Why Your Mother Was Right: How Potassium Intake Reduces Blood Pressure.

Low potassium intake, common in western diets, increases blood pressure and enhances salt-sensitivity. Most humans in "Westernized" countries also consume excess salt. In studies using mice, we found that a high-salt, low-potassium diet activates the thiazide-sensitive Na-Cl cotransporter in the kidney. This effect led to sodium retention and increased blood pressure, and was dependent on plasma potassium. We postulated that this effect was mediated by changes in intracellular chloride caused by changes in membrane voltage. We developed a model in cultured cells permitting us to confirm this hypothesis. We then confirmed, using urinary exosomes, that dietary changes in normal humans, affect the thiazide-sensitive Na-Cl cotransporter in the same way. These data show that dietary potassium deficiency increases blood pressure largely by stimulating salt reabsorption along the distal nephron. They suggest that global efforts should focus on increasing potassium intake, which will attenuate the effects of high-salt diets.

Potassium-rich diet and risk of stroke: updated meta-analysis.

Recently a few prospective population studies provided additional and heterogeneous information concerning the reported statistical associations between potassium (K) intake and stroke risk. Therefore, we updated our previous meta-analysis of K intake and risk of cerebrovascular events. Three studies were added to the previous analysis, and the results of the comparison between the event rate in the two extreme categories of K intake were used. Pooled analysis of 14 cohorts (overall 333,250 participants and 10,659 events) showed an inverse and significant association between K intake and risk of stroke (Relative Risk: 0.80; 95% CI: 0.72-0.90). Our results indicated a favorable effect of higher K intake on risk of stroke. These results confirm the appropriateness of worldwide recommendations for a population increased consumption of potassium-rich foods to prevent cardiovascular disease.

[Diet low in potassium]. / Dieta pobre en potasio. Gestión por raciones y puntos.

After confirming the high prevalence rates in our hemodialysis unit of the following nursing diagnoses: nutritional imbalances--both excesses and shortages, willingness to improve nutrition and fear related to the consequences of excessive intake of potassium and manifested by the inhibition in some people towards the enjoyment of food, we decided to plan an educational strategy which later resulted in a nursing intervention for these diagnoses, with the objective of providing adequate resources for the monitoring of balanced diets with a restriction of potassium. Inspired by dietary rations, as well as recognized dietary programs of learning by points, we decided to incorporate these ideas to design an educational tool to facilitate advice to our patients on how to follow diet plans as well as the choice of appropriate foods. The result was a set of cards incorporating nutritional information of various kinds, aimed at our patients covering different aspects of the diet appropriate food rations using household measurements, promoting good food preparation, appropriate dietary advice for different chronic diseases and a scoring system of foods according to their potassium content. Together they form a board game available during the hemodialysis sessions that also takes into consideration other issues of importance related to conditions such as cognitive stimulation, coping with the disease, improving the therapeutic performance or resources to increase patient motivation. Although initially it was only an educational exercise, the result has turned out to be both enjoyable and entertaining.

Achieving the Benefits of a High-Potassium, Paleolithic Diet, Without the Toxicity.

The average US dietary intake of K(+) is well below the current recommended nutritional requirements. This deficiency is even more striking when comparing our current intake with that of our ancestors, who consumed large amounts of dietary K(+). K(+) deficiency has been implicated in many diseases including cardiovascular disease, kidney stones, and osteoporosis. Importantly, dietary supplementation of K(+) has favorable effects on reducing blood pressure, decreasing the risk of stroke, improving bone health, and reducing the risk of nephrolithiasis. For this comprehensive review, we scanned the literature using PubMed and MEDLINE using the following search terms: potassium intake, renal potassium excretion, and prevention of hyperkalemia. Articles were selected for inclusion if they represented primary data or review articles published between 1980 and 2015 in high-impact journals. The normal kidney has the capacity to tightly regulate K(+) homoeostasis. We discuss new findings with respect to sensing mechanisms by which the kidney maintains K(+) homeostasis in the gastrointestinal tract and distal tubule. There are widely prescribed hypertensive medications that cause hyperkalemia and thus require dietary K(+) restriction. We conclude by discussing newly approved drugs capable of binding K(+) in the gastrointestinal tract and speculate that this new pharmacology might allow diet liberalization in patients at risk for hyperkalemia, affording them the numerous benefits of a K(+)-rich diet.

Potassium Intake, Bioavailability, Hypertension, and Glucose Control.

Potassium is an essential nutrient. It is the most abundant cation in intracellular fluid where it plays a key role in maintaining cell function. The gradient of potassium across the cell membrane determines cellular membrane potential, which is maintained in large part by the ubiquitous ion channel the sodium-potassium (Na+-K+) ATPase pump. Approximately 90% of potassium consumed (60-100 mEq) is lost in the urine, with the other 10% excreted in the stool, and a very small amount lost in sweat. Little is known about the bioavailability of potassium, especially from dietary sources. Less is understood on how bioavailability may affect health outcomes. Hypertension (HTN) is the leading cause of cardiovascular disease (CVD) and a major financial burden ($50.6 billion) to the US public health system, and has a significant impact on all-cause morbidity and mortality worldwide. The relationship between increased potassium supplementation and a decrease in HTN is relatively well understood, but the effect of increased potassium intake from dietary sources on blood pressure overall is less clear. In addition, treatment options for hypertensive individuals (e.g., thiazide diuretics) may further compound chronic disease risk via impairments in potassium utilization and glucose control. Understanding potassium bioavailability from various sources may help to reveal how specific compounds and tissues influence potassium movement, and further the understanding of its role in health.

Potassium depletion and salt sensitivity in essential hypertension.

