Written by Ginger Taylor http://www.canaryparty.org
In 2007 I posted a list of 16 studies that supported the vaccine/autism link, and told people that I was sick of hearing that there was NO SCIENCE that showed vaccines can cause autism. The list has now grown to 67 studies, and I am still hearing the same stupid parroting of Pharma BS talking points.
Parents… and parents to be… please pay close attention, question everything that you are being told by doctors and take charge of your health choices for your family! I wish I had known this BEFORE I had children.
Here, for your edification, the research that public health officials like to pretend does not exist, because they would likely be fired or jailed for not acting on it when it was published in the first place:
Studies supporting vaccine/autism causation
1. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism
American Journal of Clinical Nutrition, Vol. 80, No. 6, 1611-1617, December 2004
Department of Pediatrics, University of Arkansas for Medical Sciences, and the Arkansas Children’s Hospital Research Institute
Conclusions: An increased vulnerability to oxidative stress and a decreased capacity for methylation may contribute to the development and clinical manifestation of autism.
2. Porphyrinuria in childhood autistic disorder: Implications for environmental toxicity
Toxicology and Applied Pharmacology, 2006
Robert Natafa, Corinne Skorupkab, Lorene Ametb, Alain Lama, Anthea Springbettc and Richard Lathed, aLaboratoire Philippe Auguste, Paris, France, Association ARIANE, Clichy, France, Department of Statistics, Roslin Institute, Roslin, UK, Pieta Research,
This new study from France utilizes a new and sophisticated measurement for environmental toxicity by assessing porphyrin levels in autistic children. It provides clear and unequivocal evidence that children with autism spectrum disorders are more toxic than their neurotypical peers.
Excerpt: “Coproporphyrin levels were elevated in children with autistic disorder relative to control groups…the elevation was significant. These data implicate environmental toxicity in childhood autistic disorder.”
3. Uncoupling of ATP-mediated Calcium Signaling and Dysregulated IL-6 Secretion in Dendritic Cells by Nanomolar Thimerosal
Environmental Health Perspectives, July 2006.
Samuel R. Goth, Ruth A. Chu Jeffrey P. Gregg
This study demonstrates that very low-levels of Thimerosal can contribute to immune system disregulation.
Excerpt: “Our findings that DCs primarily express the RyR1 channel complex and that this complex is uncoupled by very low levels of THI with dysregulated IL-6 secretion raise intriguing questions about a molecular basis for immune dyregulation and the possible role of the RyR1 complex in genetic susceptibility of the immune system to mercury.”
4. Comparison of Blood and Brain Mercury Levels in Infant Monkeys Exposed to Methylmercury or Vaccines Containing Thimerosal
Environmental Health Perspectives, Aug 2005.
Thomas Burbacher, PhD, University of Washington.
This study demonstrates clearly and unequivocally that ethyl mercury, the kind of mercury found in vaccines, not only ends up in the brain, but leaves double the amount of inorganic mercury as methyl mercury, the kind of mercury found in fish. This work is groundbreaking because little is known about ethyl mercury, and many health authorities have asserted that the mercury found in vaccines is the “safe kind.” This study also delivers a strong rebuke of the Institute of Medicine’s recommendation in 2004 to no longer pursue the mercury-autism connection.
Excerpt: “A recently published IOM review (IOM 2004) appears to have abandoned the earlier recommendation [of studying mercury and autism] as well as back away from the American Academy of Pediatrics goal [of removing mercury from vaccines]. This approach is difficult to understand, given our current limited knowledge of the toxicokinetics and developmental neurotoxicity of thimerosal, a compound that has been (and will continue to be) injected in millions of newborns and infants.”
6. Increases in the number of reactive glia in the visual cortex of Macaca fascicularis following subclinical long-term methyl mercury exposure.
Toxicology and Applied Pharmacology, 1994
Charleston JS, Bolender RP, Mottet NK, Body RL, Vahter ME, Burbacher TM., Department of Pathology, School of Medicine, University of Washington
The number of neurons, astrocytes, reactive glia, oligodendrocytes, endothelia, and pericytes in the cortex of the calcarine sulcus of adult female Macaca fascicularis following long-term subclinical exposure to methyl mercury (MeHg) and mercuric chloride (inorganic mercury; IHg) has been estimated by use of the optical volume fractionator stereology technique. Four groups of monkeys were exposed to MeHg (50 micrograms Hg/kg body wt/day) by mouth for 6, 12, 18, and 12 months followed by 6 months without exposure (clearance group). A fifth group of monkeys was administered IHg (as HgCl2; 200 micrograms Hg/kg body wt/day) by constant rate intravenous infusion via an indwelling catheter for 3 months. Reactive glia showed a significant increase in number for every treatment group, increasing 72% in the 6-month, 152% in the 12-month, and 120% in the 18-month MeHg exposed groups, and the number of reactive glia in the clearance group remained elevated (89%). The IHg exposed group showed a 165% increase in the number of reactive glia. The IHg exposed group and the clearance group had low levels of MeHg present within the tissue; however, the level of IHg was elevated in both groups. These results suggest that the IHg may be responsible for the increase in reactive glia. All other cell types, including the neurons, showed no significant change in number at the prescribed exposure level and durations. The identities of the reactive glial cells and the implications for the long-term function and survivability of the neurons due to changes in the glial population following subclinical long-term exposure to mercury are discussed.
