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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^1,2,3,4

¹ From the Department of Medicine and Therapeutics, University of Aberdeen, Foresterhill, Aberdeen, United Kingdom (HMM, FEM, and DMR); the Centre for Nutrition and Food Safety, School of Biomedical and Molecular Sciences, University of Surrey, Guildford, Surrey, United Kingdom (SAL-N); the Department of Clinical Biochemistry, Royal Liverpool University Hospital, Liverpool, United Kingdom (WDF); and the Rheumatic Diseases Unit, Molecular Medicine Centre, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom (SHR)

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 K₁ intake, APOE polymorphisms, and markers of bone health.

Design: 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 K₁ intake (: 116 µg/d), women in the lowest quartile (: 59 µg/d) had lower BMD (analysis of variance; FN, Q1: 0.831 ± 0.122 g/cm²; Q3: 0.850 ± 0.126 g/cm²; P < 0.001; LS, Q1: 1.000 ± 0.170 g/cm²; Q3: 1.020 ± 0.172 g/cm²; 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 K₁ 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 K₁ intake was associated with markers of bone health, but no interaction was observed with APOE alleles on BMD or markers of bone turnover.