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血压、心血管结局与钠摄入:证据的批判性综述

Blood pressure, cardiovascular outcomes and sodium intake, a critical review of the evidence.

作者信息

Stolarz-Skrzypek K, Liu Y, Thijs L, Kuznetsova T, Czarnecka D, Kawecka-Jaszcz K, Staessen J A

机构信息

First Department of Cardiology and Hypertension, Jagiellonian Unversity Medical College, Kraków, Poland.

出版信息

Acta Clin Belg. 2012 Nov-Dec;67(6):403-10. doi: 10.2143/ACB.67.6.2062704.

DOI:10.2143/ACB.67.6.2062704
PMID:23340145
Abstract

Consideration of the role of NaCl (salt) in the pathogenesis and treatment of essential hypertension is one of the overriding research themes both in experimental and clinical medicine. The evidence relating blood pressure to salt intake in humans originates from population studies and randomized clinical trials of interventions on dietary salt intake. Estimates from meta-analyses of trials in normotensive subjects generally are similar to estimates derived from prospective population studies (+ 1.7-mmHg increase in systolic blood pressure per 100 mmol increment in 24‑hour urinary sodium). This estimate, however, does not translate into an increased risk of incident hypertension in subjects consuming a high-salt diet. Prospective studies relating health outcomes to 24‑h urinary sodium excretion produced inconsistent results. Taken together, available evidence does not support the current recommendations of a generalized and indiscriminate reduction of salt intake at the population level. The public should be properly educated about the pros and cons of a decrease in sodium intake, in particular if they are healthy.

摘要

考虑氯化钠(盐)在原发性高血压发病机制和治疗中的作用是实验医学和临床医学中最重要的研究主题之一。关于人类血压与盐摄入量之间关系的证据来源于人群研究以及对饮食盐摄入量进行干预的随机临床试验。对血压正常受试者进行的试验的荟萃分析估计通常与前瞻性人群研究得出的估计相似(24小时尿钠每增加100 mmol,收缩压升高1.7 mmHg)。然而,这一估计并不能转化为高盐饮食受试者发生高血压的风险增加。将健康结果与24小时尿钠排泄相关的前瞻性研究产生了不一致的结果。综合来看,现有证据不支持目前在人群层面普遍且不加区分地减少盐摄入量的建议。公众应接受关于减少钠摄入量利弊的适当教育,尤其是对健康人群而言。

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