Vitamin D consists of a group of similar molecules called vitamers, which are involved in calcium homeostasis and bone metabolism.
In the human body, vitamin D is made via a photochemical reaction of cholecalciferol in the skin. Ultraviolet light converts cholecalciferol to vitamin D. Cholecalciferol is also known as vitamin D3.
Certain mushrooms synthesize a slightly different version of vitamin D called ergocalciferol or vitamin D2; this form of the vitamin can also be used by humans. Very little vitamin D is found in natural foods.
Since vitamin D does not have to be supplied by the diet and works on specific target tissues it is by definition a hormone, and not truly a vitamin. Vitamin D hormone usually functions as a steroid.
Vitamin D is best absorbed when ingested with lipids. In the digestive tract, vitamin D is incorporated into micelles and the micelles are absorbed by the intestine via passive diffusion. In the intestinal cells, chylomicrons (particles made of proteins and fat) are formed, which enter the lymphatic system and the plasma. Vitamin D is then transported to the liver by chylomicron remnants and to specific targets with the help of carrier vitamin D binding protein (DBP) or transcalciferin.
Efficacy of absorption of dietary vitamin D is approximately 50%.
In the liver vitamin D is sequentially hydroxylated to produce 25-hydroxycholecalciferol (25(OH)D3, calcidiol), a biologically active form. In the kidney, reaction of vitamin D with alpha-1-hydroxylase yields 1,25-dihydroxyvitamin D3 (1,25(OH)D3, calcitriol), activated vitamin D. Calcitriol is the predominant form of vitamin D found in blood. The Food and Nutrition Board (FNB) at the Institute of Medicine of The National Academies appointed a panel in 2008 to review the DRI for vitamin D. The panel’s report is expected in May 2010.
Vitamin D plays an important role in calcium and phosphorus homeostasis by regulating bone resorption, affecting absorption of calcium in the gut, and by regulating calcium losses in urine.
In the kidney vitamin D works with estrogen to regulate renal tubular reabsorption of calcium and phosphorus.In bones, vitamin D works in conjunction with parathyroid hormone to regulate the release of calcium and phosphorus from the bones into the bloodstream.
Vitamin D also regulates the gene coding for synthesis of a calcium binding protein known as calbindin. Calbindin participates in calcium transport.
The generic roles of vitamin D have been confirmed in over 50 genes extending beyond balancing mineral metabolism. New findings have confirmed direct effects by vitamin D on various nuclear receptors of cells such as those of the prostate, liver, thyroid, and brain.
Cells of the prostate gland respond to vitamin D levels. These findings have lead to new potential chemotherapeutic treatments targeting specific lesions on cancer cells using doses of 1alpha25 (OH)2D3.
Another group of cells directly affected by vitamin D levels appear to be the T helper cells of the immune system.
Polymorphisms in vitamin D receptors in brain cells, (due to low levels of vitamin D early in life), also appear to be linked to schizophrenia.
In light of recent findings, many experts and professional associations have recommended an increase in the recommended amount of vitamin D intake. Most experts call for increasing vitamin D intake to 1000 IU/day for an adult, which is substantially higher than the currently recommended 600 IU. Increases in both the recommended dose as well as in the upper tolerable intakes are currently under review by the Institute of Medicine and changes in favor of increases are expected by the scientific community. Vitamin D: Dietary Reference Intake 1
Tolerable Upper Intake Levels (UL) mcg/day*
Infants* 0 to 6 months 7 to 12 months
Children 1 to 3 years 4 to 8 years
Males/Females 9 to 18 years 19 to 70 years 51 to 70 years > 70 years
5 5 10 15
600 600 600 800
100 100 100 100
Pregnancy <= 18 years 19 to 30 years 31 to 50 years
Lactation <= 18 years 19 to 30 years 31 to 50 years
Vitamin D deficiency is relatively common in the United States. Studies have demonstrated that nearly 60% of people over 70 years are vitamin D deficient. Furthermore, the average daily intake of vitamin D in the United States is only 30% of the RDA. Symptoms of vitamin D deficiency include Rickets in children, and osteomalacia in adults resulting from poor ossification of bone tissue, resulting in weak bones that bend readily.
Symptoms in adults include painful softening and bending of bones, low serum calcium concentrations, and tetany. Less severe vitamin D deficiency can result in hyperparathyroidism and increased bone turnover leading to bone loss and osteoporosis.
