Alcohol consumption and risk of dementia: 23 year follow-up of Whitehall II cohort study.

Alcohol consumption and risk of dementia: 23 year follow-up of Whitehall II cohort study.
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DOI:
10.1136/bmj.k2927
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发表时间:
2018-08-01
期刊:
BMJ (Clinical research ed.)
影响因子:
--
通讯作者:
Singh-Manoux A
Singh-Manoux A
中科院分区:
其他
文献类型:
--
作者:
Sabia S;Fayosse A;Dumurgier J;Dugravot A;Akbaraly T;Britton A;Kivimäki M;Singh-Manoux A

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研究饮酒与痴呆风险之间的关联。前瞻性队列研究。伦敦的公务员部门(Whitehall II 研究)。研究开始时(1985/88 年)有 9087 名年龄在 35-55 岁之间的参与者。截至 2017 年,通过与医院、心理健康服务和死亡率登记册联系来识别痴呆症事件。酒精消耗量是 1985/88 年至 1991/93 年(中年)期间三次评估的平均值,分为戒酒、每周 1-14 单位和每周 > 14 单位;基于 1985/88 年至 2002/04 年五次酒精消费评估的 17 年酒精消费轨迹; 1991/93 年评估的 CAGE 酒精依赖问卷; 1991 年至 2017 年间,因酒精相关慢性病入院的人数。平均随访 23 年期间,记录了 397 例痴呆病例。与每周摄入 1-14 单位相比,中年戒酒与更高的痴呆风险相关(风险比 1.47,95% 置信区间 1.15 至 1.89)。在每周饮酒量超过 14 单位的人群中,饮酒量增加 7 单位与痴呆风险增加 17%(95% 置信区间 4% 至 32%)相关。 CAGE 评分 >2(风险比 2.19、1.29 至 3.71)和酒精相关入院(4.28、2.72 至 6.73)也与痴呆风险增加相关。从中年到早年的饮酒轨迹显示,与长期每周饮酒1-14单位相比,长期戒酒(1.74、1.31至2.30)、饮酒量减少(1.55、1.08至2.22)以及长期饮酒>14单位/周(1.40、1.02至1.93)与更高的痴呆风险相关。使用多状态模型的分析表明,与中年戒酒相关的痴呆风险过高部分是由于随访期间的心脏代谢疾病所致,因为没有心脏代谢疾病的戒酒者患痴呆的风险比为 1.33(0.88 至 2.02),而整个人群的痴呆风险比为 1.47(1.15 至 1.89)。中年戒酒或每周饮酒超过 14 单位的人患痴呆症的风险会增加。在一些国家/地区,指南规定的有害酒精摄入量阈值远高于每周 14 单位。目前的研究结果鼓励向下修订此类指南,以促进老年人的认知健康。
To examine the association between alcohol consumption and risk of dementia. Prospective cohort study. Civil service departments in London (Whitehall II study). 9087 participants aged 35-55 years at study inception (1985/88). Incident dementia, identified through linkage to hospital, mental health services, and mortality registers until 2017. Measures of alcohol consumption were the mean from three assessments between 1985/88 and 1991/93 (midlife), categorised as abstinence, 1-14 units/week, and >14 units/week; 17 year trajectories of alcohol consumption based on five assessments of alcohol consumption between 1985/88 and 2002/04; CAGE questionnaire for alcohol dependence assessed in 1991/93; and hospital admission for alcohol related chronic diseases between 1991 and 2017. 397 cases of dementia were recorded over a mean follow-up of 23 years. Abstinence in midlife was associated with a higher risk of dementia (hazard ratio 1.47, 95% confidence interval 1.15 to 1.89) compared with consumption of 1-14 units/week. Among those drinking >14 units/week, a 7 unit increase in alcohol consumption was associated with a 17% (95% confidence interval 4% to 32%) increase in risk of dementia. CAGE score >2 (hazard ratio 2.19, 1.29 to 3.71) and alcohol related hospital admission (4.28, 2.72 to 6.73) were also associated with an increased risk of dementia. Alcohol consumption trajectories from midlife to early old age showed long term abstinence (1.74, 1.31 to 2.30), decrease in consumption (1.55, 1.08 to 2.22), and long term consumption >14 units/week (1.40, 1.02 to 1.93) to be associated with a higher risk of dementia compared with long term consumption of 1-14 units/week. Analysis using multistate models suggested that the excess risk of dementia associated with abstinence in midlife was partly explained by cardiometabolic disease over the follow-up as the hazard ratio of dementia in abstainers without cardiometabolic disease was 1.33 (0.88 to 2.02) compared with 1.47 (1.15 to 1.89) in the entire population. The risk of dementia was increased in people who abstained from alcohol in midlife or consumed >14 units/week. In several countries, guidelines define thresholds for harmful alcohol consumption much higher than 14 units/week. The present findings encourage the downward revision of such guidelines to promote cognitive health at older ages.
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