Does a High Salt Intake Increase Your Risk for Stroke?
Does a High Salt Intake Increase Your Risk for Stroke?
Abstract & commentary
Synopsis: An increased intake of dietary sodium is associated with an increase in the incidence of cardiovascular disease in overweight persons but not in nonoverweight persons.
Source: He J, et al. JAMA 1999;282:2027-2034.
There are a number of studies that have iden-tified a positive relationship between dietary intake of sodium and increases in hypertension and stroke. However, there are prospective cohort studies that failed to find an association between sodium intake and the risk of stroke. He and colleagues believe that "this may have been due to difficulties in measuring an individual’s usual sodium intake or the use of relatively small samples."1,2
This prospective cohort study was designed to examine the risk of cardiovascular disease associated with dietary sodium intake in overweight and nonoverweight persons. The study included those aged 25 to 74 years from the first National Health and Nutrition Examination Survey Epidemiological Follow-up Study (NHANES1). Follow-up studies were conducted in 1982-1984, 1986 and 1987, and 1992. (113,467 person-years). The study excluded individuals who: lacked 24-hour dietary recall information, had a history of heart attack or stroke, had used medication for heart disease, or were on a low-sodium diet. A total of 2688 overweight persons and 6797 nonoverweight persons were included.
A body mass index of 27.8 kg/m2 or higher for males and 27.3 mg/kg2 or higher for females was used to separate the overweight persons from the nonoverweight.
Sodium intake and total energy intake were highly correlated in the study population. Therefore, both the absolute sodium intake and sodium-to-energy ratio were used to examine the relationship between sodium intake and cardiovascular disease risk.
Sodium-to-energy ratio was expressed as 1 mmol of sodium per 7452 kJ, the average intake in the study population.
Among overweight persons, a 100 mmol higher sodium intake was associated with a 32% increase in stroke, an 89% increase in stroke mortality, a 44% increase in heart disease mortality, and a 39% increase in mortality from all causes. The P values were less than 0.001 in all instances.
Dietary sodium was not significantly associated with cardiovascular disease in nonoverweight persons.
The study concluded that a high sodium intake is strongly and independently associated with an increased risk of cardiovascular disease and all-cause mortality in overweight persons.
Comment by Ralph R. Hall, MD, FACP
He et al also divided the study group into four quartiles and demonstrated that the higher the intake of sodium, the greater the risk of an event. For instance, the cumulative mortality of stroke at age 85 was 9%, 8.9%, 14.4%, and 15. 8% among patients within the first, second, third, and fourth quartiles of sodium-to-energy ratio, respectively (P = 0.004 for trend). This held true for the other risk factors.
There was also an increase in blood pressure noted with an increase in sodium intake but, interestingly, the increase in stroke is greater than one would expect from this degree of blood pressure increase. This suggests, as other studies have, that sodium has an independent effect on stroke incidence.
It therefore behooves us to attempt to decrease the sodium intake of our obese patients. If we are not totally successful, any decrease in sodium intake that the patient is able to achieve will have a beneficial effect on the patient’s incidence of cardiovascular disease. African-American patients, because of their low renin levels, should be placed on low-salt diets regardless of their degree of obesity.3
This clinical trial required a large number of patients in order to demonstrate the effect of sodium on cardiovascular disease. The numbers of persons needed for clinical trials in the future will be much smaller. This will be because of our ability to identify genetic influences in the molecular structure of our patients’ proteins. We can then target patients with the protein structures that are responsible for the condition we are attempting to influence. Our ability to select patients who will benefit from dietary manipulation or specific pharmacologic treatment will be markedly enhanced. As suggested by Herbert,4 many of the arguments regarding whether patients should have a low- or high-carbohydrate diet or a low- or high-sodium diet, etc., will be facilitated if we place a layer labeled "Genetics" at the bottom of the food pyramid.
References
1. Grundy SM, et al. Circulation 1997;95:1683-1685.
2. Muldoon MF, et al. BMJ 1990;301:309-314.
3. He FJ, et al. Hypertension 1998;32:820-824.
4. Herbert V. Lecture. Sept. 1999.
Which one of the following statements is not correct?
a. Obese patients are more likely than nonobese patients to benefit from a low-sodium diet.
b. The higher the sodium intake, the greater the chance for a cardiovascular accident.
c. The hypertension resulting from a high sodium intake is solely responsible for the increase in cardiovascular events.
d. Even small decreases in sodium intake may reduce cardiovascular events.
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