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Background: Vitamin D deficiency is a common problem in patients with Crohn's disease (CD). The aim of this study was to determine the ability of normal subjects and patients with quiescent CD to absorb vitamin D(2) using a novel vitamin D bioavailability test. In addition, we evaluated whether the location of disease or previous surgery had any influence on the bioavailability of vitamin D(2) in CD patients., Methods: Ten normal subjects (50% female) and 37 CD patients with quiescent disease (51% female) were included in this study. Subjects who recently received any vitamin D(2) were excluded. The vitamin D bioavailability test was performed in all subjects. After a baseline blood draw, all subjects were then given a single 50,000 IU oral dose of vitamin D(2) in a capsule formulation and had their blood drawn 12 hours later to determine serum vitamin D(2), which reflected their vitamin D(2) absorption capacity., Results: Forty-two percent and 29% of CD patients were found to be either vitamin D-deficient (25-hydroxyvitamin D [25(OH)D] ≤20 ng/mL] or insufficient [25(OH)D 21-29 ng/mL], respectively. Twelve hours after ingesting 50,000 IU vitamin D(2) , vitamin D(2) levels rose from a baseline of 0.7 ± 0.7 ng/mL (mean ± SEM) to 49.8 ± 3.0 ng/mL in normal subjects. In CD patients, baseline vitamin D(2) levels rose from 0 ng/mL to 34.8 ± 2.8 ng/mL. CD patients had on average a 30% decrease in their ability to absorb vitamin D(2) (P = 0.01). Moreover, we found a wide variability of vitamin D(2) bioavailability in CD patients. Analysis of variance (ANOVA) revealed no statistical difference of vitamin D(2) bioavailability between patients in the CD subgroup stratified by the location of disease, the type of surgery, and receiving or not receiving surgery., Conclusions: More than 70% of the patients with quiescent CD were vitamin D-deficient or insufficient. The ability to absorb vitamin D(2) in CD patients is unpredictable and the only way to determine this is to perform a vitamin D bioavailability test. Use of this test may guide clinicians in administering the appropriate therapeutic dose of vitamin D for treating vitamin D deficiency in patients with CD., (Copyright © 2011 Crohn's & Colitis Foundation of America, Inc.)

Unlabelled: There are few data on the skeletal health of Hispanic men. We observed differences in vitamin D deficiency and low BMD between Hispanic ethnic subgroups that persisted with adjustment for risk factors. Our data indicate a substantial burden of low BMD and vitamin D deficiency among Hispanic men., Introduction: Disparities within ethnic groups are generally ignored, but in evolving populations they may have implications for public health. We examined ethnic variation in serum 25-hydroxyvitamin D [25(OH)D] and bone mineral density (BMD) among Hispanic American men., Methods: Three hundred and fifty-eight Hispanic males 30 to 79 years of age were studied. Logistic regression models assessed variation in odds of vitamin D deficiency (<20 ng/mL) and low BMD (T-score<-1) by ethnicity, with and without adjustment for risk factors (age, smoking, occupation, physical activity, body mass index, and sunlight exposure)., Results: Vitamin D deficiency was most common among Puerto Rican (26%), compared with Dominican (21%), Central American (11%), and South American (9%) men. Percentages with low BMD were: South American (44%), Puerto Rican (34%), Dominican (29%), and Central American (23%). Adjustment for age and risk factors failed to account for Hispanic subgroup differences in vitamin D deficiency and low BMD. Population estimates indicate a substantial burden of low BMD and vitamin D deficiency among Hispanic men., Conclusions: Our findings underscore the importance of examining the skeletal health of Hispanic subgroups, and suggest that a considerable number of Hispanic men may be at elevated risk of fracture and vitamin D deficiency.

