Vitamin K2 aktiviert zwei Proteine. Das eine leitet Calcium in den Knochen ein; das andere hält es aus den Arterienwänden fern. Deshalb wird es zusammen mit Vitamin D verkauft. Der Mechanismus ist gut belegt; die klinischen Beweise sind jedoch begrenzt, als es der Marketingauftritt nahelegt. Eine moderate tägliche Dosis von 180 mcg MK-7 verlangsamte den Knochenschwund und verbesserte die Arteriensteifigkeit bei postmenopausalen Frauen über einen Zeitraum von drei Jahren.
Die Nahrungsevidenz für das Herz ist rein beobachtend. Die randomisierten Studien zur Verkalkung haben bisher nichts ergeben. Nehmen Sie K2 zuerst aus der Nahrung auf. Ergänzen Sie eine moderate MK-7-Zusatzgabe, wenn Ihre Ernährung an fermentierten und tierischen Quellen mangelt. Bei Einnahme von Warfarin oder einem anderen Blutverdünner ist eine echte Wechselwirkung zu beachten.
Findings & Outcomes
What It Is
Vitamin K comes in two forms, and K2 is the one that works with calcium in bone and blood vessels. Vitamin K1 (phylloquinone) comes from green leaves and mostly travels to the liver, where it activates the clotting factors. Vitamin K2 (the menaquinones) comes from bacteria, fermentation, and animal tissue. It reaches bone and the artery walls, where it activates the calcium-handling proteins. Two menaquinones account for the interest in K2. MK-4 is made in animal tissue and used in Japan as a high-dose osteoporosis drug. MK-7 is made by bacteria and is richest in the fermented soybean dish natto.
Anatomy of the Practice
1From animal food and fermentation
K2 reaches you from two routes: animal foods carry MK-4, and bacterial fermentation makes the longer menaquinones, above all the MK-7 concentrated in natto. Gut bacteria make some as well. This is a different source from the K1 in leafy greens, so a diet can be adequate in one form and low in the other.
2Activating the calcium proteins
In the liver and then in bone and vessel tissue, vitamin K lets an enzyme add carbon groups to specific proteins, a step called carboxylation. That step is what turns osteocalcin and matrix Gla protein from inactive to active. Without enough K2, a fraction of these proteins stays uncarboxylated and cannot do its calcium job.
3Directing where calcium settles
Activated osteocalcin binds calcium into the bone matrix; activated matrix Gla protein sits in artery walls and blocks calcium from depositing there. This is the basis of pairing K2 with vitamin D: vitamin D raises how much calcium you absorb, and K2 is proposed to direct where that calcium ends up.
How It Works
Carboxylation is well established. Turning that biochemical step into fewer broken bones or fewer heart attacks is a different question, and it is where vitamin K2 gets oversold.
For the nutrient that raises calcium absorption, see vitamin D. For the strongest lever for building the bone this is meant to protect, see resistance training.
What The Trials Found
The firmest bone result is Knapen's three-year randomized trial. In it, 244 healthy postmenopausal women took 180 mcg a day of MK-7. That dose slowed the age-related loss of bone mineral density at the spine and femoral neck. It also improved calculated measures of bone strength against placebo. The trial measured bone density on a scan, not broken bones. A much larger pharmacological dose of MK-4, 45 mg a day, is licensed in Japan as an osteoporosis treatment. A meta-analysis of 13 trials found it reduced vertebral, hip and other fractures.
That pooled fracture result leans heavily on Japanese MK-4 trials, several of them methodologically weak, at a dose hundreds of times any nutritional amount. It has not reproduced in that form elsewhere. Not every vitamin K result is positive. The ECKO trial gave 440 women with osteopenia 5 mg a day of vitamin K1 for two to four years, and found no protection of bone density. So the bone case is modest: firmest at the surrogate of bone density, weaker the closer it gets to fractures.
For the heart, the divide is between what people eat and what trials have tested. In the Rotterdam Study, the adults who ate the most dietary K2 got it largely from cheese and meat. They had lower coronary heart disease death and less severe aortic calcification than those eating the least. Dietary K1 showed no such link. That is an association: people who eat more of these foods differ in other ways, so it cannot prove K2 caused the effect.
