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Summary of Vitamin D trials - Grant Nov 2012

Original Jan 2012 - updated Nov 2012

CLICK HERE for web page which has Jan 2012 table and associated references & abstracts

Nov 2012 document with full references is attached at the bottom of this page

List of random controlled vitamin D trials covered in version of Jan 2012:

All cause mortality
Atopic dermatitis
Bone loss in winter
Breast cancer
Colorectal cancer
Cancer, All
Cardiovascular disease event
Chronic kidney disease
CVD survival
Falls, fractures
Gastric bypass
Glucose (fasting plasma) (FPG)
Heart failure, congestive
Infections, symptomatic upper respiratory tract
Infectious diseases
Influenza type A
Insulin sensitivity
Multiple sclerosis
Muscle strength
Musculoskeletal parameters
Non-vertebrate fractures
Physical performance
Stress fractures
Tooth loss

See also by Dr. Grant

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211-RCTs abstracts, table






All cause mortality

Mean oral in take 528 IU/d

RR =  0.93 (95% CI, 0.87-0.99)

Autier and Gandini, 2007


daily vitamin D(3) (800 IU), calcium (1000 mg), both, or placebo for 24-62 months, with a follow-up of 3 yr after intervention

(HR) = 0.93; 95% confidence interval (CI) = 0.85-1.02]

Avenell, 2012

All cause mortality


Vitamin D with or without calcium reduced mortality by 7% [hazard ratio, 0.93; 95% confidence interval (CI), 0.88-0.99]. However, vitamin D alone did not affect mortality, but risk of death was reduced if vitamin D was given with calcium (hazard ratio, 0.91; 95% CI, 0.84-0.98). The number needed to treat with vitamin D plus calcium for 3 yr to prevent one death was 151. Trial level meta-analysis (24 trials with 88,097 participants) showed similar results, i.e. mortality was reduced with vitamin D plus calcium (odds ratio, 0.94; 95% CI, 0.88-0.99), but not with vitamin D alone (odds ratio, 0.98; 95% CI, 0.91-1.06).

Rejnmark, 2012

Atopic dermatitis



Sidbury, 2008

Bone loss in winter

oral cholecalciferol (500 IU/day) and calcium (500 mg/day) during the winter months

In the subjects receiving oral vitamin D3 and calcium, lumbar and femoral BMD increased significantly (lumbar spine: +0.8%, p = 0.04 versus year 1; femoral neck: +0.1%, p = 0.05 versus year 1), whereas controls continued to lose bone (intervention group versus control group: lumbar spine, p = 0.03; femoral neck, p = 0.05).

Meier, 2004

Cancer, All

1100 IU/d, 1450 mg/d calcium

When analysis was confined to cancers diagnosed after the first 12 mo, RR for the Ca + D group fell to 0.232 (CI: 0.09, 0.60; P < 0.005) but did not change significantly for the Ca-only group.

Lappe, 2007


daily vitamin D(3) (800 IU), calcium (1000 mg), both, or placebo for 24-62 months, with a follow-up of 3 yr after intervention

cancer mortality (HR = 0.85; 95% CI = 0.68-1.06), and cancer incidence (HR = 1.07; 95% CI = 0.92-1.25)

Avenell, 2012

Breast, colorectal cancer

400 IU/d vitamin D3, 1500 mg/d or placebo

In 15,646 women (43%) who were not taking personal calcium or vitamin D supplements at randomization, CaD significantly decreased the risk of total, breast, and invasive breast cancers by 14-20% and nonsignificantly reduced the risk of colorectal cancer by 17%. In women taking personal calcium or vitamin D supplements, CaD did not alter cancer risk (HR: 1.06-1.26).

Bolland, 2011


In meta-analyses of 10 trials

supplementation nonsignificantly reduced systolic blood pressure (weighted mean difference, -1.9 mm Hg [CI, -4.2 to 0.4 mm Hg]) and did not affect diastolic blood pressure (weighted mean difference, -0.1 mm Hg [CI, -0.7 to 0.5 mm Hg]).

