If there’s a single vitamin you need to know more about, it’s vitamin K 2 . The first reason is you’re probably not getting enough. The second is that it doesn’t get the attention it deserves, and it’s really hard to find reliable and easy-to-use information about it.

This resource is meant to change that. It begins by teaching you everything you need to know about the vitamin, including its benefits, how much you need, and how to get it from food. It includes shareable infographics to make the concepts fun and easy to understand. Finally, it provides reviews of the available supplements and a searchable database of the vitamin K 2 contents of foods that can’t be found anywhere else.

If you’re a beginner, you can read the article straight through or pick the parts that are most interesting or useful to you. If you are an advanced user and already know a lot about vitamin K 2 or have a strong science background, you can click on the buttons that say “click here for a more detailed explanation” in order to expand descriptions that are better suited to your level of expertise.

The Health Benefits of Vitamin K 2

Vitamin K 2 has a wide range of underappreciated health benefits:

It prevents calcium from going into all the wrong places and makes sure it gets into all the right places. For example, it keeps it out of your kidneys, where it would cause kidney stones, and keeps it out of your blood vessels, where it would cause heart disease, but helps it to get into your bones and teeth, making your bones strong and your teeth resistant to cavities. It helps you make insulin and remain very sensitive to insulin. This means it helps stabilize your blood sugar, protects against diabetes, and prevents the metabolic problems that often arise as a consequence of obesity. It promotes sexual health by helping you optimize your sex hormones. For example, it increases testosterone and fertility in males, and it helps bring the high levels of male hormones found in women with polycystic ovarian syndrome (PCOS) back down to normal. It helps improve exercise performance by enhancing your ability to utilize energy during bouts of physical activity. It protects against cancer by suppressing the genes that make cells cancerous and expressing the genes that make cells healthy.



These roles are shown in the shareable infographic below. You can share it using the button in the upper right corner, or the buttons on the bottom strip. You can even use the button in the upper right corner to generate an embed code to share it on your own site if you have one.





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Why the Form of Vitamin K You Eat Is So Important

Vitamin K comes in different forms. Vitamin K 1 is primarily found in plant foods and is most abundant in leafy greens. Vitamin K 2 is only found in animal foods and fermented plant foods. The term “vitamin K 2 ” actually refers to a collection of more specific forms known as menaquinones that are all abbreviated “MK” with a specific number attached: for example, MK-4, MK-7, MK-10, and so on.

Does it matter whether you eat one form or another? Absolutely. There are two reasons for this, so let’s deal with them one at a time.

First, once we eat foods with vitamin K in them, our bodies handle the different forms differently. Consider these examples:

Vitamin K 1 travels to our livers more effectively than it does to our bones or blood vessels. The liver is where we use vitamin K to make the proteins involved in blood clotting, so vitamin K 1 is better at supporting blood clotting than it is at providing other health benefits. MK-7 is much more effective than K 1 at reaching bone. This doesn’t just make it good for bones: our bones use vitamin K to produce a hormone known as osteocalcin, which improves metabolic and hormonal health and increases exercise performance. Thus, MK-7 better supports these health benefits than K 1 . The portion of MK-7 that reaches the liver, moreover, stays active in the liver much longer than K 1 before being broken down; as a result, MK-7 is even better than K 1 at supporting blood clotting. MK-4 is taken up by our tissues very rapidly after we consume it. While it hasn’t been studied as carefully as MK-7, it may be less effective than MK-7 at reaching liver and bone but more effective at reaching most other tissues. This would make it better at protecting those tissues from calcium deposits and cancer development and supporting sex hormone production through its direct actions within our sex organs.



Overall, then, the collection of different vitamin K 2 compounds better supports all the health benefits listed above than vitamin K 1 because they better reach the tissues that matter.



These concepts are illustrated in the shareable infographic below.

The second reason the form of vitamin K matters is that MK-4 regulates gene expression in specific ways that no other form of vitamin K does. While we tend to think of our genes as the destiny we inherited from our parents, it’s actually how they are expressed — meaning, what our cells do with the information carried by those genes — that determines our health. MK-4 turns on some genes and turns others off. For example, in our sex organs, it turns on the genes involved in sex hormone production. In a wide variety of cells, it turns on the genes that keep cells healthy and turns off the genes that make cells become cancerous. Thus, MK-4 plays an exclusive role in cancer protection and sexual health.

This special role of MK-4 probably explains why all animals break down other forms of vitamin K and convert them to MK-4. By contrast, no animal synthesizes any other form of vitamin K. This explains why MK-4 is mostly found in animal foods, and why most unfermented animal foods contain little if any of the other forms.

As humans, we also convert other forms of vitamin K to MK-4. This raises the question, do we really need to consume MK-4 directly if we can make it ourselves? My answer is yes.

There are three reasons we shouldn’t rely on the conversion:

First, we don’t actually know that much about how the conversion takes place, but it seems to be inefficient and highly variable according to genetics and health status, making it unreliable.

Second, cholesterol-lowering statin drugs and certain osteoporosis drugs inhibit the conversion, making it even less reliable in people who are taking these drugs.

Third, research shows vitamin K 2 is better than vitamin K 1 at supporting many different aspects of our health. If we easily converted as much K 1 to K 2 as we needed, we wouldn’t observe these superior benefits of K 2 .

These concepts are illustrated in the shareable infographic below.

The difference between K 1 and K 2 isn’t absolute. When we eat vitamin K 1 some of it will reach tissues outside the liver and we will convert some of it to MK-4. But the real question is: what’s the best vitamin for the job? Vitamin K 2 is clearly much better at supporting the health benefits discussed in this resource, so the resource is dedicated specifically to getting enough K 2 in its diversity of forms.

