Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The available evidence suggests that vitamin D has cardiovascular effects besides regulating calcium homeostasis. To examine the effect of 1,25-dihydroxyvitamin D(3), the major metabolite of vitamin D, on endothelium-dependent contractions, aortic rings of spontaneously hypertensive rats (SHR) were suspended in organ chambers for isometric force measurements. Rings were incubated with N(omega)-nitro-l-arginine methyl ester (l-NAME) and then exposed to increasing concentrations of acetylcholine, ATP, or the calcium ionophore to trigger contractions. This was done in the absence or presence of 1,25-dihydroxyvitamin D(3). The release of prostacyclin after acetylcholine or A-23187 stimulation was also measured. The cytosolic-free calcium concentration was measured by confocal microscopy after incubation with the fluorescent dyes fluo-4 and fura red. The presence of vitamin D receptors was confirmed using immunohistochemistry. Acetylcholine- and ATP-induced endothelium-dependent contractions were significantly reduced compared with those obtained in the absence of the drug. This effect was not present if A-23187 was used as an agonist. The acetylcholine- but not the A-23187-induced release of prostacyclin was reduced by the acute administration of 1,25-dihydroxyvitamin D(3). Exposure to 1,25-dihydroxyvitamin D(3) reduced the increase in cytosolic-free calcium concentration caused by acetylcholine but not by A-23187 in cells. Vitamin D receptors were densely distributed in the endothelium. Inecalcitol (19-nor-14-epi-23-yne-1,25-dihydroxyvitamin D(3)), a synthetic analog of vitamin D, caused a comparable depression of endothelium-dependent contractions as 1,25-dihydroxyvitamin D(3). These results demonstrate that vitamin D(3) modulates vascular tone by reducing calcium influx into the endothelial cells and hence decreasing the production of endothelium-derived contracting factors.
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PMID:Vitamin D derivatives acutely reduce endothelium-dependent contractions in the aorta of the spontaneously hypertensive rat. 1848 33

Serum 25-hydroxyvitamin D (25(OH)D) status in older adults enrolled in community-based meal programs is not well characterized. The objective was to identify predictors of poor serum 25(OH)D status and the response to vitamin D supplementation in a convenience sample from the Older Americans Act Nutrition Program (OAANP) in northeast Georgia (N = 158, mean age = 77 years, 81% women, 69% Caucasian, 31% African American). Mean serum 25(OH)D was 55nmol/l, and intakes of vitamin D and calcium from foods were very low. Vitamin D insufficiency (25(OH)D 25- < 50 nmol/l) occurred in 36.7%. Vitamin D deficiency occurred in 8.2% (25(OH)D < 25 nmol/l) and was associated with low milk intake, low sunlight exposure, receiving meals at home, tobacco use, depression, dementia, antianxiety medication, poor instrumental activities of daily living, and low calf circumference (p < or = 0.05). When non-supplement users (n = 28) were given a multivitamin with vitamin D (10 microg/d) and calcium (450 mg/d) for 4 months, 25(OH)D increased from 50 to 78 nmol/l, the prevalence of poor vitamin D status (25(OH)D < 50 nmol/l) decreased from 61% to 14%, and serum alkaline phosphatase decreased by 10% (p < 0.01). High body weight appeared to attenuate the increase in 25(OH)D in response to the multivitamin supplement (p < or = 0.05). In conclusion, OAANP services did not prevent poor vitamin D and calcium status, but a supplement with vitamin D and calcium was beneficial.
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PMID:Vitamin D deficiency and insufficiency in the Georgia Older Americans Nutrition Program. 1892 89

The main forms of renal osteodystrophy are secondary hyperparathyroidism, aluminum-induced bone disease and adynamic bone disease without aluminum intoxication. Aluminum intoxication has become rare because of control of the dialysate solution and avoidance of aluminum containing phosphate binders. Secondary hyperparathyroidism still develops early in the course of renal failure and remains the most frequent form of osteodystrophy in patients treated by maintenance hemodialysis. Several factors, including hyperphosphatemia and deficient synthesis of 1,25-dihydroxyvitamin D are involved in its pathogenesis. Secondary hyperparathyroidism is symptomatic only in severely affected patients. Prevention depends on control of serum phosphorus +/- prescription of 1-alpha-hydroxylated vitamin D derivatives or may require subtotal parathyroidectomy when hyperparathyroidism is refractory.Adynamic bone disease not related to aluminum intoxication has been increasingly recognized in recent years and is presently the most frequent form of osteodystrophy in continuous ambulatory peritoneal dialysis patients. This condition, characterized by low bone turnover and depression of bone formation, appears to be associated with an increased risk of bone fracture. The main pathophysiologic feature is excessive treatment of hyperparathyroidism leading to hypoparathyroidism. Serum immunoreactive 1,84-parathormone levels should therefore be kept at a level of 1.5-fold to 3-fold the upper limit of normal in patients treated by maintenance hemodialysis.
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PMID:Renal osteodystrophy. 1907 65

