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Vitamin K2
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In one pass Vitamin K is a family: the same naphthoquinone head with tails of different lengths, and the length changes where it goes and what it does.
Educational content, not medical advice — consult a clinician.
Inactive osteocalcin Osteoblasts secrete osteocalcin in a form that cannot grab calcium, because its 3 glutamate residues must first be modified.
Artery wall · Ca²⁺ threat Plasma Ca²⁺ is already high and the vessel wall could nucleate calcium crystals at any time, so arteries stay uncalcified only through active maintenance.
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Chapter 1
K1 clots blood, K2 routes calcium
Vitamin K is a family: the same naphthoquinone head with tails of different lengths, and the length changes where it goes and what it does. K1 (phylloquinone) comes from leafy greens and is used mainly by the liver to activate clotting factors. (menaquinones, written MK-n) has a longer tail and reaches bone and blood vessels, tissues outside the liver, more readily. There it activates two calcium-handling proteins: osteocalcin helps calcium settle into bone, and matrix Gla protein (MGP) keeps calcium out of the vessel wall. The most common K2 in supplements is , which comes from natto, not cheese.
So when people talk about K2 for bones or against arterial calcification, they mean where calcium goes, almost never clotting. Both mechanisms are well understood; whether taking K2 reduces fractures or heart disease is still thinly supported in people. The shot a newborn gets at birth is K1, because what a newborn lacks is clotting; if a baby who did not get the shot shows unexplained bleeding, or becomes drowsy, refuses feeds, or vomits repeatedly, go to the emergency department immediately.
So when people talk about K2 for bones or against arterial calcification, they mean where calcium goes, almost never clotting. Both mechanisms are well understood; whether taking K2 reduces fractures or heart disease is still thinly supported in people. The shot a newborn gets at birth is K1, because what a newborn lacks is clotting; if a baby who did not get the shot shows unexplained bleeding, or becomes drowsy, refuses feeds, or vomits repeatedly, go to the emergency department immediately.
Mechanism · How tail length splits the jobs
The vitamin K family shares one core structure (a 2-methyl-1,4-naphthoquinone head); the difference is the length of the side chain behind it:K1 (phylloquinone): in plants it is one link in the electron transport of photosynthesis, which is why leafy greens are full of it. Once eaten, K1 is taken up mainly by the liver and used to γ-carboxylate clotting factors II, VII, IX, and X; only after carboxylation can these factors bind Ca²⁺ and start clotting. Healthy people almost never lack K1. (menaquinones, MK-n): a side chain of several linked isoprenoid units, where n is the number of units; MK-4 through MK-13 are the common ones. The sources are fermented foods and animal foods, and gut bacteria also make some. Long-chain K2 is carried more readily to bone, blood vessels, and other tissues outside the liver, where the vitamin K-dependent proteins (osteocalcin, MGP) rely mainly on it.K3 (menadione): synthetic, with no side chain. Laboratory studies found it damages liver cells, so it cannot be used as a human supplement; it appears only in animal feed and in research.
So when people discuss K2 for bones or against arterial calcification, they are almost never discussing clotting. Clotting is K1's job.
Clinical · Why newborns get a K1 shot
A single intramuscular shot of vitamin K1 after birth is one of the most widespread one-off vitamin interventions in obstetrics. The American Academy of Pediatrics (AAP, 2022) recommends giving it within 6 hours of birth.Why it is needed: vitamin K barely crosses the placenta, so a newborn's liver holds very little; the gut has not yet grown the bacteria that make ; breast milk is low in vitamin K (about 1–4 µg/L, far below formula); and clotting factors II, VII, IX, and X only work after vitamin K has γ-carboxylated them.
