Calcium metabolism is the way the human body regulates, moves, and stores calcium ions (Ca²⁺) to keep blood and tissue levels within a strict, healthy range. About 99% of the calcium in your body sits in bone and teeth, locked into a mineral called hydroxyapatite. The rest circulates in blood and soft tissue, running nerve signalling, muscle contraction and clotting.
Serum calcium normally runs around 8.8 to 10.4 mg/dL, and three hormones are involved in this: Parathyroid, calcitriol and calcitonin. When calcium level falls, parathyroid hormone rises, pulling calcium back from urine in the kidney and triggering conversion of vitamin D into calcitriol, which increases gut absorption. And when calcium runs high, calcitonin from the thyroid slows the cells that break down bone.
The only missing link here is the direction system of the calcium. Nothing in that system decides whether the calcium being transported would end up in bone or in an artery wall.
Introduction to Vitamin K
Vitamin K is a fat-soluble vitamin, discovered through its role in blood clotting. It comes in two families: K1 (phylloquinones) and K2 (menaquinones).
K1 (phylloquinone) is made by plants and comes mostly from leafy greens while K2 (menaquinone) is made by bacteria and is present in fermented foods and animal products. They share the same chemical head but differ in the tail, and that tail changes the behaviour because at equal doses, MK-7 reached higher blood levels than K1, lasted for days rather than hours, and activated osteocalcin in a way K1 did not (Schurgers et al., 2007).
What does Vitamin K2 actually do?
Vitamin K2 adds a chemical group to specific proteins, giving them the ability to bind calcium. Before that step, the protein is present in an inactivated state and only gets activated by the vitamin.
These vitamin K-dependent proteins split into two groups. The clotting factors made in the liver are one while the other include osteocalcin, matrix Gla protein and Gla-rich protein. Clotting proteins carry 9 to 13 of these calcium-binding sites; osteocalcin has three.
Osteocalcin
Osteocalcin is made by bone-building cells. Once vitamin K activates it, it binds calcium and anchors the mineral into protein scaffolding of new bone. Unactivated osteocalcin (unOC) cannot bind calcium properly, and blood levels of it climb when vitamin K is short.
Matrix Gla Protein
Matrix Gla Protein (MGP) does the opposite job. MGP is made in cartilage and blood vessel walls, it blocks calcium from crystallising where it should not.
The clearest demonstration came from mice bred without the MGP gene. They calcified their arteries and cartilage and most died within two months of ruptured aorta (Luo et al., 1997). MGP, like osteocalcin, is useless until vitamin K activates it.
This is where vitamin K is very important in the picture. One activation step governs both proteins, and there is a queue to that as well. The liver takes first claim on available vitamin K for clotting factors. Someone can have entirely normal clotting while osteocalcin and MGP go partly unactivated.
The Vitamin K Cycle
Vitamin K is not used once and then discarded. Vitamin K2 acts as an essential cofactor for the enzyme γ-glutamyl carboxylase (GGCX) to activate specific proteins needed for blood clotting, bone metabolism, and the prevention of blood vessel calcification. During this process, the vitamin is oxidised to vitamin K epoxide.
A second enzyme, VKORC1, converts it back so it can be used again. Warfarin blocks VKORC1; stop the recycling and clotting proteins stop being activated.
A vitamin K shortage usually does not show up as a change in your blood calcium levels. The body keeps calcium in the blood within a narrow range by using hormones and, when necessary, drawing calcium from the bones. Instead, low vitamin K affects the activation of certain proteins. For example, more osteocalcin remains in its uncarboxylated, inactive form, while matrix Gla protein (MGP) in the artery walls becomes less effective at preventing mineral buildup. Importantly, this deficiency may not cause noticeable symptoms or appear on a routine blood test.
Because of this, researchers often look at specific protein markers rather than blood calcium levels. Undercarboxylated osteocalcin is used as an indicator of vitamin K availability in bone and has been shown to decrease with K2 supplementation (Zhang et al., 2025). For blood vessels, researchers use dephosphorylated-uncarboxylated MGP (dp-ucMGP), a marker of vitamin K status in vascular tissue. In the two-year VitaK-CAC trial, dp-ucMGP levels decreased with vitamin K supplementation, along with a slower progression of coronary calcium scores (Vossen et al., 2026). However, neither of these markers is currently part of routine clinical blood testing.
