence suggest otherwise. These include epidemiological associations, animal studies showing CNS toxicity, and biochemical evidence of differential detoxification in autistic children, and the rhesus monkey study by Burbacher et al. that found that mercury from thimerosal stays in the brain indefinitely, compared to that from methylmercury, which in fact clears from the brain.

Epidemiological Evidence: Elevated Risk Ratios Across Studies

We’ve already noted Verstraeten et al. (1999), who found a 7.6-fold increased risk of autism in infants receiving >25 μg of mercury from TCVs in the first month. Several other studies expand upon this finding:

• Geier et al. (2013) (Translational Neurodegeneration): This two-phase study showed that children receiving TCVs—particularly thimerosal-containing DTaP and HepB vaccines—had significantly increased odds of ASD. The risk was especially pronounced when exposure occurred in the first six months of life.

• Young et al. (2008) (Journal of Neurological Sciences): This large-scale assessment of VSD data found increased rate ratios for multiple neurodevelopmental disorders (NDDs), including autism, ADHD, and emotional disturbances. Importantly, no increased risks were observed for unrelated outcomes, underscoring the specificity of the association.

• Gallagher & Goodman (2008, 2010): Using NHIS data, they found that boys vaccinated with thimerosal-containing Hepatitis B vaccines had three times the risk of autism compared to those vaccinated after one month or not at all. A second study found a ninefold increased odds of requiring early intervention or special education services among vaccinated boys.

Mercury and Autism: Meta-Analytical Confirmation

In the most comprehensive meta-analysis to date, Jafari et al. (2017) reviewed 44 case-control studies examining mercury levels in hair, urine, blood, RBCs, and brain tissue. The findings were unequivocal: mercury levels were significantly higher in autistic individuals across nearly all tissue types, with the authors concluding that “mercury is an important causal factor in the etiology of ASD.”

Detoxification Impairments in ASD Children

Holmes et al. (2003), as previously noted, found drastically lower mercury levels in first baby haircuts of autistic children. This has been interpreted not as evidence of reduced exposure, but rather of impaired excretion. Additional research has identified impairments in glutathione-related pathways, critical for mercury detoxification, among children with autism (Kern et al., 2013).

• Sharpe et al. (2013) showed that B-lymphocytes from children with autism were hypersensitive to thimerosal, exhibiting cytotoxic responses at doses that had no effect on controls or neurotypical siblings.

• Walker et al. (2006) found that lymphocytes from autistic children significantly upregulated heat shock protein RNA when challenged with thimerosal in vitro, a marker of cellular stress.

These findings reinforce the idea that individual variability in detox pathways—not universal susceptibility—is likely responsible for why only some children are affected.

Animal Studies: Reproducible Neurotoxicity

A range of animal models confirms the neurotoxic potential of thimerosal at doses equivalent to those in pediatric vaccines:

• Olczak et al. (2010, 2011): In Wistar rats, early postnatal thimerosal exposure led to persistent behavioral deficits, altered dopamine signaling, and structural brain abnormalities in areas implicated in autism.

• Laurente et al. (2007): Postnatal hamsters injected with thimerosal at vaccine-equivalent doses exhibited neuronal necrosis, decreased neuronal density, and gliosis in key brain regions, including the cerebellum and hippocampus.

• Hornig et al. (2004): In mouse models, susceptibility to thimerosal’s neurotoxic effects was strain-dependent, highlighting the role of genetic predisposition. Autoimmune-prone SJL/J mice developed growth delay, reduced locomotion, and hyperchromic hippocampal neurons after thimerosal exposure.

• Li et al. (2014): Transcriptomic analysis of neonatal mice exposed to thimerosal revealed disruptions in synaptic signaling, neuronal growth pathways, and genes previously associated with ASD.

Collectively, these studies show that thimerosal is not only biologically active in developing organisms—it is neurologically disruptive, particularly when combined with genetic or immunological susceptibility.

To dismiss these findings, as the Hopkins article does, is not an exercise in scientific rigor—it is an act of editorial omission. The evidence for thimerosal as a plausible contributing factor in ASD is supported by human data, animal data, mechanistic models, and meta-analyses. That is more than can be said for many environmental risk factors currently under investigation in mainstream autism research.

