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Vitamin B12, folic acid, and bone.

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.
AuthorsKarin M A Swart, Natasja M van Schoor, Paul Lips
JournalCurrent osteoporosis reports (Curr Osteoporos Rep) Vol. 11 Issue 3 Pg. 213-8 (Sep 2013) ISSN: 1544-2241 [Electronic] United States
PMID23873438 (Publication Type: Journal Article, Review)
Chemical References
  • Homocysteine
  • Folic Acid
  • Vitamin B 12
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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