It is an often repeated fallacy that there is no research that supports the supposition that vaccine can cause autism. This talking point is most often repeated by medical personnel and public health officials who have simply never been told that these studies exist, and in some cases by those who refuse to read the information when it is offered to them, so they continue to labour under the false assumption that vaccine autism causation is merely an “internet rumour” or a result of one paper that was published in 1998.
This untruth was again testified to during the HHS Committee hearings.
In fact, the first research paper to offer evidence that vaccines may cause autism was THE first paper ever written on autism. In the 1930’s, Child Psychiatrist Leo Kanner discovered 11 children over the course of several years who displayed a novel set of neurological symptoms that had never been described in the medical literature, where children were withdrawn, uncommunicative and displayed similar odd behaviours. This disorder would become known as “autism.” In the paper, Rd. Kanner noted that onset of the disorder began following the administration of a small pox vaccine. This paper, was published in 1943, and evidence that vaccination causes an ever increasing rate of neurological and immunological regressions, including autism, has been mounting from that time until now.
Autistic Disturbances of Affective Contact Leo Kanner, Johns Hopkins University, 1943
“Since 1938, there have come to our attention a number of children whose condition differs so markedly and uniquely from anything reported so far, that each case merits – and, I hope, will eventually receive – at detailed consideration of its fascinating peculiarities.”
All of Kanners cases were born after, and began to appear following, the introduction of Eli Lilly’s new form of water soluble mercury in the late 1920s used as an anti-fungal in forestry, a wood treatment product in the lumber industry and as a disinfectant and anti-bacterial in the medical industry under the name of “Thimerosal” that was included in vaccines.
For further information on the early evidence of a vaccine/connection, I recommend reading Rd. Bryan Jepson’s book, “Changing the Course of Autism: A Scientific Approach for Parents and Physicians,” as well as Mark Blaxill and Dan Olmseted’s new book “The Age of Autism: Mercury, Medicine, and a Man-made Epidemic.”
As I testified to at the hearing, there is abundant research supporting the vaccine autism link. I have included 49 research papers for your review, and only included research published in the last ten years or so. This is by no means a complete list, but it one that I have been compiling for the last few years as relevant research came to my attention. I have ONLY included autism related information, not research on other vaccine injuries of which there are many.
As you can see, the medical professionals testifying that there is no scientific support for the vaccine/autism causation theory are uninformed about the current state of the science. When vaccination decisions are made based on an uninformed opinion, it means serious potential damage to the patient, and because of the law preventing lawsuits for vaccine injury, it also means that the uninformed medical professionals making bad recommendations CANNOT be held accountable in any way for giving the patient bad information.
Parents want to know if their child can develop autism from their vaccines. If they believe that the answer is yes, and the risk of brain injury from vaccination is higher than their risk from a disease, it is their right to decline vaccination for themselves and their children without coercion.
Patients MUST be able to make their own informed vaccine decisions, because often, they know more about potential vaccine risks that even top public health officials do.
Thank you to the Hard work of Lisa Joyce from the Thinking Mums Revolution at www.TEAMTMR.org
- 1.) Theoretical aspects of autism: Causes—A review
Journal of Immunotoxicology, January-March 2011, Vol. 8, No. 1 , Pages 68-79 Helen V. Ratajczak, PhD
Autism, a member of the pervasive developmental disorders (PDDs), has been increasing dramatically since its description by Leo Kanner in 1943. First estimated to occur in 4 to 5 per 10,000 children, the incidence of autism is now 1 per 110 in the United States, and 1 per 64 in the United Kingdom, with similar incidences throughout the world. Searching information from 1943 to the present in PubMed and Ovid Medline databases, this review summarizes results that correlate the timing of changes in incidence with environmental changes.
Autism could result from more than one cause, with different manifestations in different individuals that share common symptoms. 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.
- 2.) Neuroglia 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 Rd. 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 on-going 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."
- 3.) 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 hyper focus or reduced behavioural 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 modelled 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, behaviour 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).
Modelling 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 biologist 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 behavioural syndrome.
4.) 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 behavioural data coded from home videotapes of children with autism spectrum disorder (ASD) vs. typical development taken at 12 and 24 months of age.
