Although Vitamin K is best known for its role in normal blood clotting
function, recent research has revealed Vitamin K's beneficial effects
on bone and cardiovascular health. In bone tissue, Vitamin K is
critical for the formation of healthy, strong bone matrix. In fact,
bone quality is dependent on the presence of adequate Vitamin K.
Vitamin K's role in arterial health revolves around its ability to
support proper calcium metabolism in vascular structures. Vitamin K2 is
the most biologically active form of vitamin K. It is also the most
beneficial for bone integrity, as well as for the support of arterial
Vitamin K2 is involved in bone metabolism. Vitamin K2 homologs
(menaquinones) are characterized by the number of isoprenoid residues
comprising the side chain. Menaquinones are abbreviated MK-n, where n
represents the number of isoprenoid side chains. Thus, menaquinone-4
abbreviated MK-4 has 4 isoprene residues in the side chain. Bacteria can
produce a range of vitamin K2 forms, including the conversion of K1 to K2
(MK-7) by bacteria in the small intestines. No known toxicity exists for
vitamins K1 and K2.*
Vitamin K2 provides major protection from osteoporosis, cardiovascular
blockages, and pathological calcification.
Vitamin K's job is to put calcium in the right places and keep it from
being deposited in the wrong places. The right places are bones and blood,
and the wrong places include calcification of the vessels, bone spurs, and
calcification of soft tissues.
Vitamin K was discovered in the 1920's as a fat-soluble factor important in
blood coagulation ("K" for coagulation). Vitamin K1 is found in plants and
vitamin K2 is found in animals and bacteria, including beneficial probiotic
bacteria, aka "good bacteria," from the GI tract. The body can store about
a one-month supply of the vitamin. Antibiotics interfere with the growth of
healthy intestinal bacteria and as a result, impair vitamin K production.
The prescription anticoagulant Warfarin also interferes with the metabolism
and function of vitamin K by inhibiting critical enzymes that are involved
with the production of coagulation factors. Without this coagulation factors, excessive bleeding can occur.
Vitamin K works by acting as a cofactor in the carboxylation (adding of a
carboxyl group C02) via an enzyme (gamma-glutamyl carboxylase), of glutamic
acid (a specific amino acid) to form a modification of that amino acid
(gamma carboxyglutamic acid) in a variety of critical plasma proteins.
Without this step, these plasma proteins will not function in their role of
the regulation of calcium concentrations in various tissues.
There are several different types of GCGA proteins including osteocalcin
(OC), which is the most abundant GCGA protein in humans and is synthesized
in bone; the GCGA protein-containing blood coagulation factors are
synthesized in the liver; the matrix GCGA proteins (MGP) are synthesized in
the cartilage and in the vessel walls of arteries. 1
According to the Food and Nutrition Board of the National Academy of
Sciences National Research Council, the requirements of vitamin K in
micrograms (mcg) range from 5 micrograms for infants and up to 80 mcg for
adult males and 65 mcg for adult females. 2
When vitamin K is in short supply in the body, these proteins are formed
without the GCGA component and are inactive for their intended functions -
which play important roles in four different tissue types including 1)
liver; 2) bone; 3) cartilage; and 4) arterial vessel walls.
These four tissues are all able to pull vitamin K from the blood. However,
the uptake from the liver is much greater for K1 than for other tissues.
Very important recent findings indicate that vitamin K2, and not K1
inhibits Warfarin-induced arterial calcification. This research is
important for those on Warfarin and has implications for the majority of
us who are unaware that we are deficient in this lifesaving nutrient.
Because the liver needs so much vitamin K, this can leave the cartilage and
bone GCGA proteins with inadequate levels. Hence the dietary vitamin K
requirement for bone and the special requirements for the cardiovascular
system and cartilage may not be met even though normal clotting factor
production occurs, as this occurs in the liver. Therefore, the requirement
to keep the vasculature clear of accumulating calcium and to keep the bones
well supplied with calcium may not be adequately supplied. This is why the
recent discoveries on the value of vitamin K2 and its recent commercial
availability can make a great difference in the lives of millions -
probably a majority of the population would benefit.
