School of Public Health and Primary Care, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China; Nuffield Department of Population Health, University of Oxford, Oxford, UK.
School of Public Health and Primary Care, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.
Nutr Metab Cardiovasc Dis. 2021 Nov 29;31(12):3335-3344. doi: 10.1016/j.numecd.2021.08.051. Epub 2021 Sep 9.
Recent research demonstrated that obesity and high dietary sodium intake, the two established risk factors for hypertension, were associated with each other. The objective was to investigate the potential indirect effect of sodium intake on blood pressure via body mass index (BMI).
Using ten years data from US NHANES (2007-2016), the study included adult participants (>20 years old) who were not taking antihypertensive medications and without baseline diseases (n = 12,262). BMI was modelled as the mediator of sodium intake on systolic and diastolic blood pressure, adjusted for age, sex, socioeconomic status, smoking, drinking, physical activity, calorie intake, fluid intake and potassium intake. Mediation analysis was performed to evaluate total effect, direct effect and indirect effect via BMI. Subgroup analyses based on three age subgroups (20-40, 41-60 and ≥61 years old) were performed. The mean age was 39.29 (13.4) years and 53.1 (0.45) % were males. The mean BMI was 27.8 (6.20) kg/m. Overall, 1 g/d increase in sodium intake was associated with an increased systolic blood pressure by 0.36 (95% confidence interval 0.14 to 0.58) mmHg, with a direct effect (0.14 (0.09-0.19)) and an indirect effect via BMI (0.23 (0.02-0.44)). The indirect effect was mainly observed in participants ≤60 years old.
Sodium intake showed both direct effect and indirect effect (via BMI) on systolic blood pressure in US NHANES. The findings provide evidence for combining sodium restriction and weight reduction measures for prevention of hypertension. Cautions should be taken when generalizing the findings to other populations with lower average BMI.
最近的研究表明，肥胖和高膳食钠摄入这两个高血压的既定危险因素相互关联。本研究旨在通过体重指数（BMI）探讨钠摄入量对血压的潜在间接影响。
利用美国 NHANES（2007-2016 年）十年的数据，纳入未服用降压药物且无基线疾病的成年参与者（>20 岁，n=12262）。在调整年龄、性别、社会经济地位、吸烟、饮酒、体力活动、热量摄入、液体摄入和钾摄入后，将 BMI 建模为钠摄入对收缩压和舒张压的中介。采用中介分析评估 BMI 介导的总效应、直接效应和间接效应。基于三个年龄亚组（20-40、41-60 和≥61 岁）进行亚组分析。参与者的平均年龄为 39.29（13.4）岁，53.1（0.45）%为男性。平均 BMI 为 27.8（6.20）kg/m2。总体而言，钠摄入量增加 1g/d，收缩压增加 0.36（95%置信区间 0.14-0.58）mmHg，直接效应为 0.14（0.09-0.19），通过 BMI 的间接效应为 0.23（0.02-0.44）。间接效应主要在≤60 岁的参与者中观察到。
钠摄入量对美国 NHANES 参与者的收缩压有直接效应和间接效应（通过 BMI）。这些发现为高血压的预防提供了联合限制钠摄入和减轻体重措施的证据。在将研究结果推广到其他平均 BMI 较低的人群时应谨慎。
