Autism

Autism Spectrum Disorder (ASD) represents a major public health concern as a prevalent neurodevelopmental disorder with pronounced risk for failure of adaptation across social, educational, and psychological outcomes. The exact etiology of autism is unclear. However there is a lot of research work giving some insights about the possible predisposing factors that enhance chance of autism. Several lines of evidence suggest that prenatal and/or early life acetaminophen exposure may adversely affect neurodevelopment increasing incidence of autism. Since 1980 acetaminophen greatly has replaced aspirin as an analgesic and anti-pyretic following reports indicating that aspirin use was associated with Reye’s syndrome. Notably acetaminophen use has been associated with at least a 10-fold rise of autism epidemic since the early 1980s. Several mechanisms have been suggested to implicate the role of acetaminophen in pathogenesis of autism as altered immune function and impaired hepatic detoxification capacity resulting in accumulation of potentially neurotoxic metabolites. In early life, maturational compromises to the glucuronidation pathway in combination with the compromises to the sulfation pathway that typify autistic children, may lead to utilization of the suboptimal secondary metabolic routes with the potential for adverse neurological effects in susceptible individuals. Acetaminophen use during pregnancy has also been associated with altered metabolism increasing autism rates in born infants. The use of acetaminophen may also trigger autism by activating the endocannabinoid system thereby interfering with normal development. Accumulating evidence linking significantly increased rates of autism with prenatal and early life acetaminophen exposure strongly suggests its cautious use during these critical times.