Vitamin K2
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Wikepedia
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http://en.wikipedia.org/wiki/Vitamin_k
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Vitamin K is involved in the
carboxylation of certain
glutamate residues in proteins to form
gamma-carboxyglutamate residues (abbreviated Gla-residues). The
modified residues are often (but not always) situated within
specific
protein domains called
Gla domains. Gla-residues are usually involved in binding
calcium. The Gla-residues are essential for the biological
activity of all known Gla-proteins.
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At this time, 14 human proteins with
Gla domains have been discovered, and they play key roles in the
regulation of three physiological processes:
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Blood coagulation: (prothrombin
(factor II),
factors VII,
IX,
X,
protein C,
protein S and
protein Z).
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Bone
metabolism:
osteocalcin, also called bone Gla-protein (BGP), and
matrix gla protein (MGP).
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Vascular biology.
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Recommended amounts -
The U.S.
Dietary Reference Intake (DRI) for an Adequate Intake (AI) of
Vitamin K for a 25-year old
male is
120
micrograms/day. The Adequate Intake (AI) of this
phytonutrient for adult women is 90 micrograms/day, for infants
is 10-20 micrograms/day, for children and adolescents 15-100
micrograms/day.
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Toxicity - although
allergic reaction is possible, there is no known toxicity associated
with high doses of the phylloquinone (vitamin K1) or menaquinone
(vitamin K2) forms of vitamin K.
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Deficiency - osteoporosis
[1][2]
and coronary heart disease[3]
[4]are strongly associated with lower levels of K2 (Menaquinone).
Menaquinone is not inhibited by salicylates as happens
with K1, so Menaquinone supplimentation can alleviate the chronic
vitamin K deficiency caused by long term aspirin use.
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Vitamin K and Bone Health
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Recently vitamin K has also been lauded for its potential role
in the increase of bone mass. Studies have proved that
supplemental vitamin K promotes osteotrophic processes and slows
osteoclastic processes via calcium bonding. In Japan, a form of
vitamin K2 is recognized as a treatment for osteoporosis
[40][41].
However the long term effects and benefits are unknown and it
remains controversial.[citation
needed] Data from the 1998 Nurses Health Study
found an inverse relationship between dietary vitamin K1 and the
risk of hip fracture. After being given 110 micrograms/day of
vitamin K, the main results showed that women who consumed
lettuce one or more times per day had a significantly lower risk
of hip fracture than women who consumed lettuce one or fewer
times per week. In addition to this, high intakes of vitamin D
but low intakes of vitamin K may still pose an increased risk of
hip fracture hinting at a relationship between these two
vitamins [Kanai, T. et al. Serum Vitamin K level and Bone
Mineral Density in Postmenopausal Women. International Journal
of Gynecology and Obstetrics; 1997; 56:25-30.].
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Dr. Joseph Pizzorno -
www.drpizzorno.com
- Joseph E. Pizzorno, Jr., N.D., appointed by President
Clinton in December 2000 to the White House Commission on
Complementary and Alternative Medicine Policy and by
President Bush's administration to
the Medicare Coverage Advisory Committee in November 2002,
is one of the world's leading
authorities on science-based natural medicine.
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http://blogs.webmd.com/integrative-medicine-wellness/
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http://blogs.webmd.com/integrative-medicine-wellness/2007/11/vitamin-k-keeping-calcium-in-your-bones.html
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Vitamin K aids bone health in a number of ways: After it's carboxylated by vitamin K2, osteocalcin can latch
on to calcium and bind it to hydroxyapatite crystals forming
the bone matrix. (Think of carboxylation as adding a trailer
hitch to calcium, allowing it to be towed into and attached
to bone.) (Bügel S, Proc Nutr Soc 2003)
Vitamin K2 also teams up with vitamin D3 to increase the
production of Gla-proteins, including osteocalcin in
osteoblasts (the cells that build bone), while also
inhibiting the production of osteoclasts (the cells that
break down bone). (Plaza S, Lamson D. Alt Med Rev
2005, Masterjohn C. Med Hypotheses 2007; Yamaguchi M,
Sugimoto E, et al. Mol Cell Biochem 2001; Yamaguchi
M, Uchiyama S, et al. Mol Cell Biochem 2003)
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Research has linked osteoporotic fracture with vitamin K
insufficiency for more than 20 years. A study published in
1984 found that patients who suffered fractures caused by
osteoporosis had vitamin K levels 70% lower than age-matched
controls. This association has been repeatedly confirmed
with one recent trial involving almost 900 men and women
finding those with the lowest blood levels of vitamin K had
a 65% greater risk of hip fracture compared to those with
the highest levels of the nutrient. (Hart JP, Lancet
1984; Bitensky L, Hart JP et al, J Bone Surg Br 1988;
Hodges SJ, Pilkington MJ, et al. Bone 1991; Booth SL,
Tucker KL, et al. AJCN 2000 )
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Supplementation with vitamin K2 has been shown to be an
effective treatment against osteoporosis. A review study of
randomized controlled human trials of at least 6 months
duration that assessed the use of vitamin K1 or K2 to lower
fracture risk identified 13 trials. In all but one, vitamin
K reduced bone loss with K2 being most effective, reducing
risk of vertebral fracture by 60%, hip fracture by 77%, and
all non-vertebral fractures by 81%. (Cockayne S, Adamson J,
et al. Arch Intern Med 2006)
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Want to Check Your Vitamin K Status?
