School of Medicine, Democritus University of Thrace, Alexandroupolis, Greece.
1st Department of Neurology, Aiginition Hospital, National and Kapodistrian University of Athens, Medical School, Athens, Greece.
J Nutr Biochem. 2022 Jul;105:108994. doi: 10.1016/j.jnutbio.2022.108994. Epub 2022 Mar 25.
The aim of the present study was to investigate the association of the inflammatory potential of diet with prodromal Parkinson's disease (pPD) probability and incidence among community-dwelling older individuals without clinical features of parkinsonism at baseline. The sample consisted of 1,030 participants 65 years old or older, drawn from a population-based cohort study of older adults in Greece (Hellenic Longitudinal Investigation of Aging and Diet - HELIAD). We calculated pPD probability, according to International Parkinson and Movement Disorder Society research criteria. Dietary Inflammatory Index (DII) was used to measure the dietary inflammatory potential, with higher index score reflecting a more pro-inflammatory diet. Associations of baseline DII with pPD probability cross-sectionally, and with possible/probable pPD incidence (pPD probability ≥30%) during the follow-up period, were examined via general linear models and generalized estimating equations, respectively. Cross-sectionally, one unit increase of DII score [DII (min, max) = -5.83, 6.01] was associated with 4.9% increased pPD probability [β=0.049, 95%CI (0.025-0.090), p<0.001]. Prospectively, 62 participants developed pPD during 3.1±0.9 (mean±SD) years of follow-up. One unit increase in DII was associated with 20.3% increased risk for developing pPD [RR=1.203, 95%CI (1.070-1.351), p=0.002]. Participants in the highest tertile of DII score were 2.6 times more likely to develop pPD [β=2.594, 95%CI (1.332-5.050), p=0.005], compared to those in the lowest tertile. More pro-inflammatory diet was related with higher pPD probability and pPD incidence (pPD probability ≥30%) in a community-dwelling older adult population. Further studies are needed to confirm these findings.
本研究旨在探讨饮食的炎症潜能与社区居住的无帕金森病临床特征的老年人发生前驱帕金森病(pPD)的概率和发病的相关性。研究样本由来自希腊老年人的基于人群队列研究(希腊老龄化和饮食纵向研究-HELIAD)的 1030 名 65 岁或以上的参与者组成。我们根据国际帕金森病和运动障碍协会的研究标准计算 pPD 概率。膳食炎症指数(DII)用于衡量饮食的炎症潜能,较高的指数分数反映了更具促炎作用的饮食。通过一般线性模型和广义估计方程分别检测基线 DII 与 pPD 概率的横断面相关性,以及与随访期间可能/可能的 pPD 发病(pPD 概率≥30%)的相关性。在横断面上,DII 评分每增加一个单位[DII(最小值,最大值)=-5.83,6.01],pPD 概率增加 4.9%[β=0.049,95%CI(0.025-0.090),p<0.001]。前瞻性地,62 名参与者在 3.1±0.9(平均值±标准差)年的随访中发展为 pPD。DII 增加一个单位与 pPD 发病风险增加 20.3%相关[RR=1.203,95%CI(1.070-1.351),p=0.002]。与最低三分位组相比,DII 评分最高三分位组发生 pPD 的可能性高 2.6 倍[β=2.594,95%CI(1.332-5.050),p=0.005]。在社区居住的老年人群中,促炎饮食与更高的 pPD 概率和 pPD 发病率(pPD 概率≥30%)相关。需要进一步的研究来证实这些发现。