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Reversing calcification and the miracle of vitamin K2

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Vitamin K2 is the only known substance that can stop and reverse soft tissue calcification.

If you didn’t stop at the end of that sentence to say Wow to yourself, you should keep reading.

Soft tissue calcification is one of the most serious health problems we face as individuals, as modern societies, and, on a global scale, as a species.  Cardiovascular disease—which leads to heart attacks and strokes, and accounts for nearly half of all deaths in industrialised countries—is a disease of soft tissue calcification: the calcification of our arteries.

Arthritis, of which basically everyone past the age of 40 suffers, and increasingly more with time and with age, is a disease of soft tissue calcification.  It is caused by the calcification of the cartilage in the joints:  the joints of the knees, but also of the shoulders; the joints of the hips, but also of the wrists; the joints of the elbows, but also of the feet and the toes; the cartilage between the vertebrae of the neck and the spine all the way down the back, but also of the hands and of the fingers.

Soft tissue calcification also causes kidney stones and kidney disease.  How many people above the age of 60 don’t have kidney problems?  Hardly any.  And how many young men and women in their 20s and 30s already have kidney stones and kidney dysfunction?  More and more every year.

Every one of the processes generally associated with ageing, from heart disease and stroke, to Alzheimer’s and dementia, to arthritis and kidney disease, to stiffness in the joints and muscles, but also to the wrinkling of the skin, is intimately linked to soft tissue calcification.

And now, let me repeat the sentence with which we opened:  Vitamin K2 is the only known substance that can stop and reverse soft tissue calcification.  It is really remarkable.

Maybe you didn’t know about calcification.  And so, maybe you are wondering why it is such a major and widespread problem, why it affects everyone no matter where we are or what we do.  It’s a good question.  But because we know that only vitamin K2 can prevent this from happening, we already have our answer:  soft tissue calcification is a major and widespread problem because our intake of vitamin K2 is inadequate to provide protection from calcification.

Naturally, the next question is why?  Why is our intake of vitamin K2 so inadequate?  If it is such a crucial essential nutrient, we would surely not be here as a species if intake had always been so inadequate.  Looking at things the other way around, if we are so dependent on adequate K2 intake for staying healthy, this must necessarily mean that we evolved having plenty of it in our food supply.  What’s so different now?

To answer this question with some level of detail—meaning with an explanation more extensive than just saying that it’s industrialisation that stripped our food supply of vitamin K2 as it has for all the essential nutrients to a greater or lesser extent—we have to understand what K2 is, how it’s made, and where it’s found in food.

The short answer is that K2 is found in the fat of pastured animals that graze on fresh green grass, and produced from vitamin K1 by certain kinds of bacteria in their gut.

The longer answer is that vitamin K2 is a family of compounds called menaquinones, ranging from MK-4 to MK-13 depending on their molecular structure.  These compounds are derived from the plant analog, the sister compound, vitamin K1, called phylloquinone, and found in chlorophyll-rich plant foods.  Phylloquinone is consumed by the pastured animal, it makes its way into their intestines, and there it is transformed by the bacteria of the animal’s intestinal flora.  The resulting menaquinone is then stored in the fat cells of the animal as well as in the fat of their milk if they are milk-producing.  Consuming these animal fats in which vitamin K2 has been concentrated will provide this precious essential micronutrient.

If the grazing animal does not feed on green grass, they get no vitamin K1.  If they get no vitamin K1, their gut flora is not only compromised and negatively altered with respect to what it should be if they were consuming the grass they have evolved eating, but it produces no vitamin K2.  If their gut flora produces no vitamin K2, their fat and milk will contain no vitamin K2, and neither their offspring nor any person consuming products derived from the animal will get any vitamin K2.  Hence, no grass feeding, no vitamin K2 in the animal’s fat.

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It is most natural that grass-eating animals should be grazing on fresh green grass in open pastures.  And yet, it is rather rare.  But without green grass, there is no vitamin K1.  And without vitamin K1 there can be no vitamin K2.

Maybe you’ve already thought ahead, and wondered since it is bacteria that produces vitamin K2 from vitamin K1 in the guts of grazing animals, can’t we make vitamin K2 without the need for grass-fed animals to do it for us?  Yes, it is possible.  Fermented vegetables and dairy products like cheese can also contain vitamin K2.  In fact, in the case of cheese, there is a lot more in the finished hard cheese than in the milk used to make it.  The amount varies widely because it depends on the kind of bacteria.  For dairy products, hard cheeses like Gouda have the most, and for plant foods, even if fermented veggies have a little, the Japanese fermented soybean snack natto is the ultimate source of K2.