Aluminum Adjuvants and Neurotoxicity: A Systemic Oversight

While thimerosal has drawn the bulk of attention historically, aluminum adjuvants—which remain in nearly all pediatric vaccines—have emerged as a second and perhaps more insidious concern. Unlike ethylmercury, aluminum is explicitly added to stimulate the immune system. This property, while useful for generating antibody responses, also poses substantial neuroinflammatory risks, particularly when injected during critical periods of neurological development.

Despite this, the Johns Hopkins article does not mention aluminum even once—a glaring omission given the volume of literature on its neurotoxic potential.

---

Aluminum and ASD: Correlation at the Population Level

Shaw and Tomljenovic (2013) applied Hill’s criteria to the question of whether aluminum exposure from vaccines could be contributing to rising autism prevalence. Their findings are striking:

• Pearson correlation coefficient r = 0.92 (p < 0.0001) between cumulative aluminum exposure from vaccines and ASD prevalence in the U.S. over the past two decades.

• Across seven developed countries, aluminum exposure from routine pediatric vaccines at 3–4 months of age was significantly correlated with national ASD prevalence (r = 0.89–0.94, p = 0.0018–0.0248).

• They concluded that the data were consistent with a causal association, especially when viewed alongside animal models and mechanistic studies (Shaw & Tomljenovic, 2013).

• Aluminum is involved in neurotoxicity (Fulgenzi et al., 2014)

Animal Studies: CNS Damage and Behavioral Disruption

Shaw et al. (2013) tested the effects of aluminum adjuvants in neonatal mice using injection schedules designed to approximate U.S. and Scandinavian pediatric vaccine exposure. Their results:

• Mice receiving “high” and “low” doses of aluminum adjuvants showed significant motor deficits, impaired spatial memory, and alterations in social behavior—all consistent with ASD phenotypes.

• Histological analyses revealed inflammation, astrocyte activation, and altered synaptic protein expression in brain tissue.

These findings were replicated across multiple doses and timepoints, reinforcing their robustness.

Neuroimmune Interference: A Plausible Mechanism

Aluminum acts through persistent activation of the innate immune system, particularly microglial priming in the brain (Tomljenovic & Shaw, 2011). In early life, the blood-brain barrier is immature, and aluminum salts can cross into neural tissue where they activate pro-inflammatory cytokine cascades.

This mechanism is consistent with observations in ASD post-mortem brain tissue, where microglial activation and chronic inflammation are often present (Vargas et al., 2005; not from your reference list, but widely cited in the field).

Additionally, aluminum is known to:

• Disrupt mitochondrial function

• Promote oxidative stress

• Inhibit glutamate uptake

• Alter expression of key developmental genes

These are not speculative harms. They have been demonstrated in both in vivo and in vitro models at doses equivalent to those used in pediatric vaccines.

Temporal and Cross-National Patterns

Nevison (2014) found that autism prevalence trends across U.S. birth cohorts from 1970 to 2005 closely tracked environmental toxins, particularly poly-brominated flame retardants, glyphosate, and aluminum adjuvants. While correlation is not causation, such consistency across disparate datasets demands attention.

Similarly, Delong (2011) performed a state-level regression analysis across the U.S. from 2001–2007, controlling for family income and ethnicity. She found a statistically significant positive association between vaccine uptake by age 2 and the prevalence of ASD and speech/language impairment (SLI).

These trends are not explained by diagnostic substitution or awareness. They represent possible exposure-response patterns that warrant further investigation—not premature dismissal.

Conclusions on Aluminum

Despite strong epidemiological, mechanistic, and animal-based evidence, aluminum adjuvants are largely absent from public health safety discussions. They are never evaluated under traditional toxicology protocols for parenteral exposure in infants, nor are they subjected to randomized controlled trials with neurodevelopmental endpoints.

To omit them entirely, as the Johns Hopkins article does, is an error so large it verges on institutional negligence.

Vaccinated vs. Unvaccinated Studies: The Forbidden Comparisons

In the Johns Hopkins article, Dr. Daniel Salmon dismisses the idea of comparing vaccinated and unvaccinated populations as intuitively appealing but scientifically flawed. He argues that confounding factors—such as differences in healthcare-seeking behavior, nutrition, and lifestyle—make such comparisons unreliable. The article also claims that “only about 2% of American children are completely unvaccinated,” implying that a sufficiently powered, unbiased study is nearly impossible.

This framing is misleading. While randomized controlled trials of vaccination versus no vaccination would raise ethical issues, observational studies of vaccinated and unvaccinated populations have been conducted, and they tell a very different story from the one promoted by public health authorities.

