Department of Epidemiology, Erasmus University Medical Center, Rotterdam, Netherlands.
Nutrition and Health Innovation Research Institute, School of Medical and Health Sciences, Edith Cowan University, Royal Perth Hospital Research Foundation, Perth, Western Australia, Australia.
Am J Clin Nutr. 2023 Aug;118(2):352-359. doi: 10.1016/j.ajcnut.2023.05.027. Epub 2023 Jul 6.
Nitric oxide is a free radical that can be produced from dietary nitrate and positively affects cardiovascular health. With cardiovascular health playing an important role in the etiology of dementia, we hypothesized a link between dietary nitrate intake and the risk of dementia.
This study aimed to find the association of total, vegetable, and nonvegetable dietary nitrate intake with the risk of dementia and imaging markers of vascular brain health, such as total brain volume, global cerebral perfusion, white matter hyperintensity volume, microbleeds, and lacunar infarcts.
Between 1990 and 2009, dietary intake was assessed using food-frequency questionnaires in 9543 dementia-free participants (mean age, 64 y; 58% female) from the prospective population-based Rotterdam Study. Participants were followed up for incidence dementia until January 2020. We used Cox models to determine the association between dietary nitrate intake and incident dementia. Using linear mixed models and logistic regression models, we assessed the association of dietary nitrate intake with changes in imaging markers across 3 consecutive examination rounds (mean interval between images 4.6 y).
Participants median dietary nitrate consumption was 85 mg/d (interquartile range, 55 mg/d), derived on average for 81% from vegetable sources. During a mean follow-up of 14.5 y, 1472 participants developed dementia. A higher intake of total and vegetable dietary nitrate was associated with a lower risk of dementia per 50-mg/d increase [hazard ratio (HR): 0.92; 95% confidence interval (CI): 0.87, 0.98; and HR: 0.92; 95% CI: 0.86, 0.97, respectively] but not with changes in neuroimaging markers. No association between nonvegetable dietary nitrate intake and the risk of dementia (HR: 1.15; 95% CI: 0.64, 2.07) or changes in neuroimaging markers were observed.
A higher dietary nitrate intake from vegetable sources was associated with a lower risk of dementia. We found no evidence that this association was driven by vascular brain health.
一氧化氮是一种自由基,可从饮食中的硝酸盐中产生,并对心血管健康产生积极影响。由于心血管健康在痴呆症的发病机制中起着重要作用,我们假设饮食硝酸盐摄入量与痴呆症的风险之间存在联系。
本研究旨在探讨总膳食硝酸盐、蔬菜膳食硝酸盐和非蔬菜膳食硝酸盐摄入量与痴呆风险以及血管性脑健康的影像学标志物(如总脑容量、全脑灌注、脑白质高信号体积、微出血和腔隙性梗死)之间的关联。
1990 年至 2009 年期间,前瞻性人群为基础的鹿特丹研究中的 9543 名无痴呆症参与者(平均年龄 64 岁,58%为女性)使用食物频率问卷评估了饮食摄入情况。参与者在随访期间发生痴呆,直至 2020 年 1 月。我们使用 Cox 模型确定饮食硝酸盐摄入量与新发痴呆症之间的关联。我们使用线性混合模型和逻辑回归模型评估了饮食硝酸盐摄入量与 3 次连续检查轮次中影像学标志物变化之间的关联(图像之间的平均间隔为 4.6 年)。
参与者的平均膳食硝酸盐消耗量为 85mg/d(四分位间距为 55mg/d),平均有 81%来源于蔬菜来源。在平均 14.5 年的随访期间,有 1472 名参与者发生痴呆。每增加 50mg/d 的总膳食和蔬菜膳食硝酸盐摄入量与痴呆风险降低相关(风险比[HR]:0.92;95%置信区间[CI]:0.87,0.98;和 HR:0.92;95% CI:0.86,0.97),但与神经影像学标志物的变化无关。非蔬菜膳食硝酸盐摄入量与痴呆风险(HR:1.15;95% CI:0.64,2.07)或神经影像学标志物的变化之间没有关联。
来源于蔬菜的较高膳食硝酸盐摄入量与痴呆风险降低相关。我们没有发现这种关联是由血管性脑健康驱动的证据。