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Methylenetetrahydrofolate reductase polymorphism interacts with riboflavin intake to influence bone mineral density.

Abstract

Bone mineral density is a complex trait regulated by an interaction between genetic and environmental factors. Recent studies have identified a functional polymorphism affecting codon 677 of the methylenetetrahydrofolate reductase (MTHFR) gene that is associated with reduced bone mineral density (BMD) in Japanese and Danish postmenopausal women and increased risk of fracture in elderly Danish women. Since dietary B vitamins can influence circulating homocysteine (tHcy) levels, we examined the relationship among MTHFR genotype, B complex vitamins (folate, vitamin B12, vitamin B6 and riboflavin), BMD, and rate of change in BMD in a longitudinal study of 1241 Scottish women aged 45-54 years, at the time of initial study, who were followed up for a mean (SD) of 6.6 (0.7) years. There was no significant association between BMD and either MTHFR genotype or B complex vitamins when examined separately. However, we detected a significant interaction among quartile of energy-adjusted riboflavin intake, MTHFR 'TT' genotype, and BMD (P = 0.01 for baseline FN BMD, P = 0.02 for follow-up FN BMD). Increasing dietary riboflavin intake correlated with LS BMD and FN BMD in homozygotes for the MTHFR 'T' allele, which remained significant for FN after adjustment for confounders (r = 0.192, P = 0.036 for baseline; r = 0.186, P = 0.043 at follow-up) but not in the other genotypes. This raises the possibility that riboflavin intake and MTHFR genotype might interact to regulate BMD. Further work is required to determine if this association holds true for other populations and ethnic groups.

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  • Authors+Show Affiliations

    ,

    Department of Medicine and Therapeutics, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK. h.macdonald@abdn.ac.uk

    , , , ,

    Source

    Bone 35:4 2004 Oct pg 957-64

    MeSH

    Biomarkers
    Bone Density
    Female
    Follow-Up Studies
    Genotype
    Homocysteine
    Humans
    Methylenetetrahydrofolate Reductase (NADPH2)
    Middle Aged
    Polymorphism, Genetic
    Riboflavin

    Pub Type(s)

    Clinical Trial
    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    15454103

    Citation

    Macdonald, H M., et al. "Methylenetetrahydrofolate Reductase Polymorphism Interacts With Riboflavin Intake to Influence Bone Mineral Density." Bone, vol. 35, no. 4, 2004, pp. 957-64.
    Macdonald HM, McGuigan FE, Fraser WD, et al. Methylenetetrahydrofolate reductase polymorphism interacts with riboflavin intake to influence bone mineral density. Bone. 2004;35(4):957-64.
    Macdonald, H. M., McGuigan, F. E., Fraser, W. D., New, S. A., Ralston, S. H., & Reid, D. M. (2004). Methylenetetrahydrofolate reductase polymorphism interacts with riboflavin intake to influence bone mineral density. Bone, 35(4), pp. 957-64.
    Macdonald HM, et al. Methylenetetrahydrofolate Reductase Polymorphism Interacts With Riboflavin Intake to Influence Bone Mineral Density. Bone. 2004;35(4):957-64. PubMed PMID: 15454103.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Methylenetetrahydrofolate reductase polymorphism interacts with riboflavin intake to influence bone mineral density. AU - Macdonald,H M, AU - McGuigan,F E, AU - Fraser,W D, AU - New,S A, AU - Ralston,S H, AU - Reid,D M, PY - 2004/02/20/received PY - 2004/05/14/revised PY - 2004/05/25/accepted PY - 2004/9/30/pubmed PY - 2005/2/3/medline PY - 2004/9/30/entrez SP - 957 EP - 64 JF - Bone JO - Bone VL - 35 IS - 4 N2 - Bone mineral density is a complex trait regulated by an interaction between genetic and environmental factors. Recent studies have identified a functional polymorphism affecting codon 677 of the methylenetetrahydrofolate reductase (MTHFR) gene that is associated with reduced bone mineral density (BMD) in Japanese and Danish postmenopausal women and increased risk of fracture in elderly Danish women. Since dietary B vitamins can influence circulating homocysteine (tHcy) levels, we examined the relationship among MTHFR genotype, B complex vitamins (folate, vitamin B12, vitamin B6 and riboflavin), BMD, and rate of change in BMD in a longitudinal study of 1241 Scottish women aged 45-54 years, at the time of initial study, who were followed up for a mean (SD) of 6.6 (0.7) years. There was no significant association between BMD and either MTHFR genotype or B complex vitamins when examined separately. However, we detected a significant interaction among quartile of energy-adjusted riboflavin intake, MTHFR 'TT' genotype, and BMD (P = 0.01 for baseline FN BMD, P = 0.02 for follow-up FN BMD). Increasing dietary riboflavin intake correlated with LS BMD and FN BMD in homozygotes for the MTHFR 'T' allele, which remained significant for FN after adjustment for confounders (r = 0.192, P = 0.036 for baseline; r = 0.186, P = 0.043 at follow-up) but not in the other genotypes. This raises the possibility that riboflavin intake and MTHFR genotype might interact to regulate BMD. Further work is required to determine if this association holds true for other populations and ethnic groups. SN - 8756-3282 UR - https://www.unboundmedicine.com/medline/citation/15454103/Methylenetetrahydrofolate_reductase_polymorphism_interacts_with_riboflavin_intake_to_influence_bone_mineral_density_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S8756328204002443 DB - PRIME DP - Unbound Medicine ER -