Vitamin K1 intake and coronary calcification

In Brief Objectives The activity of matrix Gla-protein (MGP), a potent inhibitor of vascular calcification, is dependent on carboxylation using vitamin K as a co-factor. In animals, low intake of total vitamin K has been shown to accelerate vascular calcification via the MGP mechanism. This has led to the hypothesis that low levels of dietary vitamin K intake may be a risk factor for accelerated vascular calcification in humans due to decreased MGP activity. Additionally, some authors have suggested that current recommended daily intake values for vitamin K might be insufficient to fully inhibit vascular calcification via the MGP mechanism. The aim of this study was to examine the relationship between dietary vitamin K1 (the most prevalent dietary form of vitamin K) intake and premature coronary artery calcification (CAC) in an asymptomatic screening population. Methods We conducted a prospective study of 807 consecutive active-duty US Army personnel, 39–45 years of age, without known coronary heart disease. Vitamin K1 intake was measured with the Block Dietary Questionnaire and CAC was identified using electron-beam computed tomography (EBCT). Results We found no significant correlation between CAC score and vitamin K1 intake (r=0.132, P=0.106). Multivariate analysis with adjustment for cardiac risk factors showed no association between dietary vitamin K1 intake and CAC. Conclusions Dietary vitamin K1 (phylloquinone) intake appears to be unrelated to premature coronary calcification in a screening population. Further investigation into the relationship of vascular calcification and other forms of vitamin K1 (menaquinones) is indicated. Vitamin K1 is hypothesized to be protective from tissue calcification through mechanisms including carboxylation of matrix gla protein. In this cross sectional study of 807 healthy men and women, we found no association between dietary vitamin K1 (phylloquinone) intake and the presence and extent of coronary artery calcification as measured by electron-beam computed tomography. These data support the current recommended levels of vitamin K1 (phylloquinone) intake as well as the possibility that vascular tissue may preferentially use menaquinones rather than the phylloquinone form of vitamin K for MGP activity and inhibition of vascular calcification. Further investigation into the relationship of vascular calcification and other forms of vitamin K (menaquinones) is indicated.