- A normal prothrombin time (the test for
clotting activity that has been the standard used to
check vitamin K sufficiency) is not sufficient
indication that enough vitamin K is present to maintain
vascular matrix-Gla protein activity or bone osteocalcin
activity.
Request an osteocalcin test; it measures how much
uncarboxylated osteocalcin is present in the blood. High
levels of uncarboxylated osteocalin indicate
insufficient vitamin K is present to promote optimal
bone health. Similarly, high levels of undercarboxylated
matrix-Gla protein (MGP) indicate that insufficient
vitamin K is present to protect against vascular
calcification. (Berkner KL, Rune KW, J Thromb
Haemost 2004; Cranenburg EC, Schurgers LJ et al.
J Thromb Haemost 2007; Bugel S. Proc Nutr Soc
2003)
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http://blogs.webmd.com/integrative-medicine-wellness/2008/10/strong-bones-for-life-naturally.html
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How Bisphosphonates Work
- Bisphosphonates
suppress bone turnover and remodeling. Our bones, unless inhibited by bisphosphonates, are
constantly rebuilding themselves throughout our lives. Cells
called osteoclasts break down old or damaged bone, signaling
other cells called osteoblasts to replace it with strong new
bone. Bisphosphonates kill osteoclasts. Bone density goes up
on these drugs, but the bone they leave in place is worn out
tissue your body would normally clear out and replace with
strong new bone.
This is why bisphosphonates put people at risk for
osteonecrosis (jaw bone death). Because these drugs suppress
osteoclastic activity, damaged bone is left in place rather
than resorbed, so the amount of damaged old tissue
accumulates until it reaches a level when any trauma or
insult will result in extremely poor healing, the exposure
of necrotic bone to the oral environment, development of
pain, and increased risk of microbial infection, which is
precisely what is seen in bisphosphonate-associated cases of
osteonecrosis of the jaw.
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http://blogs.webmd.com/integrative-medicine-wellness/2008/10/strong-bones-for-life-naturally-part-2.html
- Vitamin K, specifically vitamin K2 or menaquinone,
activates a group of proteins (the Gla-proteins), which
are responsible for where calcium gets delivered in the
body. Vitamin K2 ensures that the calcium you consume
(and which will be getting into your circulation in
higher amounts now that you are taking vitamin D) is
deposited where you want it—in your bones, and not where
you don't—in your blood vessels and other soft tissues.
- When your vitamin K2 levels are adequate, two of the
Gla-proteins that are activated are: (1) osteocalcin,
the protein responsible for anchoring calcium within
bone, and (2) matrix Gla-protein, which prevents calcium
from depositing in the heart, arteries, breast and
kidneys.
- Both vitamin K1 (phylloquinone) and vitamin K2 (menaquinone)
are available as supplements. Vitamin K1 is primarily
involved in helping your blood clot normally, although
our bodies are able to convert a small amount of K1 into
K2.
- For bone health, K2 (menaquinone), particularly
natural menaquinone derived from natto, which may be
labeled MK-7 (menaquinone-7) is the most potent form.
You may also see K2 as menatretrenone; this is MK-4, a
synthetic version that must be taken in much higher
doses because its half-life in the body is quite a bit
shorter.
- If you are taking MK-7, a daily dose of 45 mcg is
sufficient. If taking MK-4, take 5 mg daily.
- Best food sources of vitamin K (K1) include kale,
spinach, Swiss chard, broccoli, Brussels sprouts,
parsley and romaine lettuce. Natto, from soy, is
an excellent source of K2, but is not easily available
in the U.S., nor would the taste appeal to most
Americans.
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Tufts University - Jean Mayer USDA Human Nutrition
Research Center on Aging
http://hnrc.tufts.edu/HNRCA-Page-hnrcah_index.html
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Vitamin K Laboratory -
http://hnrc.tufts.edu/1192109687036/HNRCA-Page-hnrca2ws_1192109688640.html
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About Vitamin K2
www.foodconsumer.org/newsite/2/19/the_missing_nutrient_to_blame_for_heart_attacks_and_osteoporosis.html
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Atherosclerosis - (ath-er-o-skleh-RO'sis)
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The physiology of vitamin K nutriture and vitamin
K-dependent protein function in
atherosclerosis
K. L . BERKNER and K. W. RUNGE*
Departments of Molecular Cardiology and *Molecular Biology,
Lerner Research Institute, Cleveland Clinic Lerner College
of Medicine at Case Western
Reserve University, Cleveland, OH, USA
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To cite this article: Berkner KL, Runge KW. The physiology
of vitamin K nutriture and vitamin K-dependent protein
function in atherosclerosis.
J Thromb Haemost 2004; 2: 2118–32.
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Direct link
http://www.coryi.org/cardiology/ThephysiologyofvitaminK2004.pdf
(This page was last edited on
April 15, 2011
.)
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