Health effects
Bone density
It has been suggested that vitamin K2 may play an important role in maintaining healthy levels of bone mineral density (BMD). However, data on the subject is inconclusive – some clinical trials show no improvement of BMD after vitamin K supplementation. First indications came from patients with femoral neck fractures, who demonstrated an extremely low level of circulating vitamin K2. The strong association between vitamin K2 deficiency and impaired bone health was later proved by both laboratory and clinical studies. It has been found that vitamin K2 deficiency results in a decreased level of active osteocalcin, which in turn increases the risk for fragile bones. Research also showed that vitamin K2, but not K1 in combination with calcium and vitamin D can decrease bone turnover. Moreover, a study performed by Knapen et al. clearly demonstrated that vitamin K2 is essential for the maintenance of bone strength in postmenopausal women, and was the factor for improving bone mineral content and femoral neck width.
More arguments supporting the unique function of vitamin K2 came from Japan. The Japanese population seems to be at lower risk for bone fractures compared to European and American citizens. This finding would be paradoxical, if levels of calcium consumption were the only factor determining bone density. However, Japanese studies published in 2006 and 2008 link Japan’s greater levels of BMD to that country’s widespread consumption of natto, a traditional breakfast dish made of fermented soybeans. Increased intake of MK-7 from natto seems to result in higher levels of activated osteocalcin and a significant reduction in fracture risk.
Even more striking is the research finding, reported in 2001, that there seems to be an inverse correlation between the amount of natto consumed, in different regions of Japan, and the number of hip fractures. In regions of the country where natto is not part of the daily diet, hip fractures are more common.
Heart calcification
Patients suffering from osteoporosis were shown to have extensive calcium plaques, which impaired blood flow in the arteries. This simultaneous excess of calcium in one part of the body (arteries), and lack in another (bones) – which may occur even in spite of calcium supplementation – is known as the Calcium Paradox. The underlying reason is vitamin K2 deficiency, which leads to significant impairment in biological function of MGP, the most potent inhibitor of vascular calcification presently known. Fortunately, animal research showed that vascular calcification might not only be prevented, but even reversed by increasing the daily intake of vitamin K2. The strongly protective effect of K2 and not vitamin K1 on cardiovascular health was confirmed by, among others, Geleijnse et al. in the Rotterdam Study (2004, see Figure 3) performed on a group of 4,800 subjects. Results of more than 10 years of follow-up were verified, also by Gast et al., who demonstrated that among K vitamins, the long-chain types of K2 (MK-7 through MK-9) are the most important for efficiently preventing excessive calcium accumulation in the arteries.
Vitamin K2 and children’s health
Laboratory experiments, population-based studies, and clinical trials tightly link better vitamin K status to the attainment of strong and healthy bones. The beneficial role of vitamin K in children was confirmed by van Summeren et al. that revealed a strong positive association between vitamin K status and bone mineral content. Findings from previous studies indicated also that additional vitamin K intake may improve bone geometry and positively influence the gain in bone mass. In a study of 223 healthy girls (11–12 years), O’Connor et al. found a positive relation between vitamin K status and bone mineral density.
Children have much higher bone metabolism than adults, so they need K vitamins in significantly larger quantities. Results from a number of studies suggest however a pronounced vitamin K deficiency in bone. In the majority of examined children, a marked elevation of undercarboxylated osteocalcin was observed, indicative for a poor K vitamin status. A similar observation was made by Kalkwarf et al. showing the interdependence between vitamin K status and bone turnover. This research underlined that the requirement for K vitamins may be higher than the current recommendation, which was set in accordance only with coagulation needs.
Absorption profile of different K vitamins
Vitamin K is absorbed along with dietary fat from the small intestine and transported by chylomicrons in the circulation. Most of vitamin K1 is carried by triacylglycerol-rich lipoproteins (TRL) and rapidly cleared by the liver; only a small amount is released into the circulation and carried by LDL and HDL. MK-4 is carried by the same lipoproteins (TRL, LDL, and HDL) and cleared fast as well. The long-chain menaquinones are absorbed in the same way as vitamin K1 and MK-4, but are efficiently redistributed by the liver in predominantly LDL (VLDL). Since LDL has a long half life in the circulation, these menaquinones can circulate for extended times resulting in higher bioavailability for extra-hepatic tissues as compared to vitamin K1 and MK-4. Accumulation of vitamin K in extra-hepatic tissues has direct relevance to vitamin K functions not related to hemostasis.