Studies indicate that diet and vascular calcification may be related to the occurrence of brain lesions, although the importance of dietary calcium and vitamin D has not been investigated. The objective of this study was to test the hypothesis that calcium and vitamin D intakes would be positively associated with brain lesion volumes in elderly individuals with and without late-life depression. A cross-sectional study was performed as part of a longitudinal clinical study of late-life depression. Calcium and vitamin D intakes were assessed in 232 elderly subjects (95 with current or prior depression, 137 without depression) using a Block 1998 food frequency questionnaire. Calcium, vitamin D, and kilojoule intake were determined. Brain lesion volumes were calculated from magnetic resonance imaging scan. Subjects were 60 years or older. Calcium and vitamin D intakes were significantly and positively correlated with brain lesion volume (P < .05 and P < .001, respectively). In 2 separate multivariable models, controlling for age, hypertension, diabetes, heart disease, group (depression/comparison), lesion load (high/low), and total kilocalories, these positive associations remained significant (P < .05 for calcium; P < .001 for vitamin D). In conclusion, calcium and vitamin D consumption were associated with brain lesions in elderly subjects even after controlling for potentially explanatory variables. These associations may be due to vascular calcification or other mechanism. The possibility of adverse effects of high intakes of calcium and vitamin D needs to be further explored in longitudinal studies of elderly subjects.
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PMID:Calcium and vitamin D intakes may be positively associated with brain lesions in depressed and nondepressed elders. 1908 92

Vitamin D, a multipurpose steroid hormone vital to health, has been increasingly implicated in the pathology of cognition and mental illness. Hypovitaminosis D is prevalent among older adults, and several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia. Vitamin D activates receptors on neurons in regions implicated in the regulation of behavior, stimulates neurotrophin release, and protects the brain by buffering antioxidant and anti-inflammatory defenses against vascular injury and improving metabolic and cardiovascular function. Although additional studies are needed to examine the impact of supplementation on cognition and mood disorders, given the known health benefits of vitamin D, we recommend greater supplementation in older adults.
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PMID:Some new food for thought: the role of vitamin D in the mental health of older adults. 1918 3

The understanding of the role of vitamin D in maintaining optimal health has advanced sharply in the past two decades. There is mounting evidence for beneficial roles for vitamin D in reducing the risk of bone diseases and fractures, many types of cancer, bacterial and viral infections, autoimmune diseases, and cardiovascular diseases. Recently, several reports have also been published regarding the role of vitamin D in neuroprotection. This article develops the hypothesis that vitamin D can reduce the risk of developing dementia, presenting the evidence from observational and laboratory studies. The observational evidence includes that low serum 25-hydroxyvitamin D [25(OH)D] has been associated with increased risk for cardiovascular diseases, diabetes mellitus, depression, dental caries, osteoporosis, and periodontal disease, all of which are either considered risk factors for dementia or have preceded incidence of dementia. The laboratory evidence includes several findings on the role of vitamin D in neuroprotection and reducing inflammation. Although this evidence is supportive, there do not appear to be observational studies of incidence of dementia with respect to prediagnostic serum 25(OH)D or vitamin D supplementation. Such studies now appear to be warranted.
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PMID:Does vitamin D reduce the risk of dementia? 1949 40