The FDA's current recommendations for vitamin K dosage are based solely on
the liver's requirements alone. It has been identified that a large
percentage of the enzymes that do not receive GCGA because of a vitamin K1
or K2 deficiency become unable to mobilize calcium and place it into the
bone where it belongs. This GCGA-deficient enzyme is known as
undercarboxylated osteocalcin (ucOC). It was found that this occurs in the
majority of the healthy adult population indicating subclinical vitamin
deficiency in a large portion of the population. 3,4 Though this is
subclinical in terms of obvious symptoms, the first symptoms may be
osteoporosis or acute coronary disease... the first symptom may even be
See Other LifeSource Vitamins Vitamin K Products, Articles, and
The results of a vitamin K intervention study have been examined in which
both bone mineral density and vascular elasticity were shown to increase. 5
Other studies have demonstrated consistent findings adding to the
conclusion that vitamin K1, and preferably, a good amount of vitamin K2,
may just be some of the best protection for preventing calcification of the
arteries, and for protection against osteoporosis.
Oral anticoagulant medications such as Warfarin or Coumadin, etc., which
are the most commonly used anticoagulants, are vitamin K antagonists.
Vitamin K may lessen the concentration of the anticoagulants.
Vitamin K: the overlooked bone builder and heart protector
by Dr. Susan E. Brown, PhD
At the Center for Better Bones, we have long noted the trend towards
increased arterial calcification with the use of high-dose calcium
supplementation when given without other key bone nutrients. We propose
that these trends are strongly related to vitamin K status, particularly to
the inadequacy of the menaquinone-7 (MK-7) form of vitamin K2.
Vitamin K is essential for the proper formation and full activation of the
Gla proteins. The Gla protein osteocalcin, when fully carboxylated
by vitamin K, allows for the binding of calcium to the bone matrix. The Gla
protein known as matrix-Gla protein is found in vascular smooth
muscles. Matrix Gla protein is a key inhibitor of soft tissue calcification
that binds calcium, preventing it from depositing in the vessel walls. Both
GLA proteins are essential for proper calcium metabolism, and neither can
be fully activated without adequate vitamin K.
These assertions are supported by a wide range of clinical data; for
It is well known that vitamin K antagonists such as warfarin double
arterial calcification in humans.
The decade-long, 4800-person Rotterdam study documented that people who
consumed the most vitamin K2 have a 50% reduced risk of arterial
calcification. They also exhibited a 50% reduced risk for
cardiovascular events during this 10 year period.
In 2009, a 16,000-person study by Gast and colleagues showed that a
high intake of natural vitamin K2, but not vitamin K1, protected from
cardiovascular disease. This study reported that for every 10 mcg
vitamin K2 consumed, the risk of coronary heart disease was reduced by
A recent animal study by Schurgers and colleagues (2006) showed
regression of warfarin-induced arterial calcification when given
adequate supplemental doses of vitamin K2.
As it appears vitamin K, and vitamin K2 as MK-7, in particular, play an
important role in keeping calcium in the bones and out of the arteries.
Hopefully, as we cast a broader net of understanding, clinical bone trials
will include analysis of vitamin K status along with calcium intake
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An excellent history and review of Vitamin K is offered in a number of
scientific papers - one being Vitamin K1 supplementation retards bone loss
in postmenopausal women between 50 and 60 years of age by Braam, Knapen,
Geusens, Brouns, Hamulyak, Gerichhausen, and Vermeer, epub 2003. See below
for more study results:
In 1984 it was found that patients with osteoporotic fractures had
circulating vitamin K levels which were over 70% lower than those in the
control group. 6 The data was consistent with other studies show ing that
low serum vitamin K is associated with low mineral density, which is a high
risk factor for bone fracture. 7-9
In analyzing British and American populations, it was found that they did
not meet the RDA levels of 1.5 micrograms per day per kg of body weight
(10-12) and that low intake is associated with low bone mineral density
which is associated with risk of bone fracture.
