|Autism Relevant Vaccine Dangers in Scientific Literature |
|Articles below investigate autism and/or neural changes related to vaccination or a specific vaccine ingredient. The majority are empirical reports (research with data), with a few recommended reviews by experts. Some articles are available full text and have been linked.Emphasis within summaries have been added. |
Note: control+ click on the underlined titles links to PubMed abstracts
|Click here for articles about autism and toxins broadly defined. |
Click here for articles documenting those with ASD have biological vulnerability to toxins.
Click here for documentation of the reality of autism increase.
Click here for articles about vaccine dangers and other health outcomes.
Gallagher CM, Goodman MS. (2010). Hepatitis B vaccination of male neonates and autism diagnosis, NHIS 1997-2002. J Toxicol Environ Health A. 73 (24):1665-77.
Stony Brook University Medical Center, Health Sciences Center, State University of New York at Stony Brook, Stony Brook, New York, USA
EXCERPT “Vaccination status was determined from the vaccination record. Logistic regression was used to estimate the odds for autism diagnosis associated with neonatal hepatitis B vaccination among boys age 3-17 years, born before 1999, adjusted for race, maternal education, and two-parent household. Boys vaccinated as neonates had threefold greater odds for autism diagnosis compared to boys never vaccinated or vaccinated after the first month of life. Non-Hispanic white boys were 64% less likely to have autism diagnosis relative to nonwhite boys. Findings suggest that U.S. male neonates vaccinated with the hepatitis B vaccine prior to 1999 (from vaccination record) had a threefold higher risk for parental report of autism diagnosis compared to boys not vaccinated as neonates during that same time period.”
ML Herdman, A Marcelo, Y Huang, RM Niles Dhar S & Kiningham KK. (2006). Thimerosal Induces Apoptosis in a Neuroblastoma Model via the cJun N-Terminal Kinase Pathway. Toxicological Sciences 92 (1). 246-253
Department of Pharmacology, Joan C. Edwards School of Medicine, 1542 Spring Valley Drive, Marshall University, Huntington, WV USA
EXCERPT: In recent years, controversy has surrounded the use of thimerosal in vaccines as mercury is a known neurotoxin and nephrotoxin. Since the controversy began in the late 1990’s, much of the thimerosal has been removed from vaccines administered to children in the United States. However, it remains in some, such as the influenza vaccine, and is added to multidose vials used in countries around the world. Studies concentrating on thimerosal-induced neurotoxicity are limited, and exposure guidelines, such as those set by the Food and Drug Administration, are based on research with methylmercury. Interestingly, some in vitro and in vivo studies suggest that ethylmercury may react differently than methylmercury (Aschner and Aschner, 1990;Harry et al., 2004; Magos et al., 1985). Few studies with thimerosal have focused on determining specific signaling pathways involved in neurotoxicity. Establishing these pathways may be an important step in discovering methods of alleviating toxic outcomes in patients exposed to thimerosal….Our study is the first demonstration that thimerosal can induce the activation of JNK and AP-1 in the SK-N-SH neuroblastoma cell line. We showed that activation of cJun and AP-1 transcriptional activity following thimerosal treatment does not appear to be involved in the induction of apoptosis, as demonstrated with the studies using the cJun dominant negative. Furthermore, we were able to show that JNK is an essential upstream component of this pathway through the use of the JNK inhibitor SP600125. This compound was able to attenuate activation of downstream components of mitochondrial-mediated cell death and subsequently protect the cells from apoptosis. These results are significant because identifying specific signaling pathways activated in response to thimerosal exposure presents pharmacological targets for attenuating potential toxicity in patients exposed to thimerosal-containing products. Full text or Full text
Singh VK, Lin SX, Newell E, Nelson C. (2002). Abnormal measles-mumps-rubella antibodies and CNS autoimmunity in children with autism. J Biomed Sci. 2002 Jul-Aug;9(4):359-64.
Department of Biology and Biotechnology Center, Utah State University, Logan, Utah 84322, USA. [email protected]
EXCERPT: Autoimmunity to the central nervous system (CNS), especially to myelin basic protein (MBP), may play a causal role in autism, a neurodevelopmental disorder. Because many autistic children harbor elevated levels of measles antibodies, we conducted a serological study of measles-mumps-rubella (MMR) and MBP autoantibodies. Using serum samples of 125 autistic children and 92 control children…Immunoblotting analysis revealed the presence of an unusual MMR antibody in 75 of 125 (60%) autistic sera but not in control sera….the MMR antibody in autistic sera detected measles HA protein, which is unique to the measles subunit of the vaccine. Furthermore, over 90% of MMR antibody-positive autistic sera were also positive for MBP autoantibodies, suggesting a strong association between MMR and CNS autoimmunity in autism. Stemming from this evidence, we suggest that an inappropriate antibody response to MMR, specifically the measles component thereof, might be related to pathogenesis of autism.
Holland, M. , Conte L, Krakow R. & Colin, L. (2011). Unanswered Questions: A Review of Compensated Cases of Vaccine-Induced Brain Injury
The Vaccine Injury Compensation Program (VICP) has compensated claims of vaccine injury since the inception of the program. This study found 83 cases of acknowledged vaccine-induced brain damage that include autism.
Yel L, Brown LE, Su K, Gollapudi S, Gupta S (2005). Thimerosal induces neuronal cell apoptosis by causing cytochrome c and apoptosis-inducing factor release from mitochondria. International Journal of Molecular Medicine, 16 (6) 971-977.
Department of Medicine, University of California, Irvine, CA 92697, USA.
EXCERPT: There is a worldwide increasing concern over the neurological risks of thimerosal (ethylmercury thiosalicylate) which is an organic mercury compound that is commonly used as an antimicrobial preservative. In this study, we show that thimerosal, at nanomolar concentrations, induces neuronal cell death through the mitochondrial pathway. Thimerosal, in a concentration- and time-dependent manner, decreased cell viability as assessed by calcein-ethidium staining and caused apoptosis detected by Hoechst 33258 dye. Thimerosal-induced apoptosis was associated with depolarization of mitochondrial membrane, generation of reactive oxygen species, and release of cytochrome c and apoptosis-inducing factor (AIF) from mitochondria to cytosol. Although thimerosal did not affect cellular expression of Bax at the protein level, we observed translocation of Bax from cytosol to mitochondria. Finally, caspase-9 and caspase-3 were activated in the absence of caspase-8 activation.Our data suggest that thimerosal causes apoptosis in neuroblastoma cells by changing the mitochondrial microenvironment.
Tomljenovic L, Shaw CA. Do aluminum vaccine adjuvants contribute to the rising prevalence of autism? (2011). J Inorg Biochem. 105(11):1489-99.
Neural Dynamics Research Group, Department of Ophthalmology and Visual Sciences, University of British Columbia, 828 W. 10th Ave, Vancouver, BC, Canada
Abstract: Autism spectrum disorders (ASD) are serious multisystem developmental disorders and an urgent global public health concern. Dysfunctional immunity and impaired brain function are core deficits in ASD. Aluminum (Al), the most commonly used vaccine adjuvant, is a demonstrated neurotoxin and a strong immune stimulator. Hence, adjuvant Al has the potential to induce neuroimmune disorders. When assessing adjuvant toxicity in children, two key points ought to be considered: (i) children should not be viewed as “small adults” as their unique physiology makes them much more vulnerable to toxic insults; and (ii) if exposure to Al from only few vaccines can lead to cognitive impairment and autoimmunity in adults, is it unreasonable to question whether the current pediatric schedules, often containing 18 Al adjuvanted vaccines, are safe for children? By applying Hill’s criteria for establishing causality between exposure and outcome we investigated whether exposure to Al from vaccines could be contributing to the rise in ASD prevalence in the Western world. Our results show that: (i) children from countries with the highest ASD prevalence appear to have the highest exposure to Al from vaccines; (ii) the increase in exposure to Al adjuvants significantly correlates with the increase in ASD prevalence in the United States observed over the last two decades (Pearson r=0.92, p<0.0001); and (iii) a significant correlation exists between the amounts of Al administered to preschool children and the current prevalence of ASD in seven Western countries, particularly at 3-4months of age (Pearson r=0.89-0.94, p=0.0018-0.0248). The application of the Hill’s criteria to these data indicates that the correlation between Al in vaccines and ASD may be causal. Because children represent a fraction of the population most at risk for complications following exposure to Al, a more rigorous evaluation of Al adjuvant safety seems warranted.
Olczak M, Duszczyk M, Mierzejewski P, Wierzba-Bobrowicz T, Majewska MD. (2010). Lasting neuropathological changes in rat brain after intermittent neonatal administration of thimerosal.Folia Neuropathol. 48(4): 258-69.
Abstract: Thimerosal, an organomercurial added as a preservative to some vaccines, is a suspected iatrogenic factor, possibly contributing to paediatric neurodevelopmental disorders including autism. We examined the effects of early postnatal administration of thimerosal (four i.m. injections, 12 or 240 μg THIM-Hg/kg, on postnatal days 7, 9, 11 and 15) on brain pathology in Wistar rats. Numerous neuropathological changes were observed in young adult rats which were treated postnatally with thimerosal. They included: ischaemic degeneration of neurons and “dark” neurons in the prefrontal and temporal cortex, the hippocampus and the cerebellum, pathological changes of the blood vessels in the temporal cortex, diminished synaptophysin reaction in the hippocampus, atrophy of astroglia in the hippocampus and cerebellum, and positive caspase-3 reaction in Bergmann astroglia. These findings document neurotoxic effects of thimerosal, at doses equivalent to those used in infant vaccines or higher, in developing rat brain, suggesting likely involvement of this mercurial in neurodevelopmental disorders. Full text. (Note: Below are two related follow up works which support and extend the findings above, importantly, the latter shows how investigating these effects may lead to prevention)
Olczak M, Duszczyk M, Mierzejewski P, Meyza K, Majewska MD. (2011) Persistent behavioral impairments and alterations of brain dopamine system after early postnatal administration of thimerosal in rats. Behav Brain Res. 223(1): 107-18.
