Date of Award
Master of Arts in Psychology
Mark D. Wood
Enhanced reinforcement has figured prominently in etiologic models of alcohol involvement and may be of particular relevance in adolescence and emerging adulthood. We prospectively examined an enhanced reinforcement model in a sample of emerging adults and augmented the model with a promising candidate gene, OPRMl, which has demonstrated associations with both alcohol outcomes and psychosocial factors comprising the enhanced reinforcement model. We examined whether a putatively functional polymorphism in the OPRMI gene was associated with heavy episodic drinking (HED) and negative consequences from drinking across four years via a number of intervening psychosocial factors, including behavioral undercontrol, subjective responses to alcohol, and cognitive factors (alcohol expectancies).
Participants (N = 1,0 14) were recruited prior to college matriculation for a randomized trial of two alcohol preventive interventions and were assessed via telephone surveys at baseline, and l 0-, 22-, and 46-months. Retention rates were 90.8% of randomized students at 10-months and 84.0% at 22-months. The 46-month assessment that was later added had a retention rate of 62.0%. At Wave 4, 521 students provided a saliva sample for DNA analysis. Participants were considered "at-risk" if they carried at least one copy of the OPRMI putative risk allele (the G allele of the A 118G SNP).
A series of growth curve models tested growth in two outcomes, HED and consequences, across the college years. Unconditional models suggested the functional form of HED was well captured by a quadratic growth model with an intercept, and linear and quadratic slope factors. Unconditional models suggested the functional form for the consequences outcome was linear with freely estimated time points for the linear slope factor. Gender and intervention conditions were included as exogenous factors along with family history (FH) and OPRMI statuses. Behavioral undercontrol (BU), and subjective effects (SE) were included as mediators of FH and OPRMI with activity enhancement expectancies (EXP) estimated as mediators of BU and SE effects. With the inclusion of direct paths from BU and SE to the intercept and slopes, model fit was acceptable for both models tested (CFI = .93, RMSEA = .056, for HED and CFI = 0.94, RMSEA = 0.055 for consequences). BU, EXP, and SE demonstrated significant positive associations with the intercept of HED, while only SE prospectively predicted the first growth factor. Indirect effects tested between family history and initial levels of HED were significant, indicative of partial mediation. Female gender and EXP were positively associated and SE was negatively associated with the second growth factor in the HED model. BU, EXP and SE were associated with the intercept and growth factor in the consequences model such that individuals with disinhibited personality traits and positive alcohol expectancies were susceptible to more initial problems and an increase in problems over time. However, SE was negatively associated with the growth of problems over time, suggesting that those with less sensitivity to alcohol may experience less change in problems over time. Indirect effects in the consequences model were also significant, indicative of partial mediation between FH and alcohol use consequences. OPRMI risk was not associated with any of the model's factors. Findings provide modest support for an enhanced reinforcement model and extend prospective evidence for the salience of the personality and cognitive factors tested in this model.
Martin, Scott D., "Investigating a Genetically Informed Enhanced Reinforcement Model of Alcohol Involvement: A Prospective Analysis" (2012). Open Access Master's Theses. Paper 1592.