Anyone here take Vit K2? I was hoping all the great minds of Imminst forum might weigh in on this.
There seem to be two forms of vitamin K2 available as supplements, Vitamin K2 as Menaquinone-7, (MK-7) and as Menaquinone-4 (Mk-4). There are significant differences between these two forms of vitamin K2.
(The vitamin K in plants is K1, also called phylloquinone. K1 is required for proper blood clotting. It's particularly rich in greens. It's made into K2 MK-4 by some animals, but humans seem to be bad at making the conversion.)
Some argue that MK-7 (made from natto) is more bioavailable, and has the longest serum half life; that MK-7 is superior because it stays in bloodstream 20 times longer (100h vs 5h) - which in itself has a whole host of advantages. See: http://www.menaq7.co...dex.php?s=Links
Others argue that the longer serum half life of MK-7 may be of dubious advantage. Is it positive or negative? If it stays longer in the blood stream perhaps because it is not being readily absorbed by bone and other tissue then is is not so good (thus MK-4 should be better). If on the other hand MK-4 stays so short because it is getting destroyed too quickly then MK-7 should be more benefitial in smaller doses!
So others argue that MK-4 (found mostly in animal fats/butter and in specialized supplements derived from animal fat) is far superior. See this blog: http://wholehealthso...vitamin-k2.html
K2 can be produced by bacterial fermentation, but an argument can be made that K2 MK-4, the animal form, is the most natural for humans and the most effective.
MK-4 is the type that mammals synthesize for themselves, whereas the MK-7 in natto and other bacterial menaquinones are different.
The form of K2 that Weston Price described in Nutrition and Physical Degeneration was almost certainly MK-4.
An interesting study he cites:
1: J Vasc Res. 2003 Nov-Dec;40(6):531-7. Epub 2003 Dec 3. Links
Tissue-specific utilization of menaquinone-4 results in the prevention of arterial calcification in warfarin-treated rats.
Spronk HM, Soute BA, Schurgers LJ, Thijssen HH, De Mey JG, Vermeer C.
Department of Biochemistry, Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands. email@example.com
The effects of vitamin K (phylloquinone: K1 and menaquinone-4: MK-4) on vascular calcification and their utilization in the arterial vessel wall were compared in the warfarin-treated rat model for arterial calcification. Warfarin-treated rats were fed diets containing K1, MK-4, or both. Both K1 and MK-4 are cofactors for the endoplasmic reticulum enzyme gamma-glutamyl carboxylase but have a structurally different aliphatic side chain. Despite their similar in vitro cofactor activity we show that MK-4 and not K1 inhibits warfarin-induced arterial calcification. The total hepatic K1 accumulation was threefold higher than that of MK-4, whereas aortic MK-4 was three times that of K1. The utilization of K1 and MK-4 in various tissues was estimated by calculating the ratios between accumulated quinone and epoxide species. K1 and MK-4 were both equally utilized in the liver, but the aorta showed a more efficient utilization of MK-4. Therefore, the observed differences between K1 and MK-4 with respect to inhibition of arterial calcification may be explained by both differences in their tissue bioavailability and cofactor utilization in the reductase/carboxylase reaction. An alternative explanation may come from an as yet hypothetical function of the geranylgeranyl side chain of MK-4, which is a structural analogue of geranylgeranyl pyrophosphate and could interfere with a critical step in the mevalonate pathway. Copyright 2003 S. Karger AG, Basel