Here's a question nobody asks but everyone should: if you take calcium for your bones and vitamin D to absorb it, who decides where that calcium actually goes? Because calcium in your skeleton is great. Calcium in your coronary arteries is a heart attack in slow motion.
The answer, increasingly, is vitamin K2 — a nutrient so underappreciated that most doctors couldn't tell you its food sources and most nutrition labels don't even list it.
Vitamin K1 vs. K2: A Family Divided
Vitamin K comes in two main forms:
Vitamin K1 (phylloquinone) is abundant in green leafy vegetables. Its primary role is activating clotting factors in the liver. If you eat salads regularly, you get plenty of K1. Deficiency is rare in adults.
Vitamin K2 (menaquinones) is a group of compounds (MK-4 through MK-13) found primarily in fermented foods and animal products. K2 activates a different set of proteins — ones that regulate calcium distribution in the body. The most studied forms are:
- MK-4: Short-chain menaquinone found in meat, eggs, and dairy. Rapidly absorbed but short half-life (hours).
- MK-7: Long-chain menaquinone found in natto (Japanese fermented soybeans) and some fermented cheeses. Longer half-life (days), which means more stable blood levels and more sustained tissue activation.
The critical insight: K1 and K2 are not interchangeable. Your body can convert small amounts of K1 to K2, but the conversion rate is insufficient to meet K2's tissue-specific needs. They are functionally distinct vitamins that share a name.
The Two Proteins That Matter
Vitamin K2 activates (carboxylates) two key proteins:
Osteocalcin is produced by osteoblasts (bone-building cells). When activated by K2, osteocalcin binds calcium and incorporates it into the bone matrix. Without K2, osteocalcin remains undercarboxylated — present but inactive. Your body is making the protein that builds bones, but it can't do its job without K2's activation.
Matrix Gla Protein (MGP) is the most potent inhibitor of arterial calcification known. When activated by K2, MGP binds calcium in blood vessel walls and prevents it from depositing there. A study published in The Journal of Nutrition (2004) — the Rotterdam Study — found that high dietary vitamin K2 intake was associated with a 52% reduction in severe aortic calcification and a 57% reduction in coronary heart disease mortality over a 10-year follow-up period. K1 showed no such association.
This selectivity is the crux of K2's importance: it directs calcium toward bone and away from soft tissue. It's the traffic cop of mineral metabolism.
The Evidence: Bones
Japan has been studying K2 for decades, largely because natto — the richest dietary source of MK-7 — is a staple in Eastern Japanese cuisine.
A large observational study from Japan showed that regions with higher natto consumption had significantly lower hip fracture rates. But the interventional data is also accumulating:
- A 3-year randomized controlled trial published in Osteoporosis International (2013) found that MK-7 supplementation (180 mcg/day) significantly decreased the age-related decline in bone mineral content and bone mineral density at the lumbar spine and femoral neck in postmenopausal women. It also improved bone strength.
- MK-4 at pharmacological doses (45 mg/day — note: milligrams, not micrograms) is approved in Japan as a treatment for osteoporosis and has been shown to reduce fracture risk. This dose is far above dietary levels and essentially functions as a drug.
For preventive supplementation, MK-7 at 100-200 mcg/day is the most practical and studied approach.
The Evidence: Arteries
Arterial calcification (calcium depositing in blood vessel walls) is a strong predictor of cardiovascular events. It's measured by coronary artery calcium (CAC) scoring.
The Rotterdam Study's finding that K2 reduced coronary heart disease mortality by 57% was observational, not interventional. However, a 3-year RCT published in Thrombosis and Haemostasis (2015) found that MK-7 supplementation (180 mcg/day) significantly improved arterial stiffness in healthy postmenopausal women. A subgroup analysis showed the most benefit in women who already had high arterial stiffness at baseline.
The picture is still developing, but the biological mechanism (MGP activation), the observational data (Rotterdam Study), and the early interventional evidence all point in the same direction.
