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in genetic studies pertaining to risk and vulnerability to ASD. Environmental factors,
especially the in utero milieu, likely modulate genetic vulnerabilities responsible for
the manifestation of ASD in individual children. Two seminal studies by Caspi and
his colleagues illustrated the importance of environmental as well as genetic
information in understanding human behavior. In one study, on a sample of male
children, they found that maltreated children with a genotype conferring high levels of
a neurotransmitter-metabolizing-enzyme (MAO-A) expression were less likely to
develop antisocial problems. These findings may partly explain why not all victims of
maltreatment grow up to victimize others, and they provide epidemiological evidence
that genotypes can moderate children’s sensitivity to environmental insults (Caspi et
al., 2002). In a second prospective-longitudinal study of a representative birth cohort,
they tested why stressful experiences lead to depression in some people but not in
others. In this study, differences in the serotonin transporter (5-HTT) gene were found
to moderate the influence of stressful life events on depression, thus demonstrating a
gene-by-environment interaction, in which an individual’s response to environmental
insults is moderated by his or her genetic makeup (Caspi, et al., 2003). However, Risch
et al. (2009) questioned this finding in a recent meta-analysis in which no associations
were found between serotonin transporter genotype alone or in interaction with stressful
life events on the one hand, and elevated risk for depression, on the other hand. Yet,
since ASD is a developmental disorder characterized by early onset, a likely target for
environmental risk, and interacting with genotype, are the pre-natal and peri-natal
periods.
In 1992, Hales and Barker highlighted the existence of associations between
early growth patterns and chronic adult diseases. They proposed the 'fetal programming'
concept, that describes fetus' physiological adaptation to characteristics of the