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by Dr Len Lopez

If you are over 40 years of age there is a good chance that more of your testosterone is converting into estrogen then you would like. Yes, both men and women make testosterone. The good Lord didn’t just make testosterone for men. It’s the hormone needed for both men and women to add lean muscle, keep your energy up, weight down, motivate you to get out of bed and of course give your libido a lift.

The problem that happens for a lot of men and women is that too much of their testosterone is converting into estrogen. This not only causes loss of energy, weight gain, fatigue and difficulty adding lean muscle to your body, but it also leads to what is called ‘estrogen dominance,’ which make you more susceptible to a whole host of other problems including cancer.

For men the obvious sign of too much estrogen aside from the obvious listed above is added fatty tissue around the chest…the basic men-boobs. More adipose (fatty) tissue in your chest and waist, as opposed to packing it on in your back side.

There is a big push by drug manufacturers for men to have their testosterone checked to see if that’s what is causing your erectile dysfunction, loss of stamina and libido. Unfortunately they are more interested in prescribing synthetic testosterone drugs, instead of the old fashion, inexpensive testosterone that doesn’t have a patent on it. Nor are they interested in helping you figure out why your body isn’t producing enough testosterone. Not only that – but when you take these synthetic testosterone drugs as replacements, your body will produce less on its own – so when you stop taking the drug you feel terrible and compelled to get another prescription.

FYI…Low levels of testosterone is associated with depression. Also testosterone is lowered by the use of ‘statin’ drugs, which are prescribed to lower cholesterol….can you see the vicious cycle of one drug creating another problem somewhere else, which is why trying to address the cause should be the name of the game.

For women too much estrogen is associated with PMS, fibroids, mood swings, difficulty falling asleep, menopausal symptoms and of course lack of libido and energy.

Everyone converts testosterone into estrogen. The good Lord designed it for men to retain most of their testosterone and only about a tenth of it to be converted into estrogen. For women it is just the opposite, most of their testosterone is converted into estrogen, but they should have an adequate amount of testosterone running through their body to help them get out of bed each day, feel energized, strong and maintain their desires.

What speeds up the conversion process for both men and women is the activation of an enzyme called aromatase. Too much of this enzyme and you convert more of your testosterone into estrogen for both men and women. Now the good Lord didn’t make a bad enzyme…aromatase has its function, but too much of one thing may not be good for you!

Snacks or meals that are loaded with carbohydrates, especially carbohydrates from refined, processed white flour and sugar cause the biggest surge in aromatase. Therefore, one of the last things you want to be eating are high carbohydrate meals, especially at night. This will trigger the greatest conversion of your testosterone into estrogen for both men and women

If that’s you, look at your diet. Do you eat too many high carbohydrate meals or snacks? Do you have a sweet tooth at the end of the day? If so, make some changes to your diet. Cut out all the late night snacks and treats.

A simple test anyone can do at home to check their zinc status is a zinc ‘taste-test’ It quickly and inexpensively determines if you’re low on zinc, which is an excellent clue in helping determine if you are converting your testosterone or not making enough of it.

One key function of zinc besides the need for a strong immune and reproductive system is the importance of keeping that aromatase enzyme at bay. A few herbs such as: saw palmetto, pygeum, pumpkin seeds and nettles are loaded with zinc and help keep your aromatase levels in their normal range.

These herbs are highly recommended for both men and women who are 40+ years old or have more than 20 pounds of excess body weight to lose. Both of these groups of people need testosterone and can’t afford to be losing any of it because they don’t have adequate levels of zinc.

Boost Your Testosterone

Intense exercise and sleep are the two best ways to increase your testosterone levels. With regards to sleep, make sure you are getting enough, if you are having trouble sleeping or staying asleep, get the attention and help you need to fix that problem.

With regards to exercise, the more intense the workout the more testosterone you release. Walking releases some testosterone, while jogging produces more, and running producing even more. This is again why weight training is the best way to get your testosterone levels up…it’s can be short quick and intense! You don’t have to train long, but you do have to push yourself in order to pump out more testosterone and growth hormones. Try the 5-Minute Workout, which is a quick and intense workout to help produce as much testosterone and growth hormones in the shortest amount of time, by simply performing body weight exercises.

Remember it’s not necessarily how much testosterone you make — is’t how much do you keep! Don’t let your diet or lack of zinc (less soy products and hormone-filled products) be the reason why your testosterone levels are down!

In 1945, Dr. Weston Price described   “a new vitamin-like activator” that played an influential role in the utilization of minerals, protection from tooth decay,  growth and development, reproduction, protection against heart   disease and the function of the brain.

Using a chemical test, he determined that this compound—which   he called Activator X—occurred in the butterfat, organs    and fat of animals consuming rapidly growing green grass, and   also in certain sea foods such as fish eggs.

Dr. Price died before research by Russian scientists became known  in the West. These scientists used the same chemical test to measure  a compound similar to vitamin K.

Vitamin K₂ is produced by animal tissues, including    the mammary glands, from vitamin K₁, which occurs in   rapidly growing green plants.

A growing body of published research confirms Dr. Price’s discoveries,    namely that vitamin K₂ is important for the utilization    of minerals, protects against tooth decay, supports growth and development, is involved in normal reproduction, protects against calcification of the arteries leading to heart disease, and is a major component of the brain.

Vitamin K₂ works synergistically with the two other   “fat-soluble activators” that Price studied, vitamins   A and D. Vitamins A and D signal to the cells to produce certain  proteins and vitamin K then activates these proteins.

Vitamin K₂ plays a crucial role in the development    of the facial bones, and its presence in the diets of nonindustrialized    peoples explains the wide facial structure and freedom from dental   deformities that Weston Price observed.

Main Article (On the Trail of the Elusive X-Factor)

In 1945, Weston Price published a second edition of his pioneering  work Nutrition and Physical Degeneration, to which he added  a new chapter entitled, “A New Vitamin-Like Activator.”¹ In it, he presented evidence of a theretofore unrecognized fat-soluble  substance that played a fundamental role in the utilization of minerals  and whose absence from modern nutrition was responsible for the proliferation  of dental caries and other degenerative diseases. Although Price quantified  the relative amount of this substance in thousands of samples of dairy  products sent to him from around the world, he never determined its            precise chemical identity. For want of a better means of identification,            he referred to it as “Activator X,” also sometimes referred to as the “Price Factor.”