Pittas, 2010


Vitamin D supplementation during weight loss

more pronounced decrease occurred in the vitamin D group than in the placebo group in blood concentrations of parathyroid hormone (-26.5% compared with -18.7%; P = 0.014), triglycerides (-13.5% compared with +3.0%; P < 0.001), and the inflammation marker tumor necrosis factor-alpha (-10.2% compared with -3.2%; P = 0.049).

Zittermann,  2009

Cardiovascular disease event

Pooled study

.Results of secondary analyses in 8 randomized trials showed a slight but statistically nonsignificant reduction in CVD risk (pooled relative risk, 0.90 [95% CI, 0.77 to 1.05]) with vitamin D supplementation at moderate to high doses (approximately 1000 IU/d) but not with calcium supplementation (pooled relative risk, 1.14 [CI, 0.92 to 1.41]), or a combination of vitamin D and calcium supplementation (pooled relative risk, 1.04 [CI, 0.92 to 1.18]) compared with placebo.

Wang, 2010


Participants were randomized 2:1 to vitamin D3 4,000 IU daily or placebo for 12 weeks. The primary outcome was a change in flow-mediated brachial artery dilation (FMD).


Baseline demographics were similar except for age (vitamin D versus placebo, mean ±sd 47 ±8 versus 40 ±10 years; P=0.009). Both groups had reduced FMD at baseline (median values 2.9% [IQR 1.6-4.8] for vitamin D versus 2.5% [IQR 1.7-6.4] for placebo; P=0.819). Despite an increase in the concentration of serum 25-hydroxyvitamin D from baseline to 12 weeks (5.0 ng/ml [IQR -0.9-7.4] versus -1.9 ng/ml [IQR -4.0-0.1] for vitamin D versus placebo, respectively; P=0.003), there was no difference in FMD change (0.55% [IQR -1.05-2.13] versus 0.29% [IQR -1.61-1.77]; P=0.748). Vitamin D supplementation was associated with a decrease in total and non-high-density lipoprotein cholesterol, and an increase in indices of insulin resistance.

Longenecker, 2012

CVD survival


Vitamin D supplementation conferred substantial survival benefit (odds ratio for death 0.39, 95% confidence interval 0.28 to 0.53, p <0.0001).

Vacek, 2012

Chronic kidney disease

Placebo or calcium (1,200 mg) and vitamin D(3) (800 IU) in fixed or separate combination.


Effect on parathyroid hormone

The proportion with a 30% or greater decrease in iPTH level at 6 months was 50% in all eGFR groups on treatment versus 6% to 9% for placebo (P < 0.001 for all). The effects of the intervention on iPTH levels did not differ according to baseline eGFR (interaction P > 0.1 for all times).

Kooienga, 2009


1000 IU/d vs. placebo

Mean 25(OH)D levels increased significantly higher in the treatment group (mean increase from baseline: 10.3+/-10.4 ng/mL vs. 0.8+/-6.8 ng/mL, p<0.0001).

Rucker, 2009


Successful 25OHD replacement was defined as prescription of ergocalciferol sufficient to increase serum 25OHD level by 25% from baseline within 6 months (treatment group, n = 90). Otherwise patients were considered as untreated controls (n = 36). The date when the 25OHD level was drawn was considered as the date of inclusion. All the patients were followed up from the date of inclusion until July 2009 to capture CV events prospectively.

During mean follow-up of 27.2 months, 44% of the controls had CV events, whereas only 21% of the patients in the treatment group had CV events (P = 0.001). In multivariate logistic regression analysis, adjusting for CV disease predictors age, initial parathyroid hormone level, statin use, history of CV disease, and glomerular filtration rate, the estimated odds ratio for 25OHD replacement status was 0.37 (95% confidence interval: 0.14-1.0).

Lishmanov, 2012


Cross-sectional study and randomized double blind controlled trial of 20,000 or 40,000 IU vitamin D per week versus placebo for 1 year.

In the two groups given vitamin D, but not in the placebo group, there was a significant improvement in BDI scores after 1 year. There was a significant decrease in serum parathyroid hormone in the two vitamin D groups without a concomitant increase in serum calcium.

