A Strategy for Preventing Autism Disorders

The true nature of autism is gradually coming into view as science advances. For many years we have known that the recipe for autism is an inborn predisposition followed by one or more environmental insults. It’s becoming increasingly clear that autism predisposition is associated with in-utero undermethylation that alters expression of numerous genes for the developing baby. In most cases, the result is an innate weakness or vulnerability in coping with toxic metals or other forms of oxidative stress. In about 20% of cases, autism onset occurs in the womb with autism symptoms evident soon after birth. The remaining 80% of cases involve regressive autism with typical onset between 16 and 22 months of age. The reason for heightened autism vulnerability at this time appears to be the gradual loss of immune protections after breast feeding is stopped. This presentation will summarize advances in DNA repair and epigenetic sciences that provide insights into the mechanisms of autism onset. Researchers have learned that DNA’s weak link is the nucleotide guanine, and that massive and permanent changes in human functioning can occur if oxidative assaults on guanine overwhelm DNA repair or alter epigenetic bookmarks. Once autism develops, families and clinicians are faced with a complex disorder involving dozens or hundreds of misbehaving genes that adversely impact immune function, intestinal function, brain development, and many other systems. However, if this autism-onset model is correct, autism prevention appears to be relatively easy to achieve with existing technology. This presentation will present a strategy for autism prevention that could eventually lead to elimination of autism.

 (Note: The objective is not to eliminate people; we believe that autism disorders are preventable.)