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:
- The heritable component of autism derives from a combination of DNA polymorphisms and epigenetic defects. The relative contribution of these factors is unknown.
- The primary harm from genetic/epigenetic defects involves weakened ability to cope with oxidative stress.
- In-utero environmental contributions to autism are primarily epigenetic in nature.
- Post-partum triggers for autism include toxic exposures, immune challenges, and other environmental insults that increase oxidative stress.
- 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.
- 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).
- Autism symptoms persist unless powerful antioxidant therapy is provided.
- Rampant oxidative stress impairs protein digestion and weakens intestinal and blood-brain barriers.
- Sharply reduced metallothionein activity greatly slows development of brain cells, resulting in an immature brain.
- Severity of autism depends on the relative progress in brain development prior to inundation by oxidative stress.
- If untreated, 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.