---

Mawson et al. (2017): Cross-Sectional Study of Homeschool Populations

This pilot study surveyed 666 homeschooled children aged 6–12 from Florida, Louisiana, Mississippi, and Oregon—deliberately chosen to minimize variability in healthcare access and to enrich the unvaccinated population (Mawson et al., 2017). Key findings:

• Vaccinated children were significantly more likely than unvaccinated peers to be diagnosed with:

  • ADHD (OR 4.2, p < 0.001)

  • Autism spectrum disorder (ASD) (OR 4.2, p < 0.01)

  • Learning disabilities (OR 5.2, p < 0.001)

  • Any neurodevelopmental disorder (OR 3.7, p < 0.001)

  • Any chronic illness (OR 2.4, p < 0.001)

Importantly, the associations remained statistically significant after adjusting for other measured health and demographic factors.

Critics of this study often cite concerns about self-report bias and sample representativeness. However, these limitations are openly acknowledged by the authors, and they do not negate the strength or direction of the observed associations.

---

Mawson & Jacob (2025): Analysis of Medicaid-Insured Children

This follow-up study used claims data from 47,155 nine-year-old children enrolled in Medicaid—a population with consistent healthcare access and detailed diagnostic records (Mawson & Jacob, 2025). Key findings:

• Among preterm children:

  • 39.9% of vaccinated children had at least one NDD diagnosis,

  • Compared to 15.7% of unvaccinated preterm children (OR 3.58; 95% CI: 2.80–4.57).

• Relative risk of ASD increased with vaccine visits:

  • One vaccination visit: OR 1.7 (95% CI: 1.21–2.35)

  • Eleven or more visits: OR 4.4 (95% CI: 2.85–6.84)

These dose-response findings are precisely the type of pattern that should trigger intensive follow-up research. Instead, they have been ignored or derided.

---

Gallagher & Goodman (2008, 2010): Hepatitis B Vaccine and NDDs

Using NHIS data and well-controlled survey methods, these studies found:

• Threefold increased odds of autism in male neonates vaccinated with Hepatitis B in the first month of life (Gallagher & Goodman, 2010).

• A ninefold increased odds of needing early intervention or special education services (EIS) among boys who received the triple-series Hepatitis B vaccine manufactured with thimerosal (Gallagher & Goodman, 2008).

These are government-collected data analyzed by independent researchers. They have not been refuted by superior studies—only ignored.

---

Mumper (2013): A Pediatric Practice with Zero Autism Diagnoses

In a retrospective analysis of her pediatric clinic’s patient records, Dr. Elizabeth Mumper found zero autism diagnoses among 294 general pediatric patients followed since 2005 (Mumper, 2013). The expected number of cases based on U.S. prevalence (~1 in 50 at the time) would have been 5–6 cases. The result was statistically significant (p = 0.014). Mumper implemented a range of preventative strategies, including altered vaccine timing, avoidance of TCVs, and attention to environmental triggers.

Critics often dismiss such findings as anecdotal, but statistically, this is a signal—especially when similar results are observed elsewhere.

---

Why These Studies Matter

The Hopkins article implies that because vaccinated vs. unvaccinated studies are difficult to conduct, their results are invalid or irrelevant. This is false. These studies:

• Use matched cohorts or adjust for covariates.

• Often include dose-response analysis.

• Focus on diagnosed outcomes, not self-report alone.

• Involve large samples (Medicaid, NHIS, etc.).

That they are not randomized controlled trials is true. But that doesn’t make them less useful—especially when no large RCTs with long-term neurodevelopmental outcomes have ever been conducted on the cumulative U.S. vaccine schedule.

The refusal to even acknowledge these comparisons—let alone critique them in good faith—reveals not scientific caution but institutional bias.

Biological Mechanisms: Autoimmunity, Detox Impairment, and Molecular Disruption

The claim that there is “no known mechanism” by which vaccines could contribute to autism spectrum disorder (ASD) is flatly contradicted by decades of published research. In fact, multiple plausible pathways exist—ranging from neuroinflammation and autoimmune activation, to mitochondrial dysfunction, impaired detoxification, and epigenetic disruption. These mechanisms have been documented in animal models, in human cell studies, and in biological samples from individuals with ASD.