Vitamin D deficiency can result from inadequate intake, limited exposure to sunlight, kidney or liver dysfunctions which inhibit conversion of vitamin D to its metabolically active forms, or fat-malabsorption syndromes.
Symptoms of toxicity include loss of appetite, excessive thirst, nausea, vomiting, irritability, weakness and weight loss, however these are not commonly seen. These symptoms were often seen during decades when parents would give their children massive doses of cod liver oil to prevent rickets.
The only frequently consumed dietary source of vitamin D is milk or powdered whole milk fortified with D2. Cereals, infant formulas, including soy, are usually fortified with vitamin D. Cod liver oil and fatty fish oils are excellent sources of vitamin D.
Dark skinned individuals are at risk. NHANES III reported that 41% of African American women between the ages 15-49 were vitamin D deficient.
Due to the skin’s decreased capacity to synthesize vitamin D3 with age, people over the age of 70 are at particularly high risk for developing vitamin D deficiency. The capacity of skin to synthesize vitamin D3 in these later years is approximately half what it is in younger people.
Breastfed infants who ingest only breast milk and no supplements are at risk for deficiency. Human breast milk contains approximately 25 IU/L or less of vitamin D, which is not sufficient to meet the infant’s needs. Therefore supplementation of vitamin D is recommended for all breastfed infants until they are weaned or consume 1000 mL of fortified milk or formula daily. All infant formulas sold in the United States contain at least 400 IU of vitamin D per liter.
Vegetarians are at risk for vitamin D deficiency
Obese individuals are at high risk for vitamin D deficiency. Though the skin is able to manufacture vitamin D normally, it is not able to enter into the circulation as well as it does in people with normal weight.
Use of alcohol may alter absorption of vitamin D and may lead to deficiency.
Smoking may increase the rate of bone turnover, therefore increasing the requirement of vitamin D.
Vitamin D supplements are also recommended for individuals shielded from sunlight, those who are homebound, for those who reside in northern latitudes or in areas of high atmospheric pollution. In addition they are also recommended for individuals who routinely dress in clothing which covers their entire body, for those who work nightshifts, or who tend to spend the majority of their day indoors.
Warfarin (Coumadin), an anticoagulant drug, may decrease the absorption of vitamin D.
Chronic use of laxatives that contain mineral oil can reduce intestinal absorption of many nutrients, including vitamin D. This action may be due to an increase in motility or a direct inhibition of absorption. Excessive use of mineral oil-containing drugs should be limited when taking vitamin D.
Substances that bind bile in the intestine such as bile acid sequestrants (cholestyramine (Questran) and colestipol (Colestid) reduce absorption of vitamin D. Patients using these drugs should adhere to timing regimens set by a medical expert in order to maximize efficacy. Intramuscular ergocalciferol supplements may be required.
Concurrent administration of thiazide diuretics, used for symptoms of edema and hypertension, and vitamin D analogs in patients with hypoparathyroidism may result in hypercalcemia. Hypercalcemia in these patients results from increased bone resorption.
Anticonvulsant drugs such as Phenobarbital (Luminal) and phenytoin (Dilantin) may reduce plasma concentrations of vitamin D by inhibiting enzyme activity in the liver and by preventing conversion of the vitamin to its active form. Long-term use can lead to vitamin D deficiency and eventually bone loss.
The concentrations of magnesium-containing antacids, such as aluminum/magnesium hydroxide (Maalox) and aluminum/magnesium hydroxide/simethicone (Mylanta), are increased by vitamin D.
Vitamin D may cause hypocalcaemia in patients on digitalis (Lanoxin), a cardiac drug. This may precipitate cardiac arrhythmias. Taking dietary calcium or supplements may be advisable.
Ketoconazole (Nizoral), an antifungal agent, may inhibit vitamin D synthetic and catabolic enzymes. Reductions in serum vitamin D concentrations have been observed following the administration of 300 to 1200 mg/day ketoconazole for a week to healthy men and calcium and vitamin D supplementation may be necessary in these cases.
Vitamin D may interfere with the effectiveness of verapamil (Isoptin), a calcium-channel blocker, which is used to lower high blood pressure. During this therapy, patients should consult their dhealth care provider before using vitamin D-containing supplements. Long-term therapy (longer than 2 weeks) with corticosteroids, anti-inflammatory drugs, reduces the body's ability to activate vitamin D, increasing the rate of bone loss.
