Serum 25-hydroxyvitamin D levels in vitamin D-insufficient hip fracture patients after supplementation with ergocalciferol and cholecalciferol. Ergocalciferol from mushrooms or supplements consumed with a standard meal increases 25-hydroxyergocalciferol but decreases 25-hydroxycholecalciferol in the serum of healthy adults. The Change in Plasma 25-Hydroxyvitamin D Did Not Differ between Breast-Fed Infants That Received a Daily Supplement of Ergocalciferol or Cholecalciferol for 3 Months1234 Supplementation with cholecalciferol does not result in weight reduction in overweight and obese subjects. Effect of cholecalciferol plus calcium on falling in ambulatory older men and women: a 3-year randomized controlled trial. Determinants of the Maternal 25-Hydroxyvitamin D Response to Vitamin D Supplementation During Pregnancy Effect of Vitamin D Supplementation on Obesity‐Induced Insulin Resistance: A Double‐Blind, Randomized, Placebo‐Controlled Trial Short and long-term variations in serum calciotropic hormones after a single very large dose of ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3) in the elderly. Response to Antenatal Cholecalciferol Supplementation Is Associated With Common Vitamin D–Related Genetic Variants Vitamin D supplementation has no major effect on pain or pain behavior in bedridden geriatric patients with advanced dementia Evaluation of ergocalciferol or cholecalciferol dosing, 1,600 IU daily or 50,000 IU monthly in older adults. The response of elderly veterans to daily vitamin D3 supplementation of 2,000 IU: a pilot efficacy study. Insulin-like growth factor I, growth hormone, and insulin sensitivity: the effects of a one-year cholecalciferol supplementation in middle-aged overweight and obese subjects Patients with Nonalcoholic Fatty Liver Disease Have a Low Response Rate to Vitamin D Supplementation. Impact of vitamin D supplementation during a resistance training intervention on body composition, muscle function, and glucose tolerance in overweight and obese adults. Vitamin D status and effect of low-dose cholecalciferol and high-dose ergocalciferol supplementation in multiple sclerosis Effect of Vitamin D Supplementation on Blood Pressure in Blacks Supplements of 20 microg/d cholecalciferol optimized serum 25-hydroxyvitamin D concentrations in 80% of premenopausal women in winter. Bread fortified with cholecalciferol increases the serum 25-hydroxyvitamin D concentration in women as effectively as a cholecalciferol supplement. Nutritional vitamin D supplementation in dialysis: a randomized trial. Impact of cholecalciferol treatment on biomarkers of inflammation and myocardial structure in hemodialysis patients without hyperparathyroidism. Effects of ergocalciferol added to calcium on the risk of falls in elderly high-risk women. Long-term bioavailability after a single oral or intramuscular administration of 600,000 IU of ergocalciferol or cholecalciferol: implications for treatment and prophylaxis. The level of serum anti-Müllerian hormone correlates with vitamin D status in men and women but not in boys. Cholecalciferol supplementation does not influence β-cell function and insulin action in obese adolescents: a prospective double-blind randomized trial. Maternal vitamin D supplementation to improve the vitamin D status of breast-fed infants: a randomized controlled trial. Vitamin D treatment in primary hyperparathyroidism: a randomized placebo controlled trial. Ergocalciferol supplementation in children with CKD delays the onset of secondary hyperparathyroidism: a randomized trial. The tolerability and biochemical effects of high‐dose bolus vitamin D2 and D3 supplementation in patients with vitamin D insufficiency
Vitamin D insufficiency is commonly associated with hip fracture . However , the equipotency of ergocalciferol and cholecalciferol supplementation in this patient group has not been studied in a r and omized trial using high-performance liquid chromatography ( HPLC ) measurement of serum 25-hydroxyvitamin D ( 25OHD ) . The objective of this study was to determine if ergocalciferol and cholecalciferol are equipotent therapies in vitamin D-insufficient hip fracture patients . Ninety five hip fracture in patients with vitamin D insufficiency ( 25OHD<50 nmol/L ) were r and omized , double-blind , to treatment with ergocalciferol 1000 IU/day ( n=48 ) or cholecalciferol 1000 IU/day ( n=47 ) for three months . All participants were also given a placebo matching the alternative treatment to maintain blinding of treatment allocation . The primary endpoint was total serum 25OHD measured by HPLC . Secondary endpoints included 25OHD measured by radioimmunoassay ( RIA ) , intact parathyroid hormone ( iPTH ) , and bioactive ( 1 - 84 ) whole PTH ( wPTH ) .  Seventy patients ( 74 % ) completed the study with paired sample s for analysis . Cholecalciferol supplementation result ed in a 31 % greater increase in total HPLC-measured 25OHD ( p=0.010 ) and 52 % greater rise in RIA-measured 25OHD ( p<0.001 ) than supplementation with an equivalent dose of ergocalciferol . Changes in iPTH and wPTH were not significantly different between calciferol treatments ( p>0.05 ) . In vitamin D-insufficient hip fracture patients , supplementation with cholecalciferol 1000 IU/day for three months was more effective in increasing serum 25OHD than an equivalent dose of ergocalciferol . However , the lack of difference in PTH lowering between calciferol treatments raises questions about the biological importance of this observation Few foods contain ergocalciferol or cholecalciferol . Treatment of mushrooms with UV light increases ergocalciferol content and could provide a dietary source of vitamin D. We evaluated the impact of consuming UV-treated white button mushrooms ( Agaricus bisporus ) on the vitamin D status of healthy adults . Thirty-eight volunteers were r and omized to 4 treatments consumed with a st and ard meal for 6 wk : the control ( C ) group received untreated mushrooms providing 0.85 μg/d ergocalciferol ( n = 10 ) ; groups M1 and M2 received UV-treated mushrooms providing 8.8 ( n = 10 ) and 17.1 μg/d ( n = 9 ) , respectively ; and the supplement ( S ) group received purified ergocalciferol plus untreated mushrooms , providing a total of 28.2 μg/d ( n = 9 ) . Serum total 25-hydroxyvitamin D [ 25(OH)D ] and 25-hydroxyergocalciferol [ 25(OH)D2 ] were 83 ± 38 and 2.4 ± 2.0 nmol/L , respectively , at baseline ( mean ± SD ) . At wk 6 , 25(OH)D2 had increased and was higher in all treatment groups than in the C group , whereas 25-hydroxycholecalciferol [ 25(OH)D3 ] had decreased and was lower in the M2 and S groups than in the C group . Increases in 25(OH)D2 for groups C , M1 , M2 , and S were 1.2 ± 5.2 , 13.8 ± 7.3 , 12.7 ± 3.7 , and 32.8 ± 3.3 nmol/L and decreases in 25(OH)D3 were -3.9 ± 16.3 , -10.4 ± 6.4 , -20.6 ± 14.6 , and -29.5 ± 15.9 nmol/L , respectively . Concentrations did not change in group C. In summary , ergocalciferol was absorbed and metabolized to 25(OH)D2 but did not affect vitamin D status , because 25(OH)D3 decreased proportionally The biological equivalency of ergocalciferol ( D2 ) and cholecalciferol ( D3 ) has been debated ; several comparisons have appeared in the adult literature but are scarce in pediatrics . The objective of this study was to compare increases in plasma 25-hydroxyvitamin D [ 25(OH)D ] concentrations and attainment of 50 and 75 mol/L status cutoffs following 3 mo of daily supplementation with D2 compared with D3 .  