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peakk2

Peak K2, vitamin K2 analysis, vitamin K2 and osteoporosis

PEAK
K2 - MENATETRANONE - THE "K2" THAT WORKS FOR BONES, HEART AND BRAIN

AUTHORED
BY MICHAEL RAE, RESEARCHER

 

ADVANCES in orthomolecular
research Vitamin K may be the most misunderstood vitamin in the world.

In 1929, the Danish nutritional
scientist Dr. Henrik Dam found that feeding chicks a totally fat-free diet caused
uncontrolled bleeding under their skin. Dr. Dam quickly discovered the reason
for this disturbing effect: the diet was missing a previously unknown fat-soluble
nutrient, which he appropriately named “koagulationsvitamin” –
literally, the “clotting vitamin.” The English name for the new
vitamin was taken from Dr. Dam’s Danish: “K,” for “Koagulation.”

And for over fifty years,
nearly everyone thought that the vitamin K story began and ended with blood
clotting. If doctors paid attention to it at all, it was only to make sure that
it didn’t interfere with the blood-thinning drug warfarin (Coumadin®).
But even as nutrition textbooks and mainstream medicine continued to think of
vitamin K as a one-act show, a paradigm shift had been forced onto researchers
in the late 1970s, when new vitamin K-dependent proteins associated with bone-building
osteoblast cells were discovered.

Yet as late as 1990, a
Canadian government report was still trotting out the old “ ‘K’
for ‘koagulation’ ” view of vitamin K. While noting that “a
number of non-clotting proteins” which needed vitamin K for their activation
“have been found in bone, skin, kidney, atherosclerotic plaque, lung,
spleen, placenta, and reproductive organs,” the nutrition panel quickly
shoved this evidence into a corner with the off-hand comment that the “physiological
significance and biochemical functions of these non-clotting proteins have yet
to be determined.”1

Another anomaly mentioned
in passing in the report was the fact that – except in the liver –
humans don’t use much of the vitamin K in our diet “as is.”
Instead, we biochemically convert the common plant form of the vitamin (phylloquinone,
or vitamin K1) into a different vitamin K molecule: Menatetrenone, or MK-4 (see
Figure 1). Menatetrenone is a member of a distinct family of vitamin K molecules
called the menaquinones, or vitamin K2. There are many K2 vitamins made by bacteria,
but humans and other animals specifically make Menatetrenone in our tissues,
using K1 as a raw material.

You’d think that
these facts would rouse Health Canada’s committee from its slumber and
cause them to ask some obvious questions. Why does the body need all of those
mysterious vitamin K-dependent proteins? Why are they found scattered in such
a wide range of tissues – tissues which have such disparate functions?
And above all, why does the body convert so much of its phylloquinone into Menatetrenone,
when plain old phylloquinone does a much better job of maintaining normal blood
clotting?2,3

But instead of grappling
with these enigmas, these government nutrition “experts” chose instead
to ignore them. The rest of their discussion of vitamin K is devoted to prothrombin
times, blood-thinning drugs, and the risks of hemorrhagic disease in newborns.
The report contains no call for answers to the Menatetrenone mystery.

In the ten years since
Health Canada promulgated its curiously un-curious report, research into vitamin
K – and especially Menatetrenone – has been accelerating, as revolutionary
discoveries surrounding the vitamin’s critical role in protecting you
from osteoporosis, arteriosclerosis, and perhaps Alzheimer’s disease have
been made. Science has suddenly moved Menatetrenone from being an obscure form
of a boring “blood-clotting factor” to being an orthomolecule of
crucial importance to your health and well-being.

So why have you
never heard of it?

Well, the odds are that
you have heard some of the most important news about Menatetrenone. You just
haven’t recognized what you were seeing. If you’ve caught any recent
magazine articles or books on the role of nutrition in bone health, you may
remember reading that the Japanese are now using “vitamin K,” not
just to prevent osteoporosis, but as an officially-approved treatment for the
disease. But what the people writing these articles don’t seem to realize
is that the “vitamin K” that’s prescribed as an osteoporosis-fighting
“drug” in Japan is not phylloquinone, but Menatetrenone. (Fig. 1)To
understand why the Japanese are using Menatetrenone – and not the common,
cheaper K1 form of the vitamin – to shield the bones of women and men
at risk of crippling fractures, we’ll have to look at a little history.

