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Food manufacturers are increasingly substituting potassium chloride (KCl) in food products so as to reduce the sodium chloride content. Bread and bread products are common staple foods in many Western households and are a target for recipe reformulation using KCl. Given that chronic kidney disease (CKD) is a medical condition of global importance that requires dietary potassium restriction in the later stages, we sought to evaluate the impact and safety of varying levels of KCl substitution in bread products. We undertook a secondary analysis of dietary data from the National Nutrition and Physical Activity Survey 2011–2012 for 12,152 participants (154 participants with CKD). The sodium chloride content in bread and bread-based products was substituted with 20%, 30%, and 40% of KCl. The contribution of these alterations in the dietary potassium intake to the total daily potassium intake were then examined. The replacement of sodium in bread with varying amounts of KCl (20%, 30%, and 40%) resulted in one third of people with CKD exceeding the safe limits for dietary potassium consumption (31.8%, 32.6%, and 33%, respectively). KCl substitution in staple foods such as bread and bread products have serious and potentially fatal consequences for people who need to restrict dietary potassium. Improved food labelling is required for consumers to avoid excessive consumption.

Background. The importance of dietary potassium in health and disease has been underestimated compared with that placed on dietary sodium. Larger effort has been made on reduction of sodium intake and less on the adequate dietary potassium intake, although natural food contains much more potassium than sodium. The benefits of a potassium-rich diet are known, however, the mechanism by which it exerts its preventive action, remains to be elucidated. With the hypothesis that dietary potassium reduces renal vasoconstrictor components of the renin-angiotensin system in the long-term, we studied the effect of high potassium diet on angiotensin-I converting enzyme, renin and angiotensin converting enzyme 2. Methods. Sprague Dawley male rats on a normal sodium diet received normal potassium (0.9%, NK) or high potassium diet (3%, HK) for 4 weeks. Urine was collected in metabolic cages for electrolytes and urinary volume measurement. Renal tissue was used to analyze angiotensin-I converting enzyme, renin and angiotensin converting enzyme 2 expression. Protein abundance analysis was done by Western blot; gene expression by mRNA levels by RT-qPCR. Renal distribution of angiotensin-I converting enzyme, renin and angiotensin converting enzyme 2 was done by immunohistochemistry and morphometric analysis in coded samples. Results. High potassium diet (4 weeks) reduced the levels of renin, angiotensin-I converting enzyme and angiotensin converting enzyme 2. Angiotensin-I converting enzyme was located in the brush border of proximal tubules and with HK diet decreased the immunostaining intensity (P

Potassium shifts in thrice weekly HD patients are likely a reversible cause of arrhythmia and sudden cardiac death. In general, a dialysate potassium

Background: Recent animal studies have identified that dietary salt intake may modify the risk and progression of autoimmune disorders through modulation of the IL23/TH17 pathway, which is critical in the pathogenesis of ulcerative colitis (UC) and Crohn’s disease (CD). Methods: We conducted a prospective study of U.S. women enrolled in the Nurses’ Health Study (NHS) and NHSII who provided detailed and validated information on diet and lifestyle beginning in 1984 in NHS and 1991 in NHSII. We confirmed incident cases of UC and CD reported through 2010 in NHS and 2011 in NHSII. We used Cox proportional hazards models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). In a case-control study nested within these cohorts, we evaluated the interaction between single nucleotide polymorphisms (SNPs) in genes involved in TH17 pathway and dietary potassium on risk of CD and UC. In a cohort of healthy volunteers, we also assessed the effect of supplemental potassium on development of naive and memory T cells, differentiated with TGFβ1 or TH17 conditions. Results: Among a total of 194,711 women over a follow up of 3,220,247 person-years, we documented 273 cases of CD and 335 cases of UC. Dietary intake of potassium (Ptrend = 0.005) but not sodium (Ptrend = 0.44) was inversely associated with risk of CD. Although, both dietary potassium and sodium were not significantly associated with risk of UC, there was a suggestion of an inverse association with dietary potassium (Ptrend = 0.08). The association of potassium with risk of CD and UC appeared to be modified by loci involved in the TH17 pathway that have previously been associated with susceptibility to CD, particularly SNP rs7657746 (IL21) (Pinteraction = 0.004 and 0.01, respectively). In vitro, potassium enhanced the expression of Foxp3 in both naive and memory CD4+ T cells via activating Smad2/3 and inhibiting Smad7 in TH17 cells. Conclusion: Dietary potassium is inversely associated with risk of CD with both in vitro and gene-environment interaction data suggesting a potential role for potassium in regulating immune tolerance through its effect on Tregs and TH17 pathway.

