Keep an Eye on the Sodium-Potassium Ratio

Both the medical and lay literature have entertained much discussion about the role of diet in general and sodium intake specifically to minimize population risk for cardiovascular disease and mortality. We have demonstrated that high sodium intake is associated with greater risk^[1] and that lowering sodium intake lowers blood pressure, which may translate to a decreased risk for cardiovascular events and subsequent mortality.^[2] On the other hand, we have also demonstrated that low sodium intake can be associated with greater risk.^[3] We debate these relationships and the utility of the salt-restriction intervention because the ability to reduce blood pressure and the risk for clinical events and mortality have not all been demonstrated in the same study.

Is there really controversy here, or is it that the mechanism of risk between excess sodium intake and sodium reduction are more complex than previously realized? Perhaps it is the role of potassium intake that has been underinvestigated and underpresented to the public. Multiple studies demonstrate a link between the ratio of sodium-to-potassium intake and hypertension and cardiovascular disease,^[4-8] and that this ratio is a more powerful predictor of outcomes than the intake of either separately.

A recent analysis of the Third National Health and Nutrition Examination Survey examines the association between estimated intake of sodium and potassium and both cardiovascular and all-cause mortality among adults.^[9] Dietary intake of sodium and potassium were assessed using dietary recall, with estimation of quantities based on food descriptions. In examining the distribution of sodium and potassium intakes, it is noteworthy that the mean intake of sodium, at more than 4.3 g for men and 2.9 g for women, was impressively greater than that suggested in an unselected population. While statistically significant differences in race, ethnicity, education, smoking status, and alcohol intake were present in groups, age showed the greatest clinical differences in mean intake of sodium among participants. In men, sodium intake in those over 60 years was 3.6 g compared with 4.5 g in younger men; in older women, sodium intake was 2.5 g compared with 3.0 g in younger women (P < .001). Similar trends were seen among groups when the sodium-potassium ratio was compared. As with sodium alone, the sodium-potassium ratio was higher in men than in women and, in general, higher in younger patients compared with those aged 60 years (P <.001).

When correlated with risk for all-cause mortality and adjusted for factors such as age and gender, dose-risk relationships between both sodium and potassium were demonstrated. Mortality risk increased among respondents with increasing sodium intake (comparing lowest with increasing quartiles, hazard ratio [HR] = 1.17, 1.37, and 1.73, P = .02) and decreasing potassium intake (comparing lowest quartile with increasing quartiles HR= 0.86, 0.75, and 0.61; P = .01), independently. The strongest relationship between these parameters and mortality was seen, however, when quartiles of the sodium-potassium ratio were analyzed (comparing lowest with increasing quartile HR = 1.13, 1.25, and 1.46, P <.001). Similar relationships were seen when examining cardiovascular and ischemic causes of mortality.

As is well known, observational data can only demonstrate associations and cannot establish cause and effect. If we were tempted, however, to make the cause-effect leap, this study supports that we should instruct our patients that, without an increase in potassium, just reducing sodium may not be as effective in lowering their risk.

Serum Level vs Intake: Big Difference

Of note, we need to make it very clear to both our patients and colleagues that sodium and potassium intake are not the sole determinants of, and should not be confused with, sodium and potassium levels in the blood. It is well known that both hyponatremia and hypernatremia are linked to mortality,^[10,11] but they represent a disorder of water metabolism, not a reflection of sodium intake. On the other hand, it may be easy to become potassium depleted on a potassium-wasting medication with inadequate oral intake, but the relationship between levels and risk that exists for potassium, as does for sodium, is likely related to the physiology that predisposes an individual to be unable to maintain levels within a certain range.

Most recently, an observational study demonstrated a U-shaped relationship between postadmission serum potassium levels and in-hospital mortality among persons with acute myocardial infarction.^[12] The lowest mortality rates were seen among persons with serum potassium levels between 3.5 and 4.5 mEq/L. At values greater and less than this range, mortality risk increased. It should be remembered that the kidney tightly regulates potassium concentration in the blood until a disease process or medication taxes its ability to maintain homeostasis. Therefore, whether hypokalemia is a marker of aldosterone excess or directly confers risk of dysrhythmia cannot be discerned. Regardless, these relationships between both potassium level and potassium intake are likely independent and may be additive.

References

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