stress dysregulation, anxiety, and high levels of associated stress- or alcohol cue-induced alcohol craving. For example, while naltrexone hydrochloride decreases alcohol-induced craving, to our knowledge, its effects in decreasing stress-induced alcohol craving have not been shown in human studies. The current findings suggest that targeting the identified stress-related pathophysiology with medications that decrease anxiety and high provoked craving and normalize HPA axis function could be of benefit in improving relapse outcomes as well as increasing treatment engagement after inpatient alcohol treatment. Several potential pharmacologic targets have been identified in animal models of stress-induced alcohol relapse and in addressing alcohol relapse risk in humans.42,44 For example, nonpeptide CRF1 antagonists and noradrenergic agents have shown promise in reducing stress-induced relapse in animal models and would be an important class of agents to study in human laboratory models and with further clinical trials. Such strategies to decrease stress-related pathophysiology and provoked alcohol craving could ultimately reduce alcohol relapse risk, thereby decreasing the alcohol-related disease burden associated with high relapse rates in alcohol use disorders.