 

The 1975 discovery of Bone
Gla Protein (BGP – or “ osteocalcin” as it’s sometimes
called) marked a dramatic twist in the plot of the vitamin K story. While it
wasn’t clear exactly what the new protein’s function was, it was
clear from the get-go that BGP was somehow involved in the mineralization of
bone. But it was quickly discovered that BGP can only do its job after it’s
been “activated” through a biochemical reaction called gamma-carboxylation.
Through gamma-carboxylation, the residues of the amino acid glutamine in BGP
are modified in a way that allows them to bind calcium. Without this calcium-binding
capacity, BGP is inactive.

And what nutritional factor
is needed for the gamma-carboxylation of BGP and other proteins? You guessed
it: vitamin K. And in fact, gamma-carboxylation of another protein (prothrombin)
also explained the biochemical basis for vitamin K’s involvement in blood
clotting. Once this role was discovered, however, the scientific community again
put artificial limits on the scope of vitamin K’s activity in the body:
it came to be believed that vitamin K’s biochemical actions could be explained
entirely through its role in gamma-carboxylation of proteins.

All of this got researchers
thinking. Without vitamin K, there would be no “activation” of BGP.
Without “activation,” BGP would not be able to do its bone-mineralizing
job. So might decades of low vitamin K intake lead to suboptimal mineralization,
weak bones, and osteoporosis?

Scientists went looking
for a link. And they found one. You’ll probably have heard about the studies
showing that women who get more phylloquinone in their diets have a lower risk
of suffering a fracture.4,5 Likewise, in an early study,6 levels of vitamin
K1 were found to be significantly lower in the serum of women with osteoporosis
than in women who were free of the disease. A role for vitamin K in bone health
seemed to be clear.

But some of the science
didn’t seem to mesh with the vitamin K/bone health connection. For instance,
if “activation” of BGP through gamma-carboxylation were so vital
to bone health, then you’d expect that taking warfarin (Coumadin®)
– a “blood-thinning” drug that works by blocking gamma-carboxylation
– would increase your risk of breaking a bone. But when this idea was
put to the test, the results were murky. One study found that the use of these
drugs increased the risk of a spine or rib fracture – but not the risk
of a fractured hip, or of any other kind of fracture.7

And another study found
that women taking such drugs were at no greater risk than women not taking them.8
In fact, when growing animals are given warfarin at doses so ridiculously high
that all BGP became under“activated,” there were no resulting changes
in bone mineral density, bone strength, or markers of bone metabolism.9

 

Another sticking
point: if the “activation” of BGP gave bone-protective powers to
vitamin K, then you’d expect that the body would use both forms of vitamin
K equally, since K2 is actually inferior to K1 at gamma-carboxylation of proteins
(see Figure 4).2,10,11 But instead, the body selectively concentrates Menatetrenone
in bone tissue. In fact, even when the diet contains no K2, but is adequate
in K1, bone tissue contains over twice as much menatetrenone as phylloquinone
– despite the fact that there is nearly fifteen times as much K1 as K2
circulating in the serum under these conditions!12 And when animals are actually
fed Menatetrenone itself, it quickly begins to accumulate specifically in bone
tissue – and the highest concentrations of Menatetrenone are found in
areas which are being actively remodeled.13

 

It’s just these kinds
of anomalies that forced researchers to ask a more fundamental question –
the question that the Canadian government’s 1990 nutrition panel was unwilling
to pose and unable to answer. If gamma-carboxylation is the only use for vitamin
K in the body, then why do our bodies go to the trouble of converting phylloquinone
into Menatetrenone in the first place? The situation is especially puzzling
in the heart: when you first re-feed phylloquinone to a mammal after depriving
it of vitamin K for long enough to create dangerous bleeding problems, Menatetrenone
is immediately synthesized, and accumulates more quickly in the heart than anywhere
else in the body14 – despite the fact that the heart has no gamma-carboxylase
activity!2,15-17

Acting on hints that Menatetrenone
might be the preferred form of vitamin K in mammals, researchers decided to
find out if there were any differences in the amounts of K1 and K2 in the plasma
of men and women with spinal and hip fractures.18 As you might expect, levels
of K1 and K2 were both lower in the people with fractures than in fracture-free
folk. But what was really revealing about this study was the fact that the fracture
victims’ levels of K2 were found to be over three times more depressed
than their levels of K1.

In a similar study conducted
in Japan,19 women with spinal fractures were found to have only half as much
K2 in their serums as women without fractures – yet the two groups’
levels of K1 were the same.

