Vitamin K

Vitamin K is a fat-soluble vitamin that comes in two main dietary forms — K1 (phylloquinone) from green plants, and K2 (menaquinones) from fermented foods and animal foods — which differ in how they’re distributed in the body and how long they last. The name comes from the German “Koagulationsvitamin”: the Danish scientist Henrik Dam discovered its essential role in blood clotting through experiments that began in 1929, work that earned him a share of the 1943 Nobel Prize. Clotting remains its best-known job, but it’s only part of the story: vitamin K is also needed to activate proteins that help regulate where calcium goes in the body — into bone, and away from blood vessel walls. That calcium-regulating role has made vitamin K a major focus of research on bone and heart health.

Key Mechanisms — Gamma-Carboxylation

Vitamin K’s main, best-understood job is enabling gamma-carboxylation — a chemical modification that switches certain proteins from inactive to active.

The reaction: some proteins contain glutamic acid (Glu) units that must be converted into gamma-carboxyglutamic acid (Gla) units for the protein to work. The enzyme gamma-glutamyl carboxylase makes this change, using the reduced form of vitamin K (vitamin K hydroquinone) as its cofactor. In the process, vitamin K is converted into vitamin K epoxide, and another enzyme — vitamin K epoxide reductase (VKOR, made by the VKORC1 gene) — recycles it back into the active form. This recycling lets each vitamin K molecule be reused many times.

Why carboxylation matters: Gla units bind calcium. That’s what allows clotting factors to attach to cell membranes at the site of an injury, osteocalcin to bind to bone mineral, and matrix Gla-protein (MGP) to block calcium deposits in soft tissues. Without carboxylation, these proteins are made but can’t do their jobs.

How warfarin works: warfarin blocks VKOR, stopping vitamin K from being recycled. As active vitamin K runs out, the vitamin K-dependent clotting factors are made in inactive form, and blood clots more slowly. That’s how warfarin prevents dangerous clots — and why people taking it need a consistent vitamin K intake. Vitamin K from food or supplements can still be activated through a separate route that warfarin doesn’t block, which is why extra vitamin K reverses warfarin’s effect.

The Gla-Proteins — Vitamin K’s Downstream Targets

At least 17 human proteins depend on vitamin K-driven carboxylation. The most important are:

Clotting factors: factors II (prothrombin), VII, IX, and X — key drivers of the clotting cascade — along with proteins C, S, and Z, which act as brakes on clotting. When vitamin K is lacking, both the drivers and the brakes are affected, but the main result is bleeding.

Osteocalcin (bone Gla-protein): made by bone-building cells (osteoblasts). When carboxylated, it binds calcium and bone mineral and is thought to help regulate bone mineralization. High levels of undercarboxylated osteocalcin — a sign of low vitamin K status — are linked with lower bone density and higher fracture risk, and the proportion of osteocalcin that’s undercarboxylated is used in research as a sensitive marker of vitamin K status.

Matrix Gla-protein (MGP): made in blood vessel walls and cartilage. When carboxylated, it’s one of the body’s most powerful natural inhibitors of calcium deposits in soft tissues — mice that lack MGP develop severe artery calcification and die young. In people, higher levels of inactive MGP are linked with stiffer arteries and higher cardiovascular risk. Whether vitamin K supplements can prevent or slow artery calcification is still being studied.

K1 vs K2 — The Most Important Distinction on This Page

Vitamin K is often treated as a single nutrient, but its two main forms behave quite differently.

Vitamin K1 (phylloquinone):

• Found mainly in green leafy vegetables and some vegetable oils; the main dietary form of vitamin K
• Goes mainly to the liver, where it supports the production of clotting factors
• Cleared from the blood within hours
• Poorly absorbed from vegetables, where it’s tightly bound to the plant’s chloroplasts: the body absorbs only about 4–17% as much from spinach as from a tablet, though eating vegetables with some fat helps
• The body converts some K1 into the K2 form MK-4 in tissues
• The form the Adequate Intake is based on

Vitamin K2 (menaquinones):

• Found in fermented foods (especially natto and cheese) and in smaller amounts in meat, eggs, and dairy; also made by gut bacteria
• The long-chain forms, such as MK-7, stay in the blood much longer — MK-7’s half-life is about three days, compared with hours for K1 — and reach tissues outside the liver more readily
• In studies, MK-7 activates osteocalcin and MGP more effectively than the same amount of K1
• Higher K2 intake, but not K1, was linked with less artery calcification and heart disease in a major Dutch study (see below)

