30 solid pertinent and probatory scientific studies that fully prove vaccines are linked with autism
These thirty scientific studies show a link between vaccines and autism, disproving the myth that no official research papers exist to support what alternative doctors have been saying for years.
We present you a list of 30 scientific studies that show a link between vaccines and autism, disproving the myth that no official research papers exist to support what alternative doctors have been saying for years.
These papers can be shown to medical doctors and public health officials who wish to see peer reviewed scientific studies to back up the claims that autism is a direct result from receiving a vaccination.
The first research paper that we present was the first one ever written on the subject. 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a novel set of neurological symptoms that had never been described in the medical literature, where children were withdrawn, uncommunicative and displayed similar odd behaviors.
This disorder would become known as “autism”. In the paper, Dr. 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 – a detailed consideration of its fascinating peculiarities.”
All of Kanner’s 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.
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.
1. Hepatitis B Vaccination of Male Neonates and Autism
Study published in the Annals of Epidemiology in September 2009. The authors are C. M. Gallagher and M. S. Goodman from Stony Brook University Medical Center.
Boys vaccinated as neonates had threefold greater odds for autism diagnosis compared to boys never vaccinated or vaccinated after the first month of life.
2. Porphyrinuria in childhood autistic disorder: Implications for environmental toxicity
Study published in the Toxicology and Applied Pharmacology in 2006. The authors are Robert Natafa et al from the Laboratoire Philippe Auguste, Paris, France.
These data implicate environmental toxicity in childhood autistic disorder.
3. Theoretical aspects of autism: Causes—A review
Study published in the Journal of Immunotoxicology, January-March 2011. The author is Helen V. Ratajczak, PhD.
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.
4. Uncoupling of ATP-mediated Calcium Signaling and Dysregulated IL-6 Secretion in Dendritic Cells by Nanomolar Thimerosal
Study published in the Environmental Health Perspectives in July 2006. The authors are Samuel R. Goth, Ruth A. Chu and Jeffrey P. Gregg.
This study demonstrates that very low levels of Thimerosal can contribute to immune system dysregulation.
5. Gender-selective toxicity of thimerosal
Study published in the Experimental Toxicology Pathology in March 2009. The study was conducted by a branch of researchers from the Departments of Medicine and Laboratory Medicine and Pathobiology, at University of Toronto.
A recent report shows a correlation of the historical use of thimerosal in therapeutic immunizations with the subsequent development of autism; however, this association remains controversial. Autism occurs approximately four times more frequently in males compared to females; thus, studies of thimerosal toxicity should take into consideration gender-selective effects. The present study was originally undertaken to determine the maximum tolerated dose (MTD) of thimerosal in male and female mice. However, during the limited MTD studies, it became apparent that thimerosal has a differential MTD that depends on whether the mouse is male or female.
6. Comparison of Blood and Brain Mercury Levels in Infant monkeys exposed to Vaccines Containing Thimerosal
Study published in the Environmental Health Perspectives in August 2005. The author is Thomas Burbacher, PhD, from the 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.
7. Increases in the number of reactive glia in the visual cortex of Macaca fascicularis following subclinical long-term methyl mercury exposure
Study published in the Toxicology and Applied Pharmacology, in 1994. The authors are Charleston J.S. et al, from the Department of Pathology, School of Medicine, University of Washington.
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.
8. Neuroglial Activation and Neuroinflammation in the Brain of Patients with Autism
Study published in the Annals of Neurology, in February 2005. The author is Diana L. Vargas, MD, from Johns Hopkins University.
This study, performed independently and using a different methodology than Dr. Herbert (see the following study) reached the same conclusion: the brains of autistic children are suffering from inflammation.
9. Autism: A Brain Disorder, or a Disorder That Affects the Brain?
Study published in the Clinical Neuropsychiatry, in 2005. The author is Martha R. Herbert M.D., Ph.D., from 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.
10. Activation of Methionine Synthase by Insulin-like Growth Factor-1 and Dopamine: a Target for Neurodevelopmental Toxins and Thimerosal
Study published in the Molecular Psychiatry, in July 2004. The author is Richard C. Deth, PhD, from Northeastern University.
This study demonstrates how Thimerosal inhibits methylation, a central driver of cellular communication and development.
11. Validation of the Phenomenon of Autistic Regression Using Home Videotapes
Study published in the Archives of General Psychiatry, in 2005. The authors are Emily Werner, PhD and Geraldine Dawson, PhD, from the University of Washington.
This study validates the existence of early autistic regression.
12. Blood Levels of Mercury Are Related to Diagnosis of Autism: A Reanalysis of an Important Data Set
Study published in the Journal of Child Neurology, in 2007. The authors are M. Catherine DeSoto, PhD and Robert T. Hitlan, PhD from the Department of Psychology, University of Northern 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.”