The randomized trials that tried to confirm it have not. MK-7 at 360 mcg a day for six months did not slow arterial calcification in people with type 2 diabetes. A dose of 720 mcg a day plus vitamin D for two years did not slow aortic valve calcification in older men. The one positive cardiovascular signal is softer. In Knapen's bone cohort, the same 180 mcg MK-7 improved arterial stiffness over three years, a surrogate measure, not a count of heart attacks or strokes.
If you take warfarin or a similar drug, do not start, stop or change a vitamin K2 supplement without the prescriber who manages your INR.
The Research & Studies
Everything here is based on the research we have collected and checked, sorted into groups and ordered with the strongest evidence first. Click any claim to open the studies behind it.
Bone Density
180 mcg of MK-7 daily slowed bone loss over 3 years in postmenopausal women
Taking a modest daily dose of the MK-7 form of vitamin K2 for three years slowed bone loss in healthy postmenopausal women.
Knapen 2013 (Osteoporos Int) randomized 244 healthy postmenopausal women to 180 mcg/day MK-7 (menaquinone-7) or placebo for 3 years. MK-7 significantly reduced the decline in bone mineral density at the lumbar spine and femoral neck (not the total hip) and improved bone-strength indices derived from geometry, alongside a large rise in carboxylated osteocalcin. Actual fractures were not an endpoint, so the result is a slower loss on bone densitometry, not a demonstrated reduction in broken bones.
Who this may not transfer to:Tested only in postmenopausal women; whether the same MK-7 dose slows bone loss in men or younger adults has not been measured.
The study · 1
Knapen 2013, Osteoporos Int · Osteoporos Int
5 mg Vitamin K1 täglich schützten die Knochendichte bei Frauen mit Osteopenie nicht (ECKO)
A large trial of high-dose vitamin K1 in women with thinning bones did not preserve bone density. Not every form of vitamin K and every outcome shows a benefit.
Cheung 2008 (PLoS Med), die ECKO-Studie, randomisierte 440 postmenopausale Frauen mit Osteopenie über 2 bis 4 Jahre zu 5 mg/Tag Vitamin K1 (Phyllochinon) oder Placebo. Es zeigte sich kein schützender Effekt auf die Knochenmineraldichte an der Lendenwirbelsäule oder der gesamten Hüfte, den primären Knochen-Endpunkten. Sekundäre Analysen fanden weniger klinische Frakturen (neun gegenüber 20) und weniger Krebserkrankungen (drei gegenüber 12) im K1-Arm, doch die Studie war dafür nicht ausreichend gepowert, die Zahlen waren klein, und sie bedürfen der Bestätigung. Die Studie untersuchte K1, nicht K2, bei Frauen mit Osteopenie, nicht bei manifester Osteoporose.
Who this may not transfer to:ECKO enrolled postmenopausal women with osteopenia; the K1 bone-density result has not been tested in men.
The study · 1
Cheung 2008, PLoS Med (ECKO) · PLoS Med
45 mg of MK-4 daily cut fractures, mostly in Japanese osteoporosis trials
A prescription-strength MK-4 dose used in Japan reduced fractures in women with osteoporosis, but the evidence rests mostly on Japanese trials of variable quality and a dose far above any supplement.
Cockayne 2006 (Arch Intern Med) pooled 13 RCTs of vitamin K (7 reporting fractures) and found supplementation associated with reduced vertebral, hip and all nonvertebral fractures; the fracture data were dominated by Japanese trials of high-dose MK-4 (menatetrenone). The representative RCT, Shiraki 2000 (J Bone Miner Res), an open-label study, gave 45 mg/day MK-4 to 241 patients with osteoporosis and reported fewer new clinical fractures and sustained lumbar bone mineral density versus control. The dose is roughly hundreds of times a nutritional amount and licensed as a drug in Japan; several pooled trials had methodological limitations and the fracture benefit has not reproduced at this form and dose outside that setting.
Who this may not transfer to:The MK-4 osteoporosis trials enrolled postmenopausal women; the high-dose fracture benefit has not been tested in men.
The studies · 2
Cockayne 2006, Arch Intern Med · Arch Intern Med
Shiraki 2000, J Bone Miner Res · J Bone Miner Res
Heart And Vascular
MK-7-Präparate verlangsamten in randomisierten Studien die Verkalkung von Arterien oder Herzklappen nicht
Im direkten Vergleich getestet, verlangsamten Vitamin-K2-Präparate in den bisher durchgeführten Studien den Kalziumaufbau in Arterien oder Herzklappen nicht.