Laboratory and epidemiological studies have indicated that 1alpha,25-dihydroxyvitamin D(3) [1alpha,25(OH)(2)D(3)] and dietary omega3-polyunsaturated fatty acids (PUFAs) are capable of inhibiting prostate cancer at the initiation and progression stages. The objective of this study is to investigate the influence of 1alpha,25(OH)(2)D(3) and PUFAs in the form of fish oil applied alone or in combination on cell cycle kinetics in the exponentially growing androgen-dependent and -independent prostate cancer cells. Our data indicate that the high passage androgen-independent cell line, LNCaP-c115 had a much greater inhibitory response at the level of the G(1)/S-phase transition in response to fish oil treatment than androgen-dependent low passage LNCaP-c38 cells. When LNCaP-c38 and LNCaP-c115 cells were treated with fish oil (50mug/ml), 1alpha,25(OH)(2)D(3) (10(-8)M) or fish oil (50mug/ml)+1alpha,25(OH)(2)D(3) (10(-8)M), a synergistic growth inhibitory effect was observed with 1alpha,25(OH)(2)D(3)+fish oil group in LNCaP-c115 cell line at the levels of the G(1)/S-phase transition and cell division. This interaction appears to be specific for androgen-independent prostate cancer cell lines. Based on these results, we hypothesize that dietary components, such as omega3PUFAs and Vitamin D, have the potential to delay the progression of prostate cancer cells to an aggressive and un-treatable state.

In Crohn's disease, severe skeletal demineralization, secondary hyperparathyroidism, and muscle weakness can occur. This may be caused by impaired vitamin D absorption, resulting from extensive intestinal disease and resection of duodenum and jejunum, where vitamin D is absorbed. We report a 57-year-old woman with a long history of Crohn's disease and short-bowel syndrome who had only 2 feet of small intestine remaining after 3 bowel resections. She was taking a daily multivitamin containing 400 IU of vitamin D(3) and was dependent on total parenteral nutrition that contained 200 IU of vitamin D and calcium (18 mEq in a 1-L bag infused over 8 hours daily) for a period of 36 months. Despite the above replacement, she complained of bone pain and muscle weakness, and she continued to be vitamin D-deficient with a 25(OH)D level <20 ng/mL. She was then exposed to ultraviolet B (UVB) radiation in a tanning bed wearing a 1-piece bathing suit for 10 minutes, 3 times a week for 6 months at the General Clinical Research Center, Boston University Medical Center. She tolerated the irradiation well without evidence of erythema. After 4 weeks, her serum 25(OH)D level increased by 357% from 7 to 32 ng/mL, parathyroid hormone level decreased by 52% from 92 to 44 pg/mL, and the serum calcium level increased from 7.8 to 8.5 mg/dL. After 6 months of UVB treatment, her serum 25(OH)D level was maintained in the normal range and was free of muscle weakness, and bone and muscle pain.

Background: Obesity is associated with vitamin D insufficiency and secondary hyperparathyroidism., Objective: This study assessed whether obesity alters the cutaneous production of vitamin D(3) (cholecalciferol) or the intestinal absorption of vitamin D(2) (ergocalciferol)., Design: Healthy, white, obese [body mass index (BMI; in kg/m(2)) > or = 30] and matched lean control subjects (BMI

Objectives: Because several serum studies of vitamin D metabolites have produced equivocal results on their relation to prostate cancer risk, the purpose of this study is to evaluate this association further., Methods: A nested case-control study in a cohort of 3,737 Japanese-American men examined from 1967 to 1970 was conducted in Hawaii (United States). At the time of examination, a single blood specimen was obtained, and the serum was frozen. After a surveillance period of over 23 years, 136 tissue-confirmed incident cases of prostate cancer were identified. Their stored sera and those of 136 matched controls were measured for the following: 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, calcium, phosphorus, and parathyroid hormone., Results: There were no notable differences between cases and controls in their median serum levels of the five laboratory measurements. Odds ratios (OR) for prostate cancer, based on the quartiles of serum levels in controls, were also determined. The ORs for the highest quartiles relative to the lowest were 0.8 (95 percent confidence interval [CI] = 0.4-1.8) for 25-hydroxyvitamin D and 1.0 (CI = 0.5-2.1) for 1,25-dihydroxyvitamin D., Conclusion: It is possible that the lack of sufficient numbers of study subjects with low vitamin D levels affected the results. Nonetheless, the findings suggest that there is a lack of a strong association between vitamin D and prostate cancer.

