Abstract：
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.
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.
摘要：
背景：一氧化氮是一种自由基，可以从饮食硝酸盐中产生，并积极影响心血管健康。心血管健康在痴呆的病因中起着重要作用,我们假设膳食硝酸盐摄入量与痴呆风险之间存在联系.
目的：本研究旨在发现总，蔬菜,和非植物性饮食硝酸盐摄入量与痴呆的风险和血管脑健康的成像标记，例如大脑总体积，全脑灌注，白质高强度体积，微出血，和腔隙梗死。
方法：在1990年至2009年之间，使用食物频率问卷对9543名无痴呆参与者进行了饮食摄入评估（平均年龄，64岁；58%为女性)，来自基于人口的鹿特丹前瞻性研究。参与者对痴呆症的发病率进行了随访，直到2020年1月。我们使用Cox模型来确定饮食硝酸盐摄入量与痴呆之间的关系。使用线性混合模型和逻辑回归模型，我们评估了膳食硝酸盐摄入量与连续3轮检查中成像标志物变化的相关性(图像间的平均间隔时间为4.6y).
结果：参与者的饮食硝酸盐摄入量中位数为85毫克/天（四分位数范围，55mg/d)，平均81%来自蔬菜来源。在14.5年的平均随访中，1472名参与者患上了痴呆症。总硝酸盐和蔬菜硝酸盐摄入量较高与每50mg/d增加痴呆风险较低相关[风险比(HR):0.92;95%置信区间(CI):0.87,0.98;HR:0.92;95%CI:0.86,0.97,分别],但与神经影像学指标的变化无关。观察到非植物性饮食硝酸盐摄入量与痴呆风险（HR：1.15；95％CI：0.64，2.07）或神经影像学指标变化之间没有关联。
结论：从蔬菜中摄入较高的硝酸盐与较低的痴呆风险相关。我们没有发现证据表明这种关联是由血管大脑健康驱动的。
目的：本研究旨在发现总，蔬菜,和非植物性饮食硝酸盐摄入量与痴呆的风险和血管脑健康的成像标记，例如大脑总体积，全脑灌注，白质高强度体积，微出血，和腔隙梗死。
方法：在1990年至2009年之间，使用食物频率问卷对9543名无痴呆参与者进行了饮食摄入评估（平均年龄，64岁；58%为女性)，来自基于人口的鹿特丹前瞻性研究。参与者对痴呆症的发病率进行了随访，直到2020年1月。我们使用Cox模型来确定饮食硝酸盐摄入量与痴呆之间的关系。使用线性混合模型和逻辑回归模型，我们评估了膳食硝酸盐摄入量与连续3轮检查中成像标志物变化的相关性(图像间的平均间隔时间为4.6y).
结果：参与者的饮食硝酸盐摄入量中位数为85毫克/天（四分位数范围，55mg/d)，平均81%来自蔬菜来源。在14.5年的平均随访中，1472名参与者患上了痴呆症。总硝酸盐和蔬菜硝酸盐摄入量较高与每50mg/d增加痴呆风险较低相关[风险比(HR):0.92;95%置信区间(CI):0.87,0.98;HR:0.92;95%CI:0.86,0.97,分别],但与神经影像学指标的变化无关。观察到非植物性饮食硝酸盐摄入量与痴呆风险（HR：1.15；95％CI：0.64，2.07）或神经影像学指标变化之间没有关联。
结论：从蔬菜中摄入较高的硝酸盐与较低的痴呆风险相关。我们没有发现证据表明这种关联是由血管大脑健康驱动的。
