Academic journal article Alcohol Research: Current Reviews

How Does Stress Lead to Risk of Alcohol Relapse?

Academic journal article Alcohol Research: Current Reviews

How Does Stress Lead to Risk of Alcohol Relapse?

Article excerpt

It has long been known that stress I increases the risk of alcohol relapse I (Sinha 2001). Clinical observations, surveys, and epidemiological studies document an association between self-reports of stressors and subsequent return to drinking. Studies assessing alcohol relapse after treatment completion and discharge also indicate the contribution of highly stressful events independent of alcohol use history that increase the risk of subsequent relapse (Brown et al. 1990). Furthermore, negative mood and stress are associated with increased craving, and high levels of urges to use alcohol predict relapse (Cooney et al. 2007). However, the mechanisms by which stress exposure increases alcohol relapse risk have been elusive, until recently. The last two decades have seen a dramatic increase in preclinical and clinical research to understand psychobiological and neural evidence linking stress and alcohol consumption. Evidence suggests that the neural circuits involved in stress and emotions overlap substantially with the brain systems involved in drug reward. Chronic alcohol use can result in neuroadaptive changes in stress and reward pathways. Such changes may alter an alcohol-dependent person's response to stress, particularly with respect to stress and emotion regulation and motivation for alcohol, which in turn may increase the risk of relapse (Sinha 2001, 2005).

To put the stress and alcohol relapse linkage in the clinical context, the sidebar presents sample descriptions of an acute stressful life event and an acute alcohol-related situation that led to subsequent alcohol use in a person with alcohol dependence. The patient vignettes are descriptions provided by patients currently in treatment and refer to previous experiences and episodes of alcohol use and relapse.

Chronic Alcohol-Related Changes in Emotion, Stress, and Motivational Systems

Converging lines of evidence indicate that regular and chronic alcohol use is associated with changes in emotion, stress, and motivational pathways. These changes may in turn influence alcohol craving and relapse risk. Chronic alcohol use increases stress-related symptoms and is associated with increased anxiety and negative emotions; changes in sleep and appetite; aggressive behaviors; changes in attention, concentration, and memory; and desire/craving for alcohol (Sinha 2001, 2007, 2009). Stress-related symptoms are most prominent during early abstinence from chronic alcohol use, but some of these changes also have been documented during active use of specific drugs. Chronic alcohol abuse and acute alcohol withdrawal states are associated with heightened activity in the brain stress systems, such as increased secretion of the stress hormones corticotropin-releasing factor (CRF), norepinephrine, and cortisol in a number of the brain's stress and emotion centers, such as the hypothalamus (1), amygdala, hippocampus, and prefrontal regions (Koob and Kreek 2007). Chronic alcohol abuse also alters dopaminergic signaling in the ventral striatum (VS) and the ventral tegmental area (VTA). And such changes are associated with increased alcohol seeking (craving) and alcohol self-administration in laboratory animals (Cleck and Blendy 2008; Koob and Kreek 2007; Koob et al. 2004; Rasmussen et al. 2006). Further corroboration from human neuroimaging studies indicates that chronic alcohol abuse reduces dopamine receptors (i.e., [D.sub.2] receptors) in striatal regions and dopamine transmission in the frontal lobe in alcoholics during acute withdrawal and protracted withdrawal (up to 3-4 months) (see Volkow 2004 for review). Functional imaging studies indicate increased VS activity in response to alcohol cues and altered brain response in the amygdala to emotional stimuli with chronic alcohol use (Gilman and Hommer 2008; Heinz et al. 2004, 2005; Martinez et al. 2007).

The biological stress response is most commonly detected in humans by activation of the hypothalamic-pituitary-adrenal (HPA) axis involving CRF-stimulated release of adrenocorti-cotropin (ACTH) from the anterior pituitary, which in turn stimulates the adrenal glands to release the stress hormone cortisol, which is involved in mobilizing and regulating the body's stress response. …

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