Potassium is an essential mineral in human nutrition and is one of the body's three major electrolytes: potassium, sodium, and chloride. Electrolytes are substances that dissociate to form ions in solution, allowing the solution to conduct electricity.
Potassium is the principal intracellular cation (positively charged ion). Approximately 98% of the body's potassium is in intracellular fluid. Sodium is the principal extracellular cation. The balance of potassium inside cells and sodium outside of cells is tightly controlled and essential for cell function.
Potassium in unprocessed foods is generally found coupled with organic counter ions such as citrate which may be converted to bicarbonate within the body. Many potassium supplements are in the form of potassium chloride, although other forms are available. Organic counter ions such as citrate act as buffers in the body while chloride does not.1
Inadequate dietary potassium intake has undesirable consequences which are caused by too little potassium intake of its conjugate ion.1
Both supplementary and dietary potassium are approximately 85% absorbed from the gastrointestinal tract.1
Recent dietary surveys estimated median potassium intakes for adults in the United States range from 2.8 to 3.3 g/day for men and 2.2 to 2.4 g/day for women.1 These values are low compared to the recommended potassium intake for healthy adults of 4,700 mg/day.
Potassium is lost from the body via urine and gastrointestinal secretions. Minimal and varying amounts are excreted in sweat. The kidney has a major role in regulating potassium balance.
Potassium is required for maintenance of membrane potential which is essential for nerve impulse conduction, muscle contraction, and heart function. Membrane potential is established by concentration of potassium ion (K+) inside the cell and sodium ion (Na+) outside the cell. This concentration gradient is established and maintained by the sodium-potassium ATPase pumps.
Potassium ion is essential for the function of a limited number of enzymes. These enzymes include the sodium-potassium ATPase pumps and pyruvate kinase (an enzyme involved in glycolysis that produces a molecule of ATP).
Potassium deficiency typically occurs as a result of extended use of oral diuretics, severe diarrhea, hyperaldosteronism, diabetic ketoacidosis, or long-term total parental nutrition providing inadequate potassium.
Signs and symptoms of potassium deficiency include: hypokalemia (low levels of potassium in the blood), fatigue, metabolic alkalosis, listlessness, anorexia, cardiac dysrhythmias, and weakness.
Hyperkalemia is defined as abnormally high levels of potassium in the blood. Causes of hyperkalemia include diminished renal potassium excretion, metabolic acidosis, hyperglycemia in the presence of insulin deficiency, moderately heavy exercise, and digitalis intoxication.
Hyperkalemia familial periodic paralysis is a rare inherited disorder characterized by episodic hyperkalemia due to unexpected movement of potassium out of cells, usually precipitated by exercise.
Hyperkalemia from total body potassium excess is especially common when there is reduced urine excretion as in acute renal failure. Hyperkalemia is uncommon in chronic renal failure until the glomerular filtration rate falls below 10-15 mL/min unless other sources of potassium load are present, such as diet.
The Food and Nutrition Board (FNB) of the Institute of Medicine did not set a Tolerable Upper Intake Level (UL) for potassium from foods because they found no evidence that high potassium intake from foods led to adverse effects for healthy adults.1 The FNB did find evidence for acute toxicity from supplemental potassium and recommended that supplemental potassium should be monitored by a healthcare professional.1
Oral doses greater than 18 g of potassium taken at one time may lead to severe hyperkalemia in those with normal renal function.
Symptoms of potassium toxicity include: abnormal neural sensations, weakness, irregular heartbeat, slow, weak, or absent pulse, and difficulty breathing.
Trimethoprim/sulfamethoxazole, antimicrobial agents used to treat urinary tract infections, may increase concentrations of potassium in the body. People on long-term treatment with this antibiotic, should not take potassium supplements except on advice of a physician or pharmacist. Besides potassium supplements, other sources of potassium such as high-potassium diets and salt substitutes containing potassium should be avoided.
