Early initiation and escalation of alcohol use can be attributed in part to risky decision-making, a product of hypersensitivity to reward in the context of low impulse control. As the prefrontal cortex (PFC) is involved in executive functions including impulse regulation, any delay in PFC development during adolescence may heighten an individual's propensity for risk-taking and thus alcohol initiation. Thus, identifying strategies t reinforce PFC development has important public health applications in preventing the early initiation of alcohol use. Optimal development and function of the nervous system, particularly during critical period of adolescence, may in part depend on supply of dietary docosahexaenoic acid (DHA), an omega-3 fatty acid, which is an integral component of PFC neuronal membranes where it facilitates function (neurotransmission) and supports structure (via trophic support for neurons/synapses). While low DHA has often been cited in clinical disorders of impulse control, little is known about variations in adolescent DHA status and impulsivity with respect to risk of early alcohol initiation. Preliminary analysis of pilot data suggest a trend relationship between whole blood DHA level and ability to control impulses prior to alcohol initiation. The objective of the current study is to determine to what extent DHA status is related to PFC structure and function and predicts subsequent drinking initiation in a large sample of healthy adolescents (n=135). To address this objective, three aims will be explored using a combination of neuroimaging, blood DHA (a biomarker reflecting intake), and survey measures of drug/alcohol use. Firstly, to evaluate the contribution of DHA status to prefrontal structure and risk of drinkig initiation 1.5 years later, blood levels of DHA and PFC cortical thickness prior to alcohol initiaton will be entered into a structural equation model along with socioeconomic status and IQ to determine the proportion of variance in alcohol initiation that is explained by this collective setof predictors. Secondly, we will evaluate the contribution of DHA status to prefrontal function and subsequent risk of drinking initiation 1.5 years later using a similar model. Lastly, a model incorporating DHA and both structural and functional factors will be explored. The proposed research uniquely leverages an ongoing prospective study of adolescents seeking to identify the neurobiological and cognitive antecedents of alcohol initiation. The hypothesized results would suggest that dietary modification during adolescence may be an intervention which could help catalyze morphological and functional neurodevelopment, delaying alcohol initiation and reducing longer-term alcohol misuse.
NIH ExPorter
NIH ExPorter