Orlistat (Xenical), a weight loss agent, may decrease gastrointestinal absorption of fat-soluble vitamins such as vitamin D. An interval of at least two hours (before or after) between Orlistat and vitamin D administration is recommended. However, taking multivitamins including fat-soluble vitamins did not decrease drug concentrations in clinical studies.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: a double-blind, randomized, placebo-controlled trial.
A randomized, double-blind, placebo-controlled trial investigated the effects of vitamin D supplementation for people with congestive heart failure (CHF). 93 people completed the trial. 123 CHF patients were recruited for the 9 month study; participants were only included with New York Heart Association functional class ¡Ý II. Participants were randomly assigned to receive 2000 IU cholecalciferol daily or a placebo. All participants received 500 mg calcium daily. Logarithmic transformed serum concentrations of 25(OH)D (P=0.001), parathyroid hormone (PTH, P=0.007), TNF-alpha (P=0.006), and IL-10 (P=.042) demonstrated significant treatment effects. Vitamin D supplementation increased median 25(OH)D concentrations by 26.8 ng/mL (P=0.001; paired t test). In the vitamin D supplemented group, median PTH concentrations decreased significantly by 14% (P=0.034; paired t test); PTH concentrations tended to decrease by 11% in the D(¡§C) group (P=0.092; paired t test). In the vitamin D supplemented group, median IL-10 concentrations increased by 43% (P=0.035; paired t test); medial IL-10 concentrations did not significantly change in the control group (¡§C22%, P=0.579; paired t test). Median TNF-alpha concentrations increased by 12% in the placebo group (P=0.017; paired t test) but did not change in the vitamin D supplemented group (P=0.812; paired t test). These results suggest that vitamin D supplements may beneficially affect inflammatory markers and PTH for people with CHF. 11
Vitamin D intake is inversely associated with rheumatoid arthritis: results from the Iowa Women's Health Study.
A prospective cohort study included 29,368 women of aged 55-69 years without a history of rheumatoid arthritis (RA) at study baseline to investigate relationships between vitamin D and RA. Participants completed a diet questionnaire at baseline which was used to determine the amount of vitamin D consumed. Through the 11 year follow up there 152 confirmed cases of RA were identified. Greater intake (highest versus lowest tertile) of vitamin D was inversely associated with risk of RA (RR 0.67, 95% CI 0.44-1.00, P for trend=0.05). Both dietary (RR 0.72, 95% CI 0.46-1.14, P for trend=0.16) and supplemental (RR 0.66, 95% CI 0.43-1.00, P for trend=0.03) vitamin D demonstrated inverse associations with RA. A composite measure of milk products suggested an inverse association with risk of RA (RR 0.66, 95% CI 0.42-1.01, P for trend=0.06). Vitamin D intake may be inversely associated with RA incidence. 9
Vitamin D supplement in early childhood and risk for Type I (insulin-dependent) diabetes mellitus. The EURODIAB Substudy 2 Study Group.
This case-control study focused on exposure to vitamin D in early childhood and risk of type I diabetes. Data from 820 people with type I diabetes and 2,335 healthy controls were analyzed. Vitamin D supplementation rates in different countries varied from 47 to 97% among control subjects. The Mantel-Haenszel combined odds ratio was 0.67 (95% confidence limits: 0.53, 0.86). Adjustment for a low birth weight, short duration of breast feeding, old maternal age, and study center did not affect the significant protective effect of vitamin D. Interestingly, there was no indication of heterogeneity in the association between vitamin D supplementation and decreased risk of Type I diabetes. The authors suggest that activated vitamin D might moderate immune function and thereby protect against development of type I diabetes.10
Cytokine profile in patients with multiple sclerosis following vitamin D supplementation.
A randomized, double-blind study was conducted with multiple sclerosis (MS) patients who either received 800 mg supplemental calcium plus placebo (control) or 800 mg supplemental calcium plus 1000 IU vitamin D (treatment). After six months of supplementation, serum 25-hydroxyvitamin D levels increased significantly (17±6 ng/mL at baseline to 28±8 ng/mL at 6 months). Serum transforming growth factor (TGF)-beta 1 levels were increased in the vitamin D group from 230±21 pg/mL at baseline to 295±40 pg/mL after six months. Vitamin D did not alter tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, or interleukin (IL)-13. Vitamin D supplementation of MS patients for 6 months was associated with increased vitamin D status and serum TGF-beta 1. 12
Decreased bioavailability of vitamin D in obesity.
