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The developmental period of adolescence is characterized by increasing incidence of health risk behaviors ( HRBs). Based on theoretical models that emphasize the moderating role of cognitive control, this study examined how neural correlates of cognitive control and risk sensitivity interact to predict HRBs among late adolescents (17-20 years). Neuroimaging data indicate that risk-related hemodynamic activity in the anterior insula during anticipation of uncertain outcomes predicts HRBs among late adolescents exhibiting greater dorsal anterior cingulate cortex (d ACC) activity during a cognitive interference task but not among late adolescents requiring less d ACC activity. These results present neural evidence for a significant moderating effect of cognitive control on the link between risk sensitivity and HRBs among late adolescents. [ABSTRACT FROM AUTHOR]

Individuals' risk attitudes are known to guide choices about uncertain options. However, in the presence of others' decisions, these choices can be swayed and manifest as riskier or safer behavior than one would express alone. To test the mechanisms underlying effective social 'nudges' in human decision-making, we used functional neuroimaging and a task in which participants made choices about gambles alone and after observing others' selections. Against three alternative explanations, we found that observing others' choices of gambles increased the subjective value (utility) of those gambles for the observer. This 'other-conferred utility' was encoded in ventromedial prefrontal cortex, and these neural signals predicted conformity. We further identified a parametric interaction with individual risk preferences in anterior cingulate cortex and insula. These data provide a neuromechanistic account of how information from others is integrated with individual preferences that may explain preference-congruent susceptibility to social signals of safety and risk. [ABSTRACT FROM AUTHOR]

Interpersonal factors play significant roles in the onset, maintenance, and remission of psychiatric conditions. In the current major diagnostic classification systems for psychiatric disorders, some conditions are defined by the presence of impairments in social interaction or maintaining interpersonal relationships; these include autism, social phobia, and the personality disorders. Other psychopathologies confer significant difficulties in the social domain, including major depression, posttraumatic stress disorder, and psychotic disorders. Still other mental health conditions, including substance abuse and eating disorders, seem to be exacerbated or triggered in part by the influence of social peers. For each of these and other psychiatric conditions, the extent and quality of social support is a strong determinant of outcome such that high social support predicts symptom improvement and remission. Despite the central role of interpersonal factors in psychiatric illness, the neurobiology of social impairments remains largely unexplored, in part due to difficulties eliciting and quantifying interpersonal processes in a parametric manner. Recent advances in functional neuroimaging, combined with multiplayer exchange games drawn from behavioral economics, and computational/quantitative approaches more generally, provide a fitting paradigm within which to study interpersonal function and dysfunction in psychiatric conditions. In this review, we outline the importance of interpersonal factors in psychiatric illness and discuss ways in which neuroeconomics provides a tractable framework within which to examine the neurobiology of social dysfunction. [ABSTRACT FROM AUTHOR]

Disproportionate reactions to unexpected stimuli in the environment are a cardinal symptom of posttraumatic stress disorder (PTSD). Here, we test whether these heightened responses are associated with disruptions in distinct components of reinforcement learning. Specifically, using functional neuroimaging, a loss-learning task, and a computational model-based approach, we assessed the mechanistic hypothesis that overreactions to stimuli in PTSD arise from anomalous gating of attention during learning (i.e., associability). Behavioral choices of combat- deployed veterans with and without PTSD were fit to a reinforcement learning model, generating trial-by-trial prediction errors (signaling unexpected outcomes) and associability values (signaling attention allocation to the unexpected outcomes). Neural substrates of associability value and behavioral parameter estimates of associability updating, but not prediction error, increased with PTSD during loss learning. Moreover, the interaction of PTSD severity with neural markers of associability value predicted behavioral choices. These results indicate that increased attention- based learning may underlie aspects of PTSD and suggest potential neuromechanistic treatment targets. [ABSTRACT FROM AUTHOR]