Vit k

While I am not any kind of authority on Vitamin K, my summary of the
hundreds of studies I've read are summarized here. It is a fat soluble
vitamin, usually included with A, D and E. Taken in dietary form (greens),
it normally converts to K2 while in the INTACT intestine. As with A, D and
E, people who have any form of malabsorption are missing "the converter" for
K, as well.


* K2 decalcifies the blood and the extracted calcium ends up in the
bones
* K2 as MK-4 (synthetic) "might" interfere with blood thinners, like
coumadin.
* K2 as MK-7 is safe in doses as high as 45mg (most is sold in mcg),
even for those using blood thinners
* K1 in dietary form cannot convert to K2 with any tampering of
intestines, at all
* Phytonadione and Phylloquinone appear to be used interchangeably for
K1




* My personal conclusion is that I will use the K1 1,000 mcg once
daily for myself and Don AND the K2 (as MK-7) starting at a lower dose of
50mcg twice per day, gradually increasing dosage.
* [ comments in brackets below are my own ]






Vitamin K, and the Difference Between K1 and K2

Ask doctors what vitamin K does, and most will tell you it is involved in
the clotting process...period!

As early as 1984, however, scientists reported that patients who suffered
fractures caused by osteoporosis had vitamin K levels that were 70% lower
than age-matched controls. These findings were confirmed in later studies
showing diminished bone mineral density in the presence of low serum vitamin
K levels. The most frightening statistic showed that women with the lowest
blood levels of vitamin K had a 65% greater risk of suffering a hip fracture
compared to those with the highest vitamin K levels.

One might wonder why vitamin K has such a powerful impact on bone density.
The answer is quite simple. In order for calcium to bind to the bone matrix,
a protein called osteocalcin is needed. Without adequate vitamin K,
osteocalcin is unable to transport calcium from the blood and connect it to
the bones. Tens of millions of Americans ingest calcium supplements to
reduce their risk of osteoporosis and fractures. These vitamin K studies,
however, show that people could still suffer the crippling effects of
osteoporosis if they are vitamin K deficient because the calcium would
remain in their blood and not bind to bone.

The next question is what happens to calcium if it is not taken up to form
bone mass. Regrettably, in a vitamin K deficient state, the body takes
calcium that is meant to form strong bones and instead deposits it into the
arterial wall, thereby contributing to the process of atherosclerosis. In
fact, in response to a vitamin K deficiency, the body naturally accumulates
enormous amounts of calcium in the.

This explains why so many aging individuals suffer from hardened calcified
arteries, yet have brittle bones that are markedly depleted of calcium. In a
huge European human clinical trial (The Rotterdam Study), doctors evaluated
vitamin K intake of 4807 subjects over a 7-10 year period. After adjusting
for other risk factors, coronary heart disease risk was reduced with
increased intake of vitamin K2. Those who consumed the most vitamin K2 had a
57% reduction in cardiac disease compared to those who consumed the least
K2.What has scientists most excited is that vitamin K2 is proving itself to
be superior to K1. Health enthusiasts will be pleased to learn that a new
biologically-active form of vitamin K2 has been added to the supplement
formulas used by most Foundation members today.

Vitamin K1 is obtained in the diet primarily from dark leafy vegetables
(lettuce, spinach, and broccoli). Unfortunately, vitamin K1 is tightly bound
to the chlorophyll in green plants, meaning that aging humans are not able
to benefit much from ingested K1-containing plants.10 While vitamin K1 is
not absorbed particularly well from food, it is absorbed from supplements,
provided that the supplements are taken with fat-containing meals.

Vitamin K2 is found in much smaller quantities in the diet, primarily in
dairy products. The highest level of dietary K2 is fermented soy natto.14
Human studies show that vitamin K2 is absorbed up to ten times more than
K1.15 Japanese people consume large quantities of natto, which may help
explain their lower rates of heart disease and osteoporosis compared to
Western populations.

Not only is K2 absorbed better, but it remains biologically active in the
body far more than K1. For instance, K1 is rapidly cleared by the liver
within 8 hours, whereas measurable levels of K2 have been detected 72 hours
after ingestion. This means that vitamin K2 is available to facilitate
transport of calcium into the bone and to protect the arterial wall against
calcification much longer than is K1.

Vitamin K Impedes Atherosclerosis

In rabbits with high cholesterol levels, supplemental vitamin K2 decreased
circulating cholesterol, suppressed the progression of atherosclerotic
plaque, and impeded the thickening of the inner arterial lining (intima). In
a rat model, supplemental vitamin K2 completely prevented calcification,
whereas vitamin K1 had little effect.

In a study of 188 postmenopausal women, a group known to be at high risk for
rapid decay of arterial structure, a supplement containing only 1 mg of
vitamin K1 or a placebo was administered over a three-year period. In the
vitamin K group, age-related arterial stiffening (as measured by carotid
intima-media thickness) was completely abolished, whereas the placebo group
(not receiving vitamin K) experienced a 13% worsening of arterial elasticity
during the study period.18 (Please note that some vitamin K1 is converted to
K2 in the intestine).

How Vitamin K Protects Arteries from Calcification

Vitamin K controls calcium-regulating proteins that are present in vascular
tissue. These vitamin K-dependent proteins (including osteocalcin and matrix
G1a protein) have been shown to specifically inhibit vascular calcification,
i.e. keep calcium out of the arteries.

Activation of these calcium-regulating proteins depends on the availability
of vitamin K. When there is not enough vitamin K to turn on these proteins,
the result is deposition of calcium into atherosclerotic plaque, thus
worsening cardiovascular disease risk and leading to a condition that the
lay public sometimes refers to as "hardening of the arteries." This helps
explain why patients who take anti-coagulant drugs (like Coumadin® that
deplete vitamin K in the body suffer from accelerated atherosclerosis.

