Salt Intake and Cardiovascular Mortality
Article Outline
To the Editor:
In a recent article, Cohen et al1 claim that a lower salt intake is associated with a higher cardiovascular mortality in the second National Health and Nutrition Examination Survey follow-up. However, this claim lacks substance because there is no significant relation of salt intake to either coronary heart disease or stroke mortality when analyzed separately. Furthermore, the method used to assess salt intake (one 24-hour dietary recall) is notoriously unreliable, particularly because no account is taken of discretionary salt, which in the 1970s would have contributed substantially to salt intake. The same method was used in a previous article2 that has been severely criticized. Karppanen and Mervaala3 marveled that so many women in the lowest quartile of salt intake who had a calorie intake near starvation level had survived for 20 years. It is quite extraordinary that Cohen et al choose to ignore the scientific criticisms that followed their article.
Twenty-four–hour urinary sodium is the only accurate way to measure salt intake. A study that had 24-hour urinary sodium measured while on the individuals’ usual salt intake shows that a higher salt intake is associated with higher coronary heart disease, cardiovascular, and total mortality rates.4
Cohen et al1 claim that reducing salt intake stimulates the sympathetic system and the renin-angiotensin system, and possibly increases insulin resistance. Once again they quote studies of acute salt restriction or poorly conducted studies and ignore the correspondence that followed.5 Well-controlled, longer-term randomized trials have shown that a modest reduction in salt intake has no effect on the sympathetic system6 or insulin sensitivity,7 and only a small but physiologic increase in plasma renin activity. Salt reduction works by a mechanism similar to diuretics, which have been and continue to be the most commonly prescribed drugs for the treatment of hypertension. Diuretics also stimulate the renin-angiotensin system, but outcome trials have consistently demonstrated that diuretics reduce cardiovascular mortality.
As usual, Cohen et al1 call for outcome trial evidence for salt. There are no outcome trials showing a reduction in mortality on stopping smoking, reducing fat intake alone without fish oil supplements, losing weight, increasing fruit and vegetables, or increasing exercise. Indeed, for most of these factors no attempt has been made to conduct long-term trials because of the innate difficulty of conducting and funding such trials, as well as the ethics of putting a group of people on a high salt diet for the rest of their lives. The totality of evidence for reducing salt, including epidemiologic, migration, intervention, treatment, animal, and genetic studies, is now stronger than for any other dietary or lifestyle intervention.
Increased blood pressure throughout its range is the major cause of cardiovascular disease, and decreasing blood pressure reduces strokes, heart attacks, and heart failure. As a modest reduction in salt intake decreases blood pressure, it would reduce cardiovascular mortality. The current article by Cohen et al, which is based on an entirely inadequate way of measuring salt intake, does not persuade us otherwise.
References
- . Sodium intake and mortality in the NHANES II follow-up study. Am J Med. 2006;119:275;e7-14
- . Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). Lancet. 1998;351:781–785
- . Sodium intake and mortality. Lancet. 1998;351:1509
- Urinary sodium excretion and cardiovascular mortality in Finland: a prospective study. Lancet. 2001;357:848–851
- . Salt intake and sympathetic activity. Circulation. 2003;107:e108
- . Effect of dietary counselling on blood pressure and arterial plasma catecholamines in primary hypertension. Am J Hypertens. 1995;8:704–711
- . Salt restriction: effects on lipids and insulin production in hypertensive patients. Scand J Clin Lab Invest. 1997;57:501–505
PII: S0002-9343(06)00388-3
doi:10.1016/j.amjmed.2006.03.019
© 2007 Elsevier Inc. All rights reserved.