Purchase Peak K2 (Vitamin
K2) Here
peak k2 -menatetranone

 

Look to the East:

Several other studies confirmed
that people with low serum levels of vitamin K2 have lower bone mass20,21 and
are more likely to have fractured bones22,23 than people with higher levels.
But if Menatetrenone has a special place in bone health, then you’d also
expect to see the same connections with the amount of K2 in a person’s
diet. Unfortunately, it’s hard to test this idea in the West, because
our diets contain so little Menatetrenone. Ounce-for-ounce, the best sources
are goose liver, butter, egg yolks, and fattier Emmental cheeses.24 And even
these foods provide only tiny quantities of this crucial orthomolecule, especially
granted how little of them we eat at a time. A 100 gram serving of cooked broccoli,
for instance, contains 113 micrograms of K1 – but even if you slather
it with a full tablespoon of butter, you’re only getting 2.1 micrograms
of K2.

The result is that almost
no one in the West gets a diet that’s very high in Menatetrenone, making
it hard to compare the impact on bone health provided by high- versus low-Menatetrenone
diets. But the situation is different in Japan. By an accident of cultural history,
people in eastern regions of Japan typically get a lot more of one kind of K2
(menaquinone-7) in their diets than do people in Japan’s more western
areas – and the Japanese as a whole tend to eat diets richer in K2 than
do Westerners. That’s because, along with rice, pickles, seaweed, and
grilled fish, a traditional eastern Japanese meal will often contain a fermented
soy condiment called natto – the richest known food source of this form
of the vitamin.24 So Japan is the perfect place to look for connections between
K2 in the diet and bone health.

When scientists compared
the average consumption of natto in different prefectures (provinces) of Japan
with the fracture rates in those prefectures, they found that the hip fracture
rates among women living in areas where more K2-rich natto is consumed were
consistently lower than were the rates among women living in areas where natto
consumption is lower.23 And when researchers reanalyzed the data from two previous
national dietary studies,25,26they confirmed the same association: where women
ate more K2 (in natto), there were fewer fractures.

But the investigators weren’t
satisfied with this. How could they be sure that it was the K2 that was providing
the fracture-fighting advantage? Might not some other component of natto –
say, the estrogen-like isoflavones – be responsible for the protective
effect?

Fortunately, there was an
easy way to settle the issue. Natto is, after all, just fermented soy beans.
And the Japanese eat many other soy foods, such as tofu, miso, fried bean curd,
and even soy sauce – soy foods with negligible K2 content. If something
in natto other than vitamin K2 were the key to its association with low fracture
risk, then the consumption of these other soy foods would be expected to provide
the same fracture-fighting benefit that natto does. But when the investigators
tested this idea, they found that consumption of other soy foods was not significantly
related to the regional differences in fracture risk. K2-rich natto was the
only soy food whose consumption was associated with a low risk of fracture.23

The scientists then took
the final step: they directly tested the levels of different K vitamins in the
serum of women in Tokyo (where fracture incidence is low) and in Hiroshima (where
fractures are more common). And now the results seemed indisputable. As a group,
women from low-fracture-incidence Tokyo had higher serum levels of K2 than did
women from high-risk Hiroshima. And just as revealingly, there was no significant
difference in their levels of K1.23

In fact, the same pattern
seems to hold internationally. While serum K1 levels vary only slightly between
women from the Japan and the UK, Japanese women’s levels of K2 are many
times higher than those of their British counterparts.23 That may explain why
Japanese women, taken as a whole, have much lower rates of osteoporosis than
Western women, despite their lower intake of such important bone-building nutrients
as calcium and vitamin D.

What's the Diff??

All of this evidence suggests
that K2 plays some unique role in maintaining bone health – a role not
shared by K1. And indeed, Japanese scientists have spent the last two decades
comparing the effects of the two forms of the vitamin on bone metabolism, and
have found that Menatetrenone has multiple bone-protective mechanisms that phylloquinone
simply lacks.

One of the first such discoveries
was the fact that Menatetrenone can prevent the loss of calcium from bone tissue
caused by prostaglandin E2 (PGE2), an inflammatory eicosanoid (local cellular
messenger-molecule) known to cause the resorption (breakdown) of bone.27,28
Yet the same concentration of K1 provides no protection.28 In another study,29
scientists were able to show that K2’s ability to defend bone tissue against
PGE2 is even stronger: in addition to blocking the negative impact of the eicosanoid
once it has been formed, Menatetrenone also cuts down on the bone cells’
formation of PGE2 in the first place.