Background and Purpose— Potassium intake has been inconsistently associated with risk of stroke. Our aim was to conduct a meta-analysis of prospective studies to assess the relation between potassium intake and stroke risk. Methods— Pertinent studies were identified by a search of PubMed from January 1966 through March 2011 and by reviewing the reference lists of retrieved articles. We included prospective studies that reported relative risks with 95% CIs of stroke for ≥3 categories of potassium intake or for potassium intake analyzed as a continuous variable. Study-specific results were pooled using a random-effects model. Results— Ten independent prospective studies, with a total of 8695 stroke cases and 268 276 participants, were included in the meta-analysis. We observed a statistically significant inverse association between potassium intake and risk of stroke. For every 1000-mg/day increase in potassium intake, the risk of stroke decreased by 11% (pooled relative risk, 0.89; 95% CI, 0.83 to 0.97). In the 5 studies that reported results for stroke subtypes, the pooled relative risks were 0.89 (95% CI, 0.81 to 0.97) for ischemic stroke, 0.95 (95% CI, 0.83 to 1.09) for intracerebral hemorrhage, and 1.08 (95% CI, 0.92 to 1.27) for subarachnoid hemorrhage. Conclusions— Dietary potassium intake is inversely associated with risk of stroke, in particular ischemic stroke.

Hyperkalemia is common in patients with renal disease, and is sometimes caused by dietary potassium intake. We aimed to determine and compare the content of potassium in nine brands of glucosamine supplements sold in the Japanese market and via the Internet. The potassium content was 0.165-3 mg per daily dose in Japanese products, which contained glucosamine hydrochloride or N-acetylglucosamine, while the content in foreign products, in which glucosamine was sulfated, was 197-280 mg. Our results show that the potassium content in glucosamine sulfate supplements can correspond to 20% of the maximum daily intake of potassium by patients on hemodialysis, because the products sometimes contain glucosamine as glucosamine sulfate potassium chloride for stabilization. Although it is not permitted to sell glucosamine sulfate as food in Japan, consumers can easily buy foreign products that contain glucosamine sulfate via the Internet, and those products rarely indicate the potassium content. Health professionals should pay attention to patients' use of glucosamine supplements, especially when patients' dietary potassium intake needs to be restricted.

Adequate dietary potassium intake is associated with a reduced risk of cardiovascular and other chronic diseases. The Dietary Guidelines for Americans 2005 identifies milk and milk products as a major contributor of dietary potassium and lists dairy products, along with fruits and vegetables, as food groups to encourage. This paper further examines the impact of dairy consumption on the potassium intake of the United States (US) population.Using data from the National Health and Nutrition Examination Survey (NHANES) 1999-2002 we determined potassium intakes for various age groups of individuals who met the recommended number of dairy servings compared to those who did not. We also examined the impact of dairy servings consumed on mean and median potassium intakes and compared intakes to the age-appropriate Adequate Intakes (AI).For all age groups, mean and median potassium intakes did not meet the respective AI. Mean potassium intakes were significantly greater in those subjects who met dairy intake recommendations compared to those who did not for all age groups. Mean and median potassium intakes increased with increasing dairy intake but were below current intake recommendations for all age groups analyzed. For adults age 19 to 50, 16.1% consumed the recommended number of dairy servings per day. For those 51 and older, 10.7% met current dairy intake recommendations.Consumption of dairy products is below current recommendations which contributes in part to suboptimal dietary potassium intakes among a large proportion of the US population. Since adequate potassium intake is associated with decreased risk of chronic disease, consumption of a variety of potassium-rich foods, including fruits, vegetables and low-fat and fat free dairy products, should continue to be encouraged.

Experimental studies have demonstrated that elevation of potassium concentration in the blood affects elements of renal function in ways that are known to be associated with long-term reductions in blood pressure. In a wide range of animal models of hypertension, dietary potassium supplementation has been effective in reducing blood pressure and/or prolonging survival. Potassium supplementation, in many but not all studies, reduces blood pressure in hypertensive subjects, and dietary modifications that increased potassium intake were found to substantially reduce blood pressure in hypertensive and normotensive subjects. In several of the largest population studies of factors associated with hypertension, involving subjects from all parts of the world, potassium intake was reported to be inversely and strongly related to blood pressure. The magnitude of the effect is sufficiently great to warrant recommendation by the authors of some of the studies that potassium supplementation and dietary modification to a higher potassium intake be recommended for hypertensive patients, and for normotensive subjects to reduce their risk of developing hypertension.

Potassium and sodium transport along the loop of Henle: Effects of altered dietary potassium intake. We assessed the effects of changes in potassium (K + ) balance on the function of the loop of Henle by a combination of renal clearance and microperfusion experiments. Rat superficial cortical nephrons were perfused in vivo at 20 nl · min -1 from late proximal to early distal tubule with an artificial end-proximal solution containing either 3.8 or 1.8 m M potassium. Rats were fed a control diet, a low-potassium diet for at least three weeks, or a high-potassium diet for 10 to 14 days. When compared with the appropriate end-proximal potassium concentration in the perfusion fluid, potassium absorption along the loop of Henle (J K ) increased in potassium-depletion whereas sodium (J Na ) and fluid (J v ) absorption decreased. In rats fed a high-potassium diet, absorption of potassium, sodium and fluid was depressed. We propose that changes of external potassium balance affect the transport of electrolytes and fluid along the loop of Henle in vivo by modulating the transport of potassium and sodium primarily in the thick ascending limb. Changes in potassium reabsorption may also be affected by alterations of potassium-recycling.

