Low circulating vitamin D (25(OH)D) concentrations have been associated with bone health outcomes including an increased risk of falls and low bone mineral density in some populations, suggesting that low vitamin D levels are a risk factor for osteoporosis.^[24]

A recent statement from the U.S. Preventive Services Task Force concluded that the current evidence is insufficient to conclude a benefit of vitamin D or calcium supplementation on fracture prevention in men and women who do not have a known vitamin D deficiency, osteoporosis, or prior fracture.^[25][26] However, some studies have found that vitamin D — especially when combined with calcium supplementation — can increase bone mineral density and reduce the risk of fractures and falls in certain populations.^[24]

Vitamin K is poorly understood, both by the general public and among health professionals. It has a wide range of potential benefits, but their nature and extent are still uncertain.

Why is that?

Some vitamins are more popular than others. In the past, a lot of research went into vitamin C, which became a popular supplement. Nowadays, a lot of research goes into vitamin D, whose popularity as a supplement is steadily growing.

By contrast, research on vitamin K is still scarce, having slowly developed over the past two decades. Further, it is scattered, because there exist several forms of vitamin K. Some of those forms are present only in a few foods. Others exist in various foods, but only in minute amounts. Few have been the subject of human trials.

The human trials that do exist, however, are overall promising. In order to understand their value and limitations, first you need to know a few basic facts. So let’s begin:

What is vitamin K?

Of the four fat-soluble vitamins (A, D, E, and K), vitamin K was discovered last. In 1929, Danish scientist Henrik Dam discovered a compound that played a role in coagulation (blood clotting).^[47] When he first published his findings, in a German journal, he called this compound Koagulationsvitamin, which became known as vitamin K.

Today, we know that vitamin K participates in some very important biological processes, notably the carboxylation of calcium-binding proteins (including osteocalcin and matrix GLA protein).^[48] In other words, vitamin K helps modify proteins so they can bind calcium ions (Ca²⁺). Through this mechanism, vitamin K partakes in blood clotting, as Henrik Dam discovered, but also of calcium regulation: it helps ensure that more calcium gets deposited in bones and less in soft tissues, thus strengthening bones and reducing arterial stiffness.

What complicates matters is that each vitamin has different forms, called vitamers, each of which may affect you differently. Vitamin K has natural vitamers, K₁ (phylloquinone) and K₂ (menaquinone), and synthetic vitamers, the best-known of which is K₃ (menadione).

Vitamin K1

K₁ is produced in plants, where it is involved in photosynthesis: the greener the plant, the greater its chlorophyll content; the greater its chlorophyll content, the greater its K₁ content. When it comes to foods, K₁ is especially abundant in green leafy vegetables.

K₁ makes for 75–90% of the vitamin K in the Western diet.^[49] Unfortunately, K₁ is tightly bound to chloroplasts (organelles that contain chlorophyll and conduct photosynthesis), so you could be absorbing very little of what you eat^[50] — maybe less than 10%.^[51] Since vitamin K is a fat-soluble vitamin, however, its absorption can be enhanced by the co-ingestion of fat: adding fat to cooked spinach can raise K₁ bioavailability from 5% to 13%.^[52]

Vitamin K2

Things become more complicated here, because just as there are several forms of vitamin K, there are several forms of vitamin K2. To be more precise, the side chain of K₁ always has four isoprenoid units (five-carbon structures), so there is only one form of K₁, but the side chain of K₂ has n isoprenoid units, so there are n forms of K₂, called MK-n.^[53][54]

Whereas the side chain of K₁ has four saturated isoprenoid units, the side chain of K₂ MK-4 has four unsaturated isoprenoid units. Although K₁ is directly active in your system, your body can also convert it to MK-4.^[55][56][57] How much gets converted depends notably on your genetic heritage.^[49]

MK-4 is present in animal products (meat, eggs, and dairy), though only in small quantities. Because those foods usually contain fat, dietary MK-4 should be better absorbed than dietary K₁,^[58] but future studies will need to confirm this hypothesis.