Concurrent use of an ACE inhibitor and potassium may result in elevated serum potassium concentrations. Monitoring serum potassium concentration is necessary.
Potassium-sparing diuretics, such as amiloride and triamterene that are used to treat edema, increase potassium retention and can produce severe hyperkalemia. It is not advised to increase potassium intake except on the advice of a doctor or pharmacist.
Hypokalemia is sometimes seen in patients who take digoxin, a cardiac drug. Therefore, use caution before discontinuation of a potassium preparation in these patients.
Cisplatin is a chemotherapeutic agent used with other drugs to treat various cancers. Cisplatin-induced kidney damage leads to the loss of minerals from the body, including potassium. Supplementation should be supervised by a healthcare professional.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Serum potassium level and dietary potassium intake as risk factors for stroke.
This prospective study evaluated potassium intake and serum levels as risk factors for stroke in 5,600 men and women over the age of 65 years. Participants were free of stroke at enrollment in the study and baseline data collected included serum potassium, dietary potassium intake, and diuretic use. Participants were followed for four to eight years. During the study, the incidence and type of stroke were noted for affected participants. Diuretic use was associated with increased risk for stroke with lower serum potassium (RR: 2.5, p<0.0001). Low dietary potassium intake was associated with an increased risk for stroke for people not taking diuretics (RR: 1.5, p<0.005). The results of this study suggest that low dietary potassium intake and diuretic use were associated with increased risk for stroke. Further studies are needed to determine whether potassium supplements reduce risk for stroke.6
The effects of high potassium consumption on bone mineral density in a prospective cohort study of elderly postmenopausal women.
Potassium intake and bone mineral density were evaluated in a prospective study of elderly women. Two-hundred-sixty-six women aged 70 to 80 years at baseline participated in the study. Twenty-four hour urinary potassium was determined at baseline. At one year, hip dual-energy X-ray absorptiometry bone mineral density (DXA BMD) was determined. At five years, hip and total body DXA BMD, and distal radius and tibia peripheral quantitative computed tomography volumetric bone mineral density (pQCT vBMD) were determined. BMD was higher in the highest quartile of urinary potassium excretion compared to those in the lowest quartile: total hip BMD at 1 (5%) and 5 years (6%), total body BMD (4%) and 4% distal tibia total (7%), and trabecular vBMD (11%) at 5 years. The results of this study suggest that higher potassium intake from food sources increases bone mineral density in elderly women. Further studies are needed to evaluate these results and to investigate the possibility that supplemental potassium has similar results.7
Effects of potassium citrate supplementation on bone metabolism.
A age-matched controlled trial investigated the effects of potassium citrate on bone mineral density in bone health. Thirty women (twenty-two completed the trial) and twenty-four age matched controls enrolled in the trial. Of the women who did not complete the trial, seven cited gastrointestinal symptoms and one resigned because of a concomitant disease. Participants consumed 0.08 to 0.1 g potassium citrate/kg body weight for three months; this corresponded to four to eight g potassium citrate daily. (Potassium citrate is 38.3% potassium by weight.) Net acid excretion decreased significantly in the potassium citrate group (baseline: 52.6±13.3, after supplement: 31.3±12.9, P=0.004) but did not change in the control group. Urinary deoxypyridinolines (P=0.007) and fasting urinary hydroxyproline:creatinine ratio (baseline: 23.9±9.1 mg/g uCr, after supplement: 15.3±6.7 mg/g uCr, P=0.004) decreased significantly in the potassium citrate supplemented group. Serum osteocalcin decreased in some but not all supplemented participants. These results suggest that potassium citrate may help reduce bone resorption. It is important to note that the acid lowering effects of the citrate are likely responsible for at least some of the benefits seen from this supplement study.8
Potassium citrate prevents increased urine calcium excretion and bone resorption induced by a high sodium chloride diet.
