1 1, 1alphaOHase), the enzyme that converts 25-hydroxycholecalciferol, a circulating inactive metabolit

2 ol/L, equilibrium concentrations of serum 25-hydroxycholecalciferol changed during the winter months

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

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

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

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

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

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

9 t to increase energy, calcium intake, and 25-hydroxycholecalciferol concentrations may improve bone m

10 les in the past year, lower estradiol and 25-hydroxycholecalciferol concentrations, and a higher prev

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

12                                           25-hydroxycholecalciferol deficiency may contribute to the

13                                           25-hydroxycholecalciferol deficiency was associated with ac

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

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

16 .3-6.5], p=0.008), and undetectable serum 25-hydroxycholecalciferol (<7 nmol/L) carried a higher risk

17 als with vitamin D terms: cholecalciferol or hydroxycholecalciferols or calcifediol or dihydroxychole

18                                     Serum 25-hydroxycholecalciferol was recorded in 42 contacts and 1

19 ence of genotype ff or undetectable serum 25-hydroxycholecalciferol was strongly associated with dise