7. Neuroglial Activation and Neuroinflammation in the Brain of Patients with Autism
Annals of Neurology, Feb 2005.
Diana L. Vargas, MD, Johns Hopkins University.
This study, performed independently and using a different methodology than Dr. Herbert (see above) reached the same conclusion: the brains of autistic children are suffering from inflammation.
Excerpt: “Because this neuroinflammatory process appears to be associated with an ongoing and chronic mechanism of CNS dysfunction, potential therapeutic interventions should focus on the control of its detrimental effects and thereby eventually modify the clinical course of autism.”
8. Autism: A Brain Disorder, or A Disorder That Affects the Brain?
Clinical Neuropsychiatry, 2005
Martha R. Herbert M.D., Ph.D., Harvard University
Autism is defined behaviorally, as a syndrome of abnormalities involving language, social reciprocity and hyperfocus or reduced behavioral flexibility. It is clearly heterogeneous, and it can be accompanied by unusual talents as well as by impairments, but its underlying biological and genetic basis in unknown. Autism has been modeled as a brain-based, strongly genetic disorder, but emerging findings and hypotheses support a broader model of the condition as a genetically influenced and systemic. These include imaging, neuropathology and psychological evidence of pervasive (and not just specific) brain and phenotypic features; postnatal evolution and chronic persistence of brain, behavior and tissue changes (e.g. inflammation) and physical illness symptomatology (e.g. gastrointestinal, immune, recurrent infection); overlap with other disorders; and reports of rate increases and improvement or recovery that support a role for modulation of the condition by environmental factors (e.g. exacerbation or triggering by toxins, infectious agents, or others stressors, or improvement by treatment). Modeling autism more broadly encompasses previous work, but also encourages the expansion of research and treatment to include intermediary domains of molecular and cellular mechanisms, as well as chronic tissue, metabolic and somatic changes previously addressed only to a limited degree. The heterogeneous biologies underlying autism may conceivably converge onto the autism profile via multiple mechanisms on the one hand and processing and connectivity abnormalities on the other may illuminate relevant final common pathways and contribute to focusing on the search for treatment targets in this biologically and etiologically heterogeneous behavioral syndrome.
9. Activation of Methionine Synthase by Insulin-like Growth Factor-1 and Dopamine: a Target for Neurodevelopmental Toxins and Thimerosal
Molecular Psychiatry, July 2004.
Richard C. Deth, PhD, Northeastern University.
Excerpt: “The potent inhibition of this pathway [methylation] by ethanol, lead, mercury, aluminum, and thimerosal suggests it may be an important target of neurodevelopmental toxins.”
10. Validation of the Phenomenon of Autistic Regression Using Home Videotapes
Archives of General Psychiatry, 2005
Emily Werner, PhD; Geraldine Dawson, PhD, University of Washington
Objective To validate parental report of autistic regression using behavioral data coded from home videotapes of children with autism spectrum disorder (ASD) vs typical development taken at 12 and 24 months of age.
Conclusion: “This study validates the existence of early autistic regression.”
11. Blood Levels of Mercury Are Related to Diagnosis of Autism: A Reanalysis of an Important Data Set
Journal of Child Neurology, Vol. 22, No. 11, 1308-1311 (2007)
M. Catherine DeSoto, PhD, Robert T. Hitlan, PhD -Department of Psychology, University of Northern Iowa, Cedar Falls, Iowa
Excerpt: “We have reanalyzed the data set originally reported by Ip et al. in 2004 and have found that the original p value was in error and that a significant relation does exist between the blood levels of mercury and diagnosis of an autism spectrum disorder. Moreover, the hair sample analysis results offer some support for the idea that persons with autism may be less efficient and more variable at eliminating mercury from the blood.”
12. Empirical Data Confirm Autism Symptoms Related to Aluminum and Acetaminophen Exposure
Entropy, November 7, 2012
Stephanie Seneff, Robert M. Davidson and Jingjing Liu
Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA, Internal Medicine Group Practice, PhyNet, Inc., Longview, TX
” 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.”
13. Developmental Regression and Mitochondrial Dysfunction in a Child With Autism
Journal of Child Neurology / Volume 21, Number 2, February 2006 Jon S. Poling, MD, PhD, Department of Neurology and Neurosurgery Johns Hopkins Hospital
This article showed that 38% of Kennedy Krieger Institute autism patients studied had one marker for impaired oxidative phosphorylation (mitochondrial dysfunction), and 47% had a second marker.
Excerpt: “Children who have (mitochondrial-related) dysfunctional cellular energy metabolism might be more prone to undergo autistic regression between 18 and 30 months of age if they also have infections or immunizations at the same time.”
14. Oxidative Stress in Autism: Elevated Cerebellar 3-nitrotyrosine Levels
American Journal of Biochemistry and Biotechnology 4 (2): 73-84, 2008
Elizabeth M. Sajdel-Sulkowska, – Dept of Psychiatry, Harvard Medical School
Shows a potential link between mercury and the autopsied brains of young people with autism. A marker for oxidative stress was 68.9% higher in autistic brain issue than controls (a statistically significant result), while mercury levels were 68.2% higher.
