Katarzyna Maresz¹*, Eugene J. Bruno²
*Corresponding author
1. International Science and Health Foundation, Kunickiego St. 10, 30-134 Krakow, Poland
2. Provost & Chief Academic Officer, Huntington College of Health Sciences, 117 Legacy View Way, Knoxville, TN 37918, USA

Abstract

Previously, vitamin K was recognized solely as a cofactor for blood clotting. However, the discovery of vitamin K-dependent proteins (VKDPs) led to a more comprehensive understanding of vitamin K’s role with respect to bone and cardiovascular health. Research has demonstrated that high intakes of vitamin K2 (but not K1), through its activation of the VKDP Matrix Gla Protein (MGP), is associated with reduced arterial calcification, reduced arterial stiffness, and a reduced incidence of coronary heart disease (CHD). Current data suggests that supplementation with Vitamin K2 may help correct widespread vitamin K insufficiency while improving risk parameters for cardiovascular disease in Western populations.

INTRODUCTION

Discovered in 1929, vitamin K was originally identified for its role as a haemostasiological (coagulation) cofactor. The mechanism by which vitamin K performs this function is via its involvement in several proteins, which play a role in the regulation of blood clotting (1). Vitamin K1 and K2 are the two naturally occurring forms of this fat-soluble vitamin. Plants synthesize phylloquinone (K1), and intestinal microbiota synthesizes a range of K2 forms collectively referred to as menaquinones (2). The menaquinone form of vitamin K2 is designated according to the number of repeating 5-carbon units in the side chain of the molecule. For example, if there are seven repeating 5-carbon units, the designation will be menaquinone-7, or MK-7 (3).