MK-4 vs MK-7 within K2:

K2 includes several menaquinones, numbered by the length of their side chain (MK-4 through MK-13). Two are the most relevant:

• MK-4: found in meat, eggs, and dairy, and also made by the body from K1. It’s absorbed quickly but cleared quickly. In Japan and other parts of Asia, very high doses (45mg a day) are used as a prescription osteoporosis treatment.
• MK-7: found mainly in natto (fermented Japanese soybeans). Its long half-life gives steady blood levels from a modest once-daily dose, making it the most popular and best-studied K2 supplement form. Doses around 100–200µg a day improve the activation of osteocalcin and MGP in trials. Hard cheeses also contain K2, but mostly as other long-chain forms (MK-8 and MK-9).

Vitamin K AI (Adequate Intake)

There isn’t enough evidence to set an RDA for vitamin K, so Adequate Intake (AI) values are used instead.

Source: US National Academies, via the NIH Office of Dietary Supplements. The infant values assume babies receive a vitamin K injection at birth. The daily value used on food labels is 120µg.

ODA (Optimal Daily Allowance)

Meet the AI — 90–120µg a day for adults — mainly from green vegetables, which is easy with a daily serving of leafy greens or broccoli. Adding some K2 from fermented foods, such as hard cheese or natto, is a sensible extra. K2 (MK-7) supplements, commonly 90–200µg a day, reliably improve the activation of vitamin K-dependent proteins, and Europe’s food safety authority accepts that vitamin K contributes to normal bone — but trials haven’t yet shown clear benefits of supplements for fractures or heart disease in healthy people. They’re safe for most people, with one crucial exception: anyone taking warfarin or a similar anticoagulant shouldn’t take vitamin K supplements without their doctor’s supervision.

Found In

Vitamin K1 sources (per 100g):

* Value from USDA’s SR Legacy data, where the Foundation Foods entry doesn’t include it.

Other dark leafy greens are outstanding sources too: according to the NIH, half a cup of cooked collard greens provides about 530µg, cooked turnip greens about 426µg, and a cup of raw kale about 113µg. Parsley is also very high. Some vegetable oils, particularly soybean and canola oil, provide useful amounts, while others, such as sunflower oil, contain very little.

Vitamin K2 sources (per serving):

Source: NIH Office of Dietary Supplements. Data on K2 in foods is limited, and US figures for meat, eggs, and dairy count only MK-4. Cheese also contains long-chain menaquinones (MK-8 and MK-9) that these figures leave out — Dutch analyses that measured them found roughly 50–75µg of total menaquinones per 100g in hard cheeses such as Gouda. The amounts vary with the bacteria and fermentation used.

Natto is in a class of its own for vitamin K2 — a single serving provides several times the daily value — and in Japan, eating natto has been linked with lower cardiovascular death rates in population studies. Most Western diets contain relatively little K2, mostly from cheese, meat, and eggs, which is one reason K2 supplements have become popular.

Vitamin K Helps With

• Blood clotting — activating clotting factors II, VII, IX, and X
• Normal bone — through carboxylated osteocalcin; Europe’s food safety authority accepts that vitamin K contributes to maintaining normal bone
• Limiting calcium deposits in blood vessel walls — through carboxylated MGP
• Cardiovascular health — higher K2 intake is linked with less artery calcification and heart disease, though supplement trials haven’t confirmed a benefit yet
• Wound healing — which depends on normal clotting

Vitamin K for Athletes and Active People

Vitamin K matters for athletes mainly through bone health, with some intriguing — but early — research on osteocalcin as a hormone.

Bone health: athletes such as runners, military recruits, and female endurance athletes with low bone density are at higher risk of stress fractures. Healthy bones depend on adequate calcium, vitamin D, and vitamin K, among other factors. The trial evidence on vitamin K supplements for bone is mixed: in a three-year trial in postmenopausal women, MK-7 (180µg a day) slowed bone loss and improved bone strength, and high-dose MK-4 trials in Japan reduced fractures, but other trials found no effect on bone density. There are no trials specifically in athletes, so making sure intake from food is adequate is the sensible priority.

Arteries and vitamin D: stiffer arteries make the heart work harder, and MGP helps keep artery walls free of calcium deposits. Some practitioners suggest pairing high-dose vitamin D supplements with K2, on the theory that K2 helps direct the extra calcium absorbed into bone rather than arteries. It’s a plausible idea, but it hasn’t been tested in athletes, and trials haven’t shown that the combination prevents calcification.