What happens without it: vitamin K deficiency bleeding (VKDB), which comes in three types:
Early-onset (within 24 h of birth): mostly linked to the mother taking anticoagulants or anti-seizure drugs in pregnancy; rare.Classic (1–7 days): bleeding from the gut, the nose, or the umbilical stump; overall incidence in infants given no vitamin K is about 0.25–1.7%.Late-onset (2 weeks to 6 months after birth): the most dangerous. About 50% of cases present as bleeding inside the skull (intracranial hemorrhage, ICH); once it happens, about 20% die and about 40% of survivors are left severely disabled. It occurs almost only in exclusively breastfed babies who did not get the shot at birth.
Prevention: the standard practice is a single 1 mg intramuscular dose of K1 after birth, recommended by the US CDC, the AAP, and the World Health Organization (WHO); it prevents almost all late-onset VKDB. Some countries (the Netherlands, Denmark) use an oral schedule of 2–3 doses (at birth, 1 week, and 1 month). It avoids the needle, but it works slightly less well and needs strict follow-up, and babies with a hidden absorption problem such as biliary atresia can still develop late-onset VKDB after oral doses. In the 2010s, more US parents refused the shot (mostly over worries about preservatives and other ingredients), and a cluster of newborn brain bleeds followed; the AAP restated its recommendation in 2022.
If a baby who did not get the shot shows unexplained bleeding or bruising, or becomes drowsy, refuses feeds, vomits repeatedly, or has a seizure, go to the emergency department immediately.
Newborns get K1 because what has to be protected at that age is the liver's clotting function, not bone or blood vessels. Adult diets are full of leafy greens and almost never short of K1. This shot is the clearest clinical picture of the division of labor: K1 for clotting, K2 for bone and blood vessels.
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Chapter 2
K2 sources
has few rich sources, and almost all of them are fermented. The standout is the in natto (see Natto): a small serving is far above an adult's daily adequate intake of vitamin K. The K2 in hard cheese is mostly MK-8 and MK-9, made by lactic-acid bacteria, not MK-7 (see Cheese). Leafy greens hold almost nothing but K1.
Gut bacteria make some long-chain K2 themselves, but they make it in the colon, where conditions for absorbing a fat-soluble vitamin are poor. So eating spinach and relying on gut bacteria will not cover K2. Egg yolk, chicken liver, and meat carry K2 as MK-4, only a few micrograms per serving.
Gut bacteria make some long-chain K2 themselves, but they make it in the colon, where conditions for absorbing a fat-soluble vitamin are poor. So eating spinach and relying on gut bacteria will not cover K2. Egg yolk, chicken liver, and meat carry K2 as MK-4, only a few micrograms per serving.
Numbers · Where K2 comes from in food
has few rich sources, and almost all of them are fermented foods:Natto (soybeans fermented with Bacillus subtilis natto): about 1000 µg of per 100 g, far ahead of everything else. In the food table of the US NIH Office of Dietary Supplements (ODS), a 3-ounce serving of natto holds about 850 µg; an adult's daily adequate intake of vitamin K is only 90–120 µg.Aged hard cheeses (Gouda, Edam, Brie, and others): mostly MK-8 and MK-9 made by lactic-acid bacteria, plus a little MK-4, about 50–80 µg per 100 g.Egg yolk, chicken liver, poultry, and pork: mostly MK-4, but only a few micrograms per serving; one hard-boiled egg has about 4 µg.Grass-fed butter and animal fats: small amounts of MK-4.
Ordinary leafy greens contain almost no K2, only K1. Gut bacteria make their own long-chain K2 (mainly forms like MK-10 and MK-11), but the amount is limited and depends heavily on each person's microbiome, so "I eat lots of spinach, so my K2 is covered" does not hold.
Regions with high traditional K2 intake include Japan (natto), the Netherlands (hard cheese and butter), France (cheese), and the Nordic countries (organ meats). Some people link these regions' osteoporosis and cardiovascular figures to their K2 intake, but comparisons between regions carry too many ; they are leads, not conclusions.
Myth · Is the K2 your gut makes enough?
