For decades the notion that an excessive consumption of salt (NaCl) leads to hypertension has persisted. However, this idea is based on opinion, not scientific proof. Despite this, every health organization, agency, and clinicians around the world have been advising salt restriction, especially to hypertensive patients. The present review article suggests that the consumption of a high-salt diet is not the cause of hypertension and that there are other factors, such as added sugars, which are causative for inducing hypertension and cardiovascular disease.
Hypertension is defined by a systolic blood pressure that is ≥140 mm Hg and a diastolic blood pressure that is ≥90 mm Hg.1 The etiology of hypertension is multifactorial in nature, resulting from the combination of both genetic and environmental factors.2
In recent decades hypertension has been ranked as one of the leading causes of worldwide disability-adjusted life years.3 According to a study conducted by Kearney et al,4 more than 1 billion adults worldwide (approximately 25%) have hypertension. Other estimates suggest this number will climb to 29% by 2025.
A linear relationship between blood pressure levels and cardiovascular and cerebrovascular mortality was observed by the Prospective Studies Collaboration.5Â The association between blood pressure and cardiovascular morbidity and mortality is present even below the present cut-off for hypertension, which was confirmed in the Framingham study.6
In the literature it is often said that an excessive intake of salt (NaCl) can lead to hypertension.7, 8, 9, 10, 11 In general, the average daily salt intake is more than 6 g (2400 mg of sodium), with approximately 95% of the global population consuming somewhere between 7.5 and 12.5 g of salt.12
Some European and Asian countries consume slightly more than 12 g of salt (4800 mg of sodium) per day.13 In India most people consume at least 11 g of salt per day,14, 15 but this may have to do with the hot climate of India, which can induce salt loss of up to 6 g per day (mostly from sweat).16 Despite these important nuances, various government institutions and bodies recommend population-wide sodium restriction.17, 18, 19, 20
The World Health Organization (WHO) recommends an intake of <2000 mg sodium per day.19Â Canada’s 2010 Sodium Working Group suggest sodium intake of <2300 mg/d,17Â whereas the American Heart Association suggests an even stricter sodium intake (<1500 mg/d).21Â The recently published 2015 Dietary Guidelines for Americans recommend a sodium restriction of <2300 mg/d.22Â The Food and Agricultural Organisation of the United Nations has published food-dietary guidelines for Indians, which suggested that the salt intake should be <2400 mg/d.23
India, along with other member states of the WHO, has adopted a target of reducing the mean population salt consumption up to 30% by 2025.15Â This reduction in salt intake is targeted with a belief that this will lead to a decrease in blood pressure levels, with the assumption that this will translate into a reduction in cardiovascular events.24
Previously, on the basis of a meta-analysis, it was suggested that a reduction in dietary salt intake of up to 6 g per day could help reduce the systolic/diastolic blood pressure by 7/4 mm Hg in hypertensives and 4/2 mm Hg in normotensives.24 However, recently, DiNicolantonio et al12 have proposed the idea that added sugars, not salt, is the real culprit for causing hypertension.
If this hypothesis is proved to be correct, then it would be a great relief for the entire population, especially cultures that rely on saltier dishes (such as the Indian population), probably helping them to prevent dehydration in the heat.14, 16 The present article reviews the literature and hypothesizes that 1) salt intake not may not be an important etiologic factor for hypertension; 2) salt restriction paradoxically may cause hypertension and cardiovascular events; and 3) dietary sugar is the more problematic white crystal inducing hypertension.
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-James J. DiNicolantonio, PharmD, Varshil Mehta, MBBS, James H. O’Keefe, MD
This article originally appeared in the August 2017 issue of The American Journal of Medicine.
