IngredientsThe term potash is a broad designation that refers to potassium-bearing compounds and potassium-containing materials, with potassium carbonate (K2CO3) as its most historically central form. The term potash refers to compounds of potassium and to potassium-bearing materials, usually potassium carbonate. The elemental chemical symbol for potassium, K, derives from the Latin word kalium, while the English name "potassium" itself comes from the word "potash." The name derives from the English word "potash" (pot ashes) and the Arabic word "qali" meaning alkali.
Within the broader context of dietary supplementation and health science, the term potash encompasses an entire family of potassium salts. There are eight potassium compounds with the term potash in their traditional names. The most nutritionally and pharmacologically relevant forms include:
Potassium carbonate is a dipotassium salt of carbonic acid. The compound is a hygroscopic, deliquescent white powder. It is odorless and tastes alkaline. It is readily soluble in water but insoluble in ethanol, acetone, and alcohol. It has a pH of 11.6.
From a natural-source perspective, potassium is a monovalent cation widely present in nature, where it is not in metallic form but always in combination with other substances, especially chloride. The main sources of dietary potassium are fruit and vegetables, where it is usually combined with organic acids (e.g., potassium citrate). Major dietary sources of potassium include fruits and vegetables, starchy roots and tubers, and whole grains. As a mineral element, most of the world's reserves of potassium were deposited as seawater in ancient inland oceans.
The pharmaceutical-grade production of potassium carbonate today is synthetic. The modern commercial production of potassium carbonate is by reaction of potassium hydroxide with carbon dioxide. In an alternative method, potassium chloride is treated with carbon dioxide in the presence of an organic amine to give potassium bicarbonate, which is then calcined.
The usage of the term potash dates from 1477, and derives from the Middle Dutch word potaschen, denoting pot ashes. The old method of making potassium carbonate was either by collecting or by producing wood ash, chemically leaching the ashes, and then evaporating the resulting solution in large iron pots, which yielded a white residue denominated "pot ash"; approximately 10% by weight of common wood ash can be recovered as potash. Well before potassium was recognized as an element, potassium carbonate was mixed with animal fat to make soap. The carbonate was made by extracting wood ash with water before concentration by boiling β hence the name "potash" for potassium salts.
Potash (especially potassium carbonate) has been used in bleaching textiles, making glass, ceramic, and making soap since the Bronze Age. Potash was principally obtained by leaching the ashes of wood burned for heating and cooking. Beginning in the 14th century, potash was mined in Ethiopia. One of the world's largest deposits, 140 to 150 million tons, is located in the Dallol area of the Afar Region. Potash was refined from the ashes of broadleaved trees and produced primarily in the forested areas of Europe, Russia, and North America.
Until the 18th century no distinction was made between potassium and sodium. This was because early chemists did not recognise that "mineral alkali" (Na2CO3, sodium carbonate, coming from deposits in the earth) and "vegetable alkali" (K2CO3, potassium carbonate, derived from wood ashes) are distinct from each other. Potassium was isolated in 1807 by Sir Humphry Davy, who obtained it through the electrolysis of very dry molten caustic potash (KOH, potassium hydroxide).
Potassium carbonate, historically known as "potash," has been valued for centuries not only in culinary and industrial settings but also for its medicinal properties. Dating back to ancient and medieval times, potassium carbonate was a staple in apothecaries and traditional remedies. It was commonly used as an "alkaline salt," believed to help balance bodily humors and counteract excess acidity. Physicians prescribed it to alleviate digestive discomfort, heartburn, and symptoms related to gastric hyperacidity.
Its ability to neutralize acids made it a go-to remedy for indigestion and mild dyspepsia. Furthermore, potassium carbonate was included in early formulations for cough syrups and expectorants, where its alkaline nature helped loosen phlegm and ease respiratory complaints. It also played a role in so-called "sal volatile" mixtures, which were early forms of smelling salts, offering relief for fainting and dizziness.
In the realm of herbal combinations, potassium carbonate has historically been blended with various botanicals to enhance their efficacy. Herbalists often combined it with roots such as licorice or marshmallow to improve extraction of beneficial compounds and potentiate soothing effects for the digestive and respiratory systems. In traditional Chinese medicine, alkaline salts like potassium carbonate were used to modify herbal formulas, optimizing their absorption and balancing their energetic properties.