Healthy , breast-fed , 1-mo-old infants ( n = 52 ) received 10 μg ( 400 ic ) of either D2 or D3 daily . At 1 and 4 mo of age , plasma 25-hydroxyergocalciferol and 25-hydroxycholecalciferol concentrations were determined by liquid chromatography t and em MS ( LC-MS/MS ) and total 25(OH)D by chemiluminescent immunoassay ( DiaSorin Liaison ) . Data were analyzed using t tests and χ2 by intent to treat . A total of 23 % of infants were deficient ( ≤24.9 nmol/L ) at baseline and 2 % at follow-up on the basis of LC-MS/MS . At 4 mo , 96 % were breastfed and there were no differences in compliance , breastfeeding rates , or sun exposure among groups . The change in total 25(OH)D measured by LC-MS/MS did not differ between the D2 ( 17.6 ± 26.7 nmol/L ) and D3 ( 22.2 ± 20.2 nmol/L ) groups . In the combined groups , the baseline plasma 25(OH)D concentration was inversely related to the change in total 25(OH)D ( r = −0.52 ; P < 0.001 ) . Overall , 86 % of infants met the 50 nmol/L cutoff at follow-up ; however , fewer infants in the D2 group ( 75 % ) met this level compared with the D3 group ( 96 % ) ( P < 0.05 ) . Similar results were obtained by immunoassay . In conclusion , the increase in the 25(OH)D concentration among the D2 and D3 groups did not differ , suggesting daily intake of either isoform is acceptable for infants < 4 mo OBJECTIVE Investigate whether cholecalciferol supplementation leads to weight loss in overweight and obese adults . DESIGN R and omized double blind clinical trial with 20,000 IU cholecalciferol twice a week , or 20,000 IU once a week plus placebo , or placebo twice a week , for 12 months . All subjects were given 500 mg calcium supplementation . METHODS Four hundred and forty five healthy , overweight , and obese men and women ( age 21 - 70 years , body mass index ( BMI ) 28.0 - 47.0 kg/m(2 ) ) .  Body weight , fatness , and fat distribution parameters were measured by dual-energy X-ray absorptiometry and anthropometry , blood sample s and 24-h urinary sample s were collected . RESULTS At baseline , there were no significant differences between the groups , but there was a significant inverse relation between serum 25-hydroxyvitamin D ( 25(OH)D ) levels and BMI , and a significant positive association between calorie intake and BMI .  Three hundred and thirty four subjects completed the study . During the study , there was no significant change in weight , waist-to-hip ratio ( WHR ) or percentage body fat in any of the groups , nor between them . Parathyroid hormone decreased and 25(OH)D increased significantly in both groups receiving cholecalciferol , and serum levels of 25(OH)D stabilized after 3 months . Serum calcium was unchanged in all groups . Urinary calcium excretion increased in all groups , but there was no significant difference between the groups . Weekly dosage of 20,000 - 40,000 IU cholecalciferol for 12 months was associated with a low risk of adverse effects , at least in overweight and obese adults living at latitude 70 degrees N. CONCLUSION Significant weight reduction in overweight and obese subjects is unlikely to occur with cholecalciferol supplementation BACKGROUND A recent meta- analysis found that cholecalciferol ( vitamin D ) should reduce falls by more than 20 % . However , little is known about whether supplemental cholecalciferol plus calcium citrate malate will lower the long-term risk of falling in men , active older individuals , and older individuals with higher 25-hydroxyvitamin D levels . METHODS We studied the effect of 3-year supplementation with cholecalciferol-calcium on the risk of falling  at least once in 199 men and 246 women 65 years or older and living at home . Individuals received 700 IU of cholecalciferol plus 500 mg of calcium citrate malate per day or placebo in a r and omized double-blind manner . Subjects were classified as less physically active if physical activity was below the median level . Low 25-hydroxyvitamin D levels were classified as those below 32 ng/mL ( < 80 nmol/L ) . RESULTS In 3 years , 55 % of women and 45 % of men reported at least 1 fall . Mean + /- SD baseline 25-hydroxyvitamin D levels were 26.6 + /- 12.7 ng/mL ( 66.4 + /- 31.7 nmol/L ) in women and 33.2 + /- 14.2 ng/mL ( 82.9 + /- 34.9 ) in men . Cholecalciferol-calcium significantly reduced the odds of falling in women ( 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 ) . Fall reduction was most pronounced in less active women ( OR , 0.35 ; 95 % CI , 0.15 - 0.81 ) . Baseline 25-hydroxyvitamin D level did not modulate the treatment effect . CONCLUSIONS Long-term dietary cholecalciferol-calcium supplementation reduces the odds of falling in ambulatory older women by 46 % , and especially in less active women by 65 % . Supplementation had a neutral effect in men independent of their physical activity level Context : Current approaches to antenatal vitamin D supplementation do not account for interindividual differences in 25-hydroxyvitamin D ( 25(OH)D ) response . Objective : We assessed which maternal and environmental characteristics were associated with 25(OH)D after supplementation with cholecalciferol . Design : Within-r and omization-group analysis of participants in the Maternal Vitamin D Osteoporosis Study trial of vitamin D  supplementation in pregnancy . Setting : Hospital antenatal clinics . Participants : A total of 829 pregnant women ( 422 placebo , 407 cholecalciferol ) . At 14 and 34 weeks of gestation , maternal anthropometry , health , and lifestyle were assessed and 25(OH)D measured . Compliance was determined using pill counts at 19 and 34 weeks . Interventions : 1000 IU/d of cholecalciferol or matched placebo from 14 weeks of gestation until delivery . Main Outcome Measure : 25(OH)D at 34 weeks , measured in a single batch ( Diasorin Liaison ) . Results : 25(OH)D at 34 weeks of gestation was higher in the women r and omized to vitamin D ( mean [ SD ] , 67.7 [ 21.3 ] nmol/L ) compared with placebo ( 43.1 [ 22.5 ] nmol/L ; P < .001 ) . In women r and omized to cholecalciferol , higher pregnancy weight gain from 14 to 34 weeks of gestation ( kg ) ( β = −0.81 [ 95 % confidence interval −1.39 , −0.22 ] ) , lower compliance with study medication ( % ) ( β = −0.28 [ −0.072 , −0.48 ] ) , lower early pregnancy 25(OH)D ( nmol/L ) ( β = 0.28 [ 0.16 , 0.40 ] ) , and delivery in the winter vs the summer ( β = −10.5 [ −6.4 , −14.6 ] ) were independently associated with lower 25(OH)D at 34 weeks of gestation . Conclusions : Women who gained more weight during pregnancy had lower 25(OH)D in early pregnancy and delivered in