Department of Pharmacology and Physiology of the Nervous System, Institute of Psychiatry and Neurology, Warsaw, POLAND
EXCERPT: Previously we showed that neonatal administration of THIM at doses equivalent to those used in infant vaccines or higher, causes lasting alterations in the brain opioid system in rats. Here we investigated neonatal treatment with THIM (at doses 12, 240, 1440 and 3000 μg Hg/kg) on behaviors, which are characteristically altered in autism… In animals of both sexes treated with the highest THIM dose, the frequency of prosocial interactions was reduced, while the frequency of asocial/antisocial interactions was increased in males, but decreased in females. Neonatal THIM treatment did not significantly affect spatial learning and memory. THIM-exposed rats also manifested reduced haloperidol-induced catalepsy, accompanied by a marked decline in the density of striatal D₂ receptors, measured by immunohistochemical staining, suggesting alterations to the brain dopaminergic system. Males were more sensitive than females to some neurodisruptive/neurotoxic actions of THIM. These data document that early postnatal THIM administration causes lasting neurobehavioral impairments and neurochemical alterations in the brain, dependent on dose and sex. If similar changes occur in THIM/mercurial-exposed children, they could contribute do neurodevelopmental disorders. Full text
Duszczyk-Budhathoki M, Olczak M, Lehner M, Majewska MD. (2012). Administration of thimerosal to infant rats increases overflow of glutamate and aspartate in the prefrontal cortex: protective role of dehydroepiandrosterone sulfate. Neurochem Res. 37 (2):436-47.
(note: This important research shows how investigating – rather than denying – vaccine effects may lead to prevention of vaccine injuries).
EXCERPT: We previously showed that its administration to infant rats causes behavioral, neurochemical and neuropathological abnormalities similar to those present in autism. Here we examined, using microdialysis, the effect of thimerosal on extracellular levels of neuroactive amino acids in the rat prefrontal cortex (PFC). Thimerosal administration (4 injections, i.m., 240 μg Hg/kg on postnatal days 7, 9, 11, 15) induced lasting changes in amino acid overflow: an increase of glutamate and aspartate accompanied by a decrease of glycine and alanine; measured 10-14 weeks after the injections. Four injections of thimerosal at a dose of 12.5 μg Hg/kg did not alter glutamate and aspartate concentrations at microdialysis time (but based on thimerosal pharmacokinetics, could have been effective soon after its injection). Application of thimerosal to the PFC in perfusion fluid evoked a rapid increase of glutamate overflow. Coadministration of the neurosteroid, dehydroepiandrosterone sulfate (DHEAS) prevented the thimerosal effect on glutamate and aspartate; the steroid alone had no influence on these amino acids. Coapplication of DHEAS with thimerosal in perfusion fluid also blocked the acute action of thimerosal on glutamate. In contrast, DHEAS alone reduced overflow of glycine and alanine, somewhat potentiating the thimerosal effect on these amino acids. Since excessive accumulation of extracellular glutamate is linked with excitotoxicity, our data imply that neonatal exposure to thimerosal-containing vaccines might induce excitotoxic brain injuries, leading to neurodevelopmental disorders. DHEAS may partially protect against mercurials-induced neurotoxicity. Full text
Petrik MS, Wong MC, Tabata RC, Garry RF, Shaw CA. (2007) Aluminum adjuvant linked to gulf war illness induces motor neuron death in mice Neuromolecular Med. 2007;9(1):83-100.
Department of Ophthalmology and Program in Neuroscience, University of British Columbia, Vancouver, British Columbia, Canada.
EXCERPT: Gulf War illness (GWI) affects a significant percentage of veterans of the 1991 conflict, but its origin remains unknown. Associated with some cases of GWI are increased incidences of amyotrophic lateral sclerosis and other neurological disorders. Whereas many environmental factors have been linked to GWI, the role of the anthrax vaccine has come under increasing scrutiny. Among the vaccine’s potentially toxic components are the adjuvants aluminum hydroxide and squalene. Young, male colony CD-1 mice were injected with the adjuvants at doses equivalent to those given to US military service personnel. All mice were subjected to a battery of motor and cognitive-behavioral tests over a 6-mo period postinjections. Following sacrifice, central nervous system tissues were examined using immunohistochemistry for evidence of inflammation and cell death. Behavioral testing showed motor deficits in the aluminum treatment group that expressed as a progressive decrease in strength measured by the wire-mesh hang test (final deficit at 24 wk; about 50%). Significant cognitive deficits in water-maze learning were observed in the combined aluminum and squalene group (4.3 errors per trial) compared with the controls (0.2 errors per trial) after 20 wk. Apoptotic neurons were identified in aluminum-injected animals that showed significantly increased activated caspase-3 labeling in lumbar spinal cord (255%) and primary motor cortex (192%) compared with the controls. Aluminum-treated groups also showed significant motor neuron loss (35%)and increased numbers of astrocytes (350%) in the lumbar spinal cord. The findings suggest a possible role for the aluminum adjuvant in some neurological features associated with GWI and possibly an additional role for the combination of adjuvants.
Molina V. & Shoenfeld Y. (2005). Infection, vaccines and other environmental triggers of autoimmunity. Autoimmunity. 38(3):235-45.
Department of Medicine B and The Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel. The Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel
EXCERPT: Many environmental factors are known to affect the immune system and may play a role as triggers of the autoimmune mosaic…. This was studied for some syndromes as for the association between SLE and EBV infection, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection and more. Vaccines, in several reports were found to be temporally followed by a new onset of autoimmune diseases. The same mechanisms that act in infectious invasion of the host, apply equally to the host response to vaccination. It has been accepted for diphtheria and tetanus toxoid, polio and measles vaccines and GBS. Also this theory has been accepted for MMR vaccination and development of autoimmune thrombocytopenia, MS has been associated with HBV vaccination.
DeLonga, 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: Current Issues
Department of Economics and Finance, Baruch College/City University of New York, New York, New York,USA
Abstract: The reason for the rapid rise of autism in the United States that began in the 1990s is a mystery. Although individuals probably have a genetic predisposition to develop autism, researchers suspect that one or more environmental triggers are also needed. One of those triggers might be the battery of vaccinations that young children receive. Using regression analysis and controlling for family income and ethnicity, the relationship between the proportion of children who received the recommended vaccines by age 2 years and the prevalence of autism (AUT) or speech or language impairment (SLI) in each U.S. state from 2001 and 2007 was determined. A positive and statistically significant relationship was found: The higher the proportion of children receiving recommended vaccinations, the higher was the prevalence of AUT or SLI. A 1% increase in vaccination was associated with an additional 680 children having AUT or SLI. Neither parental behavior nor access to care affected the results, since vaccination proportions were not significantly related (statistically) to any other disability or to the number of pediatricians in a U.S. state. The results suggest that although mercury has been removed from many vaccines, other culprits may link vaccines to autism. Further study into the relationship between vaccines and autism is warranted.
Sharpe MA, Gist TL, Baskin DS. (2013). B-Lymphocytes from a Population of Children with Autism Spectrum Disorder and Their Unaffected Siblings Exhibit Hypersensitivity to Thimerosal J Toxicol. 2013;2013:801517.
Department of Neurosurgery, The Methodist Neurological Institute, Houston, TX.
Abstract: The role of thimerosal containing vaccines in the development of autism spectrum disorder (ASD) has been an area of intense debate, as has the presence of mercury dental amalgams and fish ingestion by pregnant mothers. We studied the effects of thimerosal on cell proliferation and mitochondrial function from B-lymphocytes taken from individuals with autism, their nonautistic twins, and their nontwin siblings. Eleven families were examined and compared to matched controls. B-cells were grown with increasing levels of thimerosal, and various assays (LDH, XTT, DCFH, etc.) were performed to examine the effects on cellular proliferation and mitochondrial function. A subpopulation of eight individuals (4 ASD, 2 twins, and 2 siblings) from four of the families showed thimerosal hypersensitivity, whereas none of the control individuals displayed this response. The thimerosal concentration required to inhibit cell proliferation in these individuals was only 40% of controls. Cells hypersensitive to thimerosal also had higher levels of oxidative stress markers, protein carbonyls, and oxidant generation.This suggests certain individuals with a mild mitochondrial defect may be highly susceptible to mitochondrial specific toxins like the vaccine preservative thimerosal.
Goth, SR., Chu, RA. & Gregg, JP. (2006). Uncoupling of ATP-mediated Calcium Signaling and Dysregulated IL-6 Secretion in Dendritic Cells by Nanomolar Thimerosal Environmental Health Perspectives, 114(7): 1083-91.