Zwei randomisierte Studien untersuchten, ob MK-7 die Verkalkung verlangsamt. Zwakenberg 2019 (Am J Clin Nutr) gab 68 Menschen mit Typ-2-Diabetes und Herz-Kreislauf-Erkrankung über 6 Monate 360 µg/Tag MK-7 oder Placebo und fand trotz eines starken Rückgangs des inaktiven Matrix-Gla-Proteins keinen Effekt auf die per CT gemessene arterielle Verkalkung. Diederichsen 2022 (Circulation), die AVADEC-Studie, gab 365 Männern im Alter von 65 bis 74 Jahren mit Aortenklappenverkalkung über 2 Jahre 720 µg/Tag MK-7 plus 25 µg Vitamin D oder Placebo und fand keine signifikante Verlangsamung des Fortschreitens der Aortenklappenverkalkung. Beide Studien dauerten 6 Monate bis 2 Jahre und schlossen Menschen ein, die bereits eine Verkalkung oder Diabetes hatten.
The studies · 2
Zwakenberg 2019, Am J Clin Nutr · Am J Clin Nutr
Diederichsen 2022, Circulation (AVADEC) · Circulation
180 µg MK-7 täglich verbesserten über 3 Jahre die Arteriensteifigkeit bei postmenopausalen Frauen
Dieselbe MK-7-Dosis, die den Knochenabbau verlangsamte, verbesserte über drei Jahre bei postmenopausalen Frauen auch bescheiden ein Maß der Arteriensteifigkeit.
Knapen 2015 berichtete die vaskulären Endpunkte derselben Studie mit 244 Frauen über 3 Jahre mit MK-7 (180 µg/Tag). Die karotisch-femorale Pulswellengeschwindigkeit und der Steifigkeitsindex-Beta sanken in der gesamten Gruppe signifikant gegenüber Placebo, mit dem stärksten Effekt bei Frauen, deren Ausgangs-Steifigkeitsindex über dem Median von 10.8 lag, zusammen mit einem 50-prozentigen Rückgang des inaktiven (dephospho-unkarboxylierten) Matrix-Gla-Proteins. Die Arteriensteifigkeit ist ein Surrogatmarker; die Studie maß keine Herzinfarkte, Schlaganfälle oder kardiovaskuläre Todesfälle.
Who this may not transfer to:Measured only in postmenopausal women; the arterial-stiffness effect of MK-7 has not been tested in men or younger adults.
The study · 1
Knapen 2015, Thromb Haemost · Thromb Haemost
Menschen, die am meisten K2 über die Nahrung aufnahmen, hatten etwa halb so viele Todesfälle durch koronare Herzkrankheit (Beobachtungsstudie)
Menschen, die mehr Vitamin K2 über die Nahrung aufnahmen, hatten in den folgenden Jahren weniger Todesfälle durch Herzerkrankungen und weniger Verhärtung der Aorta, wobei dies eine Assoziation ist, kein getesteter Effekt.
Geleijnse 2004 (J Nutr), die Rotterdam-Studie, begleitete 4,807 Erwachsene ab 55 Jahren, die zu Studienbeginn frei von Myokardinfarkt waren. Das höchste Tertil der diätetischen Menachinon-(K2-)Zufuhr, hauptsächlich aus Käse und anderen Milchprodukten sowie aus Fleisch, war mit einer niedrigeren Mortalität durch koronare Herzkrankheit (relatives Risiko etwa 0.43 gegenüber dem niedrigsten Tertil), niedrigerer Gesamtmortalität und weniger schwerer Aortenverkalkung verbunden. Die diätetische Phyllochinon-(K1-)Zufuhr war mit diesen Ergebnissen nicht assoziiert. Als Beobachtungskohorte kann sie nicht belegen, dass K2 selbst das niedrigere Risiko verursachte.
The study · 1
How it works
K2 aktiviert Osteocalcin und Matrix-Gla-Protein – die Grundlage der Partnerschaft mit Vitamin D
Vitamin K2 aktiviert die Proteine, die Kalzium in den Knochen und von den Arterien weglenken, weshalb es als Partner von Vitamin D vorgeschlagen wird.