We determined the quantitative relationships between graded oral dosing with vitamin D3, 25(OH)D3, and 1,25(OH)2D3 for short treatment periods and changes in circulating levels of these substances. The subjects were 116 healthy men (mean age, 28 +/- 4 years, with usual milk consumption of < or = 0.47 l/day and mean serum 25(OH)D of 67 +/- 25 nmol/l). They were distributed among nine open-label treatment groups: vitamin D3 (25, 250 or 1250 micrograms/day for 8 weeks), 25(OH)D3 (10, 20 or 50 micrograms/day for 4 weeks) and 1,25(OH)2D3 (0.5, 1.0 or 1.0 microgram/day for 2 weeks). All treatment occurred between January 3 and April 3. We measured fasting serum, calcium, parathyroid hormone, vitamin D3, 25(OH)D and 1,25(OH)2D immediately before and after treatment. In the three groups treated with vitamin D3, mean values for circulating vitamin D3 increased by 13, 137 and 883 nmol/l and serum 25(OH)D increased by 29, 146 and 643 nmol/l for the three dosage groups, respectively. Treatment with 25(OH)D3 increased circulating 25(OH)D by 40, 76 and 206 nmol/l, respectively. Neither compound changed serum 1,25(OH)2D levels. However, treatment with 1,25(OH)2D3 increased circulating 1,25(OH)2D by 10, 46 and 60 pmol/l, respectively. Slopes calculated from these data allow the following estimates of mean treatment effects for typical dosage units in healthy 70-kg adults: an 8-week course of vitamin D3 at 10 micrograms/day (400 IU/day) would raise serum vitamin D by 9 nmol/l and serum 25(OH)D by 11 nmol/l; a 4-week course of 25(OH)D3 at 20 micrograms/day would raise serum 25(OH)D by 94 nmol/l; and a 2-week course of 1,25(OH)2D3 at 0.5 microgram/day would raise serum 1,25(OH)2D by 17 pmol/l.

The absorptive response to graded doses of vitamin D3, 25(OH)D, and 1,25(OH)2D was measured in healthy adult men after treatment periods of eight, four, and two weeks, respectively. While no relationship was found between baseline absorption and serum vitamin D metabolite levels, all three vitamin D compounds significantly elevated 45Ca absorption from a 300 mg calcium load given as part of a standard test meal. 1,25(OH)2D was active even at the lowest dose (0.5 microgram/day), and the slope was such that doubling of absorption would occur at an oral dose of approximately 3 micrograms/day. 25(OH)D was also active in elevating absorption and did so without raising total 1,25(OH)2D levels. On the basis of the dose response curves for 1,25(OH)2D and 25(OH)D, the two compounds exhibited a molar ratio for physiological potency of approximately 100:1. The absorptive effect of vitamin D3 was seen only at the highest dose level (1250 micrograms, or 50,000 IU/day) and was apparently mediated by conversion to 25(OH)D. Analysis of the pooled 25(OH)D data from both the 25(OH)D- and vitamin D3-treated groups suggests that approximately one eighth of circulating vitamin D-like absorptive activity under untreated conditions in winter may reside in 25(OH)D. This is a substantially larger share than has been predicted from studies of in vitro receptor binding.

We investigated the homeostatic compensation for the lower cutaneous synthesis of vitamin D in heavily melanized persons. Vitamin D2 (50,000 IU) was administered in a single oral dose to 24 young adults, 12 blacks and 12 whites, matched for age, gender, and socioeconomic status. We also included a group of eight healthy elderly white adults as representatives of a population with a nonracial mechanism for decreased cutaneous vitamin D synthesis. Plasma determinants were performed under basal conditions and at 6, 10, and 24 hours after vitamin D intake. Basal 25-hydroxyvitamin D (25-OH-D) levels were significantly lower in blacks (12.5 +/- 2.2 ng/ml (mean +/- SEM)) and in elderly whites (19.2 +/- 1.9 ng/ml), compared with young whites (30.2 +/- 3.0 ng/ml (p < 0.0001)); levels of basal 1,25-dihydroxyvitamin D (1,25(OH)2 -D) did not differ between groups. The vitamin D blood curve was similar between groups after the oral vitamin D2 load. Increases in 25-OH-D were 91.7 +/- 15.9% in blacks, 18.8 +/- 5.2% in young whites, and 28.6 +/- 6.9 in elderly whites; 1,25(OH)2-D levels increased slightly and did not differ between groups, although in blacks the change over time was significant (p < 0.05). As a whole, the study populations exhibited a strong relation between basal and peak 25-OH-D (r = -0.80; p < 0.001). Levels of intact parathyroid hormone and serum calcium of blacks and young whites did not differ within or between groups throughout the test.(ABSTRACT TRUNCATED AT 250 WORDS)

We examined two siblings who had severe rickets at ages 2 and 7 years, respectively, despite a history of adequate vitamin D intake. The patients' sera had calcium concentrations at the lower limits of normal, low phosphate concentrations, elevated alkaline phosphatase activity, and low levels of 25-hydroxyvitamin D. Treatment with high doses of vitamin D2 resulted in resolution of the biochemical abnormalities and radiographic deformities; pharmacologic doses of vitamin D2 were required to maintain normal concentrations of 25-hydroxyvitamin D in the serum even though vitamin D absorption was normal. These children may have a genetic defect of the 25-hydroxylation step in vitamin D activation.

