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

Macdonald, H M; McGuigan, F E LU ; Fraser, W D; New, S A; Ralston, S H and Reid, D M (2004) In Bone 35(4). p.64-957
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... (More)

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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published
keywords
Biomarkers, Bone Density, Female, Follow-Up Studies, Genotype, Homocysteine, Humans, Methylenetetrahydrofolate Reductase (NADPH2), Middle Aged, Polymorphism, Genetic, Riboflavin, Clinical Trial, Journal Article, Research Support, Non-U.S. Gov't
in
Bone
volume
35
issue
4
pages
8 pages
publisher
Elsevier
external identifiers
  • scopus:5344224747
ISSN
8756-3282
DOI
10.1016/j.bone.2004.05.018
language
English
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no
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db4cafc5-115b-464e-862e-e56e03e409a6
date added to LUP
2018-01-02 11:10:37
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2018-11-21 21:36:56
@article{db4cafc5-115b-464e-862e-e56e03e409a6,
  abstract     = {<p>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.</p>},
  author       = {Macdonald, H M and McGuigan, F E and Fraser, W D and New, S A and Ralston, S H and Reid, D M},
  issn         = {8756-3282},
  keyword      = {Biomarkers,Bone Density,Female,Follow-Up Studies,Genotype,Homocysteine,Humans,Methylenetetrahydrofolate Reductase (NADPH2),Middle Aged,Polymorphism, Genetic,Riboflavin,Clinical Trial,Journal Article,Research Support, Non-U.S. Gov't},
  language     = {eng},
  number       = {4},
  pages        = {64--957},
  publisher    = {Elsevier},
  series       = {Bone},
  title        = {Methylenetetrahydrofolate reductase polymorphism interacts with riboflavin intake to influence bone mineral density},
  url          = {http://dx.doi.org/10.1016/j.bone.2004.05.018},
  volume       = {35},
  year         = {2004},
}