Potassium: Benefits, Forms, Dosing, and Safety Guide

Potassium is an essential mineral and the most abundant intracellular cation in the human body. It is required for normal cell function because of its role in maintaining intracellular fluid volume and transmembrane electrochemical gradients [1][2]. This comprehensive guide covers the evidence on potassium's health benefits, the different supplemental forms, recommended dosing, safety considerations, drug interactions, and the best dietary sources.

Normal serum concentrations of potassium range from approximately 3.6 to 5.0 mmol/L [1][3]. Potassium is absorbed via passive diffusion primarily in the small intestine, with approximately 90% of ingested potassium being absorbed [1][5]. The kidneys are the primary regulators of potassium balance, and potassium deficiency is a growing public health concern — an analysis of over 50,000 Americans from 1999 to 2016 found that blood potassium levels are declining and the prevalence of deficiency has increased by 7.3% [6].

Table of Contents

• Overview
• Forms and Bioavailability
• Evidence for Benefits
• Recommended Dosing
• Safety and Side Effects
• Drug Interactions
• Dietary Sources
• References

Overview

Potassium is an essential mineral involved in proper functioning of the nervous system, skeletal system, cardiac muscle, and metabolism, as well as maintaining normal blood pressure [1][2][3]. The total amount of potassium in the adult body is approximately 45 millimole (mmol) per kilogram of body weight — roughly 140 g for a 175-pound adult [1]. Most potassium resides inside cells, with only a small amount in extracellular fluid. The intracellular concentration of potassium is about 30 times higher than the extracellular concentration, and this gradient is maintained via the sodium-potassium (Na+/K+) ATPase transporter [1][2].

This transmembrane electrochemical gradient is essential for proper nerve transmission, muscle contraction, kidney function, and cardiac rhythm [1][2][3]. Potassium also has a strong relationship with sodium — the main regulator of extracellular fluid volume — and plays a critical role in blood pressure regulation by promoting vasodilation and increasing urinary sodium excretion [1][4].

A minimum of approximately 5 mmol (about 195 mg) of potassium is excreted daily in urine, and combined with other obligatory losses, potassium balance cannot be achieved with intakes less than about 400–800 mg/day [1].

Deficiency Is Increasing

An analysis of over 50,000 men, women, and children (ages 12 to 80) from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2016 found that average annual blood levels of potassium decreased from 4.14 mmol/L to 3.97 mmol/L, and the prevalence of potassium deficiency increased by 7.3%. Deficiency was more common in non-Hispanic black than non-Hispanic white individuals [6]. The researchers suggested that a decline of potassium in crop soil and fertilizer, as well as increased consumption of processed foods and decreased consumption of fruits and vegetables, may contribute to these trends [6].

Dietary surveys consistently show that Americans consume less potassium than recommended. According to NHANES 2013-2014 data, the average daily potassium intake from foods is 3,016 mg for men and 2,320 mg for women aged 20 and over — well below the Adequate Intake levels of 3,400 mg and 2,600 mg, respectively [1][7]. Potassium is identified as a "nutrient of public health concern" by the Dietary Guidelines for Americans [7]. Average potassium intakes also vary by race, with non-Hispanic blacks consuming less (2,449 mg/day) than non-Hispanic whites (2,697 mg/day) [1].

Symptoms of Deficiency

Severe potassium deficiency causes hypokalemia (serum potassium level below 3.6 mmol/L), which affects up to 21% of hospitalized patients, most often due to diuretic use [1][8]. Symptoms progress with severity:

• Mild: Constipation, fatigue, muscle weakness, malaise, listlessness, mood changes
• Moderate: Numbness, tingling, muscle cramps, nausea, vomiting, irrational behavior
• Severe (serum potassium below ~2.5 mmol/L): Polyuria (large volume of dilute urine), muscular paralysis, poor respiration, cardiac arrhythmias, encephalopathy in patients with kidney disease. Severe hypokalemia can be life threatening due to its effects on cardiac function [1][3].

Causes of Deficiency

Hypokalemia is rarely caused by low dietary potassium intake alone. Common causes include [1][3][9]:

• Diuretic medications: Both loop diuretics (furosemide, bumetanide) and thiazide diuretics (chlorothiazide, metolazone) increase urinary potassium excretion
• Gastrointestinal losses: Prolonged vomiting, diarrhea, or laxative abuse. Vomiting produces metabolic alkalosis, leading to potassium losses in the kidneys
• Inflammatory bowel disease: Potassium secretion increases in the colon, compounded by chronic diarrhea [1]
• Beta2-receptor agonists: Albuterol, ephedrine, epinephrine [9]
• Proton-pump inhibitors: Omeprazole, esomeprazole, pantoprazole, lansoprazole [9]
• Corticosteroids: Average and large doses of hydrocortisone and cortisone, as well as large doses of synthetic derivatives such as methylprednisolone [9]
• Other medications: Xanthines (theophylline, caffeine), overdosage of insulin or verapamil [9]
• GLP-1 receptor agonists: Semaglutide (Ozempic, Wegovy) has been linked with hypokalemia in case reports. Two women in their 40s developed low blood potassium requiring hospitalization 1.5 to 6 months after starting semaglutide. Side effects such as vomiting and potential kidney effects may contribute [10]
• Refeeding syndrome: The metabolic response to initial refeeding after a starvation period, due to potassium's movement into cells [1]
• Pica: Consuming clay binds potassium in the gastrointestinal tract, increasing excretion [1]
• Heavy sweating and dialysis [1]

Magnesium and Potassium: A Critical Connection

Approximately 50% of individuals with chronically low potassium levels also have magnesium deficiency, most often due to loop or thiazide diuretics, but also from diarrhea, alcoholism, kidney disease, or medication toxicity [11][12]. If magnesium deficiency is not addressed, it may be harder to correct potassium deficiency. This is because magnesium activates the "pump" that regulates potassium levels within cells — when magnesium levels are low, pump activity decreases, resulting in loss of potassium from skeletal muscle cells and increased urinary excretion of potassium [12][13]. In people with concurrent hypomagnesemia and hypokalemia, both should be treated simultaneously [1][11].

