Youth affected by prenatal alcohol exposure (PAE) can present with a complex profile of adaptive, behavioral, cognitive and physical problems referred to as fetal alcohol spectrum disorder (FASD). FASD is completely preventable, yet is in the top 3 known causes of intellectual disability. Up to 90% of individuals with FASD may experience mental health problems over the life course. Any amount of PAE can potentially result in FASD, with an average national (US) prevalence of 2.4-4.8%, and reaching 80% of school-aged children in the Chicago area from foster or adopted homes. Further, the 2017 prevalence rates of babies who tested positive for PAE at birth reached 17.7% in some geographical regions of Texas, making PAE a major health concern. Maternal alcohol consumption can result in programming of multiple fetal systems, including the endocrine system. Although the individual with PAE is no longer connected to maternal systems postnatally, life-long endocrine alterations persist and may continue to impact the developing brain. Despite a plethora of animal literature, studies in humans examining PAE-related endocrine alterations are very limited. Indeed, a leading hypothesis in animal research is that endocrine dysregulation may underlie many of the behavioral, cognitive and mental health problems caused by PAE. My research aims to fill this translational gap in knowledge through examination of hormone-brain relationships in individuals affected by PAE using salivary biomarkers and neuroimaging. Understanding brain/endocrine alterations among individuals with FASD is essential for advancing our understanding of increased susceptibility to mental health problems as well as common cognitive, behavioral and adaptive deficits related to FASD, and may elucidate novel targets for the development of treatments.
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