What Research Shows
A 2025 meta-analysis of 9 trials covering 2,570 postmenopausal women with osteoporosis found K2 supplementation raised osteocalcin and cut its undercarboxylated fraction, meaning more of the protein was switched on. The authors noted longer studies are still needed to confirm outcomes such as increased bone mineral density (Zhang et al., 2025). On density, three years of 180 µg MK-7 daily slowed bone loss in healthy postmenopausal women (Knapen et al., 2013).
Vitamin D and calcium sit at other points in the same chain. Vitamin D increases absorption, calcium supplies the mineral which is the reasoning behind combination products. The evidence that combining them adds benefit is thinner than the marketing suggests. A trial giving K2 and vitamin D together to men with aortic valve calcification found no slowing of progression (Diederichsen et al., 2022).
MK-4 vs MK-7
| Feature | MK-4 | MK-7 |
| About | A short-chain form of vitamin K2 (menaquinone-4). | A longer-chain form of vitamin K2 (menaquinone-7). |
| Natural sources | Mainly found in animal-derived foods such as meat, eggs, and some dairy products. The body can also make MK-4 from vitamin K1. | Mainly associated with fermented foods, especially natto, a fermented soybean food. |
| How long it stays in the blood | Relatively short-lived and cleared from the circulation more quickly. | Has a longer half-life, so it remains in the bloodstream for longer. |
| Absorption | Can be absorbed effectively, although research comparing the different forms is limited. | Well-absorbed and generally produces more sustained levels in the blood because of its longer half-life. |
| Typical supplement doses | Supplements may contain higher amounts; pharmacological MK-4 doses used in some Japanese osteoporosis studies are much higher than nutritional doses. | Usually found in supplements at much smaller doses, commonly in the microgram range. |
| Bone-related role | Participates in the activation of vitamin-K-dependent proteins such as osteocalcin. | Also supports the activation of vitamin-K-dependent proteins, including osteocalcin. |
| Vascular role | Involved in the vitamin K–dependent activation of proteins such as matrix Gla protein (MGP). | Also supports MGP activation; its longer presence in circulation has made it particularly interesting in vascular research. |
| Research profile | Has been studied extensively, particularly in Japan, including at pharmacological doses for osteoporosis. | Has received considerable research attention because of its longer half-life and sustained availability. |
Safety and Drug Interactions
At usual supplement doses, MK-7 does not appear to affect clotting in healthy adults. In 40 people taking 90 µg daily for 30 days, clotting measures and vitamin K-dependent factor activity did not change (Ren et al., 2021).
Warfarin is the exception, and it follows directly from the vitamin K cycle. Since the drug works by blocking vitamin K recycling, the advice is to keep vitamin K intake steady rather than avoid it, because sudden changes shift the drug’s effect in either direction (National Institutes of Health, n.d.). Starting or stopping a K2 supplement counts as a change worth informing your doctor/prescriber about.
Common Myths
- “K2 pulls calcium out of blocked arteries”
~ No published trial shows reversal. VitaK-CAC showed slower progression of calcium scores over two years, not removal (Vossen et al., 2026).
- “K2 thins the blood”
~ Vitamin K supports clotting, not the reverse, and supplement doses did not change clotting measures in healthy adults (Ren et al., 2021).
- “K2 lowers your calcium level”
~ It does not touch blood calcium. Hormones control that number (Sahota et al., 2026).
- “Gut bacteria make all the K2 you need”
~ Absorption of bacterially produced menaquinones is poor inside the body (Lai et al., 2021).
How TerraQuino Helps
TerraQuino supplies vitamin K2-7 (MK-7) as an ingredient, produced by a controlled fermentation process, supplied allergen-free, and used in tablets, capsules, soft gels, sachets and liquids.
For brands developing supplements, TerraQuino offers flexibility in creating combined-nutrient products. Vitamin K2-7 can be paired with ingredients such as Vitamin D3, calcium salts, omega-3s, probiotics, Vitamins C and E, and zinc, making it easier for product developers to create well-rounded formulations. Its standardized processes are also designed to support consistent quality and stability from batch to batch.
Frequently Asked Questions
Does vitamin K2 lower blood calcium?
