The influence of alcohol oral intake on the effects of 35% CO2 challenge. A study in healthy volunteers

Alcohol use disorders and panic disorder co-occur at a rate that exceeds chance significantly. The reason of this comorbidity is unclear; it may be related to psychological or biological factors. First, alcohol consumption could lower anxiety by diverting attention from anxiogenic cues and because people believe in the anxiolytic effect of alcohol. On the other hand the effect of alcohol could be linked to its pharmacological properties. Although numerous studies have been devoted to the pharmacology of alcohol and the underlying mechanism of alcoholism, only a small number has examined the causes underlying its comorbidity with other disorders using experimental methodologies. The present study tested whether alcohol consumption reduces anxiety associated with a panic-challenge procedure (35% CO2 challenge) in order to evidence a direct pharmacological interaction between alcohol and experimental panic. The dose of alcohol used was small (Blood Alcohol Concentration = 50 mg/dl) to keep the subjects as far as possible below the threshold of any clinically relevant intoxication. Methods: the study was conducted according to a placebo-controlled, double-blind, randomised design. Eight healthy volunteers were enrolled (power = 95: 5 males, 3 females with a mean age of 36.63 years. All subject had a complete medical history inventory, a physical examination and an evaluation through the Mini International Neuropsychiatric Interview (MINI). Then they had an alcohol and a placebo oral intake according to a cross-over design. After each consumption, blood alcohol concentration was assessed and subjects underwent the 35% CO2 challenge and a series of anxiety and depressive symptoms assessment. Results: after alcohol intake, subjects presented a significant reduction of state anxiety associated with the challenge procedure. The Panic Symptom List score was significantly lower after alcohol intake (p = 0.032) if compared with the placebo. The Visual Analogous Anxiety Scale shows a trend to be lower after alcoholic drinking (p = 0.111). No statistically significant differences were found between the two testing days concerning the biological variables and the pre-challenge score of the PSL and the VAAS. No subject presented panic attacks during the 35% CO2 challenge. Conclusions: moderate doses of alcohol acutely decrease the response to a 35% CO2 challenge in healthy volunteers. These results lend support to the pharmacological anxiolytic effect of alcohol and to the view that this property may reinforce the drinking behaviour among those with high levels of anxiety. Related to the small dose of alcohol used, baseline anxiety did not vary significantly from the alcohol test day to the placebo test day. This means that the blunted response to CO2 observed after alcohol intake cannot be related to a decreased anticipatory anxiety, but to a specific inhibitory effect of ethanol on experimental panic. Further investigations are necessary especially referring to a larger sample including a clinical population of PD patients and using IV administration of ethanol, in order to eliminate any bias due to the act of drinking. Such investigations are presently underway in our laboratory.