Depression not reduced when vitamin D levels less than 30 nanograms – RCT Nov 2015

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.

J Nutr. 2015 Nov 25. pii: jn218883. [Epub ahead of print]
Sepehrmanesh Z1, Kolahdooz F2, Abedi F2, Mazroii N2, Assarian A3, Asemi Z4, Esmaillzadeh A5.
1Department of Psychiatry and.
2Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran;
3Department of Pharmaceutics, School of Pharmacy, and.
4Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran; asemi_r at yahoo.com.
5Food Security Research Center, and Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran; and Department of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran.

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 kIU 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 μg/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 μg/L) than in the placebo group (-0.9 μg/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 μIU/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 β 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 μmol/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.

© 2016 American Society for Nutrition.

PMID: 26609167

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