No. Blood calcium is controlled by parathyroid hormone, calcitriol and calcitonin. Vitamin K2 activates proteins that influence where calcium gets deposited.
Can a blood test tell me my vitamin K2 status?
No, a standard routine blood test cannot accurately tell you your vitamin K2 status. Vitamin K2 is fat-soluble and has a very short half-life in the blood, therefore serum levels change rapidly based on your last meal. Standard tests only measure vitamin K1. Research uses undercarboxylated osteocalcin and dp-ucMGP, neither of which is a routine clinical test.
Why do MK-4 products use milligrams and MK-7 micrograms?
MK-4 products use milligrams (mg) because the body clears it quickly, whereas MK-7 uses micrograms (mcg) because it stays active in the bloodstream much longer.
References
Berkner, K. L., & Runge, K. W. (2022). Vitamin K-dependent protein activation: Normal gamma-glutamyl carboxylation and disruption in disease. International Journal of Molecular Sciences, 23(10), Article 5759. https://doi.org/10.3390/ijms23105759
Diederichsen, A., Lindholt, J., Möller, S., Øvrehus, K. A., Auscher, S., Lambrechtsen, J., Hosbond, S., Alan, D., Urbonaviciene, G., Becker, S., Fredgart, M. H., Hasific, S., Folkestad, L., Gerke, O., Rasmussen, L., Møller, J., Mickley, H., & Dahl, J. (2022). Vitamin K2 and D in patients with aortic valve calcification: A randomized double-blinded clinical trial. Circulation, 145, 1387–1397. https://doi.org/10.1161/CIRCULATIONAHA.121.057008
Knapen, M. H. J., Drummen, N. E., Smit, E., Vermeer, C., & Theuwissen, E. (2013). Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women. Osteoporosis International, 24(9), 2499–2507. https://doi.org/10.1007/s00198-013-2325-6
Lai, Y., Masatoshi, H., Ma, Y., Guo, Y., & Zhang, B. (2021). Role of vitamin K in intestinal health. Frontiers in Immunology, 12, Article 791565. https://doi.org/10.3389/fimmu.2021.791565
Luo, G., Ducy, P., McKee, M. D., Pinero, G. J., Loyer, E., Behringer, R. R., & Karsenty, G. (1997). Spontaneous calcification of arteries and cartilage in mice lacking matrix GLA protein. Nature, 386(6620), 78–81. https://doi.org/10.1038/386078a0
National Institutes of Health, Office of Dietary Supplements. (n.d.). Vitamin K: Fact sheet for health professionals. Retrieved September 29, 2026, from https://ods.od.nih.gov/factsheets/VitaminK-HealthProfessional/
Ren, R., Liu, J., Cheng, G., & Tan, J. (2021). Vitamin K2 (menaquinone-7) supplementation does not affect vitamin K-dependent coagulation factors activity in healthy individuals. Medicine, 100(23), Article e26221. https://doi.org/10.1097/MD.0000000000026221
Sahota, R. J., Leslie, S. W., & Sharma, S. (2026). Physiology, calcium. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK482128/
Schurgers, L., Teunissen, K., Hamulyák, K., Knapen, M., Vik, H., & Vermeer, C. (2007). Vitamin K-containing dietary supplements: Comparison of synthetic vitamin K1 and natto-derived menaquinone-7. Blood, 109(8), 3279–3283. https://doi.org/10.1182/blood-2006-08-040709
Shiraki, M., Shiraki, Y., Aoki, C., & Miura, M. (2000). Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis. Journal of Bone and Mineral Research, 15(3), 515–521. https://doi.org/10.1359/jbmr.2000.15.3.515
Vossen, L. M., de Leeuw, P., Schurgers, L., Heuts, S., Adriaans, B., de Haan, C., van Varik, B., & Kroon, A. A. (2026). Two years of menaquinone-7 supplementation and coronary artery calcification: A randomized clinical trial. JAMA Cardiology. Advance online publication. https://doi.org/10.1001/jamacardio.2026.1279
Zhang, Z., Li, Y., Li, J., Yuan, Y., Liu, K., & Shi, X. (2025). The effect of vitamin K2 supplementation on bone turnover biochemical markers in postmenopausal osteoporosis patients: A systematic review and meta-analysis. Frontiers in Endocrinology, 16, Article 1703116. https://doi.org/10.3389/fendo.2025.1703116