It has been known for more than 20 years that vitamin D exerts marked effects on immune and neural cells. These non-classical actions of vitamin D have recently gained a renewed attention since it has been shown that diminished levels of vitamin D induce immune-mediated symptoms in animal models of autoimmune diseases and is a risk factor for various brain diseases. For example, it has been demonstrated that vitamin D (i) modulates the production of several neurotrophins, (ii) up-regulates Interleukin-4 and (iii) inhibits the differentiation and survival of dendritic cells, resulting in impaired allo-reactive T cell activation. Not surprisingly, vitamin D has been found to be a strong candidate risk-modifying factor for Multiple Sclerosis (MS), the most prevalent neurological and inflammatory disease in the young adult population. Vitamin D is a seco-steroid hormone, produced photochemically in the animal epidermis. The action of ultraviolet light (UVB) on 7-dehydrocholesterol results in the production of pre-vitamin D which, after thermo-conversion and two separate hydroxylations, gives rise to the active 1,25-dihydroxyvitamin D. Vitamin D acts through two types of receptors: (i) the vitamin D receptor (VDR), a member of the steroid/thyroid hormone superfamily of transcription factors, and (ii) the MARRS (membrane associated, rapid response steroid binding) receptor, also known as Erp57/Grp58. In this article, we review some of the mechanisms that may underlie the role of vitamin D in various brain diseases. We then assess how vitamin D imbalance may lay the foundation for a range of adult disorders, including brain pathologies (Parkinson's disease, epilepsy, depression) and immune-mediated disorders (rheumatoid arthritis, type I diabetes mellitus, systemic lupus erythematosus or inflammatory bowel diseases). Multidisciplinary scientific collaborations are now required to fully appreciate the complex role of vitamin D in mammal metabolism.
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PMID:Vitamin D, a neuro-immunomodulator: implications for neurodegenerative and autoimmune diseases. 1954 51

While recent laboratory-based studies have substantially advanced our understanding of the action of vitamin D in the brain, much is still unknown concerning how vitamin D relates to mood. The few epidemiological studies of vitamin D and depression have produced inconsistent results and generally have had substantial methodological limitations. Recent findings from a randomized trial suggest that high doses of supplemental vitamin D may improve mild depressive symptoms, but important questions persist concerning how vitamin D may affect monoamine function and hypothalamic-pituitary-adrenal axis response to stress, whether vitamin D supplementation can improve mood in individuals with moderate-to-severe depression, and whether vitamin D sufficiency is protective against incident depression and recurrence. At this time, it is premature to conclude that vitamin D status is related to the occurrence of depression. Additional prospective studies of this relationship are essential.
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PMID:Vitamin D and the occurrence of depression: causal association or circumstantial evidence? 1967 44

Both depressive symptoms and vitamin D insufficiency are common during winter. This study examined the association between serum 25-hydroxyvitamin D and depressive symptoms by survey season. Subjects were 527 municipal employees aged 21-67 years of two municipal offices in Japan. Overall, there was no measurable association. However, in the workplace surveyed in November, multivariate-adjusted odds ratios (95% confidence interval) of having depressive symptoms (Center for Epidemiologic Studies Depression score of >or=16) for the lowest through highest quartiles of serum 25-hydroxyvitamin D were 1.00 (reference), 0.84 (0.45-1.58), 0.83 (0.44-1.58) and 0.59 (0.30-1.15), respectively (trend P=0.14). The association with the severe depressive state was more pronounced. By contrast, there was no such association in the workplace surveyed in July. Overall, this study did not provide evidence linking higher blood vitamin D levels with decreased depressive symptoms. The suggestive inverse association in sun-deprived season warrants further investigation.
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PMID:Association between serum 25-hydroxyvitamin D and depressive symptoms in Japanese: analysis by survey season. 1969 May 78

The vitamin D hormonal system is involved in the regulation of more than 800 genes. Vitamin D deficiency, which is evaluated on the basis of the serum level of 25-hydroxycholecalciferol (25[OH]D), is frequently observed in the general population, particularly in patients with chronic kidney disease (CKD). Vitamin D deficiency is associated with an increased risk of falls and fracture and also with diabetes, malignancies, autoimmune diseases, depression and mortality. Furthermore, CKD is accompanied by a decrease in the renal production of 1,25 dihydroxycholecalciferol (1,25[OH](2)D). Such deficiencies have also been implicated in the pathophysiology of secondary hyperparathyroidism. Currently, vitamin D supplementation is not recommended in stage 5 CKD. However, since there is also significant extra-renal production of 1,25(OH)(2)D this would appear to be in favour of vitamin D treatment. We describe the disturbances of vitamin D metabolism occurring in CKD and discuss the advantages and the potential toxicity risk of vitamin D supplementation as well as the optimal serum 25[OH]D level. We then present the pharmacological properties of the various medicinal forms of vitamin D derivates and suggest therapeutic guidelines for supplementation with 25(OH)D(3) or cholecalciferol. We also examine existing guidelines for the administration of active 1-alpha-hydroxylated vitamin D. Despite the absence of strong scientific support by randomized controlled intervention studies, vitamin D supplementation should be considered in patients with CKD stages 4-5D having vitamin D insufficiency or deficiency, for the prevention of secondary hyperparathyroidism and for other potential benefits owing to its pleiotropic effects.
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PMID:[Guidelines for vitamin D prescription in dialysis patients]. 1974 43


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