Increasing evidence shows that the same calcification process involved in
normal bone formation also occurs in the linings of arteries when there is
not enough vitamin K available to activate calcium-regulating proteins (such
as matrix G1a protein, a powerful inhibitor of arterial calcification). This
means that the same biological mechanism used by bone to attract and bind
calcium can also pathologically occur in the linings of the arteries in the
presence of inadequate vitamin K.8 This explains why patients with advanced
atherosclerosis have both occluded and calcified (hardened) arteries that
have lost their youthful elasticity. The inability of arteries to readily
expand and contract with each heartbeat is a hallmark characteristic of
hypertension.

In most individuals, vitamin K from dietary sources fills the need for
proper coagulation. As people age, however, a sub-clinical vitamin K
deficiency can pose severe risks to the vascular system.
Vitamin K2 Intake Associated with Reduced Arterial Disease

In the most significant human study to date, a large group of people with no
history of heart disease were followed from 1990-1993 until year 2000. The
incidence of coronary artery disease, all cause mortality, and severe aortic
atherosclerosis was studied in relationship to the amount of vitamin K1
and/or K2 ingested over the study period.

As can clearly be seen by the table above, those who consumed the most
vitamin K2 showed significant disease reductions, compared to those who
ingested the least K2. In this study, intake of vitamin K1 from dietary
sources was not related to these risk reductions, probably due to the poor
bioavailability of K1 from plant foods. In their concluding remarks, the
scientists who conducted this study stated that adequate intake of vitamin
K2 could contribute to the prevention of coronary artery heart disease.
Vitamin K and Bone Fracture Prevention

A systemic review was made of all randomized controlled trials that gave
adults either vitamin K1 or K2 supplements for at least six months. A total
of 13 trials were identified with data on bone loss and 7 trials that
reported fracture incidences. All of these human trials except one showed
that supplemental vitamin K1 or K2 reduced bone mass loss. Vitamin K2 in
particular was associated with increased bone mineral density.

In all 7 trials to evaluate fracture risk, vitamin K2 proved most effective,
reducing the risk of vertebral fractures by 60%, hip fractures by 77%, and
an astounding reduction for all non-vertebral fractures of 81%.

For those taking calcium and vitamin D supplements to prevent osteoporosis,
adequate vitamin K intake is essential to activating proteins that bind
calcium to the bone. In the presence of inadequate vitamin K status, the
calcium that would be used to maintain strong bones is instead deposited
into the arterial wall where it accelerates the atherosclerosis process.
Summary

Since vitamin K was discovered in 1930, it was only thought to contribute to
the liver's maintenance of healthy blood coagulation. Over the past 15
years, scientists have found that vitamin K plays a crucial role in arterial
and bone health.

Recent studies indicate that vitamin K intake that is substantially above
the government's recommended reference range can slow bone loss, reduce
arterial stiffening, prevent heart attack, and reduce death rates in adult
human populations.








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http://tinyurl.com/3qph45

Originally published In Press as doi:10.1074/jbc.M702971200
<http://www.jbc.org/cgi/content/abstract/M702971200v1> on December 14, 2007


J. Biol. Chem., Vol. 283, Issue 17, 11270-11279, April 25, 2008



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Conversion of Phylloquinone (Vitamin K1) into Menaquinone-4 (Vitamin K2) in
Mice


TWO POSSIBLE ROUTES FOR MENAQUINONE-4 ACCUMULATION IN CEREBRA OF MICE*

Toshio Okano {ddagger} <http://www.jbc.org/math/Dagger.gif> 1, Yuka
Shimomura {ddagger} <http://www.jbc.org/math/Dagger.gif> , Makiko Yamane
{ddagger} <http://www.jbc.org/math/Dagger.gif> , Yo****omo Suhara {ddagger}
<http://www.jbc.org/math/Dagger.gif> , Maya Kamao {ddagger}
<http://www.jbc.org/math/Dagger.gif> , Makiko Sugiura §
<http://www.jbc.org/math/sect.gif> , and Kimie Nakagawa {ddagger}
<http://www.jbc.org/math/Dagger.gif>

From the {ddagger} <http://www.jbc.org/math/Dagger.gif> Department of
Hygienic Sciences, Kobe Pharmaceutical University, 4-19-1,
Motoyamakita-machi, Higashinada-ku, Kobe 658-8558 and the §
<http://www.jbc.org/math/sect.gif> Analytical Center, Kobe Pharmaceutical
University, Kobe 658-8558, Japan

There are two forms of naturally occurring vitamin K, phylloquinone and the
menaquinones. Phylloquinone (vitamin K1) is a major type (>90%) of dietary
vitamin K, but its concentrations in animal tissues are remarkably low
compared with those of the menaquinones, especially menaquinone-4 (vitamin
K2), the major form (>90%) of vitamin K in tissues. Despite this great
difference, the origin of tissue menaquinone-4 has yet to be exclusively
defined. It is postulated that phylloquinone is converted into menaquinone-4
and accumulates in extrahepatic tissues. To clarify this, phylloquinone with
a deuterium-labeled 2-methyl-1,4-naphthoquinone ring was given orally to
mice, and cerebra were collected for D NMR and liquid chromatography-tandem
mass spectrometry analyses. We identified the labeled menaquinone-4 that was
converted from the given phylloquinone, and this conversion occurred
following an oral or enteral administration, but not parenteral or
intracerebroventricular administration. By the oral route, the phylloquinone
with the deuterium-labeled side chain in addition to the labeled
2-methyl-1,4-naphthoquinone was clearly converted into a labeled
menaquinone-4 with a non-deuterium-labeled side chain, implying that
phylloquinone was converted into menaquinone-4 via integral side-chain
removal. The conversion also occurred in cerebral slice cultures and primary
cultures. Deuterium-labeled menadione was consistently converted into the
labeled menaquinone-4 with all of the administration routes and the culture
conditions tested. Our results suggest that cerebral menaquinone-4
originates from phylloquinone intake and that there are two routes of
accumulation, one is the release of menadione from phylloquinone in the
intestine followed by the prenylation of menadione into menaquinone-4 in
tissues, and another is cleavage and prenylation within the cerebrum.