Scientists have also compared
K1 and K2 for their effects on osteoclasts (the cells that tear down bone).
Osteoclasts, like other cell types, begin their lives as stem cells: early,
simple cells which have the potential to grow up into many different kinds of
cells, depending on the growth factors and other signals to which they are exposed.
These researchers have found that Menatetrenone is able to reduce the creation
of osteoclasts from these early, simple cell types – but again, phylloquinone
has no such power.28

In another study, researchers
again confirmed the ability of K2 – but not K1 – to prevent osteoclast
formation, this time using a different type of forerunner cell.30 In the process,
they also showed that a specific gene ([ODF]/RANK) which encourages these cells
to develop into osteoclasts is turned off by K2.30 And in further research,31
scientists demonstrated that Menatetrenone, but not phylloquinone, actually
increases the programmed cell death (“apoptosis”) of existing osteoclasts.

These effects aren’t
just test-tube results: they happen in living, breathing mammals given extra
Menatetrenone. When animals are injected with the growth factor macrophage colony-stimulating
factor (M-CSF), osteoclast formation skyrockets, reaching a bone-ravaging peak
about five days after the injection and then slowly returning to numbers which
are closer to normal: by 20 days after the injection, the animals “only”
have about a third as many excess osteoclasts as they did at the five day maximum.
But if, one day before the growth factor is injected, these animals are given
high-dose K2, Menatetrenone prevents 85% of the excess osteoclast formation
– and there are no excess osteoclasts remaining by day 20.32 The study
demonstrates that K2 both prevents most of the excess osteoclasts from being
formed, and accelerates their programmed demise.

In addition to protecting
the body against an excess number and activity of osteoclasts, studies also
show that Menatetrenone strengthens the bone-building legions of the osteoblasts.
Menatetrenone cranks up levels of a chemical marker of osteoblast maturation,30
protects osteoblasts from being pushed into cellular suicide by substances that
trigger it,33 and reduces the expression of genes involved in the cellular suicide
process.33 On top of this, K2 increases levels of DNA in osteoblasts, suggesting
that it may stimulate the creation of new osteoblast cells.34

Beyond its ability to support
higher numbers of osteoblast cells, Menatetrenone also enhances each osteoblast’s
bone-building activity. For instance, it has been found that, in addition to
“activating” the mineralizing protein BGP, K2 also increases the
amount of this protein in the osteoblast matrix.34,35 K2 also boosts levels
of alkaline phosphatase (a marker of osteoblastic metabolism and bone formation)
and of new protein.35 Interestingly, drugs which block the cell’s ability
to make new protein also interfere with some of these effects,35 suggesting
that part of K2’s unique support for bone health may lie in stimulating
the synthesis of key proteins.

While Menatetrenone’s
effects on osteoblasts are only mild compared to those recently found hidden
in the mineral Strontium (see “Strontium: The First Bone Builder”
in this special issue of Advances), this research suggests that supporting the
health of bone-building cells is at least part of the reason for Menatetrenone’s
protective effects on bone.

For more on the molecular
basis for the superior bone-building potency of Menatetrenone compared with
phylloquinone, see the page, “For Biochemistry Geeks Only.”

“K”
is for “Klinical”

By now you have a pretty
good idea of what first got Japanese scientists thinking about using Menatetrenone
– and not phylloquinone – as a treatment for osteoporosis. Before
performing clinical trials in humans, however, they first wanted to test the
effects of Menatetrenone on animal models of osteoporosis. The results have
been very encouraging: these studies have consistently found that K2 can increase
the strength, improve the structure, and boost the mineral content of bone in
animal models of menopausal osteoporosis,41-47as well as protecting their bone
health against the effects of calcium deficiency48 and of bone-wasting drugs
like cortisol 49 and phenytoin.50

All of this is good science
– but none of it is the “gold standard” of the randomized,
double-blind, controlled clinical trial. Fortunately, Japanese researchers have
moved on from preliminary research to this higher level. Over the course of
the last decade, at least sixteen clinical trials have been performed using
Menatetrenone, and every single one has found that K2 supplements protect bone
health.51- 66 Menatetrenone not only slows, halts, or even reverses loss of
bone mass: it dramatically reduces your risk of suffering a fracture.

 

The bone-building power
of Menatetrenone has been proven in women suffering with menopausal osteoporosis,52,55,56,58,61,62,65,66
and also in the similar case of younger women taking leuprolide,60 a drug used
to treat disorders like endometriosis which are triggered by excess estrogen,
and which works by blocking the release of sex hormones (and thereby mimicking
menopause’s negative effects on the bones). Additionally, however, Menatetrenone
has proven its ability to protect against bone loss caused by cirrhosis of the
liver,51,54 immobility (such as long-term confinement to bed or a wheelchair),59,63,64
and cortisol drugs.53,57 And although it wasn’t a true controlled clinical
trial, there’s even a case report of Menatetrenone (combined with vitamin
D) fighting the osteoporosis that followed graft-versus-host disease resulting
from a bone marrow transplant.67