University of California at Davis, Davis CA, USA
Abstract: Dendritic cells (DCs) , a rare cell type widely distributed in the soma, are potent antigen-presentingcells that initiate primary immune responses. DCs rely on intracellular redox state and calcium (Ca2+) signals for proper development and function, but the relationship between these two signaling systems is unclear. Thimerosal (THI) is a mercurial used to preserve vaccines and consumer products, and is used experimentally to induce Ca2+ release from microsomal stores. We tested adenosine triphosphate (ATP) -mediated Ca2+ responses of DCs transiently exposed to nanomolar THI. Transcriptional and immunocytochemical analyses show that murine myeloid immature DCs (IDCs) and mature DCs (MDCs) express inositol 1,4,5-trisphosphate receptor (IP3R) and ryanodine receptor (RyR) Ca2+ channels, known targets of THI. IDCs express the RyR1 isoform in a punctate distribution that is densest near plasma membranes and within dendritic processes, whereas IP3Rs are more generally distributed. RyR1 positively and negatively regulates purinergic signaling because ryanodine (Ry) blockade a) recruited 80% more ATP responders, b) shortened ATP-mediated Ca2+ transients > 2-fold, and c) produced a delayed and persistent rise (>/= 2-fold) in baseline Ca2+. THI (100 nM, 5 min) recruited more ATP responders, shortened the ATP-mediated Ca2+ transient (>/= 1.4-fold) , and produced a delayed rise (>/= 3-fold) in the Ca2+ baseline, mimicking Ry. THI and Ry, in combination, produced additive effects leading touncoupling of IP3R and RyR1 signals. THI altered ATP-mediated interleukin-6 secretion, initially enhancing the rate of cytokine secretion but suppressing cytokine secretion overall in DCs.DCs are exquisitely sensitive to THI, with one mechanism involving the uncoupling of positive and negative regulation of Ca2+ signals contributed by RyR1. Full text
Burbacher, TM, . Shen, DD. , N. Grant, KS, Cernichiari, E & Thomas Clarkson , T. (2005). Comparison of blood and brain mercury levels in infant monkeys exposed to methylmercury or vaccines containing thimerosal. Environmental Health Perspectives, Aug 2005. August; 113(8): 1015–1021.
University of Washington, USA; University of Rochester School of Medicine, Rochester, New York, USA
Note: A complex study, showing some similarities and differences between methyl and ethyl mercury in the body — but it documents unequivocally that thimerosal injections ( mercury found in vaccines ) get into the brain and remain there for many days after the injections end (see for example Figure 6).
EXCERPT: Thimerosal is a preservative that has been used in manufacturing vaccines since the 1930s….Monkeys were exposed to MeHg (via oral gavage) or vaccines containing thimerosal (via intramuscular injection) at birth and 1, 2, and 3 weeks of age. Total blood Hg levels were determined 2, 4, and 7 days after each exposure. Total and inorganic brain Hg levels were assessed 2, 4, 7, or 28 days after the last exposure. The initial and terminal half-life of Hg in blood after thimerosal exposure was 2.1 and 8.6 days, respectively, which are significantly shorter than the elimination half-life of Hg after MeHg exposure at 21.5 days. Brain concentrations of total Hg were significantly lower by approximately 3-fold for the thimerosal-exposed monkeys when compared with the MeHg infants, whereas the average brain-to-blood concentration ratio was slightly higher for the thimerosal-exposed monkeys (3.5 ± 0.5 vs. 2.5 ± 0.3). A higher percentage of the total Hg in the brain was in the form of inorganic Hg for the thimerosal-exposed monkeys (34% vs. 7%). The results indicate that MeHg is not a suitable reference for risk assessment from exposure to thimerosal-derived Hg. Knowledge of the toxicokinetics and developmental toxicity of thimerosal is needed to afford a meaningful assessment of the developmental effects of thimerosal-containing vaccines. Full text.
Geier DA, Geier MR. (2007). A Case Series of Children with Apparent Mercury Toxic Encephalopathies Manifesting with Clinical Symptoms of Regressive Autistic Disorder. J Toxicol Environ Health A. 70 (10): 837-51.
Institute of Chronic Illnesses, Inc., Silver Spring, Maryland, USA.
Abstract: Impairments in social relatedness and communication, repetitive behaviors, and stereotypic abnormal movement patterns characterize autism spectrum disorders (ASDs). It is clear that while genetic factors are important to the pathogenesis of ASDs, mercury exposure can induce immune, sensory, neurological, motor, and behavioral dysfunctions similar to traits defining or associated with ASDs. The Institutional Review Board of the Institute for Chronic Illnesses (Office for Human Research Protections, U.S. Department of Health and Human Services, IRB number IRB00005375) approved the present study. A case series of nine patients who presented to the Genetic Centers of America for a genetic/developmental evaluation are discussed. Eight of nine patients (one patient was found to have an ASD due to Rett’s syndrome) (a) had regressive ASDs; (b) had elevated levels of androgens; (c) excreted significant amounts of mercury post chelation challenge; (d) had biochemical evidence of decreased function in their glutathione pathways; (e) had no known significant mercury exposure except from Thimerosal-containing vaccines/Rho(D)-immune globulin preparations; and (f) had alternate causes for their regressive ASDs ruled out. There was a significant dose-response relationship between the severity of the regressive ASDs observed and the total mercury dose children received from Thimerosal-containing vaccines/Rho (D)-immune globulin preparations. Based upon differential diagnoses, 8 of 9 patients examined were exposed to significant mercury from Thimerosal-containing biologic/vaccine preparations during their fetal/infant developmental periods, and subsequently, between 12 and 24 mo of age, these previously normally developing children suffered mercury toxic encephalopathies that manifested with clinical symptoms consistent with regressive ASDs. Evidence for mercury intoxication should be considered in the differential diagnosis as contributing to some regressive ASDs.
Waly M, Olteanu H, Banerjee R, Choi SW, Mason JB, Parker BS, Sukumar S, Shim S, Sharma A, Benzecry JM, Power-Charnitsky VA, Deth RC. (2004). Activation of Methionine Synthase by Insulin-like Growth Factor-1 and Dopamine: a Target for Neurodevelopmental Toxins and Thimerosal Mol Psychiatry. 9 (4): 358-70.
Department of Pharmaceutical Sciences, Northeastern University, Boston, MA
Abstract: Methylation events play a critical role in the ability of growth factors to promote normal development. Neurodevelopmental toxins, such as ethanol and heavy metals, interrupt growth factor signaling, raising the possibility that they might exert adverse effects on methylation. We found that insulin-like growth factor-1 (IGF-1)- and dopamine-stimulated methionine synthase (MS) activity and folate-dependent methylation of phospholipids in SH-SY5Y human neuroblastoma cells, via a PI3-kinase- and MAP-kinase-dependent mechanism. The stimulation of this pathway increased DNA methylation, while its inhibition increased methylation-sensitive gene expression. Ethanol potently interfered with IGF-1 activation of MS and blocked its effect on DNA methylation, whereas it did not inhibit the effects of dopamine. Metal ions potently affected IGF-1 and dopamine-stimulated MS activity, as well as folate-dependent phospholipid methylation: Cu(2+) promoted enzyme activity and methylation, while Cu(+), Pb(2+), Hg(2+) and Al(3+) were inhibitory. The ethylmercury-containing preservative thimerosal inhibited both IGF-1- and dopamine-stimulated methylation with an IC(50) of 1 nM and eliminated MS activity. Our findings outline a novel growth factor signaling pathway that regulates MS activity and thereby modulates methylation reactions, including DNA methylation. The potent inhibition of this pathway by ethanol, lead, mercury, aluminum and thimerosal suggests that it may be an important target of neurodevelopmental toxins.
Seneff, S. Davidson, RM. & Liu J. Empirical Data Confirm Autism Symptoms Related to Aluminum and Acetaminophen Exposure Entropy, 14 (11): 2227-2253.
Abstract: Autism is a condition characterized by impaired cognitive and social skills, associated with compromised immune function. The incidence is alarmingly on the rise, and environmental factors are increasingly suspected to play a role. This paper investigates word frequency patterns in the U.S. CDC Vaccine Adverse Events Reporting System (VAERS) database. Our results provide strong evidence supporting a link between autism and the aluminum in vaccines. A literature review showing toxicity of aluminum in human physiology offers further support. Mentions of autism in VAERS increased steadily at the end of the last century, during a period when mercury was being phased out, while aluminum adjuvant burden was being increased. Using standard log-likelihood ratio techniques, we identify several signs and symptoms that are significantly more prevalent in vaccine reports after 2000, including cellulitis, seizure, depression, fatigue, pain and death, which are also significantly associated with aluminum-containing vaccines. We propose that children with the autism diagnosis are especially vulnerable to toxic metals such as aluminum and mercury due to insufficient serum sulfate and glutathione. A strong correlation between autism and the MMR (Measles, Mumps, Rubella) vaccine is also observed, which may be partially explained via an increased sensitivity to acetaminophen administered to control fever.
Humphrey ML, Cole MP, Pendergrass JC, Kiningham KK. (2005) Mitochondrial mediated thimerosal-induced apoptosis in a human neuroblastoma cell line (SK-N-SH). Neurotoxicology. 26 (3) 407–416.
Department of Pharmacology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WVGraduate Center for Toxicology, University of Kentucky, Lexington, KY USA.
