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      Cardiovascular benefits associated with higher dietary K+ vs. lower dietary Na+: evidence from population and mechanistic studies

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          Abstract

          <p class="first" id="d12266778e156">The World Health Organization ranks hypertension the leading global risk factor for disease, specifically, cardiovascular disease. Blood pressure (BP) is higher in Westernized populations consuming Na <sup>+</sup>-rich processed foods than in isolated societies consuming K <sup>+</sup>-rich natural foods. Evidence suggests that lowering dietary Na <sup>+</sup> is particularly beneficial in hypertensive individuals who consume a high-Na <sup>+</sup> diet. Nonetheless, numerous population studies demonstrate a relationship between higher dietary K <sup>+</sup>, estimated from urinary excretion or dietary recall, and lower BP, regardless of Na <sup>+</sup> intake. Interventional studies with K <sup>+</sup> supplementation suggest that it provides a direct benefit; K <sup>+</sup> may also be a marker for other beneficial components of a “natural” diet. Recent studies in rodent models indicate mechanisms for the K <sup>+</sup> benefit: the distal tubule Na <sup>+</sup>-Cl <sup>−</sup> cotransporter (NCC) controls Na <sup>+</sup> delivery downstream to the collecting duct, where Na <sup>+</sup> reabsorbed by epithelial Na <sup>+</sup> channels drives K <sup>+</sup> secretion and excretion through K <sup>+</sup> channels in the same region. High dietary K <sup>+</sup> provokes a decrease in NCC activity to drive more K <sup>+</sup> secretion (and Na <sup>+</sup> excretion, analogous to the actions of a thiazide diuretic) whether Na <sup>+</sup> intake is high or low; low dietary K <sup>+</sup> provokes an increase in NCC activity and Na <sup>+</sup> retention, also independent of dietary Na <sup>+</sup>. Together, the findings suggest that public health efforts directed toward increasing consumption of K <sup>+</sup>-rich natural foods would reduce BP and, thus, cardiovascular and kidney disease. </p>

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          Most cited references52

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          A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010

          The Lancet, 380(9859), 2224-2260
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            Links between dietary salt intake, renal salt handling, blood pressure, and cardiovascular diseases.

            Epidemiological, migration, intervention, and genetic studies in humans and animals provide very strong evidence of a causal link between high salt intake and high blood pressure. The mechanisms by which dietary salt increases arterial pressure are not fully understood, but they seem related to the inability of the kidneys to excrete large amounts of salt. From an evolutionary viewpoint, the human species is adapted to ingest and excrete <1 g of salt per day, at least 10 times less than the average values currently observed in industrialized and urbanized countries. Independent of the rise in blood pressure, dietary salt also increases cardiac left ventricular mass, arterial thickness and stiffness, the incidence of strokes, and the severity of cardiac failure. Thus chronic exposure to a high-salt diet appears to be a major factor involved in the frequent occurrence of hypertension and cardiovascular diseases in human populations.
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              Sodium and potassium intake and mortality among US adults: prospective data from the Third National Health and Nutrition Examination Survey.

              Several epidemiologic studies suggested that higher sodium and lower potassium intakes were associated with increased risk of cardiovascular diseases (CVD). Few studies have examined joint effects of dietary sodium and potassium intake on risk of mortality. To investigate estimated usual intakes of sodium and potassium as well as their ratio in relation to risk of all-cause and CVD mortality, the Third National Health and Nutrition Examination Survey Linked Mortality File (1988-2006), a prospective cohort study of a nationally representative sample of 12,267 US adults, studied all-cause, cardiovascular, and ischemic heart (IHD) diseases mortality. During a mean follow-up period of 14.8 years, we documented a total of 2270 deaths, including 825 CVD deaths and 443 IHD deaths. After multivariable adjustment, higher sodium intake was associated with increased all-cause mortality (hazard ratio [HR], 1.20; 95% confidence interval [CI], 1.03-1.41 per 1000 mg/d), whereas higher potassium intake was associated with lower mortality risk (HR, 0.80; 95% CI, 0.67-0.94 per 1000 mg/d). For sodium-potassium ratio, the adjusted HRs comparing the highest quartile with the lowest quartile were HR, 1.46 (95% CI, 1.27-1.67) for all-cause mortality; HR, 1.46 (95% CI, 1.11-1.92) for CVD mortality; and HR, 2.15 (95% CI, 1.48-3.12) for IHD mortality. These findings did not differ significantly by sex, race/ethnicity, body mass index, hypertension status, education levels, or physical activity. Our findings suggest that a higher sodium-potassium ratio is associated with significantly increased risk of CVD and all-cause mortality, and higher sodium intake is associated with increased total mortality in the general US population.
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                Author and article information

                Journal
                American Journal of Physiology-Endocrinology and Metabolism
                American Journal of Physiology-Endocrinology and Metabolism
                American Physiological Society
                0193-1849
                1522-1555
                April 2017
                April 2017
                : 312
                : 4
                : E348-E356
                Article
                10.1152/ajpendo.00453.2016
                5406991
                28174181
                9162fa58-6a52-4d38-bc3a-989c5540cab7
                © 2017
                History

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