Design Home videotapes of 56 children’s first and second birthday parties were collected from parents of young children with ASD with and without a reported history of regression and typically developing children. Child behaviours were coded by raters blind to child diagnosis and regression history. A parent interview that elicited information about parents’ recall of early symptoms from birth was also administered.
Setting Participants were recruited from a multidisciplinary study of autism conducted at a major university.
Participant’s fifteen children with ASD with a history of regression, 21 children with ASD with early-onset autism, and 20 typically developing children and their parents participated.
Main Outcome Measures Observations of children’s communicative, social, affective, repetitive behaviours, and toy play coded from videotapes of the toddlers’ first and second birthday parties.
Results Analyses revealed that infants with ASD with regression show similar use of joint attention and more frequent use of words and babble compared with typical infants at 12 months of age. In contrast, infants with ASD with early onset of symptoms and no regression displayed fewer joint attention and communicative behaviours at 12 months of age. By 24 months of age, both groups of toddlers with ASD displayed fewer instances of word use, vocalizations, declarative pointing, social gaze, and orienting to name as compared with typically developing 24-month-olds.
Parent interview data suggested that some children with regression displayed difficulties in regulatory behaviour before the regression occurred.
Conclusion this study validates the existence of early autistic regression.
UPDATE: Since the Poling Case, this has become a popular link, so I will update it with more research and better information so that you can actually find and read the articles. Below is a partial list that I will keep adding to.
- 5.) 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, Iow
Excerpt: “We have reanalysed 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.”
The question of what is leading to the apparent increase in autism is of great importance. Like the link between aspirin and heart attack, even a small effect can have major health implications. If there is any link between autism and mercury, it is absolutely crucial that the first reports of the question are not falsely stating that no link occurs. We have reanalysed 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.
- 6.) 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.”
- 7.) 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.”
- 8.) Large Brains in Autism: The Challenge of Pervasive Abnormality
The Neuroscientist, Volume 11, Number 5, 2005.
Martha Herbert, MD, PhD, Harvard University
This study helps refute the notion that the brains of autistic children are simply wired differently and notes, "neuroinflammation appears to be present in autistic brain tissue from childhood through adulthood." Rd. Herbert suggests that chronic disease or an external environmental source (like heavy metals) may be causing the inflammation.
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."
The most replicated finding in autism neuroanatomy—a tendency to unusually large brains—has seemed paradoxical in relation to the specificity of the abnormalities in three behavioural domains that define autism. We now know a range of things about this phenomenon, including that brains in autism have a growth spurt shortly after birth and then slow in growth a few short years afterward, that only younger but not older brains are larger in autism than in controls, that white matter contributes disproportionately to this volume increase and in a nonuniform pattern suggesting postnatal pathology, that functional connectivity among regions of autistic brains is diminished, and that neuroinflammation (including microgliosis and astrogliosis) appears to be present in autistic brain tissue from childhood through adulthood.
Alongside these pervasive brain tissue and functional abnormalities, there have arisen theories of pervasive or widespread neural information processing or signal coordination abnormalities (such as weak central coherence, impaired complex processing, and under connectivity), which are argued to underlie the specific observable behavioural features of autism. This convergence of findings and models suggests that a systems- and chronic disease–based reformulation of function and pathophysiology in autism needs to be considered, and it opens the possibility for new treatment targets.
- 9.)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."
- 10.) 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 Centre
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."
- 11.) 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."
Impairments in social relatedness and communication, repetitive behaviours, 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 behavioural 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, and IRB number IRB00005375) approved the present study.
A case series of nine patients who presented to the Genetic Centres 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.
- 12.) The Changing Prevalence of Autism In California
Journal of Autism and Developmental Disorders, April 2003
Mark F. Blaxill, David S. Baskin, and Walter O. Spitzer
This study helps to refute the supposition made by some researchers that autism's epidemic may only be due to "diagnostic substitution".
Excerpt: "They have suggested that 'diagnostic substitution' accounts for an apparent increase in the incidence of autism in California that is not real. This hypothesized substitution is not supported by proper and detailed analyses of the California data."
- 13.) 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.