Vitamin K is poorly understood, both by the general public and among health professionals. It has a wide range of potential benefits, but their nature and extent are still uncertain.
Why is that?
Some vitamins are more popular than others. In the past, a lot of research went into vitamin C, which became a popular supplement. Nowadays, a lot of research goes into vitamin D, whose popularity as a supplement is steadily growing.
By contrast, research on vitamin K is still scarce, having slowly developed over the past two decades. Further, it is scattered, because there exist several forms of vitamin K. Some of those forms are present only in a few foods. Others exist in various foods, but only in minute amounts. Few have been the subject of human trials.
The human trials that do exist, however, are overall promising. In order to understand their value and limitations, first you need to know a few basic facts. So let’s begin:
Of the four fat-soluble vitamins (A, D, E, and K), vitamin K was discovered last. In 1929, Danish scientist Henrik Dam discovered a compound that played a role in coagulation (blood clotting). When he first published his findings, in a German journal, he called this compound Koagulationsvitamin, which became known as vitamin K.
Today, we know that vitamin K participates in some very important biological processes, notably the carboxylation of calcium-binding proteins (including osteocalcin and matrix GLA protein). In other words, vitamin K helps modify proteins so they can bind calcium ions (Ca2+). Through this mechanism, vitamin K partakes in blood clotting, as Henrik Dam discovered, but also of calcium regulation: it helps ensure that more calcium gets deposited in bones and less in soft tissues, thus strengthening bones and reducing arterial stiffness.
What complicates matters is that each vitamin has different forms, called vitamers, each of which may affect you differently. Vitamin K has natural vitamers, K1 (phylloquinone) and K2 (menaquinone), and synthetic vitamers, the best-known of which is K3 (menadione).
K1 is produced in plants, where it is involved in photosynthesis: the greener the plant, the greater its chlorophyll content; the greater its chlorophyll content, the greater its K1 content. When it comes to foods, K1 is especially abundant in green leafy vegetables.
K1 makes for 75–90% of the vitamin K in the Western diet. Unfortunately, K1 is tightly bound to chloroplasts (organelles that contain chlorophyll and conduct photosynthesis), so you could be absorbing very little of what you eat — maybe less than 10%. Since vitamin K is a fat-soluble vitamin, however, its absorption can be enhanced by the co-ingestion of fat: adding fat to cooked spinach can raise K1 bioavailability from 5% to 13%.
Things become more complicated here, because just as there are several forms of vitamin K, there are several forms of vitamin K2. To be more precise, the side chain of K1 always has four isoprenoid units (five-carbon structures), so there is only one form of K1, but the side chain of K2 has n isoprenoid units, so there are n forms of K2, called MK-n.
Whereas the side chain of K1 has four saturated isoprenoid units, the side chain of K2 MK-4 has four unsaturated isoprenoid units. Although K1 is directly active in your system, your body can also convert it to MK-4. How much gets converted depends notably on your genetic heritage.
MK-4 is present in animal products (meat, eggs, and dairy), though only in small quantities. Because those foods usually contain fat, dietary MK-4 should be better absorbed than dietary K1, but future studies will need to confirm this hypothesis.
Other than MK-4, all forms of K2 are produced by bacteria. Your microbiota was once thought to produce three-fourths of the vitamin K you absorb. Vitamin K, however, is mostly produced in the colon, where there are no bile salts to facilitate its absorption, so the actual ratio is probably much lower.
Bacteria-produced K2 can be found in fermented foods, such as cheese and curds, but also in liver meat. The richest dietary source of K2 is natto (fermented soybeans), which contains mostly MK-7. As it stands, MK-7 is the only form of K2 that can be consumed in supplemental doses through food (i.e., natto). For that reason, MK-7 is the most-studied form of K2, together with MK-4.
K1 and MK-4 both have a side chain composed of four isoprenoid units; their half-life in your blood is 60–90 minutes. MK-7 has a side chain composed of seven isoprenoid units; it remains in your blood for several days. Due to their different side-chain lengths, the various forms tend to be transported on different lipoproteins, which are taken up at different rates by various tissues. K1 and MK-4 are used quickly (K1 in the liver, MK-4 in other specific tissues), whereas MK-7 has more time to travel and be used throughout the body (which makes it, in theory, the best option for bone health).