winter achieved a lower 25(OH)D in late pregnancy when supplemented with 1000 IU/d cholecalciferol . Future studies should aim to determine appropriate doses to enable consistent repletion of 25(OH)D during pregnancy Objective The aim was to investigate whether vitamin D supplementation , combined with a hypocaloric diet , could have an independent effect on insulin sensitivity in subjects with both overweight and hypovitaminosis D. Changes from baseline in anthropometric parameters , body composition , glucose tolerance , and insulin secretion were considered as secondary outcomes . Methods Eighteen volunteers who were nondiabetic and vitamin D deficient and had BMI > 25 kg/m2 were r and omized ( 1:1 ) in a double‐blind manner to a hypocaloric diet + either oral cholecalciferol at 25,000 IU/wk or placebo for 3 months . Hyperinsulinemic‐euglycemic clamp to measure insulin sensitivity  was performed at baseline and after intervention . Results Body weight in both groups decreased significantly ( −7.5 % in the vitamin D group and −10 % in the placebo group ; P < 0.05 for both ) , with no between‐group differences . Serum 25‐hydroxyvitamin D levels in the vitamin D group increased considerably ( from 36.7 ± 13.2 nmol/L to 74.8 ± 18.7 nmol/L ; P < 0.001 ) . Insulin sensitivity in the vitamin D group improved ( from 4.6 ± 2.0 to 6.9 ± 3.3 mg·kg−1·min−1 ; P < 0.001 ) , whereas no changes were observed in the placebo group ( from 4.9 ± 1.1 to 5.1 ± 0.3 mg·kg−1·min−1 ; P = 0.84 ) . Conclusions Cholecalciferol supplementation , combined with a weight loss program , significantly improves insulin sensitivity in healthy subjects with obesity and might represent a personalized approach for insulin‐resistant subjects with obesity CONTEXT In humans , few studies have compared the potencies of ergocalciferol and cholecalciferol in improving and maintaining vitamin D status . OBJECTIVE Our objective was to evaluate the effects of a single very large dose of both calciferols on serum changes of 25-hydroxyvitamin D [ 25(OH)D ] , 1,25-dihydroxyvitamin D [ 1,25(OH)(2)D ] , ionized calcium , and parathyroid hormone ( PTH ) at baseline , and at 3 , 7 , 30 , and 60 d. DESIGN This was a prospect i ve r and omized intervention study . SETTING The study was performed in a nursing home residence . PARTICIPANTS A total of 32 elderly female patients ( age range 66 - 97 yr ) , with vitamin D deficiency was included in the study . INTERVENTION Participants were r and omized into four groups of eight to receive a single dose of 300,000 IU ergocalciferol or cholecalciferol by oral ( os ) or i m route . RESULTS 25(OH)D levels sharply increased at d 3 only when vitamins were given os . The 30-d basal difference in serum 25(OH)D was significantly greater after cholecalciferol os administration ( 47.8 + /- 7.3 ng/ml ) compared with other forms ( D(3 ) i m : 15.9 + /- 11.3 ; D(2 ) os : 17.3 + /- 4.7 ; D(2 ) i m : 5 + /- 4.4 ; all P < 0.001 ) . The area under the curve ( AUC ) of the serum 25(OH)D against time ( AUC(60 ) ) was : D(3 ) os , 3193 + /- 759 ng x d/ml vs. D(2 ) os , 1820 + /- 512 , P < 0.001 ; and D(3 ) i m , 1361 + /- 492 vs. D(2 ) i m , 728 + /- 195 , P < 0.01 . 25(OH)D significantly influences PTH levels at 3 ( P < 0.03 ) , 7 ( P < 0.01 ) , 30 ( P < 0.01 ) , and 60 d ( P < 0.05 ) . At 60 d , the form of vitamin ( cholecalciferol ) significantly lowers PTH levels ( P = 0.037 ) . CONCLUSIONS Cholecalciferol is almost twice as potent as ergocalciferol in increasing serum 25(OH)D , when administered either by mouth or i m . 25(OH)D plays a role in modulating serum PTH Context : Single-nucleotide polymorphisms ( SNPs ) in genes related to vitamin D metabolism have been associated with serum 25-hydroxyvitamin D [ 25(OH)D ] concentration , but these relationships have not been examined following antenatal cholecalciferol supplementation . Objective : To determine whether SNPs in DHCR7 , CYP2R1 , CYP24A1 , and GC are associated with the response to gestational cholecalciferol supplementation . Design : Within-r and omization group analysis of the Maternal Vitamin D Osteoporosis Study trial of antenatal cholecalciferol supplementation . Setting : Hospital antenatal clinics . Participants : In total , 682 women of white ethnicity ( 351 placebo , 331 cholecalciferol ) were included . SNPs at rs12785878 ( DHCR7 ) , rs10741657 ( CYP2R1 ) , rs6013897 ( CYP24A1 ) , and rs2282679 ( GC ) were genotyped . Interventions : 1000 IU/d cholecalciferol from 14 weeks of gestation until delivery . Main Outcome Measure : 25(OH)D at r and omization and 34 weeks of gestation were measured in a single batch ( Liaison ; Diasorin , Dartford , UK ) . Associations between 25(OH)D and the SNPs were assessed by linear regression using an additive model [ β represents the change in 25(OH)D per additional common allele ] . Results : Only rs12785878 ( DHCR7 ) was associated with baseline 25(OH)D [ β = 3.1 nmol/L ; 95 % confidence interval ( CI ) , 1.0 to 5.2 nmol/L ; P < 0.004 ] . In contrast , rs10741657 ( CYP2R1 ) ( β = −5.2 nmol/L ; 95 % CI , −8.2 to −2.2 nmol/L ; P = 0.001 ) and rs2282679 ( GC ) ( β = 4.2 nmol/L ; 95 % CI , 0.9 to 7.5 nmol/L ; P = 0.01 ) were associated with achieved 25(OH)D status following supplementation , whereas rs12785878 and rs6013897 ( CYP24A1 ) were not . Conclusions : Genetic variation in DHCR7 , which encodes 7-dehyrocholesterol reductase in the epidermal vitamin D bio synthesis pathway , appears to modify baseline 25(OH)D. In contrast , the response to antenatal cholecalciferol supplementation was associated with SNPs in CYP2R1 , which may alter 25-hydroxylase activity , and GC , which may affect vitamin D binding protein synthesis or metabolite affinity Background and aims : In a few , earlier , uncontrolled trials , alleviation of  chronic pain  has been documented by vitamin D supplementation . This r and omized double-blind placebo controlled trial addressed the association between pain and vitamin D deficiency and the effects of vitamin D supplementation on pain in institutionalized aged patients . Methods : 216 long-term care patients were enrolled in Helsinki , Finl and . Pain was assessed by three tools : Resident Assessment Instrument ( RAI ) , Discomfort Behavior Scale , and Pain Assessment in Advanced Dementia Scale . Scores for Cognitive Performance Scale ( CPS ) and other clinical assessment s were also collected from the RAI- data base . Levels of 25-hydroxyvitamin D ( 25-OHD ) and parathyroid hormone were also determined . Patients in pain ( n=202 ) were r and omized into three treatment groups , each receiving 0 , 400 , or 1200 IU cholecalciferol per day , respectively . Assessment s were repeated after six-month vitamin D supplementation . Results : Patients were aged ( 84.5±7.5 yrs ) , demented ( CPS= 4.9±1.4 , range 1–6 ) , and chronically bedridden .  