Historically, pearl ash was created by baking potash in a kiln to remove impurities. The fine, white powder remaining was the pearl ash. The first patent issued by the US Patent Office was awarded to Samuel Hopkins in 1790 for an improved method of making potash and pearl ash. In late 18th-century North America, before the development of baking powder, pearl ash was used as a leavening agent for quick breads.
Evolutionary context is also relevant: over several million years, the physiology and metabolism of humans evolved to retain Na+ and excrete K+ in response to a diet that was low in Na+ and high in K+. With the onset of agriculture and industrialization, there has been a precipitous drop in dietary K+ consumption and an equal rise in dietary salt consumption, contributing to disease onset. Contemporarily, until recently, humans consumed a diet high in potassium. However, with the increasing consumption of processed food, which has potassium removed, combined with a reduction in the consumption of fruits and vegetables, there has been a large decrease in potassium intake which now, in most developed countries, averages around 70 mmol day-1 β only one third of our evolutionary intake.
In the context of dietary supplementation, the biologically active entity delivered by potash-family compounds is the potassium ion (K+). Potassium is an essential mineral that is needed by all tissues in the body. It is sometimes referred to as an electrolyte because it carries a small electrical charge that activates various cell and nerve functions.
Potassium carbonate contains approximately 56% elemental potassium by weight, making it a highly concentrated source. As a dietary potassium supplement, it contains 56% of elemental potassium, in tablet or powder form to address low blood potassium levels caused by inadequate nourishment, nausea and vomiting, or diarrhea.
Different potassium salt forms deliver the same cation but have distinct co-anions with additional physiological effects: potassium chloride (KCl) is the reference clinical form; potassium bicarbonate and potassium citrate also contribute alkalinizing anions; evidence is accumulating of the protective effect of adequate dietary potassium on age-related bone loss and reduction of kidney stones. These benefits depend on organic anions associated with potassium as occurs in foods such as fruits and vegetables, in contrast to similar blood pressure-lowering benefits of potassium chloride.
In the body, a large part of the potassium pool is localized in the muscles and the skeleton, but also in the central nervous system, intestines, liver, lungs, and skin. Extracellular potassium plays a key role in the regulation of cellular membrane potential and thus in the regulation of nerve and muscle activities. The transfer of potassium ions across nerve cell membranes is necessary for normal nerve transmission; potassium deficiency and excess can each result in numerous signs and symptoms, including an abnormal heart rhythm and various electrocardiographic abnormalities.
In contrast to other electrolytes, potassium is primarily an intracellular ion: only 2% of all potassium in the body is present in the extracellular fluid, so a small decrease in serum potassium may represent a significant decrease in intracellular potassium. Homeostatic challenges are overcome by regulatory mechanisms such as insulin signaling and Na+-K+-ATPase uptake that moves excess extracellular K+ into the intracellular fluid. In a healthy person, the kidneys ensure that K+ excretion is balanced with K+ intake. K+ homeostasis is achieved by balancing the extra- and intracellular distribution as well as balancing excretion with intake, primarily via urinary excretion.
Dietary potassium deficiency activates the sodium chloride cotransporter (NCC) even in the setting of high sodium intake, thus increasing sodium retention and blood pressure, while increasing potassium intake does the reverse. This is mediated via the WNK (with-no-lysine kinase) signaling pathway. Many other proposed mechanisms by which potassium can influence blood pressure have been reported, including alterations in intracellular sodium and tonicity, modulation of baroreceptor sensitivity, vasoconstrictive sensitivity to norepinephrine and angiotensin II, high sodium/potassium ATPase activity and alteration in DNA synthesis and proliferation, and decrease in cardiac diastolic dysfunction.
The underlying mechanisms linking potassium to bone health are unclear, but one hypothesis is that potassium helps protect bone through its effect on acid-base balance. Diets that are high in acid-forming foods, such as meats and cereal grains, contribute to metabolic acidosis and might have an adverse effect on bone. Alkaline components in the form of potassium salts (potassium bicarbonate or citrate, but not potassium chloride) from food or potassium supplements might counter this effect and help preserve bone tissue.