Other than MK-4, all forms of K₂ are produced by bacteria. Your microbiota was once thought to produce three-fourths of the vitamin K you absorb.^[59] Vitamin K, however, is mostly produced in the colon, where there are no bile salts to facilitate its absorption, so the actual ratio is probably much lower.^[58][60]

Bacteria-produced K₂ can be found in fermented foods, such as cheese and curds, but also in liver meat.^[61] The richest dietary source of K₂ is natto (fermented soybeans), which contains mostly MK-7.^[62][63] As it stands, MK-7 is the only form of K₂ that can be consumed in supplemental doses through food (i.e., natto). For that reason, MK-7 is the most-studied form of K₂, together with MK-4.

K₁ and MK-4 both have a side chain composed of four isoprenoid units; their half-life in your blood is 60–90 minutes. MK-7 has a side chain composed of seven isoprenoid units; it remains in your blood for several days. Due to their different side-chain lengths, the various forms tend to be transported on different lipoproteins, which are taken up at different rates by various tissues.^{[64][65][66][67][68]} K₁ and MK-4 are used quickly (K₁ in the liver, MK-4 in other specific tissues), whereas MK-7 has more time to travel and be used throughout the body (which makes it, in theory, the best option for bone health).

Vitamin K₃

K₁ and K₂ are the only natural forms of vitamin K, but there exist several synthetic forms, the best known of which is K₃. However, whereas the natural forms of vitamin K are safe, even in high doses, K₃ can interfere with glutathione, your body’s main antioxidant. K₃ was once used to treat vitamin K deficiency in infants, but it caused liver toxicity, jaundice, and hemolytic anemia. Nowadays, it is used only in animal feed, in small doses. In the animals, vitamin K₃ gets converted into K₂ MK-4,^[69] which you can consume safely.

Vitamin K is a family of fat-soluble vitamins. K₁ and K₂, the natural forms, are safe even in high doses. There is only one type of K₁; it is found in plants, notably green leafy vegetables; your body can use it directly or convert it to K₂ MK-4. Aside from MK-4, all other types of K₂ are produced by bacteria, including the bacteria populating your gut. MK-4 is present in animal products (meat, eggs, dairy), whereas other types of K₂ can be found in fermented foods and liver meat.

Vitamin K and your health

As far as we know, vitamin K mainly affects bloodclotting, cardiovascular health, and bone health. Epidemiological studies have mostly focused on K₁; cardiovascular trials, on K₁ and MK-7 (the main type present in natto, the richest dietary source of K₂); bone trials, on MK-4 (the type of K₂ your body can make out of K₁).

Blood clotting

Vitamin K deficiency impairs blood clotting, causing excessive bleeding and bruising. It is rare in adults, but more common in newborns (more than 4 cases per 100,000 births in the UK^[70]), where it can result in life-threatening bleeding within the skull. For that reason, the American Academy of Pediatrics recommends that newborns receive K₁ shortly after birth (intramuscular injections have shown greater efficacy than oral administration).^[71]

If you suffer from hypercoagulation (if your blood clots too easily), you might be prescribed a vitamin K antagonist (VKA), such as warfarin, a medication that hinders the recycling of vitamin K. Some doctors recommend that VKA users shun vitamin K entirely, but preliminary evidence suggests that, under professional supervision, vitamin K supplements might help stabilize the effects of VKAs.^[61]

Which form should be supplemented, though, and in what amount, is still uncertain. There is some evidence that K₁ enhances coagulation more than does MK-4^[72][73] but less than does MK-7.^[66] With regard to daily supplementation, 100 μg of K₁ is considered safe, but in some people 10 μg of MK-7 is enough to significantly impair VKA therapy.^[74]

Remember that natto is rich in MK-7. A single serving of natto can increase blood clotting for up to four days,^[75] so it is one food VKA users should avoid. Other foods should be safe to eat. Please note that in people who do not suffer from hypercoagulation, and thus do not need to medicate with VKA, high intakes of natto have never been correlated to excessive blood clotting. Similarly, human studies saw no increase in blood-clot risk even from 45 mg (45,000 μg) of MK-4 taken once^[76] or even thrice^[77] daily.

