1 27B1, 1alphaOHase), the enzyme that converts 25-hydroxycholecalciferol, a circulating inactive metabo

2  nmol/L, equilibrium concentrations of serum 25-hydroxycholecalciferol changed during the winter mont

3 holecalciferol input and the resulting serum 25-hydroxycholecalciferol concentration and to estimate

4 uired to achieve or maintain any given serum 25-hydroxycholecalciferol concentration are not known, p

5 in D inputs are inadequate to maintain serum 25-hydroxycholecalciferol concentration in the absence o

6 ted oral input required to sustain the serum 25-hydroxycholecalciferol concentration present before t

7 issue stores) needed to sustain the starting 25-hydroxycholecalciferol concentration was estimated at

8                     The time course of serum 25-hydroxycholecalciferol concentration was measured at

9 port to increase energy, calcium intake, and 25-hydroxycholecalciferol concentrations may improve bon

10 cycles in the past year, lower estradiol and 25-hydroxycholecalciferol concentrations, and a higher p

11 ted the interaction between serum vitamin D (25-hydroxycholecalciferol) concentrations and VDR genoty

12                                              25-hydroxycholecalciferol deficiency may contribute to t

13                                              25-hydroxycholecalciferol deficiency was associated with

14 losis, the combination of genotype TT/Tt and 25-hydroxycholecalciferol deficiency was associated with

15 tibility when considered in combination with 25-hydroxycholecalciferol deficiency.

16 I 1.3-6.5], p=0.008), and undetectable serum 25-hydroxycholecalciferol (<7 nmol/L) carried a higher r

17                                        Serum 25-hydroxycholecalciferol was recorded in 42 contacts an

18 resence of genotype ff or undetectable serum 25-hydroxycholecalciferol was strongly associated with d