K1 and K2 are the only natural forms of vitamin K, but there exist several synthetic forms, the best known of which is K3. However, whereas the natural forms of vitamin K are safe, even in high doses, K3 can interfere with glutathione, your body’s main antioxidant. K3 was once used to treat vitamin K deficiency in infants, but it caused liver toxicity, jaundice, and hemolytic anemia. Nowadays, it is used only in animal feed, in small doses. In the animals, vitamin K3 gets converted into K2 MK-4, which you can consume safely.
Vitamin K is a family of fat-soluble vitamins. K1 and K2, the natural forms, are safe even in high doses. There is only one type of K1; it is found in plants, notably green leafy vegetables; your body can use it directly or convert it to K2 MK-4. Aside from MK-4, all other types of K2 are produced by bacteria, including the bacteria populating your gut. MK-4 is present in animal products (meat, eggs, dairy), whereas other types of K2 can be found in fermented foods and liver meat.
As far as we know, vitamin K mainly affects blood clotting, vascular and heart health, and bone health. Epidemiological studies have mostly focused on K1; cardiovascular trials, on K1 and MK-7 (the main type present in natto, the richest dietary source of K2); bone trials, on MK-4 (the type of K2 your body can make out of K1).
Vitamin K deficiency impairs blood clotting, causing excessive bleeding and bruising. It is rare in adults, but more common in newborns (more than 4 cases per 100,000 births in the UK), where it can result in life-threatening bleeding within the skull. For that reason, the American Academy of Pediatrics recommends that newborns receive K1 shortly after birth (intramuscular injections have shown greater efficacy than oral administration).
If you suffer from hypercoagulation (if your blood clots too easily), you might be prescribed a vitamin K antagonist (VKA), such as warfarin, a medication that hinders the recycling of vitamin K. Some doctors recommend that VKA users shun vitamin K entirely, but preliminary evidence suggests that, under professional supervision, vitamin K supplements might help stabilize the effects of VKAs.
Which form should be supplemented, though, and in what amount, is still uncertain. There is some evidence that K1 enhances coagulation more than does MK-4 but less than does MK-7. With regard to daily supplementation, 100 mcg of K1 is considered safe, but in some people 10 mcg of MK-7 is enough to significantly impair VKA therapy.
Remember that natto is rich in MK-7. A single serving of natto can increase blood clotting for up to four days, so it is one food VKA users should avoid. Other foods should be safe to eat. Please note that in people who do not suffer from hypercoagulation, and thus do not need to medicate with VKA, high intakes of natto have never been correlated to excessive blood clotting. Similarly, human studies saw no increase in blood-clot risk even from 45 mg (45,000 mcg) of MK-4 taken once or even thrice daily.
As we saw, vitamin K partakes in calcium regulation: it helps ensure that more calcium gets deposited in bones and less in soft tissues, thus reducing arterial stiffness. This is why people who take vitamin K antagonists, such as warfarin, are more likely to suffer from vascular calcification.
Clinical trials on supplemental vitamin K have focused on K1 and MK-7. Often, those trials used a combination of vitamin D and other nutrients, but with vitamin K being the key difference between the intervention group and the control groups. Both of these forms of vitamin K seem to cause a consistent reduction in arterial stiffness (with better evidence for MK-7), and less consistent reductions in coronary calcification and carotid intima-media thickness. Judging from those trials and the epidemiological evidence, MK-7 seems the better choice.
As we have just seen again, vitamin K partakes in calcium regulation: it helps ensure that less calcium gets deposited in soft tissues and more in bones, thus strengthening the latter. This is why people who take vitamin K antagonists, such as warfarin, might be more at risk of bone fractures, though not all studies agree they are.
Current evidence suggests that supplementing with vitamin K — or, at least, with certain forms of vitamin K — can benefit bone health, especially in the elderly (who have lower levels of circulating K2). This potential should be explored, since, as the world population grows (and grows older), so does the number of osteoporotic fractures. 
