Vitamin K2

Tells calcium where to go: into bone, and out of your arteries.

Mechanisms, studies and evidence grades for each claim above.

Core mechanism

K2 enables γ-carboxylation of proteins, allowing them to bind calcium — this is what controls where calcium gets deposited in the body.

Bone (osteocalcin)

Activates osteocalcin, which binds calcium and incorporates it into the bone matrix.¹ Without K2, osteocalcin stays undercarboxylated and inactive, reducing bone mineralization.

Vascular system (matrix Gla protein, MGP)

Activates matrix Gla protein (MGP), which inhibits vascular calcification.² Without K2, inactive MGP allows calcium to accumulate in arteries — higher K2 status is associated with reduced arterial calcification and cardiovascular risk.³

Interaction with vitamin D

Vitamin D increases calcium absorption; K2 directs where that calcium goes (into bone via osteocalcin). Without sufficient K2, there's a higher risk of calcium ending up in the wrong place. See Vitamin D.

Deficiency effects

Undercarboxylated (inactive) osteocalcin and MGP, associated with vascular calcification and reduced bone quality.²

Forms: MK-4 vs. MK-7

• MK-4 — shorter half-life; found in animal tissues.
• MK-7 — longer half-life and broader tissue distribution;² found in fermented foods (e.g., natto); more stable circulating levels. This is the form the Metabolic Health hub recommends, with the explicit caveat that MK-7's long half-life doesn't license intermittent dosing — daily intake is still needed for consistent carboxylation activity.

Intake

Roughly 90–200 mcg/day, context-dependent.

Top foods

• Natto (highest)
• Fermented foods (K2-rich)
• Animal products (eggs, dairy, liver)

Key insight

Vitamin K2 activates proteins that determine where calcium goes — directing it into bone and helping prevent buildup in arteries.¹²

References