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The Many Forms of Vitamin K The names “vitamin K 1 ” and “vitamin K 2 ” are artifacts of history (Suttie, 2014). The first form of vitamin K was found in alfalfa, so it was named K 1 . The second form was found in rotten fish, so it was named K 2 . As shown in the figure below, they both have the same ring structure, but different tail structures. The tail structures are known formally as side chains. Vitamin K 1 , now known as phylloquinone, has a mostly saturated tail. Vitamin K 2 , now known as menaquinone, has an unsaturated tail. Menaquinones are actually a class of compounds with varying tail lengths, designated MK-n, where “n” indicates the number of repeating units in the tail. The specific form of vitamin K 2 found in rotten fish was MK-7. When later MKs were discovered, they all had unsaturated tails, so scientists classified them as subforms of vitamin K 2 . We now know that this is overly simplistic (Shearer, 2014). Some bacteria, such as those used to make Jarlsberg cheese, produce partially saturated menaquinones wherein some of the repeating subunits have double bonds and others don’t. For example, Jarlsberg is very rich in tetrahydromenaquinone-9, which is similar in structure to MK-9 except the second and third units of the tail are saturated. As Shearer (2014) pointed out, even phylloquinone has a double bond in the first unit of its tail and could be seen as a partially saturated form of MK-4. Thus, rather than forming two categories of K vitamins, it makes more sense to say that vitamin K comes in a wide diversity of forms that are distinguished by the length and saturation of their tails. Side Chain Length and Saturation Determines Tissue Distribution While the ring structure is what allows vitamin K to support the vitamin K carboxylase, the enzyme that activates vitamin K-dependent proteins, the tail structure determines how different forms of vitamin K reach different tissues in the body. This all begins with how they are incorporated into lipoproteins soon after we absorb them from food. When we digest fat and fat-soluble nutrients, our intestines package them into lipoproteins known as chylomicrons, which take them through the lymph and into the bloodstream. This event critically distinguishes how water-soluble and fat-soluble nutrients are distributed through the body: water-soluble nutrients travel directly to the liver through the portal vein, while fat-soluble nutrients travel through the lymph in chylomicrons to bypass the liver and nourish the other tissues first. Chylomicrons, like all other lipoproteins, have to transport fat-soluble things through the water-based environment of the blood. Therefore, they are fat-soluble on the inside and water-soluble on the outside. While all K vitamins are fat-soluble, they are not all equally soluble in fat. Those with longer tails are more fat-soluble than those with shorter tails; for tails of equal length, saturated tails are more fat-soluble than unsaturated tails. K vitamins that are more fat-soluble are carried deeper in the core of chylomicrons, while those that are less fat-soluble are carried more toward the edges. Let’s take the three forms most commonly found in supplements as examples: K 1 , MK-4, and MK-7. We would expect to find MK-7 in the center of the chylomicron, MK-4 closer to the edges, and K 1 in between the two (Schurgers and Vermeer, 2002). Chylomicrons move in and out of the bloodstream rapidly, with a half-life of 15-20 minutes (César, 2006). This means that once we eat a meal, 95% of the chylomicrons that enter our blood are fully cleared in the first hour. Very few tissues actually take up the whole chylomicron. Instead, most tissues use the enzyme lipoprotein lipase (LPL) to siphon off its nutrients bit by bit. While LPL is best known for feeding the heart, skeletal muscle, and adipose tissue, it also feeds other tissues such as the lungs, kidneys, mammary glands, and brain (Kersten, 2014). LPL spreads across the capillary beds that feed our great diversity of tissues, allowing widespread access to the fat-soluble nutrients we ingest in a meal. Presumably, these tissues all have greater access to the nutrients carried closer to the edges of the chylomicrons, such as MK-4. As these many tissues feast on the chylomicrons, the chylomicrons get smaller and smaller until they become chylomicron remnants. A small handful of tissues donate apolipoprotein E (ApoE) to the chylomicron remnants, and then use the LDL receptor and other related receptors to bind to the ApoE and take up the whole remnant. This allows them to score everything left in the particle right down to its chewy center. In this sense, ApoE is like the bait on a fishing line, and the receptor is like the hook. While the liver is best known for fishing out chylomicron remnants in this manner, our bones and spleen do as well. Our bones primarily derive nutrients through the uptake of whole lipoprotein particles, and take up about a fifth as many chylomicron remnants as our liver (Shearer, 2008). Thus, we should expect bone and liver to primarily have access to nutrients carried in the center of chylomicrons, including K 1 , but especially the MKs with longer tails, such as MK-7. This whole stream of events takes place largely in the first hour after a meal. The liver then repackages the lipids it took in from chylomicron remnants into other lipoproteins, primarily VLDL, which are sent back out into the blood. Tissues continue to siphon off nutrients using LPL. Just like chylomicrons had been digested into chylomicron remnants, VLDL particles are then digested into LDL particles until our tissues take up the LDL particles themselves. Unlike the rapid clearance of chylomicrons, clearance of LDL particles takes place slowly over the course of two weeks (Langer, 1972). Although the liver is the main tissue that takes up LDL, bone is also important; in fact, bone takes up vitamin K more effectively from LDL than from any other lipoprotein (Shearer, 2012). Thus, K vitamins that get packaged into LDL particles will have a second opportunity to nourish bone. Schurgers and Vermeer (2002) investigated how different K vitamins are transported using K 1 , MK-4, and MK-9. They fed six healthy males a mixture of one milligram of each form and took repeated blood measurements over four days, beginning at the two-hour mark. MK-4 had already peaked by the time the first blood draw was taken, when much of it was found in HDL, and disappeared most rapidly from the blood out of all the forms. K 1 peaked at the four-hour mark, was mostly gone by eight hours, and disappeared by the end of the study. K 1 was found almost exclusively in VLDL rather than in LDL or HDL. MK-9 peaked at the four-hour mark as well, but persisted in the blood for several days while carried in LDL particles. The authors suggested that MK-4 was taken up so quickly because it was carried toward the edges of the chylomicrons, making it easily accessible for LPL-mediated extraction, with the excess spilling over into HDL particles. Notably, we should expect the extended circulation of MK-9 in LDL to provide better nourishment to bone. Schurgers later collaborated with Sato (2012) to compare the bioavailability of MK-4 and MK-7 in healthy women. Compared to the 2002 study, they used less than half the dose of each vitamin and fed them separately rather than combined so that the total dose of vitamin K given at each point was over six times lower. Similar to the 2002 study, they took their first blood sample at two hours. They didn’t find MK-4 in the blood at any time point, whereas MK-7 remained elevated for two days. MK-4 vs. MK-7: What Do We Really Know? If we compare the results of the 2012 study to the earlier 2002 study, we can surmise that the dose of MK-4 in the 2012 study was low enough that the initial LPL feast in the first hour fully distributed it to a variety of tissues so that it was all gone by two hours, and that MK-7 circulated for such a long time because, like MK-9, it was redistributed in LDL particles. We should expect from this that MK-4 is good at nourishing most tissues, but not very good at nourishing liver or bone. By contrast, we should expect that MK-7 is good at nourishing the liver and even better at nourishing bone. At the present time, there is no direct support for this, but there are hints that it may be the case. Sato (2012) cited a Japanese paper as finding that 1.5 milligrams of MK-4, but not 500 μg, improved the carboxylation of osteocalcin. Not even the abstract seems to be available in English, so it is difficult to evaluate the study. Later, Nakamura (2014) showed that only 600 μg of MK-4 is needed, but in this study the researchers simply gave the same