To investigate the bioavailability of vitamin D in obese people, nineteen healthy obese people (BMI>30) and nineteen healthy lean people (BMI<25) participated in a two phase study. In phase one, participants were exposed to UV-B through a whole-body irradiation method. Vitamin D levels were monitored one hour prior to the irradiation and 24 hours after. At least one month later, participants consumed a 50,000 IU vitamin D supplement. Vitamin D levels were determined immediately prior to the supplement and six, ten, and 24 hours after. Obese participants had lower vitamin D levels and higher parathyroid hormone levels at baseline. The incremental increase in vitamin D3 was 57% lower in obese than in nonobese subjects after UV irradiation. BMI was inversely correlated with serum vitamin D3 concentrations after irradiation (r=-0.55, P=0.003). BMI was also inversely associated with peak serum vitamin D2 concentrations after vitamin D2 intake (r=-0.56, P=0.007). These results suggest that vitamin D synthesis and absorption are affected by obesity. 14
A double-blind, randomized, placebo-controlled trial of the short-term effect of vitamin D3 supplementation on insulin sensitivity in apparently healthy, middle-aged, centrally obese men.
The impact of vitamin D on insulin sensitivity in centrally obese men was investigated. Seventy-one otherwise healthy, centrally obese men without diabetes, aged 35 years or greater participated in the double-blind, placebo-controlled trial. Participants consumed 120,000 IU calcitriol orally every two weeks or a placebo during the trial (under supervision). Hepatic fasting insulin sensitivity, postprandial insulin sensitivity (oral glucose insulin sensitivity (OGIS)), insulin secretion, lipid profile and blood pressure were measured at baseline and at 6 weeks. OGIS increased with supplementation (P=0.038; intention-to-treat analysis P=0.055). The age- and baseline-25-hydroxyvitamin D level-adjusted difference in change in OGIS was highly significant (mean difference 41.1±15.5; P=0.01). No changes in insulin secretion, basal indices of insulin sensitivity, blood pressure, or lipid profile were identified in either group. These results indicate that high-dose vitamin D improved insulin sensitivity in obese men. Further studies are needed to make recommendations about vitamin D supplementation for insulin sensitivity. 17
Prevention of nonvertebral fractures with oral vitamin D and dose dependancy: a meta-analysis of randomized controlled trials.
A meta-analysis of double-blind, randomized clinical trials investigated the efficacy of vitamin D supplements with or without calcium on nonvertebral fractures. Twelve trials investigating nonvertebral fractures were included (n=42,279) and eight trials investigating hip fractures were included (n=40,886). Participants received oral vitamin D supplements with or without calcium, calcium alone, or a placebo in the included trials. For all nonvertebral fracture trials, pooled relative risk (RR) of fracture was 0.86 (95% confidence interval [CI], 0.77-0.96). For hip fracture trials, the RR was 0.91 (95% CI, 0.78-1.05). However, these data demonstrate significant heterogeneity. For all trials, antifracture efficacy increases significantly with vitamin D dosage. For 400 IU/day or more supplemental vitamin D, the RR of nonvertebral fracture was 0.80 (95% CI 0.72-0.89, n=33,265 from 9 trials). Similarly, for doses of 400 IU/day or more supplemental vitamin D, the RR of hip fracture was 0.82 (95% CI 0.69-0.97, n=31,872 from 5 trials). Doses of vitamin D greater than 400 IU/day reduced nonvertebral fractures in community-dwelling individuals (-29%) and institutionalized older individuals (-15%), independent of calcium supplementation. This meta-analysis suggests that daily vitamin D supplements of 400 IU or greater may help reduce risk for nonvertebral and hip fracture. 15
Serum 25-hydroxyvitamin D concentrations and risk for hip fractures.