Cardiovascular health

As we saw, vitamin K partakes in calcium regulation: it helps ensure that more calcium gets deposited in bones and less in soft tissues, thus reducing arterial stiffness. This is why people who take vitamin K antagonists, such as warfarin, are more likely to suffer from vascular calcification.^[78][79]

Epidemiological studies^[80][81][82] and mechanistic evidence^[83] suggest that dietary K₂ benefits cardiovascular health more than an equal dose of dietary K₁.

Clinical trials on supplemental vitamin K have focused on K₁^[84][85] and MK-7.^[86][87][88] Often, those trials used a combination of vitamin D and other nutrients, but with vitamin K being the key difference between the intervention group and the control groups. Both of these forms of vitamin K seem to cause a consistent reduction in arterial stiffness (with better evidence for MK-7), and less consistent reductions in coronary calcification and carotid intima-media thickness. Judging from those trials and the epidemiological evidence, MK-7 seems the better choice.

Bone health

As we have just seen again, vitamin K partakes in calcium regulation: it helps ensure that less calcium gets deposited in soft tissues and more in bones, thus strengthening the latter. This is why people who take vitamin K antagonists, such as warfarin, might be more at risk of bone fractures,^[89][90] though not all studies agree they are.^[91]

Current evidence suggests that supplementing with vitamin K — or, at least, with certain forms of vitamin K — can benefit bone health, especially in the elderly (who have lower levels of circulating K₂).^[92] This potential should be explored, since, as the world population grows (and grows older), so does the number of osteoporotic fractures.^{[93] [94][95]}

MK-7 appears to support the carboxylation of osteocalcin (a major calcium-binding protein in bones) more efficiently than K₁.^[66] Clinical trials suggest that, for the purpose of increasing bone density, MK-4 and MK-7 work more reliably than K₁.^[96]

More significantly, a meta-analysis of MK-4 trials found an overall decrease in fracture risk.^[97] The effect of K₁ or MK-7 supplementation on fracture risk is less clear. Only one K₁ trial looked at fracture risk; it reported a decrease, but without a concomitant increase in bone mineral density.^[98] Of the two MK-7 trials, one reported no difference in the number of fractures between the placebo group and the MK-7 group,^[99] whereas the other reported fewer fractures in the MK-7 group;^[100] there were, however, no statistical analyses for either study.

More research on vitamin K and fracture risk will be needed to clarify the effects of the different forms at different dosages. Currently, if you wish to supplement for bone health, a very high dose of MK-4 (45,000 μg) is the option best supported by human studies.^[97] Those studies, all in Japanese people, focused on the prevention of bone fractures, and yes, much smaller dosages can probably help support bone health; but how much smaller?

In a 12-month study, 20 patients suffering from a chronic kidney disorder were given a daily glucocorticoid (a corticosteroid that has for side effect to decrease bone formation and increase bone resorption). In addition, half the patients received 15 mg of MK-4 daily, while the other half received a placebo. The placebo group experienced bone-density loss (BDL) in the lumbar spine, while the MK-4 group did not.^[101]

More recently, a 12-month study in 48 postmenopausal Japanese women gave 1.5 mg of MK-4 daily to half of them and found a significant reduction in forearm BDL, but not in hip BDL, and it didn’t evaluate fractures.^[102]

So there is some evidence for dosages lower than 45 mg/day. It is, however, a lot weaker.

In healthy people, vitamin K supplementation does not increase the risk of blood clots. Judging from limited evidence, MK-7 seems to be the best form of vitamin K for cardiovascular health, and MK-4 the best form of vitamin K for bone health.

How much vitamin K do you need?

Since vitamin K is crucial to your health, why is it the subject of relatively few studies? One of the reasons is simply that vitamin K deficiency is very rare in healthy, well-fed adults. It is mostly a concern in newborns, in people who have been prescribed a vitamin K antagonist, in people who suffer from severe liver damage, and in people who have problems absorbing fat.^{[103][104][105]}

Vitamin K is abundant in a balanced diet, and the bacteria in your colon can also produce some. Moreover, your body can recycle it many times, and this vitamin K-epoxide cycle more than makes up for the limited ability your body shows for storing vitamin K.

Still, you can recycle vitamin K many times, but not forever, and so you still need to consume some regularly. But how much, exactly?

