Selenium supplementation lowers insulin resistance and markers of cardio-metabolic risk in patients with congestive heart failure: a randomised, double-blind, placebo-controlled trial
What this study found
Selenium supplementation produced favorable changes in insulin metabolism and several cardio-metabolic risk markers compared with placebo. At 12 weeks, between-group differences favored selenium for fasting plasma glucose (P = 0.04), insulin (P < 0.001), LDL-cholesterol change (P = 0.03), total-/HDL-cholesterol ratio change (P < 0.001), HDL-cholesterol change (P = 0.001), hs-CRP change (P = 0.01), TAC change (P = 0.004), and GSH change (P = 0.003). The authors concluded that selenium may improve some metabolic and inflammatory/oxidative stress markers in congestive heart failure, although…
- Study & population
- Randomized, double-blind, placebo-controlled trial in adult patients with congestive heart failure recruited from a cardiology clinic in Kashan, Iran.
- Intervention
- Participants in the active arm received 200 µg/day selenium as selenium yeast, taken orally in capsules once daily for 12 weeks, versus placebo.
- Key limitation
- Small single-center trial with only 26 participants in the selenium arm and a short 12-week duration.
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Open PDFOriginal abstract
Abstract This study was carried out to evaluate the effects of Se supplementation on metabolic profiles in patients with congestive heart failure (CHF). This randomised double-blind, placebo-controlled trial was performed among fifty-three subjects with CHF, aged 45–85 years old. Subjects were randomly allocated into two groups to take either 200 µg/d of Se as Se yeast (n 26) or placebo (n 27) for 12 weeks. Metabolic profiles were assessed at baseline and at the end of trial. Compared with the placebo, Se supplementation led to significant reductions in serum insulin (−18·41 (sd 27·53) v. +13·73 (sd 23·63) pmol/l, P<0·001), homoeostatic model of assessment for insulin resistance (−1·01 (sd 1·61) v. +0·55 (sd 1·20), P<0·001) and a significant increase in quantitative insulin sensitivity check index (QUICKI) (+0·007 (sd 0·03) v. −0·01 (sd 0·01), P=0·007). In addition, Se supplementation significantly decreased LDL-cholesterol (−0·23 (sd 0·29) v. −0·04 (sd 0·28) mmol/l, P=0·03) and total-:HDL-cholesterol ratio (−0·47 (sd 0·31) v. −0·06 (sd 0·42), P<0·001), and significantly increased HDL-cholesterol levels (+0·18 (sd 0·19) v. +0·02 (sd 0·13) mmol/l, P=0·001) compared with the placebo. In addition, taking Se supplements was associated with a significant reduction in high-sensitivity C-reactive protein (hs-CRP) (−1880·8 (sd 3437·5) v. +415·3 (sd 2116·5) ng/ml, P=0·01), and a significant elevation in plasma total antioxidant capacity (TAC) (+30·9 (sd 118·0) v. −187·9 (sd 412·7) mmol/l, P=0·004) and total glutathione levels (+33·7 (sd 130·4) v. −39·2 (sd 132·8) µmol/l, P=0·003) compared with the placebo. When we applied Bonferroni correction for multiple outcome testing, QUICKI (P=0·11), LDL-cholesterol (P=0·51), hs-CRP (P=0·17), TAC (P=0·06) and GSH (P=0·05) became non-significant, and other metabolic profiles did not alter. Overall, our study supported that Se supplementation for 12 weeks to patients with CHF had beneficial effects on insulin metabolism and few markers of cardio-metabolic risk.