Nutrition in Cardiovascular Disease

Salt in Hypertension and Heart Failure

Feng J. He; Michel Burnier; Graham A. MacGregor


Eur Heart J. 2011;32(24):3073-3080. 

In This Article

Abstract and Introduction


There is much evidence for a causal relationship between salt intake and blood pressure (BP). The current salt intake in many countries is between 9 and 12 g/day. A reduction in salt intake to the recommended level of 5–6 g/day lowers BP in both hypertensive and normotensive individuals. A further reduction to 3–4 g/day has a much greater effect. Prospective studies and outcome trials have demonstrated that a lower salt intake is associated with a decreased risk of cardiovascular disease. Increasing evidence also suggests that a high salt intake is directly related to left ventricular hypertrophy (LVH) independent of BP. Both raised BP and LVH are important risk factors for heart failure. It is therefore possible that a lower salt intake could prevent the development of heart failure. In patients who already have heart failure, a high salt intake aggravates the retention of salt and water, thereby exacerbating heart failure symptoms and progression of the disease. A lower salt intake plays an important role in the management of heart failure. Despite this, currently there is no clear evidence on how far salt intake should be reduced in heart failure. Our personal view is that these patients should reduce their salt intake to <5 g/day, i.e. the maximum intake recommended by the World Health Organisation for all adults. If salt intake is successfully reduced, there may well be a need for a reduction in diuretic dosage.


For several million years, the ancestors of humans, like all other mammals, ate a diet which contained a very small amount of salt that existed in natural foods, i.e. <0.5 g of salt (0.2 g sodium) per day.[1] Only ~5 000 years ago, the Chinese discovered that salt could be used to preserve foods. Salt then became of great economic importance and the most taxed, traded commodity in the world, with intake reaching a peak around the 1870s.[1] However, with the invention of the deep freezer and the refrigerator, salt was no longer required as a preservative. Salt intake had been declining, but with the recent large increase in the consumption of highly salted processed foods, salt intake is now increasing again. The current salt intake in many countries is between 9 and 12 g/day.[2] This large increase in salt intake is relatively recent in evolutionary terms. It presents a major challenge to the physiological systems to excrete these large amounts of salt through the kidneys. The consequence is a gradual rise in blood pressure (BP),[3,4] thereby increasing the risk of stroke, heart attack, heart failure, and renal disease. Furthermore, a high salt intake may have direct effects on stroke,[5,6] left ventricular hypertrophy (LVH),[7] progression of renal disease and proteinuria,[8] independent of but additive to the effect of salt on BP. There is also evidence that a high salt intake is indirectly related to obesity through increased soft drink consumption,[9,10] associated with a higher risk of renal stones and osteoporosis,[11] and probably a major cause of stomach cancer.[12,13] The evidence on these harmful effects of salt has been comprehensively examined in several recent review articles.[3,14] In this paper, we focus on the evidence relating salt to BP, LVH, heart failure, and total cardiovascular disease.


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