Forms and Bioavailability

Potassium is available in supplements in many forms, including potassium chloride, potassium citrate, potassium gluconate, potassium bicarbonate, potassium acetate, potassium phosphate, and potassium aspartate. More than 90% of potassium is absorbed in the gastrointestinal tract regardless of form, and nearly all common forms are absorbed equally well [3][5][14]. A 2016 dose-response trial found that humans absorb about 94% of potassium gluconate from supplements, and this absorption rate is similar to that of potassium from potatoes [15]. Liquid forms of potassium chloride are absorbed within a few hours; enteric-coated tablet forms are absorbed less rapidly than liquid forms [16].

Form	Elemental K (%)	Key Properties	Common Uses
Potassium Chloride (KCl)	52%	Highest elemental potassium per gram. Most commonly used in prescription preparations and salt substitutes. Can have bitter or metallic taste. May irritate GI tract at higher doses [3][14].	Salt substitutes, prescription hypokalemia treatment, clinical trials on blood pressure
Potassium Citrate	38.3%	Well-absorbed. Citrate component provides additional benefit for kidney stones by raising urine pH and forming complexes with calcium [17][18].	Kidney stone prevention, blood pressure support, general supplementation
Potassium Gluconate	16.7%	Less bitter taste than other forms. Good tolerability. Very low elemental potassium content means larger doses needed [3][14].	General supplementation, preferred when taste is a concern
Potassium Bicarbonate	~39%	Alkalizing effect. May support bone health via acid-base balance. Some case reports suggest it helps dissolve kidney stones [19][20].	Bone health support, kidney stone management
Potassium Phosphate	~28%	Phosphate component may reduce urinary calcium in hypercalciuria patients [21].	Kidney stone disease with hypercalciuria
Potassium Aspartate	~25%	Sometimes combined with magnesium aspartate. Limited data as standalone form.	Combined mineral supplements
Potassium Acetate	~40%	Well-absorbed. Less commonly available in over-the-counter supplements.	Specialty formulations

Key Principles for Form Selection

For general supplementation: Potassium gluconate and potassium citrate are well-tolerated choices for daily supplementation. Potassium gluconate has a less bitter taste, while potassium citrate provides additional citrate for kidney health [3][14].

For kidney stone prevention: Potassium citrate is the preferred form because the citrate component — not the potassium itself — interferes with calcium stone formation by forming complexes with urinary calcium and increasing urine pH [17][18].

For blood pressure management: Most clinical trials have used potassium chloride, though potassium-enriched salt substitutes (containing 25–75% potassium chloride) offer a practical way to increase potassium and reduce sodium simultaneously [22][23].

For bone health: Potassium citrate and potassium bicarbonate are preferred over potassium chloride because the alkaline potassium salts help counter metabolic acidosis that may contribute to bone loss. Potassium chloride does not have this alkalizing effect [24][25].

Important Label Reading Note

Product names can be misleading. A product labeled "Potassium Gluconate 595 mg" actually contains only about 99 mg of elemental potassium, because potassium makes up just 16.7% of the weight of potassium gluconate. Potassium dosage is sometimes expressed in milliequivalents (mEq), where 1 mEq equals 39.09 mg of potassium [3].

The 99 mg Supplement Limit

Most potassium supplements are limited to 99 mg of elemental potassium per pill. This is because the FDA has ruled that some oral drug products containing potassium chloride and providing more than 99 mg potassium are not safe due to associations with small-bowel lesions [26][27]. The FDA requires certain potassium salts containing more than 99 mg per tablet to carry a warning about this risk [26]. While Congress has ruled that the FDA cannot limit the amount of a nutrient in a dietary supplement except for safety reasons, most manufacturers voluntarily limit potassium to 99 mg per capsule or tablet [1][26].

This limit does not apply to liquid, powder, or effervescent tablet forms, which disperse the potassium more widely and are unlikely to cause localized intestinal irritation, provided they are taken with adequate water [3].

Evidence for Benefits

Blood Pressure

Getting adequate potassium from the diet and supplementation may help reduce hypertension, particularly in African-Americans and people who consume excessive sodium [22][28][29].

Meta-analyses of potassium supplementation:

A 2017 meta-analysis of 25 randomized controlled trials in 1,163 participants with hypertension found significant reductions in systolic blood pressure (SBP) by 4.48 mmHg and diastolic blood pressure (DBP) by 2.96 mmHg with potassium supplementation, mostly as potassium chloride at 1,173–4,692 mg/day for 4–15 weeks [30]. Another meta-analysis of 15 RCTs found that potassium supplements (mostly potassium chloride at 2,346–2,541 mg/day) for 4–24 weeks in 917 patients significantly reduced both SBP and DBP. The effect was greatest in patients with hypertension, reducing SBP by 6.8 mmHg and DBP by 4.6 mmHg [31]. Two earlier meta-analyses of 19 trials [32] and 33 trials [33] had similar findings.

A similar analysis by the NASEM committee including 16 trials found that potassium supplements significantly lowered SBP by 6.87 mmHg and DBP by 3.57 mmHg. However, these effects were stronger among studies that included participants with hypertension; for studies including only normotensive participants, the effects were not statistically significant [34].

Nuances and ceiling effects:

The American College of Cardiology (ACC) and American Heart Association (AHA) recommend that people with high blood pressure get 3,500–5,000 mg of potassium per day from foods. They note that the maximum blood pressure benefit from supplemental potassium appears to peak at approximately 1,173 mg/day, and that higher supplement doses (>3,128 mg/day) have been linked with an increase in blood pressure, particularly in people already taking antihypertensive medication [35][36].

A Cochrane Review of five clinical trials among 425 adults with primary hypertension found that potassium supplementation at 1,877–4,692 mg/day for 2–4 months did NOT significantly reduce blood pressure compared to baseline [37]. Furthermore, subsequent analysis found that high-dose potassium supplementation — enough to increase urinary potassium excretion by about 90 mmol/day (corresponding to 3,900–4,680 mg/day of supplemental potassium in addition to usual dietary intake) — may actually increase blood pressure [38].

The role of sodium reduction:

The AHRQ systematic review found that reducing sodium intake decreased blood pressure, but adding potassium via food or supplements on top of sodium reduction did not reduce blood pressure further. This suggests that at least some of the beneficial effects attributed to potassium may be driven by the accompanying reduction in sodium intake [34]. Based on 13 RCTs, potassium-containing salt substitutes significantly reduced SBP by 5.58 mmHg and DBP by 2.88 mmHg [34].