As we all know, pastured meat and dairy is not easy to come by in our modern world.  It’s actually quite hard to find.  Our supermarkets and food stores are flooded with industrially produced meat and dairy from animals that have never seen a blade of grass—grass-grazing animals living their entire lives indoors, in stalls, fed and fattened exclusively on grains, corn, and soybeans.  This is how we have stripped our food supply of vitamin K2, and this is why is this a modern phenomenon—most of our grand-parents were still eating pastured meats and animal foods.

And if this wasn’t enough of a blow to vitamin K2 status, trans-fats, which are formed when vegetable oils are hydrogenated to be made saturated and stable (for long shelf life), and which most of us consume in great quantities, contain a K2 analog called DHP (dihydrophylloquinone) that displaces the little K2 that might has found its way into our diet.

It is for all these reasons that soft tissue calcification is so widespread.  And you have at this point what you need to know in order to first stop the process by which your soft tissues are getting increasingly calcified, and then, in time, to remove the accumulated calcium from these tissues.  It’s simple: healthy grass-fed animals produce yellow butter, yellow yolks, and yellowish fat;  you need to eat plenty of pastured animal foods, making sure you eat the fat in which vitamin K2 is concentrated, and, to be sure you have enough to reverse the already present calcification, take K2 supplements.  And this might be enough for you.

If it is, you can head to your browser to find and order some K2 supplements (I currently get mine, it’s a 500 mcg per tablet, from Phoenix Nutrition).  Also, we need to know that the two main forms of K2 are MK-4 (with four double bonds) and MK-7 (with seven).  The first is the one generally found in animal fats that haven’t been fermented, while the second is the product of bacterial fermentation.  Hence, meat and butter contain mostly MK-4, whereas natto, sauerkraut, and cheese contain mostly MK-7.

There is an important difference between these two forms of K2 in terms of their effects inside the body which has to do with their half-life, not in the sense of radioactivity, but in the sense of duration of biological activity in the body.  MK-4 will be in circulation at therapeutic doses for a number of hours, while MK-7 remains in circulation between 24 and 48 hours.  Therefore, to be safe, we need to eat grass fed meat and butter, and take MK-7 supplements (I take 1000 mcg), always after a meal with plenty of fat to maximize absorption.

If you are curious to find out more, if you want to know how menaquinone does this, how vitamin K2 does its miracles inside the body, then we need to take a closer look at the biochemistry of calcium metabolism.

There are three proteins found in bone matrix that undergo gamma-carboxylation via Vitamin K-dependent enzymes: matrix-gla-protein (MGP) (Price et al., 1983), osteocalcin (bone gla-protein, BGP) (Price et al., 1976), both of which are made by bone cells, and protein S (made primarily in the liver but also made by osteogenic cells) (Maillard et al., 1992) (Table V).  The presence of di-carboxylic glutamyl (gla) residues confers calcium-binding properties to these proteins.

MGP is found in many connective tissues and is highly expressed in cartilage.  It appears that the physiological role of MGP is to act as an inhibitor of mineral deposition.  MGP-deficient mice develop calcification in extraskeletal sites such as in the aorta (Luo et al., 1997).  Interestingly, the vascular calcification proceeds via transition of vascular smooth muscle cells into chondrocytes, which subsequently hypertrophy (El-Maadawy et al., 2003).  In humans, mutations in MGP have been also been associated with excessive cartilage calcification (Keutel syndrome, OMIM 245150).

Whereas MGP is broadly expressed, osteocalcin is somewhat bone specific, although messenger RNA (mRNA) has been found in platelets and megakaryocytes (Thiede et al., 1994).  Osteocalcin-deficient mice are reported to have increased bone mineral density compared with normal (Ducy et al., 1996).  In human bone, it is concentrated in osteocytes, and its release may be a signal in the bone-turnover cascade (Kasai et al., 1994).  Osteocalcin measurements in serum have proved valuable as a marker of bone turnover in metabolic disease states.  Interestingly, it has been recently suggested that osteocalcin also acts as a hormone that influences energy metabolism by regulating insulin secretion, beta-cell proliferation, and serum triglyceride (Lee et al., 2007).