people higher and higher doses each week and waited for osteocalcin carboxylation to improve. For all we know, their lowest dose, 300 μg, would have worked if they had given it longer than a week. In seeming contrast to MK-4, MK-7 improves osteocalcin carboxylation with as little as 100 μg (Knapen, 2012; Inaba, 2015). Placing these studies side by side, they seem to suggest that improvements in osteocalcin carboxylation require much lower doses of MK-7 than of MK-4. However, the studies had different designs and were conducted in different populations that may have had different nutritional needs and different responses to vitamin K supplementation. In fact, Inaba (2015) fed MK-7 for four weeks while Nakamura (2014) only fed each dose of MK-4 for one week. This alone could explain the difference. To date, no one has compared the osteocalcin response to MK-4 and MK-7 head-to-head. On the other hand, MK-7 has been compared to K 1 . At equal doses, MK-7 is three times more potent than K 1 at carboxylating osteocalcin (Schurgers, 2007). Osteocalcin is made in bone, so its carboxylation reflects vitamin K status in that tissue. Presumably, MK-7 is better than K 1 because its recirculation in LDL particles for days after it is first taken up by the liver gives it much more opportunity to nourish bone. Since MK-4 likely has even less opportunity to reach bone than K 1 , MK-7 is probably superior to MK-4 for this purpose as well. What about other tissues? Unfortunately, we know even less about those. We know that large pharmacological doses of MK-4 given to rats (Konishi, 1973) or dogs (Sano, 1997) reach the lungs, liver, kidney, pancreas, spleen, adrenal gland, and bone very rapidly. Such large doses are also excreted into the feces in large amounts. More moderate nutritional doses could behave very differently, however, so it is difficult to form any conclusions from these studies. Until we have well designed trials comparing the ability of different MKs to support different health outcomes in humans, it makes sense to rely on what we know generally about how lipoproteins transport nutrients. This suggests K 1 would best reach the liver, MKs 7-9 would best reach liver and bone, and MK-4 would best reach most other tissues. MK-7 Supports Blood Clotting Better Than K 1 MK-7 is not just three times better than K 1 at reaching bone; it’s also five times better at supporting blood clotting (Schurgers, 2007). This may be because the greater fat-solubility of MK-7 makes it hold on more tightly to the membranes within liver cells, making it stay active in the liver much longer rather than being released and broken down (Shearer, 2008). The liver is where clotting proteins are made, so more extended activity in the liver would explain why MK-7 could better support blood clotting. If this is correct, other long-chain MKs such as MK-8 and MK-9 probably share this property as well. MK-4 Plays a Unique Role in Gene Expression MK-4 is unique among the K vitamins in its regulation of gene expression. It increases the expression of genes that regulate cell growth in osteoblasts (the cells responsible for bone growth), but MK-7 and K 1 do not (Ichikawa, 2007). MK-4 increases testosterone production when fed to male rats. Cellular experiments show that MK-4, but not K 1 , increases testosterone by increasing the expression of the enzyme that converts cholesterol to pregnenolone, which is the first step in sex hormone synthesis (Ito, 2011). MK-4 also inhibits the growth of various cancers of the liver, gut, and bone (Shearer, 2008). Remarkably, the gene that is now known to code for the enzyme that converts other K vitamins to MK-4, Ubiad1, was known years earlier as a tumor-suppressor gene (Shearer, 2014). Scientists observed that Ubiad1 was often silenced in tumors of the bladder, prostate, and kidney. Conversely, experimental overexpression of Ubiad1 inhibited the growth of prostate cancer cells. Since the enzyme that Ubiad1 codes for converts other K vitamins to MK-4, these results underscore that the anticancer properties of vitamin K belong specifically to MK-4. Can We Rely on the Conversion of Other K Vitamins to MK-4? When we consume any form of vitamin K, our intestinal cells break the side chains off of a small portion to yield the pure ring structure, known as menadione (Thijssen, 2006). Menadione then disperses through the body to many tissues that convert it to MK-4 for their own use by adding MK-4’s characteristic four-unit unsaturated side chain (Hirota, 2013). We have known that animals synthesize MK-4 from other K vitamins for over a half century. It has been clear throughout that time, however, that the conversion varies widely. Early experiments, for example, showed that birds made the conversion better than rats and pigeons made it better than other birds (Billeter, 1960). Among rats, Wistar rats (Thijssen, 1994) seem to make the conversion better than Lewis rats (Ronden, 1998). Since the conversion varies between and within species, we should not assume that we as humans can make the conversion efficiently and consistently enough to meet our needs. And just how good are we at this conversion? We really don’t know, but it stands to reason that it varies from person to person. Rare genetic defects in Ubiad1 have been identified (Yellore, 2007), and cancer is associated with epigenetic silencing of Ubiad1 (Woolston, 2015). Other genes involved in the conversion likely vary from person to person as well, but we don’t yet know what they are. One of them may be vitamin K epoxide oxidoreductase (VKOR), the target of warfarin. The normal role of VKOR is to reduce vitamin K that has been oxidized, and we know that menadione must be in a reduced state to undergo conversion to MK-4. Indeed, warfarin prevents the conversion of K 1 to MK-4 in rats (Spronk, 2003). Genetic polymorphisms in VKOR are common (Shearer, 2012), and could hypothetically contribute to variation in MK-4 synthesis. We still do not know what enzyme is responsible for cleaving the side chain within our intestinal cells, and that could be polymorphic as well. However good or bad humans may naturally be at the conversion, many people are taking medications that inhibit it (Hirota, 2015). Lipophilic statins such as lovastatin and simvastatin (and presumably atorvastatin, branded as Lipitor) inhibit the conversion. So do nitrogen-containing bisphosphonates such as alendronate (Fosamax) and zolendronate (Zometa), and presumably other nitrogenous bisphosphates as well. Ubiad1 expression depends on zinc (Funahashi, 2015) and its enzymatic activity depends on magnesium (Hirota, 2015), suggesting that deficiencies of either of these minerals could also compromise the conversion. Finally, if we converted other K vitamins to MK-4 on a “however much we need to” basis, then it shouldn’t matter what type of vitamin K we consume at all. All forms of vitamin K generate some menadione in the intestine that can be converted to MK-4 in other tissues. Whether the menadione comes from K 1 , MK-4, MK-7, or any other form of vitamin K cannot make any difference in its tissue distribution. Humans accumulate MK-4 in multiple organs including the heart, lung, brain, liver, kidney, and pancreas (Thijssen, 1996). Thus, if there are no major limitations on the conversion besides our need for it, K 1 should be perfectly capable of supplying these tissues with all the MK-4 they need, especially in populations that have high K 1 intakes. Yet this does not seem to be what we find. Consider the Dutch population, where this has been investigated most extensively. K 1 intakes are eight times higher than K 2 intakes, yet only K 2 intake is inversely correlated with heart disease (Geleijnse, 2004; Gast, 2009; Buelens, 2009; Zwakenberg, 2016). In Germany, K 1 intakes are about three times higher than K 2 intakes, yet only K 2 intake is inversely correlated with advanced prostate cancer (Nimptsch, 2008) and lung cancer (Nimptsch, 2010). These observational studies don’t offer clear evidence of cause-and-effect relationships and they don’t show correlations with health endpoints that are specific to MK-4. However, they do add to the list of reasons to believe that our ability to synthesize MK-4 is limited by much more than our specific need for MK-4 itself, and by much more than our general need for vitamin K in the tissues that unconverted K 1 has a hard time reaching. In other words, many of us probably need more MK-4 than we can make on our own, and that’s a good reason to eat foods that provide it. Altogether, the evidence suggests that the form of vitamin K we consume matters, and that we are best served by a diversity of K vitamins from leafy greens, animal foods, and fermented foods. Click here to close the detailed explanation.

