From the 1st Department of Neurology (S.C., E.N., N.S.) and Department of Medical Biopathology and Clinical Microbiology (A.N.G., K.P., S.C.), Aiginition Hospital, National and Kapodistrian University of Athens Medical School, Greece; Department of Neurology (S.C.), University of Texas Health Science Center at San Antonio; Department of Nutrition and Dietetics (E.N., M.Y., C.A.A.), Harokopio University, Athens; Lab of Cognitive Neuroscience (M.H.K.), School of Psychology, and Department of Food Science and Technology (I.M.), Faculty of Agriculture, Aristotle University of Thessaloniki; School of Medicine (E.D.), University of Thessaly, Larissa, Greece; Department of Food BioSciences (K.T.), Teagasc Food Research Centre Ashtown, Dublin, Ireland; Department of Neurology (G.H.), Medical School, University of Cyprus; Athens Association of Alzheimer's Disease and Related Disorders (P.S.), Greece; National Institute on Aging/NIH (D.K.), Baltimore, MD; and Taub Institute for Research in Alzheimer's Disease and the Aging Brain (N.S.), Gertrude H. Sergievsky Center, Department of Neurology, Columbia University, New York, NY.
Neurology. 2021 Dec 14;97(24):e2381-e2391. doi: 10.1212/WNL.0000000000012973. Epub 2021 Nov 10.
Aging is characterized by a functional shift of the immune system toward a proinflammatory phenotype. This derangement has been associated with cognitive decline and has been implicated in the pathogenesis of dementia. Diet can modulate systemic inflammation; thus, it may be a valuable tool to counteract the associated risk for cognitive impairment and dementia. The present study aimed to explore the associations between the inflammatory potential of diet, assessed with an easily applicable, population-based, biomarker-validated diet inflammatory index (DII), and the risk for dementia in community-dwelling older adults.
Individuals from the Hellenic Longitudinal Investigation of Aging and Diet (HELIAD) were included in the present cohort study. Participants were recruited through random population sampling and were followed up for a mean of 3.05 (standard deviation 0.85) years. Dementia diagnosis was based on standard clinical criteria. Those with baseline dementia or missing cognitive follow-up data were excluded from the analyses. The inflammatory potential of diet was assessed through a DII score that considers literature-derived associations of 45 food parameters with levels of proinflammatory and anti-inflammatory cytokines in the blood; higher values indicated a more proinflammatory diet. Consumption frequencies were derived from a detailed food frequency questionnaire and were standardized to representative dietary intake normative data from 11 different countries. Analysis of dementia incidence as a function of baseline DII scores was performed by Cox proportional hazards models.
Analyses included 1,059 individuals (mean age 73.1 years, 40.3% male, mean education 8.2 years), 62 of whom developed incident dementia. Each additional unit of DII score was associated with a 21% increase in the risk for dementia incidence (hazard ratio 1.21 [95% confidence interval 1.03-1.42]; = 0.023). Compared to participants in the lowest DII score tertile, participants in the highest one (maximal proinflammatory diet potential) were 3 (95% confidence interval 1.2-7.3; = 0.014) times more likely to develop incident dementia. The test for trend was also significant, indicating a potential dose-response relationship ( = 0.014).
In the present study, higher DII scores (indicating greater proinflammatory diet potential) were associated with an increased risk for incident dementia. These findings might avail the development of primary dementia preventive strategies through tailored and precise dietary interventions.
衰老的特征是免疫系统向促炎表型发生功能转变。这种失调与认知能力下降有关,并与痴呆症的发病机制有关。饮食可以调节全身炎症;因此,它可能是对抗认知障碍和痴呆相关风险的有效工具。本研究旨在探索饮食的炎症潜能与社区居住的老年人患痴呆症风险之间的关联,该炎症潜能通过一种易于应用的、基于人群的、经生物标志物验证的饮食炎症指数(DII)来评估。
本队列研究纳入了希腊老龄化和饮食纵向研究(HELIAD)的参与者。参与者通过随机人群抽样招募,并随访平均 3.05 年(标准差 0.85 年)。痴呆症的诊断基于标准临床标准。那些在基线时有痴呆症或缺失认知随访数据的人被排除在分析之外。饮食的炎症潜能通过 DII 评分来评估,该评分考虑了文献中 45 种食物参数与血液中促炎和抗炎细胞因子水平之间的关联;分值越高表示饮食的促炎作用越强。食物消耗频率来自详细的食物频率问卷,并根据来自 11 个不同国家的代表性膳食摄入规范数据进行标准化。通过 Cox 比例风险模型分析基线 DII 评分与痴呆症发生率的关系。
分析纳入了 1059 名参与者(平均年龄 73.1 岁,40.3%为男性,平均受教育年限 8.2 年),其中 62 名参与者发生了新发痴呆症。DII 评分每增加一个单位,痴呆症发病风险增加 21%(风险比 1.21[95%置信区间 1.03-1.42];=0.023)。与处于最低 DII 评分三分位的参与者相比,处于最高 DII 评分三分位(最大促炎饮食潜力)的参与者发生新发痴呆症的风险高 3 倍(95%置信区间 1.2-7.3;=0.014)。趋势检验也具有统计学意义,表明存在潜在的剂量-反应关系(=0.014)。
在本研究中,较高的 DII 评分(表示更大的促炎饮食潜力)与新发痴呆症的风险增加相关。这些发现可能有助于通过针对性和精确的饮食干预来制定预防原发性痴呆症的策略。