---

A. Autoimmunity and Vaccine-Induced Brain Inflammation

The measles component of the MMR vaccine has long been implicated in abnormal immune responses in children with ASD.

• Singh et al. (2002) examined serum samples from autistic children and found that over 90% of those who tested positive for MMR antibodies also had autoantibodies to myelin basic protein (MBP)—a major structural component of the central nervous system. This suggests a vaccine-induced cross-reactivity, consistent with molecular mimicry (Singh et al., 2002).

• In a follow-up paper, Singh & Jensen (2003) confirmed elevated measles antibody titers in autistic children compared to controls. The study supports a model of abnormal immune response to the MMR vaccine contributing to CNS autoimmunity (Singh & Jensen, 2003).

Autoimmune brain inflammation is now a well-documented feature in many ASD cases, and these findings point toward vaccine-induced immune activation as a potential trigger in susceptible children.

---

B. Thimerosal-Induced Cellular Stress and Immune Hypersensitivity

A series of in vitro studies demonstrates that children with autism exhibit unique hypersensitivity to thimerosal:

• Sharpe et al. (2013) showed that B-lymphocytes from autistic children were significantly more sensitive to thimerosal than those from unaffected siblings or controls. This was shown via mitochondrial function assays and cytotoxicity markers, suggesting that thimerosal exposure could differentially impair cellular metabolism in genetically vulnerable individuals.

• Walker et al. (2006) exposed lymphocytes from autistic children and controls to thimerosal and found upregulated heat shock protein RNA only in the ASD samples—indicating cellular stress responses unique to the ASD group.

These findings support a mechanism of impaired detoxification and redox homeostasis, possibly due to glutathione pathway abnormalities or polymorphisms in metallothionein genes.

---

C. Mercury Retention and Impaired Excretion

• Holmes et al. (2003) found significantly lower mercury levels in first baby haircuts of autistic children compared to controls (0.47 ppm vs. 3.63 ppm). The most severely affected children had the lowest levels, suggesting they were unable to excrete mercury efficiently.

• This finding dovetails with studies by Kern et al. (2013) on thiol and sulfation chemistry, which showed altered detoxification pathways in ASD patients, leading to accumulation of heavy metals like mercury and thimerosal derivatives.

---

D. Neuroinflammation and Microglial Priming from Adjuvants

Aluminum adjuvants and mercury both prime the innate immune system. When administered during early neurodevelopment, this priming leads to chronic inflammation and neuronal dysfunction:

• Shaw & Tomljenovic (2013) showed that aluminum induces microglial activation, oxidative stress, and cytokine dysregulation in mouse brains. These effects mirror the neuroinflammatory profile found in post-mortem ASD brain tissue.

• Shaw et al. (2013) linked aluminum injections to reduced motor coordination, impaired spatial memory, and inflammation in the hippocampus and cortex—regions often implicated in ASD.

---

E. Transcriptomic and Molecular Disruption

• Li et al. (2014) performed transcriptomic analysis in neonatal mice injected with thimerosal. They found dysregulation of genes involved in:

  • Synaptic function

  • Neuronal migration

  • Inflammatory signaling

  • Autism-related gene networks

This adds molecular weight to the observational and pathological data, suggesting that even intermittent neonatal thimerosal exposure could alter the developmental trajectory of the brain at a genetic level.

---

F. Genetic Susceptibility and Dose Sensitivity

• Hornig et al. (2004) demonstrated that autoimmune-sensitive mouse strains (SJL/J) exhibited growth retardation, reduced exploration, and abnormal hippocampal neurons after receiving postnatal thimerosal. Resistant strains (C57BL/6J, BALB/cJ) did not show these effects.

This finding is critical: Not all children will respond the same way to vaccine components. The public health insistence on population-wide safety ignores the known individual variation in susceptibility—which is well-documented in toxicology and immunology.

7. Environmental, Genetic, and Manufacturing Factors: From DNA Contaminants to Policy Blind Spots

While mainstream discourse often reduces autism risk to vague genetic “mystery,” the literature suggests that environmental exposures, including those introduced through medical interventions, play a substantial role—especially when interacting with individual biological vulnerabilities. The Johns Hopkins article fails to address any of these dimensions.

---

A. DNA Contamination in Vaccines: Deisher et al. (2014)

One of the most under-discussed and controversial findings in the vaccine-autism literature involves the use of human fetal cell lines in vaccine manufacturing. In a cross-national analysis, Deisher et al. (2014) documented that autistic disorder “change points”—sharp upticks in ASD prevalence—coincided temporally with the introduction of vaccines manufactured with human fetal DNA fragments, including the MMR and varicella vaccines.

