The relationship between risk-taking propensity and the COMT Val(158)Met polymorphism among early adolescents as a function of sex

Virginia Institute of Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Department of Psychiatry, 800 E. Leigh Street, P.O. Box 980126, Richmond, VA 23298-0126, USA.
Journal of Psychiatric Research (Impact Factor: 3.96). 05/2012; 46(7):940-5. DOI: 10.1016/j.jpsychires.2012.04.010
Source: PubMed


Although adolescents frequently engage in a variety of risky behaviors, much remains unknown about the specific etiologies of such tendencies. Candidate genetic variants, such as the COMT Val(158)Met polymorphism, may be related to risk-taking propensity, particularly as this variant is linked to functional enzymatic differences influencing dopamine function in regions including the prefrontal cortex. The present study aimed to examine the COMT Val(158)Met variant in relation to risk-taking propensity in a community sample of youth. As part of a larger longitudinal study on adolescent risk behaviors, 223 youths (average age 11.3 years) from the metropolitan Washington D.C. area completed a measure of risk-taking propensity, the Balloon Analog Risk Task-Youth Version (BART-Y), and provided saliva samples for DNA extraction and genotyping. Results indicate that females, but not males, who are carriers of the COMT 158Met allele had higher risk-taking propensity scores on the BART-Y compared to Val homozygotes. Analyses were also conducted in the 111 European American participants, and results were consistent with those of the full sample analyses. This study represents the first investigation of a genetic substrate of risk-taking propensity, measured by a behavioral task, in youth. Results should be taken as quite preliminary, given the small sample. Implications are discussed.

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    • "We further showed that this association led to a beneficial increase in risky decision making on the Balloon Analogue Risk Task (BART), in which the met homozygotes were more sensitive to rewards, allowing them to benefit from the rewards available during the task to a greater degree than participants with val/met and val/val genotypes. Exaggerated risky decision making by COMT met homozygotes during the BART has also been reported by other researchers (Amstadter et al. 2012). In this study, "
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    ABSTRACT: Previous studies suggest that a single nucleotide polymorphism in the COMT gene (val158met) may modulate reward-guided decision-making in healthy individuals. The polymorphism affects dopamine catabolism and thus modulates prefrontal dopamine levels, which may lead to variation in individual responses to risk and reward. We previously showed, using tasks that index reward responsiveness (measured by responses bias towards reinforced stimuli) and risk-taking (measured by the Balloon Analogue Risk Task), that COMT met homozygotes had increased reward responsiveness and thus, an increased propensity to seek reward. In the present study, we sought to replicate these effects, in a larger, independent cohort of Caucasian U.K university students and staff with similar demographic characteristics (n = 101; 54 female, mean age: 22.2 years). Similarly to our previous study, we observed a significant trial × COMT genotype interaction (P = .047; ƞ(2) = .052), which was driven by a significant effect of COMT on the incremental acquisition of response bias (response bias at block three - block one (met/met > val/val: P = .028) and block three - block two (met/met > val/val: P = .007), suggesting that COMT met homozygotes demonstrated higher levels of reward responsiveness by the end of the task. However, we failed to see main effects of COMT genotype on overall response bias or risk-seeking behaviour. These results provide additional evidence that prefrontal dopaminergic variation may have a role in reward responsiveness, but not risk-seeking behaviour. Our findings may have implications for neuropsychiatric disorders characterised by clinical deficits in reward-processing such as anhedonia. This article is protected by copyright. All rights reserved.
    Genes Brain and Behavior 06/2015; 14(6). DOI:10.1111/gbb.12228 · 3.66 Impact Factor
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    • "By uncovering the neural correlates of treatment approaches such as motivational interviewing, researchers have discovered a potential link between the active in-session ingredients of treatment with outside-of-session behavior change (Feldstein Ewing et al., 2012). Furthermore, groundbreaking research studies are also ascertaining genetic associations, including preliminary identifications of the genetic substrate of risk-taking propensity tasks among youths (Amstadter et al., 2012) and neurocognitive phenotypes that may predict treatment response for alcohol abuse (Chung, 2012). There is a growing body of research evidence for the utility of neuroscience that examines brain structure (e.g., Chung, Pajtek, & Clark, 2013; Jacobus et al., 2013; Monnig et al., 2013) and brain function (e.g., Feldstein Ewing et al., 2013; Jacobus et al., 2013; Wetherill & Tapert, 2013) to inform treatment development and tracking treatment progress for adolescents . "
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    Psychology of Addictive Behaviors 06/2013; 27(2):547-51. DOI:10.1037/a0032434 · 2.09 Impact Factor
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    • "Alterations in the dopamine system within the fronto-striatothalamic circuits have been suggested to contribute to the cognitive impairments observed in schizophrenia and normal aging (Cropley et al., 2006), while dopamine levels in the prefrontal cortex seem to be crucial for the functioning of prefrontal-related cognitive flexibility in the general population (Amstadter et al., 2012; Goldman-Rakic et al., 2000). These findings have promoted the search for genes with a role in the metabolism of dopamine that may help explain both its impairment in brain disorders and the normal variation of higher-order cognitive functions. "
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    ABSTRACT: The functional variant Val(158)Met in the coding sequence of COMT gene is involved in the modulation of dopamine availability in the prefrontal cortex in both clinical and general population samples. It has been suggested that the interplay between this genotype and early environmental factors could be used to predict the observed variation in cognitive flexibility. However, other genetic variants and environmental factors may confound the association and produce the inconsistent results commonly found in the literature. In the present study we aimed at testing putative interaction mechanisms between childhood maltreatment and COMT genotypic variability that might explain a proportion of the observed variability of cognitive flexibility in the population. Our design was based on a sample of adult monozygotic twins, which allowed us to test these effects free from potential genetic and shared-environmental confounding factors. Results showed that unique environmental effects of childhood maltreatment significantly impacted cognitive performance among Met/Met subjects. Interestingly, the direction of the association indicated that exposure to early stressful experiences was associated with enhanced cognitive flexibility in this genotype group. These results suggest that COMT may operate as a plasticity gene that provides differential cognitive capacity to respond to environmental stressors.
    Journal of Psychiatric Research 03/2013; 47(7). DOI:10.1016/j.jpsychires.2013.02.002 · 3.96 Impact Factor
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