The biological half-life of 137Cs and its organ distribution were investigated in mice fed various potassium-deficient diets. The biological half-life, which was 6.1 days in mice receiving the normal level of potassium, became longer as the dietary potassium content decreased, and 137Cs was hardly excreted from the body when dietary potassium content was restricted to 200 mg/kg or less. The muscle showed the highest concentration of 137Cs in both mice that had sufficient amounts of potassium and those that were potassium-deficient. Clearance of 137Cs from tissues was generally suppressed when mice were fed a potassium-deficient diet, but the relative distribution pattern of 137Cs was not affected by dietary potassium content. These results suggest that dietary potassium intake, which may vary with eating habits, affects the biological half-life of 137Cs in humans.

To determine whether an increase in dietary potassium intake from natural foods reduces the need for antihypertensive medication in patients with essential hypertension.Randomized, controlled trial with 1-year follow-up.Hypertension outpatient clinic of a university hospital.Fifty-four patients with well-controlled hypertension, 47 of whom completed 1 year of follow-up.Patients were randomly assigned to one of two groups and were given dietary advice aimed at selectively increasing potassium intake (group 1) or at keeping their customary diet unchanged (group 2). During a 1-year follow-up period, drug therapy was reduced in stepwise fashion, according to a fixed protocol, provided that blood pressure remained below 160/95 mm Hg.Potassium intake was checked monthly by referring to 3-day food records and by measuring 24-hour urinary potassium excretion. Potassium intake increased in group 1 but did not change in group 2 (P less than 0.001). No change was observed in either urinary sodium excretion or in body weight. After 1 year, the average drug consumption (number of pills per day) relative to that at baseline was 24% in group 1 (95% Cl, 15% to 32%) and 60% in group 2 (Cl, 44% to 76%) (P less than 0.001). By the end of the study, blood pressure could be controlled using less than 50% of the initial therapy in 81% of the patients in group 1 (Cl, 66% to 96%) compared with 29% of the patients in group 2 (Cl, 10% to 48%) (P = 0.001). Patients in group 1 ended the study with a lower number of reported symptoms compared with patients in the control group (P less than 0.001).Increasing the dietary potassium intake from natural foods is a feasible and effective measure to reduce antihypertensive drug treatment.

Adult male chickens, which were maintained on a low dietary potassium intake for 11 weeks showed no gross abnormalities, but had significantly reduced feed intake and losses of body weight. Adult male chickens had a physiological capacity to increase the biological half life of their body potassium from 18 to 134 days when the dietary potassium was reduced from .32 to .02%. However, the deficient birds were unable to balance their intake with the excretion because of the obligatory loss of potassium. The relative specific activity of different tissues in adult male chickens determined at different time intervals after the intravenous injection of potassium-42 indicated that the plasma pool potassium had the highest turnover rate of potassium in the body. In decreasing order, it was followed by the skin, heart, liver, intestine, bone, and muscle. The daily balance of potassium in adult male chickens maintained under optimum and sub-optimum dietary potassium intake gave an estimated minimum requirement for this element of .06% of the diet.

Current issues related to oral potassium supplementation are reviewed, with emphasis on recommendations for the appropriate use of potassium supplementation for both replacement and preventive therapy. Dietary potassium intake, potassium-sparing diuretics, and the various forms of oral potassium supplements are reviewed in terms of indications for use, advantages, and limitations. Attention is given to controversial areas, i.e., gastrointestinal tolerance of controlled-release potassium oral dosage preparations and the need for potassium supplementation in hypertensive patients treated with diuretics.

1. Six normal volunteers were studied on four diets (10 mEq Na/40 mEq K, 10 mEq Na/200 mEq K, 200 mEq Na/40 mEq K, and 200 mEq Na/200 mEq K) and stimulated with a continuous 48-h infusion of ACTH. 2. Aldosterone secretions were measured basically and on the days of ACTH infusion. Basal aldosterone secretion was increased by restricting sodium or by increasing potassium. 3. The mean peak response of aldosterone secretion to ACTH on the 200 mEq Na/40 mEq K diet was 241 μg/day, and 1044 μg/day on the 200 mEq Na/200 mEq K diet. The mean peak response on the 10 mEq Na/40 mEq K diet was 1803 μg/day, and on the 10 mEq Na/200 mEq K diet was 2062 μg/day. 4. These results indicate that potassium, independent of sodium and angiotensin, can regulate basal aldosterone secretion and sensitize the adrenal response to the aldosterone stimulatory properties of ACTH.

SummaryNormal rat diet supplemented with potassium at concentrations of 5, 8, or 11% increased the excretion of a single intraperitioneal dose of Cs137 from rats as compared with control rats ingesting normal rat diet without added potassium. Twenty days after injection, the Cs137 burden of rats maintained on 5% potassium diet was half that of animals fed basal diet. Animals fed a semi-synthetic low potassium diet retained Cs137 more tenaciously than animals on the normal diet.Increasing dietary potassium intake simultaneously with exposure to Cs137 does have the beneficial effect of enhancing Cs137 excretion in the rat.