An increased potassium intake lowers urinary calcium excretion and plays an important role in the management of hypercalciuria and kidney stones, and is likely to decrease the risk of osteoporosis. Getting too little potassium can deplete calcium from bones and increase the amount of calcium in urine. This calcium can form hard deposits (stones) in the kidneys, which can be very painful. Increasing the amount of potassium in the diet might reduce the risk of developing kidney stones.
The most established clinical application of potassium supplementation β including potash-derived forms β is the treatment and prevention of hypokalemia. Hypokalemia, although not formally defined, is generally considered to be when serum potassium levels fall below the normal value of 3.6 mmol/L. Individuals with mildly decreased potassium levels (3.0β3.5 mmol/L) may be asymptomatic, but patients with more pronounced decreases may report symptoms including muscle weakness, fatigue, and constipation. Very low serum potassium levels (β€ 2.5 mmol/L) can lead to muscle necrosis, paralysis, cardiac arrhythmias, and impaired respiration, which can be life-threatening.
Potassium chloride is the preferred formulation for replacement therapy in most cases. Increasing dietary potassium is usually inadequate to treat hypokalemia because most of the potassium in foods is coupled with phosphate. Most cases of hypokalemia involve chloride depletion and respond best to potassium chloride replacement. Clinical evidence for correction is strong and guideline-supported. Providing 60 to 80 mmol/day over days to weeks is usually sufficient for oral correction of mild-to-moderate hypokalemia.
Evidence strength: Strong β This is the most robustly supported clinical indication, with extensive clinical experience and guideline endorsement.
The evidence linking potassium intake to blood pressure reduction is one of the most studied areas. The Dietary Guidelines for Americans 2010 Advisory Committee concluded that there was a moderate body of evidence of the association between potassium intake and blood pressure reduction in adults, which in turn influences the risk of stroke and coronary heart disease. Potassium was identified as a shortfall nutrient.
A key systematic review with meta-analysis of randomized controlled trials in hypertensive subjects found: overall, potassium supplementation decreased systolic blood pressure by 4.48 mm Hg (95% CI 3.07β5.90) and diastolic blood pressure by 2.96 mm Hg (1.10β4.82). There was little evidence of a dose-response relation between blood-pressure decrease and potassium supplementation. However, lower (<90 mmol/day) potassium intake at baseline was associated with a higher blood-pressure lowering effect, as were higher sodium intake (particularly β₯4 g/day) and higher sodium-to-potassium ratio.
A 2025 dose-response meta-analysis of RCTs published between 2000 and 2024 (including 10 RCTs, comprising 4 studies on subjects without hypertension and 6 studies on subjects with hypertension, found that the dose-response relationship varied according to blood pressure status. In subjects without hypertension, potassium supplementation had a modest negative linear effect on blood pressure. In contrast, subjects with hypertension exhibited a markedly higher reduction. Specifically, a 50 mmol/day increase in urinary potassium excretion was associated with reductions in systolic and diastolic BP. The authors cautioned that findings are limited by the small number of RCTs included.)
Much evidence shows that increasing potassium intake has beneficial effects on human health. Epidemiological and clinical studies show that a high-potassium diet lowers blood pressure in individuals with both raised blood pressure and average population blood pressure. Prospective cohort studies and outcome trials show that increasing potassium intake reduces cardiovascular disease mortality.
Evidence strength: Moderate-to-strong for blood pressure reduction in hypertensive individuals, particularly in those with high sodium intake or low baseline potassium. Effect is more modest in normotensive individuals.
Higher potassium intakes have been associated with a decreased risk of stroke and possibly other cardiovascular diseases (CVDs). A meta-analysis of 11 prospective cohort studies in 247,510 adults found that a 1,640 mg per 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 CVD.
Similarly, a meta-analysis of nine cohort studies reported a significant 24% lower risk of stroke with higher potassium intakes and a nonsignificant reduction in coronary heart disease and CVD risk. However, the AHRQ review found inconsistent relationships between potassium intakes and risk of stroke based on 15 observational studies.
High potassium intake may have other beneficial effects independent of its effect on blood pressure β for example, reducing the risk of stroke, preventing the development of renal vascular, glomerular, and tubular damage, decreasing urinary calcium excretion, reducing formation of kidney stones, and reducing demineralisation of bone. Several prospective epidemiological studies have shown that increasing consumption of fruits and vegetables protects against stroke, but in all these studies it is difficult to separate the effects of potassium from those of other nutrients contained in fruits and vegetables β for example, fibre and antioxidants.
