In my book, I write about the use of therapeutic targets to help guide health care providers in their design and optimization of nutritional support for individuals with bone loss. By identifying “targets” such as abnormal lab results, or persistent abnormal physical signs or symptoms to improve upon (instead of just recommending a nutritional regimen and hoping for the best), providers can more effectively apply therapy for improving bone health and reducing fracture risk. Two laboratory tests for inflammation that I commonly use for this purpose are C-reactive protein and homocysteine. In this month’s issue of Bone, (Yang et al., 2012) report on their meta-analysis and systematic review that was designed to help clarify the association between blood plasma levels of homocysteine (a sulfur amino acid) and fractures.
When homocysteine increases to abnormal levels in the blood, this is a sign of chronic systemic inflammation and nutrient deficiency. These elevated homocysteine levels can result in an accumulation of the amino acid in bone which adversely affects normal collagen formation and bone strength. Normally, homocysteine is converted to methionine and cysteine in processes that require folic acid, B12, and pyridoxal-5′-phosphate (active B6). But if these nutrients are deficient (or if an individual has a genetic-related difficulty in converting vitamin B6 into its active form, pyridoxal-5′-phosphate), blood levels rise and homocysteine deposits into the bone.
The authors of this study concluded that their findings “provided strong evidence that homocysteine was associated with an increased future risk of incident fracture” and that the “risk appeared more pronounced in men.”
Yang, J., et al. (2012) Homocysteine level and risk of fracture: A meta-analysis and systemic review. Bone 51(3):376-382.