Targeting Stress Pathophysiology to Improve Alcoholism Relapse Outcomes.

Abstract

Excessive alcohol use is one of the top behavioral causes of global disease burden. A major factor contributing to this burden is the alcohol relapse risk during treatment and recovery from alcoholism. Clinical studies suggest that stress is one of the key factors that contributes to these high-relapse rates (Blaine et al, 2016). Changes in hypothalamic pituitary adrenal (HPA) axis responses, altered and blunted amygdala response to fear/threat potentiated startle in heavy drinkers compared with light social drinkers and autonomic imbalance in sympathetic/parasympathetic systems, have been reported with increased alcohol use (Sinha et al, 2011a). Furthermore, acute alcohol intake stimulates the HPA axis and increases cortisol levels (see Blaine et al (2016) for review), but chronic alcohol abuse is associated with blunted stress cortisol responses (Lovallo et al, 2000). In addition, alcohol withdrawal is associated with elevated basal cortisol (Blaine et al, 2016).