"Gut bacteria turn K1 into , so eating enough greens covers it": this claim is half right and half wrong, and it is the most common misconception in the K2 story.The right half: gut bacteria really do make K2, mainly Bacteroides and E. coli in the colon, and what they make is long-chain forms such as MK-10, MK-11, and MK-12.
The wrong half: the K2 they make is hard to absorb. K2 is fat-soluble and needs bile acids to get absorbed, but most bile acids are reabsorbed at the end of the small intestine, so few are left by the time contents reach the colon, and most of the bacterial K2 leaves in the stool. How much vitamin K the gut bacteria actually contribute to the body has no reliable human measurement. Long-term antibiotics damage the gut bacteria and cut K2 production, but they rarely cause vitamin K deficiency in practice, because most of it still comes from K1 in food. A newborn's gut has not yet grown its bacteria, which is one reason newborns bleed easily.
So what do greens do:
Some tissues (especially the testes, the pancreas, and the vessel wall) use an enzyme called UBIAD1 to rebuild dietary K1 into MK-4, a meaningful conversion inside the body.But greens cannot become long-chain forms such as or MK-9; those need bacteria-fermented foods (natto, cheese).Greens alone do not cover everything K2 does. Schurgers 2007 compared synthetic K1 with natto-derived MK-7 supplements: MK-7 stayed in the blood much longer and carboxylated osteocalcin more fully.
In practice: to cover both K1 and K2, add natto, hard cheese, or egg yolk a few times a week on top of your greens; the traditional mix of greens with egg yolk and butter is more complete than salad alone. In the week or two after a course of antibiotics, there is no need to take K2 specially; eating vitamin K foods as usual while the gut bacteria recover is enough.
Chapter 3
Helping bone take up calcium
helps bone store calcium through a protein called osteocalcin. Bone-building cells (osteoblasts) secrete it, and it is the most abundant non-collagen protein in bone. Three sites on osteocalcin must first be converted into Gla (γ-carboxyglutamate); only then can it grip calcium like a small clip and set it into bone's mineral lattice. The enzyme that makes this conversion uses vitamin K as a consumable. When vitamin K runs short, osteocalcin stays unconverted, a form called undercarboxylated osteocalcin (ucOC).
So high ucOC in the blood signals low vitamin K. In observational studies, people with high ucOC had lower and more hip fractures; that is an association. Randomized trials disagree. In 244 healthy postmenopausal women taking 180 µg of a day for 3 years, bone density fell more slowly and the vertebrae of the lower thoracic spine lost less height (that trial did not measure fractures). In another trial where everyone also took calcium and vitamin D, adding vitamin K did not raise bone density any further.
So high ucOC in the blood signals low vitamin K. In observational studies, people with high ucOC had lower and more hip fractures; that is an association. Randomized trials disagree. In 244 healthy postmenopausal women taking 180 µg of a day for 3 years, bone density fell more slowly and the vertebrae of the lower thoracic spine lost less height (that trial did not measure fractures). In another trial where everyone also took calcium and vitamin D, adding vitamin K did not raise bone density any further.
Mechanism · Is osteocalcin also a hormone?
The chemistry of how osteocalcin grips calcium: osteocalcin carries 3 glutamate (Glu) residues. The enzyme γ-glutamyl carboxylase (GGCX), working with CO₂ and O₂, adds a carboxyl group to each one, turning it into Gla. Vitamin K is the consumable in this step: it is oxidized to vitamin K epoxide, then reduced back by an enzyme called VKORC1 and used again. Each Gla carries two negative charges, and three Gla side by side form the clip that grips Ca²⁺ and sets it into the hydroxyapatite lattice; osteocalcin in this state is called carboxylated osteocalcin (cOC). When vitamin K runs short, GGCX stops and osteocalcin stays as ucOC. This is the main line of the story.A newer lead that is still debated: osteocalcin may be a hormone. From 2007 on, the Karsenty lab found in mice that uncarboxylated osteocalcin (ucOC), once released from bone into the blood, acts on other organs like a hormone:
Pancreatic beta cells: more insulin secretionFat cells: better insulin sensitivityMuscle: more glucose uptake and a role in adapting to exerciseBrain: effects on memoryTestes: more testosterone production
These results come mainly from mice. Whether the same hormonal pathway works in people, and how much it matters, is still weakly supported, and some studies have failed to reproduce it.
