CO(2) hypersensitivity in recently abstinent alcohol dependent individuals:; A possible mechanism underlying the high risk for anxiety disorder among alcoholics

Alcohol, administered acutely, is known to cause CO(2) hyposensitivity. CO(2) hypersensitivity associated with anxiogenic hyperventilation (HV) could reasonably be expected to emerge as an opponent process upon withdrawal from chronic alcohol use. To test this hypothesis, we applied two well-known methods to quantify CO(2) sensitivity in recently detoxified alcohol-dependent individuals and never alcohol-disordered individuals who are social drinkers. We found that the alcoholic group exhibited significantly greater CO(2) sensitivity than did controls in response to both challenges. Indirect evidence of chronic HV was also obtained. These findings implicate the effect of chronic alcohol use on CNS-based CO(2) sensitivity in heightening the vulnerability to disturbing anxiety symptoms and syndromes exhibited by alcoholic individuals. Future work must verify that pathological drinking actually causes the dysregulated respiratory responding observed in this study as is inferred in our conclusions.