Price found the highest concentrations of this nutrient in “the   milk of several species, varying with the nutrition of the animal” and found the combination of cod liver oil and high-Activator X butter  to be superior to that of cod liver oil alone. In the many butter samples he tested, Activator X was only present when the animals were eating  rapidly growing green grass. In most regions, this occurred in the spring and early fall.

A Sixty-Year Mystery

For over sixty years, all attempts to identify this elusive “X”  factor have failed. In the 1940s, Dr. Royal Lee, founder of the whole food supplement company Standard Process, suggested that activator X            was the essential fatty acids.² In 1980, Dr. Jeffrey Bland            suggested more specifically that it was the elongated omega-3 essential            fatty acid called EPA.³ Although these fatty acids exert  some effects on calcium metabolism,⁴ neither the distribution  of these unsaturated fatty acids in foods nor their chemical behavior  corresponds to that of Activator X. Cod liver oil is much richer than  butter in essential fatty acids including EPA, and the oils of plant seeds are even richer in these fats, but Price found little, if any,  Activator X in these foods. Moreover, Price tested for Activator X by            quantifying the ability of a food to oxidize iodide to iodine; essential            fatty acids, however, do not possess this chemical ability.

In 1982, one author wrote to the Price-Pottenger Nutrition Foundation  that after pursuing a number of false leads while attempting to identify  the X factor, he had concluded that the “peculiar behavior”  observed in Price’s chemical test might be due to a “special kind  of oxygen-containing heterocyclic ring,” and suggested a compound            called 6-methoxybenzoxazolinone (MBOA) as a likely candidate.⁵ Although researchers first identified MBOA as an antifungal agent found            in corn,⁶ later studies showed that it was found in many            other plant foods and acted as a reproductive stimulant in some animals            by mimicking the hormone melatonin.⁷ Although it is present            in young, rapidly growing grass, no research has ever established MBOA            as an essential nutrient, attributed to it any of the physiological            roles of Activator X, or demonstrated its presence in the foods that            Price considered to be the richest sources of this nutrient. MBOA, then,            was just another false lead; we will soon see, however, that the writer’s            observations about the chemical nature of Activator X were largely correct.

Vitamin K: Three Discoveries Converge

The test that Price used for Activator X, called iodometric determination,            was traditionally regarded within the English language literature as            a test for peroxides (carbon-containing molecules that have been damaged            by oxygen).^8,9 Since peroxides do not have any activity as            vitamins, the relationship between the test and any nutritional substance            remained a mystery. Although researchers publishing in other languages            were using the test to detect a class of chemicals called quinones at            least as far back as 1910,¹⁰ it was not until 1972 that Danish            researchers published a paper in the British Journal of Nutrition showing that the test could be used to detect biological quinones such            as K vitamins in animal tissues.¹²

K vitamins (Figure 1) possess oxygen-containing            ring structures that are capable of oxidizing iodide to iodine and would            therefore be detected by Price’s Activator X test. The K vitamins are            likely to go down in history as the most misunderstood group of vitamins            of the twentieth century. In many ways, however, modern researchers            are now rediscovering properties of these vitamins that Price had discovered            over sixty years ago. It has now become clear that both Activator X            and its precursor in rapidly growing grass are both members of this            group.

There are two natural forms of vitamin K: vitamin K₁ and            vitamin K₂. Vitamin K₁, also called phylloquinone,            is found in the green tissues of plants, tightly embedded within the            membrane of the photosynthesizing organelle called the chloroplast.            As the chlorophyll within this organelle absorbs energy from sunlight,            it releases high-energy electrons; vitamin K₁ forms a bridge            between chlorophyll and several iron-sulfur centers across which these            electrons travel, releasing their energy so that the cell can ultimately            use it to synthesize glucose.¹³

When animals consume vitamin K₁, their tissues convert part            of it into vitamin K₂,¹⁴ which fulfills a host            of physiological functions in the animal that we are only now beginning            to understand. The ability to make this conversion varies widely not            only between species¹⁴ but even between strains of laboratory            rats,^15,16 and has not been determined in humans. The mammary            glands appear to be especially efficient at making this conversion,            presumably because vitamin K₂ is essential for the growing            infant.¹⁷ Vitamin K₂ is also produced by lactic            acid bacteria,¹⁸ although bacteria produce forms of the vitamin            that are chemically different from those that animals produce, and researchers            have not yet established the differences in biological activity between            these forms.

Although both K vitamins were discovered and characterized over the            course of the 1930s, two fundamental misunderstandings about these vitamins            persisted for over sixty years: the medical and nutritional communities            considered blood clotting to be their only role in the body, and considered            vitamins K₁ and K₂ to simply be different forms            of the same vitamin. The first vitamin K-dependent protein relating            to skeletal metabolism was not discovered until 1978. It was not until            1997, nearly twenty years later, that the recognition that vitamin K            was “not just for clotting anymore” broke out of the confines            of the fundamental vitamin K research community.¹⁹

Since the amount of vitamin K₁ in typical diets is ten times            greater than that of vitamin K₂,²⁰ researchers            have tended to dismiss the contribution of K₂ to nutritional            status as insignificant. Yet over the last few years, a growing body            of research is demonstrating that these two substances are not simply            different forms of the same vitamin, but are better seen as two different            vitamins: whereas K₁ is preferentially used by the liver            to activate blood clotting proteins, K₂ is preferentially            used by the other tissues to place calcium where it belongs, in the            bones and teeth, and keep it out of where it does not belong, in the            soft tissues.²¹ Acknowledging this research, the United States            Department of Agriculture, in conjunction with researchers from Tufts            University, finally determined the vitamin K₂ contents of            foods in the U.S. diet for the first time in 2006.²²

Perfect Correspondence

Because vitamin K₁ is directly associated with both chlorophyll            and beta-carotene within a single protein complex and plays a direct            role in photosynthesis,¹³ the richness of the green color            of grass, its rate of growth, and its brix rating (which measures the            density of organic material produced by the plant) all directly indicate            its concentration of vitamin K₁. Animals grazing on grass            will accumulate vitamin K₂ in their tissues in direct proportion            to the amount of vitamin K₁ in their diet. The beta-carotene            associated with vitamin K₁ will also impart a yellow or orange            color to butterfat; the richness of this color therefore indirectly            indicates the amount of both vitamins K₁ and K₂ in the butter. Not only are the K vitamins detected by the Activator            X test and distributed in the food supply precisely as Price suggested,            but, as shown in Figure 2, the physiological actions            that Price attributed to Activator X correspond perfectly to those of            vitamin K₂. It is therefore clear that the precursor to Activator            X found in rapidly growing, green grass is none other than vitamin K₁,            while Activator X itself is none other than vitamin K₂.