This raises an apparent contradiction: low K2 means more ucOC, and ucOC is exactly the form with hormonal activity, so would taking K2 lose that hormonal effect? The mechanism suggests that in healthy people carboxylation and release of osteocalcin are in balance, and a small amount of ucOC may be enough to carry the signal; in severe vitamin K deficiency, the cost of damaged bone structure far outweighs the benefit of "a little more hormone". That is reasoning; human studies have not answered it directly.
Related observations in people: some studies saw blood ucOC rise briefly after strength training, but whether that improves insulin sensitivity has not been shown; in people with type 2 diabetes, lower total osteocalcin tends to go with worse insulin resistance (an observational association); bisphosphonates, which suppress bone remodeling, lower osteocalcin, and some worried this could affect metabolism, which has also not been confirmed in people.
Taken together, these leads suggest bone may be more than a scaffold and may be in contact with glucose metabolism, sex hormones, and the brain, with vitamin K as one consumable along the way. They do not change the K2 recommendation; they are a reminder that bone health and whole-body metabolism may be linked.
Chapter 4
Keeping calcium out of arteries
Smooth muscle cells in the vessel wall secrete matrix Gla protein (MGP), a kind of gatekeeper whose job is the mirror image of osteocalcin's: it keeps calcium out of the vessel wall and prevents arterial calcification. MGP also needs vitamin K to convert its glutamates into Gla before it works; inactive MGP (ucMGP) cannot grip calcium, so calcium deposits in the vessel wall more easily.
The evidence in people is observational. The Rotterdam Study in the Netherlands (Geleijnse 2004) followed 4807 residents aged 55 and over for 7–10 years. The third who ate the most had a 57% lower risk of dying of coronary heart disease than the third who ate the least, and 52% lower odds of severe aortic calcification; K1 showed no such association. That is an association and does not show that K2 caused the difference. People on long-term warfarin (which stops vitamin K from being recycled) have more vascular calcification, which also suggests this pathway operates in people.
So taking high doses of vitamin D and calcium on their own, while vitamin K is short, may send calcium somewhere it should not go. That concern follows from the mechanism; no human trial has yet shown that taking K2 prevents it.
The evidence in people is observational. The Rotterdam Study in the Netherlands (Geleijnse 2004) followed 4807 residents aged 55 and over for 7–10 years. The third who ate the most had a 57% lower risk of dying of coronary heart disease than the third who ate the least, and 52% lower odds of severe aortic calcification; K1 showed no such association. That is an association and does not show that K2 caused the difference. People on long-term warfarin (which stops vitamin K from being recycled) have more vascular calcification, which also suggests this pathway operates in people.
So taking high doses of vitamin D and calcium on their own, while vitamin K is short, may send calcium somewhere it should not go. That concern follows from the mechanism; no human trial has yet shown that taking K2 prevents it.
Clinical · Vitamin K when you take blood thinners
Warfarin (brand name Coumadin) and vitamin K are one of the most classic cases of antagonism in clinical pharmacology.Mechanism: clotting factors II, VII, IX, and X only work after GGCX converts their glutamates (Glu) into Gla. Vitamin K is used up in that step as vitamin K epoxide and must be reduced back by VKORC1 (vitamin K epoxide reductase) before it can be used again. Warfarin precisely inhibits VKORC1; once the cycle breaks, clotting factors are not γ-carboxylated, clotting takes longer, and the lab report shows a higher .
How to read INR: INR is the prothrombin time converted onto one standard scale. It is about 1.0 in most people; warfarin treatment usually targets 2.0–3.0 (atrial fibrillation, preventing deep-vein thrombosis), and people with a mechanical heart valve target 2.5–3.5.
