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A pinboard by
Michael Stone

Graduate Research/Teaching Assistant, Purdue University

PINBOARD SUMMARY

Does increased dietary potassium (K) from potato increase K bioavailability and improve CVD risk

Potassium is an essential nutrient. It is the most abundant cation in intracellular fluid where it plays a key role in maintaining cell function. Potassium is a shortfall nutrient according to the 2015 Dietary Guidelines for Americans. Only 3% of Americans meet the recommended intake of 4700 mg/d for potassium. Average potassium intake is approximately 2300mg/d, with potatoes providing the highest percentage (19-20% of potassium) in the American diet. Approximately 90% of potassium consumed is lost in the urine, with the other 10% excreted in the stool, and a very small amount lost in sweat. In setting requirements for most minerals, bioavailability is usually considered. Little is known about bioavailability of potassium, and what is known comes from studies accessing effects of potassium supplements rather than food. Less is understood on how bioavailability may affect health outcomes. 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. High blood pressure, or 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 (BP) overall is less clear. Recommended dietary potassium intakes were determined primarily to optimize protection against HTN and secondarily to protect against stroke and coronary heart disease. Evidence for the potential health benefits of adequate/increased dietary potassium is extremely limited, with the majority of the few findings coming from research implementing dietary choice coaching (e.g. instructing participants on what potassium foods to eat on their own) rather than a completely controlled diet (e.g. participants only consume meals and snacks provided by a research metabolic kitchen). The lack of control used to conduct these dietary interventions is the primary limiting factor in revealing any true potassium related effects. A complete balance study with a controlled diet is necessary to accurately assess potassium retention, and its acute and prolonged influence on BP and other health outcomes.

7 ITEMS PINNED

Increased potassium intake from fruit and vegetables or supplements does not lower blood pressure or improve vascular function in UK men and women with early hypertension: a randomised controlled trial.

Abstract: K-rich fruit and vegetables may lower blood pressure (BP) and improve vascular function. A randomised controlled trial (ISRCTN50011192) with a cross-over design was conducted in free-living participants with early stages of hypertension (diastolic BP>80 and < 100 mmHg, not receiving BP-lowering medication) to test this hypothesis. Following a 3-week run-in period on a control diet, each subject completed four dietary 6-week dietary interventions (control+placebo capsules, an additional 20 or 40 mmol K(+)/d from fruit and vegetables or 40 mmol potassium citrate capsules/d) using a Latin square design with a washout period ≥ 5 weeks between the treatment periods. Out of fifty-seven subjects who were randomised, twenty-three male and twenty-five female participants completed the study; compliance to the intervention was corroborated by food intake records and increased urinary K(+) excretion; plasma lipids, vitamin C, folate and homocysteine concentrations, urinary Na excretion, and body weight remained were unchanged. On the control diet, mean ambulatory 24 h systolic/diastolic BP were 132·3 (sd 12·0)/81·9 ((SD) 7·9) mmHg, and changes (Bonferroni's adjusted 95 % CI) compared with the control on the diets providing 20 and 40 mmol K(+)/d as fruit and vegetables were 0·8 (- 3·5, 5·3)/0·8 (- 1·9, 3·5) and 1·7 (- 3·0, 5·3)/1·5 (- 1·5, 4·4), respectively, and were 1·8 (- 2·1, 5·8)/1·4 (- 1·6, 4·4) mmHg on the 40 mmol potassium citrate supplement, and were not statistically significant. Arterial stiffness, endothelial function, and urinary and plasma isoprostane and C-reactive protein (CRP) concentrations did not differ significantly between the diets. The present study provides no evidence to support dietary advice to increase K intake above usual UK intakes in the subjects with early stages of hypertension.

Pub.: 03 Aug '10, Pinned: 01 Jul '17

Potassium Intake, Bioavailability, Hypertension, and Glucose Control.

Abstract: 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.

Pub.: 28 Jul '16, Pinned: 29 Jun '17

Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension.