The efficacy of potassium citrate supplements to prevent increased bone resorption caused by high sodium diet was evaluated in a randomized, placebo-controlled trial. Sixty postmenopausal women participated in the seven week trial. All participants consumed a low sodium chloride diet for three weeks (87 mmol daily). Participants were randomly assigned to a high salt (225 mmol/day) with or without potassium citrate (90 mmol daily; a placebo was used for the unsupplemented group) for four weeks. The high salt diet was accomplished by adding four oral sodium chloride pills, two weighed packets of salt to sprinkle on food, and one cup of bouillon per day. Urine calcium, urine N-telopeptide, urine cAMP, serum osteocalcin, and fasting serum PTH were measured at the end of the low- and high-salt diets. Urine calcium increased in the high salt plus placebo group (42±12 mg/d), but decreased (8±14 mg/d) in the high salt plus potassium citrate group (P=0.008, potassium citrate vs. placebo, unpaired t test). N-telopeptide increased 6.4±1.4 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus placebo group and 2.0±1.7 nanomoles bone collagen equivalents per millimole creatinine in the high salt plus potassium citrate group (P<0.05, potassium citrate vs. placebo, unpaired t test). The results of this study suggest that potassium citrate supplements can help attenuate bone resorption and calcium excretion due to a high sodium chloride diet.9
Effect of potassium citrate supplementation or increased fruit and vegetable intake on bone metabolism in healthy postmenopausal women: a randomized controlled trial.
A randomized, placebo-controlled trial investigated the effects of potassium citrate supplements or fruit and vegetable intake on bone metabolism for postmenopausal women. Two-hundred-seventy-six women aged 55 to 65 years participated in the two year trial. Participants were randomly assigned to one of four groups: high dose potassium citrate (55.5 mEq/day; double-blind), low dose potassium citrate (18.5 mEq/day; double-blind), placebo, or increased fruit and vegetable intake (equivalent to 18.5 mEq/day alkali; 300 g extra fruit/vegetable daily; single-blind). Urinary free deoxypyridinoline cross-links relative to creatinine (fDPD/Cr), serum N-terminal propeptide of type 1 collagen, or beta C-terminal telopeptide were not different between groups (repeated-measures ANOVA). fDPD/Cr was lower in the high dose potassium citrate group at 4-6 weeks (P=0.04). Spinal bone mineral density loss was not different in the placebo or supplement/fruit and vegetable groups (P=0.88). The results of this two-year trial indicate that potassium citrate did not alter markers of bone metabolism for healthy postmenopausal women.10
Effect of short-term supplementation of potassium chloride and potassium citrate on blood pressure in hypertensives.
A randomized, crossover trial with fourteen hypertensive participants evaluated the efficacy of potassium chloride and potassium citrate on blood pressure. Participants consumed each supplement for one week with a one week washout period between supplements. Supplements provided 96 mmol per day of potassium chloride or potassium citrate. Blood pressure was significantly reduced by potassium supplements from baseline (151+/-16/93+/-7 mm Hg) but not different between the potassium supplement groups (140+/-12/88+/-7 mm Hg with potassium chloride; 138+/-12/88+/-6 mm Hg with potassium citrate). Mean difference for blood pressures in the potassium supplemented groups compared to baseline was (95% confidence interval): 1.6 (-2.3 to 5.6) mm Hg for systolic and 0.6 (-2.4 to 3.7) mm Hg for diastolic. These results suggest that potassium supplements reduce blood pressure and that potassium citrate is as effective as potassium chloride.11
Effects of potassium chloride and potassium bicarbonate on endothelial function, cardiovascular risk factors, and bone turnover in mild hypertensives.
