Journal That Published Fatally Flawed Aluminum Study Strains Their Credibility

The reputation of Annals of Internal Medicine takes a major hit as they stand by a clearly manipulated study.

On July 15, 2025, Annals of Internal Medicine published “Aluminum-Adsorbed Vaccines and Chronic Diseases in Childhood: A Nationwide Cohort Study” (DOI: 10.7326/M24-00997), a registry-based analysis of 1,224,176 Danish children purporting to find “no evidence” that early-life aluminum adjuvant exposure increases risk for 50 autoimmune, allergic, or neurodevelopmental conditions. Within hours, major outlets heralded the paper as definitive reassurance that aluminum in vaccines is safe. That narrative—repeated by quoted “experts” who did not engage the toxicological literature—now sits in tension with a large, mechanistically consistent body of research showing aluminum hydroxide is neurotoxic, neurodevelopmentally disruptive, and immunotoxic under injection-relevant conditions.

This article examines the asymmetric epistemic value of (a) press-quote generalities from self-proclaimed authorities versus (b) detailed, experimentally grounded critiques and mechanistic evidence, alongside the methodological flaws of the Danish study.

Media Amplification of Broad-Stroke Assurances

Reuters has published an “exclusive” about the journal’s decision to not retract the obviously manipulated study.

Mainstream reports leaned heavily on general endorsements:

“It’s solid… a massive dataset and high-quality data,” — Adam Finn, University of Bristol (Reuters, Aug 11 2025)
“Rigorous and well-designed… reassuring to parents,” — Edward Belongia, Marshfield Clinic Research Institute (NBC News, July 15 2025)
“Aluminum in vaccines does not cause autism,” — Anders Hviid, lead author (media interviews, July 14 2025)

The Reuters story also quoted Michael Osterholm (CIDRAP) who used the ruse of more aluminum from other sources, such as water and food. Only a tiny %, about 0.03%, of injected aluminum actually passes through the intestine, whereas 100% of injected aluminum causes internal exposure.

Osterholms’ fallacious defense also ignores cumulative exposure. See our study from 2020 in which we show (in the Supplementary Material) that the body must deal with more aluminum from injection than ingestion.

These fallacious (but evidently believable) statements by “experts) belie the fact that large studies can dilute subgroup effects. They carry no citations, no engagement with the experimental toxicology literature, and no discussion of known mechanisms of aluminum hydroxide’s biological activity. None of this knowledge is brought forward.

In contrast, the peer-reviewed record contains decades of data showing:

• Aluminum hydroxide causes neuronal cell death, gliosis, and motor/cognitive deficits when injected into mammals PMID: 17114826PMID: 19740540.

• Aluminum persists in phagocytes and can translocate to the brain via a CCL2-dependent “Trojan horse” mechanismdoi:10.3389/fneur.2015.00004doi:10.1186/1741-7015-11-99.

• Aluminum hydroxide, the same form in pediatric vaccines, is used routinely to induce autoimmune disease in animal models so that experimental therapies can be testedPMCID: PMC3990870.

Presenting off-the-cuff reassurance as epistemically equivalent to such findings is to deny the bulk of a comprehensive body of science.

Mechanistic and Experimental Evidence on Aluminum Hydroxide Toxicity

Neurotoxicity Under Injection-Relevant Conditions

Controlled animal studies demonstrate that intramuscular or subcutaneous aluminum hydroxide produces persistent neuroinflammation, neuronal apoptosis, and behavioral deficits. Shaw and Petrik (2009) found that two intramuscular injections of aluminum hydroxide at doses scaled to human infant exposure caused motor neuron loss, microgliosis, and impaired motor function in mice PMID: 19740540. In an earlier rat model, Kawahara et al. observed aluminum-laden motor neurons with apoptosis and chromatolysis after adjuvant injections PMID: 17114826.

Biopersistence studies by Khan et al. and Crépeaux et al. tracked alum particles months after injection, demonstrating transport from the injection site to distant organs, including brain, via monocyte-lineage cells in a CCL2-dependent mannerdoi:10.3389/fneur.2015.00004doi:10.1186/1741-7015-11-99. This trafficking coincided with lysosomal damage and altered xenophagy, plausible mediators of neurotoxicity.

Neurodevelopmental Impairment

Human cerebral organoid models show that aluminum hydroxide at micromolar concentrations reduces organoid size, impairs basal neural progenitor proliferation, and drives premature neuronal differentiation in a time- and dose-dependent fashion (Zhu et al., 2023, Ecotoxicol Environ Saf, 256:114863) PMID: 37011512. Perinatal animal exposure models likewise reveal offspring neurobehavioral deficits, altered neurotransmitter levels, and oxidative stress in the developing brain PMID: 32601624.

Immunotoxicity and Autoimmunity

Alum’s adjuvanticity is inseparable from its pro-inflammatory activity. Eisenbarth et al. (2008) demonstrated that aluminum hydroxide crystals activate the NLRP3 inflammasome in macrophages, leading to caspase-1–dependent maturation of IL-1β and IL-18 PMID: 18496530. Kool et al. (2008) showed IL-1β/IL-18 signaling is required for alum-adjuvanted antibody responses PMID: 18566365.

In autoimmune-prone mouse strains, alum alone induces clinical and histological features of Sjögren’s-like disease, with salivary gland lymphocytic infiltration, reduced saliva production, and autoantibody formationPMCID: PMC3990870. Vaccine safety reviews acknowledge such adjuvant-induced autoimmunity in animal models and stress that genetic susceptibility modulates riskdoi:10.1016/j.vaccine.2015.03.062.