In the Nurses Health Study, over 72,000 women between 38 and 63 years of
age were followed for 10 years. The risk of fracture in the lower quintile
for vitamin K intake almost doubled that in the higher quintile. 13
In the Framingham study of an older group of patients, with an average age
of 75 years, the results were more dramatic. 14 Subjects in the highest
quartile for vitamin K intake had a significantly lower hip fracture risk.
Hence the critical involvement of vitamin K in bone health and its general
deficiency in our population is firmly established.
Vitamin K Supplementation Retards Postmenopausal Bone Loss
In the Maastricht osteo study, 188 postmenopausal women between 50 and 60
years old were treated for 3 years with daily supplements. 16 There was a
placebo group which received only maltodextrin and the second group
received minerals, 500 mg/day of calcium, 150 mg/day of magnesium, 10
mg/day of zinc and 320 IU/day of vitamin D3. The third group received these
minerals plus the vitamin D3 and l mg/day of vitamin K1. The group without
vitamin K benefited only transiently. In the group with vitamin K, bone
loss at the femoral neck was retarded by 35%-40% compared to the other
mineral vitamin D group. It is stated that if these effects continued over
decades, lifelong supplementation could postpone fractures by up to 10
Further research of the D-Bavis study using calcium (1000 mg), vitamin D
(10 ug) and vitamin K (200 mcg) per day, supported the previous findings.
They also found a significant increase in bone mineral content and density
in the vitamin K group. 17
The authors concluded that combined supplementation with vitamin K1 and D3
at dietary relevant levels improved bone mass density at the trabecular
bone site and that the equivalent supplementation in high osteoporotic risk
groups may be beneficial. Extremely high doses 45-90 mg/day of vitamin K2
are successfully used in the treatment of osteoporosis in Japan. 18-20
These doses of K2 exceed RDA levels by 1000 fold and no side effects were
Low Vitamin K Intake as a Risk Factor for Cardiovascular Disease
256 postmenopausal women were studied by Jie, et. al. in the EPOZ study.
They found an inverse correlation between long term vitamin K intake and
arterosclerotic aorta calcification. 21 Only vitamin K1 (phylloquinone) was
included in the study.
A subsequent study of 4500 participants of the Rotterdam study by
Gelejinse, et. al. reports a much stronger negative correlation between
long term, lower than adequate intake of vitamin K2 (menaquinone) and
aortic calcification. The data was stronger for K2 than for K1. This is
consistent with the suggestion of preferential uptake of K2 by the vessel
Vitamin K Supplementation Prevents Age Related Vascular Stiffening
In an animal study in rabbits with high cholesterol, vitamin K2 was shown
to decrease circulating cholesterol concentrations, suppress progression of
vascular plaque, thickening in the vessels, and pulmonary atherosclerosis.
23 In a study of rats on arterial calcification, vitamin K2 completely
prevented calcification, whereas vitamin K1 had little effect. 24 A three
year study involving postmenopausal women (a group which is generally known
to be at risk for vascular illness), the elastic properties of the carotid
artery were recorded using ultrasound. A supplement of 1 mg/day of vitamin
K1 completely abolished age-related arterial stiffening, whereas the
placebo group showed a decrease of 13% of elastic properties of the
vasculature during the test period. 25
Dietary & Supplemental Forms of Vitamin K1 & K2
Most of our dietary vitamin K1 comes from vegetables - about 80%. Vitamin
K2 is obtained mainly from the "good" bacteria produced in the digestive
tract and is also found in certain fermented foods. 26 The absorbability of
the vitamin K2 from the GI tract bacteria is uncertain. 27 The absorption
of vitamin K1 from vegetables is about 10%.
"However, both K1 and K2 are well absorbed from supplements as long as they
are taken with some dietary fat to stimulate bile secretion." 28
Recommendations of a European Expert Group
In November 2002, a number of European experts in the fields of vitamin K
research, bone metabolism and cardiovascular disease met to review all the
available scientific data to formulate an opinion on the amount of
recommended dietary vitamin K and the use of vitamin K-containing
supplements, for optimal bone and vascular health. Some of the conclusions
from this meeting are summarized below:
Daily intake of between 200 and 500 mcg/day of vitamin K through food
sources may be required for optimal health.