A nested case-control study investigated the relationship between serum vitamin D concentration at baseline and fracture risk. Participants were postmenopausal women (aged 50 to 79) not consuming estrogens or bone-active therapies. Four-hundred women who had suffered a hip fracture and 400 matched controls were included in the analysis. Serum vitamin D status was assessed at baseline and participants were followed for a median of 7.1 years to assess fracture risk. Mean vitamin D was lower in cases than in controls (55.95 nmol/L [SD, 20.28] vs. 59.60 nmol/L [SD, 18.05]; P=0.007). Lower vitamin D status was associated with a higher hip fracture risk (adjusted odds ratio for each 25-nmol/L decrease, 1.33 [95% CI, 1.06 to 1.68]). Comparing the lowest vitamin D concentrations (¡Ü47.5 nmol/L) to the highest concentrations (¡Ý70.7 nmol/L), revealed that women in the lowest vitamin D group had higher risk for hip fracture (adjusted odds ratio, 1.71 [CI, 1.05 to 2.79]). Risk for hip fracture increased significantly across quartiles of serum 25(OH) vitamin D concentration (P for trend=0.016). The risk reduction was found to be independent of number of falls, physical function, frailty, renal function, and sex-steroid hormone levels and seemed to be partially mediated by bone resorption. These results suggest that hip fracture risk may be increased by low vitamin D status. 20
Calcium- and vitamin D3- fortified milk reduces bone loss at clinically relevant skeletal sites in older men: a 2-year randomized controlled trial.
A two-year randomized clinical trial investigated the effects of calcium and vitamin D3 supplements on bone mineral density (BMD). One-hundred-forty-nine men aged 61.9±7.7 years completed the trial. Participants were randomly assigned to receive a daily low-fat milk product containing 1000 mg calcium and 800 IU vitamin D or no additional milk daily during the trial. The percentage change in BMD was 0.9 to 1.6% less in the milk supplemented group at the femoral neck, total hip, and ultradistal radius compared to the control group (range, p<0.08 to p<0.001 after adjusting for covariates). Compared to the control group, serum 25-(OH) D increased and parathyroid hormone decreased (31% and -18%, respectively; both p<0.001). Weight was unchanged in both groups. These results suggest that calcium plus vitamin D supplements may help to maintain BMD in older men. 22
Effect of cholecalciferol plus calcium on falling in ambulatory older men and women: a 3-year randomized controlled trial.
A randomized, double-blind, placebo-controlled trial investigated the effect of vitamin D (as cholecalciferol) plus calcium on falls in older men and women. Older adults living at home participated in the trial; 199 men and 246 women completed the trial. Participants were randomly assigned to receive 700 IU vitamin D and 500 mg calcium citrate malate or a placebo daily for three years. Low vitamin D levels were defined as serum 25-(OH) D less than 80 nmol/L. At baseline, serum vitamin D concentrations were 66.4±31.7 nmol/L in women and 82.9±34.9 in men. During the trial, 55% of women and 45% of men reported a fall. The odds of falling in women was significantly reduced by the vitamin D+calcium supplements (odds ratio [OR], 0.54; 95% confidence interval [CI], 0.30-0.97), but not in men (OR, 0.93; 95% CI, 0.50-1.72). Women who were less physically active than the median had the most pronounced reduction in risk for falling with the vitamin D+calcium supplements (OR, 0.35; 95% CI, 0.15-0.81). The results of this study indicate that long term vitamin D+calcium supplements reduce risk of falling for women but not for men. 23
Circulating vitamin D metabolites, polymorphism in vitamin D receptor, and colorectal adenoma risk.
The associations between serum levels of vitamin D, polymorphisms of the vitamin D receptor gene (VDR Taq I), and colorectal adenoma were investigated as part of the Prostate, Lung, Colorectal and Ovarian Cancer Screening trial. People with advanced adenoma of the distal large bowel and gender- and ethnicity-matched controls with a negative sigmoidoscopy were randomly selected. Genotype analysis of the VDR TaqI polymorphism was completed on 763 cases and 774 controls; serum levels of vitamin D were measured in 394 cases and 397 controls. The risk for advanced adenoma decreased by 73% in women (OR=0.27, 95% CI=0.11–0.69; P for trend=0.0002), comparing the highest quintile with the lowest quintile. The risk for advanced adenoma did not decrease in men, regardless of quintile (OR=1.10, 95% CI=0.60–2.05; P for trend=0.85). In women, current users of hormone replacement therapy (HRT) had significantly higher 25(OH)D levels than in former or never HRT users. These results suggest that higher serum 25(OH)D levels were associated with decreased adenoma risk for women. Serum 1,25(OH)2D and VDR TaqI genotype were not associated with adenoma risk. 19
Data collected in prior trials were analyzed to begin determining the dose response relationship between vitamin D and colorectal cancer. Dose-response gradients from observational studies of vitamin D intake and serum 25-hydroxyvitamin D were analyzed by plotting gradients as trend lines. The prediagnostic vitamin D intake or 25-hydroxyvitamin D concentration associated with 50% lower risk compared to <100 IU/day vitamin D or <13 ng/mL serum 25-hydroxyvitamin D was determined from the point on each linear trend line corresponding to an odds ratio of 0.50. Results suggest that intake of 1000 IU/day of vitamin D, half the safe upper intake established by the National Academy of Sciences, was associated with 50% lower risk for colorectal cancer. Serum 25-hydroxyvitamin D of 33 ng/mL, which is known to be safe, also was associated with 50% lower risk. 21
Optimal vitamin D status for colorectal cancer prevention: a quantitative meta analysis.