Excerpt: The preliminary data suggest a need for more extensive studies of oxidative stress, its relationship to the environmental factors and its possible attenuation by antioxidants in autism.”
15. Large Brains in Autism: The Challenge of Pervasive Abnormality
The Neuroscientist, Volume 11, Number 5, 2005.
Martha Herbert, MD, PhD, Harvard University.
Excerpt: “Oxidative stress, brain inflammation, and microgliosis have been much documented in association with toxic exposures including various heavy metals…the awareness that the brain as well as medical conditions of children with autism may be conditioned by chronic biomedical abnormalities such as inflammation opens the possibility that meaningful biomedical interventions may be possible well past the window of maximal neuroplasticity in early childhood because the basis for assuming that all deficits can be attributed to fixed early developmental alterations in neural architecture has now been undermined.”
“neuroinflammation appears to be present in autistic brain tissue from childhood through adulthood.” Dr. Herbert suggests that chronic disease or an external environmental source (like heavy metals) may be causing the inflammation.”
16. Evidence of Toxicity, Oxidative Stress, and Neuronal Insult in Autism
Journal of Toxicology and Environmental Health, Nov-Dec 2006.
Janet Kern, Anne Jones
“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 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.”
17. Oxidative Stress in Autism
Abha Chauhan, Ved Chauhan
This study provides a helpful overview of the growing evidence supporting the link between oxidative stress and autism.
Excerpt: “Upon completion of this article, participants should be able to: 1. Be aware of laboratory and clinical evidence of greater oxidative stress in autism. 2. Understand how gut, brain, nutritional, and toxic status in autism are consistent with greater oxidative stress. 3. Describe how anti-oxidant nutrients are used in the contemporary treatment of autism.”
18. Thimerosal Neurotoxicity is Associated with Glutathione Depletion: Protection with Glutathione Precursors
Neurotoxicology, Jan 2005.
S. Jill James, PhD, University of Arkansas.
This recent study demonstrates that Thimerosal lowers or inhibits the body’s ability to produce Glutathione, an antioxidant and the body’s primary cellular-level defense against mercury.
Excerpt: “Thimerosal-induced cytotoxicity was associated with depletion of intracellular Glutathione in both cell lines…The potential effect of Glutathione or N-acetylcysteine against mercury toxicity warrants further research as possible adjunct therapy to individuals still receiving Thimerosal-containing vaccines.”
19. Aluminum adjuvant linked to gulf war illness induces motor neuron death in mice
Neuromolecular Medicine, 2007
Christopher Shaw, Ph.D., University of British Columbia, Vancouver, Canada]
This study demonstrates the extreme toxicity of the aluminum adjuvant used as a preservative in vaccines.
Excerpt: “testing showed motor deficits in the aluminum treatment group that expressed as a progressive decrease in strength measured…Significant cognitive deficits in water-maze learning were observed in the combined aluminum and squalene group…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.
20. Environmental mercury release, special education rates, and autism disorder: an ecological study of Texas
Health & Place, 2006
Raymond F. Palmer, University of Texas Health Science Center
This study demonstrated the correlation between environmental mercury and autism rates in Texas.
Excerpt: “On average, for each 1,000 lb of environmentally released mercury, there was a 43% increase in the rate of special education services and a 61% increase in the rate of autism. The association between environmentally released mercury and special education rates were fully mediated by increased autism rates. This ecological study suggests the need for further research regarding the association between environmentally released mercury and developmental disorders such as autism.”
21. Autism Spectrum Disorders in Relation to Distribution of Hazardous Air Pollutants in the SF Bay Area
Environmental Health Perspectives – Vol. 114 No. 9, September, 2006
Gayle Windham, Div. of Environmental and Occupational Disease Control, California Department of Health Services
284 ASD children & 657 controls, born in 1994 in Bay Area, were assigned exposure levels by birth tract for 19 chemicals. Risks for autism were elevated by 50% in tracts with the highest chlorinated solvents and heavy metals. The highest risk compounds were mercury, cadmium, nickel, trichloroethylene, and vinyl chloride, and the risk from heavy metals was almost twice as high as solvents.
Excerpt: “Our results suggest a potential association between autism and estimated metal concentrations, and possibly solvents, in ambient air around the birth residence.”
22. A Case Series of Children with Apparent Mercury Toxic Encephalopathies Manifesting with Clinical Symptoms of Regressive Autistic Disorder
Journal of Toxicology and Environmental Health, 2007
David A. Geier, Mark R. Geier
This study reviewed the case histories and medical profiles of nine autistic children and concluded that eight of the nine children were mercury toxic and this toxicity manifested itself in a manner consistent with Autism Spectrum Disorders.
Excerpt: “…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.”
23. Attention-deficit hyperactivity disorder and blood mercury level: a case-control study in chinese children
Neuropediatrics, August 2006 – P.R. Kong, Department of Pediatrics and Adolescent Medicine, The University of Hong Kong.
This study demonstrates that blood mercury levels are higher for children with ADHD.
