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Bone loss occurs naturally as we age, but with sufficient Vitamin K2 intakes – particularly starting at an early age – this loss can indeed be slowed.
Poor bone metabolism is a condition characterized by loss of bone mineral density, which leads to bone that is weaker and more susceptible to fractures. According to the World Health Organization (WHO), this condition currently affects some 200 million people globally: one in three men is expected to incur bone fractures in the future because of poor bone metabolism, whereas lifetime risk of fracture for women is nearly one in two.
Bone is a living substance comprised of a hard outer shell and spongy inner tissue matrix. The skeleton “remodels” itself every 8 to 12 years. This is process is regulated by osteoblasts (cells that build up bone) and osteoclasts (cells that break down bone). Osteoblasts produce a protein called Osteocalcin, a vitamin K-dependent protein that binds calcium to the bone matrix and builds healthy bones. But Osteocalcin needs adequate Vitamin K2 to activate it.
As long as the bone-forming activity (absorption) is greater than the bone-breakdown (resorption), the process of maintaining healthy bones is kept under control. However, when this delicate process is not in balance, bones become weak and brittle. This is an unfortunate result of Vitamin K2 deficiency.
The strong association between Vitamin K2 deficiency and impaired bone health was proven in both laboratory and clinical studies. It has been found that vitamin K 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 – combined with calcium and vitamin D can decrease bone turnover. Further, a significant study clearly demonstrated that Vitamin K2 is essential for maintaining bone strength in postmenopausal women, and also improved bone mineral content and femoral neck width.
K2 for Bone Health
Bone mass or density is lost as people age, especially in women after menopause. The bones lose calcium and other minerals.
MenaQ7®’s Proven Bone Benefits
In 2013, Osteoporosis International published a groundbreaking double-blind, randomized, clinical trial that demonstrated for the first time clinically statistically significant protection of the vertebrae and the hip (femoral neck) against bone loss. This was attained with a nutritional dose of Vitamin K2 as MK-7 (MenaQ7®) taken daily for three years.
In this study of 244 healthy post-menopausal women, the MenaQ7® group took 180 mcg daily and showed significantly decreased circulating uncarboxylated osteocalcin (ucOC), a well-established biomarker for bone and vitamin K status. After 3 years, both bone mineral content and bone mineral density, as well as bone strength were statistically significantly better for the MK-7 group compared to the placebo group.
MenaQ7® is featured in quality products around the globe.
An adequate intake of Vitamin K2 has been shown to positively influence the cardiovascular system.
Calcification was once believed to be an irreversible process and a result of aging. However, it is now known that calcium accumulation is an actively regulated process involving the vitamin K-dependent Matrix Gla Protein (MGP), the most potent inhibitor of vascular calcification known, which is actively involved in recycling calcium.
Healthy arterial tissues have shown to contain 100 times more Vitamin K2 than unhealthy arteries, and the amount of calcium in the arteries is a risk factor for cardiovascular health. One might say that “you are as old as your arteries.” Studies in large population groups show that significant calcification in young persons actually make them older than their chronological age. On the contrary, older persons with little or no calcification may deduct up to 10 years from their actual age.
The Rotterdam Study (2004) shows that high dietary intake of Vitamin K2 – but not vitamin K1 – has a strong protective effect on cardiovascular health. Findings from this 10-year population-based study, which followed 4,807 initially healthy men and women >55 years of age from start, indicate that eating foods rich in natural Vitamin K2 (at least 32 mcg/day) results in 50% reduction of arterial calcification, 50% reduction of cardiovascular risk, and 25% reduction of all-cause mortality.
In 2008, these findings were confirmed by another population-based study with 16,000 persons from the Prospect-EPIC cohort population. Female participants aged 49-70 years at the start of the study, were followed up for 8 years and were free of cardiovascular diseases at the baseline. The researchers found that for every 10mcg Vitamin K2 (MK-7, MK-8, and MK-9) consumed – not K1 – the risk of coronary heart disease was reduced by 9%.
