Luft F C
Franz Volhard Clinic, Max Delbrück Center for Molecular Medicine, Medizinsche Fakultät der Charité, Humboldt University of Berlin, Federal Republic of Germany.
Wien Klin Wochenschr. 1998 Jul 31;110(13-14):459-66.
"Can that which is unsavory be eaten without salt?" This question was directed at none other than God by Job, who also had other important problems to ponder. The question posed in this review is the notion that essential hypertension is induced and/or sustained by an unnecessarily high salt intake. If this is indeed the case, then a reduction of salt intake might prevent or effectively treat essential hypertension. A cross-sectional epidemiological study of salt intake in populations showed a positive association of sodium excretion with median blood pressure and the prevalence of hypertension; however, when four disparate populations were deleted, the associations disappeared. A Scottish report on a similarly large population minimized the importance of dietary sodium. A recently analysis of the National Health and Nutrition Examination Survey (NHANES) data base does not support the idea that lower salt intake improves all-cause or cardiovascular mortality; however, the analysis is not without weaknesses. Salt-sensitivity is based on the idea that some persons might be more susceptible to salt-induced effects on blood pressure than others. Indeed, several monogenic syndromes exhibit marked salt-sensitivity and their clarification has facilitated our understanding of basic mechanisms. Allelic variants of several genes may be important in salt-sensitive patients with essential hypertension. Meta-analyses of intervention trials in patients with essential hypertension show about a 5 mm Hg decrease in blood pressure with salt restriction. Among the normotensive, this decrease is less than 2 mm Hg. In terms of efficacy, salt restriction has not been shown superior to weight loss or a "vegetable" diet. Nonpharmacological approaches in hypertensive patients should be based on a comprehensive approach.
“没有盐，那不可口的东西能吃吗？”约伯就是这样问上帝的，他还有其他重要问题需要思考。本综述所提出的问题是，原发性高血压是否由不必要的高盐摄入所诱发和/或维持。如果确实如此，那么减少盐的摄入量可能预防或有效治疗原发性高血压。一项对人群盐摄入量的横断面流行病学研究表明，钠排泄量与血压中位数及高血压患病率呈正相关；然而，剔除四个不同人群后，这种相关性就消失了。一份关于同样大量人群的苏格兰报告淡化了膳食钠的重要性。最近对美国国家健康和营养检查调查（NHANES）数据库的分析并不支持低盐摄入能改善全因死亡率或心血管死亡率这一观点；然而，该分析并非没有缺陷。盐敏感性基于这样一种观点，即有些人可能比其他人更容易受到盐对血压影响的作用。的确，几种单基因综合征表现出明显的盐敏感性，对它们的阐明有助于我们理解基本机制。几个基因的等位基因变异可能在原发性高血压的盐敏感患者中起重要作用。对原发性高血压患者干预试验的荟萃分析表明，限盐可使血压降低约5毫米汞柱。在血压正常者中，这种降低幅度小于2毫米汞柱。就疗效而言，限盐并未显示出优于减重或“素食”饮食。高血压患者的非药物治疗方法应基于综合方法。