Expert consensus:

Based on these findings, experts generally recommend that people with high blood pressure — especially those with high sodium intake (except those with chronic kidney disease or taking certain diuretics) — aim to increase potassium intake from foods to about 3,500–5,000 mg/day, rather than relying on high-dose supplements [35][39]. Substituting table salt with potassium-enriched salts (approximately 75% sodium chloride and 25% potassium chloride) is specifically recommended [35][40].

Stroke and Cardiovascular Disease

Higher potassium intakes have been associated with a decreased risk of stroke and possibly other cardiovascular diseases [4][41].

A meta-analysis of 11 prospective cohort studies in 247,510 adults found that a 1,640 mg/day higher potassium intake was associated with a significant 21% lower risk of stroke, as well as nonsignificant lower risks of coronary heart disease and total cardiovascular disease [42]. Similarly, a meta-analysis of 9 cohort studies found a 24% lower stroke risk with higher potassium intakes [43].

A 2016 meta-analysis of 16 cohort studies with 639,440 participants found that those with the highest potassium intakes (median 4,027 mg/day) had a 15% lower risk of stroke than those with the lowest intakes (median 2,053 mg/day). Participants consuming approximately 3,500 mg/day had the lowest stroke risk. Importantly, even when blood pressure was accounted for, higher potassium intakes still produced a significant 13% lower risk of stroke — suggesting that mechanisms beyond blood pressure reduction, such as improved endothelial function and reduced free radical formation, may be involved [44].

The FDA has approved the health claim: "Diets containing foods that are a good source of potassium and that are low in sodium may reduce the risk of high blood pressure and stroke" [45].

Salt Substitutes and Cardiovascular Outcomes

Replacing regular table salt with potassium-enriched salt substitutes has been shown to modestly improve blood pressure in people with hypertension. A meta-analysis found that salt substitutes (containing 25–67% potassium) reduced SBP by 4.9 mmHg and DBP by 1.5 mmHg on average [46].

The landmark SSaSS trial (Salt Substitute and Stroke Study):

A 5-year study in China among nearly 21,000 adults with a history of stroke or high blood pressure found that the use of a salt substitute (25% potassium chloride, 75% sodium chloride) resulted in a 14% reduction in risk of stroke, 13% reduction in risk of major cardiovascular events, and 12% reduction in risk of death compared to regular salt. Despite containing potassium, the salt substitute did not increase the risk of hyperkalemia [23]. Further analysis found that among people with a history of stroke specifically, the salt substitute reduced stroke-related death by 21%, mainly due to reductions in hemorrhagic stroke (−30%) and undetermined stroke (−21%). The benefit was attributed to a modest blood pressure reduction of 2.05 mmHg [47].

Elderly care facility study:

A separate study among 1,219 men and women living in an elderly care facility in China who tended to have high blood pressure (average 137.5/80.5 mmHg) found that a salt substitute (62.5% sodium chloride, 25% potassium chloride, 12.5% flavoring agents) over 2 years reduced the risk of cardiovascular events by 34% and heart disease-related death by 36% compared to usual salt. The risk of hyperkalemia was increased (7.0% vs 2.4% of participants), but there was no significant increase in kidney dysfunction [48].

Limitations: None of these studies were conducted in the U.S., where home-use table salt is not the major contributor of sodium in the diet (most comes from processed foods) [3].

Expert recommendations: Some experts recommend that all patients with hypertension consider substituting table salt for a potassium-enriched salt (~75% sodium chloride, ~25% potassium chloride), unless contraindicated. They also suggest that such products be considered for use by anyone who needs to add salt to food to help reduce blood pressure in the general population [40].

Kidney Stone Prevention

Taking certain forms of potassium may reduce the risk of kidney stones. The mechanism primarily involves citrate rather than potassium itself — citrate forms complexes with urinary calcium and increases urine pH, inhibiting calcium oxalate crystal formation [17][49].

A clinical study found that patients who took 6,480 mg (60 mEq) of potassium citrate daily (divided into three doses after meals) had no stone recurrence after one year, compared to a 28.5% stone recurrence rate in patients who did not take potassium citrate [50].

In a clinical trial of 57 patients with at least two kidney stones over the prior 2 years and hypocitraturia (low urinary citrate), supplementation with 1,173–2,346 mg potassium (as potassium citrate) for 3 years significantly reduced kidney stone formation compared with placebo [51]. This was included in a 2015 Cochrane Review of 7 studies (477 participants) that found potassium citrate salts significantly reduced the risk of new stones and decreased stone size [17].

Another clinical study found that two tablets of a patented potassium complex taken three times daily (providing 1,638 mg potassium, 252 mg magnesium, and 3,971 mg citrate daily) for up to three years reduced kidney stone recurrence by 85% in people with active stone disease compared to placebo [52].

Potassium phosphate may also help: a small clinical study found that 2,496 mg of potassium (as potassium phosphate) taken as four tablets twice daily for four years reduced urinary calcium by 30–35% in patients with absorptive hypercalciuria, the most common cause of calcium kidney stones [21].

Case reports with potassium bicarbonate: A 59-year-old man with kidney stones who took 1,173 mg (30 mEq) of potassium as potassium citrate and potassium bicarbonate one to three times daily experienced reduction in stone size after 4 months and complete disappearance of stones after 7 months [19]. Another report described a man with recurrent kidney stones who did not experience additional stones over 18 months after starting 782 mg (20 mEq) of potassium as potassium bicarbonate two to three times daily along with allopurinol [20].

Observational data: In a cohort of 45,619 men aged 40–75 with no history of kidney stones, those with the highest potassium intakes (at least 4,042 mg/day) had a 51% lower risk of kidney stones over 4 years compared to those with the lowest intakes (2,895 mg/day or less) [53]. Similarly, among more than 90,000 women aged 34–59 in the Nurses' Health Study, those consuming more than 4,099 mg potassium per day had a 35% lower risk of kidney stones over 12 years compared to those averaging less than 2,407 mg/day [54].

Note: Most potassium citrate supplements provide only 99 mg of potassium from 258 mg (2.4 mEq) of potassium citrate, far below the doses used in clinical trials for kidney stone prevention. Higher doses should be discussed with a healthcare provider [3].

Bone Health

Observational studies suggest that increased potassium intake from fruits and vegetables is associated with increased bone mineral density [55]. The underlying mechanism may involve potassium's effect on acid-base balance — diets high in acid-forming foods (meats, cereal grains) contribute to metabolic acidosis that may adversely affect bone, while alkaline potassium salts (citrate, bicarbonate — but not chloride) may help preserve bone tissue [56].