Pain was present in 38.4 % to 83.8 % of patients depending on assessment tool . Low 25-OHD levels ( < 50 nmol/L ) were very common ( 98.1 % ) . However , vitamin D deficiency was not associated with pain or pain behavior . The supplementation result ed in a marked increase in 25-OHD levels . However , neither prevalence of painlessness nor pain scores changed significantly after vitamin D supplementation . Conclusions : We were not able either to show an association between vitamin D deficiency and pain or to observe alleviation of pain by vitamin D supplementation . The independent role of vitamin D in the etiology of pain remains controversial CONTEXT Whether ergocalciferol ( D(2 ) ) and cholecalciferol ( D(3 ) ) are equally effective to increase and maintain serum 25-hydroxyvitamin D [ 25(OH)D ] concentration is controversial . OBJECTIVE The aim of the study was to evaluate the effect of daily and once monthly dosing of D(2 ) or D(3 ) on circulating 25(OH)D and serum and urinary calcium . DESIGN , SETTING AND PARTICIPANTS In a university clinical research setting , 64 community dwelling adults age 65 + were r and omly assigned to receive daily ( 1,600 IU ) or once-monthly ( 50,000 IU ) D(2 ) or D(3 ) for 1 yr . MAIN OUTCOME MEASURES Serum 25(OH)D , serum calcium , and 24-h urinary calcium were measured at months 0 , 1 , 2 , 3 , 6 , 9 , and 12 . Serum PTH , bone-specific alkaline phosphatase , and N-telopeptide were measured at months 0 , 3 , 6 , and 12 . RESULTS Serum 25(OH)D was less than 30 ng/ml in 40 % of subjects at baseline ; after 12 months of vitamin D dosing , levels in 19 % of subjects ( n = 12 , seven receiving daily doses and five monthly doses ) remained low , despite compliance of more than 91 % . D(2 ) dosing increased 25(OH)D(2 ) but produced a decline ( P < 0.0001 ) in 25(OH)D(3 ) . Substantial between-individual variation in 25(OH)D response was observed for both D(2 ) and D(3 ) . The highest 25(OH)D observed was 72.5 ng/ml . Vitamin D administration did not alter serum calcium , PTH , bone-specific alkaline phosphatase , N-telopeptide , or 24-h urine calcium . CONCLUSIONS Overall , D(3 ) is slightly , but significantly , more effective than D(2 ) to increase serum 25(OH)D. One year of D(2 ) or D(3 ) dosing ( 1,600 IU daily or 50,000 IU monthly ) does not produce toxicity , and 25(OH)D levels of less than 30 ng/ml persist in approximately 20 % of individuals . Substantial between-individual response to administered vitamin D(2 ) or D(3 ) is observed OBJECTIVES To determine the prevalence of hypovitaminosis D ( serum 25-hydroxyvitamin D<32 ng/mL ; HVD ) in a population of elderly veterans and conduct a preliminary assessment of the efficacy of supplementation with cholecalciferol in correcting HVD . DESIGN R and omized , double-blind , placebo-controlled clinical trial . SETTING Geriatric clinic at the Bruce W. Carter Veterans Affairs Medical Center , Miami , Florida . PARTICIPANTS Veterans aged 70 and older . INTERVENTION Oral cholecalciferol 2,000 IU daily or placebo for 6 months . MEASUREMENTS Serum calcium , 25-hydroxyvitamin D , parathyroid hormone , and 24-hour urinary calcium . RESULTS Of the 34 participants who completed the study , 62 % had HVD at baseline . In the treatment group , mean serum 25-hydroxyvitamin D level rose from 28.4±7.9 ng/mL at baseline to 42.7±10.5 ng/mL at the end of the trial , but levels remained less than 32 ng/mL in three of 17 ( 18 % ) of the participants . In the placebo group , the baseline level of 27.7±8.3 ng/mL remained unchanged ( 28.8±8.7 ng/mL ) . Supplementation did not alter serum or urinary calcium levels and did not result in any adverse events . CONCLUSION These initial observations suggest that , in older veterans  , cholecalciferol 2,000 IU daily for 6 months is generally safe and corrects HVD in most but not all individuals Both altered GH-IGF-I axis and low serum levels of 25-hydroxyvitamin D ( 25(OH)D ) are linked to measures of metabolic syndrome . Our hypothesis was that there is a relation between GH , IGF-I , and 25(OH)D ; and that vitamin D supplementation may have an effect on the levels of GH , IGF-I , and IGF-I/IGFBP-3 ratio . 318 overweight and obese subjects completed a one-year r and omized intervention with either 40,000 or 20,000 IU cholecalciferol per week or placebo .  GH , IGF-I , IGFBP-3 and measures of insulin resistance were evaluated at baseline and at the end of study . There was a significant relation between entities of GH-IGF-I axis and insulin resistance .  Subjects with severe obesity had significantly lower serum 25(OH)D and had a significant linear decline in IGF-I/IGFBP-3 ratio with increasing serum 25(OH)D quartiles . Vitamin D status was an independent predictor of GH-IGF-I axis and supplementation with vitamin D decreased IGF-I/IGFBP-3 ratio in subjects without severe obesity . No corresponding effect of vitamin D supplementation on BMI or insulin resistance was observed . Adverse effects of GH-IGF-I axis on glucose metabolism and the development of metabolic syndrome may be in part associated with the changes in vitamin D status Background : Hypovitaminosis D is associated with an increased severity of nonalcoholic fatty liver disease ( NAFLD ) , but reports on the response to cholecalciferol ( vitamin D3 ) supplementation are conflicting . Objective : The objective of this study was to determine if st and ard vitamin D3 supplementation is effective in NAFLD with hypovitaminosis D. Methods : Sixty-five well-characterized adults [ age ( mean ± SD ) : 51.6 ± 12.3 y ] with biopsy-proven NAFLD were screened . Forty-two patients ( the ratio of men to women was 13:29 ) had hypovitaminosis D ( plasma 25-hydroxyvitamin D [ 25(OH)D ] < 30 ng/mL ) . An observational study was performed in NAFLD patients with hypovitaminosis D treated with 2000 IU cholecalciferol ( vitamin D3 ) daily for 6 mo per clinical practice . Plasma 25(OH)D , hepatic and metabolic panels , and metabolic syndrome components were assessed before and after cholecalciferol supplementation . Body composition was measured by using bioelectrical impedance analysis . The primary outcome measure was plasma 25(OH)D ≥30 ng/mL at the end of the study . Secondary outcomes included change in serum transaminases , fasting plasma glucose , and insulin and homeostasis model assessment of insulin resistance ( HOMA-IR ) . Chi-square , Student 's t tests , correlation coefficient , and multivariate analysis were performed . Results : Twenty-six ( 61.9 % ) patients had nonalcoholic steatohepatitis ( NASH ) , and 16 ( 38.1 % ) had hepatic steatosis . After 6 mo of cholecalciferol supplementation  , plasma 25(OH)D ≥30 ng/mL was observed in 16 subjects ( 38.1 % ; responders ) whereas the remaining 26 patients ( 61.9 % ) were nonresponders with plasma 25(OH)D < 30 ng/mL. Significantly fewer ( P < 0.01 ) patients with NASH were responders ( 4 of 26 , 15.4 % ) than those with hepatic steatosis ( 12 of 16 , 75 % ) . Baseline fasting serum alanine aminotransferase , plasma glucose , and HOMA-IR were similar in the responders and nonresponders , but the NASH score on the liver biopsy was lower ( 16.5 % ) in the responders ( P < 0.001 ) . Nonresponders had a higher fat