These are the first three paragraphs of the chapter Noncollagenous Bone Matrix Proteins in Principles of Bone Biology (3rd ed.) which I found it on the web when I was searching for more info on the biochemical action of menaquinone.

And now, here is my simple explanation of how things work:

The players are the fat-soluble vitamins A, D, and K2;  three special proteins called osteocalcin, matrix gla protein, and protein S;  and an enzyme called vitamin K-dependent carboxylase.

First, vitamin D makes calcium available by allowing its absorption from the intestines into the bloodstream.  This is vital for life and health.  You know that severe vitamin D deficiency is extremely dangerous and develops into the disease that deforms bones called rickets.  Milder forms of vitamin D deficiency are much harder to detect without a blood test, but can and do lead to a huge spectrum of disorders and health problems.  However, without vitamin K2, ample or even just adequate levels of vitamin D will inevitably lead to increased soft tissue calcification.

Vitamins A and D make bone-building cells (osteoblasts) and teeth-building cells (odontoblasts) produce osteocalcin (also known as bone gla protein or BGP) and matrix gla protein (or MGP).  This is key because it is these proteins that will transport the calcium.

Vitamin K2, through the action of the vitamin K-dependent carboxylase enzyme, activates bone and matrix gla proteins by changing their molecular structure which then allows them to bind and transport calcium.

Once activated, bone gla protein brings calcium (and other minerals) into the bones;  and matrix gla protein takes calcium out of the soft tissues like smooth muscle cells of arteries, but also organs, cartilage, skeletal muscles, and skin.  Without this K2-dependent activation, BGP and MGP remain inactive, and the calcium accumulates in soft tissues all over the body.

What completes the act, is that vitamin K2 activates protein S which oversees and helps the immune system clear out the stuff of arterial plaques that remains once the calcium making the plaques structurally stable has been taken out.  And, amazingly, protein S does this without triggering a large inflammatory response.

Even though it is quite straight forward when explained in this way, this understanding of vitamin K2 and its action in the body is really quite recent: in the last 20 years or so.  For one thing, it was only 10 years ago that Chris Masterjohn solved the 60-year old mystery of Weston A. Price’s X-Factor, correctly identifying it for the first time as vitamin K2. (You can read that for yourself here.)  And although some laboratory studies and experiments on vitamin K were done several decades ago, the majority are from the last 10 years (take a look at the references in Masterjohn’s paper.)

We’ll stop here for now.  But we’ll come back to vitamin K2 because there are so many other amazing things it does for our health.

This article was inspired by Dr. Kate Rheaume-Bleue’s book entitled Vitamin K2 and the Calcium Paradox.

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We were never meant to eat simple or starchy carbohydrates

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The transition between hunting-gathering and farming took place over a period of about 1000 years between 11000 and 10000 years ago in the Fertile Crescent, a crescent-like shape of land that stretches across parts of Israel, Lebanon, Jordan, Syria, Iran and Iraq. The first people to settle were hunter-gatherers that built villages in places they found provided enough food to sustain them without having to move around. At first, these were “seasonal” villages located in different areas, to which they returned in a seasonal cycle. Finding ways to store the grain from the large seeded grasses like barley and emmer wheat growing wild but in large quantities, allowed them to settle permanently. This most likely led to a rapid growth of the population, that was matched with a proportionally rapid growth in the demand for food. The response was the development of agriculture.

The gradual decimation of the wild game over the course of about 2000 years led to the domestication of the most easily domesticable, large mammals to inhabit the region, the sheep, goat and pig, all about 8000 years ago, followed by the cow about 6000 years ago. It is very interesting and important to point out, from an anthropological point of view, that the Fertile Crescent—the seat of civilisation—is the region in the world where there were the greatest number of large-seeded grasses, as well as the greatest number of large, easily domesticable animals, by far.

The cultivation of cereal crops allowed our ancestors, some 10000 years ago, to have, for the first time in our evolutionary history, enough spare time to develop tools and technologies, as well as arts and music. For the first time in evolutionary history, a handful of people could sow, tend to, and harvest enough cereal grain to feed hundreds or even thousands of people who were, therefore, free to do a multitude of other things. Without agriculture and this shift from the hunter-gatherer lifestyle of spending most of our waking hours hunting and rummaging around looking for food, we would not have developed much of anything because we simply never would have had the time to do so.

