Department of Neurology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China; Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA, USA.
Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA.
Am J Clin Nutr. 2022 Nov;116(5):1201-1207. doi: 10.1093/ajcn/nqac193. Epub 2023 Feb 10.
BACKGROUND: The positive association of choline for cognition has been reported in both animal and human studies, yet the associations of choline with the risks of incident dementia or Alzheimer's disease (AD) in humans is unclear. OBJECTIVES: Our objective was to test the hypothesis that lower or higher dietary choline intake is associated with increased or decreased, respectively, risks of incident dementia and AD. METHODS: Data from the Framingham Heart Study Offspring Cohort exam 5 to exam 9 were used. Participants were free of dementia and stroke, with a valid self-reported 126-item Harvard FFQ at exam 5. The intakes of total choline, its contributing compounds, and betaine were estimated based on a published nutrient database. The intakes were updated at each exam to represent the cumulative average intake across the 5 exams. The associations between dietary choline intakes and incident dementia and AD were examined in mixed-effect Cox proportional hazard models, adjusting for covariates. RESULTS: A total of 3224 participants (53.8% female; mean ± SD age, 54.5 ± 9.7 y) were followed up for a mean ± SD of 16.1 ± 5.1 y (1991-2011). There were 247 incident dementia cases, of which 177 were AD. Dietary choline intake showed nonlinear relationships with incident dementia and AD. After adjusting for covariates, low choline intake (defined as ≤ 219 and ≤ 215 mg/d for dementia and AD, respectively) was significantly associated with incident dementia and incident AD. CONCLUSIONS: Low choline intake was associated with increased risks of incident dementia and AD.
背景:动物和人类研究均表明胆碱与认知呈正相关,但人类胆碱与痴呆或阿尔茨海默病(AD)风险之间的关联尚不清楚。
目的:我们旨在检验以下假设,即较低或较高的饮食胆碱摄入量分别与痴呆和 AD 风险的增加或降低相关。
方法:使用弗雷明汉心脏研究后代队列第 5 至 9 次检查的数据。参与者无痴呆和中风病史,在第 5 次检查时具有有效的 126 项哈佛 FFQ 自我报告。总胆碱及其组成化合物和甜菜碱的摄入量基于已发表的营养数据库进行估算。每次检查时更新摄入量,以代表 5 次检查期间的累积平均摄入量。在混合效应 Cox 比例风险模型中,调整协变量后,检查饮食胆碱摄入量与痴呆和 AD 发病的相关性。
结果:共有 3224 名参与者(53.8%为女性;平均年龄 ± 标准差为 54.5 ± 9.7 岁)接受了平均 ± 标准差为 16.1 ± 5.1 年(1991-2011 年)的随访。共发生 247 例痴呆病例,其中 177 例为 AD。饮食胆碱摄入量与痴呆和 AD 的发生呈非线性关系。调整协变量后,低胆碱摄入量(定义为痴呆和 AD 分别为≤219 和≤215mg/d)与痴呆和 AD 的发生显著相关。
结论:低胆碱摄入量与痴呆和 AD 的发病风险增加相关。
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