- What is Vitamin K
- What does Vitamin K do
- Vitamin K Supplements
- What are some Vitamin K Benefits on Health
- Vitamin K Deficiency
- Groups at Risk of Vitamin K Deficiency
- How much vitamin K do you need ?
- What foods provide vitamin K ?
- Are you getting enough vitamin K ?
- What happens if you don’t get enough vitamin K ?
- Vitamin E Side Effects and Toxicity
What is Vitamin K
Vitamin K is a fat-soluble vitamin that is naturally present in some foods and is available as a dietary supplement. Vitamin K is present in the diet in the forms of phylloquinone and menaquinones 1). Phylloquinone (vitamin K1), which is the major dietary source, is concentrated in leafy plants and is the vitamin K form best characterized in terms of food composition and dietary intakes. In contrast, menaquinones (vitamin K2) are the product of bacterial production or conversion from dietary phylloquinone 2). Menaquinones have unsaturated isoprenyl side chains and are designated as MK-4 through MK-13, based on the length of their side chain 3), 4). MK-4, MK-7, and MK-9 are the most well-studied menaquinones. Food composition databases are limited for menaquinones and their presence in foods varies by region. Dietary intakes of all forms of vitamin K vary widely among age groups and population subgroups. Similarly, the utilization of vitamin K from different forms and food sources appear to vary, although our understanding of vitamin K is still rudimentary in light of new developments regarding the menaquinones 5).
Phylloquinone, also referred to as vitamin K1, is a compound present in all photosynthetic plants 6). Phylloquinone is the primary dietary source of vitamin K. In general, green, leafy vegetables contain the highest known phylloquinone concentrations and contribute approximately 60% of total phylloquinone intake 7), 8). As indicated, spinach and collards, which have concomitant high concentrations of chlorophyll associated with the photosynthetic process, hence, dark leaf color have substantially higher concentrations of phylloquinone compared to the more commonly consumed iceberg lettuce, which is substantially paler, hence, lower chlorophyll concentrations. The other plant sources of phylloquinone are certain plant oils including soybean, canola (also known as rapeseed), cottonseed, and olive. Margarine, spreads, and salad dressings derived from these plant oils are important dietary sources of phylloquinone 9), 10). Plant oils are used for preparation of multiple mixed dishes, hence many commercially prepared foods including baked goods also contain small amounts of phylloquinone.
Menaquinones are the other category of vitamin K present in the food supply are primarily of bacterial origin and they are present in modest amounts in various animal-based and fermented foods 11), 12). Almost all menaquinones, in particular the long-chain menaquinones, are also produced by bacteria in the human gut 13), 14).
Menaquinone-4 (MK-4) is unique among the menaquinones in that it is produced by the body from phylloquinone via a conversion process that does not involve bacterial action. Instead, MK-4 is formed by a realkylation step from menadione present in animal feeds or is the product of tissue-specific conversion directly from dietary phylloquinone 15), 16), 17). In the United States, menadione is the synthetic form of vitamin K used in poultry feed. As such, MK-4 formed from menadione is present in poultry products in the US food supply 18). However, MK-4 formed from phylloquinone is limited to organs not commonly consumed in the diet including kidney. The exceptions are dairy products with MK-4 found in milk, butter, and cheese, albeit in modest amounts. Therefore it is unlikely that MK-4 is an important dietary source of vitamin K in food supplies that do not use menadione for poultry feed nor are rich in dairy products.
There is growing interest in the health benefits of longer-chain menaquinones, which are limited to certain foods in the food supply. Menaquinone-7 (MK-7) is primarily the product of fermentation using bacillus subtilis natto and is present in a traditional Japanese soybean-based product called natto 19). Natto contains approximately 2.5 times more MK-7 compared to the phylloquinone content of spinach. Natto also contains MK-8 and phylloquinone (84 and 35 µg/100g, respectively), although both are modest in concentration compared to MK-7 20). Some cheeses also contain MK-8 and MK-9 21), but these are dependent on cheese production practices, hence the food composition databases are limited in their ability to characterize menaquinone intake across different food supplies.
What does Vitamin K do
Vitamin K functions as a coenzyme for vitamin K-dependent carboxylase, an enzyme required for the synthesis of proteins involved in hemostasis (blood clotting) and bone metabolism, and other diverse physiological functions 22), 23). Vitamin K helps make four of the 13 proteins needed for blood clotting. Prothrombin (clotting factor II) is a vitamin K-dependent protein in plasma that is directly involved in blood clotting. Its role in maintaining the clotting cascade is so important that people who take anticoagulants such as warfarin (Coumadin) must be careful to keep their vitamin K intake stable. Warfarin (Coumadin®) and some anticoagulants used primarily in Europe antagonize the activity of vitamin K and, in turn, prothrombin 24). For this reason, individuals who are taking these anticoagulants need to maintain consistent vitamin K intakes. Coumarin anticoagulants interfere with the synthesis of vitamin–K dependent coagulation proteins (factors II, VII, IX, and X) in the liver.
Matrix Gla-protein, a vitamin K-dependent protein present in vascular smooth muscle, bone, and cartilage, is the focus of considerable scientific research because it might help reduce abnormal calcification 25).
