Vitamin K2

What is vitamin K2 and how does it differ from K1?

Vitamin K is not a single substance but a group sharing a common chemical core. Phylloquinone (K1) is made in plants; menaquinones (K2) are mostly made by bacteria and are named from MK-4 to MK-13 according to the length of their side chains. The most studied are MK-4, MK-7 and MK-9. The NIH states that menaquinones are found in modest amounts in fermented and animal foods and that MK-4 can be produced in the body from phylloquinone without needing bacteria. ^[1]

The word “K2” therefore covers not a single product but different chemical forms. According to the NIH, MK-4 and MK-7 are used in supplements; the two behave differently in the body.

Open the Deep view for details →

What does vitamin K do in the body?

Vitamin K is the cofactor of the enzyme needed for some proteins to undergo a chemical change called “carboxylation.” Foremost among these proteins are the clotting factors (such as prothrombin). Beyond this, osteocalcin in bone and matrix Gla protein (MGP) found in vascular smooth muscle, bone and cartilage are also vitamin K-dependent. The NIH states that MGP is intensively studied because it may reduce abnormal calcification, and that osteocalcin may be related to bone mineralization or turnover. ^[1]

The critical distinction here is this: that a protein is vitamin K-dependent does not show that bone will get stronger or vessels will not calcify when added K2 is given. This is information at the “mechanism” level. The sections below describe randomized trials looking at whether the mechanism is reflected in real outcomes. The NIH also says for bone that “it is unclear whether any form of vitamin K reduces osteoporosis risk.” ^[1]

Which foods contain K2?

Phylloquinone is found in green leafy vegetables, vegetable oils and some fruits. Menaquinones are found in natto (fermented soy), in fermented products such as cheese and in animal foods; however, amounts vary with the bacterial species and conditions used in fermentation. Gut bacteria are also known to produce long-chain menaquinones; the NIH states that how much vitamin K the body obtains this way is uncertain, and that it is believed to meet at least part of the requirement. ^[1]

The food table, the MK-7 content of natto and the differences among cheeses are on a separate page.

Detailed guideWhich foods contain vitamin K2? Portion table, K1–K2 difference and natto→

How much vitamin K is needed daily, and is there an upper limit?

Because an average requirement for vitamin K could not be determined, organizations give “adequate intake” (AI) values. The US Food and Nutrition Board values relayed by the NIH are 120 µg per day for men over 19 and 90 µg for women (also 90 µg in pregnancy and breastfeeding). ^[1] EFSA, in its 2017 opinion, found the data on menaquinones insufficient and so set an AI only for phylloquinone, giving a value of 70 µg per day in adults (including pregnant and breastfeeding women). ^[2] These two values belong to different organizations and different methods; the EFSA value is for phylloquinone only and should not be compared directly.

According to the NIH, the Food and Nutrition Board has not set a tolerable upper intake level (UL) for vitamin K because of its low toxicity potential; the Board relays that there are no reports that vitamin K from food or supplements has adverse effects in humans or animals. ^[1] This does not mean “risk-free in every condition”; the main risk is drug interactions (below).

Who gets vitamin K deficiency?

Clinically significant deficiency is when the clotting test (prothrombin time) is markedly prolonged. The NIH states that in healthy adults eating a varied diet, reaching an intake low enough to change standard clotting measurements is almost impossible, that deficiency is very rare in adults and is generally limited to people with malabsorption and those using drugs that affect vitamin K metabolism. Cystic fibrosis, celiac disease, ulcerative colitis and short bowel syndrome can impair absorption. ^[1]

Newborns are a separate group: transfer of vitamin K through the placenta is poor and the level in breast milk is low. The NIH notes that the American Academy of Pediatrics recommends a single intramuscular dose of K1 at birth. This is given as K1 and is unrelated to K2 supplements. ^[1]

Does K2 work for bone health?

The evidence is inconsistent and largely limited to specific populations.

