Why do vaccine officials ignore adverse effects of thimerosal, aluminum, and squalene?

Teresa Binstock
Researcher in Developmental & Behavioral Neuroanatomy
September 20, 2009

Peer-reviewed findings announced in 2009 describe an increased rate of autism-spectrum disorders (triple) among boys who as neonates had received HepB vaccination, which originally contained thimerosal (1,2). Similarly and previously, the Stony Brook medical school researchers had reported special education rates were nine times higher among boys who, early in life, had received HepB vaccinations containing thimerosal (3).

These two sets of findings are consistent (i) with outcomes in a number of other studies, and (ii) with the CDC's original findings (1999) wherein early-life vaccinations which included thimerosal were associated with autism, PDD/NOS, tics, language problems, and sleep disorders (eg, 4-7). In contrast, the 2009 findings are inconsistent with widely touted epidemiological studies that may not have had the power to reveal subgroups with increased susceptibility (8-10).

Augmenting concern are facts found in CDC documents obtained by FOIA. For instance, one CDC-investigator's email about their 1999 findings stated that making the autism-thimerosal association "go away" was not easy. Ultimately, however, the CDC team led by Thomas Verstraeten was able to dilute their own findings and did so by using large data-sets from HMOs wherein autism and other developmental disorders were under-reported. A study based upon the diluted-data findings was published by a trade-journal called "Pediatrics". This history is delineated in David Kirby's Evidence of Harm... (2; see also 5).

Why some children more than others are susceptible to adverse effects from vaccinations remains an important issue. Genetic and non-genetic factors are implicated. In other words, for any given child, increased susceptibility can be acquired and/or genetic. For instance, having one or more pro-inflammatory alleles of an immune-related gene may heighten the infant's or toddler's immune-system's reaction to vaccine ingredients (reviewed in 11). Alternatively, some children are known to have weak alleles in genes related to detoxification (eg, 12). Hypersensitivity to thimerosal has long been known, and glutathione status and glutathione pathways are implicated (eg, 13-14). 

Among the non-genetic reasons for why a child can have increased susceptibility, the vaccinating of sick or recently sick children remains problematic because an illness utilizes and may incline towards depletion of a child's reserves of glutathione (eg, 15-18), which helps detoxify mercury and other toxic metals (19). Ironically, giving Tylenol aka acetaminophen aka paracetemol increases utilization and potentiates depletion of glutathione (20).

When co-authors of the initial mercury/autism paper (21) and colleagues met with CBER personnel in their Bethesda facility (2000), I stated my concerns regarding the vaccinating of sick or recently sick children. CBER's then acting-director William Egan, M.D., responded by explaining that NOT vaccinating sick children had long been the official recommendation. However, so as to increase rates of vaccine coverage, that recommendation was changed and now stands as encouraging the vaccinating of sick children. In my opinion, this policy change has exacerbated the tendency of small subgroups of children to develop lastingly adverse traits in response to vaccinations, especially among children with pro-inflammatory and/or weak-detox alleles, especially in susceptible children given Tylenol.

As previously cited, transcripts of the CDC's Simpsonwood conference with pharmaceutical companies make clear that highly placed individuals of the CDC and and their colleagues representing companies that profit from vaccines and vaccinations knew by the year 2000 that thimerosal injections induced significant adverse effects in some children. This decade-old knowledge is consistent with the findings described by Stony Brook's Goodman and Gallagher (1,3). Given this damning track-record for early-life thimerosal injections, a question looms large: Why do government agencies continue to encourage the injection of thimerosal during vaccinations?

Towards an answer:

Since Verstraeten et al's intitial findings about thimerosal's adverse effects (CDC 1999) and despite similar findings (eg, 1,3) amid growing evidence of thimerosal's pathological mechanisms (eg, 14, 22-25), vaccinologists and regulatory agency personnel, and others (eg,  executives within the AAP and AMA) seem to have allowed themselves to accept as Sacred Truth epidemiological findings which have been described as not having sufficient design or power so as to identify small but numerically important subgroups of children with increased likelihood for adverse reactions (8-9). Indeed, declarations about thimerosal's lack of harm are not rooted in science and are based upon a deliberate ignoring of data which demonstrate thimerosal's adverse effects.

Often in scientific papers, prior findings not consistent with one another and conclusions that differ are mentioned. Contrary findings are presented and fairly summarized. In contrast, circa 2009, we have an ongoing situation wherein vaccination policies are no longer based upon the full range of peer-reviewed findings available to vaccinologists, physicians, and members of the too influential, pharmaceutical company's virtual subsidiary known as the Advisory Committee on Immunization Practices (ACIP), whose purpose seems that of promoting vaccinations regardless of evidence of adverse effects -- while deliberately ignoring that evidence.

As news reports and vaccine package inserts make clear, many and perhaps most flu and H1N1 vaccines will contain aluminum, thimerosal, and/or squalene. Each of these ingredients has been linked with neurodenegeneration (26-27) or with the induction of rheumatioid processes (28-29) and developmental disabilities (1-3).  We are reminded of Alice in Wonderland, wherein logic and reason were turned upside down and inside out. Ignoring adverse effects of thimerosal, aluminum, and squalene is not a sound basis for vaccination policies and their enforcement.