_____

Received for publication, April 9, 2007 , and in revised form, December 12,
2007.

* This work was supported by a grant-in-aid for scientific research from the
Ministry of Education, Science, Sports and Culture of Japan. The costs of
publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked "advertisement"in
accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

1 To whom correspondence should be addressed. Tel.: 81-78-441-7563; Fax:
81-78-441-7565; E-mail: [email protected] .



***************************

http://sciencelinks.jp/j-east/article/200304/000020030403A0074675.php



or



http://tinyurl.com/6elen2






Clarification of the conversion mechanism of vitamin K analogues to
menaquinone-4(MK-4) in the rats tissues without the participation of
bacterial enzyme in the intestine.

Accession number;03A0074675
Title;Clarification of the conversion mechanism of vitamin K analogues to
menaquinone-4(MK-4) in the rats tissues without the participation of
bacterial enzyme in the intestine.
Author;KOMAI MICHIO(Tohoku Univ., Graduate School of Agricultural Sci., JPN)
SHIRAKAWA HITOSHI(Tohoku Univ., Graduate School of Agricultural Sci., JPN)
EJIRI MASAHIRO(Tohoku Univ., Graduate School of Agricultural Sci., JPN)
HIWATASHI KAZUYUKI(Tohoku Univ., Graduate School of Agricultural Sci., JPN)
OSAKI YUSUKE(Tohoku Univ., Graduate School of Agricultural Sci., JPN)
MIZUTANI TAKEO(Eieruei Chuken) FURUKAWA YUJI(Tohoku Univ., Graduate School
of Agricultural Sci., JPN)
Journal Title;Journal of Germfree Life and Gnotobiology

Journal Code:L0200A

ISSN:0910-0903

VOL.32;NO.2;PAGE.94-97(2002)
Figure&Table&Reference;FIG.2, REF.5
Pub. Country;Japan
Language;Japanese
Abstract;Phylloquinone(vitamin K1=VK1) and the menaquinones(MK-n, or vitamin
K2=VK2) are naturally occurring forms of vitamin K. Most of the menaquinone
series are synthesized by microorganisms, but we have reported that MK-4 is
usual in being synthesized by the conversion of orally ingested VK1 or
menadione(=VK3) in the major tissues of germfree rats and mice which lack
their intestinal microflora. This result denies Martius' theory that
described the participation of bacterial enzyme of the intestinal flora to
this conversion. Recently MK-4 has been attracted the attention of
researchers due to its specific physiological action such as apoptotic
activity on osteoclast cells and leukemia cells, etc. The present study was
undertaken to clarify the in vivo conversion of VK1,VK3,MK-6,MK-7, and MK-10
to MK-4 in Wistar rats, and also to clarify the mechanism of the conversion
of VK3 or VK1 to MK-4 in tissue homogenate system(in vitro) of various
organs in germfree or conventional Wistar rats, and the latter part of
thestudy was summarized here. In vivo conversion studies revealed that the
increase of MK-4 level in various tissues of Wistar rats after
VK1,VK3,MK-6,MK-7, and MK-10 administration orally. In vitro conversion
studies revealed that there was the enzyme activity of MK-4 formation from
VK1 and GGPP in various tissues, and no or very low activity of MK-4
formation in the gastrointestinal mucosa in germfree rats. Results obtained
from the experiment using [8-ring]-14C-VK1 substrate indicate that the VK
analogues such as reduced-form of VK3,VK1, and MK-4 could be candidates for
intermediate products for final MK-4 formation. (author abst.)


******************

http://www.healthsalon.org/213/vitamin-k-arterial-calcification-and-atherosc
lerosis/

or

http://tinyurl.com/5qhqv7




Vitamin K, Arterial Calcification and Atherosclerosis


17th April 2007 by Rett Anderson Posted in Disease
<http://www.healthsalon.org/category/disease/> , Cardiovascular
<http://www.healthsalon.org/category/cardiovascular/> , Nutrition
<http://www.healthsalon.org/category/nutrition/>

>>>>>>>>>>>>>>>>>>>>>>>>>>>>

Researchers at the University of Maastricht in the Netherlands recently
published the results of an experiment in the journal Blood showing that
vitamin K deficiency causes arterial calcification and the death of the
smooth muscle cells that line the blood vessel wall. They have shown in
previous research that atherosclerosis is characterized by deposits of
calcium salts, lipids, white blood cells, and deformed vitamin K-dependent
proteins manufactured by cells that do not have enough vitamin K to meet
their needs. These deposits are not random -- they aggregate around the
remnants of dead ("apoptotic") smooth muscle cells.Vitamin K supports at
least two proteins that are likely to protect against atherosclerosis:
matrix Gla protein (MGP) and growth arrest specific gene product 6 (Gas6).
MGP protects soft tissues from calcification, while Gas6 increases cell
survival and helps clear away any fragments left behind by cells that do
happen to die.

In this experiment, the researchers induced a vitamin K deficiency in Wistar
Kyoto rats with warfarin, an oral anticoagulant that works by inhibiting the
recycling of vitamin K. Warfarin caused arterial calcification, a marked
increase in the death of smooth muscle cells, a loss of blood vessel
elasticity, and a decreased ability of the blood vessels to accomodate
changes in pressure. High-dose vitamin K supplementation reversed these
changes even after they were induced by warfarin. Low-dose vitamin K
supplementation not only did nothing to reverse the effects of warfarin but
the calcification actually continued at the same rate in the animals that
received the drug after it was discontinued, persisting for the entire
duration of the study, showing that the vitamin K deficiency induced by oral
anticoagulants persists long after their use is discontinued.

