Human behavior involves the unique capacities to regulate our own psychological states to pursue desired goals, bring our behavior in line with internal/external standards, manage our emotions, and cope with challenges and opportunities that arise. The term self-regulation denotes the processes through which people intentionally or automatically initiate, maintain, and terminate their own thoughts and behaviors in the service of pursuing personal goals. The importance of understanding self-regulation becomes obvious when one considers the array of public health problems that can be traced to problematic goal pursuit. Many behaviors that put people at increased risk for illness, disability, and death - such as obesity, eating disorders, smoking, alcohol abuse, suicidality, and drug addiction - involve difficulties with self-regulation. Thus, maladaptive self-regulation is an important contributory factor in a large number of psychological, social, and health-related problems. We believe that significant progress can be made in understanding and overcoming self- regulatory problems by combining existing theory and research in behavioral science with parallel findings in related disciplines. Recent developments in cognitive neuroscience (specifically, the role of the orbitofrontal cortex in self-regulation of goal pursuit) and imaging genetics (specifically, how heritable variability in the gene encoding catechol-O- methyltransferase [COMT], an enzyme that controls extracellular dopamine in the frontal cortex, influences processing of motivationally salient stimuli) offer synergistic perspectives on how failure in self-regulation could, for a particular subset of individuals, lead to chronically maladaptive behavior and increase vulnerability to a range of significant health problems.
The aims of this R01 application are: (1) to validate a hypothesized gene/environment/self-regulation risk phenotype conferring vulnerability to failures of self- regulation, and (2) to test a novel set of cognitive/behavioral techniques that we predict will acutely reverse the dysfunctions that underlie self-regulatory failure. The proposed research will be conducted in two samples: adolescents, who are vulnerable to initiation of a number of health-risking behaviors and psychological problems, and college students, some of whom already engage regularly in such behaviors and manifest psychological difficulties. We predict that a combination of three contributory factors - individual differences in regulatory focus, COMT genotype, and chronic failure to attain a particular kind of personal goal - creates a self- regulation pathway to disordered behaviors with significant public health implications.
The aims of this R01 application are: (1) to conduct a program of translational research validating a hypothesized gene/environment/self-regulation risk phenotype conferring vulnerability to failures of self-regulation, and (2) to test a novel set of cognitive/behavioral techniques that we predict will acutely reverse the dysfunctions that underlie self-regulatory failure. We predict that we will observe, in both adolescent and college student samples, that a combination of three contributory factors - individual differences in regulatory focus, COMT genotype, and chronic failure to attain a particular kind of personal goal - creates a self- regulation pathway to a broad array of disordered behaviors and psychological states with significant public health implications, including tobacco use, alcoholism, mood disorders, obesity, eating disorders, and impulsivity. Based on this model, we anticipate that the theory- based brief change techniques will prove efficacious and will ultimately provide a basis for effective broader-scale therapeutic and preventive interventions in future studies.
|Dotterer, Hailey L; Waller, Rebecca; Neumann, Craig S et al. (2016) Examining the Factor Structure of the Self-Report of Psychopathy Short-Form Across Four Young Adult Samples. Assessment :|
|Corral-FrÃas, N S; Pizzagalli, D A; CarrÃ©, J M et al. (2016) COMT Val(158) Met genotype is associated with reward learning: a replication study and meta-analysis. Genes Brain Behav 15:503-13|
|Hanson, Jamie L; Albert, Dustin; Iselin, Anne-Marie R et al. (2016) Cumulative stress in childhood is associated with blunted reward-related brain activity in adulthood. Soc Cogn Affect Neurosci 11:405-12|
|Swartz, J R; Hariri, A R; Williamson, D E (2016) An epigenetic mechanism links socioeconomic status to changes in depression-related brain function in high-risk adolescents. Mol Psychiatry :|
|Hyde, Luke W; Shaw, Daniel S; Murray, Laura et al. (2016) Dissecting the role of amygdala reactivity in antisocial behavior in a sample of young, low-income, urban men. Clin Psychol Sci 4:527-544|
|Bogdan, Ryan; Pagliaccio, David; Baranger, David Aa et al. (2016) Genetic Moderation of Stress Effects on Corticolimbic Circuitry. Neuropsychopharmacology 41:275-96|
|Nelson, E C; Agrawal, A; Heath, A C et al. (2016) Evidence of CNIH3 involvement in opioid dependence. Mol Psychiatry 21:608-14|
|Nikolova, Y S; Knodt, A R; Radtke, S R et al. (2016) Divergent responses of the amygdala and ventral striatum predict stress-related problem drinking in young adults: possible differential markers of affective and impulsive pathways of risk for alcohol use disorder. Mol Psychiatry 21:348-56|
|Trampush, Joey W; Lencz, Todd; Knowles, Emma et al. (2015) Independent evidence for an association between general cognitive ability and a genetic locus for educational attainment. Am J Med Genet B Neuropsychiatr Genet 168B:363-73|
|Victor, Elizabeth C; Sansosti, Alexandra A; Bowman, Hilary C et al. (2015) Differential patterns of amygdala and ventral striatum activation predict gender-specific changes in sexual risk behavior. J Neurosci 35:8896-900|
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