An historical insight rings true. In 1855 a journal article stated that "vaccination benefited only doctors as it produced a sicklier population" (30; see also 31-32).


1. Hepatitis B triple series vaccine and developmental disability in US children aged 1-9 years
 Gallagher C, Goodman M. Toxicol Environ Chem 2008 90(5):997-1008.
{free online}

2. Evidence of Harm
David Kirby

3. Hepatitis B vaccination of male neonates and autism
[conference abstract as published]
CM Gallagher, MS Goodman, Graduate Program in Public
Health, Stony Brook University Medical Center, Stony Brook, NY
Annals of Epidemiology, p659
Vol. 19, No. 9 Abstracts (ACE) September 2009: 651–680

4. Autism, mercury, other toxic metals, & glutathione
Teresa Binstock, Aug 12, 2009

5. Simpsonwood
Chapter II: 1999-2000

6. CDC 1999 findings summarized
Cheri Jacobus, Sallie Bernard

7. There's Mercury in Vaccines?
Chapter I: pre-1999

8. Fighting the Autism-Vaccine War
By Bernadine Healy, M.D. [former director of NIH]

9. The Vaccines-Autism War: Détente Needed - Heart to Heart
By Bernadine Healy, M.D. [former director of NIH]
Apr 14, 2009

10. Duane Alexander. M.D., NICHD director
Quoted in:  NIH Agency Head: Vaccine-Autism Research is "Legitimate"  -  by David Kirby

11. Vaccination policy lags behind vaccine science
by Teresa Binstock    December 9, 2007

12. Metabolic endophenotype and related genotypes are associated with oxidative stress in children with autism
James SJ et al. Am J Med Genet B Neuropsychiatr Genet. 2006 141B(8):947-56.
{free online}

13. Homozygous gene deletions of the glutathione S-transferases M1 and T1 are associated with thimerosal sensitization
Westphal GA et al.  Int Arch Occup Environ Health. 2000 Aug;73(6):384-8.

14. Inhibition of the human erythrocytic glutathione-S-transferase T1 (GST T1) by thimerosal
Muller M et al. Int J Hyg Environ Health. 2001 Jul;203(5-6):479-81.

15. The effects of sulfur amino acid intake on immune function in humans
Grimble RF.  J Nutr. 2006 Jun;136(6 Suppl):1660S-1665S.
{free online}

16. Glutathione levels in mental and physical illness
Cohen M et al.  AMA Arch Neurol Psychiatry. 1956 Dec;76(6):630-4.

17. Glutathione, cysteine, and ascorbate concentrations in clinically ill dogs and cats
Viviano KR et al.  J Vet Intern Med. 2009 Mar-Apr;23(2):250-7.

BACKGROUND: Oxidative stress plays a role in the pathogenesis of many systemic diseases. Hospitalized human patients are glutathione, cysteine, and ascorbate deficient, and antioxidant depletion has been correlated with poor clinical outcome. To date little is known about antioxidant concentrations in hospitalized veterinary patients. The purpose of this study was to determine whether ascorbate, cysteine, or glutathione depletion is present in ill dogs and cats compared with healthy controls. HYPOTHESIS: Clinically ill dogs and cats would be antioxidant depleted, and depletion would correlate with illness severity and clinical outcome. ANIMALS: Clinically ill client-owned dogs (n = 61) and cats (n = 37), healthy control dogs (n = 37) and cats (n = 33). METHODS: Prospective, observational, case control study. Erythrocyte reduced glutathione, plasma cysteine, and plasma ascorbate were quantified using high-performance liquid chromatography. RESULTS: Clinically ill dogs had significantly lower erythrocyte glutathione concentrations (1.22 mM, range 0.55-3.61) compared with controls (1.91 mM, range 0.87-3.51; P = .0004), and glutathione depletion correlated with both illness severity (P = .038) and mortality (P = .010). Cats had higher ascorbate concentrations when ill (10.65 microM, range 1.13-25.26) compared with controls (3.68 microM, range 0.36-13.57; P = .0009). CONCLUSIONS AND CLINICAL IMPORTANCE: Clinically ill dogs had decreased erythrocyte glutathione concentrations, which could be a marker of illness severity and prognostic of a poor outcome. Clinically ill cats had an unexpectedly high plasma ascorbate, which could represent a unique species response to oxidative stress.

18. Glutathione metabolism in sepsis
Biolo G et al.  Crit Care Med. 2007 Sep;35(9 Suppl):S591-5.

...Glutathione synthesis can be impaired by cysteine depletion, protein-energy malnutrition, hyperglycemia, glucocorticoid at pharmacologic doses, and decreased secretion of anterior pituitary hormones (growth hormones, thyrotropin, gonadotropins), as often observed in prolonged critical illness.