Background: Vitamin D has been added to milk in the United States since the 1930s to prevent rickets. We report the unusual occurrence of eight cases of vitamin D intoxication that appear to have been caused by excessive vitamin D fortification of dairy milk., Methods: Medical records were reviewed and a dietary questionnaire was sent to eight patients who had unexplained hypervitaminosis D. Vitamin D analyses with high-performance liquid chromatography were performed on samples of the patients' serum, the dairy milk they drank, and the vitamin D concentrate added to the milk., Results: All eight patients drank milk produced by a local dairy in amounts ranging from 1/2 to 3 cups (118 to 710 ml) daily. All had elevated serum 25-hydroxyvitamin D concentrations (mean [+/- SD], 731 +/- 434 nmol per liter [293 +/- 174 ng per milliliter]). Six of the eight patients had elevated serum vitamin D3 concentrations. Of the eight patients, seven had hypercalcemia and one had hypercalciuria but normocalcemia (mean serum calcium, 3.14 +/- 0.51 mmol per liter [12.6 +/- 2.1 mg per deciliter]). Analysis of the dairy's vitamin D-fortified milk revealed concentrations of vitamin D3 (cholecalciferol) that ranged from undetectable to as high as 232,565 IU per quart (245,840 IU per liter). An analysis of the concentrate that was used to fortify the milk, labeled as containing vitamin D2 (ergocalciferol), revealed that it contained vitamin D3., Conclusions: Hypervitaminosis D may result from drinking milk that is incorrectly and excessively fortified with vitamin D. Milk that is fortified with vitamin D must be carefully monitored.

Background: The fortification of milk and infant formula with vitamin D has had an important role in eliminating rickets in children and osteomalacia in adults. A recent outbreak of vitamin D intoxication caused by drinking milk fortified with excess vitamin D has led to questions about the level of vitamin D in milk from other producers., Methods: We used high-performance liquid chromatography to measure vitamin D in samples of 13 brands of milk with various fat contents and 5 brands of infant formula purchased at random from local supermarkets in five Eastern states., Results: Only 12 (29 percent) of the 42 samples of the 13 brands of milk and none of the 10 samples of the 5 brands of infant formula contained 80 to 120 percent of the amount of vitamin D stated on the label. Twenty-six of the 42 milk samples (62 percent) contained less than 80 percent of the amount claimed on the label. No vitamin D was detected in 3 of the 14 samples of skim milk tested (lower limit of assay, 4.7 IU per quart [5.0 IU per liter]). One milk sample labeled as containing vitamin D2 (ergocalciferol) contained vitamin D3 (cholecalciferol). Seven of the 10 samples of infant formula contained more than 200 percent of the amount stated on the label; the sample with the highest concentration contained 419 percent of the stated amount. None of the samples of infant formula contained less than the amount stated., Conclusions: Milk and infant-formula preparations rarely contain the amount of vitamin D stated on the label and may be either underfortified or overfortified. Since both underfortification and overfortification are hazardous, better monitoring of the fortification process is needed.

Vitamin D affects calcium metabolism and prevents proliferation of colon cells in vitro. In human beings the main circulating form of vitamin D is 25-hydroxyvitamin D; to regulate calcium homoeostasis, this form must be converted to 1alpha, 25-dihydroxyvitamin D by 1alpha-hydroxylation in the kidney with 25-hydroxyvitamin D-1alpha-hydroxylase. Cultured transformed colon cancer cells can convert 25-hydroxyvitamin D(3) to 1alpha,25-dihydroxyvitamin D(3). We identified messenger RNA (mRNA) for 25-hydroxyvitamin D-1alpha-hydroxylase in normal colon tissue and in malignant and adjacent normal colon tissue. These findings support the notion that vitamin D might have a role in cell growth regulation and cancer protection, and might be the explanation for why the risk of dying from colorectal cancer is highest in areas with the least amount of sunlight. [ABSTRACT FROM AUTHOR]