Methodological Flaws in the Danish Registry Study

Against this mechanistic backdrop, the Danish study’s design choices are not neutral:

1. No unexposed control group — Only ~2 % of Danish children in the cohort were completely unvaccinated by age 2, but rather than compare them to high-exposure children, the analysis contrasted “high” vs. “moderate” aluminum groups differing by ≈ 1 mg cumulative dose. This constricts the exposure gradient, diluting any effect.

2. Exclusion of high-exposure/high-risk children — 34,547 children with “implausible” high vaccine counts were excluded; these likely included the most aluminum-exposed individuals. Children who died or had certain serious conditions before age 2 were also excluded, removing potential early adverse outcomes from analysis.

3. Short follow-up — Outcomes were censored at age 5, well before many neurodevelopmental and autoimmune diagnoses are made.

4. Collider bias via adjustment — Adjusting for early healthcare utilization and removing patients who had to see the physicians most for potentially aluminum-induced conditions will mathematically remove true exposure-outcome associations by conditioning on variables influenced by both.

5. Data opacity — Individual-level data are not available for independent re-analysis; a July 17 2025 correction to the supplementary material added thousands of neurodevelopmental diagnoses, altering hazard ratios for autism and related outcomes, without prompting a change in the published abstract or conclusions. Rules for de-identifying the full data set no doubt exist; this would allow objective re-analysis.

These limitations bias toward null results and cannot override strong mechanistic priors and replicated experimental findings.

The journal claims they will respond to critiques of the paper sent to the journal, but not to Kennedy’s critique, because it was not sent to them. I know of critiques that were sent that they journal refused to publish; that’s narrative control, not scientific publishing. The journal believes that it exists in a silo; it does not. It is my professional opinion and recommendation that ethical physicians and scientists should eschew any article published by Annals of Internal Medicine. The games being played to obfuscate signal and access also represent lessons that the current HHS administration will not forget.

Epistemic Weight: Mechanistic Evidence vs. Narrative Authority

Risk assessment demands weighing the quality and relevance of evidence, not the rhetorical position of the source. Multi-species, injection-relevant studies demonstrating neurotoxicity, neurodevelopmental impairment, and autoimmunity from aluminum hydroxide, together with clear biological mechanisms (inflammasome activation, cytokine cascades, particle trafficking to brain), carry far more probative weight than broad-stroke assurances untethered from that literature.

A registry analysis with structural blind spots does not—and cannot—erase the toxicological reality documented in controlled experiments. Editorial decisions that elevate narrative authority while limiting or delaying publication of detailed critiques mislead readers about the true state of the science.

Conclusion

By publishing a methodologically constrained study and amplifying generalities from experts who do not address the established toxicology of aluminum hydroxide, Annals of Internal Medicine has created the appearance of narrative curation rather than neutral scientific arbitration.

In platforming arm-waving based denialism, including a comment from one “expert” who called this clearly manipulated retrospective study “high-quality” evidence, Reuters has done a disservice to their reputation as well, which has suffered massively due to their obvious complicity in COVID-19 Fauci-based HHS narrative enforcement.

Restoring credibility will require the journal to:

• Publish all substantive post-publication critiques,

• Facilitate independent re-analysis of the corrected dataset, and

• Acknowledge that existing mechanistic and experimental data establish aluminum hydroxide as a neurotoxin, neurodevelopmental disruptor, and immunotoxin in susceptible hosts.

No one claiming to refer to decades of safety studies can do so with honesty and integrity given the actual provenance of the record of how FDA came to assess that an 850 mcg dose of aluminum in adults is safe; it was based purely on aluminum of a different form than the ingected forms fed to adult mice, not injected forms injected into infant mice.

The public and the scientific community deserve a record that reflects all the evidence—not just the portions that fit a predetermined reassurance narrative.

In 2015, I published the full balance of the literature for one of the world’s greatest aluminum toxicity denialists, Paul Offit.

Key References

1. Shaw CA, Petrik MS. Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration. J Inorg Biochem. 2009;103(11):1555-62. PMID: 19740540.

2. Kawahara M, et al. Aluminum in the CNS: neurotoxic effects and autoimmunity. Neuromolecular Med. 2007;9(1):83-100. PMID: 17114826.

3. Crépeaux G, et al. Biopersistence and brain translocation of aluminum adjuvants. Front Neurol. 2015;6:4. doi:10.3389/fneur.2015.00004.

4. Khan Z, et al. Slow CCL2-dependent translocation of aluminum to brain. BMC Med. 2013;11:99. doi:10.1186/1741-7015-11-99.

5. Zhu Y, et al. Aluminum hydroxide impairs human cerebral organoid neurogenesis. Ecotoxicol Environ Saf. 2023;256:114863. PMID: 37011512.

6. Li H, et al. Developmental neurotoxicity of aluminum exposure. Chemosphere. 2020;253:126707. PMID: 32601624.

7. Eisenbarth SC, et al. Alum triggers NLRP3 inflammasome and caspase-1 activation. Nature. 2008;453:1122-6. PMID: 18496530.

8. Kool M, et al. Alum adjuvanticity via IL-1β/IL-18. J Immunol. 2008;181(1):17-21. PMID: 18566365.

9. Watad A, et al. Autoimmune induction by alum in murine Sjögren’s model. Clin Exp Rheumatol. 2014;32(2):251-255. PMCID: PMC3990870.

10. Shoenfeld Y, Agmon-Levin N. ’ASIA’—Autoimmune/inflammatory syndrome induced by adjuvants. Vaccine. 2015;33(24):2967-2971. doi:10.1016/j.vaccine.2015.03.062.