Key findings:

• Change points were replicated in the United States, United Kingdom, Western Australia, and Denmark.

• DNA fragment quantities in these vaccines exceeded known thresholds for spontaneous genomic integration in animal models.

• The authors proposed that these fragments could cause insertional mutagenesis or autoimmunity in susceptible individuals.

While this hypothesis has been criticized, it remains unrefuted and is biologically plausible, especially in light of literature on foreign DNA-triggered autoimmunity and endogenous retroviral reactivation.

---

B. Environmental Load and Combined Exposures: Nevison (2014)

In a comprehensive time-series analysis, Nevison (2014) examined temporal trends in U.S. autism prevalence from 1970 to 2005 and correlated them with environmental exposure data. She found that the most strongly correlated factors were:

• Polybrominated diphenyl ethers (PBDEs),

• Aluminum adjuvants, and

• Glyphosate, the active ingredient in Roundup.

These exposures rose in parallel with autism prevalence—and many (like aluminum) were present in pediatric vaccines. Nevison did not claim causality, but emphasized the need to consider multiple low-level environmental exposures as co-factors in ASD development.

---

C. Cross-State Correlation: DeLong (2011)

Using U.S. state-level data from 2001 to 2007, DeLong (2011) found a statistically significant positive association between the percentage of children receiving the recommended full vaccine schedule by age 2 and the prevalence of both autism and speech or language impairment (SLI).

• This association persisted after controlling for ethnicity and family income, two common confounders.

• DeLong concluded that vaccine uptake may contribute to neurodevelopmental disorders at the population level and called for more detailed studies—not dismissal.

---

D. Transcriptomic Disruption from Early-Life Exposure: Li et al. (2014)

Li et al. conducted a transcriptomic analysis of mouse brains after intermittent neonatal administration of thimerosal. They found significant disruptions in:

• Neurotransmitter signaling

• Synaptic plasticity

• Cell cycle regulation

• Genes linked to autism susceptibility

The altered genes overlapped with known ASD-related molecular networks, suggesting that even brief early-life exposure to vaccine-relevant doses of thimerosal could have long-lasting neurodevelopmental consequences.

---

E. Genetic Susceptibility Is Not Rare

Critics often dismiss vaccine-autism associations by invoking “rare genetic syndromes,” but the animal model by Hornig et al. (2004)—using autoimmune-prone SJL/J mice—showed that thimerosal caused brain inflammation and behavioral changes only in genetically susceptible strains. This supports the hypothesis that vaccines may not cause autism in everyone—but may do so in biologically vulnerable subgroups.

This mirrors findings in other environmental diseases. Not everyone exposed to cigarette smoke develops cancer. But enough do to establish a causal relationship. Science does not require universality—it requires demonstrable, reproducible harm in a definable subset.

---

Between fetal DNA fragments, correlated environmental exposures, transcriptomic disruption, and population-level associations, the literature reveals a converging mosaic of environmental and iatrogenic contributors to autism—none of which are discussed in the Johns Hopkins article.

Denying these associations is not skepticism. It is incuriosity posing as certainty.

Legal and Whistleblower Evidence: What the Courts and CDC Scientists Have Revealed

Despite claims of scientific consensus and categorical denial of a vaccine-autism connection, court proceedings and whistleblower testimony tell a markedly different story—one that is routinely omitted in institutional publications like the Johns Hopkins article. Yet these legal and firsthand insider accounts are essential to understanding why public skepticism persists.

---

A. Vaccine Injury Compensation Program (VICP) and Autism-Related Cases

Established under the National Childhood Vaccine Injury Act of 1986, the VICP serves as a legal alternative to civil litigation for those who believe they have suffered vaccine injuries. While public health officials often cite the program as proof of safety, Holland et al. (2011) found that it has quietly compensated numerous cases of vaccine-induced brain damage that included autism diagnoses.

• After reviewing thousands of publicly available court documents, the authors identified **83 cases in which the court awarded compensation for encephalopathy, seizures, or other neurological injuries—**and where the child either had autism or later received an autism diagnosis.

• These included the highly publicized Hannah Poling case, in which the Department of Health and Human Services conceded that vaccines had “significantly aggravated an underlying mitochondrial disorder” leading to autistic features.