Lately, researchers have demonstrated that vitamin K is also involved in building bone. Low levels of circulating vitamin K have been linked with low bone density, and supplementation with vitamin K shows improvements in biochemical measures of bone health 26). There is a consistent line of evidence in human epidemiologic and intervention studies that clearly demonstrates that vitamin K can improve bone health. The human intervention studies have demonstrated that vitamin K can not only increase bone mineral density in osteoporotic people but also actually reduce fracture rates. Further, there is evidence in human intervention studies that vitamins K and D, a classic in bone metabolism, works synergistically on bone density 27). Several mechanisms are suggested by which vitamin K can modulate bone metabolism. Besides the gamma-carboxylation of osteocalcin, a protein believed to be involved in bone mineralization, there is increasing evidence that vitamin K also positively affects calcium balance, a key mineral in bone metabolism. The Institute of Medicine recently has increased the dietary reference intakes of vitamin K to 90 microg/d for females and 120 microg/d for males, which is an increase of approximately 50% from previous recommendations 28). A report from the Nurses’ Health Study suggests that women who get at least 110 micrograms of vitamin K a day are 30 percent less likely to break a hip than women who get less than that 29). Among the nurses, eating a serving of lettuce or other green, leafy vegetable a day cut the risk of hip fracture in half when compared with eating one serving a week. Data from the Framingham Heart Study also shows an association between high vitamin K intake and reduced risk of hip fracture in men and women and increased bone mineral density in women 30), 31).
Vitamin K Supplements
Vitamin K is present in most multivitamin/multimineral supplements, typically at values less than 75% of the DV 32). It is also available in dietary supplements containing only vitamin K or vitamin K combined with a few other nutrients, frequently calcium, magnesium, and/or vitamin D. These supplements tend to have a wider range of vitamin K doses than multivitamin/mineral supplements, with some providing 4,050 mcg (5,063% of the DV) or another very high amount.
Several forms of vitamin K are used in dietary supplements, including vitamin K1 as phylloquinone or phytonadione (a synthetic form of vitamin K1) and vitamin K2 as MK-4 or MK-7 33). Few data are available on the relative bioavailability of the various forms of vitamin K supplements. One study found that both phytonadione and MK-7 supplements are well absorbed, but MK-7 has a longer half-life 34).
Menadione, which is sometimes called “vitamin K3,” is another synthetic form of vitamin K. It was shown to damage hepatic cells in laboratory studies conducted during the 1980s and 1990s, so it is no longer used in dietary supplements or fortified foods 35).
What are some Vitamin K Benefits on Health
Scientists are studying vitamin K to understand how it affects our health. Here are some examples of what this research has shown.
Osteoporosis, a disorder characterized by porous and fragile bones, is a serious public health problem that affects more than 10 million U.S. adults, 80% of whom are women. Consuming adequate amounts of calcium and vitamin D, especially throughout childhood, adolescence, and early adulthood, is important to maximize bone mass and reduce the risk of osteoporosis 36). The effect of vitamin K intakes and status on bone health and osteoporosis has been a focus of scientific research 37), 38), 39).
Vitamin K is a cofactor for the gamma-carboxylation of many proteins, including osteocalcin, one of the main proteins in bone 40). Some research indicates that high serum levels of undercarboxylated osteocalcin are associated with lower bone mineral density 41), 42). Some, but not all, studies also link higher vitamin K intakes with higher bone mineral density and/or lower hip fracture incidence 43), 44), 45), 46), 47), 48).
Although vitamin K is involved in the carboxylation of osteocalcin, it is unclear whether supplementation with any form of vitamin K reduces the risk of osteoporosis. In 2006, Cockayne and colleagues conducted a systematic review and meta-analysis of randomized controlled trials that examined the effects of vitamin K supplementation on bone mineral density and bone fracture 49). Most of the trials were conducted in Japan and involved postmenopausal women; trial duration ranged from 6 to 36 months. Thirteen trials were included in the systematic review, and 12 showed that supplementation with either phytonadione or MK-4 improved bone mineral density. Seven of the 13 trials also had fracture data that were combined in a meta-analysis. All of these trials used MK-4 at either 15 mg/day (1 trial) or 45 mg/day (6 trials). MK-4 supplementation significantly reduced rates of hip fractures, vertebral fractures, and all nonvertebral fractures.
A subsequent clinical trial found that MK-7 supplementation (180 mcg/day for 3 years) improved bone strength and decreased the loss in vertebral height in the lower thoracic region of the vertebrae in postmenopausal women 50). Other randomized clinical trials since the 2006 review by Cockayne et al. have found that vitamin K supplementation has no effect on bone mineral density in elderly men or women 51), 52). In one of these studies, 381 postmenopausal women received either 1 mg phylloquinone, 45 mg MK-4, or placebo daily for 12 months 53). All participants also received daily supplements containing 630 mg calcium and 400 IU vitamin D3. At the end of the study, participants receiving either phylloquinone or MK-4 had significantly lower levels of undercarboxylated osteocalcin compared to those receiving placebo. However, there were no significant differences in bone mineral density of the lumbar spine or proximal femur among any of the treatment groups. The authors noted the importance of considering the effect of vitamin D on bone health when comparing the results of vitamin K supplementation studies, especially if both vitamin K and vitamin D (and/or calcium) are administered to the treatment group but not the placebo group. The administration of vitamin D and/or calcium along with vitamin K could partly explain why some studies have found that vitamin K supplementation improves bone health while others have not.
In Japan and other parts of Asia, a pharmacological dose of MK-4 (45 mg) is used as a treatment for osteoporosis 54). The European Food Safety Authority has approved a health claim for vitamin K, noting that “a cause and effect relationship has been established between the dietary intake of vitamin K and the maintenance of normal bone” 55). The FDA has not authorized a health claim for vitamin K in the United States.
