Cover it through the diet; K2 is used as a supplement for bone and arteries.
Meta-analysis of prospective studies: higher vitamin K levels or intake were associated with somewhat fewer cardiovascular events and lower mortality. Observational association (interesting for vitamin K2 and arterial calcification); does not prove cause.
View the study (meta-analysis) →⏱ 4 min read
Vitamin K is a group of related fat-soluble compounds that share the basic biochemical function of serving as a cofactor of gamma-glutamyl carboxylase, an enzyme that activates, through post-translational carboxylation, a specific set of vitamin K-dependent proteins (clotting factors II, VII, IX, and X; anticoagulant proteins C, S, and Z; osteocalcin in bone; matrix Gla protein or MGP in vessels; others); this family of vitamins is divided into two main forms with partially distinct pharmacological and tissue profiles: vitamin K1 (phylloquinone, found in leafy green vegetables) and vitamin K2 (menaquinone, with several subtypes MK-4 to MK-13 depending on chain length, found in fermented and animal foods).
The specific profiles for vitamin K1 and vitamin K2 in this database detail the particular characteristics of each form; this article provides an integrated overview of the family and of the clinical considerations that affect both.
The most important difference between K1 and K2 is tissue distribution after absorption: K1 accumulates preferentially in the liver (where it participates in the activation of clotting factors and anticoagulant proteins), whereas K2 is distributed more efficiently to extrahepatic tissues (bone, vessels, other tissues) where it activates extrahepatic vitamin K-dependent proteins (osteocalcin, MGP, others); this tissue distinction is the basis of the epidemiological data that more consistently associate dietary K2 with cardiovascular and bone benefits than K1.
The body partially converts dietary K1 into K2 (specifically MK-4) in several tissues, but the efficiency of this conversion is variable and modest; people with diets low in fermented foods, whole-fat dairy, and organ meats (the main sources of dietary K2) may have suboptimal K2 intake even with good K1 intake from leafy green vegetables.
The clotting function (mediated mainly by hepatic K1) has the most solid and indisputable clinical indication: the prevention of hemorrhagic disease of the newborn through intramuscular or oral administration of vitamin K1 at birth, an international standard practice with extremely robust clinical data and 80-100 percent reductions in the incidence of severe neonatal bleeding.
The bone function (mediated mainly by K2 activation of osteocalcin) has moderate clinical support: several trials have documented improvements in biochemical bone markers and reductions in bone mineral density loss with specific K2 supplementation (MK-7 at 90-360 micrograms/day) over years; Japanese trials with pharmacological high-dose MK-4 (45 mg/day) show significant reductions in fractures in postmenopausal women; the data position K2 as a useful complement to vitamin D and calcium supplementation in bone health strategies, especially in postmenopausal women.
In vascular calcification (a central process in advanced atherosclerosis), K2 activates matrix Gla protein (MGP), one of the main endogenous inhibitors of arterial calcification; epidemiological data associate high dietary K2 intakes with less coronary calcification and lower cardiovascular mortality; intervention trials with supplemental doses of K2 over 3 years have shown a reduction in the progression of arterial stiffness in postmenopausal women, promising data that, together with the mechanistic basis, support the use of K2 as a complement, especially in people who are simultaneously supplementing with high doses of calcium or vitamin D (where directing mobilized calcium to bone rather than arteries is clinically relevant).
For most people, a varied diet that includes leafy green vegetables (K1) and fermented foods, whole-fat dairy, and some animal foods (K2) provides adequate amounts of both forms; specific K2 supplements (ideally MK-7 at 90-180 micrograms/day) are reasonable as a complement in people supplementing with high doses of calcium or vitamin D, in postmenopausal women for bone health, or in people at high cardiovascular risk or with documented arterial calcification; the recommended total nutritional doses of vitamin K (K1 + K2) are 90-120 micrograms daily in adults.
The most important precaution with any form of vitamin K is the interaction with anticoagulants such as warfarin and acenocoumarol: these drugs act precisely as vitamin K antagonists, and changes in dietary or supplemental vitamin K intake significantly alter the INR and the risk of bleeding or thrombosis; people taking these anticoagulants should maintain a stable vitamin K intake, not necessarily a low one, and consult their anticoagulation specialist before starting supplements; the modern direct oral anticoagulants (rivaroxaban, apixaban, edoxaban, dabigatran) do not have this interaction, and vitamin K is unrestricted with them; in pregnancy and breastfeeding, usual dietary and supplemental intakes are safe; in neonates, prophylactic supplementation with K1 at birth is standard; oral vitamin K supplements are very well tolerated, with no significant toxicities at the usual nutritional and supplemental doses.
Information, not medical advice. Scientific evidence reflects the quality of the studies.