Vitamin K

Vitamin K is a family of fat-soluble compounds required for γ-carboxylation of specific proteins — clotting factors II, VII, IX, X, protein C, protein S, plus osteocalcin and matrix Gla protein. In practical terms this means vitamin K clots blood, mineralises bone, and keeps calcium out of arteries.

K1 vs K2

Daily requirements

Deficiency

Rare in adults with normal diets. Bleeding tendency (elevated INR/PT) is the first clinical sign. Newborns routinely receive an intramuscular vitamin K injection at birth to prevent vitamin K deficiency bleeding (VKDB), which can otherwise cause fatal intracranial haemorrhage.

Bone health

Osteocalcin requires vitamin K–dependent γ-carboxylation to bind calcium to bone hydroxyapatite. Undercarboxylated osteocalcin (ucOC) is a marker of vitamin K insufficiency and correlates with fracture risk. Meta-analyses of K1 supplementation for fracture prevention are modestly positive; K2 (MK-7 45 µg/day) has stronger evidence for improving bone mineral density in postmenopausal women (Knapen 2013).

Arterial calcification

Matrix Gla protein (MGP), also vitamin K–dependent, actively inhibits arterial calcium deposition. The Rotterdam Study found high dietary K2 intake associated with lower coronary calcification and cardiovascular mortality (Geleijnse 2004). RCTs of MK-7 in kidney disease show slowed vascular calcification progression. This is the biological basis for pairing K2 with high-dose vitamin D.

Warfarin interaction

Vitamin K reverses warfarin. Patients on warfarin should keep vitamin K intake consistent, not necessarily low — sudden increases (starting a leafy-greens phase) or decreases (going low-vegetable) will destabilise INR. DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) are not affected by vitamin K.

Food sources

Supplementation

Not medical advice. Anticoagulation and vitamin K management require physician guidance. Discuss any supplement change with your prescriber, especially if you are on warfarin.

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