Ironically, Price discovered the roles of vitamin K₂ in            calcium metabolism, the nervous system and the cardiovascular system            more than sixty years before the vitamin K research community began            elucidating these roles itself, while vitamin K researchers discovered            the chemical structure of activator X several years before Price even            proposed its existence. Had Price been aware that his chemical test            had been used for decades outside of the English language scientific            community to detect quinones, a class to which the K vitamins belong,            the two independent discoveries of this one vitamin may have converged            sooner.

Instead, English-speaking researchers continued for decades to labor            under the illusion that the iodometric method detected only peroxides;            by the time this illusion was corrected, better methods for detecting            peroxides had already been developed, Activator X had been forgotten,            and the opportunity to make the connection between these three discoveries            was lost. The twenty-first century, however, is already making radical            revisions to our understanding of the K vitamins, which now make it            clearer than ever that Activator X and vitamin K₂ are one            and the same.

Synergy with Vitamins A and D

Price showed Activator X to exhibit dramatic synergy with vitamins            A and D. Chickens voluntarily consumed more butter and died more slowly            on a deficiency diet when the butter was high in both vitamin A and            Activator X than when it was high in vitamin A alone. Cod liver oil,            which is high in both vitamins A and D, partially corrected growth retardation            and weak legs in turkeys fed a deficiency diet, but the combination            of cod liver oil and high-Activator X butter was twice as effective.            Likewise, Price found that the combination of cod liver oil and a high-Activator            X butter oil concentrate was more effective than cod liver oil alone            in treating his patients for dental caries and other signs of physical            degeneration.

Vitamin K₂ is the substance that makes the vitamin A- and            vitamin D-dependent proteins come to life. While vitamins A and D act            as signaling molecules, telling cells to make certain proteins, vitamin            K₂ activates these proteins by conferring upon them the physical            ability to bind calcium. In some cases these proteins directly coordinate            the movement or organization of calcium themselves; in other cases the            calcium acts as a glue to hold the protein in a certain shape.³³ In all such cases, the proteins are only functional once they have been            activated by vitamin K.

Osteocalcin, for example, is a protein responsible for organizing the            deposition of calcium and phosphorus salts in bones and teeth. Cells            only produce this protein in the presence of both vitamins A and D;³⁴ it will only accumulate in the extracellular matrix and facilitate the            deposition of calcium salts, however, once it has been activated by            vitamin K₂.³⁵ Vitamins A and D regulate the expression            of matrix Gla protein (MGP),^36,37 which is responsible for            mineralizing bone and protecting the arteries from calcification; like            osteocalcin, however, MGP can only fulfill its function once it has            been activated by vitamin K₂.³³ While vitamins            A and D contribute to growth by stimulating growth factors and promoting            the absorption of minerals, vitamin K₂ makes its own essential            contribution to growth by preventing the premature calcification of            the cartilaginous growth zones of bones.³⁸

Vitamin K₂ may also be required for the safety of vitamin            D. The anorexia, lethargy, growth retardation, bone resorption, and            soft tissue calcification that animals fed toxic doses of vitamin D            exhibit bear a striking resemblance to the symptoms of deficiencies            in vitamin K or vitamin K-dependent proteins. Warfarin, which inhibits            the recycling of vitamin K, enhances vitamin D toxicity and exerts a            similar type of toxicity itself. Similarly, the same compounds that            inhibit the toxicity of Warfarin also inhibit the toxicity of vitamin            D. I have therefore hypothesized elsewhere that vitamin D toxicity is            actually a relative deficiency of vitamin K₂.³⁹ The synergy with which vitamin K₂ interacts with vitamins            A and D is exactly the type of synergy that Price attributed to Activator            X.

Vitamin K2 and Dental Health

Weston Price was primarily interested in Activator X because of its            ability to control dental caries. By studying the remains of human skeletons            from past eras, he estimated that there had been more dental caries            in the preceding hundred years than there had been in any previous thousand-year            period and suggested that Activator X was a key substance that people            of the past obtained but that modern nutrition did not adequately provide.            Price used the combination of high-vitamin cod liver oil and high-Activator            X butter oil as the cornerstone of his protocol for reversing dental            caries. This protocol not only stopped the progression of tooth decay,            but completely reversed it without the need for oral surgery by causing            the dentin to grow and remineralize, sealing what were once active caries            with a glassy finish. One 14-year-old girl completely healed 42 open            cavities in 24 teeth by taking capsules of the high-vitamin cod liver            oil and Activator X concentrate three times a day for seven months.

Activator X also influences the composition of saliva. Price found            that if he collected the saliva of individuals immune to dental caries            and shook it with powdered bone or tooth meal, phosphorus would move            from the saliva to the powder; by contrast, if he conducted the same            procedure with the saliva of individuals susceptible to dental caries,            the phosphorus would move in the opposite direction from the powder            to the saliva. Administration of the Activator X concentrate to his            patients consistently changed the chemical behavior of their saliva            from phosphorus-accepting to phosphorus-donating. The Activator X concentrate            also reduced the bacterial count of their saliva. In a group of six            patients, administration of the concentrate reduced the Lactobacillus            acidophilus count from 323,000 to 15,000. In one individual, the            combination of cod liver oil and Activator X concentrate reduced the            L. acidophilus count from 680,000 to 0.

In the 1940s, researchers showed that menadione and related compounds            inhibited the bacterial production of acids in isolated saliva.⁴⁷ Menadione itself is a toxic synthetic analogue of vitamin K, but animal            tissues are able to convert a portion of it to vitamin K₂.            The ability of vitamin K-related compounds to inhibit acid production            in isolated saliva had no relationship to their vitamin activity, and            the most effective of these compounds had practically no vitamin activity            at all.⁴⁸ Researchers unfortunately assumed that because            vitamin K did not have a unique role in inhibiting acid formation in            saliva within a test tube that it had no nutritional role in preventing            tooth decay within living beings.

