The purpose of this review was to identify, summarize, and critically appraise studies on dietary salt and health outcomes that were published from August 2016 to March 2017. The search strategy was adapted from a previous systematic review on dietary salt and health. Studies that meet standards for methodological quality criteria and eligible health outcomes are reported in detailed critical appraisals. Overall, 47 studies were identified and are summarized in this review. Two studies assessed all‐cause or disease‐specific mortality outcomes, eight studies assessed morbidity reduction‐related outcomes, three studies assessed outcomes related to symptoms/quality of life/functional status, 25 studies assessed blood pressure ( BP ) outcomes and other clinically relevant surrogate outcomes, and nine studies assessed physiologic surrogate outcomes. Eight of these studies met the criteria for outcomes and methodological quality and underwent detailed critical appraisals and commentary. Five of these studies found adverse effects of salt intake on health outcomes ( BP ; death due to kidney disease and initiation of dialysis; total kidney volume and composite of kidney function; composite of cardiovascular disease ( CVD ) events including, and risk of mortality); one study reported the benefits of salt restriction in chronic BP and two studies reported neutral results ( BP and risk of CKD ). Overall, these articles confirm the negative effects of excessive sodium intake on health outcomes.

The aim of this eighth Science of Salt outcomes review is to identify, summarize, and critically appraise studies on dietary sodium and health outcomes published between November 1, 2018, and August 31, 2019, to extend this series published in the Journal since 2016. The standardized Science of Salt search strategy was conducted. Studies were screened based on a priori defined criteria to identify publications eligible for detailed critical appraisal. The search strategy resulted in 2621 citations with 27 studies on dietary sodium and health outcomes identified. Two studies met the criteria for detailed critical appraisal and commentary. We report more evidence that high sodium intake has detrimental health effects. A post hoc analysis of the Dietary Approaches to Stop Hypertension (DASH) sodium trial showed that lightheadedness occurred at a greater frequency with a high sodium DASH diet compared to a low sodium DASH diet. In addition, evidence from a post‐trial analysis of the Trials of Hypertension (TOHP) I and II cohorts showed that estimates of sodium intake from methods based on spot urine samples are inaccurate and this method alters the linearity of the sodium‐mortality association. Compared to measurement of 24‐hour sodium excretion using three to seven 24‐hour urine collections, estimation of average 24‐hour sodium excretion with the Kawasaki equation appeared to change the mortality association from linear to J‐shaped. Only two high‐quality studies were identified during the review period, both were secondary analyses of previously conducted trials, highlighting the lack of new methodologically sound studies examining sodium and health outcomes.

Background: There is compelling evidence of an inverse association between potassium intake and blood pressure (BP). A potential mechanism for this effect may be dietary potassium-mediated augmentation of endothelium-dependent relaxation. To date, studies have investigated potassium intake supplementation over several weeks in healthy volunteers with variable results on vascular function. There is no assessment of the acute vascular effects of potassium supplementation achieved by the ingestion of potassium-rich food in a hypertensive population. Objective: The purpose of this study was to investigate the effect of a high potassium meal on postprandial endothelial function as measured by flow-mediated dilatation (FMD). Methods: We performed an investigator-blinded randomized crossover trial in 33 treated hypertensive individuals. Participants consumed both a high (~2400 mg) and low (~543 mg) K⁺ meal, separated by a one-week washout period. The primary endpoint was endothelial function as assessed by FMD pre-meal and postprandially at 60 and 120 min. Meals were compared at each time point using the Hills–Armitage approach. Results: 33 individuals were included in the study (48% male, mean age 68). In the fasting state (Baseline), and at 60 min postprandial, radial artery FMD was not significantly different between the participants after consumption of either meal (baseline: high K⁺ 4.2 ± 2% versus Low K⁺ 2.6 ± 3%, p = 0.93; 60 min: high K⁺ 3.8 ± 4% versus Low K⁺ 4.1 ± 3%, p = 0.69). However, at 120 min, FMD tended to be higher in participants after the high K⁺ meal (5.2 ± 4.1%) than after the low K⁺ meal (3.9 ± 4.1%) (p = 0.07). There were no differences in participants’ radial artery diameter and blood flow between meals. Conclusions: This study does not support our hypothesis that a single high K⁺ meal improves vascular function in individuals with treated hypertension. This does not contradict the clinical evidence relating greater K⁺ intake with lower BP, but suggests that mechanistic investigations of increased K⁺ intake through diet alone and its impact on endothelial function as a mediator to reducing BP are complex and not simply due to single nutrient-mediated improvement in vascular function.