Vitamin K ist der Kofaktor der Gamma-Glutamyl-Carboxylase, die Vitamin-K-abhängige Proteine carboxyliert. Osteocalcin bindet, einmal carboxyliert, Kalzium in Hydroxylapatit im Knochen; Matrix-Gla-Protein ist, einmal carboxyliert, ein starker lokaler Hemmstoff der vaskulären Verkalkung. Aaseth 2024 (Nutrients) beschreibt diesen Mechanismus und die Begründung für die Kombination von Vitamin K und D: Vitamin D erhöht die intestinale Kalziumaufnahme, während K2 die Proteine aktiviert, die bestimmen, wo Kalzium abgelagert wird. Humandaten zur Dosierung stützen den biochemischen Schritt: Shiraki 2009 (J Bone Miner Metab) zeigte, dass kurzfristiges Menatetrenon (MK-4) die Gamma-Carboxylierung von Osteocalcin bei postmenopausaler Osteoporose erhöhte. Die Carboxylierung ist ein gemessenes Surrogat; ob sie sich in weniger Frakturen oder kardiovaskulären Ereignissen niederschlägt, ist die Frage, die die klinischen Studien beantworten.
The studies · 2
Aaseth 2024, Nutrients · Nutrients
Shiraki 2009, J Bone Miner Metab · J Bone Miner Metab
MK-7 wird weit länger resorbiert und im Körper gehalten als MK-4 oder K1
MK-7 verbleibt viel länger im Blut als MK-4 oder K1, sodass eine kleine tägliche MK-7-Dosis die Wirkung erzielt, für die eine viel größere MK-4-Dosis nötig wäre.
Sato 2012 (Nutr J) verglich die Bioverfügbarkeit von MK-4 und MK-7 bei gesunden Frauen und fand, dass MK-4 in ernährungsphysiologischer Dosis im Serum nicht nachweisbar war, während MK-7 gut resorbiert wurde und die Serumkonzentrationen erhöhte, sowohl nach einer Einzeldosis als auch nach fortgesetzter Einnahme. Schurgers 2007 (Blood) zeigte, dass aus Natto gewonnenes MK-7 eine deutlich längere Halbwertszeit und stabilere Serumspiegel als K1 (Phyllochinon) hat, was bei niedrigen Dosen eine bessere Carboxylierung von Osteocalcin ergibt. Dies sind pharmakokinetische Unterschiede bei Resorption und Verbleib, keine nachgewiesene klinische Überlegenheit einer Form für Knochen- oder kardiovaskuläre Ergebnisse.
Who this may not transfer to:The head-to-head absorption comparison was done in healthy women; pharmacokinetics are not expected to differ greatly by sex but were not tested in men here.
The studies · 2
Sato 2012, Nutr J · Nutr J
Schurgers 2007, Blood · Blood
Ways to Do It
For most people this starts with food, because the foods that carry K2 are ordinary, and it pairs with whatever you already do for vitamin D. A modest MK-7 supplement is a reasonable addition if your diet is short of fermented and animal sources, at the dose the trials used.
Natto is by far the richest source of MK-7, since the bacteria that ferment it produce large amounts of K2. Aged and hard cheeses such as Gouda, Edam and Brie carry meaningful amounts, and egg yolks, chicken, and grass-fed animal fats supply MK-4. Fermented foods in general add some. If natto is not to your taste, a couple of servings of aged cheese and regular egg yolks are the everyday route.
K2's whole rationale is as vitamin D's partner. So keep the vitamin D habit you already have (sun, oily fish, or a modest supplement) and cover K2 from food alongside it. This just fills in the other half of the calcium job.
If you rarely eat natto, aged cheese or egg yolks, a generic MK-7 supplement at 90 to 180 mcg a day is the form and dose used in the bone and arterial-stiffness trials. MK-7 is fat-soluble, so take it with a meal that contains some fat. Many products combine it with vitamin D3 in one capsule, which matches how the pair is meant to work.
The 45 mg a day MK-4 drug dose is taken in divided doses. It is a medical decision for someone with diagnosed osteoporosis, made with a clinician, not a supplement to self-start. For general use, the microgram MK-7 dose is the one the everyday evidence supports.
Go Deeper
- Vitamin D: the partner nutrient, and a case study in the same gap between correcting a deficiency and an oversold routine supplement.
- Resistance training: the intervention with the strongest record for building bone, and the partner to any nutritional bone strategy.
- Omega-3 fish oil: another supplement with a strong mechanism and disappointing trials on hard outcomes, where matching dose and form to the goal is the main task.
The Chinese Medicine View
Vitamin K2 was identified in the twentieth century, so it has no entry in the classical Chinese pharmacopoeia. No channel, flavor or temperature was assigned to it by any historical text. What the tradition offers is a way to place the foods that carry K2. Treat it as a lens for thinking, since it carries no clinical weight.