In the Framingham Heart Study, higher potassium intake was associated with significantly greater bone mineral density in 628 elderly men and women [57]. The DASH diet, which provides three times more potassium than the average American diet, significantly reduced biochemical markers of bone turnover [58]. However, the DASH diet also increases magnesium and calcium intakes, so potassium's independent contribution cannot be determined.

Clinical trial evidence:

A trial of 52 healthy men and women older than 55 found that potassium citrate supplementation at 2,346 mg or 3,519 mg potassium for 6 months significantly reduced urinary calcium excretion compared to placebo [59].

In 201 healthy adults aged 65 and older who received potassium citrate (2,346 mg potassium) plus calcium (500 mg/day) and vitamin D3 (400 IU/day) for 2 years, potassium supplementation significantly increased bone mineral density at the lumbar spine and improved bone microarchitecture compared to placebo [60].

Supplemental potassium bicarbonate (mean doses of 2,893 or 4,340 mg/day potassium) for 84 days significantly reduced biochemical markers of bone turnover and urinary calcium excretion in healthy older adults [61].

Negative finding: A trial in 276 postmenopausal women aged 55–65 found that potassium citrate at 723 mg or 2,170 mg potassium for 2 years did NOT significantly reduce bone turnover or increase bone mineral density at the hip or lumbar spine compared to placebo [62].

Synthesis: Higher potassium intakes from diets emphasizing fruits and vegetables likely improve bone health, but the evidence from supplementation trials is mixed. More research is needed to determine potassium's independent contribution to bone outcomes.

Blood Glucose Control and Type 2 Diabetes

Potassium is needed for insulin secretion from pancreatic cells, and hypokalemia can impair insulin secretion and lead to glucose intolerance [1][2][63].

Numerous studies have found associations between lower potassium intakes, lower serum or urinary potassium levels, and increased rates of fasting glucose, insulin resistance, and type 2 diabetes [63][64][65][66][67]. These associations may be stronger in African Americans [64][66].

In one study of 1,066 adults aged 18–30 without diabetes, those with urinary potassium levels in the lowest quintile were more than twice as likely to develop type 2 diabetes over 15 years compared to those in the highest quintile [64]. Among the 4,754 participants with dietary intake data, African Americans with lower potassium intakes had significantly greater diabetes risk over 20 years, but this association was not found in whites.

An analysis of 84,360 women aged 34–59 in the Nurses' Health Study found that those in the highest quintile of potassium intake had a 38% lower risk of developing type 2 diabetes over 6 years compared to those in the lowest quintile [65].

Serum potassium levels were inversely associated with fasting glucose levels in 5,415 participants aged 45–84 from the Multi-Ethnic Study of Atherosclerosis, but these levels had no significant association with diabetes risk over 8 years of follow-up [67].

Clinical trial evidence: In a small trial of 29 African American adults with prediabetes and low to normal serum potassium levels (3.3–4.0 mmol/L), supplementation with 1,564 mg potassium (as potassium chloride) for 3 months significantly lowered fasting glucose levels, but did not improve glucose or insulin measures during an oral glucose tolerance test [68].

Synthesis: Observational data are promising, but clinical trial evidence is very limited. More RCTs are needed before potassium's role in blood glucose control and type 2 diabetes prevention can be confirmed.

Rheumatoid Arthritis

People with rheumatoid arthritis (RA) tend to have low blood levels of potassium and inadequate potassium intake [69]. A study among 155 people with RA and painful joints whose blood potassium was on the lower end of normal (3.9 mmol/L) found that increasing total daily potassium intake to about 5,600 mg (from food plus a ~2,000 mg supplement) modestly decreased self-reported arthritis pain by 2.23 points on a 0–10 scale, compared to a 1.31-point decrease for those following a potassium-enriched diet alone (~3,000 mg/day) and no significant reduction for those on their typical diet (~2,700 mg/day). However, high potassium intake did not decrease swollen or tender joints, erythrocyte sedimentation rate (a measure of inflammation), or analgesic use [70].

Muscle Cramps and Restless Legs

Despite common assumptions, nighttime muscle cramps and exercise-related muscle cramps do not appear to be related to potassium levels [71]. There are no published, double-blind clinical studies on the effects of potassium supplementation on muscle cramps.

A small study among people with moderate to severe restless legs syndrome suggested a benefit from 391 mg potassium (as 1,080 mg potassium citrate) daily: after one month, the majority reported having no symptoms [72]. However, this study did not include a control group, making it impossible to draw reliable conclusions.

COVID-19 and Hypokalemia

Low potassium levels have been observed in hospitalized COVID-19 patients. Among 175 patients hospitalized with COVID-19 in China, 39% had hypokalemia and 22% had severe hypokalemia. Supplementing with approximately 3 grams of potassium daily helped correct these deficiencies in most patients. The presence of underlying hypertension was associated with more severe hypokalemia [73].

A study of 290 hospitalized COVID-19 patients in Italy confirmed that hypokalemia was common but tended to be mild and was treatable with oral potassium supplements. It was not associated with poor outcomes or mortality [74].

The mechanism appears to involve the SARS-CoV-2 virus inactivating the ACE2 enzyme — which normally helps regulate sodium and potassium — leading to excess potassium excretion through the kidneys [73].

Recommended Dosing

Adequate Intakes (AIs)

The National Academies of Sciences, Engineering, and Medicine updated the AIs for potassium in 2019 [34]. These replaced older (2005) recommendations that set the AI for all adults at 4,700 mg. The current values are lower because the methodology was changed to focus specifically on nutritional adequacy in healthy individuals [34][75].

Age Group	Male (mg/day)	Female (mg/day)
1-3 years	2,000	2,000
4-8 years	2,300	2,300
9-13 years	2,500	2,300
14-18 years	3,000	2,300
19-50+ years	3,400	2,600
Pregnancy	--	2,900 (2,600 if under 19)
Lactation	--	2,800 (2,500 if under 19)

No Upper Limit Established

Tolerable Upper Intake Levels (ULs) have not been established for potassium because the kidneys excrete excess potassium in healthy individuals with normal kidney function [1][34]. However, caution against high intakes is warranted for people with — or at risk of — compromised kidney function. People requiring dialysis are generally advised to restrict potassium intake to about 2,000 mg daily [3].

