Simply restricting sodium may not be enough to reduce the risk of cardiovascular disease-associated mortality, according to US researchers — eating more potassium may also play role.

High sodium intake coupled with low potassium consumption significantly increased the risk for CVD and all-cause mortality, data from a large population-based study published this week in the Journal of the American Medical Association’s Archives of Internal Medicine indicate.

“The observed stronger and more consistent associations between the sodium-potassium ration and mortality than between each nutrient separately and mortality may be due to complex interactions between potassium and sodium at cellular levels,” Quanhe Yang, PhD of the CDC and colleagues wrote.

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They analyzed data from 12,267 adults who participated in the Third National Health and Nutrition Examination (NHANES) between 1988 and 2006.

During the median 14.8 year follow-up period, 2,270 participants died, including 825 who died of CVD and 433 who died of ischemic heart disease (IHD).

Men consumed an average of 4,323 mg of sodium and 3,373 mg of potassium per day, and women consumed an average 2,918 mg of sodium and 2,433 mg of potassium per day. On average, both men and women consumed more the American Heart Association’s current 1,500 mg sodium daily recommendation and less than  4,700 mg suggested daily potassium intake.

Although sodium intake alone was not significantly associated with either CVD or IHD mortality, it did influence all-cause mortality rates — for each 1,000-mg-a-day increase in sodium the researchers observed a 20% increase in all-cause mortality (hazard ratio= 1.20; 95% CI: 1.03-1.41).

Furthermore, the researchers found that potassium consumption was significantly and inversely associated with both ischemic heart disease mortality and cardiovascular mortality — HR was 0.39 (95% CI: 0.19 -0.80) for CVD and 0.26 (95% CI: 0.10-0.71) for IHD when comparing the highest and lowest quartiles.

Overall, each 1,000-mg-a-day increase in potassium was associated with a 20% lower all-cause mortality risk (HR=0.80; 95% CI: 0.67-0.94).

“From a public health point of view, reduced sodium intake accompanied by increased potassium intake could achieve greater health benefits than restricting sodium alone,” the researchers wrote.

They added that because sodium is added to many processed foods, lower sodium-potassium ratios may be a marker of healthy eating — signifying more plant food intake and less processed food intake.

Although an earlier analysis of NHANES data did not find a significant association between sodium and CVD mortality rates, the researchers attributed the variations in observation to a longer follow-up period and differences in study methodology, including an improved model for estimating usual nutrient intake using information form two 24-hour dietary recall periods instead of one.

However, they acknowledged certain study limitations including the self-reported nature of sodium intake measurements in lieu of more reliable urine excretion measurements, and the lack of sodium and potassium intake measurements over time.

“Caution should be taken interpretation of results from this and other similar studies,” the researchers wrote.

In an accompanying editorial, Lynn Silver, MD, and Thomas Farley, MD, both of the New York City Department of Health and Mental Hygiene, argued that these latest findings “the already compelling evidence of the relationship between sodium intake and mortality.”

In addition to continued efforts to limit the amount of added sodium in processed foods, Silver and Farley suggested additional policies requiring food manufacturers to display potassium content on packaging and increased public health efforts to promote plant-based sources of the nutrient.

Yang Q. Arch Intern Med. 2011;171: 1183-1191.

Silver AD, Farley TA. Arch Intern Med. 2011;171:1191-1192.