- Coronary heart disease
Scientists are studying whether low blood levels of vitamin K increase the risk of heart disease, perhaps by making blood vessels that feed the heart stiffer and narrower. More research is needed to understand whether vitamin K supplements might help prevent heart disease.
Vascular calcification is one of the risk factors for coronary heart disease because it reduces aortic and arterial elasticity 56). Matrix Gla-protein is a vitamin K-dependent protein that may play a role in the prevention of vascular calcification 57), 58). Although the full biological function of matrix Gla-protein is unclear, a hypothesis based on animal data suggests that inadequate vitamin K status leads to undercarboxylated matrix Gla-protein, which could increase vascular calcification and the risk of coronary heart disease. These findings might be particularly relevant for patients with chronic kidney disease because their rates of vascular calcification are much higher than those of the general population 59).
In an observational study conducted in the Netherlands in 564 postmenopausal women, dietary menaquinone (but not phylloquinone) intake was inversely associated with coronary calcification 60). Menaquinone intake was also inversely associated with severe aortic calcification in a prospective, population-based cohort study involving 4,807 men and women aged 55 years and older from the Netherlands 61). Participants in this study who had dietary menaquinone intakes in the mid tertile (21.6–32.7 mcg/day) and upper tertile (>32.7 mcg/day) also had a 27% and 57% lower risk of coronary heart disease mortality, respectively, than those in the lower tertile of intake (<21.6 mcg/day). Phylloquinone intake had no effect on any outcome.
Despite these data, few trials have investigated the effects of vitamin K supplementation on arterial calcification or coronary heart disease risk. One randomized, double-blind clinical trial examined the effect of phylloquinone supplementation in 388 healthy men and postmenopausal women aged 60–80 years 62). Participants received either a multivitamin (containing B-vitamins, vitamin C, and vitamin E) plus 500 IU vitamin D3, 600 mg calcium, and 500 mcg phylloquinone daily (treatment) or a multivitamin plus calcium and vitamin D3 only (control) for 3 years. There was no significant difference in coronary artery calcification between the treatment and control groups. However, among the 295 participants who adhered to the supplementation protocol, those in the treatment group had significantly less coronary artery calcification progression than those in the control group. Furthermore, among those with coronary artery calcification at baseline, phylloquinone treatment reduced calcification progression by 6% compared to the control group. Based on these findings, the authors did not make any clinical recommendations, and they called for larger studies in other populations 63).
At this time, the role of the different forms of vitamin K on arterial calcification and the risk of coronary heart disease is unclear, but it continues to be an active area of research in the general population and in patients with chronic kidney disease 64), 65), 66).
Vitamin K Deficiency
Inadequate intake of vitamin K is unlikely to cause symptoms. Vitamin K deficiency results from extremely inadequate intake, fat malabsorption (eg, due to biliary obstruction, malabsorption disorders, cystic fibrosis, or resection of the small intestine) or use of coumarin anticoagulants. Deficiency is particularly common among breastfed infants 67). Vitamin K deficiency is only considered clinically relevant when prothrombin time increases significantly due to a decrease in the prothrombin activity of blood 68), 69). Thus, bleeding and hemorrhage are the classic signs of vitamin K deficiency, although these effects occur only in severe cases. Because vitamin K is required for the carboxylation of osteocalcin in bone, vitamin K deficiency could also reduce bone mineralization and contribute to osteoporosis 70).
Certain antibiotics (particularly some cephalosporins and other broad-spectrum antibiotics), salicylates, megadoses of vitamin E, and hepatic insufficiency increase risk of bleeding in patients with vitamin K deficiency.
Vitamin K deficiency can occur during the first few weeks of infancy due to low placental transfer of phylloquinone, low clotting factor levels, and low vitamin K content of breast milk 71). Clinically significant vitamin K deficiency in adults is very rare and is usually limited to people with malabsorption disorders or those taking drugs that interfere with vitamin K metabolism 72), 73). In healthy people consuming a varied diet, achieving a vitamin K intake low enough to alter standard clinical measures of blood coagulation is almost impossible 74).
Neonates are prone to vitamin K deficiency because of the following:
- The placenta transmits lipids and vitamin K relatively poorly.
- The neonatal liver is immature with respect to prothrombin synthesis.
- Breast milk is low in vitamin K, containing about 2.5 mcg/L (cow’s milk contains 5000 mcg/L).
- The neonatal gut is sterile during the first few days of life.
Treatment consists of vitamin K given orally or, when fat malabsorption is the cause or when risk of bleeding is high, parenterally.
Treatment of Vitamin K Deficiency
- Phytonadione 75)
Whenever possible, phytonadione should be given orally or subcutaneously. The usual adult dose is 1 to 20 mg. (Rarely, even when phytonadione is correctly diluted and given slowly, IV replacement can result in anaphylaxis or anaphylactoid reactions.) INR usually decreases within 6 to 12 h. The dose may be repeated in 6 to 8 h if INR has not decreased satisfactorily.
Phytonadione 1 to 10 mg po is indicated for nonemergency correction of a prolonged INR in patients taking anticoagulants. Correction usually occurs within 6 to 8 h. When only partial correction of INR is desirable (eg, when INR should remain slightly elevated because of a prosthetic heart valve), lower doses (eg, 1 to 2.5 mg) of phytonadione can be given.
In infants, bleeding due to vitamin K deficiency can be corrected by giving phytonadione 1 mg sc or IM once. The dose is repeated if INR remains elevated. Higher doses may be necessary if the mother has been taking oral anticoagulants.
