Department of Nutrition and Food Hygiene, School of Public Health, Soochow University, 199 Ren'ai Road, Suzhou, 215123, China.
Department of Big Data in Health Science School of Public Health, Center of Clinical Big Data and Analytics of the Second Affiliated Hospital, Zhejiang University School of Medicine, Yuhangtang Road No.388, Hangzhou, Zhejiang Province, China.
Clin Nutr. 2023 Sep;42(9):1788-1797. doi: 10.1016/j.clnu.2023.08.006. Epub 2023 Aug 8.
Dietary advanced glycation end products (AGEs) might exert adverse effects on cognition. The associations between dietary AGEs and long-term risk of dementia are yet to be assessed in large population studies. We aimed to explore whether elevated dietary AGEs intake is associated with increased risk of dementia, and whether this association might be affected by genetic risk.
A prospective cohort study, which included a total of 93,830 participants (aged≥ 50 years) free from dementia at baseline of the UK Biobank study (2006-2010) and had at least two 24-h dietary assessments and were followed up until 2021. Dietary AGEs, including Nε-(1-Carboxyethyl)-l-lysine (CEL), Nε-(carboxymethyl) lysine (CML), and Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (MG-H1) were estimated via averaged data from the multiple 24-h food assessments according to the ultra-performance LC-tandem MS based dAGEs database. Incidence of all-cause dementia was ascertained through hospital inpatient and mortality records. Multivariable Cox regression models were utilized to estimate hazards ratios (HRs) and 95% confidence interval (CI) of dementia risk associated with dietary AGEs.
During a median follow-up of 11.9 years, 728 participants developed dementia. In multivariable adjusted model, when comparing the highest with the lowest tertile of intake level, HRs (95% CI) of dementia were 1.43 (1.16, 1.76) for total AGEs Z score, 1.53 (1.25, 1.89) for CEL, 1.27 (1.03, 1.56) for CML and 1.24 (1.02, 1.52) for MG-H1 (all P trend<0.01). There was no significant interaction between dietary AGEs intake, genetic risk and APOE ε4 carrier status for dementia.
Higher intakes of dietary AGEs including CEL, CML and MG-H1 were associated with a higher risk of dementia, independent from genetic risk, highlighting the significance of dietary AGEs restriction for dementia prevention.
饮食中晚期糖基化终产物（AGEs）可能对认知功能产生不良影响。然而，在大型人群研究中，仍需要评估饮食 AGEs 与痴呆症的长期风险之间的关联。本研究旨在探讨饮食 AGEs 摄入量的增加是否与痴呆症风险的增加有关，以及这种关联是否可能受到遗传风险的影响。
这是一项前瞻性队列研究，共纳入了 93830 名参与者（年龄≥50 岁），他们在英国生物库研究（2006-2010 年）的基线时无痴呆症，并且至少进行了两次 24 小时膳食评估，并随访至 2021 年。根据基于超高效 LC-串联 MS 的 dAGEs 数据库，通过多次 24 小时食物评估的平均值数据来估算饮食 AGEs，包括 Nε-（1-羧乙基）-l-赖氨酸（CEL）、Nε-（羧甲基）赖氨酸（CML）和 Nδ-（5-羟-5-甲基-4-咪唑啉-2-基）-鸟氨酸（MG-H1）。通过医院住院和死亡率记录确定全因痴呆的发病情况。采用多变量 Cox 回归模型来估计与饮食 AGEs 相关的痴呆风险的危害比（HR）和 95%置信区间（CI）。
在中位随访 11.9 年期间，有 728 名参与者发生了痴呆。在多变量调整模型中，与摄入水平最低三分位相比，饮食 AGEs 总得分最高三分位的 HR（95%CI）为 1.43（1.16，1.76）、CEL 为 1.53（1.25，1.89）、CML 为 1.27（1.03，1.56）和 MG-H1 为 1.24（1.02，1.52）（所有 P 趋势<0.01）。饮食 AGEs 摄入量、遗传风险和 APOE ε4 载脂蛋白状态与痴呆之间没有显著的交互作用。
较高的饮食 AGEs 摄入量包括 CEL、CML 和 MG-H1，与痴呆的风险增加有关，独立于遗传风险，这强调了限制饮食 AGEs 对预防痴呆的重要性。
