4.6 Article Retracted Publication

被撤回的出版物: Vitamin D Supplementation Affects the Beck Depression Inventory, Insulin Resistance, and Biomarkers of Oxidative Stress in Patients with Major Depressive Disorder: A Randomized, Controlled Clinical Trial (Publication with Expression of Concern. See vol. 150, pg. 3043, 2020) (Retracted article. See vol. 151, pg. 1360, 2021)

期刊

JOURNAL OF NUTRITION
卷 146, 期 2, 页码 243-248

出版社

OXFORD UNIV PRESS
DOI: 10.3945/jn.115.218883

关键词

vitamin D supplementation; glucose metabolism; lipid profiles; oxidative stress; depression

资金

  1. Kashan University of Medical Sciences
  2. Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran

向作者/读者索取更多资源

Background: Vitamin D may decrease depression symptoms through its beneficial effects on neurotransmitters, metabolic profiles, biomarkers of inflammation, and oxidative stress. Objective: This study was designed to assess whether vitamin D supplementation can reduce symptoms of depression, metabolic profiles, serum high-sensitivity C-reactive protein (hs-CRP), and biomarkers of oxidative stress in patients with major depressive disorder (MDD). Methods: This randomized, double-blind, placebo-controlled clinical trial was performed in 40 patients between 18 and 65 y of age with a diagnosis of MDD based on criteria from the Diagnostic and Statistical Manual of Mental Disorders. Patients were randomly assigned to receive either a single capsule of 50 kill vitamin D/wk (n = 20) or placebo (n = 20) for 8 wk. Fasting blood samples were taken at baseline and postintervention to quantify relevant variables. The primary [Beck Depression Inventory (BDI), which examines depressive symptoms] and secondary (glucose homeostasis variables, lipid profiles, hs-CRP, and biomarkers of oxidative stress) outcomes were assessed. Results: Baseline concentrations of mean serum 25-hydroxyvitamin D were significantly different between the 2 groups (9.2 +/- 6.0 and 13.6 +/- 7.9 mu g/L in the placebo and control groups, respectively, P = 0.02). After 8 wk of intervention, changes in serum 25-hydroxyvitamin D concentrations were significantly greater in the vitamin D group (+20.4 mu g/L) than in the placebo group (-0.9 mu g/L, P < 0.001). A trend toward a greater decrease in the BDI was observed in the vitamin D group than in the placebo group (-8.0 and -3.3, respectively, P= 0.06). Changes in serum insulin (-3.6 compared with +2.9 mu lU/mL, P= 0.02), estimated homeostasis model assessment of insulin resistance (-1.0 compared with +0.6, P= 0.01), estimated homeostasis model assessment of beta cell function (-13.9 compared with +10.3, P = 0.03), plasma total antioxidant capacity (+63.1 compared with -23.4 mmol/L, P= 0.04), and glutathione (+170 compared with -213 mu mol/L, P = 0.04) in the vitamin D group were significantly different from those in the placebo group. Conclusion: Overall, vitamin D supplementation of patients with MDD for 8 wk had beneficial effects on the BDI, indicators of glucose homeostasis, and oxidative stress. This trial was registered at www.irct.ir as IRCT201412065623N29.

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