Accumulating evidence suggests there is a synergistic effect between
vitamins K, D and calcium (and of course, magnesium). Optimal health
effects may be obtained from combined supplementation of vitamins K, D and
Any risks associated with high consumption of either vitamin K1 or K2
appear minimal, with intakes up to 1 mg/day of vitamin K1 and 45 mg/day of
vitamin K2, often having been used with no observed side effects.
The only potential problem with high levels of vitamin K supplementation
relates to interference with oral anticoagulant medications such as
Warfarin and Coumadin, which are antagonists of vitamin K. Patients on oral
anticoagulant treatment should not use vitamin K supplements and avoid
strong fluctuations in their daily dietary vitamin K intake. However, in a
systematic dose-response study of patients on oral anticoagulant therapy,
it was demonstrated that the stability of anticoagulation was not
significantly affected by vitamin K supplementation at doses below 150
mcg/day. 30 Patients on anticoagulant medications should consult with their
physician or healthcare practitioner regarding vitamin K.
Other Benefits of Vitamin K
We have discussed the beneficial effects of vitamin K on bone density,
cardiovascular health, and the Syndrome X diseases, however, there are even
more benefits to vitamin K supplementation.
Further research has demonstrated vitamin K's anti-inflammatory action. As
the body ages, levels of the inflammation-promoting cytokine interleukin-6
(IL-6) increase. Once IL-6 becomes out of ba lance with the other
cytokines, inflammation accelerates. It has been observed that people with
arthritis, Alzheimer's disease, and atherosclerosis have higher levels of
IL-6. In a study done by the National Research Institute in Italy, it was
shown that subjects with the highest levels of IL-6 were almost twice as
likely to develop mobility-related disabilities.
The second highest concentration of vitamin K in the body is in the
pancreas, which plays a major role in blood sugar and insulin regulation.
In animal studies, Japanese researchers found that when they induced
vitamin K deficiency, the test animals developed Type II diabetes. 31
Research has indicated that vitamin K has antioxidant activity comparable
to vitamin E and CoQ10. 32,33 Animal studies have demonstrated complete
hepatic (liver) protection from induced oxida tive stress using vitamin K,
and was found to be 80% as effective as vitamin E in preventing oxidation.
About 25% of the population have a genetic predisposition for developing
Alzheimer's disease - they carry the E4 form of the lipoprotein apoE.
Interestingly, people who carry this gene have been found to have low
levels of vitamin K. Calcification and the development of lesions in blood
vessels that feed the brain tissues are believed to be a component of
Alzheimer's development. Further research may reveal high-dose vitamin K
therapy to be preventive.
Japanese Study on Vitamin K2 & Viral Cirrhosis-Related Liver Cancer
Japanese researchers have recently discovered that vitamin K2 may play a
significant role in prevention of liver cancer caused by viral cirrhosis.
In a 2004 study published in the Journal of the American Medical
Association, 40 women diagnosed with viral liver cirrhosis were studied, in
which 21 were given 45 mg vitamin K2 per day. Vitamin K2 was found to
decrease the risk of the development of liver cancer in female patients
with viral cirrhosis, possibly by delaying the onset of the cancer. 34 For
over seven years, the patient's progress was closely followed. The
proportion of patients who developed liver cancer was significantly smaller
in the group of women treated with the vitamin K2 (2 of 21), compared to
the non-treated group (9 of 19). The annual incidence of liver cancer in
the treated group was 1.6%, compared to the non-treated group, which was
8.8%. The researchers believe that a substance called geranyl-geraniol (a
by-product of vitamin K2), induces cell death in tumor cells suggesting
that it may play an important role in cell growth inhibition. The
researchers wrote, "The study indicates that vitamin K2 decreases the risk
of liver cancer to about 20% compared to the control group." The
researchers also commented that these are only preliminary results and
further research needs to be done through clinical trials.