Evidence strength: Moderate for stroke reduction (observational data consistent but not uniformly so; causality not fully established; confounding by overall diet quality is a notable limitation).
A 2015 Cochrane Review of seven studies examined the effects of potassium citrate, potassium-sodium citrate, and potassium-magnesium citrate supplementation on the prevention and treatment of calcium-containing kidney stones in a total of 477 participants, most of whom had calcium oxalate stones. The potassium citrate salts significantly reduced the risk of new stones and reduced stone size. However, the proposed mechanism requires additional research to fully understand the potential link.
Evidence strength: Moderate β The Cochrane evidence favors potassium citrate forms specifically for calcium oxalate kidney stone prevention; broader evidence for other potassium forms is more preliminary.
Observational studies suggest that increased consumption of potassium from fruits and vegetables is associated with increased bone mineral density. This evidence, combined with evidence from metabolic studies and a few clinical trials, suggests that dietary potassium may improve bone health.
People who have high intakes of potassium from fruits and vegetables seem to have stronger bones. Eating more of these foods might improve bone health by increasing bone mineral density (a measure of bone strength).
Evidence strength: Preliminary β Associations in observational studies are suggestive, but larger, well-controlled clinical trials are still needed to confirm a causal effect of potassium supplementation specifically on bone mineral density outcomes.
Low intakes of potassium might increase blood sugar levels. Over time, this can increase the risk of developing insulin resistance and lead to type 2 diabetes. However, more research is needed to fully understand whether potassium intakes affect blood sugar levels and the risk of type 2 diabetes.
The findings from studies conducted to date are promising. However, more research, including randomized controlled trials, is needed before potassium's link with blood glucose control and type 2 diabetes can be confirmed.
Evidence strength: Preliminary and insufficient β While epidemiological associations exist and mechanistic hypotheses are plausible, this area lacks the robust RCT evidence needed for definitive conclusions.
Animal research has provided new evidence on potassium's renal protective effects independent of blood pressure. Results showed that dietary potassium supplementation normalized urinary Na/K ratio, hypokalemia, proteinuria, and serum creatinine, reduced renal hypertrophy, inflammations, and fibrosis, and down-regulated mRNA expression of fibronectin, collagen, TGF-Ξ², TNF-Ξ±, osteopontin, and ICAM without changes in blood pressure. The results provide new evidence that potassium and sodium may modulate pro-inflammatory and fibrotic genes, leading to chronic renal lesions independent of blood pressure.
Evidence strength: Primarily preclinical (animal models) β Human interventional evidence specifically examining kidney-protective effects of potassium supplementation as an independent variable remains limited.
Strict regulation of plasma potassium is essential for many physiologic processes, including acid-base homeostasis, systemic blood pressure control, smooth muscle tone, cardiac conduction and rhythm, and membrane potential repolarization. Potassium plays vital roles in the normal functioning of cells and organs through its involvement in nerve transmission, muscle contractions, regulation of blood pressure, and maintenance of the integrity of the skeleton.
The principal body systems and health areas associated with potassium include:
The newest Dietary Guidelines for Americans listed K+ as a "nutrient of public health concern" because of its inadequate consumption. Low K+ intake is implicated in various chronic diseases including hypertension, cardiovascular disease, osteoporosis, and nephrolithiasis.
For most adults, the recommended daily intake of potassium is 2,600β3,400 milligrams (mg). Adequate potassium intake, according to the US Panel on Dietary Reference Intake, is 4.7 g (120 mmol)/day for adults, based on the assessment of the health benefits of potassium at this level on blood pressure, bone density, and risk of kidney stones. In general, dietary intake of potassium, at least in the USA and Canada, has been found to be much lower than this recommended value.
Note: the 2019 National Academies of Sciences, Engineering, and Medicine revised the Adequate Intake (AI) downward from 4,700 mg/day to 2,600 mg/day for women and 3,400 mg/day for men, reflecting a reassessment of available evidence. In the U.S., most people get enough potassium from their diet. It is found in fruits, vegetables, beans, nuts, milk, yogurt, meat, and fish.