How Much Vitamin K 2 Do We Need?

Currently, there are no official recommendations about vitamin K 2 . In the United States, the current recommendation for total vitamin K is 90 μg per day for adults. In a typical diet, most of this would come from K 2 . These recommendations were last updated in 2001, before we learned about most of the benefits of K 2 . In fact, the USDA did not even develop a database of vitamin K 2 in foods until 2006. My recommendation, therefore, does not rely on official sources and is meant for health-conscious people who wish to take advantage of cutting-edge research.

Based on the current state of that research, I recommend 100-200 μg per day of vitamin K 2 for healthy adults. Although most of the benefit probably comes from the first 100 μg, 200 μg is harmless and may provide additional benefit. If your health is fantastic while maintaining a K 2 intake close to 100 μg, I would not worry about increasing your intake. But if you could stand to gain from the wide array of health benefits provided by the vitamin, I would use food or supplements to bring your intake closer to 200 μg.

Patients with chronic kidney disease may require doses as high as 480 μg per day and possibly much higher, but the use of high doses to treat a disease should always be done under medical supervision.

Patients using warfarin (Coumadin) or any other anticoagulant medications related to it should not make any changes to their vitamin K intake, regardless of the specific form of vitamin K, whether from food or supplements, except under the strict supervision of the prescribing physician (see below).

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Vitamin K 2 : What is the Optimal Dose? Another way to ask this question is as follows: what is the minimum effective dose to achieve the maximal desired effect? While there is no established toxicity for high doses, there are good reasons to be cautious before taking far more than we need (see below), hence the term “minimum effective dose.” At the same time, we don’t want to reap just some of the health benefit. We want to reap as much of the health benefit as we can in a safe and effective manner, hence the term “maximal desired effect.” The only rigorous way to approach this is to look at dose-finding studies, which are studies where different doses were directly compared with one another. Ideally, the studies are randomized, controlled, long enough in duration to believe the dose was able to achieve its full effect, and conducted within a context where we would expect to see a benefit. Pharmacological Doses of MK-4 A Japanese dose-finding study compared 15, 45, 90, and 135 milligrams per day (mg/d) of MK-4 to reduce fracture risk in postmenopausal women with osteoporosis and found 45 mg/d to be the minimal effective dose (Iwamoto, 2013). This is a pharmacological dose that is hundreds of times greater than what can be obtained from food. It probably works through mechanisms that are independent of the those seen for nutritional doses of vitamin K, such as overriding the body’s natural regulation of bone resorption. Thus, we should view MK-4 at these doses with the same type of cost-benefit analysis we would use for other osteoporosis drugs, like Fosamax, and we should not use these studies to determine the optimal nutritional dose of MK-4. Nutritional Doses of MK-4 Unfortunately, there is a dearth of dose-response studies for nutritional doses of MK-4. Nakamura (2014) compared the effect of 0, 300, 600, 900, and 1500 micrograms per day (μg/d) on osteocalcin carboxylation, a marker of vitamin K status in bone. They fed everyone the same doses in the same order, increasing the dose from 0 one week at a time. The carboxylation status did not change with 300 μg/d, but improved with 600 μg/d. However, it is not at all clear that 300 μg/d would not have provided the same benefit if given for longer than one week. I do not consider this study to offer any clear insight about the optimal dose of MK-4. MK-7 in Healthy Populations Dalmeijer (2012) compared 180 and 360 μg/d MK-7 to a placebo given to healthy, non-obese men and postmenopausal women aged 40-65 years over the course of twelve weeks. The mean K 2 intake from food was 25 μg/d, so these treatments effectively compared total K 2 intakes of 25, 200, and 380 μg/d. Both treatment doses lowered desphospho-uncarboxylated MGP (dp-ucMGP), a marker of vitamin K deficiency in blood vessels, and improved the carboxylation status of osteocalcin. While 360 μg seemed to cause a slightly larger effect than 180 μg, the lion’s share of benefit came from 180 μg and the difference between the two doses was not statistically significant. Thus, the study hints at a possible benefit of doses higher than 200 μg that would have to be confirmed in future studies with greater statistical power, but provides rigorous evidence only that 200 μg is better than 25 μg. Knapen (2012) reported a more extensive array of doses given to healthy men and premenopausal women aged 25-45 over the course of twelve weeks. The doses included 0, 10, 20, 45, 90, 180, and 360 μg/d MK-7 and the primary endpoint of interest reported was the carboxylation status of osteocalcin. Unfortunately, the sample size (n=42) was small for having so many groups, precluding a rigorous statistical analysis of the endpoints between each group. Additionally, while carboxylated osteocalcin levels were similar across groups at baseline, undercarboxylated osteocalcin levels were highly variable. The changes in undercarboxylated osteocalcin between baseline and the study’s end within any given group were generally about the same size as the difference in baseline values between groups. All of this makes it extremely difficult to know whether the the difference between groups for changes in undercarboxylated osteocalcin or its ratio to total osteocalcin are true biological differences or simply random variation resulting from noisy data. Doses that were 90 μg/d or greater caused statistically significant decreases in undercarboxylated osteocalcin, but only the 180 μg and 360 μg doses increased the levels of carboxylated osteocalcin or improved the ratio. From among these measurements, the increase in carboxylated osteocalcin seen with the two higher doses is most convincing because the variation in baseline values for that measurement was so low. The ending values for this measurement were higher in the 180 and 360 μg groups than in any of the the others, but they were nearly identical between groups. K 2 intake from food was not reported, but presumably would have added at least 20 μg/d to the doses. I therefore consider this study to offer limited support to 200 μg/d as the optimum dose for improving vitamin K status at bone. Inaba (2015) compared 0, 50, 100, and 200μg/d MK-7 in postmenopausal women aged 50 to 69 years over the course of four weeks. The primary endpoint of interest was the carboxylation status of osteocalcin, reported as the ratio of the carboxylated to the undercarboxylated form. The study was conducted in Hokkaido, Japan, where natto is popular. The subjects were required to avoid all MK-7-rich foods and to consume prepared meals that provided 65 μg/d of total vitamin K as a combination of K 1 and MK-4 in unspecified proportions. Whether intentional or not, this is effectively a study of how much MK-7 you need to preserve the carboxylation status of your osteocalcin when you stop eating natto. Indeed, the largest effect across all groups was for carboxylation status to significantly worsen in the 0 μg/d group. Carboxylation status was significantly different from that group in the 100 and 200 μg/d groups, but not in the 50 μg/d group. The authors did not report a statistical analysis for the difference between 100 and 200 μgd, but 200 μg/d was the only group in which carboxylation status actually improved over the course of the study. I therefore consider this study to offer limited support to 200 μg/d as the optimum dose for improving vitamin K status at bone. In further support of this conclusion, Ikeda (2006) found that postmenopasual women who reported consuming enough natto to provide 200 μg/d K 2 or more (mostly as mostly MK-7) suffered less bone loss over the course of three years than women who consumed less. Since all lower intakes of natto were grouped together for the statistical analysis, it is not clear exactly where the line of maximal benefit lies, and it may be less than 200 μg/d. As an observational study, we should also be more cautious about inferring cause and effect. Nevertheless, the fact that it measured an actual health endpoint (bone loss) instead of just a surrogate marker (osteocalcin carboxylation), and the fact that it was three years long instead of four to twelve weeks, makes it very worthy of consideration. MK-7 in Hemodialysis Patients Westenfeld (2012) and Caluwé (2014) both conducted dose-finding studies in hemodialysis patients. Patients with kidney disease have high levels of vascular calcification, which is a major contributor to mortality in this population. Since MGP protects blood vessels from calcification, dp-ucMGP was the major endpoint in both studies. Lower dp-ucMGP suggests better vitamin K status in blood vessels and a better defense against pathological calcification. Westenfeld compared 45, 135, and 360 μg/d MK-7 over six weeks. MK-7 dose-dependently decreased dc-ucMGP, with the effect almost doubling in size for each increase in the dose from 18% to 37% to 61%. However, change from baseline analysis is vulnerable to regression to the mean and it is more rigorous to compare the absolute levels of dc-ucMGP after treatment. When looked at this way, 135 and 360 μg/d had equal benefit over 45 μg/d. Nevertheless, Caluwé later tested even higher doses and provided evidence of benefit for more than 300 μg/d. They fed the patients 360, 720, or 1080 μg MK-7 three times per week for eight weeks, which equates to average daily doses of 154, 309, and 463 μg. MK-7 dose-dependently decreased dp-ucMGP by 17%, 33%, and 46%. The ending dp-ucMGP values were lower in the 463 μg/d group than in the 309 μg/d group and were lower than Westenfeld found after feeding 360 μg/d, but they were still about four times higher than that found in healthy controls. The average K 2 intakes in the Caluwé paper were 16 μg/d, making the doses compared effectively 325 and and 479 μg/d. Future studies may clarify whether even higher doses can bring dp-ucMGP levels even closer to those found in healthy controls. Thus, there is strong evidence that the K 2 requirement for kidney patients is higher than 325 μg, possibly as high as 480 μg, and may well be much higher than that. Conclusions For healthy populations, there is no smoking gun, but several studies converge towards the conclusion that 200 μg/d is the optimal dose. Most of the benefit probably comes from the first 100 μg, and the evidence for the superiority of 200 μg is limited. There may be benefits to higher doses, but there is no convincing evidence of that at this time. Thus, there is a high likelihood that I will revise my recommendation as new data comes in, but I currently recommend at least 100 μg/d and preferably 200 μg/d. For kidney disease patients, there is good reason to see 480 μg/d as better than lower doses. Since 480 μg/d almost slashes dp-ucMGP in half yet leaves it four times higher than in healthy controls, the optimal dose may well be much higher than this. I suspect it is at least 1 mg/d. Nevertheless, K 2 should only be used to augment treatment for kidney disease under medical supervision. Click here to close the detailed explanation.

