The European Fifth Framework Programme (Contract No. QLK1-CT-2000-00623).

The effect of vitamin D supplementation on bone mineral augmentation in 212 adolescent girls with adequate calcium intake was studied in a randomized placebo-controlled setting. Bone mineral augmentation determined by DXA increased with supplementation both in the femur and the lumbar vertebrae in a dose-responsive manner. Supplementation decreased the urinary excretion of resorption markers, but had no impact on formation markers.Introduction: Adequate vitamin D intake protects the elderly against osteoporosis, but there exists no indisputable evidence that vitamin D supplementation would benefit bone mineral augmentation. The aim of this 1-year study was to determine in a randomized double-blinded trial the effect of 5 and 10 g vitamin D 3 supplementation on bone mineral augmentation in adolescent girls with adequate dietary calcium intake. Materials and Methods: Altogether, 228 girls (mean age, 11.4 ± 0.4 years) participated. Their BMC was measured by DXA from the femur and lumbar spine. Serum 25-hydroxyvitamin D [S-25(OH)D], intact PTH (S-iPTH), osteocalcin (S-OC), and urinary pyridinoline (U-Pyr) and deoxypyridinoline (U-Dpyr) were measured. Statistical analysis was performed both with the intention-to-treat (IT) and compliance-based (CB) method. Results: In the CB analysis, vitamin D supplementation increased femoral BMC augmentation by 14.3% with 5 g and by 17.2% with 10 g compared with the placebo group (ANCOVA, p ‫ס‬ 0.012). A dose-response effect was observed in the vertebrae (ANCOVA, p ‫ס‬ 0.039), although only with the highest dose. The mean concentration of S-25(OH)D increased (p < 0.001) in the 5-g group by 5.7 ± 15.7 nM and in the 10-g group by 12.4 ± 13.7 nM, whereas it decreased by 6.7 ± 11.3 nM in the placebo group. Supplementation had no effect on S-iPTH or S-OC, but it decreased U-DPyr (p ‫ס‬ 0.042). Conclusions: Bone mineral augmentation in the femur was 14.3% and 17.2% higher in the groups receiving 5 and 10 g of vitamin D, respectively, compared with the placebo group, but only 10 g increased lumbar spine BMC augmentation significantly. Vitamin D supplementation decreased the concentration of bone resorption markers, but had no impact on bone formation markers, thus explaining increased bone mineral augmentation. However, the positive effects were noted with the CB method but not with IT.

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 samples 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 randomly 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: Sodium intake increases urinary calcium excretion and may thus lead to negative calcium balance and bone loss. Objective: We hypothesised that reducing sodium intake would reduce urinary calcium excretion and have a beneficial influence in bone metabolism. Design: A total of 29 subjects, 14 males and 15 females, were divided into two study groups. One group (low-sodium group (LS)) reduced sodium intake for 7 weeks by substituting low-salt alternatives for the most important dietary sources of sodium. The other group, serving as a control group (C), was given the same food items in the form of normally salted alternatives. Fasting serum samples as well as 24-h urine samples were obtained in the beginning and at the end of the study. Urinary sodium, urinary calcium, urinary creatinine, serum calcium, serum phosphate, serum creatinine, serum parathyroid hormone (s-PTH), serum C-terminal telopeptides of Type-I collagen and serum bone alkaline phosphatase (s-B-ALP) were analysed. Results: The LS group showed a significant decline (P ¼ 0.001) in urinary sodium/creatinine ratio without a significant effect on urinary calcium/creatinine ratio. In the LS group, s-PTH increased (P ¼ 0.03). The C group showed an increase in s-PTH (P ¼ 0.05) and in s-B-ALP, but no differences were observed between the study groups in the changes of serum markers of calcium and bone metabolism. Conclusions: We have shown that reducing the sodium intake of young, healthy people with adequate calcium intake over a 7-week period does not affect the markers of bone metabolism. Sponsorship: The study was supported by Tekes-National Technology Agency of Finland.