In 2012, the International Journal of Epidemiology devoted an entire issue to it, calling epigenetics “the next big thing.”
Epigenetics and Autism
Epigenetics is at the heart of the matter in autism.
Epigenetics explains why all young children exposed to today’s environmental chemical, electromagnetic, and sociological soup don’t end up with autism.
Why do some and not all children regress into autism?
Individuals with autism appear to have a genetic propensity or predisposition that manifests itself only when triggered by the “right” combination of environmental factors.
Any of the environmental exposures mentioned above can change gene expression, resulting in MTHFR or SUOX mutations.
Related to the SUOX mutation is another environmental impact: the coincidental timing during the 1980s of a recommendation by the medical community for replacing aspirin with acetaminophen for pain.
Acetaminophen is the main ingredient in Tylenol™ and some other popular painkillers.
According to recent research, acetaminophen toxicity can overload the defective sulfation pathway catalyzed by phenolsulfotransferase (PST), which is deficient in autism, leading to overproduction of the toxic metabolite N-acetylp-benzoquinone imine (NAPQI).
Increased levels of NAPQI reduce an individual’s ability to detoxify toxic chemicals, thus increasing oxidative stress and cascading into protein, lipid, and nucleic acid damage from free radicals.
Ultimately, the more “right” the genetic material combined with the more “right” environmental insults, the more severe the disability.
Those on the lesser end of the spectrum have fewer genetic variables combined with fewer environmental insults.
Those with severe autism are unfortunate enough to have a larger number of each factor.
Still Looking for Answers?
Visit the Epidemic Answers Provider Directory to find a practitioner near you.