Vitamin K1 intake is associated with higher bone mineral density and reduced bone resorption in early postmenopausal Scottish women: no evidence of gene-nutrient interaction with apolipoprotein E polymorphisms.
BACKGROUND
Polymorphisms in the apolipoprotein E (APOE) gene are associated with fracture risk, and a potential mechanism is through vitamin K transport.


OBJECTIVE
We investigated the relation between dietary vitamin K(1) intake, APOE polymorphisms, and markers of bone health.


METHODS
We measured bone mineral density (BMD) at the lumbar spine (LS) and femoral neck (FN) in a cohort of Scottish women aged 49-54 y in 1990-1994 (baseline) and in 1997-2000 (visit 2). At visit 2, bone markers (urinary pyridinoline crosslinks and serum N-terminal propeptide of type 1 collagen) were measured, 3199 women completed a food-frequency questionnaire, and 2721 women were genotyped for APOE.


RESULTS
Compared with quartile 3 (Q3) of energy-adjusted vitamin K(1) intake (mean: 116 microg/d), women in the lowest quartile (mean: 59 microg/d) had lower BMD (analysis of variance; FN, Q1: 0.831 +/- 0.122 g/cm(2); Q3: 0.850 +/- 0.126 g/cm(2); P < 0.001; LS, Q1: 1.000 +/- 0.170 g/cm(2); Q3: 1.020 +/- 0.172 g/cm(2); P = 0.009), remaining significant at the FN after adjustment for age, weight, height, menopausal status or use of hormone replacement therapy, socioeconomic status, and physical activity (P = 0.04). Vitamin K(1) intake was associated with reduced concentrations of pyridinoline crosslinks (Q1: 5.4 +/- 2.0 nmol/mmol; Q4: 5.1 +/- 1.9 nmol/mmol; P = 0.003). Carriers of the E2 allele had greater LS BMD at visit 2 and lost less BMD than did carriers of the E4 allele (E2: -0.50 +/- 1.22%/y; E4: -0.71 +/- 1.17%/y; P = 0.05). After adjustment for confounders, the P value for BMD loss (0.03 for LS and 0.04 for FN) did not reach the level of significance required for multiple testing (P = 0.012). No interaction was observed between dietary vitamin K and APOE on BMD.


CONCLUSIONS
Vitamin K(1) intake was associated with markers of bone health, but no interaction was observed with APOE alleles on BMD or markers of bone turnover.
Macdonald
Helen M
HM
Department of Medicine and Therapeutics, University of Aberdeen, Foresterhill, Aberdeen, United Kingdom. h.macdonald@abdn.ac.uk
McGuigan
Fiona E
FE
Lanham-New
Susan A
SA
Fraser
William D
WD
Ralston
Stuart H
SH
Reid
David M
DM
D015502:Absorptiometry, Photon / Q000379:methods; D000596:Amino Acids / Q000652:urine; D000704:Analysis of Variance; D001057:Apolipoproteins E / Q000235:genetics*; D015519:Bone Density / Q000187:drug effects* / Q000502:physiology; D001862:Bone Resorption; D001842:Bone and Bones / Q000000981:diagnostic imaging / Q000378:metabolism; D024042:Collagen Type I / Q000652:urine; D004032:Diet; D015444:Exercise / Q000502:physiology; D005163:Factor Analysis, Statistical; D005260:Female; D006801:Humans; D008875:Middle Aged; D010455:Peptides / Q000652:urine; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D017698:Postmenopause; D012606:Scotland; D011795:Surveys and Questionnaires; D010837:Vitamin K 1 / Q000008:administration & dosage*; D014813:Vitamin K Deficiency / Q000503:physiopathology
D000596:Amino Acids; D001057:Apolipoproteins E; D024042:Collagen Type I; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide; C015484:pyridinoline; D010837:Vitamin K 1