Kenneth S Kendler1,2,3, Henrik Ohlsson4, Jan Sundquist4, Kristina Sundquist4. 1. Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia. 2. Department of Psychiatry, Virginia Commonwealth University, Richmond, Virginia. 3. Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, Virginia. 4. Center for Primary Health Care Research, Lund University, Malmö, Sweden.
Abstract
OBJECTIVE: Most studies suggest that poor cognitive functioning in adolescence increases risk of alcohol use disorders (AUDs). We seek to clarify the causes of this association. METHOD: In Swedish individuals born from 1972 to 1990 in whom cognitive functioning was assessed by school achievement at age 16 years (males and females, N = 1,796,048) and by IQ at ages 18-20 (males, N = 554,644), we examined the hazard ratio (HR) for AUD ascertained from public registries. We examined and modeled risk of AUD in cousins, full siblings, and monozygotic twin pairs discordant for school achievement and IQ scores. RESULTS: In males and females, HRs for AUD per standard deviation of increasing school achievement equaled 0.47 (95% CI [0.46, 0.47]) and 0.52 (95% CI [0.51, 0.53]), respectively. In males, the HR for AUD per standard deviation of increasing IQ was 0.54 (95% CI [0.53, 0.55]). Excluding onsets of AUD within 5 years of the cognitive evaluation did not weaken the association, nor did controlling for alcohol intake and problems at IQ assessment. The HRs for AUD in relative pairs were higher than those observed in the population but significantly less than unity. We predicted the following HRs for AUD in discordant monozygotic twins for school achievement in males and females and for IQ in males: 0.66 (95% CI [0.62, 0.70]), 0.67 (95% CI [0.62, 0.73]), and 0.72 (95% CI [0.65, 0.79]), respectively. CONCLUSIONS: Cognitive ability in adolescence, assessed by two different measures, strongly predicts risk of AUD. This association cannot be explained by early symptoms of AUD impairing performance. Co-relative analyses suggest that this association arises partly from familial confounding and partly from a causal impact of low cognitive ability on AUD risk.
OBJECTIVE: Most studies suggest that poor cognitive functioning in adolescence increases risk of alcohol use disorders (AUDs). We seek to clarify the causes of this association. METHOD: In Swedish individuals born from 1972 to 1990 in whom cognitive functioning was assessed by school achievement at age 16 years (males and females, N = 1,796,048) and by IQ at ages 18-20 (males, N = 554,644), we examined the hazard ratio (HR) for AUD ascertained from public registries. We examined and modeled risk of AUD in cousins, full siblings, and monozygotic twin pairs discordant for school achievement and IQ scores. RESULTS: In males and females, HRs for AUD per standard deviation of increasing school achievement equaled 0.47 (95% CI [0.46, 0.47]) and 0.52 (95% CI [0.51, 0.53]), respectively. In males, the HR for AUD per standard deviation of increasing IQ was 0.54 (95% CI [0.53, 0.55]). Excluding onsets of AUD within 5 years of the cognitive evaluation did not weaken the association, nor did controlling for alcohol intake and problems at IQ assessment. The HRs for AUD in relative pairs were higher than those observed in the population but significantly less than unity. We predicted the following HRs for AUD in discordant monozygotic twins for school achievement in males and females and for IQ in males: 0.66 (95% CI [0.62, 0.70]), 0.67 (95% CI [0.62, 0.73]), and 0.72 (95% CI [0.65, 0.79]), respectively. CONCLUSIONS: Cognitive ability in adolescence, assessed by two different measures, strongly predicts risk of AUD. This association cannot be explained by early symptoms of AUD impairing performance. Co-relative analyses suggest that this association arises partly from familial confounding and partly from a causal impact of low cognitive ability on AUD risk.
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