MK-7 appears to support the carboxylation of osteocalcin (a major calcium-binding protein in bones) more efficiently than K1. Clinical trials suggest that, for the purpose of increasing bone density, MK-4 and MK-7 work more reliably than K1.
More significantly, a meta-analysis of MK-4 trials found an overall decrease in fracture risk. The effect of K1 or MK-7 supplementation on fracture risk is less clear. Only one K1 trial looked at fracture risk; it reported a decrease, but without a concomitant increase in bone mineral density. Of the two MK-7 trials, one reported no difference in the number of fractures between the placebo group and the MK-7 group, whereas the other reported fewer fractures in the MK-7 group; there were, however, no statistical analyses for either study.
More research on vitamin K and fracture risk will be needed to clarify the effects of the different forms at different dosages. Currently, if you wish to supplement for bone health, a very high dose of MK-4 (45,000 mcg) is the option best supported by human studies. Those studies, all in Japanese people, focused on the prevention of bone fractures, and yes, much smaller dosages can probably help support bone health; but how much smaller?
In a 12-month study, 20 patients suffering from a chronic kidney disorder were given a daily glucocorticoid (a corticosteroid that has for side effect to decrease bone formation and increase bone resorption). In addition, half the patients received 15 mg of MK-4 daily, while the other half received a placebo. The placebo group experienced bone-density loss (BDL) in the lumbar spine, while the MK-4 group did not.
More recently, a 12-month study in 48 postmenopausal Japanese women gave 1.5 mg of MK-4 daily to half of them and found a significant reduction in forearm BDL, but not in hip BDL, and it didn’t evaluate fractures.
So there is some evidence for dosages lower than 45 mg/day. It is, however, a lot weaker.
In healthy people, vitamin K supplementation does not increase the risk of blood clots. Judging from limited evidence, MK-7 seems to be the best form of vitamin K for cardiovascular health, and MK-4 the best form of vitamin K for bone health.
Since vitamin K is crucial to your health, why is it the subject of relatively few studies? One of the reasons is simply that vitamin K deficiency is very rare in healthy, well-fed adults. It is mostly a concern in newborns, in people who have been prescribed a vitamin K antagonist, in people who suffer from severe liver damage, and in people who have problems absorbing fat.
Vitamin K is abundant in a balanced diet, and the bacteria in your colon can also produce some. Moreover, your body can recycle it many times, and this vitamin K-epoxide cycle more than makes up for the limited ability your body shows for storing vitamin K.
Still, you can recycle vitamin K many times, but not forever, and so you still need to consume some regularly. But how much, exactly?
No one knows. There is, as yet, not enough evidence to set a Recommended Dietary Allowance (RDA) for vitamin K, so an Adequate Intake (AI) has been established at a level assumed to prevent excessive bleeding. In the United States, the AI for vitamin K is 120 mcg/day for men and 90 mcg/day for women. In Europe, the AI for vitamin K is 70 mcg/day for men and women. More recent research, however, suggests that those numbers should be increased.
Fortunately, no. Though allergic reactions have occurred with vitamin K injections, no incidence of actual toxicity has ever been reported in people taking natural vitamin K, even in high supplemental doses. For that reason, neither the FDA nor the EFSA has set a Tolerable Upper Intake Level (UL) for vitamin K. One should note, however, that we lack long-term, high-dose studies on vitamin K safety.
K1 can be found in plant products, notably green leafy vegetables. K2 MK-4 can be found in animal products (meat, eggs, and dairy). The other types of K2 can be found in fermented foods and liver meat.
Meats’ vitamin K content correlates positively but non-linearly with their fat content and will vary according to the animal’s diet (and thus country of origin). Forms of K2 other than MK-4 and MK-7 have not been well studied but are likely to have some benefit — cheeses and beef liver are notable sources of others forms of K2 and cheese consumption is associated with a reduced risk of cardiovascular disease.
