Honolulu-Asia Aging Study at Kuakini Medical Center, VA Pacific Islands Healthcare System, Honolulu, HI, USA.
J Alzheimers Dis. 2011;23(4):607-15. doi: 10.3233/JAD-2010-101428.
While animal data suggest a protective effect of caffeine on cognition, studies in humans remain inconsistent. We examined associations of coffee and caffeine intake in midlife with risk of dementia, its neuropathologic correlates, and cognitive impairment among 3494 men in the Honolulu-Asia Aging Study (mean age 52 at cohort entry, 1965-1968) examined for dementia in 1991-1993, including 418 decedents (1992-2004) who underwent brain autopsy. Caffeine intake was determined according to self-reported coffee, tea, and cola consumption at baseline. Logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI) for overall dementia, Alzheimer's disease (AD), vascular dementia (VaD), cognitive impairment (Cognitive Abilities Screening Instrument score <74), and neuropathologic lesions at death (Alzheimer lesions, microvascular ischemic lesions, cortical Lewy bodies, hippocampal sclerosis, generalized atrophy), according to coffee and caffeine intake. Dementia was diagnosed in 226 men (including 118 AD, 80 VaD), and cognitive impairment in 347. There were no significant associations between coffee or caffeine intake and risk of cognitive impairment, overall dementia, AD, VaD, or moderate/high levels of the individual neuropathologic lesion types. However, men in the highest quartile of caffeine intake (>/=411.0 mg/d) [corrected] were less likely than men in the lowest quartile (</=137.0 mg) [corrected] to have any of the lesion types (adjusted-OR, 0.45; 95% CI, 0.23-0.89; p, trend = 0.04). Coffee and caffeine intake in midlife were not associated with cognitive impairment, dementia, or individual neuropathologic lesions, although higher caffeine intake was associated with a lower odds of having any of the lesion types at autopsy.
虽然动物数据表明咖啡因对认知有保护作用，但人类的研究仍然不一致。我们研究了中年时期咖啡和咖啡因的摄入量与痴呆风险、其神经病理学相关性以及 3494 名参加檀香山-亚洲老龄化研究（队列入组时的平均年龄为 52 岁，1965-1968 年）的认知障碍之间的关系，这些人在 1991-1993 年进行了痴呆检查，包括 418 名死亡者（1992-2004 年）进行了尸检。咖啡因的摄入量是根据基线时自我报告的咖啡、茶和可乐的摄入量来确定的。使用逻辑回归计算了总体痴呆、阿尔茨海默病（AD）、血管性痴呆（VaD）、认知障碍（认知能力筛查工具评分<74）以及死亡时神经病理学病变（阿尔茨海默病变、微血管缺血性病变、皮质路易体、海马硬化、广泛萎缩）的比值比（OR）和 95%置信区间（CI），根据咖啡和咖啡因的摄入量进行计算。在 226 名男性（包括 118 名 AD、80 名 VaD）中诊断出痴呆，在 347 名男性中诊断出认知障碍。咖啡或咖啡因的摄入量与认知障碍、总体痴呆、AD、VaD 或个体神经病理学病变类型的中度/高度水平之间没有显著关联。然而，咖啡因摄入量最高四分位数（>/=411.0 mg/d）[校正]的男性比最低四分位数（</=137.0 mg）[校正]的男性更不可能有任何病变类型（校正后的 OR，0.45；95%CI，0.23-0.89；p，趋势=0.04）。中年时期的咖啡和咖啡因的摄入量与认知障碍、痴呆或个体神经病理学病变无关，尽管较高的咖啡因摄入量与尸检时任何病变类型的可能性较低相关。
