Abstract |
Vitamin B12 and folic acid deficiency are associated with a higher serum concentration of homocysteine. A high serum homocysteine is a risk factor for fractures. Both vitamins play a role in the remethylation of homocysteine to methionine. The pathophysiology from a high serum homocysteine to fractures is not completely clear, but might involve bone mineral density, bone turnover, bone blood flow, DNA methylation, and/or physical function and fall risk. Genetic variation, especially polymorphisms of the gene encoding for methylenetetrahydrofolate reductase may play a role in homocysteine metabolism and fracture risk. It is uncertain whether supplementation with vitamin B12 and folate can decrease fracture incidence. One double blind clinical trial in post- stroke patients showed that these B vitamins could decrease hip fracture incidence, but the results of further clinical trials should be awaited before a definite conclusion can be drawn.
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Authors | Karin M A Swart, Natasja M van Schoor, Paul Lips |
Journal | Current osteoporosis reports
(Curr Osteoporos Rep)
Vol. 11
Issue 3
Pg. 213-8
(Sep 2013)
ISSN: 1544-2241 [Electronic] United States |
PMID | 23873438
(Publication Type: Journal Article, Review)
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Chemical References |
- Homocysteine
- Folic Acid
- Vitamin B 12
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Topics |
- Bone Density
- Bone and Bones
(metabolism)
- Dietary Supplements
- Folic Acid
(administration & dosage, metabolism, therapeutic use)
- Fractures, Bone
(epidemiology, metabolism, prevention & control)
- Homocysteine
(metabolism)
- Humans
- Prevalence
- Vitamin B 12
(administration & dosage, metabolism, therapeutic use)
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