The real problem with diet and warfarin: it is not "no greens"; that is a common misunderstanding. The real issue is keeping intake steady. If vitamin K intake swings up and down, INR rides a rollercoaster, and both bleeding and clotting risks rise. The usual advice is to eat about the same amount of greens every day (1–2 servings) so the doctor can set the warfarin dose against that baseline. High-K foods such as kelp and Chinese broccoli do not have to be avoided entirely, but sudden big changes should be. Natto is the exception: its content is very high and stays in the blood a long time, and clinical observations in Japan (Kudo 1990) found that eating natto markedly weakened anticoagulation in patients on warfarin, so people on warfarin are generally advised not to eat natto.
Direct oral anticoagulants () changed the picture: dabigatran directly inhibits thrombin (IIa), and rivaroxaban, apixaban, and edoxaban inhibit factor Xa. None of them runs through the vitamin K cycle, so vitamin K in food does not change their effect and routine INR checks are not needed. Over the past fifteen years, many uses that once needed warfarin have moved to DOACs; a few situations, such as a mechanical heart valve, still require warfarin.
So: people on warfarin who want to add a supplement must talk to their doctor first, otherwise INR may fall noticeably and clotting risk may rise. People on a DOAC have no vitamin K food-drug interaction, and vitamin K foods and K2 supplements are fine as usual. First find out which anticoagulant you take, then decide how to eat vitamin K.
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Chapter 5
Working with vitamin D and calcium
Vitamin D, , and calcium are often discussed together because each handles one stretch of the same job:
Vitamin D: makes the gut absorb more calcium (it opens the calcium channel TRPV6 in the gut wall and increases the calcium-carrying protein calbindin)K2: activates osteocalcin and MGP, which influence whether absorbed calcium settles in bone or in the vessel wallCa²⁺: the cargo itself
Magnesium (Mg²⁺) is the often-forgotten fourth member: both hydroxylation steps that turn vitamin D into its active form (CYP2R1 and CYP27B1) need magnesium.
The mechanism predicts that a high dose of any one of them on its own may be poor value. With D and calcium but too little vitamin K, the absorbed calcium may not go to the right place; with K2 and calcium but too little D, the gut absorbs little calcium to begin with; with D and K2 but little calcium, there is no raw material. This is reasoning from mechanism; no trial has directly compared these combinations. So the safer move is to get the overall diet right first (greens, fermented foods, fish, nuts and seeds, moderate sun) rather than stacking high-dose supplements.
Vitamin D: makes the gut absorb more calcium (it opens the calcium channel TRPV6 in the gut wall and increases the calcium-carrying protein calbindin)K2: activates osteocalcin and MGP, which influence whether absorbed calcium settles in bone or in the vessel wallCa²⁺: the cargo itself
Magnesium (Mg²⁺) is the often-forgotten fourth member: both hydroxylation steps that turn vitamin D into its active form (CYP2R1 and CYP27B1) need magnesium.
The mechanism predicts that a high dose of any one of them on its own may be poor value. With D and calcium but too little vitamin K, the absorbed calcium may not go to the right place; with K2 and calcium but too little D, the gut absorbs little calcium to begin with; with D and K2 but little calcium, there is no raw material. This is reasoning from mechanism; no trial has directly compared these combinations. So the safer move is to get the overall diet right first (greens, fermented foods, fish, nuts and seeds, moderate sun) rather than stacking high-dose supplements.