In this study and in an earlier one that the same researchers published,
vitamin K1, found in plants, had no ability whatsoever to prevent
warfarin-induced calcification when the drug and the vitamin were
administered together, while vitamin K2, found in animal foods and fermented
plant foods, completely inhibited warfarin-induced calcification. The
researchers found, however, that after warfarin was discontinued, both
vitamins were equally effective at reversing calcification.

The Wistar Kyoto rats that these researchers used convert vitamin K1 to
vitamin K2 with great efficiency. Warfarin not only inhibits the recycling
of vitamin K, but also the conversion of vitamin K1 to vitamin K2. Although
it is not clear why this would be the case and the findings should therefore
be treated with caution, the results strongly suggest that only vitamin K2
protects against heart disease, and that vitamin K1 is effective only
insofar as it is converted to vitamin K2. How well humans make this
conversion compared to rats is unknown. In The Rotterdam Study, intakes of
vitamin K2 showed a powerful inverse association between calcification of
the aorta, heart disease, and heart disease mortality. Intakes of vitamin K1
by contrast -- even though they were ten times higher than intakes of vitamin
K2 -- had no relationship to any of these endpoints at all.

Schurgers LJ, Spronk HMH, Soute BAM, Schiffers PM, DeMey JGR, Vermeer C.
Regression of warfarin-induced medial alastocalcinosis by high intake of
vitamin K in rats. Blood. 2006; [Epub ahead of print].

Remember, vitamin D uses vitamin K2, so you need to make sure you get enough
of both.



***************



http://www.menaq7.com/index.php?s=Links

or

http://tinyurl.com/5c3rwy





There are two forms of vitamin K2 available as supplements, Natural Vitamin
K2 as Menaquinone-7, (MK-7) and Synthetic Menaquinone-4 (Mk-4). There are
significant differences between these two forms of vitamin K2.

<http://www.menaq7.com/img/wykres_top.gif>
<http://www.menaq7.com/img/wykres.gif>

* A single dose of 1mg of Synthetic MK-4 and Natural MK-7 were given
to healthy volunteers
* The maximum absortion levels in serum were found at 2 hours for MK4
and 4 hours for MK-7; MK-4 is excreted in approximately 8 hours
* While peak heights are comparable, MK-7 demonstrates a much longer
half-life in the blood, thus available to the body 24h/day with daily dosing

<http://www.menaq7.com/img/contact_bot.gif>

Synthetic vitamin K2 as menatetrenone (MK-4)

* Quickly appears but also disappears from the blood. Half life 1
hour! (see graph)
* As a result, high pharmacological doses (mg) are necessary; and
multiple daily doses are needed
* Importantly, large doses interact negatively with persons on
blood-thinning medications (warfarin) - very dangerous and medical
supervision is necessary

Natural Vitamin K2 as Menaquinone-7 (MK-7) from Natto

* Highly bioavailable, highly bioactive and longest serum half life
(Schurgers, et al. Blood 2007). Half life 3 days!
* Long half life will result in building up a buffer of MK-7, and
supplies MK-7 to ALL tissues 24 hours a day.
* More effective at doses that do not exceed the present
recommendations for daily vitamin K intake
* At 45mcg/daily, provides levels shown to be the highest consumption
in the Rotterdam study
* Not likely to interact negatively with blood-thinning medications
(warfarin) at 45 mcg/day!

Summary: VitaK research at the University of Maastricht, experts in vitamin
K for more than 30 years, studied the bioavailability and bioactivity of the
three K-vitamins (K1, MK-4 & MK-7) currently available for human
consumption, both in supplements and in functional foods. They have clearly
demonstrated at regular intake (once daily) of nutritional doses (20-150
mcg/day) of MK-7, its long half-life may lead to accumulation in blood and
extra-hepatic tissues (e.g. bone and vasculature) to levels that may only be
reached with more frequent supplementation (e.g. three times a day) and much
higher doses of either K1 or MK-4.

Clarification of MK-4 Claims: True or False?

Claim: MK4 is the superior form of Vitamin K2.

* MK-4 bioavailability was shown to be at least 4 times greater than
MK-7 in bone

This point is not true: the study they refer to (Yamaguchi et al., 1999) was
performed by giving first high dose of either MK-4 or MK-7. In the high
dose, both vitamins accumulated equally well in plasma and bone. All the
studies currently performed with MK-4 are done with extremely high doses.
Nothing is known about the "normal" physiological intake of MK-4. Next, they
studied the accumulation of low dose of MK-7 (combination of natural natto +
extra "pure" MK-7) in plasma and bone. THEY DID NOT STUDY LOW DOSE OF MK-4.
They found that MK-7 accumulated very well in the plasma (what we see in the
human study being published in Blood April 2007). However, they found that
MK-4 was the result in bone. This is due to the conversion of MK-7 into MK-4
(same as the conversion of K-1 into MK-4). The carboxylation (activation) of
osteocalcin was good in case of the low MK-7. When the conversion and why
and how the conversion of MK-7 (or K-1 or even MK-4.) into MK-4 is taken
place, nobody knows. We have, however, human nutritional data in the normal
range from Hodges et al (1993, JBMR) who describe that in the bones K-1 and
MK-7, 8, &9 accumulate to the same extent, but not MK-4. Recently, Dr. Sato
and colleagues have performed a rat-study, submitted recently to a Japanese
journal in which he proves that at the low dose ONLY MK-7 increase vitamin
K2 in the bone, whereas MK-4 does NOT. Also in this case he finds that some
conversion of MK-7 into MK-4 takes place (thus he only finds MK-4 after MK-7
intake whereas he does not find MK-4 after MK-4 intake in the bone...).
Taken together, we have to conclude that at the aimed physiological range
MK-7 is the most potent K-vitamin.

