Immunological Explanations for Autism Initiation From Inflammation and Neurotoxins.

Abstract

Autism initiation has been associated with genetic vulnerabilities, disruption of gastrointestinal microbes (gut dysbiosis), chemical and neurotoxin damage, maternal infections, allergies or autoimmune diseases. Ingested neurotoxin barriers protecting the central nervous system of a fetus or child include the gastrointestinal wall of the mother or child and the fetus or child's blood-brain barrier. Inflammation from gut dysbiosis or inflammation from other causes can decrease protections provided by the gastrointestinal wall and the blood-brain barrier, allowing neurotoxins to reach the fetus or child's brain. Postnatal gut dysbiosis can potentially increase inflammation to facilitate neurotoxin penetration of a child's brain. Chemical pollutants and neurotoxins continue to increase and include aluminum, mercury, lead, arsenic, cadmium, organophosphates, organochlorines, bacterial toxins and fungal mycotoxins. Gut dysbiosis can increase neurotoxin concentrations within a fetal or child's brain, potentially initiating neurodevelopmental damage to cause autism. There are three possible scenarios initiating autism. These scenarios include inflammation and neurotoxin access to fetal brains within the prenatal neurodevelopment period, inflammation and neurotoxin access to child brains within the postnatal neurodevelopment period, or a two-stage neurotoxin access to brains within the prenatal and postnatal neurodevelopment periods. In summary, a comprehensive explanation for autism causation by several distinct pathways is discussed.