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Impacts of steroid stress hormones on the brain have provided multiple opportunities for linking specific molecular phenomena to behavioral state. The negative impacts of stress on female reproductive biological processes have been documented thoroughly at the endocrine and behavioral levels. More recently, a ‘3-hit’ theory of autism has identified early stress as one of the hits. The multiple biochemical effects of endotoxin (lipopolysaccharide, LPS) indicated that it would serve as a powerful maternal immune activator. The prenatal exposure to LPS coupled with the other two ‘hits’- an autism-related mutation and the Y chromosome - - heightened certain autism-like signs in mouse behavior.
Inclusion of stress in a 3-hit theory of autism.
In the face of overwhelming degrees of heterogeneity of symptoms and time courses of autism spectrum disorders, the one feature that seems to remain constant is the large sex difference: about 80% of the children diagnosed are boys. Years ago, working with the developmental psychologist Sylvie Goldman and the pediatric neurologist Isabelle Rapin, one of us devised a “3 hit” theory of autism, concentrating on the male predominance (Pfaff et al., 2011). This theory proposed that 3 types of factors would amplify each other’s effects on the development of social behavior: prenatal stress, an autism-related genetic mutation, and having a Y chromosome (being male).
Early stress. Autism is now diagnosed in greater than 1 in 100 children, and because it begins so early in life and lasts into adulthood, it is occasioned by long-lasting emotional suffering and can entail enormous expenses for medical and psychological treatments. Sir Michael Rutter, who has participated in autism research for more than 40 years, has reviewed our current understanding of the genetic contributions to, and psychological treatments for ASDs (Rutter, 2011). For example, some decades ago, Folstein and Rutter (1977) reported 36% concordance of diagnoses of autism among monozygotic twins, compared with 0% in dizygotic twins, and in that paper anticipated the subsequent discussions of gene/environment interactions. Recently, in producing rigorous quantitative estimates of gene/environment contributions, Hallmayer et al (2011) estimated ASD diagnostic concordance rates at .77 for monozygotic male twins, with a large share (58%) of the variance in liability explained by environmental factors. He has proposed novel tests of the social problems focused on by our theory, including a theory-of-mind task (Heavey et al, 2000), and has explored the relationships between the dysphasia (i.e. severe language disorders) of autism and the evident shortcomings in social communication ( Cantwell et al, 1989). For this review, it is important to illustrate how early stress plays into some of the multiple etiologies that lead to ASDs.