Groups at Risk of Vitamin K Deficiency
The following groups are among those most likely to have inadequate vitamin K status.
- Newborns not treated with vitamin K at birth
Worldwide, vitamin K deficiency causes infant morbidity and mortality.
Vitamin K deficiency causes hemorrhagic disease of the newborn, which usually occurs 1 to 7 days postpartum. In affected neonates, birth trauma can cause intracranial hemorrhage. A late form of this disease can occur in infants about 2 to 12 wk old, typically in infants who are breastfed and are not given vitamin K supplements. If the mother has taken phenytoin anticonvulsants, coumarin anticoagulants, or cephalosporin antibiotics, the risk of hemorrhagic disease is increased.
Vitamin K transport across the placenta is poor, increasing the risk of vitamin K deficiency in newborn babies. During the first few weeks of life, vitamin K deficiency can cause vitamin K deficiency bleeding, a condition formerly known as “classic hemorrhagic disease of the newborn.” Vitamin K deficiency bleeding is associated with bleeding in the umbilicus, gastrointestinal tract, skin, nose, or other sites 76), 77), 78). VKDB is known as “early vitamin K deficiency bleeding” when it occurs in the first week of life. “Late vitamin K deficiency bleeding” occurs at ages 2–12 weeks, especially in exclusively breastfed infants due to the low vitamin K content of breast milk or in infants with malabsorption problems (such as cholestatic jaundice or cystic fibrosis) 79). Vitamin K deficiency bleeding, especially late vitamin K deficiency bleeding, can also be manifested as sudden intracranial bleeding, which has a high mortality rate 80), 81). To prevent vitamin K deficiency bleeding, the American Academy of Pediatrics recommends the administration of a single, intramuscular dose of 0.5 to 1 milligram (mg) vitamin K1 at birth 82).
- People with malabsorption disorders
People with malabsorption syndromes and other gastrointestinal disorders, such as cystic fibrosis, celiac disease, ulcerative colitis, and short bowel syndrome, might not absorb vitamin K properly 83), 84). Vitamin K status can also be low in patients who have undergone bariatric surgery, although clinical signs may not be present 85). These individuals might need monitoring of vitamin K status and, in some cases, vitamin K supplementation.
How much vitamin K do you need ?
The amount of vitamin K you need depends on your age and sex. Average daily recommended amounts are listed below in micrograms (mcg).
|Life Stage||Recommended Amount|
|Birth to 6 months||2.0 mcg|
|7–12 months||2.5 mcg|
|1–3 years||30 mcg|
|4–8 years||55 mcg|
|9–13 years||60 mcg|
|14–18 years||75 mcg|
|Adult men 19 years and older||120 mcg|
|Adult women 19 years and older||90 mcg|
|Pregnant or breastfeeding teens||75 mcg|
|Pregnant or breastfeeding women||90 mcg|
What foods provide vitamin K ?
Food sources of phylloquinone include vegetables, especially green leafy vegetables, vegetable oils, and some fruits. Meat, dairy foods, and eggs contain low levels of phylloquinone but modest amounts of menaquinones 86). Natto (a traditional Japanese food made from fermented soybeans) has high amounts of menaquinones 87), 88). Other fermented foods, such as cheese, also contain menaquinones. However, the forms and amounts of vitamin K in these foods likely vary depending on the bacterial strains used to make the foods and their fermentation conditions 89). Animals synthesize MK-4 from menadione (a synthetic form of vitamin K that can be used in poultry and swine feed) 90). Thus, poultry and pork products contain MK-4 if menadione is added to the animal feed.
The most common sources of vitamin K in the U.S. diet are spinach; broccoli; iceberg lettuce; and fats and oils, particularly soybean and canola oil 91), 92). Few foods are fortified with vitamin K 93); breakfast cereals are not typically fortified with vitamin K, although some meal replacement shakes and bars are.
Vitamin K is found naturally in many foods. You can get recommended amounts of vitamin K by eating a variety of foods, including the following:
- Green leafy vegetables, such as spinach, kale, broccoli, and lettuce
- Vegetable oils
- Some fruits, such as blueberries and figs
- Meat, cheese, eggs, and soybeans
Although multiple databases now exist that contain some phylloquinone contents of foods 94), 95), the most extensive analysis of phylloquinone in common foods using established food sampling protocols 96) are found in the United States Department of Agriculture (USDA) Nutrient Database for Standard Reference 97).
The U.S. Department of Agriculture’s (USDA’s) Nutrient Database website 98) lists the nutrient content of many foods vitamin K (phylloquinone) arranged by nutrient content 99) and by food name 100).
Data on the bioavailability of different forms of vitamin K from food are very limited 101). The absorption rate of phylloquinone in its free form is approximately 80%, but its absorption rate from foods is significantly lower. Phylloquinone in plant foods is tightly bound to chloroplasts, so it is less bioavailable than that from oils or dietary supplements 102). For example, the body absorbs only 4% to 17% as much phylloquinone from spinach as from a tablet 103). Consuming vegetables at the same time as some fat improves phylloquinone absorption from the vegetables, but the amount absorbed is still lower than that from oils. Limited research suggests that long-chain MKs may have higher absorption rates than phylloquinone from green vegetables 104).