Abstract: Environmental exposure to mercurials continues to be a public health issue due to their deleterious effects on immune, renal and neurological function. Recently the safety of thimerosal, an ethyl mercury-containing preservative used in vaccines, has been questioned due to exposure of infants during immunization. Mercurials have been reported to cause apoptosis in cultured neurons; however, the signaling pathways resulting in cell death have not been well characterized. Therefore, the objective of this study was to identify the mode of cell death in an in vitro model of thimerosal-induced neurotoxicity, and more specifically, to elucidate signaling pathways which might serve as pharmacological targets. Within 2 h of thimerosal exposure (5 microM) to the human neuroblastoma cell line, SK-N-SH, morphological changes, including membrane alterations and cell shrinkage, were observed. Cell viability, assessed by measurement of lactate dehydrogenase (LDH) activity in the medium, as well as the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay, showed a time- and concentration-dependent decrease in cell survival upon thimerosal exposure. In cells treated for 24 h with thimerosal, fluorescence microscopy indicated cells undergoing both apoptosis and oncosis/necrosis. To identify the apoptotic pathway associated with thimerosal-mediated cell death, we first evaluated the mitochondrial cascade, as both inorganic and organic mercurials have been reported to accumulate in the organelle. Cytochrome c was shown to leak from the mitochondria, followed by caspase 9 cleavage within 8 h of treatment. In addition, poly(ADP-ribose) polymerase (PARP) was cleaved to form a 85 kDa fragment following maximal caspase 3 activation at 24 h. Taken together these findings suggest deleterious effects on the cytoarchitecture by thimerosal and initiation of mitochondrial-mediated apoptosis. Full text
Maha I. Sh. Kawashti, Omnia R. Amin Nadia G. Rowehy (2006). Possible Immunological Disorders in Autism: Concomitant Autoimmunity and Immune Tolerance The Egyptian Journal of Immunology,
Abstract: Autism is a pervasive developmental disorder that affect children early in their life. Immunological disorders is one of several contributing factors that have been suggested to cause autism. Thirty autistic children aged 3-6 years and thirty non-autistic psychologically-free siblings were studied. Circulating IgA and IgG autoantibodies to casein and gluten dietary proteins were detected by enzyme-immunoassays (EIA). Circulating IgG antibodies to measles, mumps and rubella vaccine (M.M.R) and cytomeglovirus were investigated by EIA. Results revealed high seropositivity for autoantibodies to casein and gluten: 83.3% and 50% respectively in autistic children as compared to 10% and 6.7% positivity in the control group. Surprisingly, circulating anti-measles, anti-mumps and anti-rubella IgG were positive in only 50%, 73.3% and 53.3% respectively as compared to 100% positivity in the control group. Anti-CMV IgG was positive in 43.3% of the autistic children as compared to 7% in the control group. It is concluded that, autoimmune response to dietary proteins and deficient immune response to measles, mumps and rubella vaccine antigens might be associated with autism, as a leading cause or a resulting event. Further research is needed to confirm these findings.
Hewitson L, Lopresti B, Mason, NS, Stott C, Tomko J, Houser L, Klein EC, Castro C , Sackett G, Gupta S, Atwood D, Wakefield AJ, (2008) Pediatric Vaccines Influence Primate Behavior, and Amygdala Growth and Opioid Ligand Binding. Presented at the International Meeting for Autism Research, London, May 15-17.
Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA; Thoughtful House Center for Children , Austin, TX USA
Abstract Excerpt: Macaques are commonly used in pre-clinical vaccine safety testing, but the combined childhood vaccine regimen, rather than individual vaccines, has not been studied. Childhood vaccines are a possible causal factor in autism, and abnormal behaviors and anomalous amygdala growth are potentially inter-related features of this condition. The objective of this study was to compare early infant cognition and behavior with amygdala size and opioid binding in rhesus macaques receiving the recommended childhood vaccines (1994-1999), the majority of which contained the bactericidal preservative ethylmercurithiosalicylic acid (thimerosal). Macaques were administered the recommended infant vaccines, adjusted for age and thimerosal dose (exposed; N=13), or saline (unexposed; N=3).Primate development, cognition and social behavior were assessed for both vaccinated and unvaccinated infants using standardized tests developed at the Washington National Primate Research Center. Amygdala growth and binding were measured serially by MRI and by the binding of the non-selective opioid antagonist [11C]diprenorphine, measured by PET, respectively, before (T1) and after (T2) the administration of the measles-mumps-rubella vaccine (MMR). Compared with unexposed animals, significant neurodevelopmental deficits were evident for exposed animals in survival reflexes, tests of color discrimination and reversal, and learning sets. Differences in behaviors were observed between exposed and unexposed animals and within the exposed group before and after MMR vaccination. Compared with unexposed animals, exposed animals showed attenuation of amygdala growth and differences in the amygdala binding of [11C]diprenorphine. Interaction models identified significant associations between specific aberrant social and non-social behaviors, isotope binding, and vaccine exposure.
Hewitson L, Lopresti B, Stott C, Mason, NS, , Tomko J, (2010). Influence of pediatric vaccines on amygdala growth and opioid ligand binding in rhesus macaque infants: A pilot study. Acta Neurobiol Exp 70 (2): 147–164
Abstract: This longitudinal, case-control pilot study examined amygdala growth in rhesus macaque infants receiving the complete US childhood vaccine schedule (1994-1999). Longitudinal structural and functional neuroimaging was undertaken to examine central effects of the vaccine regimen on the developing brain. Vaccine-exposed and saline-injected control infants underwent MRI and PET imaging at approximately 4 and 6 months of age, representing two specific timeframes within the vaccination schedule. Volumetric analyses showed that exposed animals did not undergo the maturational changes over time in amygdala volume that was observed in unexposed animals. After controlling for left amygdala volume, the binding of the opioid antagonist [11C]diprenorphine (DPN) in exposed animals remained relatively constant over time, compared with unexposed animals, in which a significant decrease in [11C]DPN binding occurred. These results suggest that maturational changes in amygdala volume and the binding capacity of [11C]DPN in the amygdala was significantly altered in infant macaques receiving the vaccine schedule. The macaque infant is a relevant animal model in which to investigate specific environmental exposures and structural/functional neuroimaging during neurodevelopment.
Young HA, Geier DA, Geier MR. (2008). Thimerosal exposure in infants and neurodevelopmental disorders: An assessment of computerized medical records in the Vaccine Safety Datalink.
Abstract: The study evaluated possible associations between neurodevelopmental disorders (NDs) and exposure to mercury (Hg) from Thimerosal-containing vaccines (TCVs) by examining the automated Vaccine Safety Datalink (VSD). A total of 278,624 subjects were identified in birth cohorts from 1990-1996 that had received their first oral polio vaccination by 3 months of age in the VSD. The birth cohort prevalence rate of medically diagnosed International Classification of Disease, 9th revision (ICD-9) specific NDs and control outcomes were calculated. Exposures to Hg from TCVs were calculated by birth cohort for specific exposure windows from birth-7 months and birth-13 months of age. Poisson regression analysis was used to model the association between the prevalence of outcomes and Hg doses from TCVs. Consistent significantly increased rate ratios were observed for autism, autism spectrum disorders, tics, attention deficit disorder, and emotional disturbances with Hg exposure from TCVs. By contrast, none of the control outcomes had significantly increased rate ratios with Hg exposure from TCVs. Routine childhood vaccination should be continued to help reduce the morbidity and mortality associated with infectious diseases, but efforts should be undertaken to remove Hg from vaccines. Additional studies should be conducted to further evaluate the relationship between Hg exposure and NDs. Full text
Gallagher C., Goodman M (2008). Hepatitis B triple series vaccine and developmental disability in US children aged 1-9 years. Journal Toxicological & Environmental Chemistry, Volume 90, Issue 5 September 2008 , pages 997 – 1008
Graduate Program in Public Health, Stony Brook University Medical Center, Health Sciences Center, New York, USA
Abstract: This study investigated the association between vaccination with the Hepatitis B triple series vaccine prior to 2000 and developmental disability in children aged 1–9 years (n = 1824), proxied by parental report that their child receives early intervention or special education services (EIS). National Health and Nutrition Examination Survey 1999–2000 data were analyzed and adjusted for survey design by Taylor Linearization using SAS version 9.1 software, with SAS callable SUDAAN version 9.0.1. The odds of receiving EIS were approximately nine times as great for vaccinated boys (n = 46) as for unvaccinated boys (n = 7), after adjustment for confounders. This study found statistically significant evidence to suggest that boys in United States who were vaccinated with the triple series Hepatitis B vaccine, during the time period in which vaccines were manufactured with thimerosal, were more susceptible to developmental disability than were unvaccinated boys.
Minami T, Miyata E, Sakamoto Y, Yamazaki H, Ichida S. (2009). Induction of metallothionein in mouse cerebellum and cerebrum with low-dose thimerosal injection. Cell Biology and Toxicology 26 (2): 143-52.
Abstract: Thimerosal, an ethyl mercury compound, is used worldwide as a vaccine preservative. We previously observed that the mercury concentration in mouse brains did not increase with the clinical dose of thimerosal injection, but the concentration increased in the brain after the injection of thimerosal with lipopolysaccharide, even if a low dose of thimerosal was administered. Thimerosal may penetrate the brain, but is undetectable when a clinical dose of thimerosal is injected; therefore, the induction of metallothionein (MT) messenger RNA (mRNA) and protein was observed in the cerebellum and cerebrum of mice after thimerosal injection, as MT is an inducible protein. MT-1 mRNA was expressed at 6 and 9 h in both the cerebrum and cerebellum, but MT-1 mRNA expression in the cerebellum was three times higher than that in the cerebrum after the injection of 12 microg/kg thimerosal. MT-2 mRNA was not expressed until 24 h in both organs. MT-3 mRNA was expressed in the cerebellum from 6 to 15 h after the injection, but not in the cerebrum until 24 h. MT-1 and MT-3 mRNAs were expressed in the cerebellum in a dose-dependent manner. Furthermore, MT-1 protein was detected from 6 to 72 h in the cerebellum after 12 microg/kg of thimerosal was injected and peaked at 10 h. MT-2 was detected in the cerebellum only at 10 h. In the cerebrum, little MT-1 protein was detected at 10 and 24 h, and there were no peaks of MT-2 protein in the cerebrum. In conclusion, MT-1 and MT-3 mRNAs but not MT-2 mRNA are easily expressed in the cerebellum rather than in the cerebrum by the injection of low-dose thimerosal. It is thought that the cerebellum is a sensitive organ against thimerosal. As a result of the present findings, in combination with the brain pathology observed in patients diagnosed with autism, the present study helps to support the possible biological plausibility for how low-dose exposure to mercury from thimerosal-containing vaccines may be associated with autism.