How to Get Enough Vitamin K 2 From Food

You can use the searchable database we created to determine how much vitamin K 2 is in your diet. In this section, I describe a few of the simplest ways to get 200 μg per day of K 2 from foods. As noted above, most of the benefit comes from the first 100 μg, so any of the values below can be cut in half to obtain that amount.

The foods that are richest in K 2 are natto and goose liver, both of which may be difficult-to-acquire tastes. Natto is a fermented soy food popular in eastern Japan. The source of K 2 is the bacteria used in the fermentation, not the soy beans. As a result, any vegetable fermented with natto bacteria should be rich in K 2 . For example, 100 grams of traditional natto contains just under 950 μg, while 100 grams of natto made from black beans contains almost 800 μg. The value for black bean natto is a little lower than that for traditional natto, but both values are phenomenally high. Simply adding 18 grams of natto (about two-thirds of an ounce) to your diet each day would give you 200 μg, and just two ounces of goose liver would provide the same benefit.

Another excellent source of vitamin K 2 is cheese. The K 2 content of cheese varies widely according to the type of bacteria used to make it. To browse a full list of cheeses, search “cheese” in our database or leave the search box blank and select the category “Dairy Foods and Eggs.”

Jarlsberg cheese, which originates from Norway, is richest in K 2 . According to the value listed in our database, it would take nine ounces of Jarlsberg to provide 200 μg. Its true content of K 2 has likely been underestimated, however, and it may actually take as little as 4.5 ounces.

Egg yolks and the dark meat (legs and thighs) of chicken are also good sources. For example, four whole eggs provides over 20 μg and 100 grams of dark chicken meat provides 60 μg.

Ultimately, it is the way these foods are combined in your diet that determines how much K 2 you get. The first infographic provides some ideas of how to work these different foods into a meal to make a meaningful contribution to your daily K 2 intake. You can figure out how much K 2 other meals would provide by using our database.

Surprisingly, we recently learned that pork products are very high in MK-10 and MK-11. This is a newly discovered exception to the rule that fresh animal products mostly contain MK-4. Unfortunately, little is known about the bioavailability of these forms and there are some indications that we as humans largely store them in our livers rather than distributing them throughout our bodies like other forms of K 2 . However, if future research were to show that MK-10 and MK-11 have similar benefits as the other forms, that would mean most pork products are competitive sources. For example, only 4.5 ounces of baby back pork ribs would be needed to provide 200 μg, and just two ounces of pork sausage would provide the same amount.

Food quality is important. Egg yolk from The Netherlands is reported to have twice as much K 2 as egg yolk from the United States. The reasons for this are unclear, but it may relate to the ways the chickens were raised. Wherever possible, I recommend using meat, eggs, and dairy from animals raised on pasture. For egg yolks, look for the most deeply colored yolks you can find.

