Abstract P252: The Effects of Sodium Reduction on Metabolism and Thirst

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Abstract

Background: Recent studies challenge the traditional understanding of sodium physiology. Some animal studies suggest that high sodium intake may induce catabolism, leading to weight loss. Other studies suggest that high sodium intake might reduce, rather than increase, thirst.

Hypothesis: Higher sodium intake increases thirst, fluid intake, and sodium excretion without altering energy intake or lowering weight.

Methods: In the DASH-Sodium feeding study, adults with pre- or stage 1 hypertension without antihypertensive medications, were randomly assigned to the DASH diet or a control diet. On their assigned diet, participants consumed each of three sodium levels for 4 weeks (randomized crossover design). Participants were provided all meals, but could drink water freely. Throughout the trial, calorie intake was adjusted to keep weight constant. The three sodium levels (at 2100 kcal/d) were: low (1150 mg), medium (2300 mg), and high (3450 mg). Weight, energy intake, self-reported thirst, urine volume, plasma renin, serum aldosterone, urine osmolality, and urine sodium excretion were assessed at the end of each period.

Results: Among 412 participants (57% women, 57% black, mean age 48 yrs), weight increased slightly with higher sodium on the control diet, but not the DASH diet; energy intake did not vary across sodium levels in both diets (P-trends > 0.34) (Table). In contrast, participants reported more thirst with high vs low sodium (both diets P-trends < 0.001) and potentially higher fluid intake (urine volume) during the control diet (1,566 vs 1,491 ml on high vs low sodium; P-trend = 0.07). On both diets, plasma renin and serum aldosterone were lower with higher sodium (each P-trend < 0.001). Likewise, both urine osmolality and sodium excretion were higher with higher sodium intake (all P-trends < 0.001).

Conclusions: Higher sodium intake did not alter energy intake, but did increase thirst and sodium excretion. These findings are consistent with the traditional understanding of the physiology of excess dietary sodium intake.

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