Supplementation Dosing by Indication

• Preventing potassium loss: 200–400 mg (approximately 5–10 mEq) taken three to four times daily, for a total daily dose of 600–1,600 mg [3]
• Treating potassium deficiency: Approximately double the preventive dose, under physician guidance [3]
• Blood pressure support (from food): 3,500–5,000 mg/day total from dietary sources. The ACC/AHA recommend increasing potassium from foods rather than high-dose supplements, as supplemental doses above ~3,128 mg/day may paradoxically increase blood pressure [35][39]
• Kidney stone prevention (potassium citrate): Doses used in clinical trials range from 1,173–6,480 mg/day of potassium, typically as divided doses of potassium citrate. These are well above standard supplement amounts and require medical supervision [17][50][51]
• Bone health: 2,346–4,340 mg/day (as potassium citrate or bicarbonate) in clinical trials [59][60][61]. These doses are far above standard supplement levels.

Practical Considerations

Because most supplements contain only 99 mg of potassium per pill, reaching higher therapeutic doses requires taking many pills. Powder, liquid, or dissolving tablet forms may be more practical when higher doses are needed — and are likely safer because they avoid localized intestinal irritation [3].

The most practical approach for most people is to increase potassium through dietary changes (fruits, vegetables, legumes, potatoes) and the use of potassium-enriched salt substitutes, with a modest supplement to help fill gaps. Using potassium-containing dietary supplements does not significantly increase total potassium intakes in the U.S. population — supplement use adds a mean of only 87 mg to daily intakes [1].

Safety and Side Effects

Common Side Effects

Potassium supplements may cause [3][9]:

• Diarrhea, nausea, stomach pain, mild gas, vomiting (may be reduced by taking with meals)
• More serious but less common: confusion, irregular heartbeat, numbness or tingling in hands/feet/lips, shortness of breath, anxiety, tiredness or weakness
• Chest or throat pain when swallowing (take with a full glass of water)

Esophageal and Intestinal Risks

Potassium chloride can injure the esophagus by pulling water from the esophageal lining (a hyperosmolar effect) if a pill gets stuck during swallowing [76]. High doses (>99 mg) of potassium in enteric-coated pills have been linked to reports of small-bowel lesions causing obstruction, hemorrhage, and perforation [26][27]. This may result from the release of a high concentration of potassium over a small intestinal area. The FDA requires oral drugs containing 100 mg or more of potassium per coated tablet to carry a warning about this risk [26]. This concern does not pertain to liquid, effervescent, or powder forms of potassium [3].

Hyperkalemia

In healthy individuals with normal kidney function, high dietary potassium intakes do not pose a health risk because the kidneys efficiently eliminate excess amounts [1][34]. However, hyperkalemia (serum potassium above 5.0 mmol/L) can occur in people with impaired kidney function or those taking certain medications [1][34].

Very high amounts of potassium from supplements or salt substitutes could potentially exceed the kidney's capacity to excrete potassium, causing acute hyperkalemia even in healthy individuals. Chronic ingestion of supplement doses up to 15,600 mg for 5 days in healthy people can increase plasma potassium, but not beyond the normal range [1].

Symptoms of hyperkalemia progress with severity:

• Mild: Often asymptomatic
• Moderate: Muscle weakness, paresthesias (burning or prickling sensation in extremities)
• Severe: Paralysis, heart palpitations, cardiac arrhythmias that could be life-threatening [1]

Kidney Disease

Individuals with kidney disease cannot properly control electrolyte levels and should use potassium only under medical supervision [3]. However, getting too little potassium in kidney disease is also a concern. A study among 415 people undergoing dialysis (average age 56) found that those who consumed only about 543 mg of potassium per day had a two-fold greater mortality risk compared to those consuming about 2,600 mg. The risk was greater in people over 55 compared to younger patients [77].

Premenstrual Syndrome (PMS)

Higher potassium intake has been associated with increased PMS risk. A large study of U.S. women found that those consuming higher amounts of potassium (median 3,717 mg/day) had a 46% higher risk of PMS compared to those consuming less (median 2,319 mg/day) [78].

Salt Substitute Risks

Potassium-containing salt substitutes should not be used without medical supervision by people with kidney disease, as they may cause dangerously high potassium levels. In one report, an 88-year-old man with chronic kidney disease developed asymptomatic hyperkalemia (potassium blood level: 7.5 mEq/L) after frequently using a salt substitute containing 27.3% potassium for one month [79]. Salt substitutes may also increase hyperkalemia risk among people with type 1 or type 2 diabetes, coronary artery disease, or heart failure, and those taking potassium-sparing diuretics and other medications that impair potassium excretion [3].

High Potassium from Food: A Case Report

A case of leg cramps was reported in a woman in Japan who consumed a mango (a potassium-rich fruit) every night before bed for one month, developing elevated potassium levels. The cramps resolved after she stopped eating mangos and her levels returned to normal [80].

Drug Interactions

Several classes of medications interact with potassium in potentially dangerous ways. People taking these medications should discuss potassium intake with their healthcare providers.

Drugs That Increase Potassium Levels (Risk of Hyperkalemia)

Drug Class	Examples	Mechanism	Clinical Concern
ACE inhibitors	Benazepril (Lotensin), captopril, enalapril, lisinopril	Reduce urinary potassium excretion	As many as 20% experience mild potassium elevations. Severe elevations affect ~0.8%. Life-threatening elevations are rare but documented [9][81][82].
Angiotensin receptor blockers (ARBs)	Losartan (Cozaar), irbesartan, olmesartan, valsartan	Reduce urinary potassium excretion	About 31% experience mild elevations; severe elevations in ~2.8%. A 58-year-old woman on losartan developed sudden chest pressure, lightheadedness, and potassium of 9.2 mmol/L [9][83].
Potassium-sparing diuretics	Amiloride (Midamor), spironolactone (Aldactone), triamterene	Reduce renal potassium excretion	Can cause hyperkalemia. Monitor potassium levels closely, especially with impaired kidney function [1][84].
Trimethoprim/sulfamethoxazole	Bactrim, Septra	Impairs potassium excretion	Do not take potassium supplements without medical supervision [9].