13. Developmental Regression and Mitochondrial Dysfunction in a Child With Autism
Study published in the Journal of Child Neurology, in February 2006. The author is Jon S. Poling, MD, PhD, from the Department of Neurology and Neurosurgery, at Johns Hopkins Hospital.
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
Study published in the American Journal of Biochemistry and Biotechnology, in 2008. The authors are Elizabeth M. Sajdel-Sulkowska and her team from the Department of Psychiatry, Harvard Medical School.
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
Study published in the The Neuroscientist in 2005. The author is Martha Herbert, MD, PhD, from 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.”
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
Study published in the Journal of Toxicology and Environmental Health, Nov-Dec issue from 2006. The authors are Janet Kern and Anne Jones, from the Department of Psychiatry, University of Texas Southwestern Medical Center.
“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
Study published in the Pathophysiology, in 2006. The authors are Abha Chauhan and Ved Chauhan.
This study provides a helpful overview of the growing evidence supporting the link between oxidative stress and autism.
18. Thimerosal Neurotoxicity is Associated with Glutathione Depletion: Protection with Glutathione Precursors
Study published in the Neurotoxicology, in January 2005. The author is S. Jill James, PhD, from the 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.
19. Aluminum adjuvant linked to gulf war illness induces motor neuron death in mice
Study published in the Neuromolecular Medicine, in 2007. The author is Christopher Shaw, Ph.D., from the Department of Ophthalmology and Program in Neuroscience, University of British Columbia.
This study demonstrates the extreme toxicity of the aluminum adjuvant used as a preservative in vaccines.
20. Environmental mercury release, special education rates, and autism disorder: an ecological study of Texas
Study published in the Health & Place, in 2006. The author is Raymond F. Palmer, from the University of Texas Health Science Center.
This study demonstrated the correlation between environmental mercury and autism rates in Texas.
21. Autism Spectrum Disorders in Relation to Distribution of Hazardous Air Pollutants in the SF Bay Area
Study published in the Environmental Health Perspectives, in September, 2006. The authors are Gayle Windham and his team from the Division of Environmental and Occupational Disease Control, California Department of Health Services.
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
Study published in the Journal of Toxicology and Environmental Health, in 2007. The authors are David A. Geier and 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.
23. Attention-deficit hyperactivity disorder and blood mercury level: a case-control study in chinese children
Study published in the Neuropediatrics, in August 2006. The author is P.R. Kong.
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
Study published in the Journal of Autism and Developmental Disorders, in April 2003. The authors are 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”.
25. Mitochondrial Energy-Deficient Endophenotype in Autism
Study published in the American Journal of Biochemistry and Biotechnology in 2008. The authors are J. Jay Gargus and Faiqa Imtiaz, from the School of Medicine, University of California, Irvine.
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.
26. Bridging from Cells to Cognition in Autism Pathophysiology: Biological Pathways to Defective Brain Function and Plasticity
Study published in the American Journal of Biochemistry and Biotechnology in 2008. The authors are Matthew P. Anderson, Brian S. Hooker and Martha R. Herbert, from Cambridge Health Alliance/Harvard Medical School/Beth Israel Deaconess Medical Center.
Excerpt: “We review evidence to support a model where the disease process underlying autism may begin when an in utero or early postnatal environmental, infectious, seizure, or autoimmune insult triggers an immune response that increases reactive oxygen species (ROS) production in the brain that leads to DNA damage (nuclear and mitochondrial) and metabolic enzyme blockade and that these inflammatory and oxidative stressors persist beyond early development (with potential further exacerbations), producing ongoing functional consequences.”
27. Heavy-Metal Toxicity—With Emphasis on Mercury
Study conducted by 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.
28. Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment
Study published in the American Journal of Biochemistry and Biotechnology. The authors are Daniel A. Rossignol and J. Jeffrey Bradstreet.
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
Study published in the Health & Place, in 2008. The authors are Raymond F. Palmer et al, from University of Texas Health Science Center.
Excerpt: “This study should be viewed as hypothesis-generating – a first step in examining the potential role of environmental mercury and childhood developmental disorders. Nothing is known about specific exposure routes, dosage, timing, and individual susceptibility. 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
Study published in the Developmental Medicine & Child Neurology, in 2007. The authors are Guiomar Oliveira MD PhD et al, from Children’s Development Center (Centro de Desenvolvimento da Crianca), at the Children’s Hospital (Hospital Pediatrico) in Coimbra, Portugal.
The objective of this study was to estimate the prevalence of autistic spectrum disorder (ASD) and identify its clinical characterization, and medical conditions in a pediatric population in Portugal.
April 13, 2017