Kendler Kenneth S, Ohlsson Henrik, Sundquist Jan, Sundquist Kristina
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia.
Department of Psychiatry, Virginia Commonwealth University, Richmond, Virginia.
J Stud Alcohol Drugs. 2017 Mar;78(2):186-194. doi: 10.15288/jsad.2017.78.186.
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.
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.
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.
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.
大多数研究表明，青少年认知功能较差会增加酒精使用障碍（AUDs）的风险。我们试图阐明这种关联的原因。
在1972年至1990年出生的瑞典个体中，通过16岁时的学业成绩评估认知功能（男性和女性，N = 1,796,048），并通过18 - 20岁时的智商评估（男性，N = 554,644），我们从公共登记处检查了AUD的风险比（HR）。我们检查并模拟了在学业成绩和智商分数不一致的堂兄弟姐妹、全同胞和同卵双胞胎对中AUD的风险。
在男性和女性中，学业成绩每增加一个标准差，AUD的HR分别为0.47（95%CI[0.46, 0.47]）和0.52（95%CI[0.51, 0.53]）。在男性中，智商每增加一个标准差，AUD的HR为0.54（95%CI[0.53, 0.55]）。排除认知评估后5年内发生的AUD病例并没有削弱这种关联，在智商评估时控制酒精摄入量和问题也没有削弱这种关联。亲属对中AUD的HR高于总体观察值，但显著小于1。我们预测，在学业成绩不一致的同卵双胞胎中，男性和女性AUD的HR以及男性智商不一致时AUD的HR分别为：0.66（95%CI[0.62, 0.70]）、0.67（95%CI[0.62, 0.73]）和0.72（95%CI[0.65, 0.79]）。
通过两种不同测量方法评估的青少年认知能力强烈预测AUD的风险。这种关联不能用AUD损害表现的早期症状来解释。相关性分析表明，这种关联部分源于家族混杂因素，部分源于低认知能力对AUD风险的因果影响。