In 1945, American researchers conducted a double-blind, placebo-controlled            trial of menadione-laced chewing gum and showed it to reduce the incidence            of new cavities and cause a dramatic drop in the L. acidophilus count of saliva.⁴⁹ The next year, the Army Medical Department            attempted to repeat these results but failed, and research on vitamin            K and dental health in the United States was subsequently abandoned.⁵⁰ The authors of the original study assumed that the menadione exerted            its effect simply as a topical anti-bacterial agent, even though it            was highly unlikely to sustain a sufficient concentration in the saliva            to exert this effect. Ten years later, German researchers showed that            injecting menadione into the abdominal cavities of hamsters more effectively            prevented tooth decay than feeding it orally.⁵¹ Although            they could not rule out the possibility that some of this menadione            was secreted into the saliva, their results argued in favor of a nutritional            role for the vitamin K₂ that would have been produced from            it. Despite this finding, to this day no one has investigated the role            of natural K vitamins in the prevention of dental caries.

Nevertheless, our continually expanding understanding of the physiology            of both K vitamins and teeth now makes it clear that vitamin K₂ plays an essential role in dental health. Of all organs in the body,            vitamin K₂ exists in the second highest concentration in            the salivary glands (the highest concentration is found in the pancreas).            Even when rats are fed only K₁, nearly all of the vitamin            K in their salivary glands exists as K₂.¹⁵ Both            vitamin K⁵² and vitamin K-dependent proteins⁵³ are            secreted into the saliva, although their function is unknown.

We now know that the growth and mineralization of the dentin that Price            observed in response to the combination of cod liver oil and Activator            X concentrate would primarily require three essential factors: vitamins            A, D, and K₂. There are three calcified tissues of the teeth:            the cementum forms the roots, the enamel forms the surface, and the            dentin forms the support structure beneath it. Cells called odontoblasts            lining the surface of the pulp just beneath the dentin continually produce            new dentin material. If a cavity invades the dentin and reaches these            cells they can die. The pulp tissue, however, contains stem cells that            can differentiate into new odontoblasts that could regenerate the lost            dentin if the right conditions were present.⁵⁴

Dentin is unique among the tissues of the teeth for its expression            of osteocalcin, a vitamin K-dependent protein better known for its role            in organizing the deposition of calcium and phosphorus salts in bone.            In the infant rat, whose teeth grow very rapidly, dentin manufactures            much more osteocalcin than bone does, suggesting that osteocalcin plays            an important role in the growth of new dentin. Matrix Gla protein (MGP),            which is required for the mineralization of bone, is also expressed            in dentin.⁵⁵ Vitamins A and D signal odontoblasts to produce            osteocalcin,^56,57 and probably regulate their expression            of MGP as well. Only after vitamin K₂ activates these proteins’            ability to bind calcium, however, can they lay down the mineral-rich            matrix of dentin. The remarkable synergy between these three vitamins            exactly mirrors the process Price observed.

Vitamin K2 and Bone Health

Price also believed that Activator X played an important role in bone            health. Butter oil concentrate cured rickets and increased serum levels            of calcium and phosphorus in rats consuming a mineral-deficient diet.            In a four-year-old boy who suffered from rampant tooth decay, seizures            and a tendency to fracture, the combination of a large helping of this            concentrate and a meal of whole wheat and whole milk rapidly resolved            each of these symptoms.

Although the small amount of vitamin D in the butter oil was probably            sufficient to cure rickets and the combination of vitamins A and D most            likely produced the rise in serum calcium and phosphorus,⁵⁸ vitamin K₂ has a definite role in bone health. There are            at least two vitamin K-dependent proteins that fulfill important functions            in skeletal metabolism: matrix Gla protein (MGP) and osteocalcin.

In 1997, researchers from the University of Texas and the University            of Montreal developed mice that lacked the gene that codes for MGP.            These mice appeared normal for the first two weeks of their lives, after            which they developed faster heart beats, stopped growing and died within            two months with the rupture of their heavily calcified aortas. The disorganization            of their cartilage cells not only produced short stature, but also produced            osteopenia and spontaneous fractures.³⁸

The bones of mice that lack the osteocalcin gene mineralize just as            well as those of mice that do not lack the gene, but the mineral deposits            are organized differently. This could mean that osteocalcin is important            to the functional quality of bone and the ability to regulate its shape.⁵⁹ Isolated human osteoblasts, the cells that lay down the calcified matrix            of bone, secrete osteocalcin in response to vitamins A and D.³⁴ The protein-rich matrix surrounding these cells will only accumulate            this osteocalcin, however, if it is activated by vitamin K₂.            Calcification of the extracellular matrix occurs in parallel with the            accumulation of osteocalcin, but it is not clear whether this protein            plays a direct role in laying down the calcium salts or if its accumulation            simply reflects the higher amount of vitamin K₂ that is available            to activate other proteins involved more directly in mineralization            such as MGP.³⁵

When there is an insufficient amount of vitamin K to keep up with the            production of vitamin K-dependent proteins, many of these proteins are            secreted into the blood in an inactive form. Circulating cells then            take up these useless proteins and destroy them.⁴⁰ By drawing            a person’s blood and testing the percentages of circulating osteocalcin            that are active and inactive, we can determine whether that person’s            bone cells have enough vitamin K to meet their needs. People with the            highest percentages of inactive osteocalcin are at a more than five-fold            increased risk of hip fracture,60 confirming the value of the test.

By using this test, we can also show that vitamin K₂ is            the preferred K vitamin of the bones. It takes one milligram per day            of a highly absorbable pharmacological preparation of vitamin K₁ to maximally activate osteocalcin in human subjects;²⁸ it            appears, however, that humans are not capable of absorbing much more            than one fifth this amount from whole foods.²⁴ By contrast,            large amounts of vitamin K₂ are readily absorbed from foods.²⁶ Even when using highly absorbable forms of these vitamins, vitamin K₂ is much more effective. Researchers from the University of Maastricht            in the Netherlands recently showed that over the course of 40 days,            vitamin K₂ was three times more effective than vitamin K₁ at raising the percentage of activated osteocalcin. Moreover, the effect            of vitamin K₁ reached a plateau after just three days, whereas            the effect of vitamin K₂ increased throughout the entire            study. Had it lasted longer, the study may have shown an even greater            superiority of vitamin K₂.³²

We can therefore regard the percentage of inactive osteocalcin primarily            as a marker for vitamin K₂ status. In the healthy adult population,            one hundred percent of the vitamin K-dependent blood coagulants produced            by the liver are in their active form. By contrast, in this same population            between ten and thirty percent of circulating osteocalcin is in its            inactive form. Researchers rarely encounter individuals whose osteocalcin            is fully activated.³¹ This suggests that vitamin K₂ deficiency is universal, and that variation in K₂ status            within the population simply reflects varying degrees of deficiency.