To evaluate the actual role of potassium depletion on blood pressure, 11 hypertensive patients were placed on a 10-day isocaloric diet providing a daily potassium intake of either 18 or 80 mmol, with each subject serving as his or her own control; the intake of sodium (220 mmol/day) and other minerals was kept constant. On day 11 each patient was also subjected to central volume expansion by water immersion associated with either normal or low potassium intake. After a 10-day period of low potassium intake, systolic blood pressure increased (P < 0.02) by 5 mm Hg, whereas serum potassium decreased (P < 0.001) by 0.9 mmol/L; no significant changes in urinary sodium and a marked increase in urinary calcium excretion (P < 0.001) were found during the 10-day low potassium intake. PRA (P < 0.02) and plasma aldosterone (P < 0.04) concentrations also decreased during low potassium intake in hypertensive patients. Even though an identical natriuretic response was found during the water immersion experiments with either high or low potassium in the whole hypertensive group, the evaluation of hypertensive subjects in relation to salt sensitivity enabled us to disclose pronounced differences in the natriuretic and calciuretic response. In fact, although an impaired natriuretic ability and moderate calcium loss were particularly found during water immersion in those hypertensive subjects exhibiting a lower salt sensitivity index, a predominant calcium depletion appeared to be the most important consequence of potassium depletion in the hypertensive subjects with a higher salt sensitivity index. By confirming that potassium depletion may exacerbate essential hypertension, our data also suggest that not only sodium restriction, but also potassium and calcium supplementation, could be particularly advisable in salt-sensitive hypertensive patients.

Eats roots and leaves. Can edible horticultural crops address dietary calcium, magnesium and potassium deficiencies?

Human individuals require at least 20 inorganic elements ('minerals') for normal functioning. However, much of the world's population is probably deficient in one or more essential minerals and at increased risk of physiological disorders. Addressing these 'hidden hungers' is a challenge for the nutrition and agriculture sectors. Mineral deficiencies among populations are typically identified from dietary surveys because (1) minerals are acquired primarily from dietary sources and (2) (bio)assays of mineral status can be unreliable. While dietary surveys are likely to under-report energy intakes, surveys show that 9% of all UK and US adults consume Ca and Mg, and 14% of adults consume K, at quantities below the UK lower reference nutrient intake, and are therefore at risk of deficiency. Low dietary Ca, Mg and K intakes can be caused by energy-malnourishment and by cultural and economic factors driving dietary conservatism. For example, cereal grains routinely displace vegetables and fruits in the diet. Cereal grains have low concentrations of several minerals, notably Ca, as a consequence of their physiology. Low grain mineral concentrations are compounded when cereal crops are grown in soils of low mineral phytoavailability and when grain is processed. In this paper, the impact of increased vegetable consumption and horticultural biofortification, i.e. enhancing crop mineral content through breeding and agronomy, on intakes of the major minerals Ca, Mg and K is assessed. Despite low energy intake from horticultural crops generally, increased vegetable consumption and biofortification would significantly improve dietary intakes of Ca, Mg and K.

Phosphatidylcholine metabolism during renal growth and regeneration.

Phosphatidylcholine, the most abundant phospholipid in renal cellular membranes, is synthesized predominantly via the Kennedy pathway in normal and growing kidney tissue. Augmented biosynthesis of phosphatidylcholine is one of the earliest responses to growth signals in renal cells. During potassium depletion, regeneration after acute tubular necrosis, and compensatory growth after uninephrectomy increased membrane phosphatidylcholine biosynthesis precedes the appearance of new organelles and surface structures and the onset of cell division. The increment in phosphatidylcholine biosynthesis in the growing kidneys of potassium-depleted rats appears to be mediated by enhanced cellular uptake of the precursor choline and activation of the enzyme cytidine diphosphocholine:1,2-diacylglycerol cholinephosphotransferase. Specific amino acids, cations, and polyamines can modify the activity of this microsomal enzyme in normal and growing renal cells. Phospholipase A also plays a regulatory role in phosphatidylcholine metabolism because inhibition of this catabolic enzyme favors phospholipid accretion and kidney growth during potassium depletion, whereas stimulation of the enzyme leads to brisk phospholipid breakdown and a decrease in tissue mass during potassium repletion.

Zonal changes in renal structure and phospholipid metabolism during reversal of potassium depletion nephropathy.

Structural changes and membrane metabolism were studied in the enlarged kidney of potassium-depleted rats during dietary repletion with potassium. Transmission and scanning electron microscopy of kidneys revealed two patterns of involutionary change in the collecting tubules following potassium repletion. Autophagocytosis was observed within 3 hours in the hyperplastic cells of the inner red medulla, and progressive condensation and reduction in the number and size of lysosomes which had formed during potassium depletion were observed in the renal papilla. After 3 days of potassium repletion, all types of cells had a normal ultrastructural appearance. Alterations in membrane metabolism during autophagocytosis and organelle regression were assessed by measuring the in vivo breakdown of [14C]phosphatidylcholine, phospholipase A activity, and the rate of [14C]choline incorporation into phospholipid in papilla, inner red medulla, and inner cortex. In each tissue the rate of [14C]phosphatidylcholine breakdown increased and the rate of [14C]choline incorporation into phospholipid decreased during potassium repletion. Phospholipase A activity, which was depressed in potassium-depleted animals, increased in each renal zone by 12 hours after potassium repletion. The results indicate that reversal of potassium depletion nephropathy is associated with increased membrane phospholipid catabolism, loss of renal mass, and specific morphologic changes in different renal zones: lysosome regression in the papilla and autophagocytosis in the hyperplastic cells of the inner red medulla.