Excerpt: “There was significant difference in blood mercury levels between cases and controls, which persists after adjustment for age, gender and parental occupational status. The geometric mean blood mercury level was also significantly higher in children with inattentive and combined subtypes of ADHD. High blood mercury level was associated with ADHD. Whether the relationship is causal requires further studies.”
24. The Changing Prevalence of Autism In California
Journal of Autism and Developmental Disorders, April 2003 Mark Blaxill, MBA
This study helps to refute the supposition made by some researchers that autism’s epidemic may only be due to “diagnostic substitution”.
25. Mitochondrial Energy-Deficient Endophenotype in Autism
American Journal of Biochemistry and Biotechnology 4 (2): 198-207, 2008
J. Jay Gargus and Faiqa Imtiaz Department of Physiology and Biophysics and Department of Pediatrics, Section of Human Genetics, School of Medicine, University of California, Irvine, Arabian Diagnostics Laboratory, King Faisal Specialist Hospital and Research Centre
Abstract: While evidence points to a multigenic etiology of most autism, the pathophysiology of the disorder has yet to be defined and the underlying genes and biochemical pathways they subserve remain unknown. Autism is considered to be influenced by a combination of various genetic, environmental and immunological factors; more recently, evidence has suggested that increased vulnerability to oxidative stress may be involved in the etiology of this multifactorial disorder.
Furthermore, recent studies have pointed to a subset of autism associated with the biochemical endophenotype of mitochondrial energy deficiency, identified as a subtle impairment in fat and carbohydrate oxidation. This phenotype is similar, but more subtle than those seen in classic mitochondrial defects. In some cases the beginnings of the genetic underpinnings of these mitochondrial defects are emerging, such as mild mitochondrial dysfunction and secondary carnitine deficiency observed in the subset of autistic patients with an inverted duplication of chromosome 15q11-q13. In addition, rare cases of familial autism associated with sudden infant death syndrome (SIDS) or associated with abnormalities in cellular calcium homeostasis, such as malignant hyperthermia or cardiac arrhythmia, are beginning to emerge. Such special cases suggest that the pathophysiology of autism may comprise pathways that are directly or indirectly involved in mitochondrial energy production and to further probe this connection three new avenues seem worthy of exploration: 1) metabolomic clinical studies provoking controlled aerobic exercise stress to expand the biochemical phenotype, 2) high-throughput expression arrays to directly survey activity of the genes underlying these biochemical pathways and 3) model systems, either based upon neuronal stem cells or model genetic organisms, to discover novel genetic and environmental inputs into these pathways.
26. Bridging from Cells to Cognition in Autism Pathophysiology: Biological Pathways to Defective Brain Function and Plasticity
American Journal of Biochemistry and Biotechnology 4 (2): 167-176, 2008
Matthew P. Anderson, Brian S. Hooker and Martha R. Herbert Departments of Neurology and Pathology, Harvard Medical School/Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, High Throughput Biology Team, Fundamental Science Directorate, Pacific Northwest National Laboratory, Pediatric Neurology/Center for Morphometric Analysis, Massachusetts General Hospital/Harvard Medical School, and Center for Child and Adolescent Development, Cambridge Health Alliance/Harvard Medical School
“ In autism, over-zealous neuroinflammatory responses could not only influence neural developmental processes, but may more significantly impair neural signaling involved in cognition in an ongoing fashion.”
27. Heavy-Metal Toxicity—With Emphasis on Mercury
John Neustadt, ND, and Steve Pieczenik, MD, PhD
Conclusion: Metals are ubiquitous in our environment, and exposure to them is inevitable. However, not all people accumulate toxic levels of metals or exhibit symptoms of metal toxicity, suggesting that genetics play a role in their potential to damage health. Metal toxicity creates multisystem dysfunction, which appears to be mediated primarily through mitochondrial damage from glutathione depletion. Accurate screening can increase the likelihood that patients with potential metal toxicity are identified. The most accurate screening method for assessing chronic-metals exposure and metals load in the body is a provoked urine test.
28. Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment
American Journal of Biochemistry and Biotechnology 4 (2): 208-217, 2008
Daniel A. Rossignol, J. Jeffrey Bradstreet, International Child Development Resource Center,
“Exposure to environmental toxins is the likely etiology for MtD in autism. This dysfunction then contributes to a number of diagnostic symptoms and comorbidities observed in autism including: cognitive impairment, language deficits, abnormal energy metabolism, chronic gastrointestinal problems, abnormalities in fatty acid oxidation, and increased oxidative stress. MtD and oxidative stress may also explain the high male to female ratio found in autism due to increased male vulnerability to these dysfunctions.”