Drugs That Decrease Potassium Levels (Risk of Hypokalemia)

Drug Class	Examples	Mechanism	Clinical Concern
Loop diuretics	Furosemide (Lasix), bumetanide (Bumex)	Increase urinary potassium excretion	Can cause hypokalemia. Supplementation may be necessary [1][84].
Thiazide diuretics	Chlorothiazide (Diuril), hydrochlorothiazide, metolazone (Zaroxolyn)	Increase urinary potassium excretion	Can cause hypokalemia. Monitor potassium status [1][84].
Beta2-receptor agonists	Albuterol, ephedrine, epinephrine	Transcellular shift	Can lower serum potassium [9].
Corticosteroids	Hydrocortisone, cortisone, methylprednisolone	Increase potassium excretion	Average to large doses may cause potassium depletion [9].
Proton-pump inhibitors	Omeprazole, esomeprazole, pantoprazole, lansoprazole	Unclear mechanism	Can cause hypokalemia with chronic use [9].
Laxatives	Various	Increase fecal potassium loss	Repeated use or abuse increases hypokalemia risk [1].
Xanthines	Theophylline, caffeine	Multiple mechanisms	Can contribute to potassium loss [9].
GLP-1 receptor agonists	Semaglutide (Ozempic, Wegovy)	Vomiting, renal effects	Uncommon but documented cases of hypokalemia requiring hospitalization [10].

ACE Inhibitors, ARBs, and COVID-19

There are theoretical concerns that ACE inhibitors and ARBs may increase ACE2 on cell surfaces, potentially increasing the risk of severe COVID-19 [85][86]. However, there are also cautions not to stop these medications, as they may be helpful in treating COVID-19 and are essential for blood pressure control [87][88].

Dietary Sources

Foods are the best source of potassium for most people, as they provide forms of potassium (phosphate, sulfate, citrate) that are naturally well absorbed [1][4]. The body absorbs approximately 85–90% of dietary potassium [1].

Top Food Sources

Food	Serving	Potassium (mg)
Kidney beans, canned	1 cup	2,587
White potato, baked with skin	1 large	1,627
Red sockeye salmon	1 filet (~100 g)	1,037
Banana, mashed	1 cup	806
Apricots, dried	1/2 cup	755
Lentils, cooked	1 cup	731
Acorn squash, mashed	1 cup	644
Prunes, dried	1/2 cup	635
Raisins	1/2 cup	618
Potato, baked (flesh only)	1 medium	610
Orange juice	1 cup	496
Soybeans, boiled	1/2 cup	443
Banana	1 medium	422
Milk, 1%	1 cup	366
Spinach, raw	2 cups	334
Chicken breast, grilled	3 oz	332
Yogurt, fruit variety, nonfat	6 oz	330
Salmon, Atlantic, farmed	3 oz	326
Beef, top sirloin, grilled	3 oz	315
Tomato, raw	1 medium	292

Source: USDA FoodData Central [89]; NIH ODS [1][14]; ConsumerLab [3].

Additional Potassium-Rich Foods

Other notable sources include coconut water, avocados, lima beans, cantaloupes, peaches, flounder, and cod — all providing more than 300 mg of potassium per serving [3].

Practical Notes on Dietary Potassium

• Refining grains reduces potassium: Whole-wheat flour and brown rice are much higher in potassium than their refined counterparts [1].
• Top sources in the U.S.: Milk, coffee, tea, other nonalcoholic beverages, and potatoes are the top potassium sources for American adults. For children: milk, fruit juice, potatoes, and fruit [90][91].
• Food-based potassium is preferred for blood pressure: Foods rich in potassium tend to be heart-healthy overall, and experts recommend dietary strategies over high-dose supplements [35][39].
• Salt substitutes as a dietary strategy: Potassium-enriched salt substitutes (25–50% potassium chloride) provide a practical way to simultaneously reduce sodium and increase potassium intake [40][46].

References

1. National Academies of Sciences, Engineering, and Medicine. "Dietary Reference Intakes for Sodium and Potassium." Washington, DC: The National Academies Press; 2019. https://doi.org/10.17226/25353

2. Stone MS, Martyn L, Weaver CM. "Potassium intake, bioavailability, hypertension, and glucose control." Nutrients. 2016;8(7):444. https://doi.org/10.3390/nu8070444

3. ConsumerLab. "Potassium Supplements Review." Accessed 2025. https://www.consumerlab.com/reviews/potassium-supplements-review/potassium/

4. He FJ, MacGregor GA. "Beneficial effects of potassium on human health." Physiol Plant. 2008;133(4):725-35. https://pubmed.ncbi.nlm.nih.gov/18724413/

5. Bailey JL, Sands JM, Franch HA. "Water, electrolytes, and acid-based metabolism." In: Modern Nutrition in Health and Disease. 11th ed. 2014:102-32.

6. Sun H. "Potassium intake and potassium deficiency in the US population, NHANES 1999-2016." J Am Coll Nutr. 2020. https://pubmed.ncbi.nlm.nih.gov/31855136/

7. U.S. Department of Health and Human Services. "2015-2020 Dietary Guidelines for Americans." 2015.

8. Paice BJ et al. "Record linkage study of hypokalaemia in hospitalized patients." Postgrad Med J. 1986;62(725):187-91. https://pubmed.ncbi.nlm.nih.gov/3714611/

9. Makunts T et al. "Potassium-lowering effects of medications." Sci Rep. 2019. See also: Medrol Prescribing Information, 2024; Veltri KT. P T. 2015.

10. Grennan Q et al. "Hypokalemia associated with semaglutide." Cureus. 2025.

11. Huang CL, Kuo E. "Mechanism of hypokalemia in magnesium deficiency." J Am Soc Nephrol. 2007;18(10):2649-52. https://doi.org/10.1681/ASN.2007070792

12. Whang R et al. "Magnesium and potassium interrelationships." Arch Intern Med. 1992;152(1):40-5. https://pubmed.ncbi.nlm.nih.gov/1728927/

13. Rude RK. "Magnesium." In: Encyclopedia of Dietary Supplements. 2nd ed. 2010:527-37.

14. NIH Office of Dietary Supplements. "Potassium — Health Professional Fact Sheet." Updated June 2, 2022. https://ods.od.nih.gov/factsheets/Potassium-HealthProfessional/

15. Macdonald-Clarke CJ et al. "Bioavailability of potassium from potatoes and potassium gluconate." Am J Clin Nutr. 2016;104(2):346-53. https://pubmed.ncbi.nlm.nih.gov/27413130/

16. Levene DL. "The absorption of potassium chloride — liquid vs. tablet." Can Med Assoc J. 1973;108(12):1480. https://pubmed.ncbi.nlm.nih.gov/4712696/