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Vitamin K2 References:
1. Schurgers LJ, Vermeer C. Differential lipoprotein transport pathways of
K-vitamins in healthy subjects. Biochim Biophys Acta. 2002 Feb
2. Kelleys Textbook of Internal Medicine, Fourth Edition, 2000, Lippincott,
Williams and Wilkins, Philadelphia, PA.
3. Knapen MH, Jie KS, Hamulyak K, Vermeer C. Vitamin K-induced changes in
markers for osteoblast activity and urinary calcium loss. Calcif Tissue
Int. 1993 Aug;53(2):81-5.
4. Booth SL, Sokoll LJ, O'Brien ME, Tucker K, Dawson-Hughes B, Sadowski JA.
Assessment of dietary phylloquinone intake and vitamin K status in
postmenopausal women. Eur J Clin Nutr. 1995 Nov;49(11):832-41.
5. Vermeer C, Braam L, Schurgers L, Brouns F. Agro-Food Industry Hi-Tech
6. Hart JP, Catterall A, Dodds RA, Klenerman L, Shearer MJ, Bitensky L,
Chayen J. Lancet ii 283 (1984).
7. Hart JP, Shearer MJ, Klenerman L, Catterall A, Reeve J, Sambrook PN,
Dodds RA, Bitensky L, Chayen J. Electrochemical detection of depressed
circulating levels of vitamin K1 in osteoporosis. J Clin Endocrinol Metab.
8. Hodges SJ, Pilkington MJ, Stamp TC, Catterall A, Shearer MJ, Bitensky L,
Chayen J. Depressed levels of circulating menaquinones in patients with
osteoporotic fractures of the spine and femoral neck. Bone.
9. Hodges SJ, Akesson K, Vergnaud P, Obrant K, Delmas PD. Circulating
levels of vitamins K1 and K2 decreased in elderly women with hip fracture.
J Bone Miner Res. 1993 Oct;8(10):1241-5.
10. Booth SL, Pennington JA, Sadowski JA. Food sources and dietary intakes
of vitamin K-1 (phylloquinone) in the American diet: data from the FDA
Total Diet Study. J Am Diet Assoc. 1996 Feb;96(2):149-54.
11. Booth SL, Suttie JW. Dietary intake and adequacy of vitamin K. J Nutr.
12. Thane CW, Paul AA, Bates CJ, Bolton-Smith C, Prentice A, Shearer MJ.
Intake and sources of phylloquinone (vitamin K1): variation with
socio-demographic and lifestyle factors in a national sample of British
elderly people. Br J Nutr. 2002 Jun;87(6):605-13.
13. Feskanich D, Weber P, Willett WC, Rockett H, Booth SL, Colditz GA.
Vitamin K intake and hip fractures in women: a prospective study. Am J Clin
Nutr. 1999 Jan;69(1):74-9.
14. Booth SL, Broe KE, Gagnon DR, Tucker KL, Hannan MT, McLean RR,
Dawson-Hughes B, Wilson PW, Cupples LA, Kiel DP. Vitamin K intake and bone
mineral density in women and men. Am J Clin Nutr. 2003 Feb;77(2):512-6.
15. Booth SL, Tucker KL, Chen H, Hannan MT, Gagnon DR, Cupples LA, Wilson
PW, Ordovas J, Schaefer EJ, Dawson-Hughes B, Kiel DP. Dietary vitamin K
intakes are associated with hip fracture but not with bone mineral density
in elderly men and women. Am J Clin Nutr. 2000 May;71(5):1201-8.
16. Braam LAJLM, Knapen MHJ, Geusens P, Brouns F, Hamulyak K, Gerichhausen
MJW, Vermeer C. Vitamin K1 supplementation retards bone loss in
postmenopausal women between 50 and 60 years of age. Calcif. Tissue Int.
72, epub (2003).
17. Bolton-Smith C, Mole PA, McMurdo MET, Paterson CR, Shearer MJ. Ann.
Nutr. Metab. 45 Suppl. 1 246 (2001).
18. Orimo H, Shiraki M, Tomita A, Morii H, Fujita T, Ohata M. J. Bone
Miner. Metab. 16:106-112, 1998.
