A Low-Sodium DASH Dietary Pattern Affects Serum Markers of Inflammation and Mineral Metabolism in Adults with Elevated Blood Pressure

• Published in: The Journal of nutrition Vol. 151; no. 10; pp. 3067 - 3074
• Main Authors: Sullivan, Valerie K, Appel, Lawrence J, Seegmiller, Jesse C, McClure, Scott T, Rebholz, Casey M
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.10.2021; Oxford University Press; American Institute of Nutrition
• Subjects: Adult; Adults; Biomarkers; Blood Pressure; C-reactive protein; cardiovascular; DASH; Diet; Diet, Sodium-Restricted; Dietary Approaches To Stop Hypertension; Dietary intake; Dietary supplements; Fibroblast growth factor 23; Growth factors; Humans; Hypertension; Inflammation; Mineral metabolism; Minerals; Nutrient deficiency; Nutrition and Disease; Nutrition research; Phosphorus; Pressure effects; Secondary analysis; Sodium; soluble urokinase plasminogen activator receptor; U-Plasminogen activator; Urokinase; soluble urokinase plasminogen activator receptor; CRP; fibroblast growth factor-23; C-reactive protein; inflammation; suPAR; cardiovascular; DASH; FGF23; phosphorus
• ISSN: 0022-3166; 1541-6100
• DOI: 10.1093/jn/nxab236

The blood pressure–lowering effects of the Dietary Approaches to Stop Hypertension (DASH) dietary pattern and reduced sodium intake are well established. The effects on other biomarkers related to vascular health are of interest and might assist in explaining the effects of the DASH diet and sodium reduction. We hypothesized that a low-sodium DASH diet improves (lowers) biomarkers of inflammation [C-reactive protein (CRP) and soluble urokinase plasminogen activator receptor (suPAR)] and mineral metabolism [phosphorus and fibroblast growth factor-23 (FGF23)]. We conducted a secondary analysis of the DASH-Sodium trial using frozen serum samples. This controlled feeding study randomly assigned 412 adults (≥22 y) with elevated blood pressure (120–159/80–95 mmHg) to consume either a DASH diet or control diet. Within each arm, participants received 3 sodium levels [low (1150 mg), intermediate (2300 mg), high (3450 mg)] in random sequence, each for 30 d. To maximize contrast, samples collected at the end of the low-sodium DASH (n = 198) and high-sodium control (n = 194) diets were compared. Between-diet differences in serum CRP, suPAR, phosphorus, and FGF23 concentrations were assessed using linear regression adjusted for age, sex, race, income, education, smoking status, and BMI. CRP concentrations did not differ between groups (P = 0.83), but suPAR was higher after the low-sodium DASH diet than the high-sodium control [geometric mean 2470 pg/mL (95% CI: 2380, 2560 pg/mL), compared with 2290 pg/mL (95% CI: 2210, 2380 pg/mL); P = 0.006]. Phosphorus was higher after the low-sodium DASH diet [geometric mean 3.50 mg/dL (95% CI: 3.43, 3.57 mg/dL)] compared with the high-sodium control diet [geometric mean 3.39 mg/dL (95% CI: 3.33, 3.46 mg/dL); P = 0.04]. FGF23 was also higher after the low-sodium DASH diet [geometric mean 35.3 pg/mL (95% CI: 33.3, 37.3 pg/mL) compared with 28.2 pg/mL (95% CI: 26.6, 29.8 pg/mL); P < 0.001]. Contrary to our hypothesis, biomarkers of inflammation and mineral metabolism were increased or unchanged by a low-sodium DASH diet compared with a high-sodium control diet in adults with elevated blood pressure.