29. Proximity to point sources of environmental mercury release as a predictor of autism prevalence
Health & Place, 2008
Raymond F. Palmer, Stephen Blanchard, Robert Wood University of Texas Health Science Center, San Antonio Department of Family and Community Medicine, Our Lady of the Lake University, San Antonio Texas, Chair, Department of Sociology
“We suspect that persistent low-dose exposures to various environmental toxicants, including mercury, that occur during critical windows of neural development among genetically susceptible children (with a diminished capacity for metabolizing accumulated toxicants) may increase the risk for developmental disorders such as autism. ”
30. Epidemiology of autism spectrum disorder in Portugal: prevalence, clinical characterization, and medical conditions
Developmental Medicine & Child Neurology, 2007
Guiomar Oliveira MD PhD, Centro de Desenvolvimento da Criança, Hospital Pediátrico de Coimbra; Assunção Ataíde BSc, Direcção Regional de Educação do Centro Coimbra; Carla Marques MSc, Centro de Desenvolvimento da Criança, Hospital Pediátrico de Coimbra; Teresa S Miguel BSc, Direcção Regional de Educação do Centro, Coimbra; Ana Margarida Coutinho BSc, Instituto Gulbenkian de Ciência, Oeiras; Luísa Mota-Vieira PhD, Unidade de Genética e Patologia moleculares, Hospital do Divino Espírito Santo, Ponta Delgada, Açores; Esmeralda Gonçalves PhD; Nazaré Mendes Lopes PhD, Faculdade de Ciências e Tecnologia, Universidade de Coimbra; Vitor Rodrigues MD PhD; Henrique Carmona da Mota MD PhD, Faculdade de Medicina, Universidade de Coimbra, Coimbra; Astrid Moura Vicente PhD, Instituto Gulbenkian de Ciência, Oeiras, Portugal.
“ A diversity of associated medical conditions was documented in 20%, with an unexpectedly high rate of mitochondrial respiratory chain disorders.”
31. Thimerosal induces neuronal cell apoptosis by causing cytochrome c and apoptosis-inducing factor release from mitochondria.
International Journal of Molecular Medicine, 2006
Yel L, Brown LE, Su K, Gollapudi S, Gupta S.Department of Medicine, University of California, Irvine
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.
32. Mitochondrial mediated thimerosal-induced apoptosis in a human neuroblastoma cell line (SK-N-SH).
Humphrey ML, Cole MP, Pendergrass JC, Kiningham KK. Department of Pharmacology, Joan C. Edwards School of Medicine, Marshall University.
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.
33. Possible Immunological Disorders in Autism: Concomitant Autoimmunity and Immune Tolerance
The Egyptian Journal of Immunology, 2006
Maha I. Sh. Kawashti, Omnia R. Amin Nadia G. Rowehy
Microbiology Department, Faculty of Medicine (For Girls), Al Azhar University, Cairo, Egypt, Psychiatry Department, Faculty of Medicine, Cairo University, Cairo, Egypt and Serology Lab King Fahad General Hospital, Jeddah, K.S.A.
“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.”
34. Pediatric Vaccines Influence Primate Behavior, and Amygdala Growth and Opioid Ligand Binding Friday, May 16, 2008: IMFAR
L. Hewitson , Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA B. Lopresti , Radiology, University of Pittsburgh, Pittsburgh, PA C. Stott , Thoughtful House Center for Children, Austin, TX J. Tomko , Pittsburgh Development Center, University of Pittsburgh, Pittsburgh, PA L. Houser , Pittsburgh Development Center, University of Pittsburgh, Pittsburgh, PA E. Klein , Division of Laboratory Animal Resources, University of Pittsburgh, Pittsburgh, PA C. Castro , Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA G. Sackett , Psychology, Washington National Primate Research Center, Seattle, WA S. Gupta , Medicine, Pathology & Laboratory Medicine, University of California – Irvine, Irvine, CA D. Atwood , Chemistry, University of Kentucky, Lexington, KY L. Blue , Chemistry, University of Kentucky, Lexington, KY E. R. White , Chemistry, University of Kentucky, Lexington, KY A. Wakefield , Thoughtful House Center for Children, Austin, TX
Conclusions: This animal model, which examines for the first time, behavioral, functional, and neuromorphometric consequences of the childhood vaccine regimen, mimics certain neurological abnormalities of autism. The findings raise important safety issues while providing a potential model for examining aspects of causation and disease pathogenesis in acquired disorders of behavior and development.
35. Thimerosal exposure in infants and neurodevelopmental disorders: An assessment of computerized medical records in the Vaccine Safety Datalink.
Young HA, Geier DA, Geier MR.
The George Washington University School of Public Health and Health Services, Department of Epidemiology and Biostatistics, United States.
“Consistent significantly increased rate ratios were observed for autism, autism spectrum disorders, tics, attention deficit disorder, and emotional disturbances with Hg exposure from Thimerosal containing vaccines.”
36. Glutathione, oxidative stress and neurodegeneration
Schulz JB, Lindenau J, Seyfried J, Dichgans J. Neurodegeneration Laboratory, Department of Neurology, University of Tübingen, Germany.
Eur J Biochem. 2000 Aug;267(16):4904-11.
“There is significant evidence that the pathogenesis of several neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, Friedreich’s ataxia and amyotrophic lateral sclerosis, may involve the generation of reactive oxygen species and mitochondrial dysfunction.”
37. Hepatitis B triple series vaccine and developmental disability in US children aged 1-9 years
Carolyn Gallagher a; Melody Goodman, Graduate Program in Public Health, Stony Brook University Medical Center, Health Sciences Center, New York, USA
Journal Toxicological & Environmental Chemistry, Volume 90, Issue 5 September 2008 , pages 997 – 1008
” 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.”