Jorde, 2008

Falls, fractures

700-1000 IU/d

Pooled RR = 0.81 (95% CI 0.71 to 0.92)

No effect for 400 IU/d

Bischoff-Ferrari, 2009b


Our study population consisted of 242 individuals recruited by advertisements and mailing lists (mean [ +/- SD] age, 77 +/- 4 years). All serum 25-hydroxyvitamin D (25[OH]D) levels were below 78 nmol/l. Individuals received in a double blinded fashion either 1000 mg of calcium or 1000 mg of calcium plus 800 IU of vitamin D per day over a treatment period of 12 months, which was followed by a treatment-free but still blinded observation period of 8 months.

Compared to calcium mono, supplementation with calcium plus vitamin D resulted in a significant decrease in the number of subjects with first falls of 27% at month 12 (RR = 0.73; CI = 0.54-0.96) and 39% at month 20 (RR = 0.61; CI = 0.34-0.76).

Concerning secondary endpoints, we observed significant improvements in quadriceps strength of 8%, a decrease in body sway of 28%, and a decrease in time needed to perform the TUG test of 11%.

Pfeifer, 2009

Non-vertebrate fractures

700-1000 IU/d

pooled RR was 0.80 (95% CI, 0.72-0.89;

Bischoff-Ferrari, 2009a


Participants who were randomly assigned to receive vitamin D, as compared with those assigned to control groups,

had a nonsignificant 10% reduction in the risk of hip fracture (hazard ratio, 0.90; 95% confidence interval [CI], 0.80 to 1.01) and a 7% reduction in the risk of nonvertebral fracture (hazard ratio, 0.93; 95% CI, 0.87 to 0.99). By quartiles of actual intake, reduction in the risk of fracture was shown only at the highest intake level (median, 800 IU daily; range, 792 to 2000), with a 30% reduction in the risk of hip fracture (hazard ratio, 0.70; 95% CI, 0.58 to 0.86) and a 14% reduction in the risk of any nonvertebral fracture (hazard ratio, 0.86; 95% CI, 0.76 to 0.96).

Bischoff-Ferrari, 2012

Flow-mediated dilation

Following 16 weeks of placebo (n = 23; mean age 31 ± 2 years) or 60,000 IU monthly oral vitamin D(3) (n = 22; mean age 29 ± 2 years), serum concentrations of 25-hydroxyvitamin D (25(OH)D) increased from 38.2 ± 3.0 to 48.7 ± 3.2 nmol/l and 34.3 ± 2.2 to 100.9 ± 6.6 nmol/l, respectively.

No changes in serum parathyroid hormone (PTH), serum calcium, or urine calcium/creatinine were observed following either treatment. Following 16 weeks of treatment, significant improvements in FMD were only observed in the vitamin D group (1.8 ± 1.3%), whereas the placebo group had no change (-1.3 ± 0.6%). Similarly, the vitamin D group exhibited an increase in absolute change in diameter (0.005 ± 0.004 cm) and FMD/shear (0.08 ± 0.04 %/s(-1), area under the curve (AUC) × 10(3)) following treatment, whereas no change (-0.005 ± 0.002 cm and -0.02 ± 0.02 %/s(-1), AUC, respectively) was observed following placebo.

Harris, 2011

Gastric bypass

We evaluated three doses of vitamin D3 (800, 2,000, and 5,000 IU/day) in a prospective, randomized pilot trial of 45 patients undergoing Roux-en-Y gastric bypass.

At 12 months, the 800-, 2,000-, and 5,000-IU groups had a mean +/- SD increase in 25OHD of 27.5 +/- 40.0, 60.2 +/- 37.4, and 66.1 +/- 42.2 nmol/L, respectively (p = 0.09) with a maximum increase in each group of 87.4, 114.8, and 129.8 nmol/L. Forty-four percent, 78%, and 70% achieved 25OHD levels >or=75 nmol/L (p = 0.38).

Goldner, 2009

Glucose (fasting plasma) (FPG)

A total of 314 Caucasian adults without diabetes received either 500 mg calcium citrate and 700 IU vitamin D(3) or placebos daily for 3 years in a double-blind, randomized, controlled trial designed for bone-related outcomes.

