Vitamin D level predicts all-cause dementia

Q3 Medicine
H. Karl Greenblatt, C. Adler, M. Aslam, J. Welge, R. Krikorian
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引用次数: 0

Abstract

BACKGROUND: Vitamin D deficiency is common in Western societies and has been implicated in a number of health conditions including late-life dementia. OBJECTIVE: To assess whether vitamin D level is associated with all-cause dementia in late life. METHODS: This was a retrospective case control study using the electronic medical record of an urban medical center to obtain information on age, sex, body mass index, 25-hydroxy vitamin D (25-(OH)D) values, and presence of dementia diagnosis in patients 65 to 90 years old. We classified patients to quartiles according to vitamin D values and performed logistic regression analysis to determine associations between vitamin D quartiles and incidence of dementia diagnosis. RESULTS: Rates of all-cause dementia decreased with increasing levels of 25-(OH)D independent of age, sex, and BMI, factors that also predicted dementia. Vitamin D levels above 38 ng/mL were associated with the lowest rate of all-cause dementia. CONCLUSIONS: We observed dose-dependent, inverse associations of 25-hydroxy vitamin D levels with all-cause, late life dementia independent of age, sex, and BMI. There may be greater protection for supra-sufficient levels, a notion that warrants evaluation in controlled trials.
维生素D水平预测全因痴呆
背景:维生素D缺乏在西方社会很常见,并与包括老年痴呆在内的许多健康状况有关。目的:评估维生素D水平是否与晚年全因痴呆相关。方法:这是一项回顾性病例对照研究,使用城市医疗中心的电子病历,获取65至90岁患者的年龄、性别、体重指数、25-羟基维生素D (25-(OH)D)值和痴呆诊断的信息。我们根据维生素D值将患者分为四分位数,并进行logistic回归分析,以确定维生素D四分位数与痴呆诊断发生率之间的关系。结果:随着25-(OH)D水平的升高,全因痴呆的发病率下降,而这与年龄、性别和BMI无关,这些因素也可以预测痴呆。维生素D水平高于38 ng/mL与全因痴呆的最低发生率相关。结论:我们观察到25羟基维生素D水平与年龄、性别和BMI无关的全因老年痴呆呈剂量依赖性负相关。对于超充足的水平可能会有更大的保护,这一概念值得在对照试验中进行评估。
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来源期刊
Nutrition and Healthy Aging
Nutrition and Healthy Aging Agricultural and Biological Sciences-Food Science
CiteScore
1.70
自引率
0.00%
发文量
17
期刊介绍: Nutrition and Healthy Aging is an international forum for research on nutrition as a means of promoting healthy aging. It is particularly concerned with the impact of nutritional interventions on the metabolic and molecular mechanisms which modulate aging and age-associated diseases, including both biological responses on the part of the organism itself and its micro biome. Results emanating from both model organisms and clinical trials will be considered. With regards to the latter, the journal will be rigorous in only accepting for publication well controlled, randomized human intervention trials that conform broadly with the current EFSA and US FDA guidelines for nutritional clinical studies. The journal will publish research articles, short communications, critical reviews and conference summaries, whilst open peer commentaries will be welcomed.
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