38. Induction of metallothionein in mouse cerebellum and cerebrum with low-dose thimerosal injection.
Minami T, Miyata E, Sakamoto Y, Yamazaki H, Ichida S., Department of Life Sciences, School of Science & Engineering, Kinki University, 3-4-1 Kowakae, Higashi-osaka, Osaka, 577-8502, Japan.
Cell Biology and Toxicology. 2009 Apr 9.
“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.”
39. Mercury induces inflammatory mediator release from human mast cells
Duraisamy Kempuraj, Shahrzad Asadi, Bodi Zhang, Akrivi Manola, Jennifer Hogan, Erika Peterson, Theoharis C Theoharides
Journal of Neuroinflammation 2010, 7:20 doi:10.1186/1742-2094-7-20
“This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation. As a result, the findings of the present study provide a biological mechanism for how low levels of mercury may contribute to Autism Spectrum Disorder pathogenesis.”
40. Influence of pediatric vaccines on amygdala growth and opioid ligand binding in rhesus macaque infants: A pilot study
Acta Neurobiol Exp 2010, 70: 147–164 Polish Neuroscience Society – PTBUN, Nencki Institute of Experimental Biology
Laura Hewitson1,2,*, Brian J. Lopresti3, Carol Stott4, N. Scott Mason3 and Jaime Tomko1
Department of Obstetrics and Gynecology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Thoughtful House Center for Children, Austin, TX, USA; Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; 4Independent Chartered Scientist, Cambridge, UK;
“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.”
41. Cultured lymphocytes from autistic children and non-autistic siblings up-regulate heat shock protein RNA in response to thimerosal challenge.
Neurotoxicology. 2006 Sep;27(5):685-92. Epub 2006 Jun 16.
Walker SJ, Segal J, Aschner M.
Department of Physiology and Pharmacology, Wake Forest University School of Medicine.
” while cells challenged with thimerosal responded by up-regulating numerous heat shock protein transcripts, but not MTs. Although there were no apparent differences between autistic and non-autistic sibling responses in this very small sampling group, the differences in expression profiles between those cells treated with zinc versus thimerosal were dramatic.”
42. Hepatitis B Vaccination of Male Neonates and Autism
Annals of Epidemiology , Vol. 19, No. 9 ABSTRACTS (ACE), September 2009: 651-680, p. 659
CM Gallagher, MS Goodman, Graduate Program in Public Health, Stony Brook University Medical Center, Stony Brook, NY
43. 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. Epub 2009 Sep 9.
Olczak M, Duszczyk M, Mierzejewski P, Majewska MD. Department of Pharmacology and Physiology of the Nervous System, Institute of Psychiatry and Neurology, Warsaw, Poland.
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.
44. Sorting out the spinning of autism: heavy metals and the question of incidence
Acta Neurobiol Exp 2010, 70: 165–176
Mary Catherine DeSoto and Robert T. Hitlan, Department of Psychology, University of Northern Iowa.
“We argue that scientific research does not support rejecting the link between the neurodevelopmental disorder of autism and toxic exposures.”
45. Urinary Porphyrin Excretion in Neurotypical and Autistic Children
Environ Health Perspect. 2010 Oct;118(10):1450-7. Epub 2010 Jun 24.
Woods JS, Armel SE, Fulton DI, Allen J, Wessels K, Simmonds PL, Granpeesheh D, Mumper E, Bradstreet JJ, Echeverria D, Heyer NJ, Rooney JP., Department of Environmental and Occupational Health Sciences, University of Washington
BACKGROUND: Increased urinary concentrations of pentacarboxyl-, precopro- and copro-porphyrins have been associated with prolonged mercury (Hg) exposure in adults, and comparable increases have been attributed to Hg exposure in children with autism (AU).
RESULTS: Mean urinary porphyrin concentrations are naturally high in young children and decline by as much as 2.5-fold between 2 and 12 years of age. Elevated copro- (p < 0.009), hexacarboxyl- (p < 0.01) and pentacarboxyl- (p < 0.001) porphyrin concentrations were significantly associated with AU but not with PDD-NOS. No differences were found between NT and AU in urinary Hg levels or in past Hg exposure as determined by fish consumption, number of dental amalgam fillings, or vaccines received. CONCLUSIONS:These findings identify disordered porphyrin metabolism as a salient characteristic of autism. Hg exposures were comparable between diagnostic groups, and a porphyrin pattern consistent with that seen in Hg-exposed adults was not apparent.
46. Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis
Molecular Psychiatry advance online publication 25 January 2011;doi: 10.1038/mp.2010.136
D A Rossignol and R E Frye
“Overall, this evidence supports the notion that mitochondrial dysfunction is associated with ASD.”
47. Sensitization effect of thimerosal is mediated in vitro via reactive oxygen species and calcium signaling.
Toxicology. 2010 July – August;274(1-3):1-9. Epub 2010 May 10.
Migdal C, Foggia L, Tailhardat M, Courtellemont P, Haftek M, Serres M.
“In conclusion, these data suggest that thimerosal induced U937 activation via oxidative stress from mitochondrial stores and mitochondrial membrane depolarization with a primordial effect of thiol groups.”
