In case you missed the headlines last month, they railed about the increase in LDL-cholesterol and triglyceride levels and higher levels of aldosterone, renin, angiotensin, and catecholamines that occur when dietary salt is even moderately reduced. Higher levels of all these cardiovascular disease (CVD) risk factors, the authors of the article in the American Journal of Hypertension concluded, might well more than offset the small reductions in blood pressure (BP) observed in these mostly very short-term clinical trials on sodium reduction. This article is simply a rehash of the Cochrane Review of the same data last sum- mer. Specifically, Dr. Neils Gradual and his co-authors conclude: “Sodium reduction resulted in a significant decrease in BP of 1% (normotensives), 3.5% (hyperten- sives), and a significant increase in plasma renin, plasma aldosterone, plasma aldosterone, and plasma noradrenaline, a 2.5% increase in cholesterol and a 7% increase in triglyceride.”1
The headlines, no doubt, were promoted by the Salt Institute and the commercial food industry in order to prevent or at least delay public health efforts to start limiting the salt content of foods. Speculation abounded in the news media about how the significant increases in cholesterol and triglycerides and hormones associated with an increased risk of CVD might offset the modest decrease in BP from reducing salt and so might actually increase the risk of heart disease. For example, an article that appeared on msnbc.com on November 9th read “Low-salt diets may raise heart disease risk”. Other articles and reports called for more research and called into question current guidelines from the American Heart Association, Center for Disease Control, new US Dietary Guidelines, the Institute of Medicine’s expert panel, and dozens of other public health organizations around the World, which in the past several years have all called for a reduction of sodium intake to no more than 1500 mg per day for all middle-aged and older people and younger people with elevated BP.
Given that the studies reviewed were mostly very short term they provide no useful data about the long-term impact of a higher salt diet. Should we worry about the increase in renin, aldosterone, angiotensin, and catecholamines and increased blood lipids? Probably not because the decrease in these hormones is physiologically normal in response to consuming a diet with excessive added salt. While it is bad to have higher levels of these substances in your blood when salt intake is high it is perfectly normal for them to increase when salt intake is reduced. In human populations that do not add salt to their food, the levels of renin, angiotensin, and aldosterone are much higher than in those populations that salt their food. However, in the no- salt-added populations, BP does not rise with age and primary hypertension is virtually unknown. By contrast, in the US and other countries where salt is added in large amounts to most foods, BP rises throughout life and well over 90% of people end up with hypertension. What are we to make of the increased blood lipids? Not much as this increase is likely due largely to the modest expansion in blood volume seen when dietary salt is reduced. So there is not more cholesterol in the blood but rather a modest in- crease in blood volume secondary to salt and water retention that dilutes the amount present.
Bottom Line: Dr. Gradual’s suggestion that these short-term changes in CVD risk factors might negate the long term reduction in hypertension on low-salt diets makes about as much sense as claiming that cutting back on cigarette smoking for a few weeks may slightly improve lung function but this benefit may be offset by the gain of several pounds of weight. The real harm of smoking takes decades to develop and is not even close to being eliminated by the fact that smokers tend to weigh a little less than nonsmokers. In a similar fashion the big increase in BP and CVD caused by adding salt to food in large amounts are obviously not offset by minor changes in blood lipids largely from hemodilution and physiological adjustments in hormones involved in blood pressure regulation.
By James J. Kenney, PhD, FACN
1 Gradual NA, Hubeck-Gradual T, Jurgens G. Effects of low- sodium diet vs. high-sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Am J Hypertens doi:10.1038/ ajh.2011.210
Stephanie Ronco has been editing for Food and Health Communications since 2011. She graduated from Colorado College magna cum laude with distinction in Comparative Literature. She was elected a member of Phi Beta Kappa in 2008.