Vitamin K - necessary for normal bone formation and prevention of osteoporosis

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Research done by Professor Cees Vermeer at the Department of Biochemistry, Maastricht University in Holland shows that vitamin K is essential in healthy bone metabolism and is highly protective against loss of bone.

What does vitamin K do?

Vitamin K is highly protective agains osteoporosis. It is also necessary for blood to clot. So Vermeer was worried that supplements with vitamin K might increase the clotting tendency. So he set up an experiment to see how vitamin K worked (see below). He showed that when blood vessels were intact, vitamin K inhibited clotting, but when blood vessels were broken, vitamin K promoted clotting. This is a highly desirable state of affairs!

There is not just one vitamin K – there are several and it is still not certain which (if any) is the most important. However they are all present in green leafy vegetables. Vitamin K is also made by gut bacteria - see Probiotics. I often prescribe menadiione 10mgs daily for my osteoporotic patients on the grounds that it can do no harm and may well be doing good. Further research is clearly needed here.

I use vitamin K to treat any bleeding problem such as heavy periods.

An abstract of Vermeer's work:

Vitamin K serves as a cofactor in the posttranslational conversion of protein-bound glutamate into g-carboxyglutamate, also known as Gla. Since the vitamin K-dependent step is a carboxylation reaction, vitamin K deficiency leads to the synthesis of undercarboxylated proteins. Gla residues are calcium binding groups and are essential for the biological activity of the proteins in which they are found; undercarboxylated Gla-proteins have a low activity in all cases their function is known. Vitamin K-dependent proteins are known to participate in three physiological processes:

  1. in blood coagulation (coagulation factors II, VII, IX and X and proteins C and S);
  2. in bone metabolism (protein S, osteocalcin and matrix Gla-protein (MGP));
  3. in vascular biology (protein S, MGP, and growth arrest specific protein 6 (Gas 6)).

All three bone Gla-proteins are synthesized by the osteoblasts (the bone forming cells) and their importance became clear about 25 years ago, when it was realized that the use of vitamin K-antagonists (coumarin derivatives) in pregnant women was associated with serious bone defects in the foetus. Subsequent experiments in animals (rats, lambs) have shown that notably in rapidly growing (young) bone tissue coumarins interfere with calcium deposition resulting in excessive and irregular precipitation of calcium salts, bone deformations, growth reduction and severe osteopenia. Similar effects were observed in MGP knock-out mice. In 1984 it was shown by the group of Shearer that osteoporotic femur neck fractures were associated with very low circulation vitamin K levels. Similar data were observed by the group of Delmas. In 1989 data from our lab showed significant undercarboxylation of osteocalcin in postmenopausal women, which was normalized after vitamin K supplementation. These data, which strongly suggest that a mild vitamin K deficiency is common in elderly women, were confirmed by the group of Delmas, who also showed that circulating undercarboxylated osteocalcin is inversely correlated with bone mass, and that it is a strong risk factor for hip fracture. Several clinical trials showed that the daily intake of 1-10mg/day of vitamin K results in an increase of serum markers for bone formation, and in an increase of urine markers for bone resorption. Also urinary calcium loss was decreased, notably in those with high calcium excretion. Japanese studies showed that intake of vitamin K supplements results in substantial reduction of postmenopausal bone loss, but these data need verification in other populations.

In the arterial vessel wall the functions of Gla-proteins are probably associated with: local inhibition of thrombosis (protein S), inhibition of mineralisation (MGP), and stimulation of normal cell growth and prevention of apoptosis in growth arrested cells (Gas6). MGP-deficient mice were born to term but all died before the 8th week due to massive arterial calcification and rupture of the aorta. Gas6 was shown to prevent starvation-induced death of fibroblasts and smooth muscle cells, and may act as a growth-potentiating factor which acts synergistically with other known growth factors in these cells. Data presently available suggest that in humans Gas6 may play a key role in preventing the degeneration of an atherosclerotic vessel wall.

Conclusions: Vitamin K dependent proteins play a regulatory role in at least three important physiological processes: blood coagulation, bone metabolism, and vascular biology. Recent developments suggest that for normal haemostasis the nutritional vitamin K intake is adequate, but that both other processes may require intakes above the accepted RDA levels.

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