The richest K2 foods are fermented and aged: natto, aged cheeses, and cured animal products. Chinese dietary thinking has a long, specific relationship with fermented foods. It reads them as warming and as supporting the Spleen and Stomach in their work of transformation. That is why fermented and aged preparations appear across the tradition. It also reads rich, aged, fatty foods as building and moistening: useful for someone depleted, burdening for someone already damp or phlegm-laden. The Kidney in Chinese medicine governs the bones and marrow and stores Jing, the deep reserve that thins with age. K2's clearest role concerns the same territory: mineralizing bone in the older body.
A practitioner would not hand everyone the same daily portion of a rich fermented food any more than the same herb, but would ask who is in front of them. The tradition's instinct, the right amount depends on the person, parallels the modern finding that benefit depends on dose, form, and the individual.
Cautions For This Practice
Extra restraintEverything to be aware of is here, in one place. This practice suits most healthy people; a few situations call for real care.
Vitamin K2 works against warfarin and can push the INR out of range
Vitamin K antagonists (warfarin, acenocoumarol, phenprocoumon) act by inhibiting vitamin K recycling, so exogenous vitamin K directly opposes them. Violi 2016 (Medicine, Baltimore) systematically reviewed the interaction between dietary vitamin K intake and anticoagulation and concluded that everyday dietary fluctuations destabilize INR less than clinical lore holds, while noting that larger and more consistent intakes, such as supplements, are a different exposure. The clinically safe course on a vitamin K antagonist is consistency: do not start, stop or change a vitamin K supplement without the clinician who manages the INR, because a new steady dose shifts the drug's effect.Violi 2016, Medicine (Baltimore)
Warfarin and other vitamin K antagonists: do not add K2 on your own
This is the interaction that matters. Warfarin and related blood thinners work by blocking vitamin K. Any vitamin K, a K2 supplement included, is their direct counterweight: it can blunt the drug and swing your INR out of range. A systematic review found that ordinary day-to-day swings in dietary vitamin K destabilize these drugs less than long assumed. But a supplement is a higher, steadier dose than food, and the antagonism itself is not in dispute. If you take warfarin or a similar drug, do not start, stop or change a vitamin K2 supplement without the prescriber who manages your INR. Consistency is what keeps these drugs safe, and a new supplement breaks it.
K2 supplements are well tolerated, within the usual supplement caveats
At the microgram MK-7 doses sold as supplements, vitamin K2 has a good tolerability record and no established toxic upper level. That is unlike vitamin D or A. The trials that showed an effect used a low microgram dose, and higher doses have not been shown to add benefit. As with any supplement, tell a clinician what you take before surgery or if you are managing a serious condition.
Pregnancy, breastfeeding, and children
The bone and cardiovascular trials were done in adults, most of them postmenopausal women or older men. So there is little trial data on K2 supplements in pregnancy, breastfeeding, or childhood. Getting K2 from food is part of a normal diet; before taking a supplement in these situations, clear it with a clinician first, since the evidence base does not cover them.
Start slow, be smart, read the research, and consult a professional if you have any concerns. This is here to inform your choice, not make it for you.
Common Questions
Do I need K2 if I take vitamin D?
No trial has taken people already on vitamin D, added K2, and measured whether fractures or heart events then fall. That leaves it a low-risk pairing whose necessity is unconfirmed. Natto, aged Gouda and egg yolks are rich food sources of K2.
Why is the MK-7 supplement dose measured in micrograms while the Japanese osteoporosis dose is in milligrams?
The two forms leave the blood at very different speeds. MK-7, the form richest in natto, is absorbed efficiently and stays in circulation for days, so one small daily dose holds a steady level. MK-4 is cleared within hours, so the Japanese studies split a milligram-scale dose across the day to keep any in the blood.
Explore Related
Other pages this one connects to, by the evidence they share, the outcomes they touch, and the ground they cover.
All 13 sources on this page independently checked and cross-referenced.
Thomas Dehli, Founder & Editor, Sacred Lotus
Sacred Lotus has published Chinese medicine reference material since 2001. Integrative pages are held to the same standard as the herb and formula library: cite the source, grade the claim at its real strength, and say where the research has not looked. This page is educational and it is not medical advice. Last reviewed and updated August 9, 2026.
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