19. Cysteine metabolism and metal toxicity
Quig D.  Altern Med Rev. 1998 Aug;3(4):262-70.
{free online}

Chronic, low level exposure to toxic metals is an increasing global problem. The symptoms associated with the slow accumulation of toxic metals are multiple and rather nondescript, and overt expression of toxic effects may not appear until later in life. The sulfhydryl-reactive metals (mercury, cadmium, lead, arsenic) are particularly insidious and can affect a vast array of biochemical and nutritional processes. The primary mechanisms by which the sulfhydryl-reactive metals elicit their toxic effects are summarized. The pro-oxidative effects of the metals are compounded by the fact that the metals also inhibit antioxidative enzymes and deplete intracellular glutathione...

20. Glutathione, glutathione-dependent enzymes and antioxidant status in erythrocytes from children treated with high-dose paracetamol
[paracetamol = acetaminophen = Tylenol]
Kozer E et al.  Br J Clin Pharmacol. 2003 Mar;55(3):234-40.
{free online}
AIM: To investigate glutathione and antioxidant status changes in erythrocytes from febrile children receiving repeated supratherapeutic paracetamol doses. METHODS: Fifty-one children aged 2 months to 10 years participated in the study. Three groups were studied: group 1 (n = 24) included afebrile children who did not receive paracetamol; and groups 2 (n = 13) and 3 (n = 14) included children who had fever above 38.5 degrees C for more than 72 h. Patients in group 2 received paracetamol at a dose of 50 +/- 15 (30-75) mg kg(-1) day(-1) and those in group 3 received paracetamol above the recommended therapeutic dose, ie 107 28 (80-180) mg kg(-1) day(-1). A blood sample was taken for the measurement of liver transaminases, gammaglutamil transferase (GGT), reduced glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPX), glutathione S-transferase (GST), superoxide dismutase (SOD) and antioxidant status. RESULTS: Aspartate aminotransferase activity in group 3 was higher than in the other groups (P = 0.027). GSH, SOD and antioxidant status were significantly lower in group 3 compared with groups 1 and 2 (mean differences: for GSH 3.41 micromol gHb(-1), 95% confidence interval (CI) 2.10-4.72, and 2.15 micromol gHb(-1), 95% CI 0.65-3.65, respectively; for SOD 856 U min(-1) gHb(-1), 95% CI 397-1316, and 556 U min(-1) gHb(-1), 95% CI 30-1082, respectively; and for antioxidant status 0.83 mmol l(-1) plasma, 95% CI 0.30-1.36, and 0.63 mmol l(-1) plasma, 95% CI 0.02-1.24, respectively). GR activity was significantly lower in groups 3 and 2 in comparison with group 1 (mean differences 3.44 U min(-1) gHb(-1), 95% CI 0.63-6.25, and 5.64 U min(-1) gHb(-1), 95% CI 2.90-8.38, respectively). Using multiple regression analysis, paracetamol dose was found to be the only independent variable affecting GR, GST and SOD activities (P = 0.007, 0.003 and 0.008, respectively). CONCLUSIONS: In febrile children, treatment with repeated supratherapeutic doses of paracetamol is associated with reduced antioxidant status and erythrocyte glutathione concentrations. These significant changes may indicate an increased risk for hepatotoxicity and liver damage.

21. Autism: a novel form of mercury poisoning
Bernard S et al.  Med Hypotheses. 2001 Apr;56(4):462-71.

22. Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal
Waly M et al. Mol Psychiatry. 2004 Apr;9(4):358-70.

23. Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors
James SJ et al.  Neurotoxicology. 2005 Jan;26(1):1-8.

24. Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism
James SJ et al.  FASEB J. 2009 Aug;23(8):2374-83.

25. Thimerosal induces neuronal cell apoptosis by causing cytochrome c and apoptosis-inducing factor release from mitochondria
 Yel L et al.  Int J Mol Med. 2005 Dec;16(6):971-7.

26. Some aspects of astroglial functions and aluminum  implications for neurodegeneration
Aremu DA, Meshitsuka S. Brain Res Rev. 2006 Aug  30;52(1):193-200.

27. Nanomolar aluminum induces pro-inflammatory and pro-apoptotic  gene expression in human brain cells in primary culture
Lukiw WJ et al. J Inorg Biochem. 2005  Sep;99(9):1895-8.

28. [squalene]
Vaccine A: The Covert Government Experiment That's Killing Our Soldiers--And Why GI's Are Only The First Victims
Gary Matsumoto, 2004.

29. Squalene & Gulf War illnesses (GWI)

30. p3 in: Hygeist or Medical Reformer, 1955. As presented on p34 of: Bodily Matters: The anti-vaccination movement in England, 1853-1907. Nadja Durbach, 2005; Duke University Press.

31. .Delay in diphtheria, pertussis, tetanus vaccination is associated with a reduced risk of childhood asthma
McDonald KL et al. J Allergy Clin Immunol 2008;121:626-31.

32. Polymerase chain reaction detection of the hemagglutinin gene from an attenuated measles vaccine strain in the peripheral mononuclear cells of children with autoimmune hepatitis
Kawashima H et al. Arch Virol. 1996;141(5):877-84.

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