Unfortunately, the Western diet does not contain sufficient Vitamin K2, so supplementing with MenaQ7® Vitamin K2 as MK-7 is a viable alternative recommended by experts.
Breakthrough MenaQ7® Cardiovascular Study
Findings from a large clinical study, published in Thrombosis and Haemostasis, signal Vitamin K2 as MK-7 as a potential game-changer for the cardiovascular health category. Scientists at the University of Maastricht (the Netherlands) performed a double-blind, randomized, intervention study of 244 postmenopausal women given either 180 mcg of Vitamin K2 as MK-7 (as MenaQ7®) or a placebo daily for 3 years.
Using ultrasound and pulse-wave velocity measurements (recognized as standard measurements for cardiovascular health), researchers determined that carotid artery distensibility was significantly improved for a 3-year period in the MenaQ7® group as compared with that of a placebo group, especially in women having high arterial stiffness. Also, pulse-wave velocity showed a statistically significantly decrease after 3 years for the Vitamin K2 (MK-7) group, but not for the placebo group, demonstrating an increase in the elasticity and reduction in age-related arterial stiffening, again, especially in women having high arterial stiffness.
This first intervention trial on MK-7 supplements and cardiovascular endpoints showed that 3-year supplementation with a daily, nutritional dose (180 mcg) of MenaQ7® was enough to actually decreased arterial stiffness in healthy post-menopausal women.
And now a new 1-year trial has published – this time examining the impact of K2 supplementation (as MenaQ7®) on male and female populations – confirming cardiovascular benefits.
A pre-selected group of 243 vitamin K-insufficient subjects (men and women) were randomly included in a placebo-controlled, double-blind 1-year supplementation study using non-invasive diagnostic method evaluating whether an effect of vitamin K2-supplementation (180 μg MK-7 as MenaQ7®) may be demonstrated within one year.
Arterial stiffness was concluded from the carotid-femoral pulse-wave velocity (cfPWV), and other vascular characteristics were measured by echotracking of the common carotid artery. In the total study group, MK-7 induced a significant decrease of both dp-ucMGP and cfPWV.
It was concluded that high vitamin K intake decreased age-related vascular stiffening (consistent with outcomes in two previous 3-year studies), but this is the first time that vascular effect was observed within one year of treatment.
MenaQ7® is featured in quality products around the globe.
Are you getting enough Vitamin K2? If you are eating a Western diet, you likely are not.
Vitamin K occurs naturally in two major forms — Vitamin K1 and Vitamin K2. While Vitamin K1 is found in green leafy vegetables, such as broccoli, spinach and kale, and is easy to incorporate into one’s diet, the more beneficial Vitamin K2 is of bacterial origin and much more difficult to obtain through diet alone.
Vitamin K2 can be produced within the human body by beneficial bacteria colonizing the intestines. However, the intestinal absorption seems to be minimal, contributing little to the body’s vitamin K requirements especially for bones and arteries, and research now indicates that contribution is much less than previously thought.
Therefore, the daily requirement for Vitamin K2 has to be gained from dietary sources, and the most popular sources in Western diets are curd, cheeses, and other fermented dairy products shown to contain Vitamin K2. But one needs to consume extremely high amounts of these foods daily in order to get a sufficient Vitamin K2 intake.
The best source of Vitamin K2 is a traditional Japanese dish made from fermented soybeans called natto, which is uniquely rich in menaquinone-7 (MK-7). As natto remains unpopular in the Western world, supplementation with additional Vitamin K2 is viewed as the optimal alternative.
In general, the typical Western diet contains insufficient amounts of Vitamin K2 to adequately activate the K-dependent Matrix Gla Protein (MGP), which means about 30% of Vitamin K2-activated proteins remain inactive. This amount only increases with age. Further, Vitamin K2 is nearly non-existent in processed “junk” food, and even in a healthy Western diet.