High-dose MK-4 trials in Japan and the updated analysis. The NIH’s 2021 fact sheet relays that all seven trials with fracture data in a 2006 meta-analysis were conducted in Japan, that in them MK-4 was used at 15 mg per day (one trial) or 45 mg (six trials), and that hip, vertebral and non-vertebral fractures were significantly reduced. In Japan and some regions of Asia, 45 mg MK-4 is used in the treatment of osteoporosis; these doses are far above the µg-level amounts in dietary supplements. ^[1]

The authors of the same meta-analysis published a correction when the integrity of some of the included trials was questioned and updated the analysis. In the 2019 update covering 36 trials (Mott et al.), the frequency of vertebral fractures with vitamin K did not differ in postmenopausal or osteoporotic patients (OR 0.98; 95% CI 0.85–1.14). For any clinical fracture, an OR of 0.74 (0.56–0.97) was found; but when the analysis was limited to studies at low risk of bias, the OR was 0.76 (0.58–1.01) and statistical significance disappeared. The authors write that there is no evidence in this group that vitamin K affects bone density or vertebral fracture, that it may reduce clinical fracture but the evidence is not enough to confirm this. ^[3] This update evaluates different vitamin K forms (K1, MK-4, MK-7) together. ^[9]

Trials in the West. In the ECKO trial (single-center), 440 postmenopausal women with osteopenia received 5 mg K1 daily or placebo for 2 years (some up to 4 years). The change in lumbar spine and total hip bone density did not differ between groups. The number of clinical fractures was lower in the K group (nine versus twenty), but the trial was not powered for fractures and the numbers were small. ^[4] The NIH also relays that in a 12-month trial in 381 women with 45 mg MK-4 or 1 mg phylloquinone, osteocalcin carboxylation improved but there was no difference in bone density. ^[1]

Low-dose MK-7. In the study by Knapen and colleagues, 244 healthy postmenopausal women received 180 µg MK-7 daily or placebo for 3 years. MK-7 mitigated the age-related decrease in bone density at the lumbar spine and femoral neck, with no difference at the total hip. The results are valid for this population; the authors say that whether they can be generalized to men and children needs to be studied separately. ^[5]

Summary: the strong fracture results of the very high-dose MK-4 trials in Japan have not been confirmed in the current analysis; trials in the West are mixed; for low-dose MK-7, the single large randomized trial reported a region-specific difference in density. The results of the low-dose MK-7 trial are bone density and strength indicators, not fractures. The NIH states that adequate calcium and vitamin D intake is important for maximizing bone mass. ^[1]

Does K2 prevent vascular calcification?

In observational studies, high menaquinone intake has been associated with less coronary and aortic calcification; the NIH therefore states that the topic is being studied but that “the role of different forms of vitamin K in arterial calcification and coronary heart disease is unclear.” ^[1] An observational association does not show that supplementation will produce the same effect.

In randomized trials, the result is not favorable:

• AVADEC (Diederichsen, 2022): 365 men with a high aortic valve calcium score (over 300 AU) and a mean age of 71 received 720 µg MK-7 plus 25 µg vitamin D daily or placebo for 24 months. The increase in calcium score was 275 AU versus 292 AU; the difference was not significant (P=0.64). Progression of aortic and coronary calcification was also no different. The dp-ucMGP marker fell; that is, the biochemical marker changed, valve calcification did not. ^[6]
• Valkyrie (De Vriese, 2020): in 132 hemodialysis patients with atrial fibrillation, in the group given 2,000 µg K2 three times a week for 18 months together with rivaroxaban, vitamin K status improved; however, the changes in coronary, aortic and valve calcium scores and pulse wave velocity did not differ significantly between groups. ^[7]

Both trials were conducted in special populations (older men with valve calcification, dialysis patients); prevention of calcification in healthy people is not answered by these trials. However, the claim that “K2 cleans the arteries” is not supported by the current randomized data. The question of use together with D3 is on a separate page.