* Most of the published human studies supporting Vitamin K2's role in
bone health and vascular health used MK-4

This is absolutely true: However, even more evidence is present on K-1. This
is only due to the following reason: First K-1 was discovered and all the
research focussed on K-1. Later, MK-4 was discovered and even more
importantly PRESENT as synthetic compound and therefore most of the K-2
research was done with MK-4. Behind this, of course the industry was a major
driving factor: the company which produces MK-4 is Eisai Co., Tokyo, Japan
and they sponsored most of the MK-4 studies. Only since the last decade,
MK-7 as natural product from Natto was recognized as being important for
vascular health and bone health. The limited data available, however, point
towards MK-7 as most potent K-vitamin.

* MK-4 is the form the body creates from plant-source Vitamin K1

This is only partly true. MK-4 is formed out of K-1, but also out of MK-7
and even out of MK-4 itself. Why, how, and where is not known. Therefore, we
cannot draw any conclusions from this. Furthermore, no evidence is available
if the converted MK-4 (out of plant derived K-1) has an effect on bone
health or vascular health. Additionally, if the MK-4 out of the plant
derived K-1 would have an effect, all the data demonstrating that K2 is
better than K-1 would not be true since K-1 also creates MK-4. This is
definitely NOT the case since we find major advantages of K-2 over K-1.

* Vitamin K2 MK-4 is the truly natural form of Vitamin K-2. It is the
form your body uses.

Not true: All forms of vitamin K are used by the body: K-1, and all K-2
vitamins. Moreover, the definition of a vitamin is that it needs to be taken
by the food because the body cannot produce it. The MK-4 we receive is via
the food (at least with the present knowledge we have, nobody knows what the
contribution is of the converted MK-4 out of K-1), and this is via the food
products meat and eggs. The chickens and cows receive the highly toxic
vitamin K3 (menadion, not allowed for human consumption.) and they convert
MK-4 out of this K3. It accumulates in the meat and in the eggs, and this is
the food source of MK-4. As mentioned above, the low range intake of MK-4
has never been investigated, and the contribution to the vitamin K status is
rather questionable.



Further, the only supplemental form of MK-4 is the synthetic Menatetrenone.
Menatetrenone at high doses poses a risk for the general population because
any form of supplemental vitamin K daily at a dose over 100-150mcg will
impact those using the common K-antagonist blood thinning medications,
including coumarin / warfarin. Rather, menaquinone-7 at 45mcg daily is
recommended to optimally activate vitamin K dependent proteins at levels
well below this threshold.

* MK-4 benefits bone strength and protects against cardiovascular
calcification

Yes, this is correct, but only is true for the high doses: 45 mg in humans,
or very high doses in animals. No physiological dose of MK-4 has
demonstrated a beneficial effect on bone health or cardiovascular health
whereas this has been shown for MK-7: the Rotterdam study was mainly based
on 45mcg of the long-chain MKs (MK-7, 8, 9) and also the beneficial effect
of natto (= MK-7) on bone health has been accepted.

* XXX Company's Mk-4 provides a stable Vitamin K2 MK-4 in a protected
beadlet.

True, but not necessary: all K-vitamins are very stable and only degrade in
the UV light or under alkaline conditions.

*******************

http://www.truestarhealth.com/Notes/3260001.html

or

http://tinyurl.com/3oj6k8

[meds that interact with Vit K]





Vitamin K

Also indexed as: Phylloquinone, Phytonadione


Drug Interactions


Certain medicines interact with vitamin K
<http://www.truestarhealth.com/Notes/2932003.html> : Some interactions may
increase the need for vitamin K ( Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif> ), other
interactions may be negative ( Avoid
<http://www.truestarhealth.com/Notes/Images/dnicon_Avoid.gif> ) and indicate
vitamin K should not be taken without first speaking with your physician or
pharmacist, others may require further explanation ( Check
<http://www.truestarhealth.com/Notes/Images/dnicon_Check.gif> ). Refer to
the individual drug article for specific details about an interaction.

Note: The following list only includes the generic or class name of a
medicine. To find a specific brand name, use the Medicines
<http://www.truestarhealth.com/Notes/2411003.html> index.

Aminoglycoside <http://www.truestarhealth.com/Notes/1312007.html>
Antibiotics Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Amoxicillan-Potassium <http://www.truestarhealth.com/Notes/4496006.html>
Clavulanate Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Amoxicillin <http://www.truestarhealth.com/Notes/1315009.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Ampicillin <http://www.truestarhealth.com/Notes/1317001.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Antibiotics <http://www.truestarhealth.com/Notes/1081002.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Anticonvulsants <http://www.truestarhealth.com/Notes/1082009.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Azithromycin <http://www.truestarhealth.com/Notes/1094000.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Bile Acid <http://www.truestarhealth.com/Notes/1322001.html> Sequestrants
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Cephalosporins <http://www.truestarhealth.com/Notes/1344006.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Chlorhexidine <http://www.truestarhealth.com/Notes/1104006.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Ciprofloxacin <http://www.truestarhealth.com/Notes/1109001.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Clarithromycin <http://www.truestarhealth.com/Notes/1113008.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Clindamycin Oral <http://www.truestarhealth.com/Notes/1115001.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Clindamycin Topical <http://www.truestarhealth.com/Notes/1116000.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Colestipol <http://www.truestarhealth.com/Notes/1125006.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Cycloserine <http://www.truestarhealth.com/Notes/1128008.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Dapsone <http://www.truestarhealth.com/Notes/1131009.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Dicloxacillin <http://www.truestarhealth.com/Notes/1351002.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Doxycycline <http://www.truestarhealth.com/Notes/1366004.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Erythromycin <http://www.truestarhealth.com/Notes/1134001.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Gabapentin <http://www.truestarhealth.com/Notes/1390003.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Gentamicin <http://www.truestarhealth.com/Notes/1392006.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Isoniazid <http://www.truestarhealth.com/Notes/1404000.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Levofloxacin <http://www.truestarhealth.com/Notes/1419004.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Loracarbef <http://www.truestarhealth.com/Notes/1426004.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Macrolides <http://www.truestarhealth.com/Notes/1430001.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Mineral Oil <http://www.truestarhealth.com/Notes/1156003.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Minocycline <http://www.truestarhealth.com/Notes/1157007.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Neomycin <http://www.truestarhealth.com/Notes/1442006.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Nitrofurantoin <http://www.truestarhealth.com/Notes/1445008.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Ofloxacin <http://www.truestarhealth.com/Notes/1263005.html> Check
<http://www.truestarhealth.com/Notes/Images/dnicon_Check.gif>

