A co-twin-control analysis of adolescent and young adult drinking effects on learning and memory

Background and aims: Existing evidence for a link between alcohol use and memory impairments in adolescents and young adults is largely correlational. We aimed to determine whether associations between drinking and episodic memory were consistent with a causal effect of drinking or accounted for by familial factors confounding such associations. Because cannabis use is associated with a similar pattern of performance on episodic memory measures, we assessed whether any associations might be attributable to concurrent cannabis use.

Design, setting and participants: Observational study of individuals aged approximately 20-29 years, comprising two independent population-based cohorts of twins. A co-twin-control design permitted an estimate of alcohol exposure effects free of shared genetic and environmental confounding influences. Significant associations were followed-up with twin-difference analyses. Propensity scores derived from measures collected at age 11 were used to adjust for unshared confounders. Participants in both cohorts were assessed from the age of 11 (n = 1251) under the auspices of the Minnesota Center for Twin and Family Research.

Measurements: Regression analyses with cumulative alcohol use as the predictor of interest. Multiple measures of attention, learning and memory from a widely used episodic memory task constituted dependent variables.

Findings: Drinking was associated with poorer attention (P ≤ 0.003) and learning (P ≤ 0.008). Results were similar across the two cohorts. The within-pair effect in twin-difference analyses was significant only for measures of learning (P-values ≤ 0.004). Results were not due to measured unshared confounders or cannabis use. Drinking in adolescence (to age 20) and early adulthood (between 20 and 29) exerted independent effects on learning.

Conclusions: There appears to be a robust and specific association between drinking and learning that can be reproduced across cohorts, is not easily accounted for by confounding factors or concurrent cannabis use and is consistent with a causal influence of drinking.