Several food sources of vitamin K are listed in Table 2. All values in this table are for phylloquinone content, except when otherwise indicated, because food composition data for menaquinones are limited 105).
|Natto, 3 ounces (as MK-7)||850||1,062|
|Collards, frozen, boiled, ½ cup||530||662|
|Turnip greens, frozen, boiled ½ cup||426||532|
|Spinach, raw, 1 cup||145||181|
|Kale, raw, 1 cup||113||141|
|Broccoli, chopped, boiled, ½ cup||110||138|
|Soybeans, roasted, ½ cup||43||54|
|Carrot juice, ¾ cup||28||34|
|Soybean oil, 1 tablespoon||25||31|
|Edamame, frozen, prepared, ½ cup||21||26|
|Pumpkin, canned, ½ cup||20||25|
|Pomegranate juice, ¾ cup||19||24|
|Okra, raw, ½ cup||16||20|
|Salad dressing, Caesar, 1 tablespoon||15||19|
|Pine nuts, dried, 1 ounce||15||19|
|Blueberries, raw, ½ cup||14||18|
|Iceberg lettuce, raw, 1 cup||14||18|
|Chicken, breast, rotisserie, 3 ounces (as MK-4)||13||17|
|Grapes, ½ cup||11||14|
|Vegetable juice cocktail, ¾ cup||10||13|
|Canola oil, 1 tablespoon||10||13|
|Cashews, dry roasted, 1 ounce||10||13|
|Carrots, raw, 1 medium||8||10|
|Olive oil, 1 tablespoon||8||10|
|Ground beef, broiled, 3 ounces (as MK-4)||6||8|
|Figs, dried, ¼ cup||6||8|
|Chicken liver, braised, 3 ounces (as MK-4)||6||8|
|Ham, roasted or pan-broiled, 3 ounces (as MK-4)||4||5|
|Cheddar cheese, 1½ ounces (as MK-4)||4||5|
|Mixed nuts, dry roasted, 1 ounce||4||5|
|Egg, hard boiled, 1 large (as MK-4)||4||5|
|Mozzarella cheese, 1½ ounces (as MK-4)||2||3|
|Milk, 2%, 1 cup (as MK-4)||1||1|
|Salmon, sockeye, cooked, 3 ounces (as MK-4)||0.3||0|
|Shrimp, cooked, 3 ounces (as MK-4)||0.3||0|
*DV = Daily Value. DVs were developed by the U.S. Food and Drug Administration (FDA) to help consumers compare the nutrient contents of products within the context of a total diet. The DV for vitamin K is 80 mcg for adults and children age 4 and older. However, the FDA does not require food labels to list vitamin K content unless a food has been fortified with this nutrient. Foods providing 20% or more of the DV are considered to be high sources of a nutrient.
Are you getting enough vitamin K ?
In most cases, vitamin K status is not routinely assessed, except in individuals who take anticoagulants or have bleeding disorders. The only clinically significant indicator of vitamin K status is prothrombin time (the time it takes for blood to clot), and ordinary changes in vitamin K intakes have rarely been shown to alter prothrombin time 109). In healthy people, fasting concentrations of phylloquinone in plasma have been reported to range from 0.29 to 2.64 nmol/L 110). However, it is not clear whether this measure can be used to quantitatively assess vitamin K status. People with plasma phylloquinone concentrations slightly below the normal range have no clinical indications of vitamin K deficiency, possibly because plasma phylloquinone concentrations do not measure the contribution of menaquinones from the diet and the large bowel 111). No data on normal ranges of menaquinones are available 112).
Vitamin K deficiency is very rare. People who do not regularly eat a lettuce salad or green, leafy vegetables are likely to be deficient in their intake of vitamin K; national data suggests that only about one in four Americans meets the goal for vitamin K intake from food 113). The current US dietary guidelines for intakes of vitamin K are 90 and 120 µg/day for women and men, respectively 114).
Most people in the United States get enough vitamin K from the foods they eat. Also, bacteria in the colon make some vitamin K that the body can absorb. However, certain groups of people may have trouble getting enough vitamin K:
- Newborns who don’t receive an injection of vitamin K at birth
- People with conditions (such as cystic fibrosis, celiac disease, ulcerative colitis, and short bowel syndrome) that decrease the amount of vitamin K their body absorbs
- People who have had bariatric (weight loss) surgery
What happens if you don’t get enough vitamin K ?
Severe vitamin K deficiency can cause bruising and bleeding problems because the blood will take longer to clot. Vitamin K deficiency might reduce bone strength and increase the risk of getting osteoporosis because the body needs vitamin K for healthy bones.
Vitamin E Side Effects and Toxicity
The Food and Nutrition Board did not establish ULs for vitamin K because of its low potential for toxicity 115). In its report, the Food and Nutrition Board stated that “no adverse effects associated with vitamin K consumption from food or supplements have been reported in humans or animals.”
Can vitamin K be harmful ?
Vitamin K has not been shown to cause any harm. However, it can interact with some medications, particularly warfarin (Coumadin®).
