The link between dietary salt intake and risk for CVD has become an exceedingly contentious issue. The defensive/aggressive authoritarianism commonly exuded over recommendations regarding salt intake in hypertension seems more suited to medieval theologians than to contemporary scientists. This is perhaps not surprising in view of the fact that a comprehensive Medline search from 1966 to the present using the terms high blood pressure, hypertension,salt, and sodium revealed more than 10,000 articles dealing with these topics. As the reader may remember, the link between dietary salt and high BP was raised more than 100 years ago by Ambard and Beaujard. The Medline search covers, therefore, only one-third of the time during which this link has been researched and discussed.
Given such a plethora of information, a thorough, comprehensive, yet objective, analysis of the literature pertaining to salt and hypertension is most likely beyond the intellectual capacity of even the most skilled scientists. Information overload engenders helplessness and frustration, and the most common defensive mechanism consists in selective reading of the literature (cherry-picking). Thus, the reaction in view of this scientific fog covers the whole spectrum, from apathy on one side, to fervent evangelism on the other. Because most dietary salt intake originates from processed food, the world's major food manufacturers are interested in keeping the controversy alive. It is then of little surprise that pecuniary interests have taken the salt debate far beyond a purely scientific level. Debate over population-wide benefit
In a position paper of the American Society of Hypertension, Appel and colleagues concluded: In view of the age-related rise in BP in both children and adults, the direct, progressive relationship of BP with CV-renal disease throughout the usual range of BP, and the worldwide epidemic of BP-related disease, efforts to reduce BP in non-hypertensive as well as hypertensive individuals are warranted. A variety of national and international guidelines for the treatment of CVD take a similar viewpoint. Thus, there seems to be consensus that population-wide reduction in salt intake could possibly translate into an impressive reduction in CV morbidity and mortality. Indeed, a recent study in The New England Journal of Medicine has estimated that a national effort to reduce daily salt intake by 3 g could reduce the annual number of strokes by 32,000, to 66,000; MI by 54,000, to 99,000; and reduce the annual number of deaths from any cause by 44,000, to 92,000. This intervention could also save $10 billion to $24 billion in health care costs annually. However, a study in the May issue of JAMA has rekindled controversy. Stolarz-Skrzypek found that systolic BP correlated positively with 24-hour urinary sodium excretion (similar to what has been reported in previous studies). In contrast to most previous studies, lower sodium excretion predicted higher CV mortality. The authors stated that their findings did “not support the current recommendations of the generalized and indiscriminate reduction of salt intake at the population level.
Not surprisingly, these findings stirred the leaves in the teapot, and in view of the 50% higher mortality that was found in the lowest tertile of sodium excretion in the Stolarz-Skrzypek study, news media reported that sodium reduction was ineffective and useless. As to the possible pathophysiologic mechanism accounting for the increase in CV morbidity and mortality, the authors speculated that salt intake low enough to decrease BP was prone to stimulate sympathetic activity, to decrease insulin sensitivity, to activate the renin angiotensin system and also to stimulate aldosterone release from the adrenal cortex.
When salt is detrimental
The paper by Stolarz-Skrzypek was extensively criticized by several scientists. The most pertinent criticisms were perhaps that salt intake as estimated by just one calculation of urinary sodium excretion at the start would hardly reflect salt intake during several years of the study. The inherent paradox of the study, that BP increased with salt intake but that morbidity and mortality fell with salt intake, was impossible to explain. Incomplete and unreliable 24-hour urine collections may have hampered the study. The Lancet commented that “this study is disappointingly weak and constitutes little to our understanding of salt and disease. It is likely to confuse public perceptions of the importance of salt as a risk factor for high BP, heart disease and stroke. Perhaps the exact relationship between sodium intake and BP is difficult to establish, but we should remember that a high salt intake also has been shown to cause target organ disease independent of BP. In the INTERSALT study, median 24-hour urinary sodium excretion strongly correlated with stroke mortality. Experimental studies have shown that rates of stroke and death are higher on a high salt intake than on a low salt intake, despite similar BP levels. High salt intake has also been related to hypertensive heart disease. Independent of BP, dietary salt is a determinant of left ventricular hypertrophy. Similarly, a link between hypertensive renal disease and salt intake has been established. A high salt intake in salt-sensitive patients seems to accentuate the risk for proteinuria and glomerular injury. Thus, there is solid evidence that a high salt intake may not only raise BP but have a BP independent detrimental effect on heart, kidneys and brain.
Take-home message for the physician
Ever since the lively debates of Sir George Pickering and Lewis Dahl, scientists have continued to waste ink on the relationship between dietary salt intake and BP. In doing so, most of them were oblivious to the possibility that dietary salt may exert direct harmful effects on the CV system independent of arterial pressure. Given the uncertainty and the quasi-religious fervor of proponents and opponents alike, what then should be the take-home message, if any, for the practicing physician? Is salt a powerful poison and, as such, the culprit of a major plague of humankind, causing millions of heart attacks and strokes every year, or, indeed, is it Mother Nature’s own best inhibitor of the renin-angiotensin system? As with other issues, physicians should attempt to weigh the general evidence against the particular needs of the individual patient. The general evidence suggests that a reduction of dietary salt intake may have some CV benefits that extend beyond those (if any) conferred by the small decrease in BP. Self-monitoring of BP will allow patients to appreciate the effects of a low-salt diet. A modest salt reduction interferes little, if at all, with the needs of the individual and therefore should be recommended as a simple measure for the prevention of CVD, certainly in hypertensive patients and their offspring, but possibly in normotensive patients as well.
Ambard L. Arch Gen Med. 1904;193:520-533.
Appel L. J Clin Hypertens (Greenwich). 2009;11:358-368.
Bibbins-Domingo K. N Engl J Med. 2010;362:590-599.
Stolarz-Skrzypek K. JAMA. 2011;305:1777-1785.
Salt and cardiovascular disease mortality. Lancet. 2011;377:1626.
Disclosure: Dr. Messerli reports no relevant financial disclosures.
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