Vitamin K₁ supplements produce modest decreases in bone            loss in the elderly. A number of Japanese trials, on the other hand,            have shown that vitamin K₂ completely reverses bone loss            and in some cases even increases bone mass in populations with osteoporosis.³¹ The pooled results of seven Japanese trials show that vitamin K₂ supplementation produces a 60 percent reduction in vertebral fractures            and an 80 percent reduction in hip and other non-vertebral fractures.⁶¹ These studies used extremely high amounts of vitamin K₂ and            did not observe any adverse effects over the course of several years.            Since they used such high doses of K₂, however, and no studies            have tested lower doses, they do not constitute definitive proof that            the vitamin activity rather than some drug-like action unique to the            high dose produced such dramatic results. The balance of the evidence,            however, suggests that vitamin K₂ is essential to skeletal            health and that it is a key substance that modern diets do not adequately            provide.

Vitamin K2 and Heart Disease

Price analyzed more than 20,000 samples of dairy products sent to him            every two to four weeks from various districts of the United States,            Canada, Australia, Brazil and New Zealand. Dividing the total area into            many districts, each producing dairy products with different patterns            of seasonal fluctuation in vitamin A and Activator X content, he found            an inverse relationship in each district between the vitamin content            of butterfat and the mortality from pneumonia and heart disease.

The role of vitamin A in the immune system is well established. We            do not currently know, however, whether vitamin K₂ plays            an important role in the immune system. Nevertheless, lymph glands and            bone marrow accumulate large amounts of it⁶² and a vitamin            K-dependent protein called gas6 plays a role in phagocytosis,³³ a process wherein immune cells destroy and consume foreign cells or            the body’s own cells when they are infected or no longer needed. It            is therefore possible that K vitamins could play an important role in            protecting against infectious diseases such as pneumonia.

Vitamin K₂‘s ability to protect us from heart disease is            much more clearly established. Research is in fact rapidly redefining            heart disease largely as a deficiency of this vitamin. While it is most            clearly established that vitamin K₂ deficiency causes calcification            of the cardiovascular system, vitamin K₂ appears to protect            against the inflammation and accumulation of lipids and white blood            cells that characterize atherosclerosis as well.

Cardiovascular calcification can begin as early as the second decade            of life, and is nearly ubiquitous in the population by the age of 65.³³ There are primarily two types: calcification of the heart valves and            tunica media constitutes one type, while calcification of the tunica            intima constitutes the second. The tunica media is the middle layer            of the artery; it contains elastic fibers that allow the artery to stretch            and accommodate varying degrees of pressure. The elastic fibers of the            tunica media and the valves of the heart calcify during diabetes, kidney            disease and aging. The tunica intima is the innermost layer of the artery            and is the site where atherosclerosis develops. In atherosclerosis,            calcified deposits rich in lipids and white blood cells accumulate on            the debris left behind by the blood vessel’s smooth muscle cells once            they have died.⁶³

In healthy arteries, the vitamin K-dependent matrix Gla protein (MGP)            congregates around the elastic fibers of the tunica media and guards            them against the formation of crystals by the calcium that circulates            in the blood. The inactive form of MGP, which cells produce when they            do not have sufficient K vitamins to meet their needs, does not exist            in healthy arteries. In early atherosclerosis, by contrast, most MGP            exists in its inactive form and associates with calcified structures            containing lipids, white blood cells, and the remnants of dead smooth            muscle cells. Inactive MGP also accumulates within the calcified deposits            of the medial sclerosis that occurs during diabetes, kidney disease            and aging. Although blood tests for the percentage of inactive and active            MGP are not available, patients with severe calcifications have high            percentages of inactive osteocalcin, indicating a general deficiency            of vitamin K₂.⁶³

Two other vitamin K-dependent proteins are likely to play a role in            the development of atherosclerosis: gas6 and protein S. Gas6 promotes            the survival of the smooth muscle cells that line the intima and the            rapid clearance of those that die. The rapid clearance of these dead            cells may be important for preventing the accumulation of the calcified            lipids and white blood cells that gather around them. Protein S guides            the immune system to clear away this debris from the intima gently rather            than mounting a dangerous inflammatory attack against it.³³ As these observations all predict, experimental and epidemiological            evidence both show that vitamin K₂ is a powerful inhibitor            of cardiovascular disease.

Mice that lack the gene for MGP develop extensive calcification of            the aorta, aortic valves and arteries soon after birth and bleed to            death within two months when their heavily calcified aortas rupture.³⁸ Warfarin, which inhibits the recycling of K vitamins⁴⁰ and            the conversion of K₁ to K₂,⁶⁴ causes            calcification of the tunica media in rats within two weeks,²¹ increases arterial stiffness, decreases the ability of the artery to            accommodate moderately high levels of blood pressure, and causes the            death of the artery’s smooth muscle cells.65 Marcoumar, a similar drug,            doubles the degree of aortic valve calcification in humans over the            course of one to three years.⁴²

Large amounts of vitamin K₂ completely inhibit the ability            of Warfarin to cause arterial calcification in rats. Vitamin K₁,            by contrast, has no inhibitory effect at all.²¹ Researchers            from the University of Maastricht recently showed that both K vitamins            can reverse calcification that has already occurred in Wistar Kyoto            rats.⁶⁵ The K vitamins also reduced the number of dead smooth            muscle cells after Warfarin treatment, showing that vitamin K-dependent            proteins not only promote cell survival but also facilitate the safe            clearance of cells that have died. Although both K vitamins were effective,            these rats convert vitamin K₁ to vitamin K₂ with            great efficiency. In the absence of Warfarin, two-thirds of the vitamin            K in the blood vessels of the rats that consumed K₁ alone            existed as K₂. In the presence of Warfarin, however, which            inhibits the conversion, none of the vitamin K in these blood vessels            existed as K₂. Apparently, vitamin K₁ is effective            after but not during Warfarin treatment because it can only protect            against arterial calcification insofar as it is converted to vitamin            K₂.