In practice · Who might need supplements on top
The vitamin D, , calcium, and magnesium "four-piece set" is the hottest combination in the influencer supplement market. Translated into actual food and supplement doses, it looks roughly like this. A caveat first: these doses are common practice, not a combined prescription from any guideline, so check your own amounts with a doctor or dietitian.Diet and sunlight first (most people do not need the full set of supplements):
Vitamin D: in spring and summer, 10–15 min of outdoor sun 2–3 times a week, fatty fish 2–3 times a week, plus egg yolksK2: natto, hard cheese, or egg yolk 2–3 times a week, plus some animal fat (such as grass-fed butter)K1: 100–200 g of dark leafy greens a dayCalcium: dairy, tofu, sardines, and greens, 1000–1200 mg a dayMagnesium: pumpkin seeds, almonds, dark greens, and whole grains, 320–420 mg a day
When to consider adding supplements (by situation):
Situation A · an ordinary adult with a basically adequate diet and above 50 nmol/L: usually no supplements needed; in winter, 1000 of vitamin a day is reasonable insurance.Situation B · 25(OH)D below 50 nmol/L and no fermented foods: vitamin D3 2000–4000 IU a day, 90–180 µg a day, and 200–350 mg of supplemental magnesium a day; calcium preferably from food unless the diet is truly very short.Situation C · a postmenopausal woman with borderline and cardiovascular risk: vitamin D3 2000–4000 IU, MK-7 180 µg, 1000–1200 mg of calcium from food, 300–350 mg of supplemental magnesium, plus strength training 2–3 times a week. Each item has its own rationale, but as a package no trial has shown that it reduces fractures or cardiovascular events.Situation D · taking warfarin: do not start K2 on your own; talk to your doctor first, since the dose usually needs adjusting and rechecking. Vitamin D, calcium, and magnesium can still be used.Situation E · chronic kidney disease ( stages 3–5): do not take magnesium, potassium, or calcium on your own; the kidneys excrete less, so these build up easily. Whether to take vitamin D, and in which form, is for a kidney specialist to decide.
About the magnesium ceiling: by the standard quoted by the US NIH Office of Dietary Supplements (ODS), the tolerable upper intake level () for magnesium from supplements is 350 mg a day for adults; magnesium from food does not count. That is why the supplemental magnesium above stays within 350 mg; higher doses are treatment doses and belong under a doctor's guidance.
Some traps to avoid:
Cheap all-in-one vitamin D, K2, magnesium, and calcium tablets: some are short on every ingredient, with only 400–600 IU of vitamin D and less than 50 µg of K2.A high-dose calcium supplement (1000 mg) with no thought for K2 and D: by the mechanism, the calcium may go to the wrong place.K2 alone, with no exercise and little calcium: with no raw material, K2 is an engineer with nothing to build.
The mechanism behind the four-piece set holds, but most healthy adults who eat a varied diet and get moderate sun do not need to take all four as supplements. The logic of supplements is filling a gap, not stacking on top.
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Chapter 6
Two forms of K2 in supplements
Supplement comes mainly in two forms, which differ in the number of isoprenoid units on the side chain (chemical name menaquinone, written MK-n):
MK-4 (4 units): found in animal foods such as egg yolk, meat, and milk, and it stays in the blood only 1–3 hours. Japanese trials that used it to treat osteoporosis mostly gave 45 mg a day in 3 doses, and one gave 15 mg; that is a drug-level dose, it is expensive, and taking it several times a day is hard to keep up.
(7 units): comes from natto and takes about 3 days to fall by half in the blood, so 90–180 µg once a day keeps plasma levels steady. It is the mainstream supplement form, cheap and easy to stick with.
So if you do take K2, MK-7 is the more convenient form, though no large trial has yet shown that it reduces fractures. The high-dose MK-4 regimen is osteoporosis treatment and a doctor's decision. Ordinary people without a clotting problem do not need a K1 supplement.
Anyone on warfarin should talk to a doctor before taking any form of vitamin K, because every form weakens warfarin's anticoagulant effect.
MK-4 (4 units): found in animal foods such as egg yolk, meat, and milk, and it stays in the blood only 1–3 hours. Japanese trials that used it to treat osteoporosis mostly gave 45 mg a day in 3 doses, and one gave 15 mg; that is a drug-level dose, it is expensive, and taking it several times a day is hard to keep up.