17. Phillips R et al. "Citrate salts for preventing and treating calcium containing kidney stones." Cochrane Database Syst Rev. 2015;(10):CD010057. https://doi.org/10.1002/14651858.CD010057.pub2

18. Soygur T et al. "Potassium citrate in preventing kidney stone recurrence." J Endourol. 2002;16(9):687-90. https://pubmed.ncbi.nlm.nih.gov/12490024/

19. Barbera M et al. "Potassium bicarbonate and kidney stone dissolution." Arch Ital Urol Androl. 2016;88(3):236-8. https://pubmed.ncbi.nlm.nih.gov/27711109/

20. Pak CYC et al. "Potassium bicarbonate and kidney stones." Kidney Int. 1986;30(3):422-8.

21. Heller HJ et al. "Potassium phosphate reduces urinary calcium in hypercalciuria." J Urol. 1998;159(5):1451-6. https://pubmed.ncbi.nlm.nih.gov/9554332/

22. Chan Q et al. "Potassium and blood pressure." Hypertension. 2023. https://doi.org/10.1161/HYPERTENSIONAHA.122.20017

23. Neal B et al. "Effect of salt substitution on cardiovascular events and death." N Engl J Med. 2021;385(12):1067-77. https://doi.org/10.1056/NEJMoa2105675

24. Tucker KL et al. "Potassium and bone mineral density." Am J Clin Nutr. 1999;69(4):727-36. https://pubmed.ncbi.nlm.nih.gov/10197575/

25. Dawson-Hughes B et al. "Potassium bicarbonate supplementation lowers bone turnover." J Bone Miner Res. 2015;30(11):2103-11. https://pubmed.ncbi.nlm.nih.gov/25989378/

26. U.S. FDA. Code of Federal Regulations Title 21. 21CFR201.306. Potassium salt preparations. 2017.

27. Allen AC et al. "Potassium-induced small bowel lesions." JAMA. 1965;193:1001-6. https://pubmed.ncbi.nlm.nih.gov/14325113/

28. Suh A et al. "Potassium and blood pressure in African Americans." Kidney Int. 2004.

29. Matlou SM et al. "Potassium and blood pressure." J Hypertens. 1986;4(suppl 6):S61-S63.

30. Filippini T et al. "Potassium supplementation on blood pressure in hypertensive subjects: meta-analysis." Int J Cardiol. 2017;230:127-35. https://pubmed.ncbi.nlm.nih.gov/28024910/

31. Binia A et al. "Daily potassium intake and blood pressure: meta-analysis." J Hypertens. 2015;33(8):1509-20. https://pubmed.ncbi.nlm.nih.gov/26039623/

32. Cappuccio FP, MacGregor GA. "Potassium supplementation and blood pressure: meta-analysis." J Hypertens. 1991;9(5):465-73. https://pubmed.ncbi.nlm.nih.gov/1649867/

33. Whelton PK et al. "Effects of oral potassium on blood pressure: meta-analysis." JAMA. 1997;277(20):1624-32. https://pubmed.ncbi.nlm.nih.gov/9168293/

34. AHRQ. "Sodium and Potassium Intake: Effects on Chronic Disease Outcomes." 2018. See also: NASEM, DRIs for Sodium and Potassium, 2019.

35. Jones DW et al. "Potassium and blood pressure guidelines." Hypertension. 2025. See also: McEvoy JW et al. Eur Heart J. 2024.

36. Azizi M et al. "Salt substitution and blood pressure." JAMA. 2026.

37. Dickinson HO et al. "Potassium supplementation for primary hypertension." Cochrane Database Syst Rev. 2006;(3):CD004641. https://pubmed.ncbi.nlm.nih.gov/16856051/

38. Filippini T et al. "High-dose potassium supplementation and blood pressure." J Am Heart Assoc. 2020. https://doi.org/10.1161/JAHA.119.015719

39. Whelton PK et al. "2017 ACC/AHA Guideline for High Blood Pressure." Hypertension. 2018;71(6):e13-e115. https://doi.org/10.1161/HYP.0000000000000065

40. Xu J et al. "Potassium-enriched salt substitutes for hypertension." Hypertension. 2024.

41. Aaron KJ, Sanders PW. "Dietary salt and potassium in cardiovascular health." Mayo Clin Proc. 2013;88(9):987-95. https://pubmed.ncbi.nlm.nih.gov/24001491/

42. D'Elia L et al. "Potassium intake, stroke, and cardiovascular disease: meta-analysis." J Am Coll Cardiol. 2011;57(10):1210-9. https://pubmed.ncbi.nlm.nih.gov/21371638/

43. Aburto NJ et al. "Increased potassium intake and cardiovascular risk: meta-analyses." BMJ. 2013;346:f1378. https://doi.org/10.1136/bmj.f1378

44. Vinceti M et al. "Potassium Intake and the Risk of Stroke: meta-analysis." J Am Heart Assoc. 2016;5(10):e004210. https://doi.org/10.1161/JAHA.116.004210

45. U.S. FDA. "Food Labeling: Revision of the Nutrition and Supplement Facts Labels." Federal Register. 2016;81(103):33894-33895.

46. Raquel G et al. "Salt substitutes and blood pressure: meta-analysis." Hypertension. 2020.

47. Ding J et al. "Salt substitute and stroke outcomes." JAMA Cardiol. 2025. https://doi.org/10.1001/jamacardio.2024.5264

48. Yuan Y et al. "Salt substitute and cardiovascular events in elderly care." Nat Med. 2023. https://doi.org/10.1038/s41591-023-02435-x

49. Maalouf NM et al. "Hypercalciuria and dietary protein." J Clin Endocrinol Metab. 2011;96(12):3733-40. https://pubmed.ncbi.nlm.nih.gov/21937618/

50. Soygur T et al. "Potassium citrate prevents kidney stone recurrence." J Endourol. 2002;16(9):687-90. https://pubmed.ncbi.nlm.nih.gov/12490024/

51. Barcelo P et al. "Potassium citrate in calcium nephrolithiasis." J Urol. 1993;150(6):1761-4. https://pubmed.ncbi.nlm.nih.gov/8230497/

52. Ettinger B et al. "Potassium complex and kidney stone recurrence." J Urol. 1997;158(6):2069-73. https://pubmed.ncbi.nlm.nih.gov/9366314/

53. Curhan GC et al. "Dietary calcium and kidney stone risk." N Engl J Med. 1993;328(12):833-8. https://pubmed.ncbi.nlm.nih.gov/8441427/

