I wrote this section of 589 words this morning as an introduction to more detailed information that will follow.
Structure
Similar to “vitamin E” which represents a group of distinct molecules (eg, DL/alpha/gamma-tocopherols, vitamin E succinate, tocotrienols), the term “vitamin K” includes several forms of the vitamin, each with different dosage, effects, and therapeutic applications. All types of vitamin K are quinones (conjugated nonaromatic six-carbon rings with reductive ability), specifically with a 2-methyl-1,4-naphthoquinone nucleus (two six-carbon rings), while the vitamin K2 group (menaquinones, vK2) are distinguished by the number of isoprenyl (C[5]H[8]) units. Vitamin K1 (phylloquinone, phytonadione, vK1) is the form of vitamin K found in plants. Produced by intestinal bacteria and also present in some foods, vitamin K2 (menaquinone) with four isoprenyl units is menaquinone-4 (MK-4, menatetrenone, vK4) and with seven isoprenyl units is menaquinone-7 (MK-7, vK7), which can be converted to vK4. Vitamin K3 (menadione, vK3) is a synthetic/unnatural form of the vitamin which, among other characteristics, is converted into vK4; vK3 has been used as an experimental anticancer agent but is not commonly used as a source of vitamin K. Note that my use of vK1, vK4, vK7 is my personal preference for efficiency of communication/differentiation.
Function
A common biochemical theme of different forms of vitamin K is that they are cofactors for the carboxylase enzyme that gamma-carboxylates glutamic acid residues to form gamma-carboxyglutamate (Gla) on specific proteins in order to create calcium-binding sites, thereby activating specific functions of those proteins (vitamin K-dependent proteins), such as blood-clotting factors II (2), VII (7), IX (9), X (10), the anticlotting proteins C and S, osteocalcin (bone Gla protein, which binds calcium in bone, promoting bone calcification), and vK2-dependent matrix Gla protein (MGP, which binds calcium in soft tissues including vasculature, inhibiting soft tissue and vascular calcification).
Politics
Official government-endorsed recommendations for vitamin K intake are sufficient to prevent hemorrhage but are not sufficient to optimize osteocalcin nor matrix Gla protein[1]; this is to be expected as government/academic institutions are selectively unwilling to advance beyond acknowledgement of acute deficiency disease to endorse prevention of “long-latency deficiency diseases” (classic concept and article by Robert Heaney, Am J Clin Nutr 2003 Nov[2]) which would advance the human population toward improved/optimal health.