Abstract: Angiotensin II (AngII) hypertension increases distal tubule Na-Cl cotransporter (NCC) abundance and phosphorylation (NCCp), as well as epithelial Na(+) channel abundance and activating cleavage. Acutely raising plasma [K(+)] by infusion or ingestion provokes a rapid decrease in NCCp that drives a compensatory kaliuresis. The first aim tested whether acutely raising plasma [K(+)] with a single 3-hour 2% potassium meal would lower NCCp in Sprague-Dawley rats after 14 days of AngII (400 ng/kg per minute). The potassium-rich meal neither decreased NCCp nor increased K(+) excretion. AngII-infused rats exhibited lower plasma [K(+)] versus controls (3.6±0.2 versus 4.5±0.1 mmol/L; P<0.05), suggesting that AngII-mediated epithelial Na(+) channel activation provokes K(+) depletion. The second aim tested whether doubling dietary potassium intake from 1% (A1K) to 2% (A2K) would prevent K(+) depletion during AngII infusion and, thus, prevent NCC accumulation. A2K-fed rats exhibited normal plasma [K(+)] and 2-fold higher K(+) excretion and plasma [aldosterone] versus A1K. In A1K rats, NCC, NCCpS71, and NCCpT53 abundance increased 1.5- to 3-fold versus controls (P<0.05). The rise in NCC and NCCp abundance was prevented in the A2K rats, yet blood pressure did not significantly decrease. Epithelial Na(+) channel subunit abundance and cleavage increased 1.5- to 3-fold in both A1K and A2K; ROMK (renal outer medulla K(+) channel abundance) abundance was unaffected by AngII or dietary K(+) In summary, the accumulation and phosphorylation of NCC seen during chronic AngII infusion hypertension is likely secondary to potassium deficiency driven by epithelial Na(+) channel stimulation.

Pub.: 08 Sep '16, Pinned: 29 Jun '17

Bioavailability of potassium from potatoes and potassium gluconate: a randomized dose response trial.

Abstract: The bioavailability of potassium should be considered in setting requirements, but to our knowledge, the bioavailability from individual foods has not been determined. Potatoes provide 19-20% of potassium in the American diet.We compared the bioavailability and dose response of potassium from nonfried white potatoes with skin [targeted at 20, 40, and 60 milliequivalents (mEq) K] and French fries (40 mEq K) with potassium gluconate at the same doses when added to a basal diet that contained ∼60 mEq K.Thirty-five healthy, normotensive men and women with a mean ± SD age of 29.7 ± 11.2 y and body mass index (in kg/m(2)) of 24.3 ± 4.4 were enrolled in a single-blind, crossover, randomized controlled trial. Participants were partially randomly assigned to the order of testing for nine 5-d interventions of additional potassium as follows: 0 (control; repeated at phases 1 and 5), 20, 40, and 60 mEq K/d consumed as a potassium gluconate supplement or as unfried potato or 40 mEq K from French fries completed at phase 9. The bioavailability of potassium was determined from the area under the curve (AUC) of serial blood draws and cumulative urinary excretion during a 24-h period and from a kinetic analysis. The effects of the potassium source and dose on the change in blood pressure and augmentation index (AIx) were determined.The serum potassium AUC increased with the dose (P < 0.0001) and did not differ because of the source (P = 0.53). Cumulative 24-h urinary potassium also increased with the dose (P < 0.0001) and was greater with the potato than with the supplement (P < 0.0001). The kinetic analysis showed the absorption efficiency was high across all interventions (>94% ± 12%). There were no significant differences in the change in blood pressure or AIx with the treatment source or dose.The bioavailability of potassium is as high from potatoes as from potassium gluconate supplements. Future studies that measure the effect of dietary potassium on blood pressure will need to evaluate the effect of various dietary sources on potassium retention and in both normal and hypertensive populations. This trial was registered at clinicaltrials.gov as NCT01881295.

Pub.: 15 Jul '16, Pinned: 29 Jun '17