Oral Corticosteroids <http://www.truestarhealth.com/Notes/1346008.html>
Check <http://www.truestarhealth.com/Notes/Images/dnicon_Check.gif>

Penicillin V <http://www.truestarhealth.com/Notes/1454006.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Penicillins <http://www.truestarhealth.com/Notes/1455007.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Phenobarbital <http://www.truestarhealth.com/Notes/1460006.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Quinolones <http://www.truestarhealth.com/Notes/1478001.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Sulfamethoxazole <http://www.truestarhealth.com/Notes/1503009.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Sulfasalazine <http://www.truestarhealth.com/Notes/1504003.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Sulfonamides <http://www.truestarhealth.com/Notes/1505002.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Tetracycline <http://www.truestarhealth.com/Notes/1514007.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Tetracyclines <http://www.truestarhealth.com/Notes/1515008.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Tobramycin <http://www.truestarhealth.com/Notes/1522000.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Trimethoprim <http://www.truestarhealth.com/Notes/1530004.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Trimethoprim/Sulfamethoxazole
<http://www.truestarhealth.com/Notes/1531000.html> Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Valproic Acid <http://www.truestarhealth.com/Notes/1535009.html>
Beneficial
<http://www.truestarhealth.com/Notes/Images/dnicon_Beneficial.gif>

Warfarin <http://www.truestarhealth.com/Notes/1539003.html> Check
<http://www.truestarhealth.com/Notes/Images/dnicon_Check.gif>



*****************

http://www.nutriherb.net/vitamin_K.html

or

http://tinyurl.com/6x49dg






Vitamin K




Also Known as: Phylloquinone, Phytonadione, Menadiol

Vitamin K Facts
Vitamin K is a fat-soluable vitamin that is stored in the liver in minute
amounts. It derives its name from the term "koagulation vitamin" due to its
role in blood clotting. Natural forms of this vitamin come from the
chlorophyll in plants that give them their green color. The body does not
store Vitamin K in large amounts, but deficiences are rare among healthy
individuals.

How Vitamin K Works
Vitamin K helps the body transport calcium, to be utilized for bone
formation and normal blood clotting. It is responsible for setting in motion
the blood clotting process as soon as a wound occurs.

Possible Benefits

*

Reduces hemorrhaging risks and protects against bleeding after
surgery
*

Useful treatment for osteoporosis; decreases risk of fractures
*

Aids normal liver functioning
*

May help with cancer prevention
*

Radiation therapy support
*

Aids vitality and longevity
*

May reduce LDL cholesterol and reduce build-up of arterial plaque
*

May help with excessive menstrual bleeding
*

May reduce LDL cholesterol and reduce build-up of arterial plaque
*

Helpful with morning sickness
*

May aid in Chrohn's disease and Cystic Fibrosis

Usage Guidelines
RDA for Vitamin K is 80 mcg per day. Common dosages found in multivitamins
range from 65 - 80 mcg. Take with meals to enhance absorption. Side effects
are rare.

Some Natural Sources
Spinach, kale, collards, broccoli, swiss chard, turnip greens, spring
onions, brussel sprouts, alfalfa, kelp, liver, soybeans, pistachios, soybean
oil, olive oil, cottonseed oil, canola oil, safflower oil, fish liver oils,
and in lesser amounts - dairy products, fruits, cereals, meats, and eggs

*************

[use of vitamin K + D3 for 2 bone density studies below shows positive
result of this comabo. please note that the low doses mentioned here are
for people whose intestinal arrangement is still in original condition and
would not apple to malabsorptive people]





http://www.druglib.com/abstract/sc/schaafsma-a_eur-j-clin-nutr_20000800.html

or

http://tinyurl.com/6dgjvr




Vitamin D(3) and vitamin K(1) supplementation of Dutch postmenopausal women
with normal and low bone mineral densities: effects on serum
25-hydroxyvitamin D and carboxylated osteocalcin.


Author(s): Schaafsma A, Muskiet FA, Storm H, Hofstede GJ, Pakan I, Van der
Veer E

Affiliation(s): Department of Research & Development Leeuwarden, Friesland
Coberco Dairy Foods, Leeuwarden, The Netherlands. [email protected]

Publication date & source: 2000-08, Eur J Clin Nutr., 54(8):626-31.

