Abstract
BackgroundPolymorphisms in the apolipoprotein E (APOE) gene are associated with fracture risk, and a potential mechanism is through vitamin K transport. ObjectiveWe investigated the relation between dietary vitamin K1 intake, APOE polymorphisms, and markers of bone health. DesignWe 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. ResultsCompared with quartile 3 (Q3) of energy-adjusted vitamin K1 intake (x̄: 116 μg/d), women in the lowest quartile (x̄: 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. ConclusionsVitamin K1 intake was associated with markers of bone health, but no interaction was observed with APOE alleles on BMD or markers of bone turnover.
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