mass ( 10.5 % ) and lower fat-free mass ( 10.4 % ) than responders did . End-of-treatment alanine aminotransferase and HOMA-IR improved only in responders . The baseline HOMA-IR and histological NASH score were independent predictors of nonresponse to cholecalciferol supplementation . Conclusions : Daily supplementation with 2000 IU cholecalciferol for 6 mo did not correct hypovitaminosis D in the majority of patients with NASH . Further studies are needed to determine if higher doses are effective . This trial was registered at clinical trials.gov as 13 - 00153 BACKGROUND & AIMS The impact of vitamin D supplementation in overweight and obese adults during resistance training on body composition , muscle function , and glucose tolerance was investigated . METHODS Twenty-three overweight and obese ( age : 26.1±4.7 y ; BMI : 31.3±3.2 kg/m(2 ) ; 25-hydroxyvitamin D : 19.3±7.2 ng/mL ) adults were recruited for participation in a double-blind , placebo-controlled trial . Participants were r and omly divided into vitamin D ( VitD , 4000 IU/d ; 5 females , 5 males ) and placebo ( PL ; 7 females , 6 males ) groups . Both groups completed 12 weeks of resistance training . 25-hydroxyvitamin D , parathyroid hormone , body composition , and glucose tolerance were assessed at baseline and 12 weeks . Muscle function ( strength and power ) was assessed at baseline , 4 , 8 , and 12 weeks . RESULTS During the intervention , 25-hydroxyvitamin D increased and parathyroid hormone decreased in the VitD group ( P<0.05 ) . Peak power was significantly increased at 4 weeks in the VitD group only ( P<0.05 ) . Regression analysis revealed an inverse association between the change in 25-hydroxyvitamin D with the change in waist-to-hip ratio ( R(2)=0.205 , P=0.02 ) . No other improvements were observed with supplementation . CONCLUSIONS Vitamin D supplementation in overweight and obese adults during resistance training induced an early improvement in peak power , and elevated vitamin D status was associated with reduced waist-to-hip ratio . CLINICAL TRIAL REGISTRATION NUMBER NCT01199926 Background Vitamin D is important for bone health and immune regulation , and has been shown to be low in multiple sclerosis ( MS ) . We sought to determine the effect of over the counter low dose cholecalciferol ( LDC ) and high dose ergocalciferol ( HDE ) on the vitamin D levels in MS patients . Methods We retrospectively evaluated serum 25-hydroxy-vitamin D [ 25(OH)D ] levels of 199 patients ( CIS , n = 32 ; RRMS , n = 115 ; PPMS , n = 10 ; SPMS , n = 16 ; Transverse Myelitis ( TM ) , n = 9 ; other neurological diseases , n = 16 ) attending our clinic between 2004 and 2008 . We examined the change in  25(OH)D levels in 40 MS patients who took either LDC ( ≤800 IU/day ) or HDE ( 50,000 IU/day for 7 - 10 days , followed by 50,000 IU weekly or biweekly ) . Results The average 25(OH)D level was 71 ± 39 nmol/L ( Mean ± SD ) , and 167(84 % ) patients had insufficient levels ( ≤100 nmol/L ) of 25(OH)D. The patients supplemented with LDC did not have a significant increase in their 25(OH)D levels . However , 25(OH)D levels increased by 42 nmol/L ( P = 0.01 ) in the patients originally taking LDC and then prescribed HDE . Optimal levels ( ≥100 nmol/L ) were only achieved in less than 40 % of patients . Conclusions We conclude that large numbers of patients with MS and TM in our cohort are deficient in vitamin D. HDE significantly elevated 25(OH)D levels in MS patients and was more effective at increasing 25(OH)D levels than LDC . Prospect i ve studies are required to determine appropriate dosing regimen to achieve optimal levels in the majority of MS patients and to ascertain the safety , immunological response , and ultimately the clinical efficacy of vitamin D replacement therapy Blacks have significantly higher rates of hypertension than whites , and lower circulating levels of 25-hydroxyvitamin D. There are few data about the effect of vitamin D3 ( cholecalciferol ) supplementation on  blood pressure in blacks . During 2 winters from 2008 to 2010 , 283 blacks ( median age , 51 years ) were r and omized into a 4-arm , double-blind trial for 3 months of placebo , 1000 , 2000 , or 4000 international units of cholecalciferol per day . At baseline , 3 months , and 6 months , systolic and diastolic pressure and 25-hydroxyvitamin D were measured . The 3-month follow-up was completed in 250 ( 88 % ) participants . The difference in systolic pressure between baseline and 3 months was + 1.7 mm Hg for those receiving placebo , −0.66 mm Hg for 1000 U/d , −3.4 mm Hg for 2000 U/d , and −4.0 mm Hg for 4000 U/d of cholecalciferol ( −1.4 mm Hg for each additional 1000 U/d of cholecalciferol ; P=0.04 ) . For each 1-ng/mL increase in plasma 25-hydroxyvitamin D , there was a significant 0.2-mm Hg reduction in systolic pressure ( P=0.02 ) . There was no effect of cholecalciferol supplementation on diastolic pressure ( P=0.37 ) . Within an unselected population of blacks , 3 months of oral vitamin D3 supplementation significantly , yet modestly , lowered systolic pressure . Future trials of vitamin D supplementation  on blood pressure are needed to confirm these promising results , particularly among blacks , a population for whom vitamin D deficiency may play a more specific mechanistic role in the pathogenesis of hypertension The serum 25-hydroxyvitamin D [ 25(OH)D ] response to daily supplementation with 20 microg cholecalciferol ( D3 ) during winter in predominantly white premenopausal women living in Maine was measured and the effects of body composition and hormonal contraceptive use on baseline serum 25(OH)D concentrations and the response to supplementation were examined . A total of 112 women ( 22.2 + /- 3.7 y old ) received placebo from March 2005 until September 2005 when they were r and omized to receive either placebo or 20 microg/d D3 through February 2006 . Eighty-six women completed the study .  Actual mean D3 content of the supplements was 22 microg per capsule . In February 2005 the serum 25(OH)D concentration was 62.0 + /- 23.4 nmol/L ( mean + /- SD ) . Serum 25(OH)D concentrations increased by 35.3 + /- 23.2 nmol/L from February 2005 to February 2006 in the treatment group , significantly more than the 10.9 + /- 16.9 nmol/L increase in the placebo group . Treatment group , magnitude of summer increase in 25(OH)D , estrogen dose , and baseline serum 25(OH)D concentrations , but not body fat , were significant predictors of the 1-y change in 25(OH)D concentrations used to assess the magnitude of the response to supplementation . Daily supplementation with 20 microg D3 during winter achieved optimal 25(OH)D concentrations ( > or = 75 nmol/L ) in 80 % of participants , indicating that this dose is adequate to optimize vitamin D status in most young women in Maine Fortification of foods is a feasible way of preventing low vitamin D status .  