Among participants with IFG at baseline, those who took combined calcium-vitamin D supplements had a lower rise in FPG at 3 years compared with those on placebo (0.02 mmol/l [0.4 mg/dl] vs. 0.34 mmol/l [6.1 mg/dl], respectively, P = 0.042) and a lower increase in HOMA-IR (0.05 vs. 0.91, P = 0.031).

Pitas, 2007


HD patients were included in this study if their serum 25(OH)D level was <75 mmol/L. Oral 25(OH)D(3) was administered daily at 10-30 microg/day based on the severity of the deficiency.

After 6 months of treatment [mean daily 25(OH)D(3): 16 +/- 5 microg/day], the serum 25(OH)D level increased (30 +/- 19 to 126 +/- 46 nmol/ L, P < 0.001), with 13% of patients in group 1, 57% in group 2 and 30% in group 3. The serum intact parathyroid hormone (iPTH) level decreased (235 +/- 186 to 189 +/- 137 pg/mL, P = 0.05), except in group 1. Bone alkaline phosphatase (BALP) showed a tendency to normalize (23 +/- 16 to 18.3 +/- 11 microg/L, P < 0.05), leading to a decrease in alfacalcidol administration from 66% to 43% (P < 0.05), except in group 1. The KDOQI targets achieved increased significantly for serum calcium (76% to 85%) and phosphate levels (66% to 77%) in all patients. The serum albumin level increased in all groups (34.6 +/- 4 to 36.8 +/- 4 g/L, P < 0.05), without any significant improvement in normalized protein catabolic rate (nPCR) or C-reactive proteins (CRP).

Jean, 2008

Heart failure, congestive

either 50 mug vitamin D(3)/d plus 500 mg Ca/d [D(+) group] or placebo plus 500 mg Ca/d [D(-) group] for 9 mo

Compared with baseline, parathyroid hormone was significantly lower and the antiinflammatory cytokine interleukin 10 was significantly higher in the D(+) group after 9 mo. The proinflammatory cytokine tumor necrosis factor alpha increased in the D(-) group but remained constant in the D(+) group. The survival rate did not differ significantly between the study groups during the follow-up period.

Schleithoff, 2006

Infectious diseases



Yamshchikov, 2009

Infections, symptomatic upper respiratory tract

50 microg vitamin D3 (2000 IU) daily or matching placebo for 12 weeks.

The mean 25-hydroxyvitamin D level at baseline was similar in both groups (64.3+/-25.4 nmol/l in the vitamin D group; 63.0+/-25.8 nmol/l in the placebo group; n.s.). After 12 weeks, 25-hydroxyvitamin D levels increased significantly to 88.5+/-23.2 nmol/l in the vitamin D group, whereas there was no change in vitamin D levels in the placebo group. There was no benefit of vitamin D3 supplementation in decreasing the incidence or severity of symptomatic URIs during winter.

Li-Ng,  2009



Vitamin D status was the sole determinant of circulating MMP9 (inversely) and an independent determinant of CRP (inversely). Determinants of TIMP-1 were MMP9, systolic blood-pressure (directly) and VDR genotype (TaqI). Significant reductions in MMP9 (-68%), TIMP-1 (-38%) and CRP (-23%) concentrations followed vitamin-D supplementation.

Timms, 2002


2000 IU/d vitamin D3 given to diabetics

Vitamin D deficiency was common, affecting 36% of patients. There was no impact of hypovitaminosis D on metabolic syndrome status, HbA1c or insulin use (p >or= 0.4 for all) and no association between 25OHVitD and ferritin or hsCRP (p >or= 0.3 for all). Neither BMI nor the metabolic syndrome affected the incremental rise in 25OHVitD levels during supplementation.

Luo, 2009


800 or 2000 IU/d

40 or 90% reduction

Aloia & Li-Ng, 2007

Influenza type A

1100 IU/d, no other oral intake

RR: 0.36; 95% CI: 0.17, 0.79; P = 0.006

No effect for type B

Urashima, 2010

Insulin sensitivity

120,000 IU/fortnight

Seventy-one of the recruited subjects completed the study (35 in supplemented group, 36 in control group). There was an increase in oral glucose insulin sensitivity (OGIS) with supplementation by per protocol analysis (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 secondary outcome measures (insulin secretion, basal indices of insulin sensitivity, blood pressure or lipid profile) were found with supplementation.