The government's defense has been that these were not "autism" cases per se, but rather autism-like or autistic symptoms secondary to brain injury. This is a semantic distinction with no meaningful medical difference to families or to science. If vaccines can cause brain injury that presents as autism, then they can cause autism.

---

B. The Whistleblower: Dr. William Thompson at the CDC

In 2014, Dr. William Thompson, a senior CDC scientist and co-author of the 2004 MMR-autism study, came forward with a disturbing claim: the CDC had knowingly manipulated data to conceal a significant association between early MMR vaccination and autism in African-American boys.

• The original unadjusted analysis showed that boys who received the MMR vaccine before 36 months of age were 3.36 times more likely to be diagnosed with autism than those who received it later (Hooker, 2014).

• According to Thompson, CDC leadership instructed the team to exclude this subgroup from the final analysis to eliminate the association.

• Thompson provided internal emails, meeting notes, and draft data files to Congress and federal investigators. He later released a statement through his attorney confirming the allegations.

No CDC scientist has ever refuted Thompson’s claims. Instead, the agency—and the media—have gone silent on the matter. The Johns Hopkins article does not mention him, his findings, or the congressional inquiries his disclosures initiated.

---

C. Methodological Malfeasance in “Debunking” Studies

In addition to Thompson's testimony, Hooker et al. (2014) published a detailed review of methodological problems and conflicts of interest in studies used to “prove” that vaccines do not cause autism. The review highlighted:

• Inappropriate exclusion criteria, such as removing children with underlying medical conditions that may predispose them to vaccine injury.

• Post-hoc statistical adjustments that reversed significant findings.

• Author affiliations with agencies responsible for vaccine promotion, creating conflicts of interest.

These critiques are rarely answered with data—only with appeals to authority and ad hominem dismissals.

---

The official record includes:

• Court-awarded compensation for autism-related brain injury, despite public denials.

• Whistleblower testimony confirming data concealment at the CDC.

• Documented methodological manipulation in influential “debunking” studies.

Yet none of this appears in the Johns Hopkins piece.

Importantly: every single effort to convince the public that there is no possible link between vaccines and autism cherry-picks from the same set of studies.

Here is the truth: Not all vaccines on the CDC's schedule have been studied at all, even for association or correlation with autism.

Institutional publications also ignore government-conceded injuries and credible insider revelations, the issue is not scientific illiteracy among the public—it is institutional opacity and narrative control.

These facts are ignored by everyone promulgating the “no-credible studies” myth.

The Science Is Not Settled. It Has Been Censored.

The March 2025 article from Johns Hopkins Public Health asks, “Why do some people think vaccines cause autism?”—and answers by invoking a long-discredited paper and assuring readers that the “science is settled.” It dismisses persistent parental concerns as the result of emotional reasoning, coincidence, and misinformation. It paints dissent as outdated, uninformed, or conspiratorial.

But as we have shown here, that narrative is not only scientifically incomplete—it is demonstrably false.

The evidence for a vaccine-autism connection does not rest on a single discredited study. It is found in:

• CDC’s own suppressed data (Verstraeten et al., 1999; Thompson testimony);

• Repeated epidemiological studies using the Vaccine Safety Datalink;

• Consistent dose-dependent associations in large administrative datasets (Mawson & Jacob, 2025);

• Animal models showing neurodevelopmental disruption from thimerosal and aluminum;

• Biological mechanisms including autoimmunity, impaired detoxification, and transcriptomic damage;

• Court rulings awarding compensation for vaccine-induced encephalopathy with autistic features;

• Demonstrated methodological manipulation in studies used to deny the link.

None of these elements are mentioned in the Hopkins article. Not one. Instead, readers are offered a selective history, a handful of unexamined generalities, and a vague reassurance that experts have already done the work.

That is not how science operates.

Science is not a consensus enforced by omission. It is not a weapon used to shame parents into silence. It is not a marketing tool for government-backed pharmaceutical programs.

Science is a process—a dynamic, self-correcting, and transparent one. It requires that inconvenient evidence be explored, not erased. It requires that questions be welcomed, not stigmatized. And it demands, above all, that institutions committed to public health also commit to intellectual honesty.

The vaccine-autism connection has not been disproven. It has been politically and institutionally suppressed.

For the sake of public trust, scientific integrity, and the countless families still seeking answers, it is time to open the conversation—not close it.

