A smaller emergent literature has focused on the contributions of a corticolimbic circuit supporting threat processing in the emergence of AUD risk. Several studies provide convergent evidence that relatively reduced threat-related reactivity of the amygdala, which functions as the information processing hub of the corticolimbic circuit, may increase AUD risk, possibly via diminished recognition of, and reaction to, the hazards of excessive drinking. Specifically, one prior study has demonstrated blunted threat-related amygdala reactivity in currently healthy individuals at high familial risk for AUD.18 Along similar lines, genetic liability for substance use19 has been linked to relatively reduced threat-related amygdala reactivity in a normative population of middle-aged adults.20 Conversely, we recently demonstrated that relatively increased threat-related amygdala reactivity may be a protective factor against stress-related problem drinking associated with relative VS hyper-activity in university students.21 Interestingly, heightened threat-related amygdala reactivity is characteristic of mood and anxiety disorders,22, 23 which are frequently comorbid with, and contribute to the emergence of, AUD.24, 25 Thus, as may be true with reward-related VS activity, both hypo- and hyper-reactivity of the amygdala to threat may contribute to AUD risk.
