Observations Heads Up

Dethroning the king of condiments

BMJ 2013; 347 doi: https://doi.org/10.1136/bmj.f7192 (Published 04 December 2013) Cite this as: BMJ 2013;347:f7192
  1. Krishna Chinthapalli, associate editor, BMJ
  1. kchinthapalli{at}bmj.com

What is the link between salt, hypertension, and mortality?

Killing an elephant is not easy. The Waliangulu tribesmen in Kenya use an arrow a metre long and dipped in the poisonous sap of the Acokanthera plant. They shoot from a few steps away into an elephant’s underbelly so that the active toxin, ouabain, can rapidly enter the bloodstream. Ouabain molecules bind to and inhibit the sodium pump in cardiac muscle. Intracellular sodium thus increases, which stimulates another pump (the sodium-calcium exchanger) to get rid of sodium and take in calcium instead. The calcium ions make the myocyte contract permanently and can stop a 20 kg heart from beating again.

Ouabain circulates naturally in our own bloodstream too, but instead of stopping the heart it seems to make arteriolar smooth muscle contract and thus raise blood pressure. The theory is that increased dietary salt intake leads to sodium and water retention, which stimulates ouabain, which causes hypertension.1 But in practice the role of salt has been highly controversial.

Twenty five years ago the BMJ published the cross sectional Intersalt study of Kenyan villagers and 51 other populations from around the world.2 Within each population a person’s urinary sodium excretion (a reliable surrogate for salt intake) correlated with systolic blood pressure. Across populations higher salt intake was linked to a faster increase in blood pressure over time. In 2001 the DASH-sodium study, a randomised controlled trial of low, intermediate, or high …

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