50. Theoretical aspects of autism: Causes—A review
Journal of Immunotoxicology, January-March 2011, Vol. 8, No. 1 , Pages 68-79
Helen V. Ratajczak, PhD
“Documented causes of autism include genetic mutations and/or deletions, viral infections, and encephalitis following vaccination. Therefore, autism is the result of genetic defects and/or inflammation of the brain. The inflammation could be caused by a defective placenta, immature blood-brain barrier, the immune response of the mother to infection while pregnant, a premature birth, encephalitis in the child after birth, or a toxic environment.”
51. 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 Volume 74, Issue 14, 2011, Pages 903 – 916 Author: Gayle DeLonga
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. To read the abstract click HERE.
52. Ancestry of pink disease (infantile acrodynia) identified as a risk factor for autism spectrum disorders.
J Toxicol Environ Health A. 2011 Sep 15;74(18):1185-94. Shandley K, Austin DW.
Swinburne Autism Bio-Research Initiative (SABRI), Brain and Psychological Sciences Research Centre , Swinburne University of Technology , Hawthorn , Victoria , Australia.
Abstract Pink disease (infantile acrodynia) was especially prevalent in the first half of the 20th century. Primarily attributed to exposure to mercury (Hg) commonly found in teething powders, the condition was developed by approximately 1 in 500 exposed children. The differential risk factor was identified as an idiosyncratic sensitivity to Hg. Autismspectrum disorders (ASD) have also been postulated to be produced by Hg. Analogous to the pink disease experience, Hg exposure is widespread yet only a fraction of exposed children develop an ASD, suggesting sensitivity to Hg may also be present in children with an ASD. The objective of this study was to test the hypothesis that individuals with a known hypersensitivity to Hg (pink disease survivors) may be more likely to have descendants with an ASD. Five hundred and twenty-two participants who had previously been diagnosed with pink disease completed a survey on the health outcomes of their descendants. The prevalence rates of ASD and a variety of other clinical conditions diagnosed in childhood (attention deficit hyperactivity disorder, epilepsy, Fragile X syndrome, and Down syndrome) were compared to well-established general population prevalence rates. The results showed the prevalence rate of ASD among the grandchildren of pink disease survivors (1 in 22) to be significantly higher than the comparable general population prevalence rate (1 in 160). The results support the hypothesis that Hg sensitivity may be a heritable/genetic risk factor for ASD.
53. Do aluminum vaccine adjuvants contribute to the rising prevalence of autism?
J Inorg Biochem. 2011 Nov;105(11):1489-99. Epub 2011 Aug 23. Tomljenovic L, Shaw CA.
Neural Dynamics Research Group, Department of Ophthalmology and Visual Sciences, University of British Columbia, 828 W. 10th Ave, Vancouver, BC, Canada V5Z 1L8.
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, pThe 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.
54. Lasting neuropathological changes in rat brain after intermittent neonatal administration of thimerosal.
Folia Neuropathol. 2010;48(4):258-69. Olczak M, Duszczyk M, Mierzejewski P, Wierzba-Bobrowicz T, Majewska MD.
Department of Pharmacology and Physiology of the Nervous System, Institute of Psychiatry and Neurology, ul. Sobieskiego 9, Warsaw, Poland.
“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.”
55. Persistent behavioral impairments and alterations of brain dopamine system after early postnatal administration of thimerosal in rats.
Behav Brain Res. 2011 Sep 30;223(1):107-18. doi: 10.1016/j.bbr.2011.04.026. Epub 2011 Apr 28.
Olczak M, Duszczyk M, Mierzejewski P, Meyza K, Majewska MD. Department of Pharmacology and Physiology of the Nervous System, Institute of Psychiatry and Neurology, 02-957 Warsaw, Poland.
“These data document that early postnatal Thimerosal (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.”
56. Risk Factors for Autistic Regression: Results of an Ambispective Cohort Study.
J Child Neurol. 2012 Jan 30. [Epub ahead of print]
Zhang Y, Xu Q, Liu J, Li SC, Xu X., Department of Child Health Care, Children’s Hospital of Fudan University,Shanghai, China.
“This study suggests that febrile seizures and family history of neuropsychiatric disorders are correlated with autistic regression.”
57. Adverse events following 12 and 18 month vaccinations: a population-based, self-controlled case series analysis.
PLoS One. 2011;6(12):e27897. Epub 2011 Dec 12.
Wilson K, Hawken S, Kwong JC, Deeks S, Crowcroft NS, Van Walraven C, Potter BK, Chakraborty P, Keelan J, Pluscauskas M, Manuel D. Department of Medicine, Ottawa Hospital Research Institute, University of Ottawa.
“There were an additional 20 febrile seizures for every 100,000 vaccinated at 12 months.”
58. Administration of thimerosal to infant rats increases overflow of glutamate and aspartate in the prefrontal cortex: protective role of dehydroepiandrosterone sulfate.
Neurochem Res. 2012 Feb;37(2):436-47. Epub 2011 Oct 21.
Duszczyk-Budhathoki M, Olczak M, Lehner M, Majewska MD. Marie Curie Chairs Program, Department of Pharmacology and Physiology of Nervous System, Institute of Psychiatry and Neurology, 02-957, Warsaw, Poland.
“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.”
59. Neonatal Administration of Thimerosal Causes Persistent Changes in Mu Opioid Receptors in the Rat Brain
Neurochem Res. 2010 November; 35(11): 1840–1847.