In the Nurses’ Health Study, the risk of heart disease was a modest            16 percent lower for those consuming more than 110 micrograms per day            of vitamin K₁, but there was no benefit from consuming any            more than this.⁶⁶ This small amount is equivalent to consuming            only three servings of kale per month. The Health Professionals Follow-Up            Study generated a similar finding in men, although it lost significance            after adjustment for other dietary risk factors.⁶⁷ It isn’t            clear whether the slight increase in risk associated with only the lowest            intakes reflects the possibility that only very small amounts of vitamin            K₁ are absorbed, or simply reflects the association between            K₁ intake and a healthy lifestyle. People who consume more            vitamin K₁ weigh less, smoke less, eat more fruits, vegetables,            fish, folate, vitamin E and fiber,⁶⁸ and are more likely            to use vitamin supplements.⁶⁷

The inverse association between heart disease and vitamin K₂ intake is more straightforward. In The Rotterdam Study, which prospectively            followed just over 4,600 men aged 55 or older in the Netherlands, the            highest intake of vitamin K₂ was associated with a 52 percent            lower risk of severe aortic calcification, a 41 percent lower risk of            coronary heart disease (CHD), a 51 percent lower risk of CHD mortality,            and a 26 percent lower risk of total mortality. Even though the study            population consumed ten times more K₁ than K₂,            vitamin K₁ had no association with either the degree of aortic            calcification or the risk of heart disease.²⁰ The profound            effects of variations in such small amounts of dietary K₂ emphasize just how powerful this substance is in the prevention of degenerative            disease.

Vitamin K2 and the Brain

Price supplied several anecdotes suggesting that Activator X plays            an important role in the nervous system. Price administered a daily            meal of nutrient-dense whole foods supplemented with high-vitamin cod            liver oil and high-Activator X butter oil to the children of impoverished            mill workers who suffered from rampant tooth decay. The treatment not            only resolved the tooth decay without the need for oral surgery, but            resolved chronic fatigue in one boy and by the report of their school            teachers produced a marked increase in learning capacity in two others.

Price also administered the butter oil concentrate to a four-year-old            who suffered from rampant tooth decay, a fractured leg and seizures.            A dessert spoonful of the butter oil served over whole wheat gruel with            whole milk once before bed and five times over the course of the following            day immediately resolved his seizures. Rapid healing of his fracture            and dental caries followed soon after. The fact that these three symptoms            appeared together and resolved following the same treatment suggests            a common cause for each of them. Sixty years later, modern research            is now elucidating the essential role that vitamin K₂ plays            not only in the dental and skeletal systems, but in the nervous system            as well. This strongly suggests it was the key unidentified factor in            Price’s protocol.

The brain contains one of the highest concentrations of vitamin K₂ in the body; only the pancreas, salivary glands, and the cartilaginous            tissue of the sternum contain more. When male Wistar rats consume vitamin            K₁ alone, 98 percent of the vitamin K in their brains exists            as K₂, demonstrating the overwhelming preference of the nervous            system for this form. The K₂ contents of these four tissues            remain remarkably high on a vitamin K-deficient diet, suggesting either            that the vitamin is so essential to their function that they have developed            a highly efficient means of preserving it, or that it plays a unique            role in these tissues that does not require as high a rate of turnover            as is required by the roles it plays in most other tissues.¹⁵

An analysis of three autopsies showed that vitamin K₂ makes            up between 70 and 93 percent of the vitamin K in the human brain.⁶⁹ It is not clear why humans exhibit greater variation in this percentage            than rats, although it could be that we convert K₁ less efficiently            and are therefore more dependent on dietary K₂.

Vitamin K₂ supports the enzymes within the brain that produce            an important class of lipids called sulfatides. The levels of vitamin            K₂, vitamin K-dependent proteins and sulfatides in the brain            decline with age; the decline of these levels is in turn associated            with age-related neurological degeneration.⁴⁶ Comparisons            of human autopsies associate the early stages of Alzheimer’s disease            with up to 93 percent lower sulfatide levels in the brain.⁷⁰ Warfarin treatment or dietary vitamin K deficiency causes lack of exploratory            behavior and reduced physical activity in rats that is suggestive of            fatigue.⁷¹ Animals that completely lack the enzymes to make            sulfatides and a related class of lipids, cerebrosides, progressively            suffer from growth retardation, loss of locomotor activity, weak legs            and seizures.⁷²

These observations suggest that deficiencies in vitamin K, especially            vitamin K₂, could result in fatigue and learning difficulties            in humans, and that rare, extreme deficiencies of vitamin K₂ in the brain could result in seizures. If this is the case, it would            explain why Price observed tooth decay, bone fracture, learning difficulties            and seizures to share a common cause and a common solution.

Other Roles of Vitamin K2

Our understanding of the K vitamins is rapidly expanding and we are            likely to discover many new roles for them as the twenty-first century            progresses.

The highest concentration of vitamin K₂ exists in the salivary            glands and the pancreas. These organs exhibit an overwhelming preference            for K₂ over K₁ and retain high amounts of the            vitamin even when animals consume a vitamin K-deficient diet.¹⁵ The high presence of the vitamin in both of these organs suggests a            role in activating digestive enzymes, although its apparent role in            the regulation of blood sugar could explain its presence in the pancreas.⁷⁶ The testes of male rats also exhibit a high preference for and retention            of vitamin K₂,¹⁶ and human sperm possess a vitamin            K-dependent protein with an unknown function.⁷⁷ The kidneys            likewise accumulate large amounts of vitamin K₂⁶⁹ and secrete vitamin K-dependent proteins that inhibit the formation            of calcium salts. Patients with kidney stones secrete this protein in            its inactive form, which is between four and twenty times less effective            than its active form at inhibiting the growth of calcium oxalate crystals,            suggesting that vitamin K₂ deficiency is a major cause of            kidney stones.⁷⁷

The use of Warfarin during pregnancy produces developmental malformations            of the face; as the nasal cartilage calcifies, growth of the nose comes            to an early end, resulting in a stubby appearance.⁷⁸ Vitamin            K₂ therefore most certainly played a role in the development            of beautiful faces with broad features that Price observed among primitive            peoples.

