Neurobiological mechanisms of early life adversity, blunted stress reactivity and risk for addiction

Abstract

Blunted stress reactivity resulting from early exposure to stress during childhood and adolescence may increase vulnerability to addiction. Early life adversity (ELA) affects brain structure and function and results in blunted stress axis reactivity. In this review, we focus on the underlying neurobiological mechanisms associated with a blunted response to stress, ELA, and risk for addictive disorders. ELA and blunted reactivity are accompanied by unstable mood regulation, impulsive behaviors, and reduced cognitive function. Neuroimaging studies reveal cortical and subcortical changes in persons exposed to ELA and those who have a genetic disposition for addiction. We propose a model in which blunted stress reactivity may be a marker of risk for addiction through an altered motivational and behavioral reactivity to stress that contribute to disinhibited behavioral reactivity and impulsivity leading in turn to increased vulnerability for substance use. Evidence supporting this hypothesis in the context of substance use initiation, maintenance, and risk for relapse is presented. The effects of ELA on persons at risk for addiction may lead to early experimentation with drugs of abuse. Early adoption of drug intake may alter neuroregulation in such vulnerable persons leading to a permanent dysregulation of motivational responses consistent with dependence. This article is part of the special issue on 'Vulnerabilities to Substance Abuse'.

Keywords: Addiction risk; Early life adversity; HPA axis; Neurobiological mechanisms; Stress reactivity.

Fig. 1.

The influence of early life stress and genetic predisposition in modifying brain development and stress response systems leading to poor decision making and increased vulnerability for substance use. The gradient oval indicates that a range of protective factors may confer either low or high levels of protection to individuals, with the result that risk for substance use disorders is manifested to different degrees in downstream outputs.