While well-conducted controlled trials provide the most reliable evidence, most such trials used amounts of vitamin K2 that far exceed what could be obtained through foods, save for natto. This leaves us wondering if dietary K2 has any effect.
Fortunately, it seems to be the case: a high dietary intake of K2 (≥33 mcg/day seems optimal) may reduce the risk of coronary heart disease — an effect a high dietary intake of K1 doesn’t appear to have. It doesn’t mean, of course, that foods rich in K1 are valueless: dietary K1 intake will protect you from excessive bleeding and is inversely associated with risk of bone fractures.
Observational studies, however, are less reliable than controlled trials, so we know less about the effects of dietary intake than about the effects of supplemental intake. If you wish to supplement with vitamin K, here are the dosages supported by the current evidence:
Although much more research needs to be performed, there is early evidence that vitamin K, whether in food or in supplemental form, can benefit cardiovascular health and bone health.
If you’d like to peruse the full body of research, our vitamin K page has over 450 references. If you are interested in an a step-by-step, evidence-based approach to supplementation, then check out our Supplement Guides.
- The antihaemorrhagic vitamin of the chick. Biochem J. (1935) Dam H.
- Roles for vitamin K beyond coagulation. Annu Rev Nutr. (2009) Booth SL.
- Recent trends in the metabolism and cell biology of vitamin K with special reference to vitamin K cycling and MK-4 biosynthesis. J Lipid Res. (2014) Shearer MJ, Newman P.
- Comparison of phylloquinone bioavailability from food sources or a supplement in human subjects. J Nutr. (1999) Garber AK, et al.
- Effect of food composition on vitamin K absorption in human volunteers. Br J Nutr. (1996) Gijsbers BL, Jie KS, Vermeer C.
- Oral anticoagulant therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. (2012) Ageno W, et al.
- Vitamin K: food composition and dietary intakes. Food Nutr Res. (2012) Booth SL.
- Vitamin K2 in electron transport system: are enzymes involved in vitamin K2 biosynthesis promising drug targets?. Molecules. (2010) Kurosu M, Begari E.
- Metabolism and cell biology of vitamin K. Thromb Haemost. (2008) Shearer MJ, Newman P.
- Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not dependent on gut bacteria. J Nutr. (1998) Davidson RT, et al.
- Intestinal flora is not an intermediate in the phylloquinone-menaquinone-4 conversion in the rat. Biochim Biophys Acta. (1998) Ronden JE, et al.
- The role of menaquinones (vitamin K₂) in human health. Br J Nutr. (2013) Beulens JW, et al.
- Vitamin K-controlled diet: problems and prospects. Clin Ter. (2005) Miggiano GA, Robilotta L.
- Colonic absorption of menaquinone-4 and menaquinone-9 in rats. J Nutr. (1992) Ichihashi T, et al.
- The role of dietary vitamin K in the management of oral vitamin K antagonists. Blood Rev. (2012) Holmes MV, Hunt BJ, Shearer MJ.
- Intake of fermented soybeans, natto, is associated with reduced bone loss in postmenopausal women: Japanese Population-Based Osteoporosis (JPOS) Study. J Nutr. (2006) Ikeda Y, et al.
- Usual dietary intake of fermented soybeans (Natto) is associated with bone mineral density in premenopausal women. J Nutr Sci Vitaminol (Tokyo). (2002) Katsuyama H, et al.
- Comparison of menaquinone-4 and menaquinone-7 bioavailability in healthy women. Nutr J. (2012) Sato T, Schurgers LJ, Uenishi K.
- Vitamin K: the effect on health beyond coagulation - an overview. Food Nutr Res. (2012) Vermeer C.
- Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7. Blood. (2007) Schurgers LJ, et al.
- Differential lipoprotein transport pathways of K-vitamins in healthy subjects. Biochim Biophys Acta. (2002) Schurgers LJ, Vermeer C.
- Determination of phylloquinone and menaquinones in food. Effect of food matrix on circulating vitamin K concentrations. Haemostasis. (2000) Schurgers LJ, Vermeer C.