Mieszko Olczak, Michalina Duszczyk, Pawel Mierzejewski, Teresa Bobrowicz, and Maria Dorota Majewska1, Department of Pharmacology and Physiology of the Nervous System, Institute of Psychiatry and Neurology,02-957 Warsaw, Poland, Department of Forensic Medicine, Medical University of Warsaw, Department of Neuropathology, Institute of Psychiatry and Neurology, Department of Biology and Environmental Science, University of Cardinal Stefan Wyszynski, Warsaw, Poland
“These data document that exposure to thimerosal during early postnatal life produces lasting alterations in the densities of brain opioid receptors along with other neuropathological changes, which may disturb brain development.”
60. Unanswered Questions: A Review of Compensated Cases of Vaccine-Induced Brain Injury
Pace Environmental Law Review, vol. 28, no. 2, 2011
Mary Holland, Louis Conte, Robert Krakow and Lisa Colin
“This empirical investigation, published in a peer-reviewed law journal, examines claims that the VICP compensated for vaccine-induced encephalopathy and seizure disorder. The VICP has compensated approximately 2,500 claims of vaccine injury since the inception of the program. This study found 83 cases of acknowledged vaccine-induced brain damage that include autism, a disorder that affects speech, social communication and behavior.”
61. Abnormal measles-mumps-rubella antibodies and CNS autoimmunity in children with autism.
J Biomed Sci. 2002 Jul-Aug;9(4):359-64.
Singh VK, Lin SX, Newell E, Nelson C., Department of Biology and Biotechnology Center, Utah State University.
“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.”
62. Serological association of measles virus and human herpesvirus-6 with brain autoantibodies in autism.
Clin Immunol Immunopathol. 1998 Oct;89(1):105-8.
Singh VK, Lin SX, Yang VC. College of Pharmacy, University of Michigan, Ann Arbor, Michigan, 48109-1065, USA.
“This study is the first to report an association between virus serology and brain autoantibody in autism; it supports the hypothesis that a virus-induced autoimmune response may play a causal role in autism.”
63. Integrating experimental (in vitro and in vivo) neurotoxicity studies of low-dose thimerosal relevant to vaccines.
Neurochem Res. 2011 Jun;36(6):927-38. doi: 10.1007/s11064-011-0427-0. Epub 2011 Feb 25.
Dórea JG, Faculty of Health Sciences, Universidade de Brasília.
There is a need to interpret neurotoxic studies to help deal with uncertainties surrounding pregnant mothers, newborns and young children who must receive repeated doses of Thimerosal-containing vaccines (TCVs). 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. The persisting use of TCV (in developing countries) is counterintuitive to global efforts to lower Hg exposure and to ban Hg in medical products; its continued use in TCV requires evaluation of a sufficiently nontoxic level of ethylmercury compatible with repeated exposure (co-occurring with adjuvant-Al) during early life.
64. Hepatitis B vaccine induces apoptotic death in Hepa1-6 cells
Apoptosis. 2012 Jan 17. Hamza H, Cao J, Li X, Li C, Zhu M, Zhao S.
Key Lab of Agricultural Animal Genetics, Breeding, and Reproduction of Ministry of Education, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan, 430070, People’s Republic of China.
“Vaccines can have adverse side-effects, and these are predominantly associated with the inclusion of chemical additives such as aluminum hydroxide adjuvant… 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.”
65. Maternal thimerosal exposure results in aberrant cerebellar oxidative stress, thyroid hormone metabolism, and motor behavior in rat pups; sex- and strain-dependent effects.
Cerebellum. 2012 Jun;11(2):575-86. doi: 10.1007/s12311-011-0319-5.
Sulkowski ZL, Chen T, Midha S, Zavacki AM, Sajdel-Sulkowska EM, Department of Psychiatry, Harvard Medical School and Brigham and Women’s Hospital.
Methylmercury (Met-Hg) and ethylmercury (Et-Hg) are powerful toxicants with a range of harmful neurological effects in humans and animals… Our data thus demonstrate a negative neurodevelopmental impact of perinatal TM exposure which appears to be both strain- and sex-dependent.
66. The rise in autism and the role of age at diagnosis.
Epidemiology. 2009 Jan;20(1):84-90. doi: 10.1097/EDE.0b013e3181902d15.
Hertz-Picciotto I, Delwiche L., Department of Public Health Sciences, University of California, Davis.
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.
67. Enrichment of Elevated Plasma F2t-Isoprostane Levels in Individuals with Autism Who Are Stratified by Presence of Gastrointestinal Dysfunction
PLoS ONE 8(7): e68444.
Gorrindo P, Lane CJ, Lee EB, McLaughlin B, Levitt P (July 3, 2013)
Funding: This work was supported in part by National Institutes of Health awards National Institute of Child Health and Human Development..
Excerpt: Elevation in peripheral oxidative stress is consistent with, and may contribute to, the more severe functional impairments in the ASD-GID group. With unique medical, metabolic, and behavioral features in children with ASD-GID, the present findings serve as a compelling rationale for both individualized approaches to clinical care and integrated studies of biomarker enrichment in ASD subgroups that may better address the complex etiology of ASD.