A randomized, double-blind, placebo-controlled, crossover-design trial examined the effects of potassium chloride and potassium bicarbonate on cardiovascular and bone health. Forty-two untreated mildly hypertensive people participated in the 12 week trial. Participants consumed 10 placebo capsules per day for 4 weeks, 10 potassium bicarbonate capsules per day (potassium: 6.4 mmol per capsule) for 4 weeks, or 10 potassium chloride capsules per day (potassium: 6.4 mmol per capsule) for 4 weeks in random order. Endothelial function (measured by brachial artery flow-mediated dilatation) was significantly improved by both potassium supplements (p<0.001). Both potassium supplements also significantly increased arterial compliance as assessed by carotid-femoral pulse wave velocity compared to placebo (p<0.001). Potassium supplements also decreased left ventricular mass (p=0.016) and improved left ventricular diastolic function (p<0.001 for E/A ratio). Potassium chloride reduced 24-hour urinary albumin (p=0.001) and albumin:creatinine ratio (p=0.005) while potassium bicarbonate decreased 24-hour urinary calcium (P=0.009) calcium:creatinine ratio (P=0.002), and plasma C-terminal cross-linking telopeptide of type 1 collagen. The results of this study suggest that potassium supplements may beneficially affect cardiovascular health and that potassium bicarbonate may help to improve bone health. Further studies are needed to further evaluate these findings.12
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 randomized, placebo-controlled trial investigated the effects of potassium citrate or increased fruit and vegetable intake on blood pressure and vascular function. Forty-eight people with early, untreated hypertension completed the trial. All participants consumed a control diet for three weeks. Then, participants were randomly assigned to one of four interventions: control diet plus placebo capsules, 20 or 40 mmol extra potassium from fruits and vegetables, or 40 mmol potassium citrate daily. All participants completed each intervention for six weeks with at least five weeks washout between interventions. Blood pressure averaged 132.3 (sd 12.0)/81.9 (7.9) mmHg on the control diet. Blood pressure changes (Bonferroni's adjusted 95 % CI) compared with the control for diets providing 20 and 40 mmol potassium per day from 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. Blood pressure changes for the 40 mmol potassium citrate supplement were 1.8 (-2.1, 5.8)/1.4 (-1.6, 4.4) mmHg, also not statistically significant. Additionally, arterial stiffness, endothelial function, and urinary and plasma isoprostane and CRP concentrations did not change. The results of this study suggest that extra potassium, either from foods or from supplements, do not improve blood pressure or vascular function. Further studies are needed to clarify the function of potassium in blood pressure and vascular function.13
The effect of a dietary supplement of potassium chloride or potassium citrate on blood pressure in predominantly normotensive volunteers.
A double-blind, randomized, placebo-controlled trial investigated the effects of potassium chloride and potassium citrate on blood pressure. Eighty-five healthy, young people with normal blood pressures participated in the six week trial. Participants completed a two week run-in period and were then randomly assigned to receive 30 mmol potassium citrate, 30 mmol potassium chloride, or a placebo daily. Each treatment consisted of two capsules taken three times daily. Both potassium supplements lowered mean arterial pressure compared to control: for potassium citrate, -5.22 mmHg (95% CI -8.85, -4.53; P<0.005) and for potassium chloride, -4.70 mmHg (-6.56, -2.84; P<0.005). Systolic and diastolic blood pressure were also reduced by potassium supplements compared to control and were not statistically different between the potassium citrate (changes in systolic and diastolic BP were -6.69 (95% CI -8.85, -4.43) and -4.26 (95% CI -6.31, -2.21) mmHg) and potassium chloride (5.24 (95% CI -7.43, -3.06) and -4.30 (95% CI -6.39, -2.20) mmHg). The results of this study suggest that potassium citrate and potassium chloride reduce blood pressure in healthy people with normal blood pressures.14
The dietary supplement information contained on this site has been compiled from published sources thought to be reliable, but it cannot be guaranteed. Efforts have been made to assure this information is accurate and current. However, some of this information may be purported or outdated due to ongoing research or discoveries. The authors, editors and publishers cannot accept responsibility for errors or omissions or for any consequences from applications of the information in this site and make no warranty, expressed or implied, with respect to the contents herein.
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