- Identification of UBIAD1 as a novel human menaquinone-4 biosynthetic enzyme. Nature. (2010) Nakagawa K, et al.
- Vitamin K. Lancet. (1995) Shearer MJ.
- Controversies concerning vitamin K and the newborn. American Academy of Pediatrics Committee on Fetus and Newborn. Pediatrics. (2003) American Academy of Pediatrics Committee on Fetus and Newborn.
- Tissue-specific utilization of menaquinone-4 results in the prevention of arterial calcification in warfarin-treated rats. J Vasc Res. (2003) Spronk HM, et al.
- The relative effects of phylloquinone and menaquinone-4 on the blood coagulation factor synthesis in vitamin K-deficient rats. Biochem Pharmacol. (1993) Groenen-van Dooren MM, et al.
- Effect of low-dose supplements of menaquinone-7 (vitamin K2 ) on the stability of oral anticoagulant treatment: dose-response relationship in healthy volunteers. J Thromb Haemost. (2013) Theuwissen E, et al.
- Effect of vitamin K intake on the stability of oral anticoagulant treatment: dose-response relationships in healthy subjects. Blood. (2004) Schurgers LJ, et al.
- Effect of continuous combined therapy with vitamin K(2) and vitamin D(3) on bone mineral density and coagulofibrinolysis function in postmenopausal women. Maturitas. (2002) Ushiroyama T, Ikeda A, Ueki M.
- Vitamin K administration to elderly patients with osteoporosis induces no hemostatic activation, even in those with suspected vitamin K deficiency. Osteoporos Int. (2001) Asakura H, et al.
- Desphospho-uncarboxylated matrix Gla-protein is associated with mortality risk in patients with chronic stable vascular disease. Atherosclerosis. (2014) Mayer O Jr, et al.
- Vascular calcification: the price to pay for anticoagulation therapy with vitamin K-antagonists. Blood Rev. (2012) Chatrou ML, et al.
- A high menaquinone intake reduces the incidence of coronary heart disease. Nutr Metab Cardiovasc Dis. (2009) Gast GC, et al.
- High dietary menaquinone intake is associated with reduced coronary calcification. Atherosclerosis. (2009) Beulens JW, et al.
- Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study. J Nutr. (2004) Geleijnse JM, et al.
- Vitamin k dependent proteins and the role of vitamin k2 in the modulation of vascular calcification: a review. Oman Med J. (2014) El Asmar MS, Naoum JJ, Arbid EJ.
- Vitamin K supplementation and progression of coronary artery calcium in older men and women. Am J Clin Nutr. (2009) Shea MK, et al.
- Beneficial effects of vitamins D and K on the elastic properties of the vessel wall in postmenopausal women: a follow-up study. Thromb Haemost. (2004) Braam LA, et al.
- Effect of vitamin K2 on progression of atherosclerosis and vascular calcification in nondialyzed patients with chronic kidney disease stages 3-5. Pol Arch Med Wewn. (2015) Kurnatowska I, et al.
- Menaquinone-7 supplementation improves arterial stiffness in healthy postmenopausal women. A double-blind randomised clinical trial. Thromb Haemost. (2015) Knapen MH, et al.
- Effect of Vitamin K on Vascular Health and Physical Function in Older People with Vascular Disease--A Randomised Controlled Trial. J Nutr Health Aging. (2016) Fulton RL, et al.
- Long-term use of oral anticoagulants and the risk of fracture. Arch Intern Med. (1999) Caraballo PJ, et al.
- Risk of osteoporotic fracture in elderly patients taking warfarin: results from the National Registry of Atrial Fibrillation 2. Arch Intern Med. (2006) Gage BF, et al.
- Warfarin use and risk for osteoporosis in elderly women. Study of Osteoporotic Fractures Research Group. Ann Intern Med. (1998) Jamal SA, et al.
- Age-related changes in the circulating levels of congeners of vitamin K2, menaquinone-7 and menaquinone-8. Clin Sci (Lond). (1990) Hodges SJ, et al.
- Major osteoporotic fragility fractures: Risk factor updates and societal impact. World J Orthop. (2016) Pisani P, et al.
