K2 is one of the most genuinely confusing nutrients in the bone health space. Here's what it actually does, what the research shows (and where it falls short), and how Canadians can realistically get more of it.
If you've spent any time researching bone health, you've probably seen vitamin K2 mentioned alongside calcium and vitamin D. But unlike those two, K2 tends to get buried in vague claims. What does it actually do? Is it the same as the vitamin K your doctor tests for? And does the evidence support supplementing it?
These are reasonable questions. The answers are nuanced — some good evidence, some clear gaps, and a few important distinctions that most popular sources blur together.
This is where most confusion starts. "Vitamin K" gets treated as a single nutrient, but K1 (phylloquinone) and K2 (menaquinones) have very different roles in the body.
Vitamin K1 is abundant in leafy greens — kale, spinach, broccoli. Its primary function is blood clotting. When doctors test your vitamin K levels, they're testing K1. When warfarin (Coumadin) works by inhibiting vitamin K, it's K1-dependent clotting it's interfering with.
Vitamin K2 is primarily involved in calcium regulation. It activates proteins that direct calcium into bone and keep it out of soft tissues like arteries. K2 is largely absent from plant foods; it comes from fermented foods and animal products. Most Canadians get far less K2 than K1 from their diet, and the two don't reliably convert to each other.
So when someone asks "does vitamin K help bones?" — they usually mean K2 specifically. K1 plays a minor supporting role in bone metabolism, but K2 is the one with the more direct and interesting mechanism.
K2 is a cofactor for a process called gamma-carboxylation, which activates certain proteins by adding calcium-binding sites to them. Two proteins matter most for bone and vascular health:
Osteocalcin is produced by osteoblasts (bone-building cells) and plays a key role in mineralizing the bone matrix. But it only binds calcium effectively when it's been carboxylated — and that requires vitamin K2. Uncarboxylated osteocalcin (ucOC) circulates in the blood and is sometimes used as a biomarker of vitamin K2 insufficiency. Several studies show elevated ucOC is associated with lower bone density and higher fracture risk, though the relationship is correlational and the causality isn't fully established.
MGP is one of the most potent known inhibitors of vascular calcification. It's produced in arterial wall cells and, when activated by K2, prevents calcium from depositing in blood vessel walls. When K2 is insufficient, MGP remains uncarboxylated and can't do its job. Uncarboxylated MGP (ucMGP) has been proposed as a cardiovascular risk marker, and several population studies — notably the Rotterdam Study from the Netherlands — found associations between higher dietary K2 intake and lower rates of aortic calcification and cardiovascular mortality. That study, published in 2004 in the Journal of Nutrition, is widely cited; its finding was that high K2 (but not K1) intake was associated with reduced coronary heart disease risk and less aortic calcification.
The practical implication: K2 may help direct calcium to bone while simultaneously protecting arteries from calcification. This is why it's often framed as particularly important for people supplementing calcium — though the direct evidence for this specific claim in supplement contexts is still being built.
K2 exists as several menaquinones (MK-4 through MK-13), but MK-4 and MK-7 are the two you'll actually encounter in supplements and research.
| Feature | MK-4 | MK-7 |
|---|---|---|
| Half-life in body | ~1–2 hours | ~72 hours |
| Dosing frequency needed | Multiple times daily | Once daily |
| Research doses used | Often 45 mg 3×/day (pharmacological) | 90–200 mcg/day (nutritional range) |
| Food sources | Butter, egg yolk, dark poultry meat | Natto (primary), hard fermented cheese |
| Population studied most | Japanese postmenopausal women | European postmenopausal women |
MK-4 is the form most studied in Japan, where pharmacological doses (15 mg three times a day) were used as a licensed treatment for osteoporosis. Several Japanese RCTs showed fracture reduction with this approach. But here's the critical nuance: these were pharmacological doses — milligrams, not micrograms. The typical supplement capsule contains 100 or 200 mcg of MK-4, which is 100–200 times smaller than the research doses. Whether low-dose MK-4 from supplements produces equivalent benefits is not established. Additionally, MK-4's short half-life means once-daily dosing likely produces blood level peaks and troughs that differ substantially from the research protocols.
