Age of Autism
May 9, 2011
By J.B. Handley
In the most recent issue of the Journal of Immunotoxicology, Helen V. Ratajczak, PhD , had two separate reviews published. The first review, Theoretical Aspects of-Autism Causes a Review tackles a seemingly taboo topic in mainstream health: the many potential environmental causes of autism. Dr. Ratajczak writes:
“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.”
Perhaps more controversially, Dr. Ratajczak also proposes a novel theory regarding the mechanism of action for a vaccine to cause autism:
“The MMR II vaccine is contaminated with human DNA from the cell line in which the rubella virus is grown. This human DNA could be the cause of the spikes in incidence. An additional increased spike in incidence of autism occurred in 1995 when the chicken pox vaccine was grown in human fetal tissue (Merck and Co., Inc., 2001; Breuer, 2003). The current incidence of autism in the United States, noted above, is approximately 1/100.
The human DNA from the vaccine can be randomly inserted into the recipient’s genes by homologous recom- bination, a process that occurs spontaneously only within a species. Hot spots for DNA insertion are found on the X chromosome in eight autism-associated genes involved in nerve cell synapse formation, central nervous system devel- opment, and mitochondrial function (Deisher, 2010). This could provide some explanation of why autism is predomi- nantly a disease of boys. Taken together, these data support the hypothesis that residual human DNA in some vaccines might cause autism.”
Her conclusion is something I’m sure many parents wish more researchers were willing to embrace:
“It is possible that autism results from more than one cause, with different manifestations in different individuals that share common symptoms. Integrating the data presented here, a hypothesis is that autism is the result of genetic defects, with the contributory effect of advancing age of the parents, and/or inflammation of the brain. The inflammation could be caused by a defective placenta, an immature blood- brain barrier, the immune response of the mother to a viral or bacterial infection, a premature birth, encephalitis in the child after birth, or a toxic environment. Also, intracellular pathogens could induce an immune response, resulting in neuro-inflammation, autoimmune reactions, brain injury, and autism.”
Dr. Ratajczak’s second paper is called Theoretical aspects of autism: biomarkers—a review. Here, Dr. Ratajczak seeks to summarize many of the previously established biomarkers of autism present in the “gastrointestinal, immunologic, neurologic, and toxicologic systems” of children with autism. She writes:
“Covering the literature from 1943 to the present in the PubMed and Ovid Medline databases, this review summarizes evidence of hormones, metabo- lites, amino acids, and other biomarkers present in significantly different quantities in autistic subjects compared to age- and sex-matched controls. These differences can be measured in the gastrointestinal, immunologic, neu- rologic, and toxicologic systems of the body, with some biomarkers showing ubiquitous application. In addition, there are unifying concepts, i.e., increased vulnerability to oxidative stress, immune glutamatergic dysfunction, and pineal gland malfunction. The variances of the biomarkers from the norm present the opportunity to create biomarker arrays that when properly developed and analyzed could result in an objective diagnosis with a ranking of the severity of autism for each subject. The contribution of each biomarker to the overall diagnosis could be calculated, thus providing a profile pattern unique to the individual. This profile could consequently provide information for therapeutic interventions on an individual basis.”
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