• DOI:10.1097/WCO.0b013e328336a01f
• Corpus ID: 17280526

Contributions of the environment and environmentally vulnerable physiology to autism spectrum disorders

@article{Herbert2010ContributionsOT,
  title={Contributions of the environment and environmentally vulnerable physiology to autism spectrum disorders},
  author={Martha Reed Herbert},
  journal={Current Opinion in Neurology},
  year={2010},
  volume={23},
  pages={103–110}
}

• M. Herbert
• Published 1 April 2010
• Biology, Psychology, Medicine
• Current Opinion in Neurology

Purpose of reviewThis review presents a rationale and evidence for contributions of environmental influences and environmentally vulnerable physiology to autism spectrum disorders (ASDs). Recent findingsRecent studies suggest a substantial increase in ASD prevalence above earlier Centers for Disease Control figures of one in 150, only partly explicable by data artifacts, underscoring the possibility of environmental contributors to increased prevalence. Some gene variants in ASD confer altered vulnerability to environmental stressors and exposures. De-novo mutations and advanced parental age as a risk factor for ASD also suggest a role for environment. Systemic and central nervous system pathophysiology, including oxidative stress, neuroinflammation, and mitochondrial dysfunction can be consistent with a role for environmental influence (e.g. from air pollution, organophosphates, heavy metals) in ASD, and some of the underlying biochemical disturbances (such as abnormalities in glutathione, a critical antioxidant and detoxifier) can be reversed by targeted nutritional interventions. Dietary factors and food contaminants may contribute risk. Improvement and loss of diagnosis in some with ASD suggest brain circuitry amenable to environmental modulation. SummaryPrevalence, genetic, exposure, and pathophysiological evidence all suggest a role for environmental factors in the inception and lifelong modulation of ASD. This supports the need for seeking targets for early and ongoing medical prevention and treatment of ASD.