A number of cell experiments have shown that vitamin K₂ has powerful anti-carcinogenic properties that may make it useful in            preventing or treating cancer in humans.⁷⁹

Researchers have recently discovered a whole new class of vitamin K-dependent            proteins called transmembrane Gla (TMG) proteins. Their functions are            unknown.³³

The K vitamins perform all of their well understood roles in the part            of the cell responsible for the modification of proteins. Only a portion            of the vitamin K within a cell exists in this area, however. Even more            exists in the inner membrane of the mitochondria where the cell produces            its energy.⁴⁵ The greatest concentration exists in the nucleus,            which possesses a receptor for vitamin K that may be involved in regulating            the expression of genes.⁴⁴ Vitamin K₂ has a greater            affinity than vitamin K₁ for both the mitochondrial membrane            and the nuclear receptor. We presently know virtually nothing about            these functions of the K vitamins and the plot will only thicken as            the story unfolds.

Vitamin K2 in Foods

Figure 4 shows the distribution of vitamin K₂ in selected foods. Precise values for the organ meats that would be            richest in K₂ are not available. The pancreas and salivary            glands would be richest; reproductive organs, brains, cartilage and            possibly kidneys would also be very rich; finally, bone would be richer            than muscle meat.^15,16,69 Analyses of fish eggs, which Price            found to be rich in Activator X, are not available.

Commercial butter is only a moderate source of vitamin K₂.            After analyzing over 20,000 samples of butter sent to him from around            the world, however, Price found that the Activator X concentration varied            50-fold. Vitamin K-rich cereal grasses, especially wheat grass, and            alfalfa in a lush green state of growth produced the highest amounts            of Activator X, but the soil in which the pasture was grown also profoundly            influenced the quality of the butter. The concentrations were lowest            in the eastern and far western states where the soil had been tilled            the longest, and were highest in Deaf Smith County, Texas, where excavations            proved the roots of the wheat grass to pass down six feet or more through            three feet of top soil into deposits of glacial pebbles cemented together            with calcium carbonate. It was this amazingly vitamin-rich butter that            had such dramatic curative properties when combined with high-vitamin            cod liver oil and nutrient-dense meals of whole milk, whole grains,            organ meats, bone broths, fruits and vegetables.

For over 50 years after Price described his discovery of Activator            X, the medical and nutritional communities saw vitamin K merely as a            requirement for blood clotting. The poor understanding of the functions            of the K vitamins within the body and the apparent lack of any relationship            between Price’s chemical test and the structure of any known vitamin            made it impossible to determine the identity of this mysterious substance.            We now know, however, that vitamin K₂ and Activator X are            one and the same. Like Price’s X factor, vitamin K₂ is synthesized            by animal bodies from its precursor in rapidly growing grass. Cereal            grasses and alfalfa are rich in this precursor, and these plants accumulate            it in direct proportion to their photosynthetic activity. It is critical            to the ability of teeth and bones to lay down mineralized tissue, and            to the prevention of degenerative diseases of the cardiovascular and            nervous systems. It is the key factor that acts in synergy with vitamins            A and D: these vitamins command cells to make proteins, but vitamin            K brings these proteins to life. It is an “activator,” then,            in the truest sense of the word, and it is therefore fitting that we            knew it for so many decades simply as “Activator X.”

Thank you to Michael Eiseike, a health researcher from Hokkaido            Japan, for originally bringing the Rotterdam Study to our attention            and suggesting that vitamin K₂ may be the X Factor of Weston            Price; and also to David Wetzel of Green Pasture Products for his input            and advice.

Figures

Figure 1: The Structure of K Vitamins and Their            Chemical Behavior

Single lines represent single bonds between carbon atoms; double lines            represent double bonds between carbon atoms. Hydrogen atoms are attached            to most of the carbons but are not shown.

a.

Vitamin K₁. The side chain extending to the right of the            molecule is monounsaturated.

b.

Vitamin K₂. The nucleus, composed of two ring structures,            is the same as that of vitamin K₁. The side chain, however,            is polyunsaturated rather than monounsaturated.

c.

Either K vitamin would be expected to react with hydriodic acid (HI)            by absorbing hydrogen atoms and liberating diatomic iodine (I2). The            side chain is abbreviated by the letter “R.”

d.

If the mixture of the vitamin K and hydriodic acid is combined with            a starch indictor, the diatomic iodine liberated by the reaction would            turn the starch blue.

Figure 3. Vitamin K-Dependent Carboxylation

<!–

a. O=C=O O(-1) | b.C=O

O(-1) | C=O | c. —Glutamate— (Glu)

CO2 | \/ Vitamin K- -Dependent Carboxylase

Ca(+2) (-1)O   O(-1) |   | O=C  C=O \  / —γ-Carboxy— Glutamate (Gla)

–>

a.) A carbon dioxide molecule b.) a carboxyl group c.) Vitamin K-dependent carboxylation

The vitamin K-dependent carboxylase rearranges the chemical bonds            within carbon dioxide molecules. Carboxyl groups contain carbon and            oxygen atoms and carry a charge of negative one. Calcium carries a charge            of positive two. The side chains of the amino acid glutamate normally            carry one carboxyl group; the vitamin K-dependent addition of a second            carboxyl group gives these side chains a charge of negative two and            thus allows them to bind to calcium, which has the equal and opposite            charge. This process transforms glutamate into γ-carboxyglutamate,            abbreviated Gla. For this reason, many vitamin K-dependent proteins,            such as matrix Gla protein (MGP), contain “Gla” in their name.

Figure 4: Vitamin K2 Contents of Selected Foods^{22,            26}

The percentage of vitamin K₂ present as MK-4 represents            that synthesized by animal tissues, while the remainder represents that            synthesized by bacteria during fermentation.

SIDEBARS

The Activator X Test

The chemical test that Price eventually came to use for the quantification            of Activator X in foods was originally suggested as an indirect test            for vitamin D by Lester Yoder of the Agricultural Experiment Station            of Iowa State College in 1926.⁸ The basic principle of the            test, called iodometric determination, was most commonly utilized in            the United States for detecting the presence of organic peroxides.⁹ Since peroxides are capable of oxidizing ionic iodide to diatomic iodine,            researchers can detect them by combining the test substance with hydriodic            acid and a starch indicator. Hydriodic acid releases iodide ions into            a solution. If peroxides are present, they convert these iodide ions            to diatomic iodine, which then turns the starch blue or purple.

This is somewhat similar to the amylase test that is used as a demonstration            in many high school or college biology classes. In that test, however,            preformed iodine is used; in the absence of amylase, the iodine turns            the starch blue, while in the presence of amylase, the starch is broken            down into sugar and the color change does not occur.