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Vitamin K 2 in Foods: A Closer Look Vitamin K 2 in foods comes either from the conversion of other K vitamins to MK-4 in animals or from bacterial production of various MKs. A good example that ties these concepts together is cheese. A cow eats grass that contains K 1 . The cow converts a portion of that K 1 to MK-4. Both K 1 and MK-4 are found in the milk. Humans take the milk and ferment it into cheese. During the fermentation process, bacteria proliferate that synthesize a variety of MKs, mainly MK-7 through MK-10, and especially MK-8 and MK-9. A comparison of different cheeses illustrates the importance of the specific type of bacteria used in the fermentation. For example, in each 100 gram serving, Jarlsberg contains 74 μg while blue cheese contains 36, cheddar contains 21, Swiss contains 8, and mozzarella only contains 4. This variation can also be seen among fermented plant foods. For example, sauerkraut has only 5 μg, compared to nearly 1000 for natto. Within a particular type of cheese, ripening has little effect. For example, gamalost increases from 38 to 51 in the first ten days of ripening, but this level remains mostly stable over the course of 20, 30, and 60 days. This is probably because the bacteria that produced the K 2 during the initial stage of fermentation die off during the ripening (Hojo, 2007). The data for cheese also provide a window into the possibility that some of our current food data are gross underestimates. For example, most cheeses are made with lactic acid bacteria that produce mostly MK-8 and MK-9, but some cheeses are made with proprionibacteria that also produce tetrahydro-MK-9 (Hojo, 2007), which has a structure that is the same as MK-9 except it lacks some double bonds in its side chain. These include the Swiss cheeses Emmental and Gruyère, the French cheese Comté, and the Norwegian cheese Jarlsberg. Whether tetrahydro-MKs might be present in other foods is somewhat unclear because virtually all analyses of vitamin K in foods have ignored them. No analysis has yet evaluated both tetrahydro-MKs and all the regular MKs in any food at the same time, strongly suggesting that the total K 2 in foods that contain tetrahydro-MKs is grossly underestimated. To take Jarlsberg as an example, Hojo (2007) showed that, per 100 grams, it contains 8 μg MK-4 and 65 μg tetrahydro-MK-9, and cited evidence that it also contains another ~50 μg of MK-8 and MK-9. In our database, we only report values that were measured in a single scientific paper for any given sample, so our data for Jarlsberg reflects what was actually measured in the Hojo paper, 74 μg, but the true value may be over 130 μg. Our own gut microbiota also synthesize K 2 : Bacterioides synthesize MK-10 and MK-11, Enterobacteria synthesize MK-8, Veillonella synthesize MK-7, and Eubacterium lentum synthesizes MK-6 (Shearer, 2014). However, this probably makes little if any contribution to our own vitamin K status for two reasons: first, most of this occurs in the large intestine, which is well past the sites of vitamin K absorption in the small intestine, and all the K 2 is stuck in bacterial membranes that would have to be digested to release it. MKs produced during the fermentation of foods such as cheese or natto are also bound in bacterial membranes, but when we eat them we digest those membranes to release the K 2 in the small intestine where it can be absorbed. Some animals eat their own feces, a practice known as coprophagia, and this allows the the microbiota-derived K 2 to be released and absorbed in the same way as when we eat cheese or natto. This may explain the recent finding that pork products are extremely rich in MK-10 and MK-11 (Fu, 2016). The meat was obtained from supermarkets in Eastern Massachusetts, so it presumably came from commercial farms. Perhaps pigs on those farms whether by instinct, necessity, or accident, consume feces.The only other possibility would seem to be that the pigs are fed rotten or fermented food. The question arises whether MK-10 and MK-11 provide similar bioavailability to the MKs in other foods, which are generally much richer in MK-4 (animal foods), MK-7 (natto) or MK-8 and MK-9 (cheese) than in MK-10 or MK-11. In humans, MK-10 and MK-11 tend to predominate in the liver rather than in other tissues, and in the mitochondria rather than in the endoplasmic reticulum where vitamin K-dependent carboxylation takes place (Thijssen, 1996). Thus, we should be cautious before making a conclusion about how interchangeable the MKs in pork products are with the MKs in most other foods. Ultimately this can be resolved with studies comparing the abilities of the different MKs to support different biological functions of vitamin K. Click here to close the detailed explanation.

The Three Best Vitamin K 2 Supplements

Supplements should never be used to replace a good diet. A well-rounded nutrient-dense diet not only provides vitamin K itself in a greater diversity of forms than can be found in any supplement, but it also provides a full spectrum of other nutrients that work together with vitamin K to produce good health. As such, a good diet provides the context needed for a supplement to be both safe and effective.

When evaluating K 2 supplements, I look for the following things:

Dose: I prefer a dose from which it is easy to obtain approximately 200 ug. While it is probably effective to take a larger dose less than once a day (for example, taking 1 mg every five days), it is easier to maintain the habit of taking a daily dose.

Form: Since different forms of vitamin K 2 are distributed differently in the body, it is best to obtain a diversity of forms. In supplements, the best diversity we can obtain is to combine MK-4 and MK-7. The only supplemental MK-4 available is synthetic, but it is bioidentical, meaning it has the same chemical structure as the natural form. MK-7 on the market can be natural or synthetic; some synthetic MK-7 is bioidentical and some is not. Out of caution, I would only choose bioidentical options. Those who wish to have an entirely natural supplement should opt for MK-7 derived from the fermentation of soybeans or chickpeas.

Cost and convenience: For any two products that are substantially equivalent, I prefer lower cost, easy online ordering, quick delivery, and the opportunity for free shipping.

Here are my top three recommendations:

Innovix Labs Full Spectrum Vitamin K 2 — This supplement wins on its diversity of forms (without going overboard on its total dose). It contains both MK-4 (500 μg) and MK-7 (100 μg). The MK-7 appears to be synthetic but bioidentical. It costs $21.97 on Amazon , is fulfilled by Amazon, and is eligible for Prime. Taken once a day, it costs 24 cents per day. Taken once every three days to achieve an average dose of 200 μg, it costs 9 cents per day.

Thorne Research MK-4 — This supplement wins on cost. Its cost is nearly identical between Amazon and Iherb ($64.62 and $64.65), and if ordered on Amazon it is fulfilled by Amazon and eligible for Prime. It contains one milligram of MK-4 per drop. While the label recommends a daily dose of 45 drops, this is based on studies using pharmacological doses to treat osteoporosis. It is easy to instead take one drop per day to obtain a nutritional dose. Taken like that, it costs 5 cents per day. Taken once every five days to achieve an average dose of 200 μg, it costs one cent per day. They also make a combination of vitamin D and K 2 that is more expensive but easier to get a consistent daily dose of 200 μg from. This is described in more detail in the comprehensive review below.

Nested Naturals K 2 — This is free of GMOs, soy, and other common allergens. It is made from fermented chickpeas. The MK-7 is made by another company, MenaQ7, whose MK-7 is sold under many different names and has also been used successfully in scientific research. This is the least expensive of all of the natural MK-7 products. It contains 100 μg of MK-7 and costs 12 cents per capsule. Taken twice per day to achieve 200 μg, it costs 24 cents per day.

An interesting runner-up is Nature’s Plus, which is an affordable MK-7 supplement that is interesting mostly for its long list of features, like its background blend of plant, mushroom, and algae extracts, and its substantial list of third party certifications. It is described in more detail in the comprehensive review below.

If you have the time for home fermentation, Dr. Mercola created a starter culture that is designed to generate K 2 during the fermentation of vegetables. While I do not believe this will provide a standardized amount of K 2 like a commercial supplement will, I would expect it to substantially augment the K 2 content of your diet.

These are my top recommendations from a much more extensive review of over twenty supplements. If you want more details, click below for the comprehensive review.

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Light and Heat Stability, and Proper Storage of Vitamin K 2

Vitamin K is only slightly sensitive to heat, but is extremely sensitive to light. So much so that when we measure vitamin K in a laboratory we work under yellow lamps. In food oils exposed to daylight, 80 percent of the vitamin K disappears within two days. To make sure that your food and supplements retain their vitamin K content over time, keep them in the refrigerator, behind cabinets, or otherwise out of the light when not in use. If you keep them in plain daylight, they should be in amber glass or in opaque containers such as the white plastic used for most supplements.