Osteocalcin as a hormone — early research: work led by Gerard Karsenty, mostly in mice, suggests that osteocalcin — particularly its undercarboxylated form — also acts as a hormone. In mouse studies, exercise increases osteocalcin release from bone, and osteocalcin helps muscles take up and use glucose and fatty acids during exercise; it has also been linked with memory. If this holds true in humans, it would mean some undercarboxylated osteocalcin is useful, and that the relationship between vitamin K and osteocalcin is more complex than “more carboxylation is better.” But human studies have been inconsistent, and there are no practical supplement implications yet.

Practical considerations for athletes:

• Eat green vegetables regularly — deficiency is rare in athletes eating varied diets
• K2 (MK-7) is a reasonable, low-risk option if you take high-dose vitamin D, though its benefits are unproven
• If you take warfarin or a similar anticoagulant, keep your vitamin K intake consistent and don’t take vitamin K supplements without medical advice. Newer anticoagulants (DOACs, such as apixaban, rivaroxaban, and dabigatran) aren’t affected by vitamin K

Vitamin K Deficiency

Vitamin K deficiency is very rare in healthy adults. In people eating a varied diet, it’s almost impossible to get so little vitamin K that blood clotting is affected. Deficiency matters mainly in specific situations.

Deficiency risk is higher in:

• Newborns: the most important case. Babies are born with very little vitamin K, because little crosses the placenta, and breast milk contains little. This can cause vitamin K deficiency bleeding (VKDB). Early VKDB occurs in the first week; late VKDB occurs between about 2 and 12 weeks, especially in exclusively breastfed babies, and often involves sudden bleeding in the brain, which can cause permanent damage or death. A single vitamin K injection at birth (0.5–1mg) prevents it, and is recommended by the American Academy of Pediatrics and health authorities worldwide. Babies who don’t receive it are far more likely to develop late VKDB. The injection is safe — an early concern about a link with childhood cancer was not confirmed by later studies.
• People with malabsorption conditions: such as celiac disease, Crohn’s disease, ulcerative colitis, cystic fibrosis, cholestatic liver disease, or short bowel syndrome, or after weight-loss surgery
• People taking long courses of antibiotics while eating little vitamin K: antibiotics can reduce vitamin K-producing gut bacteria, and some (certain cephalosporins) also interfere with vitamin K’s action
• People on warfarin: warfarin deliberately blocks vitamin K recycling — which also affects osteocalcin and MGP, and some studies have linked long-term use with more fractures and artery calcification
• People with severe liver disease: who may not make enough clotting factors even with adequate vitamin K

Symptoms of vitamin K deficiency:

• Easy or excessive bruising
• Prolonged bleeding from cuts
• Nosebleeds and bleeding gums
• Heavy menstrual bleeding
• Blood in the urine or stool
• In severe cases, internal bleeding
• Lower, longer-term vitamin K status is linked with lower bone density, though standard clotting tests can be normal

Excessive Doses of Vitamin K

No upper limit (UL) has been set for vitamin K1 or K2, because no harmful effects have been reported from vitamin K in food or supplements in healthy people.

Vitamin K3 (menadione): a synthetic form that isn’t used in supplements or fortified foods. It damaged liver cells in laboratory studies and can destroy red blood cells and cause jaundice, particularly in newborns. It’s still used in some animal feed — which is why chicken and pork contain some MK-4. It’s mentioned here only to distinguish it clearly from K1 and K2, which are safe.

The warfarin interaction: this isn’t toxicity from vitamin K itself, but it’s the most important practical concern. More vitamin K reduces warfarin’s effect (lowering the INR blood test result) and raises clotting risk, while less vitamin K increases warfarin’s effect and bleeding risk. The key is consistency: big sudden changes in intake — such as suddenly eating lots of leafy greens after weeks without them — destabilize the INR. Keeping intake steady works better than avoiding vitamin K.

The Rotterdam Study: a landmark observational study of 4,807 older Dutch adults found that those with the highest K2 intake had a 57% lower risk of dying from heart disease, 41% lower risk of heart disease, 26% lower overall mortality, and about half the risk of severe aortic calcification compared with those with the lowest intake. K1 intake showed no link. This finding redirected vitamin K research toward K2 and blood vessel health. Because it was observational — and K2 in the Netherlands comes mostly from cheese — it can’t prove cause and effect, and supplement trials so far have been small, with mixed results.