For instance, in a recent
double-blind, placebo-controlled trial,62 eighty women with osteoporosis took
either a megadose Menatetrenone supplement (90 milligrams – twice the
dose used in most clinical trials), or a lookalike pill with no effect on bone
health, for 24 weeks. At the end of the study, women who took the Menatetrenone
supplement increased their bone mineral density by an impressive 2.2%, even
as the women taking the dummy pill lost 7.31% of their bone density. (Fig. 2)

 

Even more exciting results
came from a later trial in which the power of Menatetrenone was put to the test
in a direct comparison against both the bisphosphonate drug etidronate (Didrocal®)
and a plain calcium supplement.52 A group of 75 menopausal, osteoporotic women
were first given help to improve their diets, ensuring that they got at least
800 milligrams of calcium and 400 IU of vitamin D a day from food sources. (This
amount of calcium would not be enough for most Westerners, but it meets the
needs of Japanese women, because of their shorter stature and lower body mass:
the average woman in this study weighed just 100 pounds).

Then the women were divided
into three groups. One group took a 45 milligram Menatetrenone supplement every
day; a second group took the drug, following the on again/off again cycle that
is standard with bisphosphonates; and a third group of women took a daily low-dose
(260 milligram) calcium supplement.

Despite an adequate calcium
and vitamin D intake, the women receiving only the calcium supplement lost 1.7%
of their bone mineral density (BMD) over the course of the two-year trial. In
the group taking etidronate, by contrast, BMD increased by 2.1%. Meanwhile,
the women in the Menatetrenone group held steady: over the course of two years,
no significant change in BMD occurred.

Now we come to another surprise
– a new twist in the vitamin K research. If all you had to go by was the
bone mineral density numbers, you’d think that Menatetrenone would provide
less anti-fracture protection than the drug. But instead, Menatetrenone proved
to be just as effective at reducing fractures as etidronate, slashing women’s
odds of breaking a bone by about two thirds as compared to women taking the
calcium supplement! See Figure 2. These results closely parallel the findings
of a third trial involving 241 osteoporotic women,58 in which women taking Menatetrenone
supplements sustained nearly no bone loss over two years (a reduction of 0.5%
in bone mineral density, versus a 3.3% reduction in the control group), while
cutting fracture risk by 64% as compared with non-supplementing women. In an
extension of this trial,68 women have continued to benefit from this dramatic
bone-shielding effect through an additional year of testing.

Once again, Menatetrenone
presented researchers with a mystery – a paradox. How can Menatetrenone
cut fracture risk as effectively as drugs whose effects on bone mineral density
are much more marked? Answers have not been long in coming. As it turns out,
the most important bone-shielding power of Menatetrenone is not its capacity
to preserve the quantity of bone, but its ability to improve bone quality.

Quantity vs. Quality

Bone mineral density (BMD)
is a measure of the amount of calcium and other minerals in a given amount of
bone, and it tells you something about the quantity and rigidity of bone tissue.
But when it comes to predicting your risk of actually suffering a fracture,
bone mineral density doesn’t tell you the whole story. That’s because
the ability of bone to resist breakage is also strongly determined by bone quality:71
the structural soundness of the living tissue.

We tend to think of bone
as being a solid mass, like steel girders or stone columns. But bone is actually
a complex honeycomb, composed of an interpenetrating network of plates woven
together by rods of tissue (see Figure 3a). This is especially true of trabecular
bone, the mineralized, regularly-ordered bone type found at the end of long
bones. The integrity of this network – its “connectivity”
– is a major contributor to the overall architecture of bone, and to the
bone’s ability to withstand fracture. So even if you have a high bone
mineral density, your bones can still be easily broken if weak structure –
poor bone quality – makes them brittle.

vitamin k2 and osteoporosis

Along with loss of bone
mineral density, osteoporosis causes the deterioration of bone connectivity
– especially in trabecular bone (see Figure 3b). In fact, loss of bone
connectivity is the most dangerous part of the disease process, and is also
the most difficult to restore.72 Simply increasing BMD does nothing to re-establish
the architectural integrity of the bone. As a result, the National Institutes
of Health and other scientific bodies now define osteoporosis in terms of the
overall fragility of the bone – whether this fragility is due to lower
bone mineral density, or lower bone quality, or both. A recent consensus conference
therefore defined osteoporosis as “a disease characterized by low bone
mass and microarchitectural deterioration of bone tissue, leading to enhanced
bone fragility and a consequent increase in fracture risk”73 – a
definition now used in standard osteoporosis textbooks74 and by the Merck manual.

