Vitamin K in the Treatment and Prevention of Osteoporosis and Arterial Calcification

Jamie Adams; Joseph Pepping

Disclosures

Am J Health Syst Pharm. 2005;62(15):1574-1581. 

In This Article

Discussion

Over the past decade it has become evident that vitamin K plays a far greater role in human health than previously thought. Vitamin K is essential for the activation, via γ-carboxylation, of VKD proteins. These proteins have various functions and are found throughout the body. Some of these proteins, such as those involved in blood coagulation, have been thoroughly researched. Others, notably those involved in bone metabolism and the inhibition of arterial calcification, have drawn new attention to vitamin K.

Numerous studies have demonstrated the importance of vitamin K in bone health. Cell studies have helped delineate the mechanism by which menaquinone promotes bone mineralization and inhibits resorption.[35] Human and animal studies have clearly demonstrated that vitamin K can improve bone health by increasing bone mass and reducing bone loss.[12,37,46,54]

The results of two dose-response studies have indicated that (1) the amount of vitamin K needed for optimal γ-carboxylation of osteocalcin is significantly higher than what is provided by diet alone and (2) there is a need to increase current dosage recommendations to optimize bone mineralization.[32,33]

The combination of menaquinne and vitamin D3 has additive beneficial effects on sustaining lumbar BMD and preventing osteoporotic vertebral fractures in postmenopausal women with osteoporosis.[12,50]

The role of vitamin K in the prevention of arterial calcification is not as well researched. Several epidemiologic studies,[5,6,7,8] as well as a recent clinical trial of postmenopausal women,[63] have implicated phylloquinone deficiency as a risk factor for arterial calcification and have alluded to a connection between the deficiency and osteoporosis.

Additional research is needed to address several important questions: What is the optimal intake of phytonadione, menaquinone, and vitamin D3 to support bone mineralization and reduce fracture risk? What is the optimal dosage of phytonadione and menaquinone to preserve the elasticity of arterial endothelial tissue by decreasing the calcification of the intima and media? Do phytonadione, menaquinone, and vitamin D3 have additive bone mineralization effects with bisphosphonates, selective estrogen-receptor modulators, or hormone therapies (e.g., estrogen for women and testosterone for men)? Is menaquinone more efficacious in reducing fracture risk than phytonadione? Does vitamin K play a role in immune modulation with respect to cytokine expression? Is there a potential relationship between chronic inflammation (as seen in both vascular calcification and osteoporosis) and vitamin K deficiency? For example, is synthesis or the activities of inflammatory cytokines, such as tumor necrosis factor, prostaglandin E2, and interleukin-1, affected by vitamin K levels?

Because of their very low toxicity and potentially beneficial effects on both bone mineralization and attenuation of arterial calcification, phytonadione and menaquinone should be strongly considered as nutritional adjuncts in patients most susceptible to these disorders, such as postmenopausal women, diabetics, and hemodialysis patients.

Conclusion

Phytonadione and menaquinone may be effective for the prevention and treatment of osteoporosis and arterial calcification.

Comments

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