Dietary sodium and the human gut microbiota
Date
2021
Authors
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Journal ISSN
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Publisher
University of Delaware
Abstract
A disrupted gut microbial profile mediates pathogenesis of hypertension (HTN) and cardiovascular disease (CVD), and humans with HTN present with lower microbial diversity than their normotensive counterparts. High sodium intake is a modifiable risk factor for HTN and CVD but only 11% of the United States (U.S.) adults meet the recommended dietary sodium intake set by the Dietary Guidelines for Americans (2,300 vs 3,400 mg/d). High sodium diets (HSDs) disrupt the microbial profile through increased inflammation, in particular by activating proinflammatory T helper 17 (TH17) cells and suppressing anti-inflammatory T regulatory cells (Treg). OBJECTIVES: 1.a) Determine the effect of an HSD on gut microbiota composition in healthy adults. 1.b) Determine the effect of an HSD on gut microbiota composition in men and women. 2. Determine the effect of an HSD on the abundance of TH17 and Treg cells in the peripheral blood of healthy adults. HYPOTHESES: 1.a) Gut microbial composition will exhibit more deleterious changes following an HSD compared to a recommended sodium diet (RSD) as evidenced by a reduction in microbial diversity. 1.b) Gut microbial composition in men will exhibit more deleterious changes following an HSD compared to women, as evidenced by greater reductions in gut microbial diversity. 2) An HSD would increase the serum abundance of TH17 cells and reduce abundance of Treg cells compared to an RSD. METHODS: Healthy, non-hypertensive and non-obese young adults were recruited. Subjects underwent a 10-day HSD (6,900mg sodium/d) and a 10-day RSD (2,300 mg sodium/d) intervention in random order. Microbial diversity (Shannon diversity index) was assessed from a fecal sample that subjects provided on Day 0 and Day 10 of each intervention. A blood sample was obtained on Day 10 of each intervention to quantify TH17 and Treg cells. Compliance was assessed from urinary sodium excretion obtained via 24-hour urine collection on Day 9, and blood pressure (BP) was measured using a 24-hour ambulatory BP monitor on the same day. RESULTS: Thirty-one subjects completed both interventions. Day 10 fecal samples were analyzed from 20 subjects (8M/12W, 25 ± 1 yrs, body mass index 23.1 ± 0.5 kg/m2), and day 0 and day 10 samples (complete sets) were analyzed from a subset of 16 subjects. Urinary sodium excretion and serum sodium levels were increased following an HSD (p = <0.001, p = <0.002, respectively; n = 20). Systolic BP remained stable (p = 0.222). Shannon diversity index was comparable between RSD and HSD in all subjects (RSD: 2.62 ± 0.18; HSD: 3.11 ± 0.21; p = 0.088; n = 20). There were also no significant differences in Shannon diversity index between sexes (men: RSD: 2.52 ± 0.29, HSD: 3.01 ± 0.27; women: RSD: 2.69 ± 0.23, HSD: 3.18 ± 0.32; diet * sex interaction p = 0.937). There were no differences in diversity within and between each intervention in samples from complete sets (RSD: Day 0: 2.91 ± 0.35, Day 10: 2.54 ± 0.27; HSD: Day 0: 3.36 ± 0.33, Day 10: 3.19 ± 0.33; diet * day interaction p = 0.062; n = 16). Inclusion of sex in the analysis revealed no significant differences in Shannon diversity index (diet * day * sex interaction p = 0.925). TH17 and Treg cells were quantified from 22 subjects (13M/9W, 25 ± 1 yrs, BMI 22.9 ± 0.5 kg/m2). Urinary sodium excretion and serum sodium levels were increased following an HSD (p = <0.001, p = <0.010, respectively). Systolic BP remained stable (p = 0.129). Abundance of TH17 cells did not differ between HSD and RSD (RSD: 0.35 ± 0.06%, HSD: 0.28 ± 0.02%, p = 0.262). Abundance of Treg also remained unchanged (RSD: 0.99 ± 0.11%, HSD: 0.28 ± 0.02%, p = 0.552). CONCLUSION: An HSD did not affect the gut microbial diversity nor the abundance of TH17 and Treg cells in the peripheral blood. Further studies should investigate the influence of HSD in a larger sample and target individual characteristics, such as salt sensitivity and middle to advanced age, that may be mediating changes in the gut microbial composition on HSD.
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Keywords
Dietary sodium, Gut microbiota, Immune function, Salt, T cells