Department of Preventive Medicine and Public Health, University of Valencia, Valencia, Spain.
J Alzheimers Dis. 2010;20(2):577-86. doi: 10.3233/JAD-2010-1399.
The roles of smoking and alcohol on the development of Alzheimer's disease (AD) remain unclear. We performed a case-control study on the effects of both exposures before the age of onset of the disease in the cases (and same reference age for their age-matched controls) on disease risk. Interviews were conducted with population controls (n=246) and relatives of cases (n=176) identified through local Alzheimer's Disease Associations. Logistic regression models were built adjusting by gender, age, residence, education, economic situation, employment, and history of dementia in close relatives. Risk of AD was unaffected by any measure of tobacco consumption. Alcohol consumers showed a lower risk of AD than never consumers (adjusted odds ratio, aOR = 0.53, 95% CI 0.32, 0.88), with differences by gender (women aOR =0.48, 95% CI 0.27, 0.84; men aOR=0.80, 95% CI 0.23, 2.80). Mean daily total consumption of alcohol and time consuming alcohol showed increasingly protective dose-response relationships in women. Lower AD risk was observed in alcohol drinkers of both genders who never smoked (aOR= 0.37, 95% CI 0.21, 0.65). All these associations were independent of the presence of apolipoprotein E4 allele(s) in the cases. Although the sample was small for some analyses addressing these interactions, our results suggest a protective effect of alcohol consumption, mostly in non-smokers, and the need to consider interactions between tobacco and alcohol consumption, as well as interactions with gender, when assessing the effects of smoking and/or drinking on the risk of AD.
吸烟和饮酒对阿尔茨海默病(AD)发展的作用仍不清楚。我们在病例(以及与他们年龄匹配的对照者的相同参考年龄)发病前进行了一项病例对照研究,以研究这两种暴露对疾病风险的影响。通过当地的阿尔茨海默病协会,对人群对照者(n=246)和病例的亲属(n=176)进行了访谈。使用逻辑回归模型对性别、年龄、居住地、教育、经济状况、就业和近亲痴呆史进行了调整。任何吸烟量的衡量都不会增加 AD 的风险。饮酒者患 AD 的风险低于从不饮酒者(调整后的比值比,aOR=0.53,95%可信区间 0.32,0.88),且存在性别差异(女性 aOR=0.48,95%可信区间 0.27,0.84;男性 aOR=0.80,95%可信区间 0.23,2.80)。女性中,每日总酒精摄入量和饮酒时间与风险呈逐渐保护的剂量反应关系。无论性别,从不吸烟的饮酒者 AD 风险均降低(aOR=0.37,95%可信区间 0.21,0.65)。所有这些关联都与病例中载脂蛋白 E4 等位基因的存在无关。尽管一些分析这些相互作用的样本量较小,但我们的结果表明,饮酒具有保护作用,主要在不吸烟者中,并且需要考虑吸烟和/或饮酒对 AD 风险的影响,以及与性别之间的相互作用。