A protective role for
vitamin K in
cardiovascular disease (CVD), a leading cause of morbidity and mortality, has been proposed because
vitamin K-dependent
proteins, such as matrix Gla (γ-carboxyglutamic
acid)
protein (MGP), are present in vascular tissue. MGP functions as a
vascular calcification inhibitor-but only when it is carboxylated, which requires
vitamin K. There is more than one naturally occurring form of
vitamin K.
Phylloquinone (
vitamin K1) is found in plant-based foods, whereas
menaquinones (
vitamin K2) are a class of
vitamin K compounds found in animal-based and fermented foods.
Phylloquinone and
menaquinones are capable of carboxylating MGP and other
vitamin K-dependent
proteins. In rodent models, high intakes of either
phylloquinone or
menaquinone reduced
vascular calcification. Evidence of the relative importance of
phylloquinone and
menaquinone to CVD in humans is limited and controversial. In some observational studies, higher dietary
menaquinone intake, but not
phylloquinone intake, was associated with less coronary artery calcification (a subclinical manifestation of CVD) and a lower risk for clinical CVD events. These findings have led to claims that
menaquinones have unique cardiovascular health benefits compared with
phylloquinone. However, this claim is not supported by the results of the limited number of intervention trials conducted to date. The purpose of this review is to evaluate the strengths and limitations of the available evidence regarding the role of
vitamin K in
vascular calcification, CVD, and mortality.