Potassium supplements are used to increase potassium levels. They come in various salts, forms, and strengths. Some are available only by prescription, while others are available over the counter as a dietary supplement.
Common pharmaceutical forms include:
Doses reported in clinical and research contexts:
In healthy people with normal kidney function, high dietary potassium intakes do not pose a health risk because the kidneys eliminate excess amounts in the urine. Although case reports indicate that very large doses of potassium supplements can cause heart abnormalities and death, the National Academies committee concluded that these reports do not provide sufficient evidence to set a tolerable upper limit (UL). In addition, there is no evidence that high intakes of potassium cause hyperkalemia in adults with normal kidney function or other adverse effects. Therefore, the committee did not set a UL for potassium.
All carbonate salts are on the FDA generally regarded as safe (GRAS) list.
Common side effects include nausea, vomiting, diarrhea, gas, and stomach pain. Oral supplementation can irritate the gastrointestinal mucosa and cause bleeding or ulceration. However, oral potassium replacement is associated with a lower risk of rebound hyperkalemia compared to intravenous forms.
Potassium in supplement form can lead to acute toxicity, even in generally healthy adults. The evidence is based on trials conducted between 1980 and 1990 which reported gastrointestinal discomfort in healthy individuals and patients receiving 0.8 to 2.3 g (20β60 mmol/day) of supplemental potassium chloride. The AHRQ panel rated the strength of evidence for potassium-related adverse outcomes as low.
In people with impaired urinary potassium excretion due to chronic kidney disease or the use of certain medications, such as ACE inhibitors or potassium-sparing diuretics, even dietary potassium intakes below the AI can cause hyperkalemia. Hyperkalemia can also occur in people with type 1 diabetes, congestive heart failure, adrenal insufficiency, or liver disease.
Very high amounts of potassium supplements or salt substitutes that contain potassium could exceed the kidney's capacity to excrete potassium, causing acute hyperkalemia even in healthy individuals.
Very low serum potassium levels can be life-threatening; conversely, severe hyperkalemia can equally lead to muscle necrosis, paralysis, cardiac arrhythmias, and impaired respiration.
ACE Inhibitors and Angiotensin Receptor Blockers (ARBs): Potassium supplements, K+-sparing diuretics, and salt substitutes (approximately 60 mmol/tsp of potassium chloride) increase the probability of developing hyperkalemia if combined with an ACE inhibitor or an ARB. Nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase inhibitors can also exaggerate the rise in serum K+ seen with either an ACE inhibitor or an ARB by reducing aldosterone concentrations and thereby decreasing K+ excretion.
Potassium-Sparing Diuretics: Potassium-sparing diuretics cause the kidneys to hold potassium in the body. Persons taking these medications generally should not take potassium supplements because potassium levels might rise too high. These medications can lead to potentially harmful drug interactions, particularly when combined with potassium supplements, with elevated potassium levels posing health risks.
Diuretics (Loop and Thiazide) β Potassium-Depleting: Disturbances in plasma potassium are more common in patients with chronic kidney disease compared to the general population. This typically presents as hypokalemia as a consequence of diuretic administration. In such cases, potassium supplementation may be clinically indicated, but requires monitoring.
Chronic Kidney Disease: In subjects with CKD, both hypo- and hyperkalemia are associated with higher risk of all-cause mortality, major cardiovascular events, and hospitalization. Supplementation in the CKD population requires close medical supervision. A study in CKD patients found that plasma potassium increased by approximately 0.4 mmol/L over baseline when using oral KCl supplements at 40 mmol K+ per day to increase potassium intake to recommended levels, but 89% of participants remained normokalemic over the 14-day study period. Those developing hyperkalemia were older or had a higher baseline plasma potassium concentration.
Severity gradient of hypokalemia and treatment decisions: Prolonged diarrhea or vomiting, laxative abuse, diuretic use, eating clay, heavy sweating, dialysis, or using certain medications can cause severe potassium deficiency. In this condition, called hypokalemia, blood levels of potassium are very low. Symptoms include constipation, tiredness, muscle weakness, and not feeling well. More severe hypokalemia can cause increased urination, decreased brain function, high blood sugar levels, muscle paralysis, difficulty breathing, and irregular heartbeat. Severe hypokalemia can be life threatening.
Health conditions that Potash may help support.
Body systems that Potash may help support.
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