N° 34 | May 2009

Potassium is beneficial to human health

For several million years the ancestors of humans ate a diet that contained large amounts of potassium. However, with the advent of civilized societies, cooking and processing of food have greatly reduced the potassium content, and this in combination with a large increase in the consumption of processed foods and a reduction in the consumption of fruit and vegetables, have led to a significant decrease in potassium intake.

In most developed countries, the average potassium intake is now around 70 mmol/day, i.e. approximately one third of our evolutionary intake1. This low potassium intake causes a rise in blood pressure, increases the risk of cardiovascular disease, renal disease and bone demineralization. Much evidence has shown that an increase in potassium intake is beneficial to human health2.

Effect on blood pressure

Both epidemiological studies and randomised trials have shown that a higher potassium intake was related to a lower blood pressure. A meta-analysis of 32 randomised trials demonstrated that potassium supplementation, with an average increase of approximately 50 mmol in 24-hour urinary potassium excretion, resulted in a fall in blood pressure of 4.4/2.5 mmHg in individuals with high blood pressure and 1.8/1.0 mmHg in those with normal blood pressure3.

Most of the randomised trials have used potassium chloride, which is convenient for making a study double blinded by using wax encapsulated potassium chloride (Slow-K) against Slow-K placebo. However, the best way to increase potassium intake is to increase the consumption of food high in potassium, e.g. fruit and vegetables. In the DASH (Dietary Approaches to Stop Hypertension) trial, an increase in fruit and vegetable intake from an average of 3.6 to 8.5 serving/day, with a subsequent increase of approximately 30 mmol/24-hour in urinary potassium excretion, resulted in a fall of 2.8/1.1 mm Hg in blood pressure in individuals with normal or mildly raised blood pressure4.

Effect on cardiovascular disease

A number of epidemiological studies have shown an inverse association between potassium intake and cardiovascular disease. For example, in a 12 year prospective study, Khaw et al demonstrated that an increase of 10 mmol/day in potassium intake was associated with a 40% reduction in the risk of stroke mortality 5. This association was independent of other dietary variables and also independent of other known cardiovascular risk factors including age, sex, blood pressure, blood cholesterol, obesity, fasting blood glucose and cigarette smoking.

The consumption of fruit and vegetables has also been shown to be inversely related to cardiovascular disease in a dose-response manner6, 7. Meta-analyses of prospective cohort studies showed that, compared with those who consumed less than 3 servings/day of fruit and vegetables, individuals who ate 3-5 servings/day had an 11% reduction in stroke risk and 7% reduction in coronary heart disease risk, and people who consumed more than 5 servings/day had a reduction of 26% and 17% in stroke and coronary heart disease risk respectively6, 7. It was estimated that, worldwide, up to 2.6 million deaths per year were attributable to inadequate consumption of fruit and vegetables8.

Although several nutrients, e.g. potassium, folate, fibre, antioxidants, may contribute to the beneficial effects of fruit and vegetables on cardiovascular disease, much evidence suggests that potassium plays an important role. As raised blood pressure is a major cause of cardiovascular disease, the blood pressure-lowering effect of potassium is likely to be an important mechanism. Additionally, increasing evidence suggests that potassium may have a direct effect on reducing vascular lesions associated with cardiovascular disease9.

A recently published outcome trial demonstrated that an increase in potassium intake reduced cardiovascular mortality. The trial was carried out by Chang et al. in 1981 elderly veterans who lived in a veteran's retired home in northern Taiwan10. Five kitchens of the veteran retirement home were randomised into 2 groups (experimental or control) and veterans assigned to those kitchens were given either potassium-enriched salt (experimental group) or regular salt (control group) for approximately 31 months. With this intervention there was a 76% increase in potassium intake and a 17% reduction in salt intake in the experimental group, as measured by urinary potassium/creatinine ratio and sodium/creatinine ratio. Compared to those in the control group, individuals in the experimental group had a 40% reduction in cardiovascular disease mortality.

Other beneficial effects

Experimental studies in animals have shown that a high potassium diet may prevent or at least slow the progression of renal disease11. An increased potassium intake lowers urinary calcium excretion and could play an important role in the management of hypercalciuria and kidney stones, and is also likely to decrease the risk of osteoporosis12. Low potassium concentration in serum is strongly related to glucose intolerance and increasing potassium intake could prevent the development of diabetes that occurs in hypertensive patients who receive prolonged treatment with thiazide diuretics13.

Reduced serum potassium increases the risk of lethal ventricular arrhythmias in patients with coronary heart disease, heart failure and left ventricular hypertrophy, and increasing potassium intake may prevent this14.
The best way of increasing potassium intake is to increase the consumption of fruit and vegetables, which in themselves may have beneficial effects on health (e.g. antioxidants, folic acid, etc) independent of potassium intake.

  1. Intersalt Cooperative Research Group. BMJ. 1986;297:319-28.
  2. He FJ, et al. Physiol Plant. 2008;133:725-35.
  3. Whelton PK, et al. JAMA. 1997;277:1624-32.
  4. Appel LJ, et al. N Engl J Med. 1997;336:1117-24.
  5. Khaw KT, et al. N Engl J Med. 1987;316:235-40.
  6. He FJ, et al. Lancet. 2006;367:320-6.
  7. Dauchet L, et al. Neurology. 2005;65:1193-7.
  8. Lock K, et al. Bulletin of the World Health Organization. 2005;83:100-8.
  9. Young DB, et al. Semin Nephrol. 1999;19:477-86.
  10. Chang HY, et al. Am J Clin Nutr. 2006;83:1289-96.
  11. Tobian L, et al. Hypertension. 1984;6:I170-6.
  12. New SA, et al. Am J Clin Nutr. 1997;65:1831-9.
  13. Zillich AJ, et al. Hypertension. 2006;48:219-24.
  14. Gheeraert PJ, et al. Eur Heart J. 2006;27:2499-510.
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