Nagpal, 2009


double-blind intervention administering 100 microg (4000 IU) vitamin D(3) (n 42) or placebo (n 39) daily for 6 months to South Asian women, aged 23-68 years, living in Auckland, New Zealand

Significant improvements were seen in insulin sensitivity and IR (P = 0.003 and 0.02, respectively), and fasting insulin decreased (P = 0.02) with supplementation compared with placebo.

Von hurst, 2010


Only subjects in the intervention group received one intramuscular injection of 300,000 IU of vitamin D3. HbA(1c), serum 25-hydroxyvitamin D3, fasting insulin and blood glucose, C-peptide, homeostasis model assessment insulin resistance index (HOMA-IR), β-cell function, insulin sensitivity and the Quantitative Insulin Sensitivity Check Index (QUICKI) were measured at baseline and after 3 months of intervention.


Approximately 80% of the mothers had a degree of vitamin D deficiency. Post-intervention, this was found in 4.2 and 71.4% in the intervention and control groups, respectively. The medians of HOMA-IR indices before and after intervention were 0.6 and 0.5 (P = 0.7), respectively, in subjects in the intervention group, and 0.5 and 0.9 (P = 0.01) in subjects in the control group. The mean of the QUICKI fell only in the control group (P = 0.008). In the control group, β-cell function increased by ~8% (P = 0.01) and insulin sensitivity decreased after 3 months (P = 0.002). Post-intervention, the median C-peptide decreased in the intervention group and increased in the control group, but the change was significant only in the control group (P = 0.03).

Mozaffari-Khosravi, 2012


participants with low serum 25(OH)D levels were thereafter randomized to receive capsules of 20,000 IU vitamin D(3) or identical-looking placebo twice weekly for 6 months.

The 52 participants with high serum 25(OH)D levels (85.6 ± 13.5 nmol/L [mean ± SD]) had significantly higher insulin sensitivity index (ISI) and lower HbA(1c) and triglycerides (TGs) than the 108 participants with low serum 25(OH)D (40.3 ± 12.8 nmol/L), but the differences in ISI and TGs were not significant after adjustments. After supplementation, serum 25(OH)D was 142.7 ± 25.7 and 42.9 ± 17.3 nmol/L in 49 of 51 completing participants randomized to vitamin D and 45 of 53 randomized to placebo, respectively. At the end of the study, there were no statistically significant differences in the outcome variables between the two groups.

Grimnes, 2011


cholecalciferol (2000 IU once daily) or calcium carbonate (400 mg twice daily) for 16 wk.

The disposition index increased in the vitamin D group and decreased in the no-vitamin D group (adjusted mean change ± SE: 300 ± 130 compared with -126 ± 127, respectively; P = 0.011), which was explained by an improvement in insulin secretion (62 ± 39 compared with -36 ± 37 mU · L(-1) · min, respectively; P = 0.046). Hb A(1c) increased less, but nonsignificantly, in the vitamin D group than in the no-vitamin D group (0.06 ± 0.03% compared with 0.14 ± 0.03%, respectively; P = 0.081).

Mitri, 2011

Muscle strength

6-month supplementation (December to May) of daily calcium plus monthly placebo (calcium/placebo group) or daily calcium plus oral cholecalciferol (150,000 IU once a month during the first 2 months, followed by 90,000 IU once a month for the last 4 months; calcium/vitamin D group)

SHF was increased in the calcium/vitamin D group by 16.4% (p = 0.0001) and SKE by 24.6% (p = 0.0007).

[strength of hip flexors (SHF) and knee extensors (SKE)]


Moreira-Pfrimer, 2009


800 or 1600 IU/d plus vibration

Same improvements with both doses

Verschueren, 2011


Twenty-six (87%) patients completed 3 months of therapy. The percent increase in serum 25OHD (compared to baseline) was 82.7% in 2,000-IU group and 219.5% in 5,000-IU group. All participants (100%) achieved a serum 25OHD concentration >50 nmol/L; only 5 subjects (45.4%) in 2,000-IU group compared to 14 subjects (93.3%) in 5,000-IU group achieved final 25OHD concentration ≥75 nmol/L (p<0.01).