No one knows. There is, as yet, not enough evidence to set a Recommended Dietary Allowance (RDA) for vitamin K, so an Adequate Intake (AI) has been established at a level assumed to prevent excessive bleeding. In the United States, the AI for vitamin K is 120 μg/day for men and 90 μg/day for women. In Europe, the AI for vitamin K is 70 μg/day for men and women. More recent research, however, suggests that those numbers should be increased.^[65]

Since 100 g of collards contain, on average, 360 μg of vitamin K,^[106][53] getting enough vitamin K looks easy. But can’t you just as easily get too much?

Fortunately, no. Though allergic reactions have occurred with vitamin K injections,^{[107][108][109]} no incidence of actual toxicity has ever been reported in people taking natural vitamin K, even in high supplemental doses.^[110] For that reason, neither the FDA nor the EFSA has set a Tolerable Upper Intake Level (UL) for vitamin K. One should note, however, that we lack long-term, high-dose studies on vitamin K safety.

Sources of vitamin K

K₁ can be found in plant products, notably green leafy vegetables. K₂ MK-4 can be found in animal products (meat, eggs, and dairy). The other types of K₂ can be found in fermented foods and liver meat.

Table references: ^{[111][112][53][113][114][68][106][115][116]}

Meats’ vitamin K content correlates positively but non-linearly with their fat content and will vary according to the animal’s diet (and thus country of origin). Forms of K₂ other than MK-4 and MK-7 have not been well studied but are likely to have some benefit — cheeses and beef liver are notable sources of others forms of K₂^[112][116] and cheese consumption is associated with a reduced risk of cardiovascular disease.^[117]

While well-conducted controlled trials provide the most reliable evidence, most such trials used amounts of vitamin K2 that far exceed what could be obtained through foods, save for natto. This leaves us wondering if dietary K₂ has any effect.

Fortunately, it seems to be the case: a high dietary intake of K₂ (≥33 μg/day seems optimal) may reduce the risk of coronary heart disease — an effect a high dietary intake of K₁ doesn’t appear to have.^{[80][82][81][118]} It doesn’t mean, of course, that foods rich in K₁ are valueless: dietary K₁ intake will protect you from excessive bleeding and is inversely associated with risk of bone fractures.^[119]

Observational studies, however, are less reliable than controlled trials, so we know less about the effects of dietary intake than about the effects of supplemental intake. If you wish to supplement with vitamin K, here are the dosages supported by the current evidence:

Summary

Although much more research needs to be performed, there is early evidence that vitamin K, whether in food or in supplemental form, can benefit cardiovascular health and bone health.

More protein in the diet has been linked to more calcium in the urine. Two reasons have been suggested to explain this phenomenon:

• Your body draws from its calcium stores (in bones) to buffer the acid load caused by dietary protein. This has led researchers to suggest that higher protein intake could increase bone loss.^[13]
• Most studies that looked at protein intake and calcium excretion list dairy products as a protein source,^[14] so higher urinary calcium could simply be the result of higher calcium intake (i.e., more calcium in, more calcium out).

Therefore, looking only at calcium excretion wasn’t enough. Subsequent studies showed that dietary protein promotes dietary-calcium absorption^[15] and that high protein intake “promotes bone growth and retards bone loss whereas low-protein diet is associated with higher risk of hip fractures.”^[16] High-protein diets have also been shown to modestly suppress the decrease in bone mineral density caused by weight loss.^[17]

What happens is that when you ingest more protein, you absorb more of the calcium in your food, so less calcium ends up in your feces. Later, your body gets rid of the calcium it doesn’t need, so more calcium ends up in your urine, but not as much as would have otherwise ended in your feces.^[18] Therefore, an increase in protein intake leads to an overall decrease in calcium excretion, which points to an increase in calcium retention. High-protein diets also raise your insulin-like growth factor-1 (IGF-1),^[19] which notably promotes bone growth.^[20]

All in all, current evidence suggests that protein’s effect on bones is either neutral or beneficial.^[18][21]