How Much Fat to Eat With Vitamin K 2 and What Kind

Vitamin K is fat-soluble so fat helps us absorb it from foods and supplements. If your fat intake varies from meal to meal, it makes sense to eat your K 2 -rich foods or take your K 2 supplements with the meal that contains the most fat. The optimal amount of fat to maximize absorption of K 2 from a single meal is probably about 35 grams. The true optimal amount of fat has not been precisely determined and may be higher than this, but I consider it adequate.

For the best effect, the fat should be low in polyunsaturated fatty acids, which means that butter and other animal fats, tropical oils, olive oil, avocado oil, macadamia nut oil, and the high-oleic varieties of sunflower and safflower oil would help the most. By contrast, soybean oil, canola oil, the regular varieties of sunflower and safflower oil, grape seed oil, and most other oils derived from nuts and seeds would help the least.

Notably, many of the foods richest in K 2 like cheese, meat, and egg yolks are themselves rich in fat. The total fat content of the meal is what is important, so the more natural fats within the foods, the less you have to add.

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Vitamin K Absorption and Fat: A Closer Look Dietary fat is important for the absorption of all fat-soluble vitamins partly because it helps dissolve the vitamins and partly because it helps stimulate the machinery involved in fat digestion, such as bile acids and lipases. Studies have generally suggested the following rule: the more fat you eat, the more fat-soluble vitamins you absorb. For example, 28 grams of fat allows better absorption of carotenoids from a salad than 6 grams of fat (Brown, 2004), and 30 grams of fat allows better absorption of vitamin E from a supplement than 11 grams of fat (Bruno, 2006). Studies have also shown that oils lower in polyunsaturated fatty acids (PUFAs) promote better absorption of fat-soluble vitamins than high-PUFA oils. For example, beef tallow allows better absorption of beta-carotene from a standardized test meal than safflower oil (Hu, 2000). These rules appear to apply to vitamin K just the same. For example, 35 grams of fat allows better absorption of MK-4 than 20 grams of fat (Uematsu, 1996), and more K 1 is absorbed from spinach with 25 grams of butter than without butter (Gijsbers, 1996). More K 1 was absorbed from a “cosmopolitan” meal or an “animal-oriented” meal than from a “convenience meal,” with one possible explanation being the two-fold greater PUFA content of the convenience meal (Jones, 2009). None of these studies showed a ceiling to the fat effect, and none of them tested more than 35 grams of fat. So, there may not be any ceiling to the effect. What we can say with confidence is that 30-35 grams of fat will provide for better absorption than lower amounts. Even still, absorption will probably never reach 0% or 100%, and for any given percent absorption one can always absorb a greater total amount of a vitamin by consuming more of it. Therefore, there is no sense in chasing after complete absorption and there is no intrinsic danger of a low-fat diet. If you have a good reason to eat less than 35 grams of fat per meal, it just becomes more important to spend the fat you do eat wisely by allocating it to K 2 -rich foods. It is fine to be flexible about fat intake, but it is important to be aware that any given amount of K 2 in the diet will provide more nutrition to our bodies if consumed with a good dose of healthy fat. Click here to close the detailed explanation.

How to Test Your Vitamin K 2 Status

Unfortunately, there are no useful tests for measuring vitamin K status that are available to the general public at this time. However, good tests are on the horizon. VitaK will be releasing innovative medical devices to allow health care practitioners to monitor vitamin K status in patients, and ImmunoDiagnostic Systems will be releasing a blood test for dp-ucMGP, a protein that circulates in the blood when blood vessels become deficient in vitamin K.

If you would like me to notify you when these tests become available in the United States, please join my newsletter.

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Tests for Vitamin K Status: A Closer Look Vitamin K travels through the blood almost entirely as a means of being delivered to our other tissues, so blood levels of vitamin K only reflect recent intake rather than long-term nutritional status. Red blood cells lack the organelles in which vitamin K function is important (the endoplasmic reticulum, mitochondria, and nucleus). Lymphocyte vitamin K concentrations could, perhaps, reflect long-term vitamin K status, but practically nothing is known about what vitamin K does in lymphocytes in the context of human nutrition, and such tests have never been validated to show anything important. The appropriate way to test vitamin K status is to look at the carboxylation status of vitamin K-dependent proteins. These tests can be validated by showing that they respond to vitamin K depletion or supplementation and that they correlate with known health outcomes that respond in the same way. For example, the ability of the blood to clot reflects vitamin K status in the liver, where clotting factors are made; the carboxylation status of osteocalcin reflects vitamin K status in bone, where osteocalcin is made; and the carboxylation status of matrix Gla protein (MGP) reflects vitamin K status in blood vessels, where MGP is made. Clotting disorders are life threatening and we have known about the role of vitamin K in this process for almost a century. As a result, a whole battery of tests for the different vitamin K-dependent clotting factors are readily available (for example, Ohishi, 2014). Vitamin K 1 is perfectly good at supporting the production of clotting factors, and since hemorrhage can be life-threatening, clotting factors will always get priority over a limited pool of vitamin K. Thus, most people consume enough vitamin K for their clotting factors to be fully carboxylated and these tests are not useful measures of whether vitamin K status is adequate to support its other functions in other tissues. The most common marker of vitamin K status in research studies is the carboxylation status of osteocalcin, which reflects vitamin K status in bone. This test is only useful if the proportion of osteocalcin in the carboxylated and undercarboxylated forms can be measured. Unfortunately, this is not available outside of research studies. Quest offers total osteocalcin, but doesn’t measure its carboxylation status; Genova offers undercarboxylated osteocalcin, but doesn’t measure the total. One could “hack” its carboxylation status by getting both, but this would require each “half” of the correct marker to be measured from separate blood samples analyzed by separate laboratories, making the interpretation highly questionable. Were it available, we would still have to interpret it with caution, because, independent of vitamin K status, bone resorption decarboxylates osteocalcin and releases the undercarboxylated form into the bloodstream where it has beneficial hormonal roles, so it isn’t a black-and-white marker of vitamin K status. The most promising marker of vitamin K status on the horizon is desphospho-uncarboxylated matrix Gla protein (dc-ucMGP), which reflects vitamin K status in blood vessels and the risk of soft tissue calcification. It’s just a matter of time before it becomes available. Click here to close the detailed explanation.

Is Vitamin K 2 Dangerous?

Very high doses of vitamin K 2 have proved remarkably safe in large clinical trials, but there are safety concerns for people taking prescription anticoagulants, and there are reasons to be cautious about high doses even for healthy people.

This is Critical If You Are Taking Prescription Anticoagulants

The most common anticoagulants used in medicine are warfarin and its relatives. As a class, they are known as 4-hydroxycoumarins. These go by a number of brand names, the most common of which is Coumadin. As a class, these drugs act as vitamin K antagonists, and it is absolutely critical that anyone taking them avoid making any changes to their diet or supplements that would be expected to change their vitamin K intake except under the strict supervision of the physician who prescribed the medication.