References [ + ]
|1, 3, 11, 19, 87.||↵||Booth SL. Vitamin K: food composition and dietary intakes. Food Nutr Res 2012;56. https://www.ncbi.nlm.nih.gov/pubmed/22489217?dopt=Abstract|
|2.||↵||Thane C, Paul A, Bates C, Bolton-Smith C, Prentice A, Shearer M. Intake and sources of phylloquinone (vitamin K-1): variation with socio-demographic and lifestyle factors in a national sample of British elderly people. Brit J Nutr. 2002;87:605–13. https://www.ncbi.nlm.nih.gov/pubmed/1206743|
|4, 29, 103, 112.||↵||Ferland G. Vitamin K. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012:230-47.|
|5.||↵||National Institute of Health, Office of Dietary Supplements. Vitamin K. https://ods.od.nih.gov/factsheets/VitaminK-HealthProfessional/|
|6.||↵||Gross J, Cho WK, Lezhneva L, Falk J, Krupinska K, Shinozaki K, et al. A plant locus essential for phylloquinone (vitamin K1) biosynthesis originated from a fusion of four eubacterial genes. J Biol Chem. 2006;281:17189–96. https://www.ncbi.nlm.nih.gov/pubmed/16617180|
|7.||↵||Thane C, Paul A, Bates C, Bolton-Smith C, Prentice A, Shearer M. Intake and sources of phylloquinone (vitamin K-1): variation with socio-demographic and lifestyle factors in a national sample of British elderly people. Brit J Nutr. 2002;87:605–13. https://www.ncbi.nlm.nih.gov/pubmed/12067431|
|8.||↵||McKeown NM, Jacques PF, Gundberg CM, Peterson JW, Tucker KL, Kiel DP, et al. Dietary and nondietary determinants of vitamin K biochemical measures in men and women. J Nutr. 2002;132:1329–34. https://www.ncbi.nlm.nih.gov/pubmed/12042454|
|9.||↵||Piironen V, Koivu T, Tammisalo O, Mattila P. Determination of phylloquinone in oils, margarines and butter by high-performance liquid chromatography with electrochemical detection. Food Chem. 1997;59:473–80.|
|10.||↵||Peterson JW, Muzzey KL, Haytowitz D, Exler J, Lemar L, Booth SL. Phylloquinone (vitamin K-1) and dihydrophylloquinone content of fats and oils. JAOCS. 2002;79:641–46.|
|12, 31, 86, 106.||↵||Elder SJ, Haytowitz DB, Howe J, Peterson JW, Booth SL. Vitamin K contents of meat, dairy, and fast food in the U.S. Diet. J Agric Food Chem 2006;54:463-7. https://www.ncbi.nlm.nih.gov/pubmed/16417305?dopt=Abstract|
|13, 23, 41, 54, 57, 64, 83, 91, 93, 109.||↵||Suttie JW. Vitamin K. In: Coates PM, Betz JM, Blackman MR, et al., eds. Encyclopedia of Dietary Supplements. 2nd ed. London and New York: Informa Healthcare; 2010:851-60.|
|14.||↵||Conly JM, Stein K, Worobetz L, Rutledge-Harding S. The contribution of vitamin K2 (menaquinones) produced by the intestinal microflora to human nutritional requirements for vitamin K. Am J Gastroenterol 1994;89:915-23. https://www.ncbi.nlm.nih.gov/pubmed/8198105?dopt=Abstract|
|15, 69, 71, 73, 76, 79, 80, 92, 104.||↵||Suttie JW. Vitamin K. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:305-16.|
|16.||↵||Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not dependent on gut bacteria. Davidson RT, Foley AL, Engelke JA, Suttie JW. J Nutr. 1998 Feb; 128(2):220-3. https://www.ncbi.nlm.nih.gov/pubmed/9446847/|
|17.||↵||Menadione is a metabolite of oral vitamin K. Thijssen HH, Vervoort LM, Schurgers LJ, Shearer MJ. Br J Nutr. 2006 Feb; 95(2):260-6. https://www.ncbi.nlm.nih.gov/pubmed/16469140/|
|18.||↵||Vitamin K contents of meat, dairy, and fast food in the U.S. Diet. Elder SJ, Haytowitz DB, Howe J, Peterson JW, Booth SL. J Agric Food Chem. 2006 Jan 25; 54(2):463-7. https://www.ncbi.nlm.nih.gov/pubmed/16417305/|
|20, 21, 94.||↵||Schurgers LJ, Vermeer C. Determination of phylloquinone and menaquinones in food. Effect of food matrix on circulating vitamin K concentrations. Haemostasis. 2000;30:298–307. https://www.ncbi.nlm.nih.gov/pubmed/11356998|
|22.||↵||Institute of Medicine. Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, DC: National Academy Press; 2001.|
|24.||↵||Ufer M. Comparative pharmacokinetics of vitamin K antagonists: warfarin, phenprocoumon and acenocoumarol. Clin Pharmacokinet 2005;44:1227-46. https://www.ncbi.nlm.nih.gov/pubmed/1637282?dopt=Abstract|
|25, 59, 65.||↵||Schurgers LJ. Vitamin K: key vitamin in controlling vascular calcification in chronic kidney disease. Kidney Int2013;83:782-4. https://www.ncbi.nlm.nih.gov/pubmed/23633049?dopt=Abstract|
|26, 27, 28.||↵||Weber P. Vitamin K and bone health. Nutrition. 2001; 17:880–7. https://www.ncbi.nlm.nih.gov/pubmed/11684396?dopt=Citation|
|30, 35, 68, 72, 74, 115.||↵||Institute of Medicine. Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, DC: National Academy Press; 2001.|
|32, 33.||↵||National Institutes of Health. Dietary Supplement Label Database 2014. https://dsld.nlm.nih.gov/dsld/|
