Potassium

Keeps nerves and muscles firing

Potassium is the main ion inside cells, the mirror image of sodium outside them. About 98% of the body's potassium is inside cells, at roughly 140 mmol/L, against only 3.5–5 mmol/L in blood. The sodium-potassium pump keeps this up by bringing 2 potassium in for every 3 sodium it pushes out, using ATP each time. Jens Skou won a Nobel Prize for identifying the pump in 1957.¹

Cell membranes have channels that let potassium leak out slowly, and those channels are always partly open. As positively charged potassium leaks out, it leaves negative charge behind until the inside of the cell sits at about −70 to −90 mV. That is the resting membrane potential, and it's set mostly by the ratio of potassium inside to potassium outside. Every nerve signal starts from that baseline. Sodium rushes in to fire the cell, then potassium flows out to reset it for the next signal.²

Because the resting voltage depends on a ratio, small changes in blood potassium shift it a lot. Low blood potassium (hypokalemia) pulls the resting voltage further negative, so nerves and muscles are harder to fire. The result is weakness, cramps, constipation (sluggish gut muscle) and, when severe, paralysis.³ High potassium does the opposite and is just as dangerous.

Steady heart rhythm

The heart is where potassium's narrow safe range matters most. After each beat, heart cells reset by letting potassium out through several kinds of potassium channel. When blood potassium is low, those channels pass less current, which seems backwards. So the reset slows and becomes uneven between cells. On an ECG this shows as flattened T waves, U waves and a longer QT interval. Uneven resetting lets stray electrical activity trigger extra beats, and in the worst case ventricular fibrillation.⁴ High potassium instead flattens the resting voltage until the heart can't fire at all.

The safe zone is narrow. Among 38,689 heart attack patients, the lowest death rate was at blood potassium of 3.5–4.5 mEq/L. Death rates were higher below 3.5 and doubled at 4.5–5.0. Ventricular fibrillation or cardiac arrest rose below 3.0 and at 5.0 or above.⁵ That's why potassium supplements are sold in small doses and why intravenous potassium is given slowly. The kidneys handle large amounts from food easily, but a big dose taken all at once can outpace them.

Low magnesium makes low potassium hard to fix. Magnesium normally blocks a potassium channel in the kidney (ROMK) from inside the cell. Without it the channel leaks potassium into the urine, and potassium replacement doesn't work until magnesium is replaced too.⁶ See Magnesium.

Balances sodium

The kidneys control sodium and potassium as a pair. Aldosterone, the same hormone that holds onto sodium when blood volume falls, also makes the kidney push potassium out in exchange. A potassium-rich meal raises aldosterone and quickly increases potassium excretion. Potassium also makes the kidney excrete more sodium. So eating more potassium partly offsets a high salt intake.⁷

Outcome evidence. This is the strongest reason to care about potassium, and it doesn't depend on a few mmHg of blood pressure:

• A WHO-commissioned meta-analysis found that higher potassium intake went with a 24% lower risk of stroke and no harm to the kidneys, blood lipids or stress hormones in people with normal kidney function.⁸
• In the PURE study, people who excreted more potassium (a measure of how much they ate) had fewer deaths and cardiovascular events than those under 1.5 g/day.⁹
• The best evidence is a randomised trial. In the Salt Substitute and Stroke Study, 20,995 older villagers in China were given either regular salt or a substitute that was 25% potassium chloride. Over about 5 years the substitute cut stroke by 14%, major cardiovascular events by 13% and death from any cause by 12%, with no rise in serious high-potassium events.¹⁰ The substitute both added potassium and removed some sodium, so the trial can't fully separate the two. But its participants started at very high sodium and very low potassium intakes, and the shift in the potassium-to-sodium ratio is what changed.

Most people in Western diets eat well under the 2,600–3,400 mg target. The usual cause is eating little fruit, vegetables and potatoes, not salting food too much.

Intake

The adequate intake is 2,600 mg/day for women and 3,400 mg/day for men. Get it from food. Over-the-counter supplements are limited to 99 mg per pill because concentrated potassium can irritate the gut and, in people whose kidneys can't clear it, raise blood potassium dangerously. People with kidney disease, or taking ACE inhibitors, ARBs, spironolactone or other potassium-sparing drugs, should check before using potassium salt substitutes.

Top foods

• Baked potato with skin: about 925 mg (medium)
• Spinach, cooked: about 840 mg per cup
• Avocado: about 690 mg per fruit
• Orange juice: about 500 mg per cup
• Banana: about 420 mg (medium)
• Tomato: about 290 mg (medium)

Deficiency effects

Low blood potassium rarely comes from diet alone. It usually comes from losses: diuretics, vomiting, diarrhoea, heavy sweating or low magnesium.³ Mild cases cause fatigue, weakness, cramps and constipation. Severe cases (under about 3.0 mEq/L) cause muscle paralysis and dangerous heart rhythms, and need medical treatment. A diet that is low in potassium without a low blood level is far more common. It doesn't cause symptoms, but over years it shows up as higher stroke risk.