Now, although it is well known to most anthropologists, it is not a well appreciated fact that the cultivation and eating of cereal crops as an important source of calories, is possibly the most negatively impacting evolutionary mistake to have been made in regards to the health and robustness of our species as a whole. There was, indeed, plenty of free time, and we did develop technologies extremely quickly considering how slowly things had changed before then. But the price to pay was high.

Within as little as one or two generations, our powerful stature shrank markedly, our strong teeth rotted, our massive bones became thin and brittle, our thick hair grew thin and fell out at an early age. In fact, evidence indicates that while our hunter-gatherer ancestors were tall, strong, robust, with hard teeth and bones, and apparently healthy to their death—usually of a violent nature instead of progressive degradation through “ageing” as later became the norm, our oldest cereal-eating ancestors in contrast, were the exact opposite: small, weak, fragile, with rotten teeth, and advanced osteoporosis in their bones at the time of their death in their early 50’s. (For a lot more details about all the points discussed up to here, I strongly recommend Jared Diamond’s fascinating books: The Third Chimpanzee; Guns, Germs and Steel; and Collapse).

Today, at the beginning of the 21st century some 10000 years later, we know exactly why we were never meant to consume carbohydrates on a regular basis, let alone in large quantities as we do today, such that they provide a significant part of our daily calories—sometimes even the majority! We know exactly why because we have pretty clearly understood the primary effect of phytic acids or phytates, the importance of dietary fats, and the insulin mechanism.

Phytates are compounds that exist in all grains and legumes—where they are found in the greatest concentration—as well as in all nuts and seeds. Some animals like rats, for example, have evolved the necessary digestive mechanisms to break down phytates, but humans have not. The consequence is these bind to minerals in the gut and in so doing prevent their absorption into the bloodstream. The regular consumption of grains and legumes—and we believe that many of our first agrarian ancestors lived almost exclusively from grains—leads to severe mineral deficiencies that result in demineralisation of the teeth and bones, exactly as is seen in the remains of these ancestors.

Moreover, any diet consisting primarily of grains (and legumes) as was theirs, will also inevitably be extremely deficient in fat, that is now know to be essential for the proper function of every cell, tissue and organ in the body (especially the brain), but also crucial in the absorption of minerals. So, the combination of a high concentration of phytates together with an almost complete absence of fat, made for an extremely effective demineralisation, which is indeed seen in the smaller statures, weakened bones and teeth, and considerably shortened lifespan of our agrarian ancestors. This obviously still applies today: the more phytates, the faster the demineralisation; and the less fat; the faster the demineralisation.

Finally, insulin is a hormone secreted by the pancreas. There is always a certain concentration of glucose in the blood, and there is also always a certain concentration of insulin. If there isn’t a major metabolic disorder, then the higher the glucose concentration, the higher the insulin concentration. And conversely, the lower the glucose concentration, the lower the insulin concentration. But since the body is programmed to always keep glucose concentrations to a minimum, as soon as there is a simple carbohydrate in our mouth, insulin is secreted into the bloodstream. As the glucose—either from the simple carbohydrates or from the breakdown of starches—enters the bloodstream through the intestinal wall, and as its concentration continues to rise, the pancreas continues to secrete insulin to match the concentration of glucose; but always a little more, just to be on the safe side.

Why? If glucose were good for us, then why should we have this highly sensitive mechanism to always try to get rid of it?

Insulin’s primary role is storage of “excess” nutrients, and regulation of fat storage and fat burning: when insulin is high, there is fat storage; when insulin is low, there is fat burning. It’s very simple. This, in turn, means that insulin is the primary regulator of energy balance, and therefore of metabolism. From an evolutionary perspective, the importance of insulin is perfectly clear. Firstly, it is a mechanism that is common to almost if not all living creatures, from the simplest to the most complex, because all living creatures depend for their survival on a mechanism that allows them to store nutrients when they are available for consumption but not needed by their metabolism, in order to live through periods where food is not available. This is why the role of insulin is so fundamental and why it is a master hormone around which most others adjust themselves. But when glucose levels are higher than a minimum functional threshold, what insulin is trying to do, in fact, is to clear away the glucose circulating in our bloodstream.

Why? Because the body simply does not want large amounts of glucose in circulation. In fact, it wants blood glucose to be low, very low, as low as possible. And beyond this very low threshold of glucose concentration between 60 and 80 mg/dl, it always tries to store it away, to clear it from the bloodstream, to make it go away. It tries to store as much as possible in the muscles and the liver as glycogen, and converts the rest to fat stored away in fat cells. That the body does not want glucose in circulation is most certainly related to the fact that the insulin mechanism even exists: very small amounts of glucose in the bloodstream is essential for life, but large amounts of glucose in the bloodstream is toxic. And all simple and starchy carbohydrates stimulate the secretion of insulin from the pancreas.