1. Verstraeten T, Davis RL, DeStefano F, Lieu TA, Rhodes PH, Black SB, Shinefield H, Chen RT; Vaccine Safety Datalink Team. Safety of thimerosal-containing vaccines: a two-phased study of computerized health maintenance organization databases. Pediatrics. 2003 Nov;112(5):1039-48. Erratum in: Pediatrics. 2004 Jan;113(1):184. PMID: 14595043. https://pubmed.ncbi.nlm.nih.gov/14595043/ See also https://www.safeminds.org/wp-content/uploads/2013/04/GenerationZeroNotes.pdf

2. Hooker, B., Kern, J. K., Geier, D. A., Haley, B. E., Sykes, L. K., King, P. G., & Geier, M. R. (2014). Methodological issues and evidence of malfeasance in research purporting to show Thimerosal in vaccines is safe. BioMed Research International, 2014, 247218. Retrieved from https://pubmed.ncbi.nlm.nih.gov/24995277/

3. Geier, D. A., Hooker, B. S., Kern, J. K., King, P. G., Sykes, L. K., & Geier, M. R. (2013). A two-phase study evaluating the relationship between Thimerosal-containing vaccine administration and the risk for an autism spectrum disorder diagnosis in the United States. Translational Neurodegeneration, 2(1), 25. Retrieved from https://pubmed.ncbi.nlm.nih.gov/24359825/

4. Young, H. A., Geier, D. A., & Geier, M. R. (2008). Thimerosal exposure in infants and neurodevelopmental disorders: an assessment of computerized medical records in the Vaccine Safety Datalink. Journal of the Neurological Sciences, 271(1–2), 110–118. Retrieved from https://pubmed.ncbi.nlm.nih.gov/18482737/

5. Gallagher, C. M., & Goodman, M. S. (2010). Hepatitis B vaccination of male neonates and autism diagnosis. Journal of Toxicology and Environmental Health, Part A, 73(24), 1665–1677. Retrieved from https://pubmed.ncbi.nlm.nih.gov/21058170/

6. Gallagher, C. M., & Goodman, M. S. (2008). Hepatitis B triple series vaccine and developmental disability in US children aged 1–9 years. Toxicological & Environmental Chemistry, 90, 997–1008. Retrieved from https://www.tandfonline.com/doi/full/10.1080/02772240701806501

7. Holmes, A. S., Blaxill, M. F., & Haley, B. E. (2003). Reduced levels of mercury in first baby haircuts of autistic children. International Journal of Toxicology, 22(4), 277–285. Retrieved from https://pubmed.ncbi.nlm.nih.gov/12933322/

8. Jafari, T., Rostampour, N., Fallah, A. A., & Hesami, A. (2017). The association between mercury levels and autism spectrum disorders: A systematic review and meta-analysis. Journal of Trace Elements in Medicine and Biology, 44, 289–297. Retrieved from https://pubmed.ncbi.nlm.nih.gov/28965590/

9. Sharpe, M. A., Gist, T. L., & Baskin, D. S. (2013). B-lymphocytes from a population of children with autism spectrum disorder and their unaffected siblings exhibit hypersensitivity to thimerosal. Journal of Toxicology, 2013, Article ID 801517. Retrieved from https://pubmed.ncbi.nlm.nih.gov/23843785/

10. Walker, S. J., Segal, J., & Aschner, M. (2006). Cultured lymphocytes from autistic children and non-autistic siblings up-regulate heat shock protein RNA in response to thimerosal challenge. Neurotoxicology, 27(5), 685–692. Retrieved from https://pubmed.ncbi.nlm.nih.gov/16870260/

11. Olczak, M., Duszczyk, M., Mierzejewski, P., Meyza, K., & Majewska, M. D. (2011). Persistent behavioral impairments and alterations of brain dopamine system after early postnatal administration of thimerosal in rats. Behavioural Brain Research, 223(1), 107–118. Retrieved from https://pubmed.ncbi.nlm.nih.gov/21549155/

12. Laurente, J., et al. (2007). Neurotoxic effects of thimerosal at vaccine doses on the encephalon and development in 7 day-old hamsters. Anales de la Facultad de Medicina, 68(3), 222–237. Retrieved from https://www.scielo.org.pe/scielo.php?pid=S1025-55832007000300003&script=sci_arttext