Olczak M, Duszczyk M, Mierzejewski P, Majewska MD. (2009). Neonatal administration of a vaccine preservative, thimerosal, produces lasting impairment of nociception and apparent activation of opioid system in rats. Brain Res. 2009 Dec 8;1301:143-51.
Abstract: Thimerosal (THIM), an organomercury preservative added to many child vaccines is a suspected factor in pathogenesis of neurodevelopmental disorders. We examined the pharmacokinetics of Hg in the brain, liver and kidneys after i.m. THIM injection in suckling rats and we tested THIM effect on nociception. THIM solutions were injected to Wistar and Lewis rats in a vaccination-like mode on PN days 7, 9, 11 and 15 in four equal doses. For Wistar rats these were: 12, 48, 240, 720, 1440, 2160, 3000 microg Hg/kg and for Lewis: 54, 216, 540 and 1080 microg Hg/kg. Pharmacokinetic analysis revealed that Hg from THIM injections accumulates in the rat brain in significant amounts and remains there longer than 30 days after the injection. At the 6th week of age animals were examined for pain sensitivity using the hot plate test. THIM treated rats of both strains and sexes manifested statistically significantly elevated pain threshold (latency for paw licking, jumping) on a hot plate (56 degrees C). Wistar rats were more sensitive to this effect than Lewis rats. Protracted THIM-induced hypoalgesia was reversed by naloxone (5 mg/kg, i.p.) injected before the hot plate test, indicative of involvement of endogenous opioids. This was confirmed by augmented catalepsy after morphine (2.5 mg/kg, s.c.) injection. Acute THIM injection to 6-week-old rats also produced hypoalgesia, but this effect was transient and was gone within 14 days. Present findings show that THIM administration to suckling or adult rats impairs sensitivity to pain, apparently due to activation the endogenous opioid system.
Bernard Rimland, PhD, Woody McGinnis, MD (2002). Vaccines and Autism. Laboratory Medicine 33 (9).
Autism Research Institute, San Diego, CA
Note: It is important to note that the late Dr. Rimland was the founder (1967) of the Autism Research Institute, and the founder of the Autism Society of America in 1965. According to Wikipedia, “Rimland was long an internationally recognized authority on autism spectrum disorders.” His opinion speaks to the range and reality of actual expert and scientific opinions.
Excerpts: “Vaccinations may be one of the triggers for autism. Substantial data demonstrate immune abnormality in many autistic children consistent with impaired resistance to infection, activation of inflammatory response, and autoimmunity. Impaired resistance may predispose to vaccine injury in autism.” And, “we submit that MMR (usually at 15 months) may result in chronic infection of the gut by vaccinial measles and trigger regressed autism. Thimerosal injections in series prior to or at the time of MMR may potentiate injury…” Full text
Wilson K, Hawken S, Kwong JC, Deeks S, Crowcroft NS, Van Walraven C, Potter BK, Chakraborty P, Keelan J, Pluscauskas M, Manuel D. (2011). Adverse events following 12 and 18 month vaccinations: a population-based, self-controlled case series analysis. PLoS One. 6(12):e27897.
EXCERPT: Live vaccines have distinct safety profiles, potentially causing systemic reactions one to 2 weeks after administration. Using the self-controlled case series design we examined 271,495 12 month vaccinations and 184,312 18 month vaccinations to examine the relative incidence of the composite endpoint of emergency room visits or hospital admissions in consecutive one day intervals following vaccination. These were compared to a control period 20 to 28 days later. In a post-hoc analysis we examined the reasons for emergency room visits and the average acuity score at presentation for children during the at-risk period following the 12 month vaccine. Four to 12 days post 12 month vaccination, children had a 1.33 (1.29-1.38) increased relative incidence of the combined endpoint compared to the control period, or at least one event during the risk interval for every 168 children vaccinated. Ten to 12 days post 18 month vaccination, the relative incidence was 1.25 (95%, 1.17-1.33) which represented at least one excess event for every 730 children vaccinated. The primary reason for increased events was statistically significant elevations in emergency room visits following all vaccinations. There were non-significant increases in hospital admissions. There were an additional 20 febrile seizures for every 100,000 vaccinated at 12 months…. Future studies should examine whether these events could be predicted or prevented. Full text with illustrations.
Dórea JG, (2011). Integrating experimental (in vitro and in vivo) neurotoxicity studies of low-dose thimerosal relevant to vaccines. Neurochem Res. 36(6): 927-38.
Faculty of Health Sciences, Universidade de Brasília, BRAZIL
EXCERPT: This review integrates information derived from emerging experimental studies (in vitro and in vivo) of low-dose Thimerosal (sodium ethyl mercury thiosalicylate). Major databases (PubMed and Web-of-science) were searched for in vitro and in vivo experimental studies that addressed the effects of low-dose Thimerosal (or ethylmercury) on neural tissues and animal behaviour.Information extracted from studies indicates that: (a) activity of low doses of Thimerosal against isolated human and animal brain cells was found in all studies and is consistent with Hg neurotoxicity; (b) the neurotoxic effect of ethylmercury has not been studied with co-occurring adjuvant-Al in TCVs; (c) animal studies have shown that exposure to Thimerosal-Hg can lead to accumulation of inorganic Hg in brain, and that (d) doses relevant to TCV exposure possess the potential to affect human neuro-development. Thimerosal at concentrations relevant for infants’ exposure (in vaccines) is toxic to cultured human-brain cells and to laboratory animals.
Hamza H, Cao J, Li X, Li C, Zhu M, Zhao S.(2012). Hepatitis B vaccine induces apoptotic death in Hepa1-6 cells. Apoptosis. 17(5):516-27.
EXCERPT: Vaccines can have adverse side-effects, and these are predominantly associated with the inclusion of chemical additives such as aluminum hydroxide adjuvant. The objective of this study was to establish an in vitro model system amenable to mechanistic investigations of cytotoxicity induced by hepatitis B vaccine, and to investigate the mechanisms of vaccine-induced cell death. The mouse liver hepatoma cell line Hepa1-6 was treated with two doses of adjuvanted (aluminium hydroxide) hepatitis B vaccine (0.5 and 1 μg protein per ml) …Vaccine exposure was accompanied by significant increases in the levels of activated caspase 3, a key effector caspase in the apoptosis cascade.Upregulation of cleaved caspase 3,7 were detected by western blot in addition to Apaf-1 and caspase 9 expressions argues that cell death takes place via the intrinsic apoptotic pathway in which release of cytochrome c from the mitochondria triggers the assembly of a caspase activation complex. We conclude that exposure of Hepa1-6 cells to a low dose of adjuvanted hepatitis B vaccine leads to loss of mitochondrial integrity, apoptosis induction, and cell death, apoptosis effect was observed also in C2C12 mouse myoblast cell line after treated with low dose of vaccine (0.3, 0.1, 0.05 μg/ml). In addition In vivo apoptotic effect of hepatitis B vaccine was observed in mouse liver.
Sulkowski ZL, Chen T, Midha S, Zavacki AM, Sajdel-Sulkowska EM (2012). Maternal thimerosal exposure results in aberrant cerebellar oxidative stress, thyroid hormone metabolism, and motor behavior in rat pups; sex- and strain-dependent effects. Cerebellum. 11(2):575-86.
Department of Psychiatry, Harvard Medical School and Brigham and Women’s Hospital, Boston, MA, USA.
Abstract: Methylmercury (Met-Hg) and ethylmercury (Et-Hg) are powerful toxicants with a range of harmful neurological effects in humans and animals. While Met-Hg is a recognized trigger of oxidative stress and an endocrine disruptor impacting neurodevelopment, the developmental neurotoxicity of Et-Hg, a metabolite of thimerosal (TM), has not been explored. We hypothesized that TM exposure during the perinatal period impairs central nervous system development, and specifically the cerebellum, by the mechanism involving oxidative stress. To test this, spontaneously hypertensive rats (SHR) or Sprague-Dawley (SD) rat dams were exposed to TM (200 μg/kg body weight) during pregnancy (G10-G15) and lactation (P5-P10). Male and female neonates were evaluated for auditory and motor function; cerebella were analyzed for oxidative stress and thyroid metabolism. TM exposure resulted in a delayed startle response in SD neonates and decreased motor learning in SHR male (22.6%), in SD male (29.8%), and in SD female (55.0%) neonates. TM exposure also resulted in a significant increase in cerebellar levels of the oxidative stress marker 3-nitrotyrosine in SHR female (35.1%) and SD male (14.0%) neonates. The activity of cerebellar type 2 deiodinase, responsible for local intra-brain conversion of thyroxine to the active hormone, 3′,3,5-triiodothyronine (T3), was significantly decreased in TM-exposed SHR male (60.9%) pups. This coincided with an increased (47.0%) expression of a gene negatively regulated by T3, Odf4 suggesting local intracerebellar T3 deficiency. Our data thus demonstrate a negative neurodevelopmental impact of perinatal TM exposure which appears to be both strain- and sex-dependent.
Blaxill MF, Redwood L, Bernard S. Thimerosal and autism? A plausible hypothesis that should not be dismissed. Med Hypotheses. 2004;62(5):788-94.