Also of note is that there are currently no recommended intake levels for Vitamin K2 – the only recommended levels are for vitamin K1.
Even the healthiest diets fall short on delivering all the nutrients the body requires to operate optimally.
It has long been believed that vitamin K deficiency is rare due to dietary intake and contribution from microbial biosynthesis in the gut. Yet published studies show that the majority of both children and adults are vitamin K deficient.
Consider that dietary intake data from the 1950s and early 2000 in the UK show that consumption of vitamin K is now lower than it once was – a likely a consequence of changing diets, as well as food supply. For example, between the 1950s and the 1990s, fats and oils became a larger part of most Western diets than vegetables.
Further, changes in food composition and different preparation practices can also explain deficiencies. 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.
And while it was thought that bacterial synthesis of menaquinones in the colon was a significant contributor to the body’s systemic needs, research now indicates that contribution is much less than previously thought.
Published studies strongly indicate that better Vitamin K2 status contributes to non-calcified, flexible arteries and strong, healthy bones. With a shifting emphasis to fast and processed foods, it is conceivable that vitamin K intakes have been on a significant decline since 1950, which may have serious implications for bone and cardiovascular health.
Vitamin K2 Unrecognized in RDAs
Current daily recommendations for K vitamins are based exclusively on vitamin K1 and the requirement for proper blood clotting, which is presently 1 mcg vitamin K1/kg of body weight (daily). This amount is insufficient for the optimal function of vitamin K-dependent proteins in other tissues like bone and vasculature.
Further complicating the issue is that very few foods contain Vitamin K2 as MK-7. For those that do, we need to eat substantial amounts of those foods daily just to obtain the minimum dosage of 45 mcg to experience any sort of bone or cardiovascular benefit.
Vitamin K was discovered in 1929. The Danish scientist Henrik Dam and colleagues were investigating the role of dietary cholesterol by feeding chickens a diet without fat. After several weeks the animals started to suffer from frequent bleedings. This could not be stopped by adding cholesterol to the diet, so Dam postulated that – together with fat – there had to be another compound in the diet that prevented the bleedings. After years of research he found a factor in hempseed that prevented bleeding, and decided to call it the coagulation vitamin. It was designated in German as “Koagulations” vitamin and that is how the new vitamin got the letter K.
This monumental discovery of Vitamin K earned Professors Henrik Dam and Edward Doisy the Nobel Prize in 1943.
1975
Esmon et al. published the mechanism of action of vitamin K and identified the vitamin K cycle as vital for the activity of carboxylase enzyme.
1989
Vermeer et al. published that vitamin K deficiency influences the ratio of serum uncarboxylated to carboxylated osteocalcin.
1997
Sokoll et al. published that the US dietary vitamin K intake is not sufficient to fully carboxylate osteocalcin.
2001
Schurgers et al. published that inhibition of vitamin K-dependent carboxylation of MGP promotes vascular calcification.
2006
Tsugawa et al. published that MK-7 is the vitamin K form found in serum of women with reduced risk of bone fractures. Later that year Ikeda et al. published that intake of MK-7 is associated with reduced bone loss in post menopausal women in a population-based study (JPOS study).
2007
Schurgers et al. used rats to demonstrate that that arterial calcification and the resulting decreased arterial distensibility are reversible by high intake of vitamin K.
2008
Nimptsch et al. published a large population-based study showing that consuming dairy products containing higher menaquinones like MK-7 reduces the risk of prostate cancer substantially. No such reduction was observed with vitamin K1-containing food. Later, van Summeren et al. showed that a better vitamin K status was associated with more pronounced increase in bone mass in healthy children.
2009
Beulens et al. found among 564 post-menopausal women that intake of Vitamin K2 – but not vitamin K1 – was associated with reduced coronary calcification, and that adequate Vitamin K2 intake could be important for prevention of cardiovascular disease. Shortly thereafter van Summeren et al. demonstrated that modest MK-7 supplementation increases circulating concentrations of MK-7 and increases osteocalcin carboxylation in healthy children, while Gast et al. found that a high menaquinone intake reduces the incidence of coronary heart disease.
