Mahedy Liam, Suddell Steph, Skirrow Caroline, Fernandes Gwen S, Field Matt, Heron Jon, Hickman Matthew, Wootton Robyn, Munafò Marcus R
School of Psychological Science, University of Bristol, Bristol, UK.
MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.
Addiction. 2021 Feb;116(2):292-302. doi: 10.1111/add.15100. Epub 2020 Jun 10.
There have been few longitudinal studies of association between alcohol use and cognitive functioning in young people. We aimed to examine whether alcohol use is a causal risk factor for deficient cognitive functioning in young adults.
Linear regression was used to examine the relationship between longitudinal latent class patterns of binge drinking and subsequent cognitive functioning. Two-sample Mendelian randomization (MR) tested evidence for the causal relationship between alcohol use and cognitive functioning.
South West England.
The observational study included 3155 adolescents and their parents (fully adjusted models) from the Avon Longitudinal Study of Parents and Children (ALSPAC). Genetic instruments for alcohol use were based on almost 1 000 000 individuals from the genome-wide association studies (GWAS) and Sequencing Consortium of Alcohol and Nicotine use (GSCAN). Genome-wide association studies for cognitive outcomes were based on 2500 individuals from ALSPAC.
Binge drinking was assessed at approximately 16, 17, 18, 21 and 23 years. Cognitive functioning comprised working memory, response inhibition and emotion recognition assessed at 24 years of age. Ninety-nine independent genome-wide significant single nucleotide polymorphisms (SNPs) associated with 'number of drinks per week' were used as the genetic instrument for alcohol consumption. Potential confounders were included in the observational analyses.
Four binge drinking classes were identified: 'low-risk' (41.3%), 'early-onset monthly' (19.1%), 'adult frequent' (22.5%) and 'early-onset frequent' (17.0%). The association between early-onset frequent binge drinking and cognitive functioning: working memory (b = -0.42, 95% confidence interval (CI) = -1.24 to 0.41), response inhibition (b = 31.9, 95% CI = -25.3 to 89.2), and emotion recognition (b = 0.02, 95% CI = -0.07 to 0.10) in comparison to low-risk drinkers were inconclusive as to whether a difference was present. Two-sample MR analyses similarly provided little evidence that alcohol use is associated with deficits in working memory using the inverse variance weight (b = 0.29, 95% CI = -0.42 to 0.99), response inhibition (b = -0.32, 95% CI = -1.04 to 0.39) and emotion recognition (b = 0.03, 95% CI = -0.55 to 0.61).
Binge drinking in adolescence and early adulthood may not be causally related to deficiencies in working memory, response inhibition or emotion recognition in youths.
关于年轻人饮酒与认知功能之间关联的纵向研究较少。我们旨在探讨饮酒是否是年轻成年人认知功能缺陷的因果风险因素。
采用线性回归分析来研究暴饮暴食的纵向潜在类别模式与随后认知功能之间的关系。双样本孟德尔随机化（MR）检验饮酒与认知功能之间因果关系的证据。
英格兰西南部。
观察性研究纳入了来自埃文亲子纵向研究（ALSPAC）的3155名青少年及其父母（完全调整模型）。饮酒的遗传工具基于来自全基因组关联研究（GWAS）和酒精与尼古丁使用测序联盟（GSCAN）的近100万人。认知结果的全基因组关联研究基于来自ALSPAC的2500名个体。
在大约16、17、18、21和23岁时评估暴饮暴食情况。认知功能包括在24岁时评估的工作记忆、反应抑制和情绪识别。与“每周饮酒量”相关的99个独立的全基因组显著单核苷酸多态性（SNP）被用作饮酒的遗传工具。观察性分析中纳入了潜在混杂因素。
确定了四个暴饮暴食类别：“低风险”（41.3%）；“早发每月一次”（19.1%）；“成人频繁”（22.5%）；“早发频繁”（17.0%）。与低风险饮酒者相比，早发频繁暴饮暴食与认知功能之间的关联：工作记忆（b = -0.42，95%置信区间（CI）= -1.24至0.41）、反应抑制（b = 31.9，95% CI = -25.3至89.2）和情绪识别（b = 0.02，95% CI = -0.07至0.10），关于是否存在差异尚无定论。双样本MR分析同样几乎没有提供证据表明饮酒与使用逆方差权重的工作记忆缺陷有关（b = 0.29，95% CI = -0.42至0.99）、反应抑制（b = -0.32，95% CI = -1.04至0.39）和情绪识别（b = 0.03，95% CI = -0.55至0.61）。
青少年和成年早期的暴饮暴食可能与年轻人的工作记忆、反应抑制或情绪识别缺陷没有因果关系。
