The anti-cramp commander. Balances sodium to control blood pressure, helps muscles contract and relax properly, and keeps your nerves firing. It's a fundamental electrolyte.
Reviewed March 2026
Source: NIH ODS + He 2006 blood pressure meta
In a fully controlled randomised placebo-controlled crossover in 36 untreated adults with elevated blood pressure, 3 g a day of supplemental potassium for 4 weeks lowered 24 hour blood pressure by 3.9/1.6 mmHg and central pulse pressure by 2.9 mmHg; arterial stiffness measures did not change over the 4 weeks. A meta-analysis restricted to trials of 4 weeks or longer in hypertensive participants measured systolic pressure 4.48 mmHg lower and diastolic 2.96 mmHg lower. In generally normotensive participants a 2024 meta-analysis measured a smaller 2.80 mmHg systolic fall at durations beyond one month.
Where a trial measured an actual number, we show it next to the claim. It is the average across the trials, never a promise about one person.
About 3.5 mmHg lower systolic and 2 mmHg lower diastolic, on average, in adults with hypertension.
Adults; the effect was seen in those with hypertension, not those without.
About 24 percent lower risk of stroke in the cohort studies.
Adults, higher versus lower potassium intake.
Read at the source. The magnitude sits beside the same trial the claim already cites. It describes what the trials measured, never what any one person will feel.
These words describe the research, not the molecule's worth. Research strength is how much work stands behind one claim, and it is never a product score.
Essential electrolyte.
About 3.5 mmHg lower systolic and 2 mmHg lower diastolic, on average, in adults with hypertension.
Adults; the effect was seen in those with hypertension, not those without. Confidence interval systolic 1.8 to 5.2 mmHg lower.
About 24 percent lower risk of stroke in the cohort studies.
Adults, higher versus lower potassium intake. Confidence interval risk ratio 0.76, 0.66 to 0.89.
Why these belong in the same formula. Each row says what the basis is, from settled biochemistry through to a trial that measured the pair.
Magnesium powers the pump that pulls potassium into cells and holds it there, so the body needs enough magnesium to keep potassium where it works. Magnesium also helps the kidneys retain potassium instead of losing it in urine, which is why the two minerals are usually balanced together.
Potassium promotes sodium excretion at the kidney while sodium pulls in the opposite direction on fluid balance and normal blood pressure regulation. The ratio between the two matters more than either amount on its own, so they are a counterbalanced pair.
Glycyrrhizin blocks the enzyme that inactivates cortisol in the kidney, producing mineralocorticoid-like signalling that holds sodium and excretes potassium. Licorice therefore works directly against potassium status and the pairing is a caution.
Dandelion increases urine output, which moves electrolytes including potassium, though the leaf is itself unusually potassium rich. Any ingredient that changes urine volume changes what potassium balance looks like.
Caffeine has a modest diuretic effect that raises urinary electrolyte loss, potassium among them. The interaction is on renal handling rather than on absorption.
Dietary nitrate raises nitric oxide availability and relaxes vessel walls, while potassium works through natriuresis and membrane potential. Both support normal blood pressure regulation by unrelated routes.
Renal potassium retention depends on magnesium, because low intracellular magnesium opens the ROMK channel and potassium is lost in urine. Correcting magnesium is what allows a potassium load to be held.
Taurine acts as an intracellular osmolyte and influences potassium currents in cardiac and skeletal muscle. The overlap is on cell volume and membrane excitability rather than on potassium absorption.
Potassium sets the resting membrane potential across cell membranes while calcium entry drives the contraction itself, so the two sit on opposite sides of the same contraction and relaxation cycle. Diets and formulas that raise potassium usually raise calcium too, which is why the two are so often reported together in intake work. Nothing here is a shared transporter, and the pairing does not change how much of either is absorbed.
Every cell in the body runs a sodium potassium pump, and the kidney trades one ion for the other in the distal nephron, so intake of one changes the handling of the other. A higher potassium intake increases urinary sodium loss, which is the physiology behind the widely reported sodium to potassium ratio. This is settled pharmacology rather than a combination trial result, and it describes ion handling, not a clinical outcome.
Raising blood pH pushes potassium into cells in exchange for hydrogen ions, so an alkali load lowers the measured serum potassium without changing total body potassium. Citrate and bicarbonate potassium salts carry both the mineral and the alkali, which is why they behave differently in the body from the chloride salt. The relevant reading here is a laboratory value, not a symptom.