The problem is that restoring
BMD doesn’t necessarily restore bone quality. The most extreme example
of this is the effects of fluoride on the skeletal system. It’s long been
known that fluoride drugs can increase the mineral content in bone, because
fluoride is absorbed into the bone structure in basically the same way that
calcium is. But while fluoride can increase bone mineral density, it can actually
degrade the quality of bone75,76 because the incorporation of fluoride into
the bone mineral crystals warps their structure. As a result, fluoride drugs
don’t actually reduce a woman’s risk of broken bones.77 In fact,
some trials have even found that a woman who takes fluoride drugs actually increases
her fracture risk,78,79 especially if she hasn’t already suffered a broken
bone before she starts taking the drug! Some scientists believe that newer fluoride
drugs may limit these problems, but whether these revised versions are either
effective or safe is still an unresolved question 80, and the quality-versus-quantity
tradeoff will continue to be a concern. To this day, no fluoride drug has ever
been approved for use in the United States, although Canada allows the sale
of the fluoride drug Fluotic.®

Even the widely-hailed bisphosphonate
drugs like alendronate (Fosamax®), etidronate (Didrocal®) and risedronate
(Actonel®) appear to increase BMD at the cost of bone quality, because they
reduce the activity of osteoclasts (the cells that tear down old bone), without
having any effect on osteoblasts (the cells that build up new bone). Because
old bone is not torn down as quickly, but the bone-building osteoblasts continues,
the total mass of bone slowly increases. But by allowing old bone tissue to
hang around longer without speeding its replacement, bisphosphonate use results
in bone tissue that is, on average, older – and thus, of poorer quality.
Because this older bone tends to be more brittle, the overall architectural
quality of the bone is decreased.71,81,82

For women whose bone mineral
density is very low, and whose bone connectivity has already decayed, bisphosphonates
clearly reduce the odds of a fracture. For these women, a slight decrease in
quality is a small price to pay for a considerable increase in bone quantity.
But recent clinical trials suggest that the same can’t be said for women
who have osteopenia – that is, who have lost significant (but not extreme)
amounts of bone mineral density, but who haven’t yet suffered a fracture.
Such women’s bone structure is usually still intact, and the decay of
this quality appears to neutralize the benefits of an increased BMD numbers.

There was no clear anti-fracture
benefit from taking Fosamax® in a trial involving such women.83 Their rate
of hip fractures was apparently reduced by 21%, but their risk of suffering
a wrist fracture risk actually appeared to increase by 19% – and neither
result was strong enough to rule out a statistical fluke. As was emphasized
in an editorial in the Journal of the American Medical Association, “the
antifracture benefit of bisphosphanates in women with low bone mass but without
prevalent fracture must be judged to be small.”84

Unfortunately, all of the
mainstream drug treatments for osteoporosis – including hormone replacement
therapy, selective estrogen receptor modulators (SERMs, such as raloxifene (Evista®)),
or calcitonin (Calcimar ® or Miacalcin ®) and even calcium and vitamin
D85 – share this problem to one extent or another: they slow down the
resorption of bone, but don’t support the formation of new bone mass.86
Fluoride is a pseudo-exception: it directly increases the formation of new bone
mineral crystals – but those crystals are of inferior quality. So the
integrity of the architecture of your skeleton continues to degrade.

A “fantasy molecule”
for bone health, then, would be a safe, natural substance which would address
both sides of the osteoporosis coin: quantity and quality. It would maintain
or increase bone mass, but would also improve the structural integrity of the
bone tissue itself.

It turns out that this molecule
isn’t a fantasy at all. It manifests in reality as Menatetrenone.

‘K’
is for ‘Kwality’

We’ve already seen
that K2 stops – or even reverses – bone mineral loss in clinical
trials. Its effects on BMD are not as strong as those of bisphosphonates (or
of the newly-rediscovered bone-building powerhouse mineral, strontium (see “Strontium:
The First Bone Builder” in this special issue of Advances)), and yet clinical
trials prove that Menatetrenone slashes fracture risk by much more than you’d
expect from a glance at the BMD numbers. This “extra” protection
would make sense if it could be shown that Menatetrenone improves bone quality
as well as quantity. Looking into this possibility, scientists recently demonstrated
that, indeed, Menatetrenone improves the quality, architecture, and “connectivity”
of bone in animal models of menopausal osteoporosis.41,42,43

In one study,43 four groups
of experimental animals were compared. Two groups underwent surgery to prevent
estrogen production (thereby mimicking the hormonal environment of menopause).
One of these “menopausal” groups was given no treatment, while another
group was given Menatetrenone supplements. At the same time, a third group was
kept in its natural, youthful hormonal condition as a control group, and a fourth
group was kept non-“menopausal” but consumed Menatetrenone supplements
anyway.