Publication type: Clinical Trial; Randomized Controlled Trial

OBJECTIVE: Improvement of vitamin D and K status of about 60 -y-old
postmenopausal Dutch women. DESIGN: In a randomized study postmenopausal
women with normal (T-score >-1; n=96) and low (T-score< or =-1; n=45) bone
mineral density (BMD) of the lumbar spine, were supplemented with 350-400 IU
vitamin D(3), 80 microg vitamins K(1) vitamins K(1)+D(3), or placebo for 1
y. Serum 25-hydroxyvitamin D [25(OH)D] and percentage carboxylated
osteocalcin (%carbOC) were measured at baseline and after 3, 6 and 12
months. RESULTS: Baseline %carbOC of the entire study population was
positively correlated with BMD of the lumbar spine and femoral neck.
Correspondingly, women with low BMD had lower %carbOC at baseline than women
with normal BMD but this difference disappeared after 1 y of supplementation
with vitamin K(1) ((mean+/-s.d.) 68+/-11% (95% CI, 64. 5-71.2%) vs 72+/-6%
(95% CI, 70.1-72.9%), respectively). One year of supplementation with
vitamin D(3) showed maximum increases in 25(OH)D of 33+/-29% (95% CI,
24.8-41.8%) and 68+/-58% (95% CI, 50.1-84.6%) in women with normal and low
BMD, respectively. During winter, however, a 29% decline in maximum 25(OH)D
levels was not prevented in women with low BMD. CONCLUSION: Daily
supplementation of Dutch postmenopausal women with >400 IU vitamin D(3) is
indicated to prevent a winter decline in 25(OH)D and to control serum
parathyroid hormone levels. Daily supplementation with 80 microg vitamin
K(1) seems to be necessary to reach premenopausal %carbOC levels. A
stimulatory effect of calcium and/or vitamin D on %carbOC cannot be
excluded. European Journal of Clinical Nutrition (2000) 54, 626-631.

***************



[specifically K2 in this study]



http://www.druglib.com/abstract/ad/adams-j_am-j-health-syst-pharm_20050801.h
tml

or



http://tinyurl.com/5z2bcx





Vitamin K in the treatment and prevention of osteoporosis and arterial
calcification.


Author(s): Adams J, Pepping J

Affiliation(s): Castle Medical Center, Kailua, HI 96814, USA.

Publication date & source: 2005-08-01, Am J Health Syst Pharm.,
62(15):1574-81.

Publication type: Review

PURPOSE: The role of vitamin K in the prevention and treatment of
osteoporosis and arterial calcification is examined. SUMMARY: Vitamin K is
essential for the activation of vitamin K-dependent proteins, which are
involved not only in blood coagulation but in bone metabolism and the
inhibition of arterial calcification. In humans, vitamin K is primarily a
cofactor in the enzymatic reaction that converts glutamate residues into
gamma-carboxyglutamate residues in vitamin K-dependent proteins. Numerous
studies have demonstrated the importance of vitamin K in bone health. The
results of recent studies have suggested that concurrent use of menaquinone
and vitamin D may substantially reduce bone loss. Menaquinone was also found
to have a synergistic effect when administered with hormone therapy. Several
epidemiologic and intervention studies have found that vitamin K deficiency
causes reductions in bone mineral density and increases the risk of
fractures. Arterial calcification is an active, cell-controlled process that
shares many similarities with bone metabolism. Concurrent arterial
calcification and osteoporosis have been called the "calcification paradox"
and occur frequently in postmenopausal women. The results of two
dose-response studies have indicated that the amount of vitamin K needed for
optimal gamma-carboxylation of osteocalcin is significantly higher than what
is provided through diet alone and that current dosage recommendations
should be increased to optimize bone mineralization. Few adverse effects
have been reported from oral vitamin K. CONCLUSION: Phytonadione and
menaquinone may be effective for the prevention and treatment of
osteoporosis and arterial calcification.

*************

http://www.nowfoods.com/?action=itemdetail
<http://www.nowfoods.com/?action=itemdetail&item_id=73282> &item_id=73282

or

http://tinyurl.com/5av34r






Vitamin K1, Phytonadione




By Nilesh Patel, NOW Quality Assurance Dept.

Vitamins are, by definition, essential for human growth and health. They are
usually found in the foods we eat. Vitamin K is necessary for normal
clotting of the blood. Although Vitamin K deficiencies are rare, they can
lead to problems with blood clotting and excessive bleeding.

Fat-soluble vitamins [for example: Vitamin A (trans-Retinol), Vitamin D
(Calciol), Vitamin E (á-tocopherol), and Vitamin K (Phylloquinone)] are all
polyprenyl compounds (similar to steroids) synthesized from a five-carbon
molecule (isoprene). Phylloquinone (C31H46O2), the most common form of
Vitamin K, is found in plants as a photosynthetic electron carrier (mostly
isolated from alfalfa, commercially), and is the preparation of choice
marketed under the generic name of phytonadione. In other words,
Phylloquinone is also called phytonadione; both terms refer to the
fat-soluble natural Vitamin K (Vitamin K1) used for nutritional
supplementation.

(Technical note: The term Vitamin K refers to a group of
2-methyl-1,4-napthoquinone derivatives which can fulfill an essential
co-factor function in humans, aiding in the biosynthesis of a number of
calcium-binding proteins, some of which are essential for homeostasis
(normal biological equilibrium). The natural forms are substituted in
position 3 with an alkyl side chain. Vitamin K1 (phylloquinone) has a phytyl
side chain in position 3, where as Vitamin K­2 has an isoprenyl side chain
at position 3.)

Vitamin K is essential since the 1,4-napthoquinone compound cannot be
synthesized in the body. In nature, Vitamin ****urs as phylloquinone in
plants and as menaquinones produced by bacteria, another significant source.
There are three notable forms of Vitamin K:

K1 (phytonadione/ phylloquinone/ phytonactone);

K2 (menaquinones), which can be formed naturally by the bacteria in the
intestines (note: K1 is converted to K2 in the body); and

K3 (menadione), which is the most active of the synthetic forms of Vitamin K
and is a water-soluble vitamin not used as a prophylaxis (preventative
vitamin) because of its potential to cause hemolytic anemia with jaundice.

Absorption of K1 is from the gut (duodenum and jejunum) via the lymphatic
system. Thus, conditions that impair the fat absorption will also affect the
absorption of Vitamin K. Antibiotics destroy the beneficial bacteria in the
intestine needed for Vitamin K synthesis. All forms of Vitamin K have a
common basic structure that acts as a cofactor for the enzymes essential for
normal blood clotting, namely, in forming the blood clotting chemical
prothrombin (Factor II).

