Autism, Theory of Cause

*Oxidative Stress *Undermethylation *Genetics

Adopted from the "Bermuda Triangle Theory" as presented by Walsh Research Institute based on more than 50,000 chemical assays of blood and urine in autistic children and adults:

1. The heritable component of autism derives from a combination of DNA polymorphisms and epigenetic defects. The relative contribution of these factors is unknown.
2. The primary harm from genetic/epigenetic defects involves weakened ability to cope with oxidative stress.
3. In-utero environmental contributions to autism are primarily epigenetic in nature.
4. Post-partum triggers for autism include toxic exposures, immune challenges, and other environmental insults that increase oxidative stress.
5. The body's natural protectors against oxidative stress (e.g., glutathione, metallothionein, selenium, super oxide dismutase, ceruloplasmin, and cysteine) are gradually weakened until a threshold is reached in which their effectiveness collapses. This event results in a sudden increase in oxidative stress and inflammation within the brain.
6. In regressive autism, the sudden increase in oxidative stress and inflammation can cause a rapid decline in mental functioning (e.g., loss of speech, behavioral changes, and divergent gaze).
7. Autism symptoms persist unless powerful antioxidant therapy is provided.
8. Rampant oxidative stress impairs protein digestion and weakens intestinal and blood-brain barriers.
9. Sharply reduced metallothionein activity greatly slows development of brain cells, resulting in an immature brain.
10. Severity of autism depends on the relative progress in brain development prior to inundation by oxidative stress.
11. If not addressed, excessive oxidative stress can result in gradual loss of brain cells and mental retardation by age 20.

Antioxidant therapies together with applied behavior analysis (ABA) offer the promise of a better life for autistic children. If started in earnest prior to age four, a greater possibility of recovery exists.