Detailed guideAre D3 and K2 taken together? Evidence and the warfarin warning→

Can people taking warfarin take K2?

This is the most important safety topic for vitamin K. The NIH states that warfarin and vitamin K antagonists commonly used in Europe such as phenprocoumon, acenocoumarol and tioclomarol act by reducing vitamin K-dependent clotting factors; that people using these drugs should keep their vitamin K intake from food and supplements consistent, because sudden changes can increase or decrease the anticoagulant effect. ^[1] This risk is not theoretical for menaquinone supplements either: Schurgers and colleagues stated that preparations providing 50 µg or more of MK-7 per day can impair oral anticoagulant treatment in a clinically significant way. ^[8]

Direct oral anticoagulants such as rivaroxaban are not vitamin K antagonists; in the Valkyrie trial, rivaroxaban was tested as a drug replacing a vitamin K antagonist and was given together with K2. ^[7] The NIH’s interaction warning was not written for this drug group; still, use of a specific product with a drug depends on the assessment of the physician who prescribes the drug. The NIH also relays that bile acid binders and orlistat can reduce vitamin K absorption, that orlistat may markedly prolong prothrombin time with warfarin, and that long-term antibiotic use can affect vitamin K production by gut bacteria. ^[1]

How is the label read on a K2 supplement?

Three pieces of information on the label are separate: the form (MK-4, MK-7 or K1), the amount in µg, and what the serving is. The NIH states that K1 (including phytonadione) and MK-4 and MK-7 are used in supplements, that the content of products varies over a very wide range; that in multivitamin products it is generally below 75% of the Daily Value, while in products containing only K or combined with calcium, magnesium and vitamin D, very high amounts such as 4,050 µg can be found. ^[1] The amount is decisive especially for warfarin users. Phrases such as “directs calcium to the bone” or “cleans the arteries” are marketing language that does not match the evidence above. This guide does not recommend a product or brand.

Common misunderstandings about K2

• “Everyone is deficient in K2.” The NIH states that clinical vitamin K deficiency is very rare in adults. The NIH relays that in some NHANES analyses about one-third of the US population had intake above the AI, but that, because the AI is only an estimate and vitamin K is also synthesized in the body, the meaning of this remains uncertain. ^[1]
• “MK-7 is superior to MK-4.” The half-life difference was measured in biochemical markers; it has not been shown to translate into superiority in bone or vascular outcomes. The NIH states that there are few data on the relative bioavailability of vitamin K forms. ^{[8] [1]}
• “Because it is a natural vitamin, it is safe in every condition.” No UL has been established, but there is a serious interaction for those using anticoagulants. ^[1]

Evidence table: claim, population and limits

Detailed guideVitamin K2 benefits: which claims are supported and which are not?→

This guide does not recommend a daily or weekly personal dose. For people who use warfarin or a similar drug, have kidney disease or have a malabsorption disorder, the suitability of a K-containing product is assessed by the treating physician.

Why the 2020 correction matters

Mott and colleagues removed the YOPS trial after concerns about data integrity. The corrected odds ratio was 0.74 (95% CI 0.56–0.97) for clinical fractures and 0.98 (0.85–1.14) for vertebral fractures. Low-risk-of-bias estimates and the authors’ overall interpretation were unchanged. These results do not establish that K2 prevents fractures in everyone. The numerical summary above uses the corrected values. ^[9]

The 2026 VitaK-CAC trial: positive imaging, uncertain clinical benefit

In symptomatic coronary artery disease, 180 people were randomized; 85 received MK-7 and 82 received placebo. Coronary calcium-score progression was slower with MK-7 over two years (between-group p=0.02). Scores increased in both groups, so this is not evidence of “cleaning arteries.” The trial measured imaging; implications for plaque stability, heart attacks and survival remain uncertain. It studied a different population from earlier valve and dialysis trials, so those findings should not be collapsed into one universal efficacy claim. ^[10]