BENEDETTA RASPINI, BENVENUTO CESTARO, ROBERTA CAZZOLA*
*Corresponding author
University of Milan, Dept. Biomedical and Clinical Sciences “L. Sacco”, Graduate School of Nutrition Science, Via G. B. Grassi 74, 20157 Milan, Italy

Abstract

Osteoporosis and cardiovascular diseases present similar etiopathogenic mechanisms. The presence of a “bone-vascular cross talk” is pointed out by several studies. This altered balance is due to an association between increased mortality due to cardiovascular disease and bone fractures related to osteoporosis. Recent researches revealed that vitamin K2 deficiency could be responsible of a disrupted calcium regulation and that low levels of this vitamin are connected with an enhanced risk of heart disease and atherosclerosis, because of a lack of calcium in bones and an excessive storage of calcium in arteries.

INTRODUCTION

Vitamin K is known as the “Koagulation vitamin“ since it was discovered by the Danish scientist Dr. Henrik Dam in 1929. In the last decades, it has been determined that vitamin K is not a single molecule, but a family of compounds with similar chemical structure and characteristics, fundamental for the maintenance of adequate levels of some coagulation factors. These compounds include phylloquinone (K1 vitamin) and menaquinones (K2 vitamin) (1). Some studies have described alternative functions for vitamin K in addition to its classic role in coagulation, including modulation of vascular calcification, taking out calcium from arteries, decreasing cardiovascular risk, and the improvement of bone health (2-5). Moreover, several studies have suggested that menaquinones could be more efficient in these functions than the phylloquinone (2-5). The purpose of this work is to review the biological effects of vitamin K2 and how it could play a role in the prevention of cardiovascular disease and osteoporosis.

Mechanism of action of Vitamin K
Vitamin K is a cofactor of γ-glutamyl carboxylase (GGCX), an enzyme that ...