cholecalciferol and Depressive-Disorder--Major

Traditional methods of depression treatment with the use of pharmacotherapy with antidepressants have limited effectiveness. Biological, psychological and environmental causes of depressive disorders are known, but pathophysiology of depression has not been fully explained. Many factors and mechanisms play role in the pathophysiology of depression, one of which may be vitamin D3 deficiency. Deficiency or border level of vitamin D3 is fairly common in the general population and may occur even in one billion people globally. Epidemiological studies show that vitamin D3 or its metabolites do not reach an optimal level in most adults. Even lower than the optimal level may cause clinical symptoms and be one of the risk factors for depression. In the population of patients suffering from depressive disorders deficiency or insufficiency of vitamin D3 occur more frequently than in the general population. The use of vitamin D3in patients with depression may have antidepressant effect. Continuous supplementation may also reduce the risk of recurrence. This article is a review of literature on the possible impact of vitamin D3 deficiency on the prevalence of depression and antidepressant effect of the supplementation. Selection of articles was made by searching the Medline and PubMed databases using specific keywords: depression, vitamin D3 deficiency. Previous studies on the use of vitamin D3 and its role in prevention and treatment of depressive disorders included too small number of people to clearly assess the effectiveness and safety of supplementation used as adjunctive therapy to antidepressants, as well as and dose range which should be used.

Topics: Cholecalciferol; Depressive Disorder, Major; Dietary Supplements; Female; Humans; Hydroxycholecalciferols; Male; Vitamin D Deficiency

Randomized controlled trials (RCTs) of vitamin D (VitD) supplementation for depression have yielded inconsistent results. We conducted the first RCT of VitD supplementation with multipoint serum 25(OH)D assessments in major depressive disorder (MDD) patients with concurrent severe VitD deficiency.. We randomized antidepressant-free depressed adults with mean baseline 25(OH)D of 11.5 ng/ml to VitD (60,000 IU every 5 days; n = 31) or placebo (n = 28) for 12 weeks. All patients also received escitalopram (10-20 mg/day). Patients were rated at baseline and at the end of weeks 4, 8, and 12. Serum 25(OH)D was estimated at baseline, week 8, and week 12.. In an intent-to-treat analysis, mean Hamilton Depression Scale scores dropped from 25.7 to 5.7 and from 25.8 to 5.0 in VitD and placebo groups, respectively (primary outcome; P = 0.92). VitD and placebo groups did not differ on other objective and subjective ratings of depression, or on global ratings. Similar findings characterized completer analyses. No significant correlations were observed between 25(OH)D levels and depression ratings across the course of the study. Importantly, endpoint escitalopram doses were 4 mg/day higher in placebo than in VitD patients, and 4 mg/day higher in VitD deficient than in VitD sufficient patients.. A ceiling effect with escitalopram may have prevented the discovery of benefits with VitD supplementation.. VitD supplementation does not improve antidepressant outcomes with flexibly dosed escitalopram. VitD deficient depressed patients may require higher antidepressant doses to experience benefits similar to those whose deficiency is corrected by VitD supplementation.

Topics: Adult; Cholecalciferol; Depressive Disorder, Major; Dietary Supplements; Double-Blind Method; Humans; Vitamin D; Vitamin D Deficiency; Vitamins

Psychological problems are common among end-stage renal disease patients undergoing dialysis. We aim to evaluate whether high-dose vitamin D3 (VD3) supplementation has beneficial effects on depressive symptoms in dialysis patients. This prospective, randomized, and double-blind trial includes 746 dialysis patients with depression treated in 3 hospitals in Southeast China. Depression was diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders criteria. Patients were randomly assigned to 52-week treatment of oral 50,000 IU/wk VD3 (cholecalciferol) (test group) or a placebo (control group). The presence of depressive symptoms was evaluated using the Chinese version of Beck Depression Inventory (BDI) II both before and after treatment. Sociodemographic data, clinical data, nutritional indexes, inflammatory biomarkers, and plasma VD3 concentrations were also determined. Finally, 726 patients completed the experiments, including 362 tested patients and 364 controls. After 52 weeks, the depressive symptoms were not significantly improved in the test group (mean BDI II scores changed from -1.1 ± 0.3 to -3.1 ± 0.6) versus the control group. Multivariable logistic regression showed BDI scores were not significantly improved in the test group versus the control group with adjustment for age, sex, comorbidity index, dialysis modality, or (OH)D levels (multivariable-adjusted mean change or MAMC [95% confidence interval (CI)], -2.3 [-2.48 to -1.83]) in the whole dialysis population. After stratification by depression types, the findings do support a significant relationship between the VD3 supplementation and the improvement in BDI II scores in dialysis patients with vascular depression (MAMC [95% CI], -4.4 [-5.08 to -2.76]), but the effect was not significant for major depressive disorders (MAMC [95% CI], -0.9 [-1.52 to -0.63]). The high-dose VD3 supplementation did not significantly reduce the depressive symptoms in our total dialysis population, but a beneficial effect on vascular depression was found, probably mainly based on the improvement of cardiovascular risk factors.