54. Curhan GC et al. "Dietary calcium and kidney stone risk in women." Ann Intern Med. 1997;126(7):497-504. https://pubmed.ncbi.nlm.nih.gov/9092314/

55. Weaver CM. "Potassium and health." Adv Nutr. 2013;4(3):368S-77S. https://pubmed.ncbi.nlm.nih.gov/23674806/

56. Hanley DA, Whiting SJ. "Dietary acid and bone loss." J Clin Densitom. 2013;16(4):420-5. https://pubmed.ncbi.nlm.nih.gov/24063846/

57. Tucker KL et al. "Potassium and bone mineral density." Am J Clin Nutr. 1999;69(4):727-36. https://pubmed.ncbi.nlm.nih.gov/10197575/

58. Lin PH et al. "DASH diet and bone turnover." J Nutr. 2003;133(10):3130-6. https://pubmed.ncbi.nlm.nih.gov/14519796/

59. Moseley KF et al. "Potassium citrate and calcium balance." J Bone Miner Res. 2013;28(3):497-504. https://pubmed.ncbi.nlm.nih.gov/23060044/

60. Jehle S et al. "Potassium citrate on bone density in older adults." J Clin Endocrinol Metab. 2013;98(1):207-17. https://pubmed.ncbi.nlm.nih.gov/23162100/

61. Dawson-Hughes B et al. "Potassium bicarbonate and bone turnover." J Bone Miner Res. 2015;30(11):2103-11. https://pubmed.ncbi.nlm.nih.gov/25989378/

62. Macdonald HM et al. "Potassium citrate and bone in postmenopausal women." Am J Clin Nutr. 2008;88(2):465-74. https://pubmed.ncbi.nlm.nih.gov/18689384/

63. Zillich AJ et al. "Thiazide diuretics, potassium, and diabetes." Hypertension. 2006;48(2):219-24. https://pubmed.ncbi.nlm.nih.gov/16801488/

64. Chatterjee R et al. "Potassium and type 2 diabetes: the CARDIA Study." Diabetologia. 2012;55(5):1295-303. https://pubmed.ncbi.nlm.nih.gov/22322920/

65. Colditz GA et al. "Diet and diabetes risk in women." Am J Clin Nutr. 1992;55(5):1018-23. https://pubmed.ncbi.nlm.nih.gov/1315120/

66. Chatterjee R et al. "Potassium and diabetes: the ARIC study." Arch Intern Med. 2010;170(19):1745-51. https://pubmed.ncbi.nlm.nih.gov/20975023/

67. Chatterjee R et al. "Potassium and diabetes risk: the MESA study." PLoS One. 2016;11(7):e0157252. https://pubmed.ncbi.nlm.nih.gov/27391103/

68. Chatterjee R et al. "Potassium supplements and glucose in prediabetes." Am J Clin Nutr. 2017;106(6):1431-8. https://pubmed.ncbi.nlm.nih.gov/29070559/

69. Nuki G et al. "Potassium and rheumatoid arthritis." Ann Rheum Dis. 1975;34(suppl):52-3.

70. Toktam F et al. "Potassium supplementation in rheumatoid arthritis." medRxiv. 2022. (Preprint.)

71. Allen RE, Kirby KA. "Nocturnal leg cramps." Am Fam Physician. 2012;86(4):350-5. https://pubmed.ncbi.nlm.nih.gov/22963024/

72. Rauf M et al. "Potassium citrate in restless legs syndrome." Pharm Pharmacol Int J. 2016.

73. Chen D et al. "Hypokalemia and COVID-19." medRxiv. 2020. (Preprint.)

74. Alfano G et al. "Hypokalemia in COVID-19 patients in Italy." medRxiv. 2020. (Preprint.)

75. National Academies of Sciences. "DRIs for Sodium and Potassium." 2019. (Previous AI for adults was 4,700 mg in 2005.)

76. Hey H et al. "Potassium chloride and esophageal injury." Br Med J. 1982;285(6343):717-8.

77. Narasaki Y et al. "Potassium intake and mortality in dialysis." J Renal Nutr. 2020. https://pubmed.ncbi.nlm.nih.gov/31753764/

78. Chocano-Bedoya PO et al. "Potassium and PMS risk." Am J Epidemiol. 2013;177(10):1118-27. https://doi.org/10.1093/aje/kws363

79. Kusunoki T et al. "Salt substitute-induced hyperkalemia." Cureus. 2025.

80. Abe T et al. "Mango-induced hyperkalemia." Case Rep Neurol Med. 2012. https://doi.org/10.1155/2012/926152

81. Raebel MA. "Hyperkalemia with ACE inhibitors and ARBs." Cardiovasc Ther. 2012;30(3):e156-66. https://pubmed.ncbi.nlm.nih.gov/21883995/

82. Epstein M. "Hyperkalemia and RAAS blockade." J Clin Hypertens. 2009;11(1):55-60. https://pubmed.ncbi.nlm.nih.gov/19125861/

83. Dockery MA et al. "Life-threatening hyperkalemia from losartan." Mil Med. 2022.

84. Sarafidis PA et al. "Diuretics and electrolyte disorders." Expert Opin Drug Saf. 2010;9(2):259-73. https://pubmed.ncbi.nlm.nih.gov/20095753/

85. Fang L et al. "ACE inhibitors and COVID-19." Lancet Respir Med. 2020;8(4):e21. https://doi.org/10.1016/S2213-2600(20)30116-8

86. Diaz JH. "ACE inhibitors, ARBs, and COVID-19." J Travel Med. 2020;27(3):taaa041. https://doi.org/10.1093/jtm/taaa041

87. Danser AHJ et al. "RAAS blockers and COVID-19." Hypertension. 2020;75(6):1382-5. https://doi.org/10.1161/HYPERTENSIONAHA.120.15082

88. de Simone G et al. "ESC position on ACE-inhibitors and ARBs." European Society of Cardiology. 2020.

89. USDA, Agricultural Research Service. "FoodData Central." https://fdc.nal.usda.gov/

90. O'Neil CE et al. "Food sources of nutrients among US adults." Nutrients. 2012;4(12):2097-120. https://pubmed.ncbi.nlm.nih.gov/23363999/

91. Keast DR et al. "Food sources of nutrients among US children." Nutrients. 2013;5(1):283-301. https://pubmed.ncbi.nlm.nih.gov/23340318/