Eight weeks of this extreme
“menopause” caused the first group to suffer the loss of 20.4% of
their BMD, 77% of the volume in their trabecular bone – and 78% of their
bone connectivity, as compared with the control group. But giving the “menopausal”
animals Menatetrenone supplements kept their bone mineral density at a level
which was not significantly different from the level of the controls, protected
against 51% of the loss in trabecular bonevolume, and prevented 74.5% of the
loss of bone connectivity! 43

Just as excitingly, when
the animals that were not placed in the menopausal hormonal milieu were given
Menatetrenone-fortified diets, Menatetrenone supplements actually increased
BMD and bone connectivity, to levels which were above those of the control group!43

So where can you get
more of this remarkable nutrient?
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Little K2 in Food

As we mentioned earlier,
the richest Western food sources for Menatetrenone, per gram, are goose liver,
butter, egg yolks, and fattier Emmental cheeses.24 The problem is that the amounts
of K2 even in these “high-Menatetrenone” foods is pretty minimal,
especially compared to the dosages proven to be effective in clinical trials.
Goose liver paté appears to be the best dietary source of K2 in the West,
and its Menatetrenone content is just 48 micrograms per serving – not
much more than a thousandth of the 45 milligrams (45 000 micrograms) proven
to protect against fracture. And it hardly makes good health sense to start
eating a few dozen egg yolks every day in hopes of increasing your Menatetrenone
intake!

On the other hand, if you
have a more adventuresome palate, you might see if you enjoy natto, the stringy
Japanese condiment. For a food source, natto is very rich in the bacterial forms
of K2 (longer-chain menaquinones, such as MK-7): one tablespoon serving contains
193 micrograms of these forms of the nutrient. This is still well below the
kinds of megadoses used to treat women with existing osteoporosis: even natto
can’t give you the standard dose of 45 milligrams of K2 used in clinical
trials, which is what’s needed to get your tissue levels high enough to
manifest the full range of Menat e t r enone’ s powerful effects at the
cellular level. Also, it isn’t certain that the bacterial forms of K2
(such as MK-7) will give the full benefits of Menatetrenone (MK-4), the form
of K2 made specifically by mammals (including people) for their use. But as
the dietary studies in Japan show,23,25,26 years of such lower-dose K2 intake
(as MK-7), beginning in your youth and continuing as a lifelong habit, clearly
provides some bone-healthy benefits.

One important heads-up on
natto: you’ll want to make sure that you’re getting authentic, traditional
natto, which is fermented using the Bacillus subtilis bacterium (the specific
strain is sometimes called “Bacillus subtilis (natto)” or even “Bacillus
natto”). Because of excessive concern about this bacterium “contaminating”
other foods, some North American food companies are selling a product labeled
“natto,” which looks and tastes much like the real thing but is
actually fermented using Lactobacillus species. Also, some supplement companies
offer fermented soy supplements as a rich source of highly-bioavailable soy
isoflavones. But neither of these fermented soy products contain any appreciable
amount of K2.

The Myth of the
Probiotic K2 Source

“But,” you
may ask, “isn’t K2 made in abundance by the friendly bacteria in
the colon?” Yes, it is – but unfortunately, you can’t absorb
this K2.

It first came to be believed
that the vitamin K made by probiotic bacteria in the gastrointestinal tract
was a significant source of the nutrient when it was observed that rodents fed
vitamin K-free lab chow did not develop severe deficiency of the vitamin. It
turned out, however, that these rodents were staving off bleeding disorders
through a cunning (if repulsive) act of desperation: they were consuming their
own K2-containing feces.87 When this tactic was blocked by using barriers which
keep the rats from accessing their stool, dangerous deficiency states quickly
set in.12,88 Stronger evidence was provided by studies in which the colon was
directly flooded with different K vitamins: virtually no vitamin K was absorbed,
even when very high concentrations of vitamin K were used.88,89

Another reason that it was
once believed that the K2 from colonic probiotics was absorbed was the fact
that people on antibiotics often develop a vitamin K deficiency. By killing
off a person’s probiotic bacteria, the theory went, the antibiotics eliminated
a major source of vitamin K, and deficiency set in. But it’s now known
that these deficiency states are not caused by the effects of the antibiotics
on colonic bacteria, but by the fact that some kinds of antibiotics prevent
the body from recycling “used” vitamin K into the form which is
active in gamma-carboxylation.90,91