|34.||↵||Schurgers LJ, Teunissen KJ, Hamulyak K, Knapen MH, Vik H, Vermeer C. Vitamin K-containing dietary supplements: comparison of synthetic vitamin K1 and natto-derived menaquinone-7. Blood 2007;109:3279-83. https://www.ncbi.nlm.nih.gov/pubmed/17158229?dopt=Abstract|
|36.||↵||National Institutes of Health. Osteoporosis prevention, diagnosis, and therapy. NIH consensus statement 2000;17:1-45. https://www.ncbi.nlm.nih.gov/pubmed/11525451?dopt=Abstract|
|37.||↵||Booth SL, Tucker KL, Chen H, et al. Dietary vitamin K intakes are associated with hip fracture but not with bone mineral density in elderly men and women. Am J Clin Nutr. 2000; 71:1201–8. https://www.ncbi.nlm.nih.gov/pubmed/10799384?dopt=Citation|
|38.||↵||Booth SL, Broe KE, Gagnon DR, et al. Vitamin K intake and bone mineral density in women and men. Am J Clin Nutr. 2003; 77:512–6. https://www.ncbi.nlm.nih.gov/pubmed/12540415?dopt=Citation|
|39.||↵||Feskanich D, Weber P, Willett WC, Rockett H, Booth SL, Colditz GA. Vitamin K intake and hip fractures in women: a prospective study. Am J Clin Nutr. 1999; 69:74–9. https://www.ncbi.nlm.nih.gov/pubmed/9925126?dopt=Citation|
|40, 42.||↵||Gundberg CM, Lian JB, Booth SL. Vitamin K-dependent carboxylation of osteocalcin: friend or foe? Adv Nutr 2012;3:149-57. https://www.ncbi.nlm.nih.gov/pubmed/22516722?dopt=Abstract|
|43.||↵||Yaegashi Y, Onoda T, Tanno K, Kuribayashi T, Sakata K, Orimo H. Association of hip fracture incidence and intake of calcium, magnesium, vitamin D, and vitamin K. Eur J Epidemiol 2008;23:219-25. https://www.ncbi.nlm.nih.gov/pubmed/18214692?dopt=Abstract|
|44.||↵||Rejnmark L, Vestergaard P, Charles P, Hermann AP, Brot C, Eiken P, et al. No effect of vitamin K1 intake on bone mineral density and fracture risk in perimenopausal women. Osteoporos Int 2006;17:1122-32. https://www.ncbi.nlm.nih.gov/pubmed/16683180?dopt=Abstract|
|45.||↵||Feskanich D, Weber P, Willett WC, Rockett H, Booth SL, Colditz GA. Vitamin K intake and hip fractures in women: a prospective study. Am J Clin Nutr 1999;69:74-9. https://www.ncbi.nlm.nih.gov/pubmed/9925126?dopt=Abstract|
|46.||↵||Booth SL, Broe KE, Gagnon DR, Tucker KL, Hannan MT, McLean RR, et al. Vitamin K intake and bone mineral density in women and men. Am J Clin Nutr 2003;77:512-6. https://www.ncbi.nlm.nih.gov/pubmed/12540415?dopt=Abstract|
|47.||↵||Booth SL, Tucker KL, Chen H, Hannan MT, Gagnon DR, Cupples LA, et al. Dietary vitamin K intakes are associated with hip fracture but not with bone mineral density in elderly men and women. Am J Clin Nutr 2000;71:1201-8. https://www.ncbi.nlm.nih.gov/pubmed/10799384?dopt=Abstract|
|48.||↵||Chan R, Leung J, Woo J. No association between dietary vitamin K intake and fracture risk in chinese community-dwelling older men and women: a prospective study. Calcif Tissue Int 2012;90:396-403. https://www.ncbi.nlm.nih.gov/pubmed/22451220?dopt=Abstract|
|49.||↵||Cockayne S, Adamson J, Lanham-New S, Shearer MJ, Gilbody S, Torgerson DJ. Vitamin K and the prevention of fractures: systematic review and meta-analysis of randomized controlled trials. Arch Intern Med 2006;166:1256-61. https://www.ncbi.nlm.nih.gov/pubmed/16801507?dopt=Abstract|
|50.||↵||Knapen MH, Drummen NE, Smit E, Vermeer C, Theuwissen E. Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women. Osteoporos Int 2013;24:2499-507. https://www.ncbi.nlm.nih.gov/pubmed/23525894?dopt=Abstract|
|51.||↵||Booth SL, Dallal G, Shea MK, Gundberg C, Peterson JW, Dawson-Hughes B. Effect of vitamin K supplementation on bone loss in elderly men and women. J Clin Endocrinol Metab 2008;93:1217-23. https://www.ncbi.nlm.nih.gov/pubmed/18252784?dopt=Abstract|
|52, 53.||↵||Binkley N, Harke J, Krueger D, Engelke J, Vallarta-Ast N, Gemar D, et al. Vitamin K treatment reduces undercarboxylated osteocalcin but does not alter bone turnover, density, or geometry in healthy postmenopausal North American women. J Bone Miner Res 2009;24:983-91. https://www.ncbi.nlm.nih.gov/pubmed/19113922?dopt=Abstract|
|55.||↵||European Food Safety Authority. Scientific opinion on the substantiation of health claims related to vitamin K and maintenance of bone pursuant to Article 13(1) of Regulation (EC) No 1924/2006. The EFSA Journal 2009;7:1228.|
|56.||↵||Demer LL, Tintut Y. Vascular calcification: pathobiology of a multifaceted disease. Circulation 2008;117:2938-48. https://www.ncbi.nlm.nih.gov/pubmed/18519861?dopt=Abstract|
|58, 61.||↵||Geleijnse JM, Vermeer C, Grobbee DE, Schurgers LJ, Knapen MH, van der Meer IM, et al. Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study. J Nutr 2004;134:3100-5. https://www.ncbi.nlm.nih.gov/pubmed/15514282?dopt=Abstract|
