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Sep 2026

Supplement: Vitamine K2

My Plan

Vitamin K2 activeert twee eiwitten. Het ene zet calcium in het bot; het andere houdt het buiten de wanden van de slagaders. Daarom wordt het verkocht samen met vitamine D. Het mechanisme is goed vastgesteld; het klinische bewijs is beperkter dan de marketing suggereert. Een bescheiden dagelijkse dosis van 180 mcg MK-7 vertraagde botverlies en verbeterde arteriële stijfheid bij postmenopauzale vrouwen over een periode van drie jaar.

Het voedselbewijs voor het hart is alleen waarnemend. De gerandomiseerde studies over calcificatie hebben tot nu toe niets gevonden. Haal K2 eerst uit voeding. Voeg een bescheiden MK-7-supplement toe als uw dieet tekortschiet in gefermenteerde en dierlijke bronnen. Bij gebruik van warfarine of een ander bloedverdunner is er een echte interactie waar rekening mee moet worden gehouden.

Cost
LowLow · Inexpensive MK-7 capsule · once daily · bone and artery changes measured over months to years
Effort
EasyEasy
Results In
Months to LongerMonths to Longer

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 womenModerate
In plain terms

Taking a modest daily dose of the MK-7 form of vitamin K2 for three years slowed bone loss in healthy postmenopausal women.

In detail

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 of vitamin K1 daily did not protect bone density in women with osteopenia (ECKO)Moderate · no effect
In plain terms

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.

In detail

Cheung 2008 (PLoS Med), the ECKO trial, randomized 440 postmenopausal women with osteopenia to 5 mg/day vitamin K1 (phylloquinone) or placebo for 2 to 4 years. There was no protective effect on bone mineral density at the lumbar spine or total hip, the primary bone endpoints. Secondary analyzes found fewer clinical fractures (nine versus 20) and fewer cancers (three versus 12) in the K1 arm, but the trial was not powered for these, the numbers were small, and they need confirmation. The trial tested K1, not K2, in women with osteopenia, not established osteoporosis.

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 trialsEmerging
In plain terms

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.

In detail

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 supplements did not slow artery or heart-valve calcification in randomized trialsModerate · no effect
In plain terms

When tested head to head, vitamin K2 supplements did not slow the buildup of calcium in arteries or heart valves in the trials done so far.

In detail

Two randomized trials tested whether MK-7 slows calcification. Zwakenberg 2019 (Am J Clin Nutr) gave 68 people with type 2 diabetes and cardiovascular disease 360 mcg/day MK-7 or placebo for 6 months and found no effect on arterial calcification measured on CT, despite a large fall in inactive matrix Gla protein. Diederichsen 2022 (Circulation), the AVADEC trial, gave 365 men aged 65 to 74 with aortic valve calcification 720 mcg/day MK-7 plus 25 mcg vitamin D or placebo for 2 years and found no significant slowing of aortic valve calcification progression. Both were 6 months to 2 years and enrolled people who already had calcification or diabetes.

The studies · 2

Zwakenberg 2019, Am J Clin Nutr · Am J Clin Nutr

Diederichsen 2022, Circulation (AVADEC) · Circulation

180 mcg of MK-7 daily improved arterial stiffness over 3 years in postmenopausal womenEmerging
In plain terms

The same MK-7 dose that slowed bone loss also modestly improved a measure of artery stiffness over three years in postmenopausal women.

In detail

Knapen 2015 reported the vascular endpoints from the same 244-woman, 3-year MK-7 (180 mcg/day) trial. Carotid-femoral pulse wave velocity and the stiffness index beta decreased significantly versus placebo across the whole group, with the effect strongest in women whose baseline stiffness index was above the median of 10.8, alongside a 50 percent fall in inactive (dephospho-uncarboxylated) matrix Gla protein. Arterial stiffness is a surrogate marker; the trial did not measure heart attacks, strokes or cardiovascular death.

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

People eating the most K2 in food had about half the coronary heart disease deaths (observational)Emerging
In plain terms

People who ate more vitamin K2 in food had less heart disease death and less hardening of the aorta over the following years, though this is an association, not a tested effect.

In detail

Geleijnse 2004 (J Nutr), the Rotterdam Study, followed 4,807 adults aged 55 and over free of myocardial infarction at baseline. The highest tertile of dietary menaquinone (K2) intake, mainly from cheese and other dairy and from meat, was associated with lower coronary heart disease mortality (relative risk about 0.43 versus the lowest tertile), lower all-cause mortality, and less severe aortic calcification. Dietary phylloquinone (K1) intake was not associated with these outcomes. As an observational cohort it cannot establish that the K2 itself produced the lower risk.

The study · 1

Geleijnse 2004, J Nutr (Rotterdam Study) · J Nutr

How it works

K2 activates osteocalcin and matrix Gla protein, the basis of the vitamin D partnershipModerate · mixed
In plain terms

Vitamin K2 activates the proteins that route calcium into bone and away from arteries, which is why it is proposed as the partner to vitamin D.

In detail

Vitamin K is the cofactor for gamma-glutamyl carboxylase, which carboxylates vitamin K-dependent proteins. Osteocalcin, once carboxylated, binds calcium into hydroxyapatite in bone; matrix Gla protein, once carboxylated, is a potent local inhibitor of vascular calcification. Aaseth 2024 (Nutrients) reviews this mechanism and the rationale for combining vitamins K and D: vitamin D increases intestinal calcium absorption while K2 activates the proteins that determine where calcium is deposited. Human dosing data support the biochemical step: Shiraki 2009 (J Bone Miner Metab) showed short-term menatetrenone (MK-4) increased the gamma-carboxylation of osteocalcin in postmenopausal osteoporosis. Carboxylation is a measured surrogate; whether it translates into fewer fractures or cardiovascular events is the question the clinical trials address.

The studies · 2

Aaseth 2024, Nutrients · Nutrients

Shiraki 2009, J Bone Miner Metab · J Bone Miner Metab

MK-7 is absorbed and retained far longer than MK-4 or K1Emerging · mixed
In plain terms

MK-7 stays in the blood much longer than MK-4 or K1, so a small daily MK-7 dose does the work a much larger MK-4 dose would.

In detail

Sato 2012 (Nutr J) compared MK-4 and MK-7 bioavailability in healthy women and found that MK-4 given at a nutritional dose was not detectable in serum, whereas MK-7 was well absorbed and raised serum concentrations, both after a single dose and after continued intake. Schurgers 2007 (Blood) showed natto-derived MK-7 has a substantially longer half-life and more stable serum levels than K1 (phylloquinone), giving better carboxylation of osteocalcin at low doses. These are pharmacokinetic differences in absorption and retention, not a demonstrated clinical superiority of one form for bone or cardiovascular outcomes.

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.

1
Eat the Foods That Carry ItFreeEasy

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.

2
Pair It With What You Already Do For Vitamin DFreeEasy

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.

3
A Modest MK-7 Supplement$Easy

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.

4
The MK-4 Drug Dose Is a Separate Thing$ to $$Easy

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 restraint

Everything 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.

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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.