Types of Vitamin K

• Vitamin K1 (phylloquinone or phytonadione): found in leafy greens and vegetable oils, and in many multivitamins. Diet usually provides enough for clotting. Also the form used for the newborn injection and to reverse warfarin.
• Vitamin K2 MK-7: made from natto fermentation or synthetically. The most popular K2 supplement — effective once a day at around 100–200µg, and the best-studied form for activating osteocalcin and MGP. Very potent for its dose, so it’s the form most likely to interfere with warfarin.
• Vitamin K2 MK-4: found in animal foods and made in the body from K1. Short-lived in the blood. Used at 45mg a day as a prescription osteoporosis treatment in Japan; available in some supplements at lower doses.
• Full-spectrum vitamin K2 (MK-4 + MK-7): combined menaquinone products.
• Vitamin K3 (menadione): synthetic; not used in human supplements — avoid.

Which form for your goal:

How to Take Vitamin K

Take it with a meal that contains fat: vitamin K is fat-soluble and needs dietary fat and bile to be absorbed well. The same applies to vitamin K in vegetables — a little oil or other fat with your greens helps.

MK-7 once a day is enough: with a half-life of about three days, a single daily dose keeps blood levels steady.

The vitamin D and K2 pairing: many people take K2 alongside vitamin D supplements, especially at higher vitamin D doses, on the reasoning that vitamin D increases calcium absorption and vitamin K activates the proteins that direct calcium into bone and away from arteries. The reasoning is sound, and the combination is low-risk for most people, but trials haven’t yet shown that it improves bone or heart outcomes beyond vitamin D and calcium alone.

Warfarin users — the most important instruction: vitamin K is the antidote to warfarin. Don’t start or stop vitamin K supplements, or make big changes to how many leafy greens you eat, without talking to your doctor or anticoagulation clinic. Be particularly careful with MK-7: it’s so potent that even 10–20µg a day has measurably changed INR results in studies. If a vitamin K supplement is used at all, it should be at a consistent daily dose with close INR monitoring.

K1 from food: for most people who eat green vegetables regularly, food provides plenty of vitamin K1 for blood clotting. If you’re considering a supplement for bone or heart reasons, K2 is the form usually chosen.

Interactions

Warfarin and similar anticoagulants (such as acenocoumarol and phenprocoumon, used in parts of Europe): vitamin K directly opposes how these drugs work — one of the most important drug–nutrient interactions — so consistent vitamin K intake is essential for stable INR results. Newer anticoagulants (DOACs) aren’t affected by vitamin K. Long courses of antibiotics, particularly some cephalosporins, can lower vitamin K status. Orlistat, cholestyramine, and mineral oil reduce absorption of fat-soluble vitamins, including vitamin K — and orlistat combined with warfarin can increase warfarin’s effect. High-dose vitamin E (400 IU or more) can interfere with vitamin K’s role in clotting, which matters most for people taking anticoagulants.

Synergy

• Works with vitamin D and calcium in bone — vitamin D increases calcium absorption, calcium provides the mineral, and vitamin K activates the proteins that help put calcium into bone and keep it out of arteries.
• Works alongside magnesium, which is also important for bone and blood vessel health.
• Complements vitamin E at normal intakes — though high-dose vitamin E can interfere with vitamin K’s role in clotting.
• Interacts with vitamin A in bone — very high vitamin A intake may work against vitamin K’s effects on bone.

Antagonistic Interactions

• Warfarin blocks the VKOR enzyme that recycles vitamin K — the drug’s intended effect.
• High-dose vitamin E (400 IU a day or more) can interfere with vitamin K-dependent clotting — an added concern for people on anticoagulants.
• Very high vitamin A intake may work against vitamin K’s effects on bone.
• Long courses of antibiotics can lower vitamin K status.
• Orlistat and bile acid sequestrants (such as cholestyramine) reduce vitamin K absorption.

Sources: vitamin K1 values from USDA FoodData Central — spinach, boiled (SR Legacy, FDC ID 168463); spinach, mature, raw (Foundation Foods, 1999633, vitamin K from SR Legacy); broccoli raab, cooked (SR Legacy, 170382); broccoli, boiled (SR Legacy, 169967); Brussels sprouts, boiled (SR Legacy, 169971); broccoli, raw (Foundation Foods, 747447); asparagus, boiled (SR Legacy, 168390); edamame, prepared (SR Legacy, 168411); pumpkin, canned (SR Legacy, 168450); grapes (SR Legacy, 174683). Vitamin K2 values, per-serving greens figures, and Adequate Intakes from the NIH Office of Dietary Supplements, Vitamin K Fact Sheet for Health Professionals. % Daily Values use the FDA’s current Daily Value of 120µg.