Stress, Social Processes, and Health Over the Lifecourse

Shelley E. TaylorUniversity of California, Los Angeles

May 21, 2009Advancing Integrative Psychological

Research on Adaptive and Healthy AgingUniversity of California, Berkeley

Significant Contributions1) 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: 402-409)

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 andCortisol 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 Polymorphismand 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 forregulation 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, 296-301.

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