Dietary sources and adequate intake
In 2012, Canadian health writer Kate Rhéaume-Bleue suggested the Recommended Daily Allowance (RDA) for K vitamins (range of 80-120 µg) might be too low. Earlier suggestions in the scientific literature, which note that the RDA is based on hepatic (i.e. related to the liver) requirements only, date back as far as 1998. This hypothesis is supported by the fact that the majority of the Western population exhibits a substantial fraction of undercarboxylated extra-hepatic proteins. Thus, complete activation of coagulation factors is satisfied, but there doesn’t seem to be enough vitamin K2 for the carboxylation of osteocalcin in bone and MGP in the vascular system. Highest concentrations of vitamin K1 are found in green leafy vegetables, but significant concentrations are also present in non-leafy green vegetables, several vegetable oils, fruits, grains and dairy. In Europe and the USA 60%, or more, of total vitamin K1 intake is provided by vegetables, the majority by green leafy vegetables. National surveys reveal that K1 intakes vary widely. Intakes determined by weighed-dietary Intakes are similar in mainland Britain to the USA with average daily intakes of around 70–80 μg, which is less than the adequate intake for vitamin K. Apart from animal livers, the richest dietary source of long-chain menaquinones are fermented foods (from bacteria not moulds or yeasts) typically represented by cheeses (MK-8, MK-9) in Western diets and natto (MK-7) in Japan. Food frequency questionnaire-derived estimates of relative intakes in the Netherlands suggest that ~90% of total vitamin K intakes are provided by K1, ~7.5 % by MK-5 through to MK-9 and ~ 2.5% by MK-4. Most food assays measure only fully unsaturated menaquinones; accordingly cheeses have been found to contain MK-8 at 10–20 μg/100g and MK-9 at 35–55 μg/100 g.
Dietary intake sources
Vitamin K2 is preferred by the extra-hepatic tissues (bone, cartilage, vasculature) and is of bacterial origin. Scientific discussions are ongoing as to what extent K2 produced by our intestinal bacteria contributes to our daily vitamin K2 needs. If, however, intestinal bacterial supply was enough to supplement all tissues needing K2, we would not find high fractions of undercarboxylated Gla-proteins in human studies.
Natural K2 is also found in bacterial fermented foods, like mature cheeses and curd. The MK-4 form of K2 is often found in relatively small quantities in meat and eggs. The richest source of Natural K2 is the traditional Japanese dish natto made of fermented soybeans and Bacillus subtilis, which provides an unusually rich source of Natural K2 as long-chain MK-7: its consumption in North Japan has been linked to significant improvement in K vitamin’s status and bone health in many studies. The intense smell and strong taste, however, make this soyfood a less attractive source of Natural K2 for Westerners’ tastes, but supplement food companies sell nattō in capsules. It is not known whether B. Subtilis will produce K2 with other legumes (chickpeas, beans, lentils).
Other sources
Accumulating evidence suggests that Western society is affected by subclinical deficiency of vitamin K. Moreover, it has been scientifically proven that for optimal bone and vascular health, relatively high in-takes of vitamin K are required. The synthetic (and less effective)
Vitamin K deficiency
There are two kinds of vitamin K deficiency: acute and chronic.
Widely recognized, acute deficiency is characterized by unusual bleeding from gums, nose, or the gastrointestinal tract. Consequences can be severe, including internal clogging, strokes, lung damage, and death caused by immoderate blood loss. Newborn infants are at increased risk for acute vitamin K deficiency, because vitamin K is not transported sufficiently across the placenta, and the newborn gut is sterile at the beginning. Thus, there are no bacteria to produce the required amount of vitamin K. Vitamin K deficiency may also occur with the use anticoagulant drugs (i.e., warfarin or other coumarins), prolonged use of antibiotics, gallbladder disease, and Crohn’s disease.
Chronic vitamin K deficiency is less obvious than acute deficiency. It is actually more dangerous because there are no alarming symptoms and the results – impairments in bone, cardiovascular health, and other disease of aging – might be severe.
It had been long believed that vitamin K deficiency is rare. Requirements could be easily met via diet and microbial biosynthesis by bacteria living in the gut. However, recent scientific data show that the amount of vitamin K is not as abundant in the diet as once thought. Even a well-balanced diet might not provide vitamin K in the amounts sufficient for satisfying the body’s needs. This is especially concerning given that, according to researcher CJ Prynne, mean dietary intake of vitamin K is currently significantly lower than it was 50 years ago, while the daily consumption of vitamin K has gradually decreased since 1950.
This shortage can be partly explained by alterations in food composition (people eat much less green-leafy vegetables, which are rich in vitamin K1) and different preparation practices. Food used to be made in the presence of various bacteria species (synthesizing vitamin K2). Now, sterile conditions introduced by international standards of food manufacturing stop microorganisms, including beneficial flora, from multiplying and penetrating the human body.
Dietary patterns have also changed over decades. For example, children in 1950 derived around 15% of their vitamin K intake from fats and oil sources and 55% from vegetables (excluding potatoes). In the 1990s, 35% came from fats and oils, and just 30% from vegetables.
Moreover, it was shown that all K vitamins are absorbed from the gastrointestinal tract in the small intestine. Bacterial colonies producing menaquinones are located in the colon (large intestine), where the bile salts required for vitamin K uptake are not present. As stated earlier, the efficacy of intestinal vitamin K absorption might be questionable. Further, the presently used Recommended Dietary Intake for vitamin K might be too low. The need for complete activation of coagulation factors is satisfied, but it’s not enough to fulfill all of vitamin K’s benefits.
Excerpted from a Wikipedia article as it appeared on April 7, 2015 under a Creative Commons license. This excerpt is available under the same license. Citations and hyperlinks have been removed from this version.