Why can’t you absorb
the K2 supply created by your probiotics? Partly, it’s because those friendly
bacteria don’t release the K2 that they make: it’s tightly bound
into their cell walls.92 But it also has to do with the way that the body absorbs
all fat-soluble nutrients, such as CoQ10, lycopene, or vitamin k. Simply put,
oil and water don’t mix. To be absorbed, Menatetrenone and other K vitamins
must first be dissolved in fat, and then incorporated into micelles, which are
tiny transport globules (not unlike a simple cell membrane) formed in the small
intestines from bile salts. Micelles must then be moved through the small intestine
wall by special transport proteins before they can be released into the lymphatic
system and, from there, work their way into the bloodstream.

Low down in the intestinal
tract where probiotic bacteria live, there is little fat available into which
K2 can be dissolved, no bile salts available for micelle formation, and no transport
proteins to move any micelles that might be formed into the lymph. As a result,
little or none of the K2 made by these bacteria is absorbed. In fact, the need
for active transport is so strong that little or no K2 is absorbed into the
lymphatic system even if unbound K2 and bile are specially injected into the
colon.89

Bottom line: for protection
against the risk of a broken hip, you’ll want to consider a supplement.

K1 Won’t Get
You There

We’ve seen the reasons
to choose Menatetrenone over phylloquinone as the vitamin K for bone health
– and, in future issues, we’ll explore the similar evidence for
K2’s ability to protect heart health and the brain. But some will wonder:
if the body converts K1 into Menatetrenone, won’t an extra-large dose
of phylloquinone do just as well?

vitamin k2 analysis

 

Unfortunately, this strategy
won’t work, because in addition to phylloquinone’s lower bioavailability24,93,94
as compared with Menatetrenone, careful animal feeding experiments have shown
that the body’s ability to make Menatetrenone from K1 is limited, and
the percentage conversion in vital tissues like bone and heart gets lower and
lower as intake of phylloquinone increases. As a result, total levels of K2
formed from K1 grind to a halt well before megadose levels are reached2 (see
Table 1).

On top of this, the body’s
ability to upgrade phylloquinone into menatetrenone falls with age, plummeting
during the first half of life and then continuing to slowly peter out as old
age advances.95 The result is that tissue levels of K2 get lower the older you
get,96 even if you continue to get the same amount of K1 in your diet and supplements
(see Table 2).95 By contrast, when megadoses of Menatetrenone itself are provided
(as in clinical trials), the extra K2 is eagerly absorbed and incorporated into
these organs (Table 1). Clearly, getting the equivalent of the megadose levels
of Menatetrenone used in clinical trials from phylloquinone just isn’t
feasible.

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Finally, it’s important
to note that no clinical trial has ever been performed to show that K1 supplements
actually increase bone mass or protect women from fractures.97 Since it’s
now clear (as we’ve seen) that K2 protects bone mass through several mechanisms
which do not involve gamma-carboxylation or boosting bone mineralization, and
that these mechanisms are not shared with phylloquinone, the two cannot be considered
equivalent.

In other words: to experience
the results seen in the clinical trials, do what the women in the clinical trials
did. At the end of the day, the only thing equivalent to Menatetrenone is Menatetrenone
itself – the clinically-proven supplement, at the clinically-proven dose.

 

And if Protecting
Your Bones Weren’t Enough …

For many people, Menatetrenone’s
potent support of bone health – its undeniable ability to not only preserve
(or even increase) bone mass, but to improve bone quality and reduce the risk
of suffering a fracture – will be reason enough to supplement with this
powerful orthomolecule. And that one facet of Menatetrenone’s role in
health has been the only aspect for which we’ve had the room to explore
in this article.

But Menatetrenone’s
health benefits extend well beyond the skeletal system. Emerging science is
now documenting the role of vitamin k – and specifically of Menatetrenone
– in protecting our cardiovascular health, and the health of that all-important
organ, the brain. And while it won’t mean much to most people, evidence
has recently come to light that Menatetrenone (and not phylloquinone) can help
restore normal blood cell development in people suffering with myelodysplastic
syndrome (MDS) – a rare disorder caused by damage to blood stem cells,
leading to low levels of many blood cell types and (too often) to leukemia.
We’ll get into these other powers in an upcoming issue of Advances.

Until then, know that, when
you choose to support the health of your bones using Menatetrenone, you’ll
also be giving much-needed support to the health of your heart, and also of
your brain – the biological home of your identity.

Flesh and blood.

, Body and soul.

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