Topics: Administration, Oral; Adolescent; Adult; Aged; China; Cholecalciferol; Depression; Depressive Disorder, Major; Dietary Supplements; Double-Blind Method; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Prospective Studies; Renal Dialysis; Treatment Outcome; Vitamin D Deficiency; Young Adult

To compare the therapeutic effects of vitamin D3 plus fluoxetine and fluoxetine alone in patients with major depressive disorder.. In the present double-blind, randomized, placebo-controlled trial, 42 patients with a diagnosis of major depressive disorder based on DSM-IV criteria were randomly assigned into two groups to receive daily either 1500 IU vitamin D3 plus 20 mg fluoxetine or fluoxetine alone for 8 weeks. Depression severity was assessed at 2-week intervals using the 24-item Hamilton Depression Rating Scale (HDRS) as a primary outcome measure and the 21-item Beck Depression Inventory (BDI) as a secondary outcome measure. Serum 25(OH) vitamin D was measured at baseline and after intervention.. Forty patients completed the trial. A two-way repeated-measures analysis of variance showed that depression severity based on HDRS and BDI decreased significantly after intervention, with a significant difference between the two groups. The vitamin D + fluoxetine combination was significantly better than fluoxetine alone from the fourth week of treatment.. In the present 8-week trial, the vitamin D + fluoxetine combination was superior to fluoxetine alone in controlling depressive symptoms.

Topics: Adolescent; Adult; Aged; Calcifediol; Cholecalciferol; Depressive Disorder, Major; Double-Blind Method; Drug Therapy, Combination; Female; Fluoxetine; Humans; Male; Middle Aged; Psychiatric Status Rating Scales

This study: 1) examined cross-sectional and longitudinal relations of serum brain-derived neurotrophic factor (BDNF) to late-life depression (LLD); 2) tested effects of vitamin D3 and omega-3s on change in BDNF; 3) explored modifying or mediating roles of BDNF on effects of vitamin D3 and omega-3s for LLD. We selected 400 adults from a completed trial of vitamin D3 and omega-3 supplements for LLD prevention. BDNF was measured using an enzyme-linked immunosorbent assay. We administered semi-structured diagnostic interviews and Patient Health Questionnaire [PHQ]-9 to ascertain outcomes at baseline (depression caseness vs. non-caseness; PHQ-9) and at 2-year follow-up among baseline non-depressed individuals (incident vs. no incident MDD; change in PHQ-9). At baseline, while there were no significant differences in mean serum BDNF comparing depression cases and non-cases, being in the lowest vs. highest serum BDNF quartile was significantly associated with worse depressive symptoms. There were no significant longitudinal associations between serum BDNF and LLD. Neither supplement significantly affected change in BDNF; serum BDNF did not appear to modify or mediate treatment effects on LLD. In conclusion, we observed significant cross-sectional but not longitudinal associations between serum BDNF levels and LLD. Vitamin D3 or omega-3s did not alter serum BDNF over 2 years.

Topics: Adult; Brain-Derived Neurotrophic Factor; Cholecalciferol; Cross-Sectional Studies; Depression; Depressive Disorder, Major; Fatty Acids, Omega-3; Humans

Major depressive disorder is a serious neuropsychiatric disease that leads to significant impairment in social functioning and increased morbidity and mortality. Low vitamin D (25-OH D) levels have been hypothesized to contribute to the pathophysiology of MDD. To investigate the therapeutic role of vitamin D in MDD, we recruited 62 male and female patients diagnosed with MDD and randomized them into two groups: the first group (49 patients) received vitamin D supplementation as cholecalciferol vitamin D

Topics: Adolescent; Adult; Case-Control Studies; Cholecalciferol; Combined Modality Therapy; Depressive Disorder, Major; Female; Humans; Male; Middle Aged; Psychotherapy; Vitamins

Low bone mineral density, which increases the risk of stress fragility fractures, is a frequent, often persistent finding in patients with major depressive disorder (MDD). The clinical association between major depressive disorder and osteopenia is still unclear, although several factors are associated with a loss of bone mass. The aim of our study, therefore, was to evaluate bone mineral density and bone metabolism in patients with MDD. Bone mineral density was evaluated in fifty postmenopausal women with MDD, and in 50 matched postmenopausal control women by dual-energy X-ray absorptiometry of the lumbar spine and femur, and by ultrasonography of the calcaneus and phalanges. Serum levels of 25-hydroxivitamin D, parathyroid hormone, Osteoprotegerin/Receptor Activator for Nuclear Factor κB Ligand ratio, bone turnover markers, serum and urinary cortisol were examined. Bone mineral density of the lumbar spine (BMD: 0.72 ± 0.06 vs. 0.82 ± 0.09 g/cm(2), p < 0.001), femoral neck (BMD: 0.58 ± 0.04 vs. 0.71 ± 0.07 g/cm(2), p < 0.001) and total femur (BMD 0.66 ± 0.09 vs. 0.54 ± 0.06 g/cm(2), p < 0.001); and ultrasound parameters at calcaneus (SI: 81.30 ± 6.10 vs. 93.80 ± 7.10, p < 0.001) and phalanges (AD-SOS: 1915.00 ± 37.70 vs. 2020.88 ± 39.46, p < 0.001; BTT : 1.30 ± 0.8 vs. 1.45 ± 0.9, p < 0.001) are significantly lower in patients with MDD compared with controls. Moreover bone turnover markers, parathyroid hormone levels and Receptor Activator for Nuclear Factor κB Ligand are significantly higher in MDD patients compared with controls, while serum levels of 25-hydroxivitamin D and osteoprotegerin are significantly lower. There are no differences in urinary excretion and serum cortisol between groups. Postmenopausal women with depressive disorder have an elevated risk for osteoporosis. Our data suggest that a high level of parathyroid hormone may play a role in the pathogenetic process underlying osteopenia in these patients.

Topics: Bone Density; Bone Diseases, Metabolic; Bone Remodeling; Calcaneus; Cholecalciferol; Comorbidity; Depressive Disorder, Major; Disease Progression; Female; Finger Phalanges; Humans; Middle Aged; Parathyroid Hormone; Postmenopause; Risk Factors; Ultrasonography