Mechanisms linking early life stress to adult health outcomes

Abstract

Research relating stress to health has progressed from anecdotal evidence in the 1930s and 1940s to complex multivariate models that identify underlying longitudinal mechanisms. Enduring questions that have guided our research are: How does the early life environment affect health outcomes into adulthood? How is the latent damage stored and what processes are set into motion that link early life stress to health disorders in the later years? An emerging perspective focuses on the accumulation of interacting dysregulations in multiple physiological systems that compromise the systems' abilities to respond flexibly to stressful circumstances. Our research explores: the antecedents of these processes, including genetic predispositions, the harshness of the early environment, and their interaction; the mediating roles of neural regulation in the brain and psychological and social resources; and health-related outcomes, such as metabolic functioning and inflammatory processes.

Fig. 1.

Stress and health across the lifespan.

Fig. 2.

Neural activity in the left and right amygdala for people from nurturant and harsh families.

Fig. 3.

Relationship of the 5-HTTLPR and the quality of the early family environment to depressive symptomatology. [Reprinted from Biological Psychiatry, vol. 60, Taylor SE, et al., Early family environment, current adversity, the serotonin transporter polymorphism, and depressive symptomatology, 672, Copyright (2006), with permission from Elsevier; http://journals.elsevierhealth.com/periodicals/bps.]

Fig. 4.

Relationship between daily social support and cortisol reactivity during the Trier Social Stress Task (TSST).

Fig. 5.

(A) RVLPFC activity during labeling of emotions as a function of psychosocial resources; (B) Left amygdala activation during threat task as a function of psychosocial resources; (C) Relation of left amygdala during threat task to cortisol reactivity during TSST.