Psychosocial processes are implicated in health decisions and in mental and physical health outcomes across the lifespan. However, little research has explored their origins in genetic, early environment, and neurocognitive processes in conjunction with these consequences. The proposed research examines genetic, SES, and family environment origins of psychosocial resources/risk factors and the neural mechanisms (ACC, amygdala, hypothalamus, RFC) that link them to poor health behaviors and psychological and biological (cardiovascular, HPA axis, proinflammatory cytokine) stress responses. Young adults (N= 120) complete assessments of early environment and psychosocial resources/risk factors and are genotyped for genes related to the serotonin and dopamine systems. In a neuroimaging sub-study, half the sample completes tasks previously demonstrated to evoke ACC, amygdala, and PFC responses to threatening tasks. All participants participate in the Trier Social Stress Task (TSST), during which cardiovascular responses, cortisol, and proinflammatory cytokines (IL-6 and sTNF-RII) are assessed. We test predictions that 1) Psychosocial resources/risk factors derive, in part, from individual differences in genes related to dopaminergic and serontonergic functioning, from an early family environment, and from their interaction; 2) Psychosocial resources (optimism, mastery, self-esteem, social support) are evident at the neural level in lower dACC, amygdala, and hypothalamic responses to threat and greater PFC responses to threats; 3) Poor health decisions and psychosocial risk factors (e.g., negative emotionality, low SES, early adverse environment) are evident at the neural level in higher dACC, amygdala, and hypothalamic, and lower PFC responses to threat; and 4) Deficits in psychosocial resources will be associated with poor health decisions through pathways implicating genetic differences, early environment, and neural differences in responsivity to threat-related stimuli as predictors, and enhanced biological/psychological responses to stress as consequences. Evidence in support of these hypotheses will provide an integrated assessment of the early environment, genetic, and neural mechanisms that underlie health decision making and mental and physical health outcomes. As such, the research brings a lifespan approach to an integration of genetics, psychoneuroimmunology, health psychology, and social neuroscience. ? ? ?
| Chiang, Jessica J; Taylor, Shelley E; Bower, Julienne E (2015) Early adversity, neural development, and inflammation. Dev Psychobiol 57:887-907 |
| Moons, Wesley G; Way, Baldwin M; Taylor, Shelley E (2014) Oxytocin and vasopressin receptor polymorphisms interact with circulating neuropeptides to predict human emotional reactions to stress. Emotion 14:562-72 |
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| Chiang, Jessica J; Eisenberger, Naomi I; Seeman, Teresa E et al. (2012) Negative and competitive social interactions are related to heightened proinflammatory cytokine activity. Proc Natl Acad Sci U S A 109:1878-82 |
| Way, Baldwin M; Taylor, Shelley E (2011) A polymorphism in the serotonin transporter gene moderates cardiovascular reactivity to psychosocial stress. Psychosom Med 73:310-7 |
| Saphire-Bernstein, Shimon; Way, Baldwin M; Kim, Heejung S et al. (2011) Oxytocin receptor gene (OXTR) is related to psychological resources. Proc Natl Acad Sci U S A 108:15118-22 |
| Taylor, Shelley E; Way, Baldwin M; Seeman, Teresa E (2011) Early adversity and adult health outcomes. Dev Psychopathol 23:939-54 |
| Tomiyama, A Janet; Mann, Traci; Vinas, Danielle et al. (2010) Low calorie dieting increases cortisol. Psychosom Med 72:357-64 |
| Taylor, Shelley E (2010) Inaugural article: mechanisms linking early life stress to adult health outcomes. Proc Natl Acad Sci U S A 107:8507-12 |
| Pluess, Michael; Belsky, Jay; Way, Baldwin M et al. (2010) 5-HTTLPR moderates effects of current life events on neuroticism: differential susceptibility to environmental influences. Prog Neuropsychopharmacol Biol Psychiatry 34:1070-4 |
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