A meta-analysis of five studies evaluating the associations between serum vitamin D status and colorectal cancer incidence was completed. Data from the studies were pooled for analysis. Serum 25(OH) D concentrations were divided into quintiles with median concentrations of 6, 16, 22, 27, and 37 ng/mL. The lowest quintile was used as the reference. Odds ratio for colorectal cancer were 1.00, 0.82, 0.66, 0.59, and 0.46 (p(trend)<0.0001) for the quintiles from lowest to highest, respectively. Risk of colorectal cancer was reduced by 50% for a serum 25(OH)D level ±33 ng/mL, compared to ±12 ng/mL. The authors suggest that daily intake of 1000-2000 IU/day of vitamin D3 could significantly reduce risk for colorectal cancer. Since the results of this study contradict those of some other studies, further evaluation is necessary. However, the suggested daily intake is within the range of safe daily intake established by the National Academy of Sciences and may have significant benefits. 24
Fall prevention with supplemental and active forms of vitamin D: a meta-analysis of randomised controlled trials.
A meta-analysis of double-blind, randomized clinical trials investigated the efficacy of vitamin D supplements for fall prevention in elderly persons. The study included eight trials involving a total of 2,426 people with an average age of 65 years. Supplemental vitamin D (cholecalciferol or ergocalciferol) at a higher dose (700 to 1000 IU/day) was compared to a lower dose (200 to 600 IU/day). Heterogeneity was indicated for these two dose ranges (P=0.02). Higher intake of vitamin D decreased fall risk by 19% (pooled relative risk (RR) 0.81, 95% confidence interval (CI) 0.72 to 0.92; n=1921). Achieved serum 25(OH)D of 60 nmol/L or higher reduced risk of a fall by 23% (pooled RR 0.77, CI 0.65 to 0.90). The lower doses of vitamin D (200 to 600 IU/day) did not reduce fall risk. Active forms of vitamin D (1alpha-hydroxyvitamin D(3) or 1,25-dihydroxyvitamin D(3) reduced fall risk by 22% (pooled RR 0.78, 95% CI 0.64 to 0.94; n=624). The results of this meta-analysis indicate that supplemental vitamin D (cholecalciferol, ergocalciferol, or active forms) at a daily dose of 700 to 1000 IU significantly reduced risk for falls. Doses lower than 700 IU/day did not reduce risk.6
A higher dose of vitamin D reduces the risk of falls in nursing home residents: a randomized, multiple-dose study.
In a secondary analysis of data collected in a randomized, placebo-controlled trial investigated the effects of various doses of vitamin D on risk of falling in nursing home residents. One-hundred-twenty-four nursing home residents, average age 89 years, participated in the five month study. Participants were randomly assigned to receive 200, 400, 600, or 800 IU vitamin D or a placebo for the duration of the trial. The adjusted fall rate for the 800 IU group was decreased 72% relative to the placebo group (adjusted incidence rate ratio 0.28, 95% CI 0.11-0.75). No significant differences in adjusted fall rate versus placebo were found for the other supplement groups. This study indicated that a higher supplemental intake of vitamin D decreased falls in a high risk group. 16
Effects of ergocalciferol added to calcium on the risk of falls in elderly high-risk women.
