An abundance of human clinical data reveals that vitamin K plays a critical role in maintaining healthy bone density by facilitating the transport of calcium from the bloodstream into the bone. Vitamin K is also required by calcium-regulating proteins in the arteries. Matrix Gla-protein (MGP) is a vitamin K-dependent protein, and it must be carboxylated to function properly. Poor vitamin K status leads to inactive uncarboxylated MGP (ucMGP), which accumulates at sites of arterial calcification. Since MGP is a potent local inhibitor of arterial calcification, MGP is important in relation to the health of the entire cardiovascular system. Without adequate vitamin K, calcium in the blood can bind to the arterial wall resulting in calcification. As people age, even a subclinical vitamin K deficiency can pose risks to the vascular system. Poor vitamin K status also results in increased circulating levels of undercarboxylated osteocalcin that is shown to be associated with increased bone loss in postmenopausal women. Humans get most of their vitamin K from green vegetables in the form of vitamin K1. The problem is that K1 is tightly bound to plant fiber and only a small fraction absorbs into the bloodstream. Vitamin K2 (menaquinones) is found in meat, eggs, and dairy products and is also made by bacteria in the human gut, which provides a certain amount of the human vitamin K requirement. Human studies show that vitamin K2 is up to ten times more bioavailable than is K1. Vitamin K2 remains biologically active in the body far longer than K1. For instance, K1 is rapidly cleared by the liver within eight hours, whereas measurable levels of K2 have been detected 72 hours after ingestion.

Individuals taking anticoagulant drugs, such as Coumadin or Heparin, should avoid vitamin K supplements, unless otherwise directed by a physician.*

Bones, Osteoporosis