Are Your Bones Getting Enough of This Important Vitamin?

by VRP Staff

If you're beginning to have concerns about maintaining your bone health, you might think that an extra glass of milk every day will deliver all the nutrients you need. But the truth is that calcium and vitamin D alone can't support the dynamic metabolism of your bones—and new research is shining a spotlight on the vital importance of another vitamin in the effort to support overall bone strength.

As part of a recent study, researchers set out to identify the influence that vitamin K2 (also known as menaquinone) has on osteoclasts and osteoblasts—two types of cells that work in tandem to break down and form bone tissue, respectively. This continual process of resorption and regeneration—called "remodeling"—is essential to maintaining maximum, lifelong bone density and strength.

There are several factors, however, that can throw your body's bone remodeling process off balance—and as the results of this new study show, vitamin K2 may play a critical role in keeping the cycle on track.

The researchers discovered that vitamin K2 is able to block the activation of nuclear factor kappa-B (NF-kappaB) and tumor necrosis factor alpha (TNF-alpha)—two inflammatory mediators that simultaneously increase the activity of bone-degrading osteoclasts while decreasing the activity of bone-building osteoblasts. By keeping NF-kappaB and TNF-alpha at bay, vitamin K2 tips your body's scales back toward regeneration, promoting normal bone tissue formation and supporting maximum bone density.¹

These findings support previous research on vitamin K2's benefits for bone density support, with the study authors touting its unique bone-building mechanism as an effective potential tool in the quest to maintain a strong skeleton. And that's just one more reason to add a daily dose of this nutrient—available as Ultra K2 from Vitamin Research Products®—to your bone health regimen today.

Reference:

1. Yamaguchi M, Weitzmann MN. Vitamin K2 stimulates osteoblastogenesis and suppresses osteoclastogenesis by suppressing NF-kB activation. Int J Mol Med. 2010 Nov 11. Published Online Ahead of Print.

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