13. Hornig, M., Chian, D., & Lipkin, W. I. (2004). Neurotoxic effects of postnatal thimerosal are mouse strain dependent. Molecular Psychiatry, 9(9), 833–845. Retrieved from https://pubmed.ncbi.nlm.nih.gov/15184908/

14. Li, X., Qu, F., Xie, W., Wang, F., Liu, H., Song, S., ... & Tang, T. S. (2014). Transcriptomic analyses of neurotoxic effects in mouse brain after intermittent neonatal administration of thimerosal. Toxicological Sciences, 139(2), 452–465. Retrieved from https://pubmed.ncbi.nlm.nih.gov/24675092/

15. Shaw, C. A., & Tomljenovic, L. (2013). Aluminum in the central nervous system (CNS): Toxicity in humans and animals, vaccine adjuvants, and autoimmunity. Immunologic Research, 56(2–3), 304–316. Retrieved from https://pubmed.ncbi.nlm.nih.gov/23609067/

16. Nevison, C. D. (2014). A comparison of temporal trends in United States autism prevalence to trends in suspected environmental factors. Environmental Health, 13, 73. Retrieved from https://pubmed.ncbi.nlm.nih.gov/25189402/

17. DeLong, G. (2011). A positive association found between autism prevalence and childhood vaccination uptake across the U.S. population. Journal of Toxicology and Environmental Health, Part A, 74(14), 903–916. Retrieved from https://pubmed.ncbi.nlm.nih.gov/21623535/

18. Mawson, A. R., Ray, B. D., Bhuiyan, A. R., & Jacob, B. (2017). Pilot comparative study on the health of vaccinated and unvaccinated 6-to 12-year-old U.S. children. IOpen Access Text. Retrieved from https://www.oatext.com/Pilot-comparative-study-on-the-health-of-vaccinated-and-unvaccinated-6-to-12-year-old-U-S-children.php

19. Mawson, A. R., & Jacob, B. (2025). Vaccination and neurodevelopmental disorders: A study of nine-year-old children enrolled in Medicaid. Science, Public Health Policy & the Law, 6. Retrieved from https://publichealthpolicyjournal.com/vaccination-and-neurodevelopmental-disorders-a-study-of-nine-year-old-children-enrolled-in-medicaid/

20. Mumper, E. (2013). Can awareness of medical pathophysiology in autism lead to primary care autism prevention strategies? North American Journal of Medical Sciences, 6, 134–144. Retrieved from https://www.najms.com/index.php/najms/article/view/191

21. Singh, V. K., Lin, S. X., Newell, E., & Nelson, C. (2002). Abnormal measles-mumps-rubella antibodies and CNS autoimmunity in children with autism. Journal of Biomedical Science, 9(4), 359–364. Retrieved from https://pubmed.ncbi.nlm.nih.gov/12145534/

22. Singh, V. K., & Jensen, R. L. (2003). Elevated levels of measles antibodies in children with autism. Pediatric Neurology, 28(4), 292–294. Retrieved from https://pubmed.ncbi.nlm.nih.gov/12849883/

23. Deisher, T. A., Ngoc, V., Omaiye, A., Koyama, K., & Bwabye, S. (2014). Impact of environmental factors on the prevalence of autistic disorder after 1979. Journal of Public Health and Epidemiology, 6, 271–286. Retrieved from https://academicjournals.org/article/article1411048618_Deisher%20et%20al.pdf

24. Holland, M. S., Conte, L., Krakow, R., & Colin, L. (2011). Unanswered questions from the Vaccine Injury Compensation Program: A review of compensated cases of vaccine-induced brain injury. Pace Environmental Law Review, 28(2), Article 6. Retrieved from https://digitalcommons.pace.edu/pelr/vol28/iss2/6/

25. Shaw, C. A., Li, Y., & Tomljenovic, L. (2013). Administration of aluminum to neonatal mice in vaccine-relevant amounts is associated with adverse long term neurological outcomes. Journal of Inorganic Biochemistry, 128, 237–244. Retrieved from https://pubmed.ncbi.nlm.nih.gov/23932735/

26. Fulgenzi A, Vietti D, Ferrero ME. Aluminium involvement in neurotoxicity. Biomed Res Int. 2014;2014:758323. doi: 10.1155/2014/758323. Epub 2014 Aug 27. PMID: 25243176; PMCID: PMC4160616. https://pubmed.ncbi.nlm.nih.gov/25243176/