Folic Acid Supports Blood Flow to Bone and Bone Density

According to a new study, folic acid supplementation supports blood flow to bone and bone density in mice with imbalances in homocysteine. Homocysteine is an amino acid, and imbalanced levels are associated with suboptimal cardiovascular health. Homocysteine has also been associated with changes in bone and bone strength. Vitamin B12, vitamin B6 and folic acid have been shown to optimize serum homocysteine concentrations.

Normal mice and mice genetically predisposed to have imbalanced homocysteine levels were evaluated in this study. Some of the mice were supplemented with 300 mg/kg of folic acid in their drinking water for 6 weeks. The mice were then evaluated for blood flow to the tibial bone, which is a bone in the lower leg, using dual energy X-ray absorptiometry (DEXA). The bone was also assessed for the marker of oxidative stress, NOX-4, and the antioxidant marker thioredoxin-1. Bone remodeling was evaluated by measuring matrix metallopeptidase 9 (MMP-9), which is an enzyme involved in the breakdown of collagen. Availability of nitric oxide, which is a molecule that dilates blood vessels, was also measured.

The researchers found that the mice genetically predisposed to having imbalanced homocysteine had suboptimal blood flow to the bone and suboptimal bone density compared to the normal mice. The genetically predisposed mice also showed MMP-9 imbalances, indicating bone remodeling, suboptimal antioxidant marker thioredoxin-1, imbalances in oxidative stress marker NOX-4, and suboptimal nitric oxide bioavailability.

Mice that received folic acid supplementation had more optimized function in these specific areas.

The researchers concluded that folic acid may contribute to healthy bone density in cases of genetically imbalanced homocysteine levels.

Reference:

Tyagi N, Kandel M, Munjal C, Qipshidze N, Vacek JC, Pushpakumar SB, Metreveli N, Tyagi SC. Homocysteine mediated decrease in bone blood flow and remodeling: Role of folic acid. J Orthop Res. 2011 Apr 5. Published Online Ahead of Print.