|60.||↵||Beulens JW, Bots ML, Atsma F, Bartelink ML, Prokop M, Geleijnse JM, et al. High dietary menaquinone intake is associated with reduced coronary calcification. Atherosclerosis 2009;203:489-93. https://www.ncbi.nlm.nih.gov/pubmed/18722618?dopt=Abstract|
|62, 63.||↵||Shea MK, O’Donnell CJ, Hoffmann U, Dallal GE, Dawson-Hughes B, Ordovas JM, et al. Vitamin K supplementation and progression of coronary artery calcium in older men and women. Am J Clin Nutr 2009;89:1799-807. https://www.ncbi.nlm.nih.gov/pubmed/19386744?dopt=Abstract|
|66.||↵||Gallieni M, Fusaro M. Vitamin K and cardiovascular calcification in CKD: is patient supplementation on the horizon? Kidney Int 2014;86:232-4. https://www.ncbi.nlm.nih.gov/pubmed/25079019?dopt=Abstract|
|67, 75.||↵||Merck Sharp & Dohme Corp., Merck Manual. Vitamin K. https://www.merckmanuals.com/professional/nutritional-disorders/vitamin-deficiency,-dependency,-and-toxicity/vitamin-k|
|70, 84.||↵||Jagannath VA, Fedorowicz Z, Thaker V, Chang AB. Vitamin K supplementation for cystic fibrosis. The Cochrane database of systematic reviews 2013;4:CD008482. https://www.ncbi.nlm.nih.gov/pubmed/25596954?dopt=Abstract|
|77, 82.||↵||American Academy of Pediatrics Committee on F, Newborn. Controversies concerning vitamin K and the newborn. American Academy of Pediatrics Committee on Fetus and Newborn. Pediatrics 2003;112:191-2. https://www.ncbi.nlm.nih.gov/pubmed/12837888?dopt=Abstract|
|78, 81.||↵||Pichler E, Pichler L. The neonatal coagulation system and the vitamin K deficiency bleeding – a mini review. Wien Med Wochenschr. 2008;158:385-95. https://www.ncbi.nlm.nih.gov/pubmed/18677590?dopt=Abstract|
|85.||↵||Heber D, Greenway FL, Kaplan LM, Livingston E, Salvador J, Still C, et al. Endocrine and nutritional management of the post-bariatric surgery patient: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2010;95:4823-43. https://www.ncbi.nlm.nih.gov/pubmed/21051578?dopt=Abstract|
|88, 107.||↵||Schurgers LJ, Vermeer C. Determination of phylloquinone and menaquinones in food. Effect of food matrix on circulating vitamin K concentrations. Haemostasis 2000;30:298-307. https://www.ncbi.nlm.nih.gov/pubmed/11356998?dopt=Abstract|
|89.||↵||Walther B, Karl JP, Booth SL, Boyaval P. Menaquinones, bacteria, and the food supply: the relevance of dairy and fermented food products to vitamin K requirements. Adv Nutr 2013;4:463-73. https://www.ncbi.nlm.nih.gov/pubmed/23858094?dopt=Abstract|
|90.||↵||U.S. Food and Drug Administration. CFE – Code of Federal Regulations Title 21, Sec. 573.620 Menadione dimethylpyrimidinol bisulfite. 2014. https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm?fr=573.620|
|95.||↵||Bolton-Smith C, Price RJ, Fenton ST, Harrington DJ, Shearer MJ. Compilation of a provisional UK database for the phylloquinone (vitamin K1) content of foods. Br J Nutr. 2000;83:389–99. https://www.ncbi.nlm.nih.gov/pubmed/10858697|
|96.||↵||Pehrsson P, Haytowitz D, Holden J, Perry C, Beckler D. USDA’s National Food and Nutrient Analysis Program: food sampling. J Food Compos Anal. 2000;13:379–90.|
|97, 98.||↵||The USDA Food Composition Databases. https://ndb.nal.usda.gov/ndb/|
|99.||↵||The USDA Food Composition Databases. Vitamin K Content. https://ods.od.nih.gov/pubs/usdandb/VitK-Menaquinone-Content.pdf|
|100.||↵||The USDA Food Composition Databases. Foods Vitamin K Content. https://ods.od.nih.gov/pubs/usdandb/VitK-Menaquinone-Food.pdf|
|101, 102, 105.||↵||Booth SL. Vitamin K: food composition and dietary intakes. Food Nutr Res 2012;56. www.ncbi.nlm.nih.gov/pubmed/22489217?dopt=Abstract|
|108.||↵||U.S. Department of Agriculture, Agricultural Research Service. USDA National Nutrient Database for Standard Reference, Release 28. Nutrient Data Laboratory Home Page, 2015. https://ndb.nal.usda.gov/ndb/|
|110, 111.||↵||Sadowski JA, Hood SJ, Dallal GE, Garry PJ. Phylloquinone in plasma from elderly and young adults: factors influencing its concentration. Am J Clin Nutr 1989;50:100-8. https://www.ncbi.nlm.nih.gov/pubmed/2750682?dopt=Abstract|
|113.||↵||Moshfegh A, Goldman, J., Cleveland, L. . What We Eat In America. NHANES 2001–2002: Usual Nutrient Intakes from Food Compared to Dietary Reference Intakes. U.S. Dept. of Agriculture, Agricultural Research Service. 2005.|
|114.||↵||Dietary reference intakes: vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Trumbo P, Yates AA, Schlicker S, Poos M. J Am Diet Assoc. 2001 Mar; 101(3):294-301. https://www.ncbi.nlm.nih.gov/pubmed/11269606/|