Acute alcohol response phenotype in heavy social drinkers is robust and reproducible.
- Authors
- Roche, Daniel J O; Palmeri, Michael D; King, Andrea C
- Year
- 2014
- Journal
- Alcoholism, clinical and experimental research
- PMID
- 24117681
- DOI
- 10.1111/acer.12280
- PMCID
- PMC4167376
BACKGROUND: In 3 previously published works (Brumback et al., 2007, Drug Alcohol Depend 91:10-17; King et al., 2011a, Arch Gen Psychiatry 68:389-399; Roche and King, 2010, Psychopharmacology (Berl) 212:33-44), our group characterized acute alcohol responses in a large group of young, heavy binge drinkers (n = 104) across a variety of subjective, eye-tracking, and psychometric performance measures. METHODS: The primary goal of the current study was to directly replicate prior findings of alcohol response in heavy social drinkers (HD) in a second independent cohort (n = 104) using identical methodology. A secondary goal was to examine the effects of family history (FH) of alcohol use disorders (AUD) on acute alcohol response in both samples. Participants attended 2 randomized laboratory sessions in which they consumed 0.8 g/kg alcohol or a taste-masked placebo. At pre- and post-drink time points, participants completed subjective scales, psychomotor performance and eye-movement tasks, and provided salivary samples for cortisol determination. RESULTS: Results showed that the second cohort of heavy drinkers exhibited a nearly identical pattern of alcohol responses to the original cohort, including sensitivity to alcohol's stimulating and hedonically rewarding effects during the rising breath alcohol content (BrAC) limb, increases in sedation during the declining BrAC limb, a lack of cortisol response, and psychomotor and eye-tracking impairment that was most evident at peak BrAC. The magnitude and temporal pattern of these acute effects of alcohol in the second cohort were similar to the first cohort across all measures, with the exception of 3 eye-movement measures: pro- and antisaccade accuracy and antisaccade velocity. FH of AUD did not affect alcohol response in the first cohort, and this was replicated in the second cohort. CONCLUSIONS: In sum, in 2 independent samples, we have demonstrated that HD display a consistent and reliable sensitivity to alcohol's subjective effects and impairment of eye-tracking and psychomotor performance, which is not affected by FH status. This acute alcohol response phenotype in heavy, frequent binge drinkers appears to be robust and reproducible.
Subjective MeasuresSubjective response to alcohol and placebo in Cohort 1 and Cohort 2 heavy drinkers as measured by (a) BAES Stimulation, (b) BAES Sedation, (c) DEQ Like, & (d) DEQ Want More. Alcohol significantly increased all subjective measures in both cohorts (dose × time, p’s < 0.0001 for both cohorts on stimulation, sedation, like, and want more). The data presented from Cohort 1 was previously published in King et al., (2011a).
Eye Tracking ResultsThe effect of alcohol and placebo on (a) smooth pursuit gain, (b) pro-saccade latency (msec.), & (c) anti-saccade latency (msec.) in Cohort 1 and Cohort 2 HD. Alcohol significantly decreased smooth pursuit gain and increased pro- and anti-saccade latency in both cohorts (dose × time, p’s < 0.0001 for gain, pro-saccade latency, and anti-saccade latency). The data presented from Cohort 1 was previously published in Roche and King (2010).
Performance MeasuresThe effect of alcohol and placebo on (a) DSST & (b) Grooved Pegboard performance in Cohort 1 and Cohort 2 heavy drinkers. Alcohol significantly decreased DSST (# correct) and Grooved Pegboard (sec.) performance in both cohorts (dose × time, p’s < 0.0001 for DSST and Pegboard). The data presented from Cohort 1 was previously published in Brumback et al., (2007).
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