One randomised trial gave an olive leaf extract with potassium to participants whose blood pressure sat in the mildly to moderately elevated range, so the pairing has been studied as a combination rather than inferred. Because the two arms are not separable in a single trial of this size, the contribution of each part is not established. Read it as one trial of a combination that supports normal blood pressure regulation, not as a settled additive effect.
Potassium phosphate is a single salt that carries both minerals, so any formula using it changes phosphate intake as well. When cells take up glucose and build ATP they pull potassium and phosphate inward at the same time, which is why both fall together in plasma during a strong anabolic shift. This is ion movement between compartments, described as a marker and not as an effect a person feels.
Sweat carries sodium, chloride, potassium and magnesium, so rehydration blends include potassium to match what is lost rather than to add a separate action. The potassium share of sweat is small compared with sodium, which is why these products are sodium led. The pairing is about matching a loss profile, and it supports normal fluid and electrolyte balance.
Potassium acts mostly through renal sodium handling and vascular smooth muscle repolarisation, while aged garlic preparations are studied through nitric oxide and vascular tone pathways, so the routes differ. Taken together the effects could add, but the candidate literature here holds no trial of the two given as a pair. Anyone tracking blood pressure while using both should know the direction of both inputs is the same.
Talk to a doctor before taking Potassium if any of these apply to you: Kidney disease. These are flags to check first, not effects Potassium is known to cause.
Not medical advice. Show the label to your pharmacist.Potassium is the main mineral inside your cells. A pump in every cell membrane pushes three sodium out for every two potassium in, and it burns ATP doing it.
The gap between potassium inside and outside a cell sets the resting electrical charge across the membrane. That charge is what makes nerve signals and muscle contraction possible.
Your kidneys do most of the balancing. A hormone called aldosterone tells them to hold on to sodium and let potassium go, so the two move in opposite directions.
Insulin and adrenaline-type signals both push potassium out of blood and into cells. So a blood potassium reading shows where it's parked as much as how much you took in.
It starts as rock. Potash is mined or dissolved out of old seabed deposits, cleaned up into potassium chloride, then reacted with something like citric acid to make the version on your label. The potassium is the same either way, and the second half of the name tells you what it is paired with.
From a mineral source, then refined and usually bound to a carrier so the body can take it up.
Potassium is mined as potash from ancient evaporated seabed deposits, mainly the minerals sylvite and carnallite, either by conventional shaft mining or by solution mining with brine injected into the seam.
Sylvite is separated from sodium chloride either by froth flotation of the crushed ore or by fractional crystallisation of the brine, which exploits how differently the two salts drop out of solution as temperature changes.
Purified potassium chloride is the common starting point. It is reacted with citric acid, gluconic acid, malic acid, phosphoric acid or carbonate chemistry, or neutralised with potassium hydroxide, to give citrate, gluconate, malate, phosphate or bicarbonate salts.
The salt is recrystallised, washed and dried to food or pharmaceutical grade, with residual sodium, heavy metals and insoluble matter as the specifications that get tested.
The dried salt is milled to a target particle size, sometimes granulated for flow, then blended into a powder or filled into capsules or tablets. Doses per unit are usually kept modest because concentrated potassium salts irritate the gut lining.
Which mine or region the potash came from is almost never stated on a supplement label, and the salt conversion is usually done by a separate chemical supplier from the miner.
The whole-food sources on file. A supplement closes the gap, it does not replace dinner.
A gram-for-gram figure (how much of each you would eat to match a dose) will appear here once it is sourced and reviewed. This page will not print a number it cannot cite.
Same mineral in different salts. Each is its own molecule with its own page, and absorption and feel differ from one to the next.
These are the studies our verdict leans on, chosen from the 7,041 we read for Potassium. The full linked list is below.
6 sources behind our Potassium verdict: peer-reviewed studies and registered clinical trials. Every one links straight to PubMed, the journal, or ClinicalTrials.gov. Read them yourself.
Evidence surfaced via Semantic Scholar (Allen Institute for AI) and ClinicalTrials.gov. Ranked by study type and citation weight, not cherry-picked.
Read this carefully. These are 1,133,200 voluntary, unverified reactions reported to the FDA (openFDA). The number mostly reflects how popular Potassium is, not how risky it is. A report is not proof Potassium caused anything. It is a signal of what to watch for, nothing more.
Source: openFDA adverse-event reports. Voluntary reporting, not an incidence rate.
FDA Disclaimer: These statements have not been evaluated by the Food and Drug Administration. This information is for educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before starting any supplement regimen.
