# Vitamin K2

> Vitamin K2 (menaquinone) is the vitamin that determines where calcium goes. It is the cofactor for the γ-carboxylation of osteocalcin, which binds calcium into the bone matrix, and of matrix Gla…

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Section: Substances and pharmacology
Last updated: 2026-10-20
Publisher: Library of Ashurbanipal (Van Kush Family Research Institute), https://wiki.soapbox.community

**Vitamin K2** (menaquinone) is the vitamin that determines **where calcium goes**. It is the cofactor for the γ-carboxylation of **osteocalcin**, which binds calcium into the bone matrix, and of **matrix Gla protein**, which actively inhibits calcification of arteries and soft tissue.

That dual role is the entire argument for the nutrient: without adequate K2, calcium is deposited less reliably in bone and more readily in vessel walls — the direction nobody wants.

## K1 and K2 are not interchangeable

- **K1 (phylloquinone)** — from green leaves; taken up preferentially by the liver for the clotting cascade. Most dietary vitamin K is K1.
- **K2 (menaquinone)** — from fermented foods and animal products; reaches bone and vessel tissue.

Within K2 the **subtype governs the half-life**, and the difference is large:

- **MK-4** — half-life of **hours**. Occurs in animal tissue; the form the body makes by converting K1. Studied at pharmacological doses (45 mg/day) in Japanese osteoporosis trials.
- **MK-7** — half-life of **about three days**. From *Bacillus subtilis* fermentation; **nattō** is the dietary source. Maintains a steady blood level from a single daily dose, which is why it is the form in most bone formulations, typically 90–180 μg.

MK-7's long half-life is the whole reason it displaced MK-4 in supplements: MK-4 at supplement doses is cleared before it does much.

## Evidence

- **Rotterdam Study** — higher dietary K2 (not K1) associated with less coronary calcification and lower cardiovascular mortality. Observational.
- **Knapen (2013)**, 3 years, MK-7 180 μg/day in postmenopausal women — reduced bone-mineral-density loss and reduced vertebral height loss.
- Japanese MK-4 osteoporosis trials at 45 mg/day are positive but at doses three orders of magnitude above supplement levels and have not consistently replicated outside Japan.

Reasonable summary: the mechanism is solid, the bone evidence is decent, the cardiovascular evidence is largely observational.

## The one interaction that matters

**Warfarin.** Warfarin works *by* antagonising vitamin K. Adding K2 opposes the drug directly and changes INR. This is not a caution to be careful — it is a reason not to start it without the prescriber's involvement. It does **not** apply to the direct oral anticoagulants (apixaban, rivaroxaban, dabigatran), which do not act on vitamin K.

## Other cautions

- Fat-soluble — take with fat; deficiency is likelier after bariatric surgery or with fat malabsorption.
- K2 is frequently combined with **high-dose vitamin D**, which raises calcium absorption. The pairing has a rationale — D brings calcium in, K2 directs it — but a high-dose D regimen has its own risks that K2 does not cancel.
- No established toxicity for K1 or K2 at supplemental doses; synthetic **K3 (menadione)** is a different matter and is not used in human supplements.

See also: Creatine · Chelated Minerals · Stack Substances