Keep in mind that the presence of insulin promotes the storage of glucose, but also of proteins as well as fats. Once more, its role is to store away and deplete the “excess” nutrients in the bloodstream for later times of food scarcity. Once the insulin molecule has delivered its load (glucose, protein or fat) through the receptor on the cell, it can either be released back into circulation or degraded by the cell. Degradation of circulating insulin is done by the liver and kidneys, and a single molecule will circulate for about 1 hour from the time it was released into the bloodstream by the pancreas until it is broken down.

It is important to add that stress stimulates the secretion of stress hormones that in turn stimulates the release from and production of glucose by the liver, just in case we need to sprint or jump on someone to save ourselves. Obviously, the presence of glucose—now not from ingested carbohydrates but from the liver itself—will trigger the secretion of insulin in exactly the same way as if we had eaten sugar. This means that stress mimics the physiological effects of a high sugar diet. And that’s not good. In fact, it’s pretty bad.

Chronically elevated glucose levels lead to chronically elevated insulin levels. And this is much worse. Like for any kind of messenger mechanism—as is insulin, if there are too many messengers repeating the same message over and over again, very soon they are not heard well because their efforts at passing on the message becomes more like background noise. Frustrated that they are not taken seriously, the messengers seek reinforcements in numbers to be able to pass on their message more forcefully. This, however, leads to even more annoyance on the part of the listeners—the message recipients—that now start to simply ignore the message and the messengers. This process continues to gradually escalate up to the point where the terrain is completely flooded by messengers yelling the same thing, but there is no one at all that is listening because they have insulated their windows and doors, and closed them tightly shut.

Here, the messengers are the insulin hormone molecules secreted by the pancreas and coursing throughout the body in our veins and arteries; the message recipients are our cells: muscle tissue, liver and fat cells; and the message itself is “Take this sugar from the bloodstream, and store it away. We don’t want this stuff circulating around.” The desensitisation—the not-listening—to different, progressively higher degrees with time, is called insulin resistance. Finally, the complete ignoring by the cells of the message and the messengers is called type II diabetes.

Furthermore, insulin resistance—not in the muscle, liver and fats cells, but in the brain cells—clearly leads to neurological degradation identified as cognitive impairment, dementia, Alzheimer’s or whatever other terms are used. Because beyond the fact that type II diabetes and Alzheimer’s disease are both increasing together at an alarming rate in the US and other western countries, and beyond the fact that diabetics are at least twice as likely to develop Alzheimer’s compared to non-diabetics, the basic condition of insulin resistance inevitably leads to chronically elevated glucose concentrations simply because the cells do not allow the glucose to enter. And it is well known that glucose in the blood simply and straight forwardly damages to the lining of the blood vessels, which then leads to plaque formation—the body’s repair mechanism for the damaged cells underneath. Thus, as are the coronary arteries of advanced atherosclerotic heart disease sufferers (and diabetics): riddled with plaques, so are the arteries and blood vessels in the brains of Alzheimer’s sufferers (and diabetics).

Now, although many claim that these and other issues related to the development of Alzheimer’s disease and other kinds of neurological degradation are still relatively poorly understood, as far as I’m concerned, it’s all the evidence I need: Do you want the vessels supplying blood to the brain fill up with plaque in response to the damage caused by glucose circulating in the bloodstream? Do you want the coronary arteries fill up with plaque in response from the damage caused by glucose circulating in the bloodstream? I certainly don’t. How could anyone?

What do we need to do? Very simple: just eliminate  simple and starchy carbohydrates from the diet. Concentrate on eating a lot of green vegetables, tons of green leafy salad greens; plenty of fat from coconut milk, coconut oil, nuts and seed of all kinds; and a little animal protein from eggs, raw cheese, wild fish and meat (if you chose to do so). Blood sugar will drop to its minimum, insulin will follow suit, and the body’s own repair and maintenance mechanisms will clear out the plaques, repair damaged tissues, degraded unneeded scar tissues and small tumours and recycle these proteins into useful muscle tissue, and many, many more amazing things will happen to the body that it will gradually look and feel younger and stronger as time passes. Sounds too good to be true? Just try it, and you’ll see for yourself. I guarantee it.