Safe Minds (Sensible Action For Ending Mercury-Induced Neurological Disorders), New Jersey USA.
Abstract: The autism-mercury hypothesis first described by Bernard et al. has generated much interest and controversy. The Institute of Medicine (IOM) reviewed the connection between mercury-containing vaccines and neurodevelopmental disorders, including autism. They concluded that the hypothesis was biologically plausible but that there was insufficient evidence to accept or reject a causal connection and recommended a comprehensive research program. Without citing new experimental evidence, a number of observers have offered opinions on the subject, some of which reject the IOM’s conclusions. In a recent review, Nelson and Bauman argue that a link between the preservative thimerosal, the source of the mercury in childhood vaccines, is improbable. In their defense of thimerosal, these authors take a narrow view of the original hypothesis, provide no new evidence, and rely on selective citations and flawed reasoning. We provide evidence here to refute the Nelson and Bauman critique and to defend the autism-mercury hypothesis.
Christian LM, Iams JD, Porter K, Glaser R. (2011). Inflammatory Responses to Trivalent Influenza Virus Vaccine Among Pregnant Women Vaccine. 8;29(48):8982-7.
Department of Psychiatry, The Ohio State University Medical Center, Columbus, OH
EXCERPT: In the U.S., seasonal trivalent influenza vaccination (TIV) is currently universally recommended for all pregnant women. However, data on the maternal inflammatory response to vaccination is lacking and would better delineate the safety and clinical utility of immunization. Women were assessed prior to and at one day (n=15), two days (n=10), or approximately one week (n=21) following TIV. Serum interleukin (IL)-6, tumor necrosis factor (TNF)-α, C-reactive protein (CRP), and macrophage migration inhibitory factor (MIF) were determined by high sensitivity immunoassay. Significant increases in CRP were seen at one and two days post-vaccination (ps <.05). A similar effect was seen for TNF-α, for which an increase at two days post-vaccination approached statistical significance (p = .06). There was considerable variability in magnitude of response; coefficients of variation for change at two days post-vaccination ranged from 122% to 728%, with the greatest variability in IL-6 responses at this timepoint. The inflammatory response elicited by vaccination is substantially milder and more transient than seen in infectious illness, arguing for the clinical value of vaccination. However, further research is needed to confirm that the mild inflammatory response elicited by vaccination is benign in pregnancy.
These articles are not an exhaustive list of scientific publications (by any means!). These are intended to represent good places to start reading if the goal is to understand why experts are seeking the reasons for increasing rates of developmental disabilities.
Additional articles may be added from time to time.Check back.
| Diagnostic Substitution, Changing Age of Diagnosis, and Increases in Incidence |
Blaxill MF. (2004) What’s going on? The question of time trends in autism. Public Health Rep. 119(6):536-51.
Abstract: Increases in the reported prevalence of autism and autistic spectrum disorders in recent years have fueled concern over possible environmental causes. The author reviews the available survey literature and finds evidence of large increases in prevalence in both the United States and the United Kingdom that cannot be explained by changes in diagnostic criteria or improvements in case ascertainment. Incomplete ascertainment of autism cases in young child populations is the largest source of predictable bias in prevalence surveys; however, this bias has, if anything, worked against the detection of an upward trend in recent surveys. Comparison of autism rates by year of birth for specific geographies provides the strongest basis for trend assessment. Such comparisons show large recent increases in rates of autism and autistic spectrum disorders in both the U.S. and the U.K. Reported rates of autism in the United States increased from < 3 per 10,000 children in the 1970s to > 30 per 10,000 children in the 1990s, a 10-fold increase. In the United Kingdom, autism rates rose from < 10 per 10,000 in the 1980s to roughly 30 per 10,000 in the 1990s. Reported rates for the full spectrum of autistic disorders rose from the 5 to 10 per 10,000 range to the 50 to 80 per 10,000 range in the two countries. A precautionary approach suggests that the rising incidence of autism should be a matter of urgent public concern. Full text
DeSoto, MC & Hitlan RT (2010). Sorting out the spinning of autism: Heavy metals and the question of incidence. Acta Neurobiol Exp 70: 165–176
Abstract: The reasons for the rise in autism prevalence are a subject of heated professional debate. Featuring a critical appraisal of some research used to question whether there is a rise in cases and if rising levels of autism are related to environmental exposure to toxins (Soden et al. 2007, Thompson et al. 2007, Barbaresi et al. 2009) we aim to evaluate the actual state of scientific knowledge. In addition, we surveyed the empirical research on the topic of autism and heavy metal toxins. Overall, the various causes that have led to the increase in autism diagnosis are likely multi-faceted, and understanding the causes is one of the most important health topics today. We argue that scientific research does not support rejecting the link between the neurodevelopmental disorder of autism and toxic exposures.
Gurney JG, Fritz MS, Ness KK, Sievers P, Newschaffer CJ, Shapiro EG. (2003). Analysis of prevalence trends of autism spectrum disorder in Minnesota. Arch Pediatr Adolesc Med.157(7):622-7.
EXCERPT: Alarming increases in the prevalence of autism spectrum disorder have been reported recently in the United States and Europe.We conducted an age-period-birth cohort analysis of special educational disability data from the Minnesota Department of Children, Families & Learning from the 1981-1982 through the 2001-2002 school years. Prevalence rates of autism spectrum disorder rose substantially over time within single-age groups and increased from year to year within birth cohorts. Autism spectrumdisorder prevalence among children aged 6 to 11 years increased from 3 per 10 000 in 1991-1992 to 52 per 10 000 in 2001-2002. All other special educational disability categories also increased during this period, except for mild mental handicap, which decreased slightly from 24 per 10 000 to 23 per 10 000. We found that federal and state administrative changes favoring identification ofautism spectrum disorders corresponded in time with the increasing rates. We observed dramatic increases in the prevalence of autism spectrum disorder as a primary special educational disability starting in the 1991-1992 school year, and the trends show no sign of abatement. We found no corresponding decrease in any special educational disability category to suggest diagnostic substitution as an explanation for the autism trends in Minnesota. We could not assess changes in actual diseaseincidence with these data, but federal and state administrative changes in policy and law favoring better identification and reporting of autism are likely contributing factors to the prevalence increases and may imply that autism spectrum disorder has been underdiagnosed in the past.
Altadottir, H.O., Schendel, D., Dalsgaard, S., Thomsen, P.H. and Thorsen, P. (2007) Time trends in reported diagnoses of childhood neuropsychiatric disorders: A Danish cohort study. Archives of Pediatrics and Adolescent Medicine, 161, 193-199.
Note: This is cumulative incidence using all children born in a large circumscribed region, with autism diagnosed the same way, across time. The increase was clear for both full autism than for autism spectrum disorders, which were considered separately.
Excerpt:….Children were identified in the Danish Medical Birth Registry…..All children born in Denmark from 1990 through 1999, a total of 669 995 children….Cumulative incidence proportion by age, stratified by year of birth, for each disorder. Statistically significant increases were found in cumulative incidence across specific birth years for autism spectrum disorder, childhood autism, hyperkinetic disorder, and Tourette syndrome. No significant change in cumulative incidence was observed for obsessive-compulsive disorder. Recent increases in reported autism diagnoses might not be unique among childhoodneuropsychiatric disorders and might be part of a more widespread epidemiologic phenomenon. The reasons for the observed common pattern of change in reported cumulative incidence could not be determined in this study, but the data underscore the growing awareness of and demand for services for children with neurodevelopmental disorders in general…. the cumulative incidence proportion was significantly higher for children born in 1998-1999 than for both the 1994-1995 (P<.001) and 1996-1997 (P = .02) birth cohorts; for example, at 5 years of age, the cumulative incidence for the 1998-1999 cohort was 62% and 28% higher, respectively, than the cumulative incidences for the 1994-1995 and 1996-1997 cohorts.
DeSoto, M.C. & Hitlan, R.T. (2013). Professional opinion on the question of changes in autism incidence. Open Journal of Psychiatry 3 (2A), 61-67.
Abstract: The question of whether the prevalence increase observed in autism due to an actual increase in the incidence of autism is a matter of concern to professional psychologists, and has been a matter of debate. As professionals trained in diagnosis and research methodology, the opinions of psychologists are of interest. We report the results of what we believe to be the first survey of professional opinion on the topic. Results suggest that among professional psychologists with a terminal degree (n = 88), the majority believe that diagnostic changes can not fully account for the observed increase; 72% reported either the true rate may have, or definitely has, increased. In this sample, the professionals who are certain about the occurrence of a real increase (n=20) are five times as many as those who do not think the increase has occurred (n=4). These results are not meant to document whether or not an increase has or has not occurred, but instead speak to the question of consensus opinion among professional psychologists. What experts believe is an empirical question, and statements about what experts believe should be empirically based. full rext.
Hertz-Picciotto I, Delwiche L. (2009) The rise in autism and the role of age at diagnosis. Epidemiology. 20(1):84-90.
EXCERPT: Autism cases were identified from 1990 through 2006 in databases of the California Department of Developmental Services, which coordinates services for individuals with specific developmental disorders. The main outcomes were population incident cases younger than age 10 years for each quarter,cumulative incidence by age and birth year, age-specific incidence rates stratified by birth year, and proportions of diagnoses by age across birth years. Autism incidence in children rose throughout the period. Cumulative incidence to 5 years of age per 10,000 births rose consistently from 6.2 for 1990 births to 42.5 for 2001 births. Age-specific incidence rates increased most steeply for 2- and 3-year olds. The proportion diagnosed by age 5 years increased only slightly, from 54% for 1990 births to 61% for 1996 births. Changing age at diagnosis can explain a 12% increase, and inclusion of milder cases, a 56% increase. Autism incidence in California shows no sign yet of plateauing. Younger ages at diagnosis, differential migration, changes in diagnostic criteria, and inclusion of milder cases do not fully explain the observed increases. Other artifacts have yet to be quantified, and as a result, the extent to which the continued rise represents a true increase in the occurrence of autism remains unclear.