A one-year population based study investigated the efficacy of vitamin D supplementation for risk of falling in elderly women. Three-hundred-two community dwelling women with serum 25-hydroxyvitamin D less than 24.0 ng/mL (aged 70 to 90 years) participated in the double-blind, randomized, placebo-controlled trial. Participants were randomly assigned to receive 1000 IU vitamin D (ergocalciferol) or a placebo daily for the duration of the trial. All participants received 1000 mg calcium citrate daily. Baseline height was significantly different between the vitamin D and placebo groups; results for falls were adjusted for this difference. Vitamin D supplements significantly reduced the risk of having at least 1 fall over 1 year (vitamin D group, 53.0%; control group, 62.9%; odds ratio (OR), 0.61; 95% confidence interval (CI), 0.37-0.99). When stratified by season, vitamin D supplements reduced the risk of having the first fall in winter and spring (vitamin D group, 25.2%; control group, 35.8%; OR, 0.55; 95% CI, 0.32-0.96). Vitamin D reduced the risk of having one fall (vitamin D group, 21.2%; control group, 33.8%; OR, 0.50; 95% CI, 0.28-0.88). Vitamin D did not reduce the risk for multiple falls. This study suggests that vitamin D supplementation can reduce the risk of falling in elderly women, especially during the winter. 13
Association between 25-hydroxyvitamin D levels and cognitive performance in middle-aged and older European men.
A population based, cross-sectional study investigated the associations between vitamin D and cognitive performance in 3,133 men aged 40 to 79 years. Participants were recruited from eight centers enrolled in the European Male Ageing Study. Serum 25(OH)D levels were measured by radioimmunoassay and cognitive function was assessed using the Rey-Osterrieth Complex Figure (ROCF) test, the Camden Topographical Recognition Memory (CTRM) test and the Digit Symbol Substitution Test (DSST). In age-adjusted regression with correction for confounders, 25(OH)D levels were associated with scores on the DSST (beta per 10 nmol/L=0.152; 95% CI 0.051 to 0.253). Further analysis indicated that this relationship was most pronounced at concentrations below 35 nmol/L. This study suggests that low levels of vitamin D may contribute to poor cognitive functioning. Further studies in this area are warranted. 7
Effects of vitamin D supplementation on symptoms of depression in overweight and obese subjects: randomized double blind trial.
This randomized double blind trial investigated the relationship between serum 25-hydroxyvitamin D (25-(OH) D) and depression in overweight and obese people. Overweight and obese men and women aged 21 to 70 years were recruited for the study; 441 people were enrolled in the trial. Participants consumed 20,000 IU vitamin D (as cholecalciferol), 40,000 IU vitamin D, or a placebo weekly for the duration of the one year trial. At baseline, participants with <40 nmol 25-(OH) D/L demonstrated more depressive symptoms than those with 40 nmol/L or higher [BDI total 6.0 (0–23) versus 4.5 (0–28) (median and range); BDI subscale 1–13 [2.0 (0–15) versus 1.0 (0–29.5)] (P < 0.05)]. After one year the vitamin D supplemented groups demonstrated significant improvements in depressive symptoms (p<0.01); the placebo group did not experience an improvement in symptoms. These results suggest that vitamin D status may play a role in depression, particularly in overweight or obese people. Both doses of vitamin D in this trial improved depressive symptoms. Additional trials are necessary to define the amount of vitamin D needed to improve symptoms. 18
Vitamin D supplementation enhances the beneficial effects of weight loss on cardiovascular disease risk markers.
A randomized, placebo-controlled, double-blind study investigated the effects of vitamin D supplementation on cardiovascular disease risk factors during weight loss. Two-hundred healthy overweight people (mean 25-hydroxy-vitamin D concentration 30 nmol/L at baseline) participated in the study. Participants were randomly assigned to receive either 83 mcg vitamin D daily or a placebo for 12 months. Vitamin D supplementation did not affect weight loss during the study (vitamin D –5.7 ± 5.8 kg vs placebo –6.4 ± 5.6 kg). In the vitamin D group, the decrease in parathyroid hormone was more pronounced than in the placebo group (-26.5% vs -18.7%, respectively, P=0.014). Tumor necrosis factor alpha decreased more in the vitamin D group than the placebo group (-10.2% vs. -3.2%, respectively, P=0.049). Triglycerides were reduced in the vitamin D group but increased slightly in the placebo group (-13.5% vs +3.0%, respectively, P<0.001). However, LDL cholesterol was significantly increased in the vitamin D group relative to placebo (+5.4% vs. -2.5%, respectively, P<0.001). In this study, vitamin D did not alter weight loss but had beneficial effects on markers of cardiovascular disease risk. 8
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