Background:
Elevated aldosterone promotes inflammation, insulin resistance, and hypertension. These effects are particularly important in obesity because adipocytes secrete factors that increase aldosterone production. Weight loss is thought to lower aldosterone levels, but little longitudinal data is available. We aimed to determine if, independent of changes in sodium intake, reductions in circulating aldosterone are associated with weight loss and improvements in inflammation, adipokines, insulin resistance, and blood pressure in normotensive overweight and obese young adults undergoing lifestyle modification.
Methods:
Participants were overweight/obese adults aged 20–45 years (20% male, 15% black) from the Slow Adverse Vascular Effects of excess weight trial, a study evaluating the relationships between weight loss, dietary sodium, and vascular health. Subjects were randomly assigned to a regular or reduced sodium diet, and all received a one-year nutrition and physical activity intervention. For this study, individuals providing valid baseline 24hr urine collections were included (n=281). Linear mixed models were used to evaluate associations between changes in aldosterone and changes in weight, blood pressure, and obesity-related factors.
Results:
Weight loss was significant at 6 months (∼7%), 12 months (∼6%), and 24 months (∼4%) (p<0.0001 for all). Within-subject decreases in aldosterone were associated with decreases in C-reactive protein, leptin, and homeostasis assessment of insulin resistance (HOMA-IR) and with increases in adiponectin (p<0.01 for all) in models including baseline age, sex, race, intervention arm, time since baseline, and baseline and concurrent changes in BMI, urinary sodium and potassium, and the obesity-related factor of interest. Decreases in aldosterone were associated with weight loss only in the subgroup (n=98) with metabolic syndrome (MetS) at baseline (MetS x percent weight loss p=0.02); a 10% weight reduction in this subgroup was associated with a 9% (95% CI 1–16) reduction in aldosterone. Though no association was detected between changes in aldosterone and mean arterial pressure (MAP), a significant association was found between reductions in MAP and 24hr urinary sodium in those with MetS (MetS x urinary sodium reduction p=0.02). Independent of weight loss, a 30% reduction in urinary sodium was associated with a 0.9 mm Hg (95% CI 0.2–1.6) decrease in MAP in those with MetS.
Conclusions:
Changes in aldosterone are associated with changes in obesity-related factors in overweight/obese normotensive young adults. In persons with MetS, weight loss and dietary sodium restriction are particularly useful to reduce aldosterone and MAP respectively. Given the adverse effects of excess aldosterone on cardiac and vascular remodeling, future studies should investigate the benefits of aldosterone antagonists in individuals with MetS.