Mechanical loading of bone through weight-bearing exercise is one of the best ways to increase bone mineral density and therefore, exercise has been suggested to prevent and treat osteoporosis — but the type of exercise matters. Running, weight training, and high-impact aerobic exercise can increase bone mineral density in the hips and spine. Gentle, low-impact aerobic exercise and walking protect against further losses in bone mineral density, while swimming does not seem to have a beneficial effect.^[27] It appears that adolescents and prepubertal girls derive the greatest benefit from weight-bearing exercise when it comes to increasing their peak bone mass. Jumping, hopping, weight training, and high-impact exercise are the most effective forms of activity for increasing bone mineral density in most populations. In terms of duration, 2-4 exercise sessions per week lasting 30 minutes or less can be effective for maintaining and improving bone quality.^[28]

Lifting weights, or resistance training, has numerous benefits to the muscles and skeleton that are uniquely attributed to this form of training.

There are some cognitive benefits associated with exercise in general, but this FAQ entry will be more focused on what resistance training can give that other forms of exercise cannot.

Resistance training?

Resistance training is a form of training where the muscles and skeleton are pit against a large force, either induced by external resistance (lifting weights) or by gravity (maximal jumping or sprinting). Resistance training tends to be focused on power, and tends to be anaerobic (intense) in nature.

Anything with maximal exertions can be considered resistance training. Things like Tennis and racquetball show some benefits as well due to some strides being full exertion, but weightlifting tends to have the most dramatic effects.

Benefits to Muscles

Most notably weight lifting, but all forms of resistance training, can increase muscle mass.

This can reduce the occurrence of sarcopenia (the age-related decline in muscle mass not associated with pro-inflammatory cytokines)^[29] when elderly,^[30][31] although all activity can reduce rates of sarcopenia, resistance training seems most effective.^[32][33]

Benefits to Bone

Exercise in general tends to be associated with better bone mineral density and/or bone width in athletes when compared to a non-athletic control group.^[34][35][36] Greater bone health and an exercise regimen are inversely associated with falls in the elderly, which suggests that exercise is a good preventative measure.^[37][38][39]

It might also slightly protect against further reductions in bone mineral density in those already diagnosed with osteoporosis or osteopenia,^[40] although in general activity is encouraged.^[41]

In older age, those who practice Sprinting have been shown to have better bone density and size relative to jogging and walking activities.^[42] Although beneficial bone adaptations seem to be better in the young, they can still occur even if one starts a physical exercise program later in life.^[43]

It should be noted that swimming does not tend to increase bone density or mass, as the person is suspended in a pool of water rather than actively forcing power against gravity. It may increase bone health slighty in some persons, but is much less reliable than other forms of exercise.^[41][44][45]

Health Promoting effects

Involvement in exercise for at least 150 minutes a week in associated with a reduced risk of diabetes in men, with a protective effect existing for both aerobic exercise and weight training with persons participating in both having least risk.^[46]

Bone mass is, for the most part, regulated by the activity of two specialized cell types. Osteoblasts are tasked with adding bone mass, while osteoclasts actively digest it and cause bone resorption. In the context of diseases like osteoporosis, increasing osteoclast number or activity shifts the balance toward bone resorption, causing a progressive loss of bone density over time.^[8] Bone is capable of sensing mechanical stress, which lessens in response to weight loss. This shifts the balance of bone remodeling cells. Calorie restriction also alters a number of hormones that play a role in the regulation of bone mass. Reductions in body fat have been linked to reduced levels of estrogen and other sex hormones,^[9] and increased sex hormone binding globulin (SHBG), a protein that binds to and sequesters hormones, blocking their function. Although shifts in overall hormone levels during calorie restriction and weight loss can be subtle, small changes in hormone levels (particularly estrogens, and IGF-1)^[10][11][12] can work through both direct and indirect mechanisms to alter the balance of osteoblast vs. osteoclasts activity to promote bone resorption and decreased bone density.

It is a common misconception that osteoporosis is a “woman’s disease.” Although women do tend to experience osteoporosis more than men and experience the condition at a younger age, men can also get osteoporosis. Osteoporosis tends to begin at a later age in men — around 70 years of age or so compared to 50 years in women.^[22] Risk factors for male osteoporosis include low testosterone levels, vitamin D deficiency, poor calcium intake, tobacco and heavy alcohol use, and prolonged use of some medications, including glucocorticoids (a type of steroid).^[23]