Sodium reduction was associated with a nonsignificant reduction in long-term mortality (HR 0.85; 95% CI 0.66-1.09; p=0.19), while higher average sodium intake directly increased mortality risk.
RCT (n=3,126)
randomized
Does sodium reduction reduce long-term all-cause mortality in pre-hypertensive adults?
Long-term follow-up demonstrates a direct linear relationship between higher sodium intake and increased all-cause mortality, supporting the benefits of sodium reduction and challenging the existence of a J-shaped curve.
Hazard Ratio: 0.85 (95% CI 0.66–1.09)
p-value: p=0.19
Background While several studies suggest beneficial effects of lower sodium on cardiovascular disease, the relationship with total mortality remains controversial. Some have reported a J-shaped curve, but this may be due to poor quality measurement of sodium or confounding bias. Objective To examine the relationship of well-characterized measures of sodium intake, estimated from urinary sodium excretion, with long-term mortality. Methods Two trials Phase I (1987-90) over 18 month and Phase II (1990-5) over 36 months in the Trials of Hypertension Prevention implemented sodium reduction interventions. Multiple 24-hour urines were collected from pre-hypertensive adults aged 30-54 during these trial periods. Post-trial deaths were ascertained over a median 24 years through December 31, 2013 using the National Death Index. The association of mortality with both the randomized intervention and average sodium intake was examined. Results Among 744 Phase I and 2382 Phase II participants randomized to sodium reduction or control, 251 deaths occurred, with a nonsignificant 15% lower risk in the active intervention (hazard ratio (HR)=0.85, 95% CI=0.66-1.09, p=0.19). Among 2,974 participants not assigned to an active sodium intervention, 272 deaths occurred. There was a direct linear association of average sodium intake with mortality, with HR=0.75, 0.95, 1.00 (reference), and 1.07 (p-trend = 0.30) for =4800 mg/24hr, respectively, with HR=1.12 per 1000 mg/24hr (95% CI = 1.00-1.26, p=0.05) and no evidence of a J-shape or nonlinear relation. The HR per unit increase in sodium/potassium ratio was 1.13 (95% CI = 1.01-1.27, p=0.04). Conclusions This study, with carefully characterized measures of sodium intake, found an increased risk at high sodium intake and a direct relation with total mortality even at the lowest levels of sodium intake. Overall, these results are consistent with a benefit of reduced sodium and sodium/potassium on total mortality over a period of over 20 years.
“Sodium is an essential nutrient. It's not tobacco. Without sodium, you die. The body needs sodium. The optimal level of tobacco is zero, but with sodium, it's not zero. The question is, how much sodium? Every essential nutrient in the body tends to have the so-called U-shaped relationship with mortality—calcium, magnesium, vitamin D, and so on and so forth. Why would sodium be any different? The researchers are making it seem like there's a linear relationship when in fact it violates the laws of biology. It doesn't make any sense.”
Cook et al. (2016) conducted an RCT in Pre-hypertension (n=3,126). Sodium reduction vs. Control was evaluated on long-term mortality (HR 0.85, 95% CI 0.66-1.09, p=0.19). Sodium reduction was associated with a nonsignificant reduction in long-term mortality (HR 0.85; 95% CI 0.66-1.09; p=0.19), while higher average sodium intake directly increased mortality risk.