Stress, Social Processes, and Health Over the Lifecourse Shelley E. Taylor University of California, Los Angeles May 21, 2009 Advancing Integrative Psychological Research on Adaptive and Healthy Aging University of California, Berkeley

Significant Contributions 1) Animal Research (Meaney, Coplan & Rosenbloom, Suomi) 2) Clinical Research Maltreatment, abuse, and PTSD (e.g., Yahuda, Pollak) 3) Developmental Research Risky families (Repetti, Taylor) 4) Childhood SES Research Health implications into adulthood (Chen, Miller)

Focal Questions  Why do events early in life lead to health consequences not evident for decades? What processes are set into effect? How is the damage stored?

Metatheoretical Perspectives  Socioemotional skills and deficits (poor emotion regulation, low social support)  Allostatic load (accumulating physiological costs)  Early programming/critical periods – e.g., Barker hypothesis; Meaney’s HPA axis work  More tonic models – e.g., positive emotional functioning

Pathways  Goal: Integrative approaches across multiple levels of analysis  Examples: Genes Neural processes in the brain Neuroendocrine and immune functioning

Early-Life SES & GR mRNA in Adolescence Values adjusted for current age, ethnicity, social class, health practices (Miller & Chen, Psychosom Med, 2007; 69: )

People homozygous for the short allele had greater depressive symptomatology if they had experienced early adversity but significantly less depressive symptomatology if a supportive early environment

People homozygous for the short allele had greater depressive symptomatology if they were currently experiencing adversity but less depressive symptomatology if current positive experiences

The 5-HTTLPR and Cortisol Response to Social Stress (Way, Taylor et al. in preparation) Evaluation Condition:Control Condition: (F (6,333) =2.75, p =.013)(F (6,165) =1.68, p =.13)

(F (3,335) =2.91, p =.035)(F (3,180) =.14, p =.93) The A118G Polymorphism and Social Stress Evaluation Condition:Control Condition:

Risky Families Values adjusted for age, ethnicity, SES, smoking, adiposity (Miller, in preparation)

Risky Families, Stress-Responsive Phenotype Values adjusted for age, ethnicity, smoking, adiposity

Family Environment and Coping  Children from risky families show High levels of avoidant coping Overly aggressive responses to stressors perceived by others to be only moderately challenging Ineffective coping (Coping that does not reduce experienced stress) Question: Any neural evidence for these processes?

Brain candidates for regulation of stress responses  Amygdala, tied to threat detection and fear responses  RVLPFC (right ventrolateral prefrontal cortex), believed to regulate amygdala responses to threat

Observe Only Label Emotions Label Gender (Control Task)

In the observe only task, offspring from harsh environments show significantly lower amygdala activity, suggesting they are tuning out the stimuli

Implications  Growing up in a risky family environment marked by harsh parenting has effects on neural processes involved in threat detection and regulation of responses to threat  Offspring from risky families may not have effective threat detection and emotion regulation skills for coping with stressful circumstances Taylor, S. E., Eisenberger, N. I., Saxbe, D., Lehman, B. J., & Lieberman, M. D. (2006). Biological Psychiatry, 60,

Conclusions  Several not mutually exclusive metatheoretical models are available for understanding the impact of stress and socioemotional functioning on health across the lifespan  Multi-level approaches that integrate psychological and biological processes have the greatest potential to elucidate the underlying mechanisms