(7 units): comes from natto and takes about 3 days to fall by half in the blood, so 90–180 µg once a day keeps plasma levels steady. It is the mainstream supplement form, cheap and easy to stick with.
So if you do take K2, MK-7 is the more convenient form, though no large trial has yet shown that it reduces fractures. The high-dose MK-4 regimen is osteoporosis treatment and a doctor's decision. Ordinary people without a clotting problem do not need a K1 supplement.
Anyone on warfarin should talk to a doctor before taking any form of vitamin K, because every form weakens warfarin's anticoagulant effect.
Evidence · How far the K2 supplement evidence goes
The right stance on supplements is: the mechanism is clear, observational studies point the same way, and the randomized trials are early and small. It is neither a miracle drug nor a gimmick. By type of evidence:Mechanism and observational studies (consistent in direction, but associations only): in several prospective cohorts, people with high undercarboxylated osteocalcin (ucOC) had more hip fractures; people with high inactive MGP (dp-ucMGP) had more cardiovascular events and more aortic calcification (the Rotterdam, PREVEND, and EPIC-NL cohorts, among others); and people on long-term warfarin, whose vitamin K cycle is blocked, have more vascular calcification, a side effect seen in clinical practice.
Small randomized trials (): in Knapen 2013, 244 postmenopausal women took 180 µg of a day for 3 years. Their fell more slowly, the vertebrae of the lower thoracic spine lost less height, and vitamin K status (the ucOC/cOC ratio) improved, but fractures were not an endpoint. Knapen 2015, in the same women (same dose, 3 years), found improved measures of arterial stiffness. Several Japanese trials of MK-4 at 45 mg a day reduced fractures in postmenopausal women, but that is a treatment dose, not an ordinary supplement; other randomized trials giving vitamin K to older adults saw no change in bone density.
Still unanswered: whether K2 on its own lowers cardiovascular deaths. The epidemiological association is strong, but the large randomized trials are not finished. Osteoporosis drugs (such as bisphosphonates) are backed by large trials with fractures as the endpoint; K2 is not, so it cannot replace them.
In practice:
If your diet already includes natto, hard cheese, or egg yolks, you do not need K2.If you eat a near-vegan diet and also take high-dose vitamin D and calcium supplements, MK-7 at 90–180 µg a day is reasonable insurance.Postmenopausal women with borderline bone density can consider K2 with vitamin D and calcium under a doctor's guidance.People on warfarin (Coumadin) must not start it on their own and must ask their doctor first, because it weakens the drug.
K2's role is not treating disease on its own but making sure the calcium you have already absorbed goes to the right place. It is a fairly cheap insurance policy, not a miracle.
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References · 5
- National Institutes of Health, Office of Dietary Supplements. (2021). Vitamin K — Fact Sheet for Health Professionals. Fact sheet (updated March 29, 2021; Wayback snapshot 19 September 2026): free phylloquinone is about 80% absorbed, but absorption from food is much lower - the body absorbs only 4% to 17% as much from spinach as from a tablet; Table 2: natto, 3 ounces, 850 mcg (as MK-7); egg, hard boiled, 1 large, 4 mcg (as MK-4) (fact sheet). ods.od.nih.gov/factsheets/VitaminK-HealthProfessional
- Beulens, J. W. J., et al. (2013). The role of menaquinones (vitamin K₂) in human health. British Journal of Nutrition, 110(8), 1357–1368. 10.1017/S0007114513001013
- Schurgers, L. J., et al. (2007). Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7. Blood, 109(8), 3279–3283. 10.1182/blood-2006-08-040709
- Geleijnse, J. M., et al. (2004). Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study. Journal of Nutrition, 134(11), 3100–3105. 10.1093/jn/134.11.3100
- Uwitonze, A. M., & Razzaque, M. S. (2018). Role of magnesium in vitamin D activation and function. Journal of the American Osteopathic Association, 118(3), 181–189. 10.7556/jaoa.2018.037