Hypothetical Side Effects of High Doses

Long-term use of 45 mg per day of MK-4 has not revealed any established toxicity syndrome or risk of serious side effects. This is 225 times the dose I recommend. Nevertheless, the biochemistry of vitamin K suggests that unnecessarily high doses could rob the body of antioxidants or interfere with blood sugar regulation, insulin sensitivity, and hormonal health. The real question, though, is at what dose these potential side effects kick in. Since 45 mg per day has not shown any clear syndrome of toxicity and the dose I recommend is more than 200 times lower than this, I think we have a very large window of safety to work within. The potential for hypothetical side effects, however, should lead us to avoid supplementing with doses that are much larger than those that provide clear benefits.

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Hypothetical Side Effects of High-Dose Vitamin K There are several aspects of vitamin K’s biochemistry that suggest high doses could have adverse effects on our health: Vitamins E and K are broken down in similar pathways ( Shearer, 2008 ). High doses of either one elicit an increase in these catabolic pathways by activating a common receptor known as the steroid and xenobiotic receptor (SXR) or the pregnane X receptor (PXR). As a result, high doses of one will elicit the destruction of the other. Thus, high-dose vitamin K could contribute to vitamin E deficiency.

Second, a small portion of vitamin K is broken down to a compound known as menadione ( Thijssen, 2006 ). Some of the menadione is used to synthesize MK-4, but high concentrations are toxic. We therefore conjugate a portion of the menadione to glutathione, the master antioxidant and detoxifier of the cell, and excrete the complex into our urine. High doses of vitamin K could therefore deplete glutathione. This would impair detoxification, and along with vitamin E depletion it would hurt antioxidant activity.

High doses of vitamin K can inhibit bone resorption, which is probably the mechanistic basis by which 45 mg/day reduce fracture risk ( Iwamoto, 2013 ). While bone resorption sounds like a bad thing, we need to use it every day to help our bones remodel themselves and adapt their structures to our lifestyles, and to keep blood levels of calcium within a precisely controlled range. We also use bone resorption to release osteocalcin into the blood, where it acts on multiple tissues to improve our metabolic and hormonal health ( Ferron, 2007 ; Oury, 2013 ). Ironically, one of the benefits of vitamin K 2 is to support proper production of osteocalcin, but high doses of the vitamin could hypothetically prevent us from using it. That would be expected to hurt blood sugar control, insulin sensitivity, our metabolic rate, and, in males, testosterone production. Japanese trials using 45 mg/day MK-4 to treat osteoporosis have not established any risk of severe side effects (Iwamoto, 2013). Most of them, however, had between 20 and 120 subjects per group. One very large two-year trial with over 2,000 subjects per group (Inoue, 2009) reported 23 percent more adverse drug reactions in the MK-4 group than in the control group. The report did not include any description of what those side effects were, but confirmed that there was no difference in “serious” adverse effects or deaths. Such high doses are pharmacological in nature and not nutritional. We should look at their costs and benefits in the same way we look at other pharmaceutical drugs. In this light, high-dose MK-4 is remarkably safe and effective. We nevertheless have hints that negative side effects of some sort occur when using extended pharmacological doses and we have several biochemical rationales for why high doses would cause harm. This provides a basis for caution in using doses outside of the nutritional range. Click here to close the detailed explanation.

Vitamin K 2 : A Critical Component of a Well Rounded Nutrient-Dense Diet

Vitamin K 2 is something most of us could use a lot more of. The best way to obtain it is to consume K 2 -rich foods in the context of a well rounded, nutrient-dense diet. The many other nutrients contained in a good diet provide the context that makes vitamin K 2 safe and effective. Supplements can be very helpful, as long as they are used as adjuncts to support a good diet rather than as replacements for a good diet.

From here, you can leave a comment, scroll on for my suggestions for further reading, or search for some K 2 rich foods in our database to plan out your next K 2 -rich meal.

Suggestions for Further Reading

In spring of 2007, I wrote “On the Trail of the Elusive X Factor: Vitamin K 2 Revealed.” This is an extensive article arguing that vitamin K 2 was the “activator X” that Weston Price claimed to have discovered in 1945. Weston Price was one of the pioneers of nutritional anthropology, and many people had speculated about the identity of his “activator X” for decades. The article tells the history of that mystery and in the process extensively reviews the many roles of vitamin K and its interactions with other important nutrients like vitamins A and D.

For more about how vitamin K interacts with other nutrients in the diet, see my 2013 article, “Nutritional Adjuncts to the Fat-Soluble Vitamins.”

For my other writings on vitamin K 2 , see Start Here for Vitamin K 2 .

Some other sources that I recommend include Chris Kresser’s Vitamin K 2 : The Missing Nutrient, and Stephan Guyenet’s writings on the topic. Kate Rheaume-Bleue wrote a great book, Vitamin K 2 and the Calcium Paradox: How a Little-Known Vitamin Could Save Your Life.

For a more advanced understanding of vitamin K, I would start with the vitamin K chapter by John Suttie in Modern Nutrition in Health and Disease. I consider this textbook so valuable as a general scientific reference that I buy it again every time there is a new edition. Reviews by important figures in the field such as Martin Shearer, John Suttie, Sarah Booth, Cees Vermeer, and Leon Schurgers are also highly valuable and can be found on pubmed. On the specific topic of the hormonal functions of osteocalcin, I recommend reviews by Gerard Karsenty, also found on pubmed. Finally, the expandable “detailed explanation” sections within this resource are rich in scientific references that provide additional opportunities for advanced learning.

I’d Like to Hear From You

I would like to make this a multi-purpose resource for all things related to vitamin K 2 that can be constantly improved over time. Therefore, I’d like to hear from you: what is most useful? What can be improved? What topics would you like to see included in the future? What features would you like to see added to the searchable database? Please let me know in the comments.



The Database: Search for the Vitamin K 2 Contents of Foods

Here’s the icing on the cake. We scoured the literature for data on the K 2 contents of foods and found many publications that haven’t been included in databases elsewhere. There are almost 200 foods included. You can search by keyword, or you can submit a blank search to browse through everything. You can pick a food category and search it by keyword or submit a blank search to browse through just the foods in that category. Every food entry gives you the opportunity to click for more details, including a breakdown of its different vitamin K forms and the reference from which the data comes. Have fun searching!

Vitamin K2 Advanced Search Form If you are human, leave this field blank. FOOD CATEGORY All Foods Bread Dairy Foods and Eggs Fast Foods Fats and Oils Fish and ShellFish Fruits, Vegetables, and Beans (Plant Foods) Meat (Muscle Meats) Organ Meats (Offal) Processed Meats Seasonings, spices, dressings SPECIFIC VITAMIN K VALUES MK-4 MK-5 MK-6 MK-7 MK-8 MK-9 MK-10 MK-11 MK-12 MK-13 Vitamin K1 Total Vitamin K Sum of MK4 and MK7 Total Vitamin K2

This resource is continually updated so that it will remain the most useful resource on vitamin K2 over time. Click below for a list of updates.