In the regression analysis, the reflexion point at which the PTH level increased above the normal range was calculated to be 63.8 nmol/L 25OHD. All parameters of muscle strength showed trends in improvements following the administration of both the 2,000 and 5,000 IU doses. No patient reported untoward side effects and no patient developed

Diamond, 2012

Musculoskeletal parameters

One hundred seventy-nine girls, ages 10-17 yr, were randomly assigned to receive weekly oral vitamin D doses of 1,400 IU (equivalent to 200 IU/d) or 14,000 IU (equivalent to 2,000 IU/d) in a double-blind, placebo-controlled, 1-yr protocol.

In the overall group of girls, lean mass increased significantly in both treatment groups (P < or = 0.05); bone area and total hip BMC increased in the high-dose group (P < 0.02). In premenarcheal girls, lean mass increased significantly in both treatment groups, and there were consistent trends for increments in BMD and/or BMC at several skeletal sites, reaching significance at lumbar spine BMD in the low-dose group and at the trochanter BMC in both treatment groups. There was no significant change in lean mass, BMD, or BMC in postmenarcheal girls.

El-Hajj, 2006

Multiple sclerosis

6000 IU/d vitamin D2 vs. 1000 IU/d vitamin D2

There were 4 relapses with high-dose D2 vs none with low-dose D2 (p = 0.04).

Stein, 2011


8400 IU/week

significantly reduced sway compared with treatment with placebo (P = 0.047) in patients with elevated baseline sway but not in patients with normal baseline sway.

Lips, 2010

Periodontal disease

A cohort of 51 subjects receiving periodontal maintenance therapy was recruited from two dental clinics; 23 were taking vitamin D (>or=400 IU/day) and calcium (>or=1,000 mg/day) supplementation, and 28 were not taking such supplementation. All subjects had at least two interproximal sites with >or=3 mm clinical attachment loss. Daily calcium and vitamin D intake (from food and supplements) were estimated by nutritional analysis.

Compared to subjects who did not take vitamin D and calcium supplementation, supplement takers had shallower probing depths, fewer bleeding sites, lower gingival index values, fewer furcation involvements, less attachment loss, and less alveolar crest height loss. The repeated-measures analysis indicated that collectively these differences were borderline significant (P = 0.08).

Miley, 2009

Physical performance


gait speed was higher among subjects supplemented with vitamin (whether trained or not) than in non-supplemented subjects (838+/-147 and 768+/-127 m/12 min, respectively, p=0.02).

Bunout, 2006


Children, 100,000 IU D3 once

Children in the vitamin D(3) group survived longer without experiencing a repeat episode (72 days vs. 59 days; HR 0.71; 95% CI 0.53-0.95; P = 0.02).

Manaseki-Holland, 2010


Oral vitamin D (1000 IU for <1 year and 2000 IU for >1 year) (n=100) or placebo (lactose) (n=100) once a day for 5 days, from enrolment.

Median duration (SE, 95% CI) of resolution of severe pneumonia was similar in the two groups [vitamin D: 72 (3.7, 64.7-79.3) hours; placebo: 64 (4.5, 55.2-72.8)hours]. Duration of hospitalization and time to resolution of tachypnea, chest retractions, and inability to feed were also comparable between the two groups.

Choudhary & Gupta, 2011


4000 IU/d

No adverse effects on serum or urine calcium

Hollis, 2011


Maternal 25(OH)D (n = 161) increased from 22.7 ng/mL (SD 9.7) at baseline to 36.2 ng/mL (SD 15) and 37.9 ng/mL (SD 13.5) in the 2000 and 4000 IU groups, respectively. While maternal 25(OH)D change from baseline did not differ between groups, 25(OH)D monthly increase differed between groups (P < .01). No supplementation-related adverse events occurred. Mean cord blood 25(OH)D was 22.1 ± 10.3 ng/mL in 2000 IU and 27.0 ± 13.3 ng/mL in 4000 IU groups (P = .024).