These articles are not presented as an exhaustive list of scientific publications (by any means!). These are intended to represent good places to start reading if the goal is to understand expert views regarding how and why developmental disabilities occur in predisposed individuals.
Additional articles may be added from time to time.Check back.
|Persons with ASD may have a biological vulnerability to toxins. |
Obviously not everyone exposed to a toxin develops a lifelong disability, the idea is that some do — and — that the vulnerability can be discovered leading to prevention.
Sharpe MA, Gist TL, Baskin DS.(2013). B-Lymphocytes from a Population of Children with Autism Spectrum Disorder and Their Unaffected Siblings Exhibit Hypersensitivity to Thimerosal J Toxicol.
Abstract: The role of thimerosal containing vaccines in the development of autism spectrum disorder (ASD) has been an area of intense debate, as has the presence of mercury dental amalgams and fish ingestion by pregnant mothers. We studied the effects of thimerosal on cell proliferation and mitochondrial function from B-lymphocytes taken from individuals with autism, their nonautistic twins, and their nontwin siblings. Eleven families were examined and compared to matched controls. B-cells were grown with increasing levels of thimerosal, and various assays (LDH, XTT, DCFH, etc.) were performed to examine the effects on cellular proliferation and mitochondrial function. A subpopulation of eight individuals (4 ASD, 2 twins, and 2 siblings) from four of the families showed thimerosal hypersensitivity, whereas none of the control individuals displayed this response. The thimerosal concentration required to inhibit cell proliferation in these individuals was only 40% of controls. Cells hypersensitive to thimerosal also had higher levels of oxidative stress markers, protein carbonyls, and oxidant generation. This suggests certain individuals with a mild mitochondrial defect may be highly susceptible to mitochondrial specific toxins like the vaccine preservative thimerosal.
James, SJ, Cutler, P, Melnyk, S, Jernigan, S, Janak, L, Gaylor, DW, Neubrander JA, (2004). Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. American Journal of Clinical Nutrition, 80 (6), 1611-1617.
EXCERPT: Although abnormal metabolism of methionine and homocysteine has been associated with other neurologic diseases, these pathways have not been evaluated in persons with autism. Plasma concentrations of methionine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), adenosine, homocysteine, cystathionine, cysteine, and oxidized and reduced glutathione were measured in 20 children with autism and in 33 control children. On the basis of the abnormal metabolic profile, a targeted nutritional intervention trial with folinic acid, betaine, and methylcobalamin was initiated in a subset of the autistic children. Relative to the control children, the children with autism had significantly lower baseline plasma concentrations of methionine, SAM, homocysteine, cystathionine, cysteine, and total glutathione and significantly higher concentrations of SAH, adenosine, and oxidized glutathione. This metabolic profile is consistent with impaired capacity for methylation (significantly lower ratio of SAM to SAH) and increased oxidative stress (significantly lower redox ratio of reduced glutathione to oxidized glutathione) in children with autism. The intervention trial was effective in normalizing the metabolic imbalance in the autistic children.
Kern JK, Jones AM. (2006). Evidence of Toxicity, Oxidative Stress, and Neuronal Insult in Autism J Toxicol Environ Health B Crit Rev. 9(6):485-99.
Abstract: According to the Autism Society of America, autism is now considered to be an epidemic. The increase in the rate of autism revealed by epidemiological studies and government reports implicates the importance of external or environmental factors that may be changing. This article discusses the evidence for the case that some children with autism may become autistic from neuronal cell death or brain damage sometime after birth as result of insult; and addresses the hypotheses that toxicity and oxidative stress may be a cause of neuronal insult in autism. The article first describes the Purkinje cell loss found in autism, Purkinje cell physiology and vulnerability, and the evidence for postnatal cell loss. Second, the article describes the increased brain volume in autism and how it may be related to the Purkinje cell loss. Third, the evidence for toxicity and oxidative stress is covered and the possible involvement of glutathione is discussed. Finally, the article discusses what may be happening over the course of development and the multiple factors that may interplay and make these children more vulnerable to toxicity, oxidative stress, and neuronal insult.
James SJ, Slikker W 3rd, Melnyk S, New E, Pogribna M, Jernigan S. (2005). Thimerosal Neurotoxicity is Associated with Glutathione Depletion: Protection with Glutathione Precursors Neurotoxicology. 2005 Jan;26(1):1-8.
Abstract: Thimerosol is an antiseptic containing 49.5% ethyl mercury that has been used for years as a preservative in many infant vaccines and in flu vaccines. Environmental methyl mercury has been shown to be highly neurotoxic, especially to the developing brain. Because mercury has a high affinity for thiol (sulfhydryl (-SH)) groups, the thiol-containing antioxidant, glutathione (GSH), provides the major intracellular defense against mercury-induced neurotoxicity. Cultured neuroblastoma cells were found to have lower levels of GSH and increased sensitivity to thimerosol toxicity compared to glioblastoma cells that have higher basal levels of intracellular GSH. Thimerosal-induced cytotoxicity was associated with depletion of intracellular GSH in both cell lines. Pretreatment with 100 microM glutathione ethyl ester or N-acetylcysteine (NAC), but not methionine, resulted in a significant increase in intracellular GSH in both cell types. Further, pretreatment of the cells with glutathione ethyl ester or NAC prevented cytotoxicity with exposure to 15 microM Thimerosal. Although Thimerosal has been recently removed from most children’s vaccines, it is still present in flu vaccines given to pregnant women, the elderly, and to children in developing countries. The potential protective effect of GSH or NAC against mercury toxicity warrants further research as possible adjunct therapy to individuals still receiving Thimerosal-containing vaccinations.
Rossignol DA & Frye RE (2011) Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis Molecular Psychiatry
Abstract: A comprehensive literature search was performed to collate evidence of mitochondrial dysfunction in autism spectrum disorders (ASDs) with two primary objectives. First, features of mitochondrial dysfunction in the general population of children with ASD were identified. Second, characteristics of mitochondrial dysfunction in children with ASD and concomitant mitochondrial disease (MD) were compared with published literature of two general populations: ASD children without MD, and non-ASD children with MD. The prevalence of MD in the general population of ASD was 5.0% (95% confidence interval 3.2, 6.9%), much higher than found in the general population (~0.01%). The prevalence of abnormal biomarker values of mitochondrial dysfunction was high in ASD, much higher than the prevalence of MD. Variances and mean values of many mitochondrial biomarkers (lactate, pyruvate, carnitine and ubiquinone) were significantly different between ASD and controls. Some markers correlated with ASD severity. Neuroimaging, in vitro and post-mortem brain studies were consistent with an elevated prevalence of mitochondrial dysfunction in ASD. Taken together, these findings suggest children with ASD have a spectrum of mitochondrial dysfunction of differing severity. Eighteen publications representing a total of 112 children with ASD and MD (ASD/MD) were identified. The prevalence of developmental regression (52%), seizures (41%), motor delay (51%), gastrointestinal abnormalities (74%), female gender (39%), and elevated lactate (78%) and pyruvate (45%) was significantly higher in ASD/MD compared with the general ASD population. The prevalence of many of these abnormalities was similar to the general population of children with MD, suggesting that ASD/MD represents a distinct subgroup of children with MD. Most ASD/MD cases (79%) were not associated with genetic abnormalities, raising the possibility of secondary mitochondrial dysfunction. Treatment studies for ASD/MD were limited, although improvements were noted in some studies with carnitine, co-enzyme Q10 and B-vitamins. Many studies suffered from limitations, including small sample sizes, referral or publication biases, and variability in protocols for selecting children for MD workup, collecting mitochondrial biomarkers and defining MD. Overall, this evidence supports the notion that mitochondrial dysfunction is associated with ASD. Additional studies are needed to further define the role of mitochondrial dysfunction in ASD.
Nataf R, Skorupka C, Amet L, Lam A, Springbett A, Lathe R. (2006). Porphyrinuria in childhood autistic disorder: Implications for environmental toxicity Toxicology and Applied Pharmacology, 2006 Jul 15;214(2):99-108. Epub 2006 Jun 16.
Abstract: To address a possible environmental contribution to autism, we carried out a retrospective study on urinary porphyrin levels, a biomarker of environmental toxicity, in 269 children with neurodevelopmental and related disorders referred to a Paris clinic (2002–2004), including 106 with autistic disorder. Urinary porphyrin levels determined by high-performance liquid chromatography were compared between diagnostic groups including internal and external control groups. Coproporphyrin levels were elevated in children with autistic disorder relative to control groups. Elevation was maintained on normalization for age or to a control heme pathway metabolite (uroporphyrin) in the same samples. The elevation was significant (P < 0.001). Porphyrin levels were unchanged in Asperger’s disorder, distinguishing it from autistic disorder.The atypical molecule precoproporphyrin, a specific indicator of heavy metal toxicity, was also elevated in autistic disorder (P < 0.001) but not significantly in Asperger’s. A subgroup with autistic disorder was treated with oral dimercaptosuccinic acid (DMSA) with a view to heavy metal removal. Following DMSA there was a significant (P = 0.002) drop in urinary porphyrin excretion. These data implicate environmental toxicity in childhood autistic disorder.
