Vitamin K2: The Forgotten Vitamin That Protects Your Bones and Heart

K1 vs K2: A Critical Distinction

Vitamin K1 (phylloquinone) is found in dark green vegetables. The UK diet is generally adequate in K1. Its primary function is blood clotting.

Vitamin K2 (menaquinones, MK-4 to MK-13) is found in fermented foods and certain animal products. UK intakes are typically low. K2 has distinct functions from K1: - Activates matrix Gla-protein (MGP), which prevents arterial calcification - Activates osteocalcin, which binds calcium into bone mineral

The Rotterdam Heart Study (1999, n=4,800) found that high K2 intake (but not K1) was associated with a 57% reduction in death from cardiovascular disease. This seminal finding sparked significant research interest.

The Calcium Paradox

A paradox exists in cardiovascular medicine: high calcium intake is associated with both better bone density AND, in some studies, increased cardiovascular events.

The resolution: calcium without adequate K2 and vitamin D may deposit in soft tissue (arteries) rather than bone. This is the "calcium paradox."

K2 activates MGP, the most potent inhibitor of vascular calcification known. Without K2, MGP remains inactive — calcium can accumulate in arterial walls.

A 2019 RCT (Journal of Bone and Mineral Research) showed that K2 supplementation significantly reduced arterial stiffness in healthy postmenopausal women over 3 years.

K2 and Bone Density

Osteocalcin is a protein produced by osteoblasts (bone-building cells). It binds calcium into hydroxyapatite crystals in bone matrix — but only when carboxylated (activated) by vitamin K2.

Without adequate K2, osteocalcin is undercarboxylated and cannot effectively mineralise bone. Studies measuring ucOC (undercarboxylated osteocalcin) as a K2 insufficiency biomarker find high ucOC associated with fracture risk.

Key studies: - A 2006 meta-analysis (Archives of Internal Medicine, 13 RCTs) found vitamin K2 supplementation reduced hip fracture risk by 77% and vertebral fracture risk by 45% - Japan has used MK-4 (45mg) as a prescription osteoporosis treatment since 1995

MK-4 vs MK-7

The two main supplemental forms of K2:

| Feature | MK-4 | MK-7 | |---------|------|------| | Food source | Certain animal products | Natto (fermented soybean) | | Half-life | 1–2 hours | 72 hours | | Tissue distribution | Liver, brain | Liver, bone, arteries | | Effective dose | 45mg (pharmacological) or 1,000mcg | 90–360mcg | | Bioavailability | Lower | Higher (more sustainable blood levels) |

MK-7 is generally preferred for supplementation because of its longer half-life and lower dose requirement. Look for natural MK-7 (trans-MK-7 from natto) rather than synthetic.

UK Dietary Sources of K2

| Food | K2 content | |------|-----------| | Natto (fermented soy, 85g) | 850mcg MK-7 | | Hard cheese (Gouda, 50g) | 45mcg MK-4/MK-7 | | Soft cheese (Brie, 50g) | 25mcg | | Egg yolk (1) | 10–15mcg MK-4 | | Chicken liver (100g) | 30–60mcg | | Butter (10g) | 2–5mcg |

UK intakes are typically 10–60mcg/day — well below the levels showing benefits in studies (90–360mcg MK-7 or 1,000–45,000mcg MK-4).

When to Supplement

K2 supplementation is particularly relevant when: - Taking vitamin D at doses above 1,000 IU (high-dose D increases calcium absorption — K2 directs it appropriately) - Post-menopausal women (bone loss accelerates) - People with cardiovascular risk factors - Those with arterial calcification on imaging - People with osteoporosis or osteopenia

Dose: 100–200mcg MK-7 daily is the range used in most positive RCTs.

Drug Interactions

Anticoagulants (warfarin, acenocoumarol): K2 can interfere with warfarin's mechanism. If you take anticoagulants, do not supplement K2 without GP advice. The dose can be managed with INR monitoring, but requires clinical oversight.

Non-warfarin anticoagulants (DOACs like rivaroxaban, apixaban): no significant interaction. K2 supplementation is generally safe.

This is educational information. Discuss supplementation with your GP if you take anticoagulants or have cardiovascular disease.