Bread could be a suitable vehicle for fortification because it is a common part of diets worldwide . The bioavailability of cholecalciferol from bread is not known . We studied cholecalciferol stability , the concentration of the added cholecalciferol , the dispersion of cholecalciferol in bread , and the bioavailability of cholecalciferol from fortified bread . Three batches of fortified low-fiber wheat and high-fiber rye breads were baked ; from each batch , 3 sample s of dough and bread were analyzed for their cholecalciferol content . In a single-blind bioavailability study , 41 healthy women , 25 - 45 y old , with mean serum 25-hydroxyvitamin D concentration 29 nmol/L ( range 12 - 45 nmol/L ) , were r and omly assigned to 4 study groups . Each group consumed fortified wheat bread , fortified rye bread , regular wheat bread ( control ) , or regular wheat bread and a cholecalciferol supplement ( vitamin D control ) daily for 3 wk . The daily dose of vitamin D was 10 mug in all groups except the control group . The vitamin dispersed evenly in the breads and was stable . Both fortified breads increased serum 25-hydroxyvitamin D concentration as effectively as the cholecalciferol supplement . Supplementation or fortification did not affect serum intact parathyroid hormone concentration or urinary calcium excretion . In conclusion , fortified bread is a safe and feasible way to improve vitamin D nutrition BACKGROUND AND OBJECTIVES Vitamin D ( 25-hydroxyvitamin D ; 25[OH]D ) deficiency is common in patients initiating long-term hemodialysis , but the safety and efficacy of nutritional vitamin D supplementation in this population remain uncertain . DESIGN , SETTING , PARTICIPANTS , & MEASUREMENTS This r and omized , placebo-controlled , parallel-group multicenter trial compared two doses of ergocalciferol with placebo between October 2009 and March 2013 . Hemodialysis patients ( n=105 ) with 25(OH)D levels ≤32 ng/ml from 32 centers in the Northeast United States were r and omly assigned to oral ergocalciferol , 50,000 IU weekly ( n=36 ) or monthly ( n=33 ) , or placebo ( n=36 ) for a 12-week treatment period . The primary endpoint was the achievement of vitamin D sufficiency ( 25[OH]D > 32 ng/ml ) at the end of the 12-week treatment period . Survival was assessed through 1 year . RESULTS Baseline characteristics were similar across all arms , with overall mean±SD 25(OH)D levels of 21.9±6.9 ng/ml . At 12 weeks , vitamin D sufficiency ( 25[OH]D > 32 ng/ml ) was achieved in 91 % ( weekly ) , 66 % ( monthly ) , and 35 % ( placebo ) ( P<0.001 ) . Mean 25(OH)D was significantly higher in both the weekly ( 49.8±2.3 ng/ml ; P<0.001 ) and monthly ( 38.3±2.4 ng/ml ; P=0.001 ) arms compared with placebo ( 27.4±2.3 ng/ml ) . Calcium , phosphate , parathyroid hormone levels , and active vitamin D treatment did not differ between groups . All-cause and cause-specific hospitalizations and adverse events were similar between groups during the intervention period . Lower all-cause mortality  among ergocalciferol-treated participants was not statistically significant ( hazard ratio , 0.28 ; 95 % confidence interval , 0.07 to 1.19 ) . CONCLUSIONS Oral ergocalciferol can increase 25(OH)D levels in incident hemodialysis patients without significant alterations in blood calcium , phosphate , or parathyroid hormone during a 12-week period INTRODUCTION Vitamin D ( 25-hydroxyvitamin D , 25(OH)D ) deficiency , hypovitaminosis D , is highly prevalent in chronic kidney disease patients and is potentially involved with complications in the hemodialysis ( HD ) population . The aim of this study was to evaluate the impact of cholecalciferol supplementation on biomarkers of mineral metabolism , inflammation , and cardiac function in a group of HD patients presenting with hypovitaminosis D and low intact parathyroid hormone ( iPTH ) levels . MATERIAL AND METHODS HD patients with iPTH levels of < 300 pg/mL , not receiving vitamin D therapy , and presenting with 25(OH)D levels of < 30 ng/mL were enrolled in this prospect i ve study . Oral cholecalciferol was prescribed once a week in the first 12 weeks ( 50,000 IU ) and in the last 12 weeks ( 20,000 IU ) of the study . High-sensitivity C-reactive protein , interleukin-6 , and serum albumin were used as inflammatory markers .  Echocardiograms were performed on a midweek interdialytic day at baseline and after 6 months of cholecalciferol supplementation . RESULTS In all , 30 patients were included in the final analysis . We observed a significant increase in serum 25(OH)D levels after 3 months ( 46.2 ± 14.4 ng/mL vs. 18.1 ± 6.6 ng/mL ; P < .001 ) and after 6 months ( 40.4 ± 10.4 ng/mL vs. 18.1 ± 6.6 ng/mL ; P < .001 ) of cholecalciferol supplementation . There were no significant changes in alkaline phosphatase , iPTH , phosphorus , and serum albumin levels , but there was a slight but significant increase in calcium levels after 6 months of cholecalciferol supplementation ( 9.4 ± 0.6 mg/dL vs. 9.0 ± 0.6 mg/dL ; P = .02 ) . Additionally , we observed a significant reduction in high-sensitivity C-reactive protein levels after 3 months ( median : 0.62 [ 0.05 to 29.6 ] mg/L vs. 0.32 [ 0.02 to 3.13 ] mg/L ; P = .02 ) and after 6 months ( median : 0.62 [ 0.05 to 29.6 ] mg/L vs. 0.50 [ 0.02 to 5.66 ] mg/L ; P = .04 ) of cholecalciferol supplementation , as well as a significant reduction in interleukin-6 levels ( median : 6.44 pg/mL vs. 3.83 pg/mL ; P = .018 ) after 6 months of supplementation . Left ventricular mass index was significantly reduced at the end of supplementation ( 159 ± 55 g/m(2 ) vs. 175 ± 63 g/m(2 ) ; P = .03 ) . CONCLUSIONS Cholecalciferol supplementation in HD patients was found to be safe and efficient to correct hypovitaminosis D and established little impact on mineral metabolism markers . Additionally , we observed a reduction in important surrogate markers of cardiovascular risk , namely systemic inflammation and left ventricular hypertrophy , suggesting an anti-inflammatory action and possibly an improvement of cardiac dysfunction BACKGROUND Ergocalciferol ( vitamin D(2 ) ) supplementation plays a role in fall prevention , but the effect in patients living in the community in sunny climates remains uncertain . We evaluated the effect of ergocalciferol and calcium citrate supplementation compared with calcium alone on the risk of falls in older women at high risk of falling . METHODS A 1-year population -based , double-blind , r and omized controlled trial of 302 community-dwelling ambulant older women aged 70 to 90 years living in Perth , Australia ( latitude , 32 degrees S ) , with a serum 25-hydroxyvitamin D concentration of less than 24.0 ng/mL and a history of falling in the previous year . Participants were r and omized to receive ergocalciferol , 1000 IU/d , or identical placebo ( hereinafter , ergocalciferol and control groups , respectively ) . Both groups received calcium citrate , 1000 mg/d . Fall data were collected every 6 weeks . RESULTS Ergocalciferol therapy reduced the risk of having at least 1 fall over 1 year after adjustment for baseline height , which was significantly different between the 2 groups ( ergocalciferol