In the liver, Vitamin K plays an important role in the actions of
coagulation (blood clotting) factors [Proconvertin (Factor VII),
Stuart-Power factor (Factor X), & Christmas factor (Factor IX)]. The
following are also dependent on Vitamin K: protein C, protein S, and protein
Z, along with anti-coagulants proteins C, S, and Z. Phytonadione (K1) is an
analogue of Vitamin K, but it has the quickest onset of action, the most
prolonged duration, and is the most potent of all the Vitamin K forms. K1 is
safer than menadione (K3) to use on newborns. Vitamin K3 is the only form
that could cause toxicity, causing hemolytic anemia (due to dying red blood
cells), causing jaundice, liver damage and severe neurological damage.

Natural Vitamin K is required for two bone matrix proteins: osteocalcin and
matrix-Gla (gamma carboxyglutamic acid). Gla is an amino acid that is part
of certain proteins that control calcium. Vitamin K is shown to be
beneficial in bone health because it helps to produce the natural protein
osteocalcin. Vitamin K adds carboxyl groups to osteocalcin and other
proteins that build and maintain bones by binding to ("chelating") calcium.
This is a self-limiting process (similar to hydroxylation of collagen by
Vitamin C). Calcium needs these proteins to crystallize and strengthen bone
tissue. Vitamin K has been approved for the treatment of osteoporosis in
Japan. Thus, Vitamin K is required for proper bone formation and blood
clotting. In both cases, Vitamin K accomplishes the job by assisting the
body in transporting calcium*.

Green leafy vegetables (spinach, kale, parsley, cilantro, and broccoli) and
certain vegetable oils (soybean oil, olive oil, cottonseed oil and canola
oil) are good food sources of Vitamin K1. Hydrogenation of oils produces a
biologically non-active form of Vitamin K called dihydrophylloquinone. The
RDA for Vitamin K ranges from about 65mcg for adult females to 80mcg for
adult males, per day.

Deficiency symptoms of Vitamin K manifest as decreased clotting, nosebleeds,
increased blood pressure, hemorrhages, and diarrhea.

Precautions: Vitamin K should not be taken without prior medical
consultation if pregnancy is suspected or if one is breast-feeding.
Antibiotics and certain steroidal preparations may deplete or interfere with
Vitamin K. Blood-thinning medications like warfarin and dicumarol will
adversely interact with Vitamin K. Vitamin K inhibitors include: x-rays,
radiation, aspirin, mineral oil, and laxatives. High amounts of Vitamins A
and E can actually block Vitamin K, necessitating supplementation to
compensate.

Selected References:

1 http://www.drugs.com/enc/congenital_protein_c_or_s_deficiency.html

2 http://www.cdc.gov/genomics/info/reports/research/protein_c.html

3 J P Hanley Warfarin Reversal, Journal of Clinical Pathology
2004;57:1132-1139

4 http://www.nlm.nih.gov/medlineplus/druginfo/medmaster/a682659.html

5 Raj G, et al. Time course of reversal of anticoagulant effect of warfarin
by intravenous and subcutaneous phytonadione. Arch Intern Med December
13/27, 1999;159: 2721-4

6 Kodaka K, Ujiie T, Ueno T, Saito M. Contents of Vitamin K1 and
chlorophyll in green vegetables. J Jpn Soc Nutr Food Sci 1986;39:124-6

7 Food and Nutrition Board, National Research Council. Recommended Dietary
Allowances, 10th ed. Washington, DC: National Academy Press, 1989

8 Booth SL, Suttie JW. Dietary intake and adequacy of Vitamin K. J Nutr
2000;130 (1S Suppl):785-8

9 http://my.webmd.com/drugs/drug-726-Vitamin+K+Oral.aspx?drugid=726
<http://my.webmd.com/drugs/drug-726-Vitamin+K+Oral.aspx?drugid=726&drugname=
Vitamin+K+Oral> &drugname=Vitamin+K+Oral


10 http://www.merck.com/product/usa/pi_circulars/m/mephyton/mephyton_pi.pdf

*These statements have not been evaluated by the FDA. This product is not
intended to diagnose, treat, cure or prevent any disease. All information
is given for educational purposes ONLY and should not replace the advice of
a physician.

*******
None of this is to be construed as medical advice, and taking or changing of
any supplements should be discussed with your medical professional.
<http://www.druglib.com/druginfo/aquamephyton/abstracts/>

With all that info Michelle, it looks like I should add K2, 50 mcg, 1 or 2 a day, to my vitamin order list. Whew! A lot to take in. Thanx as always for your expertise.
Karen

I should say that I'm not on as firm a footing with K. Much more conversant in vit D, for example. But I suspect that there is a lot to know that we NEED to know. but we don't. Yet.

Wow!!! I am so glad that i take the K2 every day Michelle!! Thanks for all the great info as usual!! happy holidays Vitalady!!

Yorkie xx

How are you doing Nikki. I know it must be tough for you to bear, but know you are in my thoughts. Is your mum with you yet?

Hi Karen, I am doing as best I can under the cir****tances ya know?? The holidays are pretty tough, but I am holding up. My Mom is here with me til 30th Dec and then she has to go home as she has a business to run in the UK. She plans to come out and visit agin in Feb which will be nice for me.
I am trying to sell the business but it is not easy, once that happens, I can concentrate on getting on with my life KWIM?
anyhow, you look after yourself andhave a great holiday okay??
lots of love
Yorkie xx

Many thanks.  I booked marked this.   I've been taking about 300mcg or more of K2 for around 6 months.  I'm still alive.  :)  

I think the Vitamin Ks are interesting.

Thank you for all the info!!

 
*Bump* for anyone like me who is having trouble with osteocalcin and whatever else.  I got some crazy blood work back recently and had to do some research.   I'm totally freaking out, but glad for the expertise of Vitalady, Major Mom and others.

My new year's resolution is to take my vitamins and stay on my bloodwork.  I have been, but still...