End Of Vitamin Research Articles

Reduction of Parathyroid Hormone with Vitamin D Supplementation in Blacks: A Randomized Controlled Trial.

Response of parathyroid hormone (PTH) to vitamin D supplementation is determined by the baseline PTH level and change in vitamin D status. Conflicting reports in Blacks exist on the PTH response to vitamin D to supplementation. During 3 winters from 2007-2010, 328 healthy Blacks (median age, 51 years) living in Boston, MA were randomized into a 4-arm, double-blind trial for 3 months of placebo, 1000, 2000, or 4000 IU of vitamin D3. PTH was measured in 254 participants at baseline and at the end of vitamin D supplementation period. The differences in PTH between baseline and 3 months were 3.93 pg/mL for those receiving placebo, -3.37 pg/mL for those receiving 1000 IU/d, -6.76 pg/mL for those receiving 2000 IU/d, and -8.99 pg/mL for those receiving 4000 IU/d ( -2.98 pg/mL for each additional 1000 IU/d of vitamin D3; p<0.001). We found a significant decrease in PTH with increasing doses of vitamin D supplementation up to intakes of 4000 IU/d in Blacks. Clinical Trials.gov: NCT00585637.

Abstract P173: Serum 25-hydroxyvitamin D and Mortality in Middle-aged Men and Women: Results from the MONICA/KORA Augsburg Study

Background: Recent studies found an inverse association between vitamin D status and both morbidity and mortality from major chronic diseases such as cardiovascular diseases (CVD) and cancer. In contrast, some studies have suggested adverse health effects such as increased all-cause mortality at the high end of vitamin D levels. Therefore, the aim of the present study was to further elucidate the relationship between 25-hydroxyvitamin D (25[OH]D) and all-cause as well as CVD and non-CVD mortality. Methods: Our study population comprised 851 men and 774 women aged 35-74 years at baseline selected randomly, stratifying by sex and survey out of 9,531 subjects with available blood samples. All had participated in at least one of the three population-based MONICA/KORA Augsburg surveys between 1984-1995. Participants were followed-up for a mean of 16.8 ± 5.4 years. During this period 197 persons died from CVD (ICD9 390-459, 798) and 226 from non-cardiovascular causes. For three participants the cause of death was missing. 25[OH]D was measured in serum samples collected at baseline using an enzyme immunoassay from IDS, Frankfurt. Results: After adjustment for age, sex, survey, and season of blood sampling we observed a significant inverse association between serum 25[OH]D and all-cause mortality. The hazard ratio (HR) and 95% confidence interval (CI) comparing subjects with levels &gt;75 nmol/l to those with levels ≤25 nmol/l was 0.59 (0.38-0.93); P trend =0.007 across the following four categories: ≤25 nmol/l; &gt;25-≤50 nmol/l; &gt;50-≤75 nmol/l; &gt;75 nmol/l, assigning the median value within each category to the respective category. Further adjustment for BMI, education and lifestyle factors attenuated the association and it became non-significant (HR [95% CI]: 0.78 [0.48-1.27]; P trend =0.205). For CVD mortality, we also observed an inverse association which persisted after adjustment for the above mentioned confounders (HR [95% CI]: 0.49 [0.21-1.11]; P trend =0.012). After further multivariable adjustment including potential intermediate risk factors such as systolic blood pressure, total cholesterol/HDL-cholesterol, diabetes and markers of inflammation the association became non-significant (HR [95% CI]: 0.63 [0.26-1.51]; P trend =0.122). We did not observe any significant association between 25[OH]D and non-CVD mortality regardless of the degree of adjustment. However, there was a trend towards increased non-CVD mortality in women with 25[OH]D &gt;75 nmol/l compared to those with concentrations ≤25 nmol/l (HR [95% CI]: 2.87 [0.99-8.33]; P trend =0.111 for the fully adjusted model). Conclusions: Our data indicate that vitamin D status is inversely related to CVD mortality. However, before large scale measures to improve vitamin D status should be initiated, further studies should evaluate potentially harmful effects of very high levels of 25[OH]D on other outcomes especially among women.

P3.148 Common genetic variants at the 5′ end of vitamin D receptor (VDR) gene are associated with Parkinson disease (PD) susceptibility

P3.148 Common genetic variants at the 5′ end of vitamin D receptor (VDR) gene are associated with Parkinson disease (PD) susceptibility

Assessment of vitamin E concentrations in serum and cerebrospinal fluid of horses following oral administration of vitamin E

To determine concentrations of alpha-tocopherol in serum and CSF of healthy horses following administration of supplemental vitamin E in feed. 10 healthy adult horses. Horses were allocated to receive supplemental d-alpha-tocopherol (1,000 U/d [group A; n=5] or 10,000 U/d [group B; 5]) in feed for 10 days. Blood samples were collected before (baseline), during, and at intervals for 10 days after discontinuation of vitamin E administration for assessment of serum alpha-tocopherol concentration. Cerebrospinal fluid samples were collected prior to and 24 hours after cessation of vitamin E administration. Alpha-tocopherol concentrations in serum and CSF samples were analyzed via high-performance liquid chromatography; changes in those values during the treatment period were compared between groups, and the relationship of serum and CSF alpha-tocopherol concentrations was evaluated. In both groups, serum alpha-tocopherol concentration increased significantly from baseline during vitamin E administration; values in group B were significantly greater than those in group A during and after treatment. At the end of vitamin E administration, CSF alpha-tocopherol concentration was not significantly greater than the baseline value in either group; however, the increase in CSF concentration was significant when the group data were combined and analyzed. Serum and CSF alpha-tocopherol concentrations were significantly correlated at baseline for all horses, but were not strongly correlated after 10 days of vitamin E administration. In healthy horses, daily oral administration of supplemental vitamin E in feed resulted in increases in serum and CSF alpha-tocopherol concentrations.

Vitamin E and Dapsone-Induced Hemolysis

Sixteen patients, each receiving 100 mg of dapsone per day, were studied for evidence of hemolysis. Vitamin E (dl-alpha tocopherol acetate), 800 mg/day, was then administered for up to three months, and dapsone therapy was continued at the same dose. Hemolysis factors were reexamined immediately prior to cessation of vitamin E therapy. No substantial change was demonstrable for levels of hemoglobin, reticulocyte count, and haptoglobin at the end of vitamin E therapy, despite a significant rise in serum vitamin E levels. Erythrocyte survival measured in four patients before and at the end of vitamin E therapy also showed no substantial change. Erythrocyte Heinz body count, however, fell in nine of 15 patients studied, and none showed an increase in this measurement while receiving vitamin E. We conclude that in patients receiving dapsone at 100 mg/day, vitamin E therapy at 800 mg/day does not substantially ameliorate the hemolytic effect of this drug.