MRC Integrative Epidemiology Unit (IEU), University of Bristol, Bristol, UK.
UK Centre for Tobacco and Alcohol Studies, School of Experimental Psychology, University of Bristol, Bristol, UK.
Addiction. 2018 Jan;113(1):148-157. doi: 10.1111/add.13975. Epub 2017 Sep 29.
To evaluate the utility of coffee-related genetic variants as proxies for coffee consumption in Mendelian randomization studies, by examining their association with non-alcoholic beverage consumption (including subtypes of coffee and tea) and a range of socio-demographic and life-style factors.
Observational study of the association of genetic risk scores for coffee consumption with different types of non-alcoholic beverage consumption.
UK general population.
Individuals of European ancestry aged 40-73 years from the UK Biobank between 2006 and 2010 (n = 114 316).
Genetic risk scores were constructed using two, four and eight independent single nucleotide polymorphisms (SNPs) identified in genome-wide association studies (GWAS) of coffee consumption. Drinks were self-reported in a baseline questionnaire (all participants) and in detailed 24 dietary recall questionnaires in a subset (n = 48 692).
Genetic risk scores explained up to 0.38, 0.19 and 0.76% of the variance in coffee, tea and combined coffee and tea consumption, respectively. Genetic risk scores demonstrated positive associations with both caffeinated and decaffeinated coffee and tea consumption, and with most subtypes of coffee consumption, but only with standard tea consumption. There was no clear evidence for positive associations with most other non-alcoholic beverages, but higher genetic risk for coffee consumption was associated with lower daily water consumption. The genetic risk scores were associated with increased alcohol consumption, but not consistently with other socio-demographic and life-style factors.
Coffee-related genetic risk scores could be used as instruments for combined coffee and tea consumption in Mendelian randomization studies. However, associations observed with alcohol consumption require further investigation to determine whether these are due to causal effects of coffee and tea consumption or biological pleiotropy.
通过研究咖啡相关遗传变异与非酒精饮料(包括咖啡和茶的不同类型)以及一系列社会人口学和生活方式因素的关联,评估其作为孟德尔随机化研究中咖啡摄入量替代指标的效用。
观察性研究,研究咖啡消费遗传风险评分与不同类型非酒精饮料消费的关联。
英国普通人群。
2006 年至 2010 年间,英国生物库中年龄在 40-73 岁之间的欧洲血统个体(n=114316)。
使用两项、四项和八项在咖啡消费全基因组关联研究(GWAS)中鉴定的独立单核苷酸多态性(SNP)构建遗传风险评分。饮料在基线问卷(所有参与者)和一个亚组的 24 项详细饮食回忆问卷中进行自我报告(n=48692)。
遗传风险评分分别解释了咖啡、茶和咖啡与茶混合消费的变异的 0.38%、0.19%和 0.76%。遗传风险评分与含咖啡因和脱咖啡因咖啡和茶的消费均呈正相关,与大多数咖啡消费类型均呈正相关,但仅与标准茶消费呈正相关。遗传风险评分与大多数其他非酒精饮料之间没有明显的正相关,但咖啡消费的遗传风险越高,每日水的摄入量越低。遗传风险评分与饮酒量增加有关,但与其他社会人口学和生活方式因素的关系并不一致。
咖啡相关的遗传风险评分可作为孟德尔随机化研究中咖啡与茶混合消费的工具。然而,与酒精消费相关的关联需要进一步研究,以确定这些关联是由于咖啡和茶消费的因果效应还是由于生物学的多效性。