Poling JS, Frye, RE, Schoffer J, Zimmerman AW (2006). Developmental Regression and Mitochondrial Dysfunction in a Child With Autism J Child Neurol. 2006 Feb;21(2):170-2.
Note : this is a case study of the first author’s child, Hannah Poling, who received significant media attention.
Abstract: Autistic spectrum disorders can be associated with mitochondrial dysfunction. We present a singleton case of developmental regression and oxidative phosphorylation disorder in a 19-month-old girl. Subtle abnormalities in the serum creatine kinase level, aspartate aminotransferase, and serum bicarbonate led us to perform a muscle biopsy, which showed type I myofiber atrophy, increased lipid content, and reduced cytochrome c oxidase activity. There were marked reductions in enzymatic activities for complex I and III. Complex IV (cytochrome c oxidase) activity was near the 5% confidence level. To determine the frequency of routine laboratory abnormalities in similar patients, we performed a retrospective study including 159 patients with autism (Diagnostic and Statistical Manual of Mental Disorders-IV and Childhood Autism Rating Scale) not previously diagnosed with metabolic disorders and 94 age-matched controls with other neurologic disorders. Aspartate aminotransferase was elevated in 38% of patients with autism compared with 15% of controls (P <.0001). The serum creatine kinase level also was abnormally elevated in 22 (47%) of 47 patients with autism. These data suggest that further metabolic evaluation is indicated in autistic patients and that defects of oxidative phosphorylation might be prevalent. Full text
…still under construction
These articles are not an exhaustive list of scientific publications (by any means!). These are intended to represent good places to start reading if the goal is to understand why experts are seeking the reasons for increasing rates of developmental disabilities.
Additional articles may be added from time to time.Check back.
|Links between autism and toxins broadly defined. |
….Still Under Construction
DeSoto, M.C. (2009). Ockham’s Razor and Autism: The case for developmental neurotoxins contributing to a disease of neurodevelopment. Neurotoxicology, 30 (3). 331-337.
Abstract: Much professional awareness regarding environmental triggers for ASD has been narrowly focused on a single possible exposure pathway (vaccines). Meanwhile, empirical support for environmental toxins as a broad class has been quietly accumulating. Recent research has shown that persons with ASD have comparatively higher levels of various toxins and are more likely to have reduced detoxifying ability, and, that rates of ASD may be higher in areas with greater pollution. This report documents that within the state with the highest rate of ASD, the rate is higher for schools near EPA Superfund sites, t (332)=3.84, p=.0001. The reasons for the rise in diagnoses likely involve genetically predisposed individuals being exposed to various environmental triggers at higher rates than in past generations. Full text.
Shelton JF, Hertz-Picciotto I, Pessah IN. (2012). Tipping the balance of autism risk: potential mechanisms linking pesticides and autism. Environ Health Perspect. 120(7):944-51
EXCERPT: Autism spectrum disorders (ASDs) have been increasing in many parts of the world and a portion of cases are attributable to environmental exposures. Conclusive replicated findings have yet to appear on any specific exposure; however, mounting evidence suggests gestational pesticides exposures are strong candidates. Because multiple developmental processes are implicated in ASDs during gestation and early life, biological plausibility is more likely if these agents can be shown to affect core pathophysiological features. On the basis of experimental and observational research, certain pesticides may be capable of inducing core features of autism, but little is known about the timing or dose, or which of various mechanisms is sufficient to induce this condition. In animal studies, we encourage more research on gene × environment interactions, as well as experimental exposure to mixtures of compounds. Similarly, epidemiologic studies in humans with exceptionally high exposures can identify which pesticide classes are of greatest concern, and studies focused on gene × environment are needed to determine if there are susceptible subpopulations at greater risk from pesticide exposures.
B. Eskenazi, A.R. Marks, A. Bradman, K. Harley, D.B. Barr, C. Johnson et al. (2007). Organophosphate pesticide exposure and neurodevelopment in young Mexican-American children Environmental Health Perspectives, 115 (2007), pp. 792–798
EXCERPT: Organophosphate (OP) pesticides are widely used in agriculture and homes. Animal studies suggest that even moderate doses are neurodevelopmental toxicants, but there are few studies in humans. We investigated the relationship of prenatal and child OP urinary metabolite levels with children’s neurodevelopment. We measured six nonspecific dialkylphosphate (DAP) metabolites in maternal and child urine as well as metabolites specific to malathion (MDA) and chlorpyrifos (TCPy) in maternal urine. We examined their association with children’s performance at 6 (n = 396), 12 (n = 395), and 24 (n = 372) months of age on the Bayley Scales of Infant Development [Mental Development (MDI) and Psychomotor Development (PDI) Indices] and mother’s report on the Child Behavior Checklist (CBCL) (n = 356). Generally, pregnancy DAP levels were negatively associated with MDI, but child measures were positively associated. At 24 months of age, these associations reached statistical significance [per 10-fold increase in prenatal DAPs: β = −3.5 points; 95% confidence interval (CI), −6.6 to −0.5; child DAPs: β = 2.4 points; 95% CI, 0.5 to 4.2]. Neither prenatal nor child DAPs were associated with PDI or CBCL attention problems, but both prenatal and postnatal DAPs were associated with risk of pervasive developmental disorder [per 10-fold increase in prenatal DAPs: odds ratio (OR) = 2.3, p = 0.05; child DAPs OR = 1.7, p = 0.04].
Palmer RF, Blanchard S, Wood R (2009). Proximity to point sources of environmental mercury release as a predictor of autism prevalence. Health and Place 15 (1) 18-24.
Abstract: The objective of this study was to determine if proximity to sources of mercury pollution in 1998 were related to autism prevalence in 2002. Autism count data from the Texas Educational Agency and environmental mercury release data from the Environmental Protection Agency were used. We found that for every 1000 pounds of industrial release, there was a corresponding 2.6% increase in autism rates (p<.05) and a 3.7% increase associated with power plant emissions (p<.05). Distances to these sources were independent predictors after adjustment for relevant covariates. For every 10 miles from industrial or power plant sources, there was an associated decreased autism Incident Risk of 2.0% and 1.4%, respectively (p<.05). While design limitations preclude interpretation of individual risk, further investigations of environmental risks to child development issues are warranted. Full text
|These articles are not an exhaustive list of scientific publications on the topic. Rather, this represents an attempt to provide a partial answer to why ‘some people say’ there are concerns about vaccines. These are intended to represent good places to start reading if someone is curious. |
Additional articles may be added from time to time. Check back.
Vaccine concerns broadly defined.
…still Under Construction
.….a few to start….
In 1995 as published in Lancet by Thompson et al, 3545 MMR vaccinated persons were compared to some 11,000 non vaccinated MMR persons. Total risk of inflammatory bowel disease was 3 fold higher in those who received vaccination.Lancet. 1995 Apr 29;345(8957):1071-4. Read it
In 1999, Fisher and Ekland reported in the journal Epidemiology: “we calculated the risk of liver problems among hepatitis B vaccinated and non-hepatitis b vaccinated children using logistic regression. Hepatitis B vaccinated children…” were found to have 3 fold increase in liver problems compared to non vaccinated children. Read it
Dr. McDonald and colleagues of the University of Manitoba (2008) published in the J. of Allergy and Clinical Immunology on the effect of delaying DPT vaccination so that the vaccination occurred- but was given later rather than earlier in infancy. A total of 11,531 kids were studied. A delay of two months in the initial DPT shot was associated with a 50% cut in asthma diagnosis. Read it
Granoff and colleagues publishing in the New England Journal of Medicine (1986) studied a group of children who got HIB Meningitis even though they were vaccinated. These kids were compared to other kids who did not get the vaccine, but also got HIB meningitis. The idea was to try and figure out why the vaccine failed. Kids who were vaccinated had very low immune responses to the disease compared to kids who had not been vaccinated. Read it
Daum et al reported corroborating findings in the Journal of Pediatrics. They measured antibodies in 48 persons after they got an HIB shot and antibodies (immune response) did not increase, they dropped. Read it
Petrik and colleagues documented that vaccine ingredients (adjuvants) injected in mice at levels equivalent to those given to humans caused motor deficits, cognitive deficits, and neural loss. This was a controlled experiment documenting harm from vaccine ingredients. It is important to further the finding because sometimes vaccine safety studies that report no effects use “control groups” for comparison who get injected with adjuvants, rather than injected with placebo. Neuromolecular Medicine. 2007; 9(1):83 – 100.
Classen and colleagues published (2002) in the journal Autoimmunity. First, they gave the HIB vaccine to mice and showed that the vaccine itself triggered insulin-dependent diabetes in mice… and then also a comparison: 116,000 HIB vaccinated children had a significantly higher rate of diabetes compared to 128,000 children who did not have the vaccine. Read it
Experimental research examined whether acquisition of neonatal reflexes in newborn rhesus macaques was influenced by receipt of a single neonatal dose of hepatitis B vaccine containing the preservative thimerosal. Yes, adverse effects were found. J Toxicol Environ Health A. 2010;73(19):1298-313. doi: 10.1080/15287394.2010.484709.
Sood and colleagues, writing in the Journal of Pediatrics, gave HIB vaccines to animals and then exposed them to the HIB virus. This is what is called a controlled experiment. It is the kind that allows cause and effect statements to be made: this kind of control cannot be usually be done with humans…..Know that approximately 90% of the vaccinated group came down with HIB. And – there was a control group of unvaccinated rats who also were exposed to the same HIB virus. but only 17% of the unvaccinated rats got HIB. Read it