group , 53.0 % ; control group , 62.9 % ; odds ratio [ OR ] , 0.61 ; 95 % confidence interval [ CI ] , 0.37 - 0.99 ) . When those who fell were grouped by the season of first fall or the number of falls they had , ergocalciferol treatment reduced the risk of having the first fall in winter and spring ( ergocalciferol group , 25.2 % ; control group , 35.8 % ; OR , 0.55 ; 95 % CI , 0.32 - 0.96 ) but not in summer and autumn , and reduced the risk of having 1 fall ( ergocalciferol group , 21.2 % ; control group , 33.8 % ; OR , 0.50 ; 95 % CI , 0.28 - 0.88 ) but not multiple falls . CONCLUSION Patients with a history of falling and vitamin D insufficiency living in sunny climates benefit from ergocalciferol supplementation in addition to calcium , which is associated with a 19 % reduction in the relative risk of falling , mostly in winter CONTEXT We previously showed that a single high dose of oral ( po ) cholecalciferol ( D₃ ) sharply increases serum 25-hydroxyvitamin D [ 25(OH)D ] . OBJECTIVE We evaluated the long-term bioavailability and metabolism of a single po or intramuscular ( i m ) high dose of ergocalciferol ( D₂ ) or D₃. DESIGN This was a prospect i ve intervention study . SETTING The study was conducted in an ambulatory care setting . PATIENTS Participants were 24 subjects with hypovitaminosis D. INTERVENTIONS A single dose of 600,000 IU of po or i m D₂ or D₃ was administered . MAIN OUTCOME MEASURES Serum 25(OH)D and 1,25-dihydroxyvitamin D [ 1,25(OH)₂D ] were measured at baseline and at days 30 , 60 , 90 , and 120 by RIA . Serum 1,25(OH)₂D₂ , 1,25-dihydroxyvitamin D₃ [ 1,25(OH)₂D₃ ] , 24,25-hydroxyvitamin D₂ [ 24,25(OH)D₂ ] , and 24,25-hydroxyvitamin D₃ [ 24,25(OH)D₃ ] were measured by liquid chromatography-t and em mass spectrometry in a subgroup of patients receiving the po formulations . RESULTS The areas under the curve of 25(OH)D after D₃ were significantly higher than those after D₂ ( P < .0001 ) . Serum 25(OH)D basal difference significantly increased at day 30 with po D₂ and D₃ ( P < .01 and P < .0001 ) and up to day 90 with po D₃ ( P < .01 ) . The i m formulations produced a slow increased , and values peaked at day 120 relative to the other time points ( P < .0001 ) . We found a decrease in 1,25(OH)₂D at day 30 ( P < .05 ) and up to day 120 ( P < .001 ) and an increase in 1,25(OH)₂D₂ at day 30 ( P < .01 ) and up to day 120 ( P < .01 ) after po D₂. Oral D₂ and D₃ produced increases in 24,25(OH)D₂ and 24,25(OH)D₃ , respectively , at day 30 ( P < .001 ) . CONCLUSIONS A po dose of 600,000 IU of D₂ or D₃ is initially more effective in increasing serum 25(OH)D than the equivalent i m dose and is rapidly metabolized . Our RIA assay for 1,25(OH)₂D may not recognize CONTEXT Anti-Müllerian hormone ( AMH ) is a gonad-specific hormone , which is extensively used as a marker of gonadal status . The level of serum AMH has a high variance in similar individuals for reasons that are unknown . The AMH gene promoter contains a vitamin D response element that may cause vitamin D status to influence serum AMH levels . AIM The objective of the study was to determine whether serum levels of AMH are related to 25-hydroxyitamin D [ 25(OH)D ) ] status . SETTING This was a correlative and intervention study . PARTICIPANTS Three cohorts of participants were analyzed ; mature men ( n = 113 ) , premenopausal women ( n = 33 ) , and 5- to 6-yr-old boys ( n = 74 ) . Women were given a daily supplement of ergocalciferol , cholecalciferol , or a placebo for 6 months and provided baseline and posttreatment blood sample s. MAIN OUTCOME MEASURES Serum AMH and 25(OH)D were measured and analyzed for covariation . RESULTS Serum AMH positively correlated with 25(OH)D in men ( r = 0.22 , P = 0.02 ) but not boys . Both 25(OH)D and AMH levels exhibited seasonal variation in women , with an 18 % decrease in AMH levels in winter compared with summer ( P = 0.01 ) . Change in AMH level correlated with the initial AMH level and the magnitude of change in vitamin D levels ( r = 0.36 , P = 0.004 ) . Cholecalciferol supplementation prevented seasonal AMH change . CONCLUSION Vitamin D may be a positive regulator of AMH production in adults , and vitamin D deficiency may confound clinical decisions based on AMH . Vitamin D deficiency should be considered when serum AMH levels are obtained for diagnosis BACKGROUND There is increasing interest in the extraskeletal effects of vitamin D , particularly in the obese state with regard to the development of insulin resistance and diabetes . OBJECTIVE The objective of the study was to determine the effect of 2 doses of cholecalciferol ( vitamin D3 ) supplementation on insulin action ( Si ) and pancreatic β-cell function in obese adolescents . METHODS We performed a 12-wk double-blind , r and omized comparison of the effect of vitamin D3 supplementation on Si and β-cell function in obese Caucasian adolescents ( body mass index > 95(th ) percentile ) . The subjects were r and omly assigned to receive either 400 IU/d ( n = 25 ) or 2000 IU/d ( n = 26 ) of vitamin D3 . Each subject underwent a 7- sample 75 g oral glucose tolerance test , with glucose , insulin , and C-peptide measurements , to calculate Si and β-cell function as assessed by the disposition index ( DI ) , with use of the oral minimal model before and after supplementation . A total of 51 subjects aged 15.0 ± 1.9 y were enrolled . Included for analysis at follow-up were a total of 46 subjects ( 20 male and 26 female adolescents ) , 23 in each group .  RESULTS Initial serum 25-hydroxyvitamin D [ 25(OH)D ] was 24.0 ± 8.1 μg/L. There was no correlation between 25(OH)D concentrations and Si or DI . There was a modest but significant increase in 25(OH)D concentration in the 2000 IU/d group ( 3.1 ± 6.5 μg/L , P = 0.04 ) but not in the 400 IU/d group ( P = 0.39 ) . There was no change in Si or DI  following vitamin D3 supplementation in either of the treatment groups ( all P > 0.10 ) . CONCLUSIONS The current study shows no effect from vitamin D3 supplementation , irrespective of its dose , on β-cell function or insulin action in obese nondiabetic adolescents with relatively good vitamin D status . Whether obese adolescents with vitamin D deficiency and impaired glucose metabolism would respond differently to vitamin D3 supplementation remains unclear and warrants further studies . This trial was registered at clinical trials.gov as NCT00858247 OBJECTIVE To determine whether a single monthly supplement is as effective as a daily maternal supplement in increasing breast milk vitamin D to achieve vitamin D sufficiency in their infants . PATIENTS AND METHODS Forty mothers with exclusively breast-fed infants were r and omized to receive oral cholecalciferol ( vitamin D3 ) 5000 IU/d for 28 days or 150,000 IU once . Maternal serum , breast milk , and urine were collected on days 0 , 1 , 3 , 7 , 14 , and 28 ; infant serum was obtained on days 0 and 28 . Enrollment occurred between January 7 , 2011 , and July 29 , 2011 . RESULTS In mothers given daily cholecalciferol , concentrations of serum and breast milk cholecalciferol attained steady levels of 18 and 8 ng/mL , respectively , from day 3 through 28 . In mothers given the single dose , serum and breast milk cholecalciferol peaked at 160 and 40 ng/mL , respectively , at day 1 before rapidly declining . Maternal milk and serum cholecalciferol concentrations were related ( r=0.87 ) . Infant mean serum 25-hydroxyvitamin D concentration increased from 17±13 to 39±6 ng/mL in the single-dose group and from 16±12 to 39±12 ng/mL in the daily-dose group ( P=.88 ) . All infants achieved serum 25-hydroxyvitamin D concentrations of more than 20 ng/mL. CONCLUSION Either single-dose or daily-dose cholecalciferol supplementation of mothers provided breast milk concentrations that result in vitamin D sufficiency in breast-fed infants . CLINICAL TRIAL REGISTRATION clinical trials.gov NCT01240265 CONTEXT Low 25-hydroxyvitamin D levels are common in patients with primary hyperparathyroidism ( PHPT ) and associated with higher PTH levels and hungry bone syndrome after parathyroidectomy ( PTX ) . However , concerns have been raised about the safety of vitamin D supplementation in PHPT . OBJECTIVE We aim ed to assess safety and effects on calcium homeostasis and bone metabolism of supplementation with high doses of vitamin D in PHPT patients . DESIGN , SETTING This was an investigator-initiated double-blind , r and omized , placebo-controlled , parallel-group trial from a single center . PATIENTS Forty-six PHPT patients were recruited , with a mean age of 58 ( range 29 - 77 ) years , and 35 ( 76 % ) were women . INTERVENTIONS Intervention included daily supplementation with 70 μg ( 2800 IU ) cholecalciferol or identical placebo for 52 weeks . Treatment was administered 26 weeks before PTX and continued for 26 weeks after PTX . MAIN OUTCOME MEASURES PTH , calcium homeostasis , and bone metabolism were evaluated . RESULTS Preoperatively , 25-hydroxyvitamin D increased from 50 to 94 nmol/L in the treatment group and decreased from 57 to 52 nmol/L in the placebo group ( P < .001 ) . Compared with placebo , vitamin D  decreased PTH significantly by 17 % before PTX ( P = .01 ) , increased lumbar spine bone mineral density by 2.5 % ( P = .01 ) , and decreased C-terminal β-CrossLaps by 22 % ( P < .005 ) . The trabecular bone score did not change in response to treatment , but improved after PTX . Postoperatively , PTH remained lower in the cholecalciferol group compared with the placebo group ( P = .04 ) . Plasma creatinine and plasma and urinary calcium did not differ between groups . CONCLUSIONS Daily supplementation with a high vitamin D dose safely improves vitamin D status and decreases PTH in PHPT patients . The vitamin D treatment is accompanied by reduced bone resorption and improved bone mineral density before operation BACKGROUND AND OBJECTIVES Vitamin D deficiency is an important contributor to the development of hyperparathyroidism and is independently associated with cardiovascular and bone disease . The hypothesis was that nutritional vitamin D ( ergocalciferol ) supplementation in children with CKD stages 2 - 4 delays the onset of secondary hyperparathyroidism . DESIGN , SETTING , PARTICIPANTS , & MEASUREMENTS A r and omized , double-blinded , placebo-controlled study in children with CKD2 - 4 who had 25-hydroxyvitamin D [ 25(OH)D ] deficiency was conducted . Ergocalciferol ( or a matched placebo ) was given daily as per Kidney Disease Outcomes Quality Initiative guidelines . The primary endpoint was the time to development of hyperparathyroidism . RESULTS Seventy-two children were screened . Forty-seven children were 25(OH)D-deficient and r and omly assigned to receive ergocalciferol or placebo .  Twenty children in each arm completed the study ; median follow-up was 12 months . Groups were well matched for age , race , estimated GFR , and season when recruited . Nine of 20 children on placebo and 3 of 20 children on ergocalciferol developed hyperparathyroidism ( odds ratio , 4.64 ; 95 % confidence interval , 1.02 - 21.00 ) . The time to development of hyperparathyroidism was significantly longer with ergocalciferol treatment compared with placebo ( hazard ratio , 0.30 ; 95 % confidence interval , 0.09 - 0.93 , P=0.05 ) . With ergocalciferol treatment , normal 25(OH)D levels were achieved in all 8 children with CKD2 , 8 of 11 children with CKD3 , but not in the single patient with CKD4 . There were no  ergocalciferol-related adverse events . 25(OH)D levels > 100 nmol/L were required to achieve normal levels of 1,25-dihydroxyvitamin D. CONCLUSIONS Ergocalciferol is an effective treatment that delays the development of secondary hyperparathyroidism in children with CKD2 - 3 Objectives : To investigate the practicality and tolerability of high‐dose intramuscular ( i.m . ) vitamin D2 or oral vitamin D3 replacement in vitamin D‐insufficient patients , and to evaluate the biochemical efficacy of each formulation . Methods : Sixty‐nine patients with vitamin D insufficiency [ 25‐hydroxyvitamin D ( 25(OH)D ) < 40 nmol/L ] were recruited from the Rheumatology Outpatient Department of St George 's Hospital , London . In study 1 , 50 patients received 300 000 IU i.m . vitamin D2 ( ergocalciferol ) . In study 2 , 19 patients received 300 000 IU oral vitamin D3 ( cholecalciferol ) under observation . Biochemical response was measured at baseline , and at 12 and 24 weeks . Results : Bolus i.m . vitamin D2 or oral vitamin D3 was well tolerated . The change from baseline in serum 25(OH)D was significantly greater at 6 and 12 weeks in study 2 ( p<0.0001 and < 0.0001 , respectively ) . In study 1 , a modest increase in mean serum 25(OH)D at 6 , 12 , and 24 weeks was observed but no patients achieved a serum 25(OH)D concentration ⩾50 nmol/L. PTH remained elevated in 42 % of patients with secondary hyperparathyroidism at 12 weeks . In study 2 , 100 % and 89 % of patients had serum 25(OH)D>50 nmol/L at 6 and 12 weeks , respectively . All patients with elevated baseline PTH were fully suppressed at 12 weeks . No cases of hypercalcaemia were observed in either group . Conclusion : The 300 000‐IU bolus of vitamin D2 or D3 was practical , well tolerated , and safe . Vitamin D3 had greater potency than equimolar vitamin D2 , with a higher , sustained serum 25(OH)D response and efficacious PTH suppression . To adequately treat vitamin D insufficiency we would recommend administering 300 000 IU oral vitamin D3 approximately three times per year
Meta- analysis of BMI values at end of trial showed no statistically significant difference in BMI change by use of 25[OH]D supplementation .
Based on existing published trials , oral 25[OH]D supplementation does not significantly impact BMI change
The impact of 25-hydroxyvitamin D ( 25[OH]D ) supplementation on weight change remains controversial .
The objective of this study was to summarize the effects of 25[OH]D supplementation ( cholecalciferol or ergocalciferol ) on BMI change through a meta- analysis of published clinical trials .