From the Laboratory of Epidemiology and Population Sciences (M.A.B., S.H., M.K.E., A.B.Z.), National Institute on Aging, Intramural Research Program, NIA/NIH/IRP, Baltimore, MD; Department of Research Programs (H.A.B.), Fort Belvoir Community Hospital, VA; Department of Behavioral Health and Nutrition (M.T.F.-K.), University of Delaware, Newark; Department of Demography (J.W.), University of California, Berkeley; and Department of Pediatrics (J.A.C.), Johns Hopkins Medical Institutions, St. Petersburgh, FL.
Neurology. 2022 May 24;98(21):e2150-e2162. doi: 10.1212/WNL.0000000000200289. Epub 2022 May 4.
Serum antioxidant vitamins and carotenoids may protect against neurodegeneration with age. We examined associations of these nutritional biomarkers with incident all-cause and Alzheimer disease (AD) dementia among US middle-aged and older adults.
Using data from the third National Health and Nutrition Examination Surveys (1988-1994), linked with Centers for Medicare & Medicaid follow-up data, we tested associations and interactions of serum vitamins A, C, and E and total and individual serum carotenoids and interactions with incident AD and all-cause dementia. Cox proportional hazards regression models were conducted.
After ≤26 years follow-up (mean 16-17 years, 7,283 participants aged 45-90 years at baseline), serum lutein+zeaxanthin was associated with reduced risk of all-cause dementia (65+ age group), even in the lifestyle-adjusted model (per SD: hazard ratio [HR] 0.93, 95% CI 0.87-0.99; = 0.037), but attenuated in comparison with a socioeconomic status (SES)-adjusted model (HR 0.92, 95% CI 0.86-0.93; = 0.013). An inverse relationship was detected between serum β-cryptoxanthin (per SD increase) and all-cause dementia (45+ and 65+) for age- and sex-adjusted models (HR 0.86, 95% CI 0.80-0.93; < 0.001 for 45+; HR 0.86, 95% CI 0.80-0.93; = 0.001 for 65+), a relationship remaining strong in SES-adjusted models (HR 0.89, 95% CI 0.82-0.96; = 0.006 for 45+; HR 0.88, 95% CI 0.81-0.96; = 0.007 for 65+), but attenuated in subsequent models. Antagonistic interactions indicate putative protective effects of 1 carotenoid may be observed at lower levels other carotenoids or antioxidant vitamin.
Incident all-cause dementia was inversely associated with serum lutein+zeaxanthin and β-cryptoxanthin levels. Further studies with time-dependent exposures and randomized trials are needed to test neuroprotective effects of supplementing the diet with select carotenoids.
This study provides Class II evidence that incident all-cause dementia was inversely associated with serum lutein+zeaxanthin and β-cryptoxanthin levels.
血清抗氧化维生素和类胡萝卜素可能有助于预防与年龄相关的神经退行性变。我们研究了这些营养生物标志物与美国中老年人全因和阿尔茨海默病(AD)痴呆的发病风险之间的关联。
使用第三次国家健康和营养检查调查(1988-1994 年)的数据,并与医疗保险和医疗补助中心的随访数据进行了关联,我们测试了血清维生素 A、C 和 E 以及总血清和个体类胡萝卜素与 AD 和全因痴呆发病风险的关联和相互作用。采用 Cox 比例风险回归模型进行分析。
在 ≤26 年的随访期内(平均随访 16-17 年,基线时年龄为 45-90 岁的 7283 名参与者),叶黄素+玉米黄质与全因痴呆(65 岁以上年龄组)的发病风险降低相关,即使在调整生活方式的模型中也是如此(每标准差:风险比[HR]0.93,95%置信区间 0.87-0.99;P=0.037),但与调整社会经济地位(SES)的模型相比有所减弱(HR 0.92,95%置信区间 0.86-0.93;P=0.013)。血清β-隐黄质(每标准差增加)与全因痴呆(45+ 和 65+)之间呈负相关,这在年龄和性别调整模型中是显著的(HR 0.86,95%置信区间 0.80-0.93;P<0.001 用于 45+;HR 0.86,95%置信区间 0.80-0.93;P=0.001 用于 65+),在 SES 调整模型中仍然很强(HR 0.89,95%置信区间 0.82-0.96;P=0.006 用于 45+;HR 0.88,95%置信区间 0.81-0.96;P=0.007 用于 65+),但在后续模型中有所减弱。拮抗相互作用表明,一种类胡萝卜素的潜在保护作用可能在其他类胡萝卜素或抗氧化维生素水平较低时显现出来。
全因痴呆的发病风险与血清中叶黄素+玉米黄质和β-隐黄质水平呈负相关。需要进一步进行具有时间依赖性暴露的研究和随机试验,以测试用特定类胡萝卜素补充饮食的神经保护作用。
本研究提供了 II 级证据,表明全因痴呆的发病风险与血清中叶黄素+玉米黄质和β-隐黄质水平呈负相关。