Univ. Bordeaux, Inserm, BPH, U1219, F-33000 Bordeaux, France.
Univ. Bordeaux, Inserm, BPH, U1219, F-33000 Bordeaux, France.
Environ Int. 2024 Oct;192:109033. doi: 10.1016/j.envint.2024.109033. Epub 2024 Sep 23.
Diet is a major route of exposure to potentially neurotoxic chemicals, yet the epidemiological association of diet contaminants with dementia is unknown. We studied the link between dietary exposure to multiple chemicals and dementia risk in older persons, considering interaction with dietary fat content, which may modify the bioavailability and toxicity of (lipophilic) chemicals.
We included 1,288 non-demented participants from the French Three-City cohort who answered a food frequency questionnaire and 24-hour recall at baseline and were followed for incident dementia. Dietary exposure to 167 contaminants was assessed by combining food intakes with food chemical content from the French second Total Diet Study. We assessed the relation of each individual contaminant with dementia risk using multivariable-adjusted Cox models, exploring effect modification by high-fat diet (>35 % energy from fat). Among high-fat diet consumers, we looked for a signature of contaminants associated with dementia using elastic-net penalization and assess their joint effect.
Participants were 76 years-old on average at baseline and 62 % were women. In total, 314 individuals developed dementia over a median 10 years. No contaminant was associated with dementia in the whole population. However, having a high-fat diet was a strong effect modifier for 85 contaminants (FDR-corrected p < 0.05 for interactions) in single-chemical analyses, so that higher intakes were significantly associated with higher dementia risk among high-fat consumers only (n = 386). Among them, a multi-chemical approach revealed a signature of 9 contaminants related to dementia, including 4 perfluoroalkyl substances, 2 flame retardants hexabromocyclododecane (HBCDD) congeners, 2 mycotoxins, and nitrites. This selection included two top hits from the single-chemical analyses (α-HBCDD and perfluorooctanesulfonic acid [PFOS]), and was mainly provided by delicatessen meat, seafood and bread/crispbread.
In this large population-based study, dietary exposure to several chemicals was associated with higher dementia risk among older persons consuming > 35 % energy from fat in diet.
饮食是接触潜在神经毒性化学物质的主要途径，但饮食污染物与痴呆症的流行病学关联尚不清楚。我们研究了老年人饮食暴露于多种化学物质与痴呆症风险之间的联系，同时考虑了饮食脂肪含量的相互作用，因为它可能会改变（亲脂性）化学物质的生物利用度和毒性。
我们纳入了法国三城队列中的 1288 名非痴呆参与者，他们在基线时回答了一份食物频率问卷和 24 小时膳食回忆，并随访了新发痴呆症。通过结合法国第二次总膳食研究中的食物摄入量和食物化学含量，评估了 167 种污染物的饮食暴露情况。我们使用多变量调整的 Cox 模型评估了每种污染物与痴呆症风险的关系，探索了高脂肪饮食（脂肪供能比>35%）的效应修饰作用。在高脂肪饮食消费者中，我们使用弹性网络惩罚寻找与痴呆症相关的污染物特征，并评估它们的联合效应。
参与者在基线时的平均年龄为 76 岁，62%为女性。共有 314 人在中位 10 年内患上痴呆症。在整个人群中，没有一种污染物与痴呆症有关。然而，高脂肪饮食是 85 种污染物的强效应修饰因素（交互作用的 FDR 校正 p<0.05），因此仅在高脂肪消费者中，较高的摄入量与更高的痴呆症风险显著相关（n=386）。在这些人中，一种多化学物质方法揭示了与痴呆症相关的 9 种污染物特征，包括 4 种全氟烷基物质、2 种阻燃剂六溴环十二烷（HBCDD）同系物、2 种霉菌毒素和亚硝酸盐。这种选择包括单化学物质分析中的两个热门结果（α-HBCDD 和全氟辛烷磺酸[PFOS]），主要来自熟食肉、海鲜和面包/脆饼。
在这项大型基于人群的研究中，饮食中暴露于多种化学物质与老年人中高脂肪饮食（>35%的能量来自脂肪）的痴呆症风险增加有关。