2012
Westenfeld et al. confirmed that most hemodialysis patients have a functional vitamin K deficiency. More importantly, they found that inactive MGP levels can be decreased markedly by daily Vitamin K(2) supplementation.
2013
Knapen et al. showed that after three years of supplementation of 180 mcg Vitamin K2 as MK-7 (MenaQ7®) daily, improvements in both bone mineral content and bone mineral density were statistically significant in the MenaQ7® group. Moreover, bone strength was statistically improved. Later that year Theuwissen et al. established the vitamin K status across age groups based on circulating levels of ucOC and dp-ucMGP, i.e. markers for the vitamin K status of bone and the vasculature, respectively. Accordingly, the study classified healthy children and adults above 40 years as groups with prominent vitamin K deficiency and thus appropriate groups for vitamin K supplementation.
2015
Knapen et al. published the first double-blind, randomized, intervention trial where the results confirm that Vitamin K2 intake is linked to cardiovascular risk. Researchers found that, after three years of daily supplementation with 180 mcg Vitamin K2 as MK-7 (as MenaQ7®), it not only inhibited age-related stiffening of the artery walls, but also made a statistically significant improvement of vascular elasticity, especially in women having high arterial stiffness. To date, the effects of increased menaquinone intake on markers of vascular health have been investigated using predominantly food supplements. Therefore, Knapen et al. sought to study the effects of a menaquinone-fortified yogurt drink (as MenaQ7®) on vitamin K status and markers of vascular health in healthy men and postmenopausal women. Results showed MK-7 was efficiently absorbed from the fortified yogurt drink, improving vitamin K status, which contributed to improved cardiovascular health.
K-dependent proteins in the body need to be activated in order to function.
Vitamin K1 is known for its blood-clotting activity. Vitamin K2 also contributes to this process, but Vitamin K2 is now recognized as essential for helping the body to properly utilize calcium in order to build healthy, strong bones and to stop calcium from depositing in the arteries and blood vessels.
Vitamin K2 “makes calcium work” through its ability to activate certain K-dependent proteins already present in the body:
- Osteocalcin is the protein responsible for binding calcium ions to the matrix of bone, making bones stronger.
- Matrix Gla Protein (MGP) is the most potent modulator of arterial calcification known today, and the amount of arterial calcification is an indicator of one’s cardiovascular health.
Natural vitamin K2 as MK-7 is the essential cofactor for the enzyme γ-carboxylase which is able to carboxylate these calcium-regulating proteins making them able to form calcium-binding groups essential for their biological activity. By controlling these proteins in vascular tissue, vitamin K2 keeps calcium out of the arteries and drive it to bones.
Research has found that osteocalcin was undercarboxylated by 40% in postmenopausal women when compared with premenopausal women. Uncarboxylated matrix Gla-protein is associated with the increased vascular calcification and cardiovascular disease.
When the body has sufficient Vitamin K2, calcium is directed to where it is needed, and kept away from where it is not.
Vitamin K deficiency results in impaired bone strength and mineral density.
Calcification increases vessels’ stiffness and fragility, impeding healthy blood flow to and from the heart.
However, inadequate Vitamin K2 may result in what is known as the “Calcium Paradox.” This is where the bones receive too little calcium (leaving them weak and brittle) as excess calcium deposits in the arteries and blood vessels (making them stiff and inelastic).
Vitamin K2 is the powerful component in transporting “excess” calcium out of the arteries and blood and depositing it into our bones.
The link between Calcium, Vitamin D3 and Vitamin K2
While Vitamin K2 as MK-7 is essential for activating calcium-binding proteins, Vitamin D3 plays a vital Role in synthesizing these proteins and aiding with calcium absorption.