19. Shiraki M, Shiraki Y, Aoki C, Miura M. Vitamin K2 (menatetrenone)
effectively prevents fractures and sustains lumbar bone mineral density in
osteoporosis. J Bone Miner Res. 2000 Mar;15(3):515-21.
20. Iwamoto J, Takeda T, Ichimura S. Effect of menatetrenone on bone
mineral density and incidence of vertebral fractures in postmenopausal
women with osteoporosis: a comparison with the effect of etidronate. J
Orthop Sci. 2001;6(6):487-92.
21. Jie KS, Bots ML, Vermeer C, Witteman JC, Grobbee DE. Vitamin K intake
and osteocalcin levels in women with and without aortic atherosclerosis: a
population-based study. Atherosclerosis. 1995 Jul;116(1):117-23.
22. Geleijnse JM, Vermeer C, Schurgers LJ, Grobbee DE, Pols HAP, Witteman
JCM. Thromb. Haemostas. (Suppl July) P473, 2001.
23. Kawashima H, Nakajima Y, Matubara Y, Nakanowatari J, Fukuta T, Mizuno
S, Takahashi S, Tajima T, Nakamura T. Effects of vitamin K2 (menatetrenone)
on atherosclerosis and blood coagulation in hypercholesterolemic rabbits.
Jpn J Pharmacol. 1997 Oct;75(2):135-43.
24. Spronk HM, Soute BA, Schurgers LJ, Thijssen HH, De Mey JG, Vermeer C.
Tissue-specific utilization of menaquinone-4 results in the prevention of
arterial calcification in warfarin-treated rats. J Vasc Res. 2003
Nov-Dec;40(6):531-7. Epub 2003 Dec 3.
25. Braam LAJLM. Thesis, Maastricht ISBN 90-5681-145-2, 2002.
26. Schurgers LJ, Vermeer C. Determination of phylloquinone and
menaquinones in food. Effect of food matrix on circulating vitamin K
concentrations. Haemostasis. 2000 Nov-Dec;30(6):298-307.
27. Ronden JE, Drittij-Reijnders MJ, Vermeer C, Thijssen HH. Intestinal
flora is not an intermediate in the phylloquinone-menaquinone-4 conversion
in the rat. Biochim Biophys Acta. 1998 Jan 8;1379(1):69-75.
28. Vermeer C, Braam L, Knapen M and Schurgers L; Vitamin K
supplementation: a simple way to improve vascular health. Agr Food Industry
hi Tech Nov 2003.
29. Vermeer C, Shearer MJ, Zittermann A, Bolton-Smith C, Szulc P, Hodges S,
Walter P, Rambeck W, Stocklin E, Weber P. Beyond deficiency: potential
benefits of increased intakes of vitamin K for bone and vascular health.
Eur J Nutr. 2004 Dec;43(6):325-35. Epub 2004 Feb 5.
30. Schurgers LJ. Thesis, Maastricht ISBN 90-5681-138-X, 2002.
31. Sakamoto N, Wakabayashi I, Sakamoto K. Low vitamin K intake effects on
glucose tolerance in rats. Int J Vitam Nutr Res. 1999 Jan;69(1):27-31.
32. Mukai K, Itoh S, Morimoto H. Stopped-flow kinetic study of vitamin E
regeneration reaction with biological hydroquinones (reduced forms of
ubiquinone, vitamin K, and tocopherolquinone) in solution. J Biol Chem.
1992 Nov 5;267(31):22277-81.
33. Mukai K, Morimoto H, Kikuchi S, Nagaoka S. Kinetic study of
free-radical-scavenging action of biological hydroquinones (reduced forms
of ubiquinone, vitamin K and tocopherol quinone) in solution. Biochim
Biophys Acta. 1993 Jul 11;1157(3):313-7.
34. Habu D, Shiomi S, Tamori A, Takeda T, Tanaka T, Kubo S, Nishiguchi S.
Role of vitamin K2 in the development of hepatocellular carcinoma in women
with viral cirrhosis of the liver. JAMA, 2004 Jul 21;292(3):358-61.