Early life adversity reduces stress reactivity and enhances impulsive behavior: implications for health behaviors

Abstract

Altered reactivity to stress, either in the direction of exaggerated reactivity or diminished reactivity, may signal a dysregulation of systems intended to maintain homeostasis and a state of good health. Evidence has accumulated that diminished reactivity to psychosocial stress may signal poor health outcomes. One source of diminished cortisol and autonomic reactivity is the experience of adverse rearing during childhood and adolescence. The Oklahoma Family Health Patterns Project has examined a cohort of 426 healthy young adults with and without a family history of alcoholism. Regardless of family history, persons who had experienced high degrees of adversity prior to age 16 had a constellation of changes including reduced cortisol and heart rate reactivity, diminished cognitive capacity, and unstable regulation of affect, leading to behavioral impulsivity and antisocial tendencies. We present a model whereby this constellation of physiological, cognitive, and affective tendencies is consistent with altered central dopaminergic activity leading to changes in brain function that may foster impulsive and risky behaviors. These in turn may promote greater use of alcohol other drugs along with adopting poor health behaviors. This model provides a pathway from early life adversity to low stress reactivity that forms a basis for risky behaviors and poor health outcomes.

Keywords: 5-HT; ASPD; Addiction; Affect; COMT; CPI-So; California Personality Inventory Sociability Scale; Cognition; Cortisol; Early life adversity; FH+; FH−; HPA; Impulsivity; MAOA; OFHP; Oklahoma Family Health Patterns; SES; Stress reactivity; antisocial personality disorder; catechol-o-methyltransferase; hypothalamic–pituitary–adrenocortical axis; monoamineoxidase A; negative family history of alcoholism; positive family history of alcoholism; serotonin; socioeconomic status.

Published by Elsevier B.V.

Figures

Figure 1

Cortisol and heart rate responses to psychosocial stress in persons low, medium, and high (0, 1, > 1) in lifetime adverse experience (Right Panels), and diurnal patterns of cortisol secretion in the men and women from the same adversity groups on a nonstress day (Left Panels). Subjects were exposed to 30 min of speech preparation and delivery (3 4-min speeches) and 15 min of mental arithmetic. Reprinted from “Lifetime adversity leads to blunted stress axis reactivity: studies from the oklahoma family health patterns project,” by W.R. Lovallo, N.H. Farag, K.H. Sorocco, A.J. Cohoon, and A.S. Vincent, 2012, Biological Psychiatry, 71, pp. 344–349.

Figure 2

Pathway from adverse life experience to risky health behaviors. This conceptual model summarizes a series of steps through which the experience of stressful events in childhood and adolescence may alter behavior patterns in a way that can lead to adverse health outcomes. Life experience is seen as being processed through regions of the brain that evaluate ongoing events and shape coping behaviors and bodily responses that support these coping behaviors. These frontolimbic structures include key portions of the limbic system and the prefrontal cortex. Because these are areas whose functional connectivity is highly modifiabe by experience, there are at least three consequences of adverse experience based on empirical findings: 1) Stress reactivity is reduced; 2) Cognitive processing is shifted toward a focus on short term goals and a more impulsive response selection; 3) Regulation of affect is less stable and prone to negative states. It appears that these three immediate consequences of modified frontolimbic functions may result in an impulsive behavioral style that includes a tendency toward risk taking. Over the course of a lifetime, this behavioral style may have an impact on health through a tendency to use alcohol and other drugs and to engage in unhealthy behaviors such as smoking.