- Epidemiology of hip fracture: Worldwide geographic variation. Indian J Orthop. (2011) Dhanwal DK, et al.
- An estimate of the worldwide prevalence and disability associated with osteoporotic fractures. Osteoporos Int. (2006) Johnell O, Kanis JA.
- Effect of vitamin K on bone mineral density: a meta-analysis of randomized controlled trials. J Bone Miner Metab. (2012) Fang Y, et al.
- Vitamin K and the prevention of fractures: systematic review and meta-analysis of randomized controlled trials. Arch Intern Med. (2006) Cockayne S, et al.
- Vitamin K supplementation in postmenopausal women with osteopenia (ECKO trial): a randomized controlled trial. PLoS Med. (2008) Cheung AM, et al.
- Vitamin K2 supplementation does not influence bone loss in early menopausal women: a randomised double-blind placebo-controlled trial. Osteoporos Int. (2010) Emaus N, et al.
- Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women. Osteoporos Int. (2013) Knapen MH, et al.
- Vitamin K2 inhibits glucocorticoid-induced bone loss partly by preventing the reduction of osteoprotegerin (OPG). J Bone Miner Metab. (2005) Sasaki N, et al.
- Low-dose vitamin K2 (MK-4) supplementation for 12 months improves bone metabolism and prevents forearm bone loss in postmenopausal Japanese women. J Bone Miner Metab. (2013) Koitaya N, et al.
- Prevalence and correlates of vitamin K deficiency in children with inflammatory bowel disease. Sci Rep. (2014) Nowak JK, et al.
- Vitamin K supplementation for cystic fibrosis. Cochrane Database Syst Rev. (2013) Jagannath VA, et al.
- Association of vitamin K deficiency with bone metabolism and clinical disease activity in inflammatory bowel disease. Nutrition. (2011) Nakajima S, et al.
- Food sources and dietary intakes of vitamin K-1 (phylloquinone) in the American diet: data from the FDA Total Diet Study. J Am Diet Assoc. (1996) Booth SL, Pennington JA, Sadowski JA.
- Severe Dextran-Induced Anaphylactic Shock during Induction of Hypertension-Hypervolemia-Hemodilution Therapy following Subarachnoid Hemorrhage. Case Rep Crit Care. (2015) Shiratori T, et al.
- The incidence of anaphylaxis following intravenous phytonadione (vitamin K1): a 5-year retrospective review. Ann Allergy Asthma Immunol. (2002) Riegert-Johnson DL, Volcheck GW.
- Skin reactions caused by vitamin K in patients with liver disease. Br J Dermatol. (1978) Bullen AW, et al.
- Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. .
- Measurement of Multiple Vitamin K Forms in Processed and Fresh-Cut Pork Products in the U.S. Food Supply. J Agric Food Chem. (2016) Fu X, et al.
- Quantitative measurement of vitamin K2 (menaquinones) in various fermented dairy products using a reliable high-performance liquid chromatography method. J Dairy Sci. (2013) Manoury E, et al.
- Vitamin K content of foods and dietary vitamin K intake in Japanese young women. J Nutr Sci Vitaminol (Tokyo). (2007) Kamao M, et al.
- Vitamin k contents of meat, dairy, and fast food in the u.s. Diet. J Agric Food Chem. (2006) Elder SJ, et al.
- Purification of Chlamydomonas 28-kDa ubiquitinated protein and its identification as ubiquitinated histone H2B. Arch Biochem Biophys. (1992) Shimogawara K, Muto S.
- Measurement of K vitamins in animal tissues by high-performance liquid chromatography with fluorimetric detection. J Chromatogr. (1989) Hirauchi K, et al.
- Cheese consumption and risk of cardiovascular disease: a meta-analysis of prospective studies. Eur J Nutr. (2017) Chen GC, et al.
- Vitamin K1 intake and coronary calcification. Coron Artery Dis. (2005) Villines TC, et al.
- Vitamin K intake and the risk of fractures: A meta-analysis. Medicine (Baltimore). (2017) Hao G, et al.