Food Sources
| Food | Serving | K2 Content (mcg) | Form |
|---|---|---|---|
| Natto | 3.5 oz | 1,000+ | MK-7 |
| Gouda cheese | 1 oz | 20 | MK-7, MK-9 |
| Brie cheese | 1 oz | 15 | MK-7 |
| Egg yolk | 1 large | 5-10 | MK-4 |
| Chicken liver | 3 oz | 12 | MK-4 |
| Butter (grass-fed) | 1 tbsp | 2-5 | MK-4 |
| Sauerkraut | 1/2 cup | 5 | Mixed MK |
Natto is in a league of its own — a single serving provides over 1,000 mcg of MK-7. The catch: natto has a texture and flavor that many Western palates find challenging (sticky, stringy, pungent fermented soybeans). If you love it, you're set. If you can't tolerate it, supplementation is the practical alternative.
European-style cheeses, particularly aged varieties like Gouda and Brie, are the best Western food sources but still provide relatively modest amounts.
Why Most People Are Probably Low in K2
Unlike K1 (which is abundant in any green vegetable), K2 requires specific dietary choices that many people don't make:
- Fermented foods aren't a staple in most Western diets
- Modern animal products from grain-fed livestock contain less K2 than those from grass-fed animals (the animal converts K1 from grass into K2)
- No official RDA exists for K2 specifically (vitamin K recommendations are based on K1 clotting needs)
Subclinical K2 insufficiency — enough K1 for clotting but not enough K2 for best calcium regulation — is likely widespread but difficult to measure with standard lab tests.
Supplementation Guidance
Form: MK-7 is preferred for supplementation due to its longer half-life and more consistent blood levels. A single daily dose maintains steady-state activation of osteocalcin and MGP.
Dose: 100-200 mcg of MK-7 per day. This is the range used in positive clinical trials for bone and arterial health.
Timing: K2 is fat-soluble. Take it with a meal containing dietary fat for best absorption.
Pairing: K2 works together with vitamin D3 and calcium. Many practitioners recommend supplementing all three together, particularly for bone health in postmenopausal women and older adults.
The Warfarin Question
Warfarin (Coumadin) works by blocking vitamin K recycling, which inhibits K-dependent clotting factors. This has led to blanket advice to "avoid vitamin K" for warfarin users.
The nuance: warfarin primarily targets K1-dependent clotting factors in the liver. K2 (particularly MK-7) has a stronger affinity for extrahepatic tissues (bones, arteries). However, MK-7 does affect INR at supplemental doses. If you take warfarin, do NOT start K2 supplementation without consulting your prescriber. The interaction is real and needs monitoring.
When to Talk to a Pro
Consult a healthcare provider if:
- You take warfarin or other vitamin K-dependent anticoagulants
- You have osteoporosis or osteopenia and are considering K2 as part of your treatment plan
- You have existing cardiovascular calcification and want to know if K2 might help
- You take high-dose vitamin D and want to add K2 (generally sensible, but discuss it)
- You have a clotting disorder
FAQ
Does vitamin K2 thin or thicken the blood? Vitamin K2 supports normal blood clotting — it doesn't thin the blood. At typical supplemental doses (100-200 mcg MK-7), it's unlikely to cause excessive clotting in healthy people. The concern is specifically for warfarin users, where any vitamin K can counteract the drug's anticoagulant effect.
Can I get enough K2 from a multivitamin? Most multivitamins contain K1, not K2 — or contain very small amounts of K2 (10-25 mcg). This is typically insufficient for the calcium-directing benefits discussed here. A dedicated K2 supplement is usually necessary.
Is K2 safe during pregnancy? Vitamin K is generally considered safe during pregnancy at recommended levels. In fact, adequate vitamin K status supports fetal bone development. However, specific research on K2 supplementation during pregnancy is limited. Discuss with your prenatal care provider.
How long does it take for K2 to work? Osteocalcin and MGP activation begins within weeks of starting supplementation. However, measurable changes in bone density or arterial stiffness require months to years — consistent with the 2-3 year durations of the positive clinical trials.
A note from Living & Health: We're a lifestyle and wellness magazine, not a doctor's office. The information here is for general education and entertainment — not medical advice. Always talk to a qualified healthcare professional before making changes to your health routine, especially if you have existing conditions or take medications.