After controlling for race and study site, preterm birth and labor were inversely associated with predelivery and mean 25(OH)D, but not baseline 25(OH)D.


Wagner, 2012

Respiratory infections

At baseline, the median serum 25(OH)D level was 7 ng/mL (interquartile range: 5-10 ng/mL). At the end of the trial, follow-up was 99% (n = 244), and the median 25(OH)D levels of children in the control versus vitamin D groups was significantly different (7 vs 19 ng/mL; P < .001).

Compared with controls, children receiving vitamin D reported significantly fewer ARIs during the study period (mean: 0.80 vs 0.45; P = .047), with a rate ratio of 0.52 (95% confidence interval: 0.31-0.89). Adjusting for age, gender, and history of wheezing, vitamin D continued to halve the risk of ARI (rate ratio: 0.50 [95% confidence interval: 0.28-0.88]). Similar results were found among children either below or above the median 25(OH)D level at baseline (rate ratio: 0.41 vs 0.57; P(interaction) = .27).

Camargo, 2012

Stress fractures

Navy females, 800 IU/d, 2000 mg/d calcium

21% lower incidence

Lappe, 2008


Participants received either 83 μg (3,332 IU) vitamin D daily for 1 year (n = 31) or placebo (n =2 3).

Compared to baseline values, a significant increase in total testosterone levels (from 10.7 ± 3.9 nmol/l to 13.4 ± 4.7 nmol/l; p < 0.001), bioactive testosterone (from 5.21 ± 1.87 nmol/l to 6.25 ± 2.01 nmol/l; p = 0.001), and free testosterone levels (from 0.222 ± 0.080 nmol/l to 0.267 ± 0.087 nmol/l; p = 0.001) were observed in the vitamin D supplemented group. By contrast, there was no significant change in any testosterone measure in the placebo group

Pilz, 2011

Tooth loss

Elderly, taking supplements or not

During the randomized trial, 11 of the 82 subjects (13%) taking supplements and 17 of the 63 subjects (27%) taking placebo lost one or more teeth (OR = 0.4; 95% CI: 0.2 to 0.9).

Krall, 2001


The subjects were randomised to receive vitamin D (0.25 mg/day) or placebo in a double blind method, during the 6th initial week of Tb treatment.

One hundred percent of the vitamin D group and only 76.7% of the placebo group had sputum conversion. This difference is statistically significant (p=0.002).


Nursyam, 2006


The intervention was 100,000 IU of cholecalciferol or placebo at inclusion and again 5 and 8 months after the start of treatment.

Overall mortality was 15% (54 of 365) at 1 year of follow-up and similar in both arms (30 of 187 for vitamin D treated and 24 of 178 for placebo; relative risk, 1.19 [0.58-1.95]).

Wejse, 2009


A single oral dose of 2.5 mg (100,000 IU) vitamin D

significantly enhanced the ability of participants' whole blood to restrict BCG-lux luminescence in vitro without affecting antigen-stimulated IFN-gamma responses.

Martineau, 2011


At baseline, the mean (±SD) 25(OH)D concentration was 7 ± 4 ng/mL, and all concentrations were <20 ng/mL. Vitamin D supplementation increased serum 25(OH)D by a mean of 12.7 ng/mL compared with placebo (P < 0.0001). At baseline, 16 children in the vitamin D group and 18 in the placebo group were TST positive (P = 0.7).

Over 6 mo, TSTs converted to positive in 5 (11%) children receiving vitamin D compared with 11 (27%) receiving placebo (RR: 0.41; 95% CI: 0.16, 1.09; P = 0.06). Only one TST conversion occurred among those whose serum 25(OH)D concentration increased to >20 ng/mL, whereas 8 TST conversions occurred in those whose final 25(OH)D concentration remained <10 ng/mL (P = 0.05). The mean increase in stature was 2.9 ± 1.6 cm in the vitamin D group and 2.0 ± 1.7 cm in the placebo group (95% CI: 2.16, 2.81; P < 0.003).


Ganmaa, 2012



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