MK-7 is derived primarily from natto (fermented soybeans), though smaller amounts appear in other fermented foods. Its long half-life makes it practical for once-daily supplementation — blood levels remain relatively stable. A 2013 Dutch study published in Osteoporosis International (Knapen et al.) followed 244 healthy postmenopausal women for three years and found that 180 mcg/day of MK-7 significantly slowed the rate of bone loss at the spine and femoral neck compared to placebo. This is one of the cleaner Western-population RCTs on MK-7 specifically. A 2020 review in Nutrients found that MK-7 at nutritional doses can promote carboxylation of both osteocalcin and MGP, while MK-4 at equivalent doses is less effective at the extrahepatic (non-liver) level.
Here's an honest summary rather than a rosy one:
Fracture reduction in Japanese populations: Several RCTs have shown K2 supplementation (mostly high-dose MK-4) reduces fracture rates in Japanese postmenopausal women with osteoporosis. These results are relatively consistent. But Japan is unusual: natto consumption is high, baseline K2 intake is higher, and genetic and dietary factors differ from Western populations. These studies don't translate directly.
Bone density (BMD) outcomes in Western populations: More mixed. Some RCTs show modest improvements in lumbar spine BMD or reductions in bone loss rate; others show no significant effect. The Knapen MK-7 study noted above showed bone loss reduction without dramatic BMD gains. Part of the issue is that K2 may improve bone quality (strength, microarchitecture) without large changes in density — and most trials measure BMD rather than fracture outcomes directly.
Vascular calcification: Observational evidence (especially from Rotterdam) is suggestive. Intervention studies are fewer. A 2015 study published in Thrombosis and Haemostasis found that MK-7 supplementation increased activated MGP and modestly reduced vascular stiffness in healthy postmenopausal women. Promising, but not definitive.
The overall picture: the biological mechanism is plausible and well-characterized; the population evidence has meaningful gaps, particularly for fracture endpoints in non-Japanese populations. K2 supplementation appears safe; the main question is whether it produces meaningful clinical benefit beyond adequate calcium and vitamin D.
This is the question Canadians most commonly ask, since D3+K2 combined supplements are widely marketed. The reasoning is coherent: D3 increases calcium absorption from the gut; K2 helps direct that calcium into bone and away from arteries. In theory, they're complementary.
The evidence is suggestive but not conclusive. There's a small number of trials looking at D3+K2 combinations versus D3 alone, and some show additional bone-related benefits (better ucOC correction, for example), but the trial quality and sample sizes are modest. What the research does not yet clearly show is that combining them reduces fracture risk better than D3 alone in Western populations over the timescales and doses relevant to most supplementers.
Editorially: if you're already taking D3, adding MK-7 at 100–200 mcg/day is a low-risk addition with a biologically reasonable rationale. The downside is cost and one more capsule. The evidence isn't strong enough to call it essential, but it's strong enough that many physicians and dietitians don't discourage it.
Most Canadians are low in dietary K2. This isn't surprising: our food patterns don't include the main K2 sources. Here's what's actually realistic:
Natto (fermented soybeans) contains 800–1,000 mcg of MK-7 per 100g serving. A single 50g serving provides 400–500 mcg — several times the 100–200 mcg target. In Canada, natto is available at Japanese grocery stores. In Metro Vancouver and the Lower Mainland, T&T Supermarket (multiple locations) and Oceans Fresh Food Market typically carry it in the frozen section. In Toronto, T&T and smaller Japanese grocery stores stock it. It's an acquired taste — pungent, sticky, with strong umami. If you like it, it's by far the most efficient dietary source.
Gouda (aged), Brie, and Edam contain meaningful amounts of MK-9, a longer-chain menaquinone. Canadian-available Gouda (including Bothwell, Ivanhoe, and various imports) contains roughly 60–75 mcg of K2 per 100g. This is modest compared to natto but meaningful if you eat cheese regularly. Soft cheeses and fresh cheeses contain very little K2.
Egg yolks provide MK-4 in modest amounts — roughly 30–40 mcg per yolk, varying by diet of the hens. Pasture-raised eggs likely provide more. Not a major source, but contributes.
Dark chicken meat (thighs, legs) contains MK-4 at levels of roughly 8–10 mcg per 100g — meaningful if you eat it frequently. White breast meat contains less.
The honest assessment: unless you're regularly eating natto and aged cheese, most Canadians don't come close to the 100+ mcg/day range studied in research. This is the primary argument for supplementation.
For supplementation, MK-7 is the more practical form:
Based on the evidence, K2 supplementation makes the most sense if:
For younger adults eating a varied diet including dairy and eggs, K2 deficiency is less likely to be a limiting factor in bone health. Calcium adequacy and vitamin D are usually the more pressing considerations.