At the time, the only way to test a food for vitamin D was to feed            it to rats on a mineral-deficient diet, kill the rats, and analyze the            mineral content of their bones. The richer the food was in vitamin D,            the more it would stimulate absorption of the small amounts of calcium            and phosphorus in the diet and the higher the bone mineral content would            be. Yoder suggested, however, that there was a general correlation between            the ability of an oil to peroxidize (become rancid) and its vitamin            D content, and advocated testing an oil’s ability to oxidize iodide            as an indirect indicator of its level of vitamin D. Having no other            convenient chemical test, Price adopted this as his test for vitamin            D.

The test was far from perfect. Yoder found peroxidation in substances            with no vitamin D activity such as turpentine, a thirteen-year-old sample            of cholesterol, and an aged sample of mineral oil. He further found            that irradiating foods to the point at which their vitamin D activity            was destroyed actually increased their score on the test.⁸

As Price used this test on over 20,000 samples of dairy foods sent            to him from around the world, he realized that the physiological effects            that correlated with a food’s ranking were different from those attributable            to isolated vitamin D, and began using the term “Activator X”            to describe the nutritional substance that the test was measuring. He            observed that the vitamin content of these butter samples varied fifty-fold,            and that the samples richest in Activator X were the most potent for            controlling dental caries. Clearly, Price’s test was detecting something            besides rancid oils.

While researchers who published in English language journals traditionally            used this test to detect peroxides, researchers publishing in Russian            and German language journals had been using it to detect the synthetic            compound benzoquinone all along.^10,11 Benzoquinone belongs            to a class of chemicals called quinones that includes biological molecules            such as coenzyme Q₁₀ and the K vitamins. These quinones possess            oxygen-containing ring structures whose oxygens will steal electrons            and hydrogen ions from hydriodic acid and thereby oxidize ionic iodide            to diatomic iodine, causing the starch to become a bluish purple color            (see Figure 1).

In the 1970s, researchers from Britain and Denmark were debating whether            or not healthy rat tissues contained lipid peroxides. The British researchers            used the iodometric method to determine peroxide levels and argued that            healthy rat tissues did contain peroxides, while the Danish researchers            used a different method and argued that they did not. In a 1972 paper            published in the British Journal of Nutrition, the Danish researchers            demonstrated that the iodometric method was not showing the existence            of peroxides in the rat tissues, but rather the existence of coenzyme            Q₁₀ and probably other quinones.¹²

Price’s test, therefore, was not specific to any one particular chemical            compound. When used for fresh oils, however, it would be able to detect            a number of nutrients that include coenzyme Q₁₀ and the K            vitamins. As shown in this article, it is the K vitamins that we should            expect to vary in direct proportion to the amount of richly green grass            in the diet of the animals, while the physiological effects Price identified            with Activator X are specifically attributable to vitamin K₂.

Interactions between            Vitamins A, D, and K2

Is Vitamin K2 an Essential Nutrient?

Vitamins K₁ and K₂ are both effective cofactors            for the enzyme that activates vitamin K-dependent proteins,²³ but the liver preferentially uses vitamin K₁ to activate            clotting factors while most other tissues preferentially use vitamin            K₂ to activate the other vitamin K-dependent proteins.²¹ Although animals can convert vitamin K₁ to vitamin K₂,¹⁴ there are a number of lines of evidence strongly suggesting that humans            require preformed K₂ in the diet to obtain optimal health.

Humans appear to have a finite ability to absorb vitamin K₁ from plant foods. In the United States, where the mean intake of vitamin            K₁ is less than 150 micrograms per day, blood levels increase            with increasing dietary intake until the latter reaches two hundred            micrograms per day, after which they plateau. In the Netherlands, where            the mean intake of vitamin K₁ is much higher (250 micrograms            per day), plasma levels of vitamin K₁ have no relationship            to dietary intake at all.²⁴ These results suggest that humans            do not possess the ability to absorb much more than 200 micrograms of            vitamin K₁ per day from vegetables.

This interpretation is also supported by feeding experiments. Whereas            the absorption of vitamin K₂ from natto, a fermented soy            food, is nearly complete, the absorption of vitamin K₁ from            servings of green vegetables ranging from two hundred to four hundred            grams consumed without added fat is only between five and ten percent.            The absorption of similarly sized servings of vegetables with added            fat is still only between ten and fifteen percent.^25-26 By            contrast, smaller servings are absorbed more efficiently. For example,            the absorption from a 150-gram serving of spinach is 17 percent and            the absorption from a 50-gram serving of spinach is 28 percent.²⁷ These results show that our absorption of the vitamin declines as the            amount we consume increases and strengthens the interpretation that            we might only be able to absorb about 200 micrograms per day. When study            subjects consume a highly absorbable pharmacological preparation of            vitamin K₁, a dose of 1000 micrograms per day is required            to maximize the activation of proteins important to bone metabolism.²⁸ If we can only absorb one-fifth of this amount from vegetables, we cannot            support our skeletal system with vitamin K₁ regardless of            how efficiently we may be able to convert it to vitamin K₂.

The ability to convert K₁ to K₂ varies widely            between species and breeds of animals. The German researchers who first            reported this conversion found that rats made it poorly compared to            birds and that pigeons made it most efficiently.¹⁴ Every            tissue tested in male Wistar rats is capable of making the conversion,¹⁵ whereas the liver, kidneys and heart of male Lewis rats will preferentially            accumulate preformed K₂, but, unlike the pancreas and testes            of these same animals, will not synthesize it from K₁.¹⁶ The K₂ content of human breast milk increases when mothers            consume pharmacological preparations of K₁, but the K₂ content of their blood does not;¹⁷ since the conversion takes            place in the target tissues rather than the blood, however, we do not            know how efficiently other human tissues make this conversion.

Vitamins K₁ and K₂ share a common ring-structured            nucleus but possess different types of side chains. The first step in            the conversion of K₁ to K₂ appears to be the cleavage            of its side chain in either the liver or the gastrointestinal tract,            yielding a toxic oxidizing agent called menadione; much of this metabolite            is detoxified by the liver and excreted in the urine, while the remaining            portion can be used to synthesize K₂ in tissues.²⁹ After this cleavage takes place, menadione must be transported to its            target tissues where cellular enzymes can add a side chain to it, completing            the transformation to K₂. Because they are transported in            different types of lipoproteins, vitamin K₁ is primarily            sent to the liver, whereas vitamin K₂ is primarily sent to            the other tissues;³⁰ we know very little, however, about            the transport of menadione in the blood. We also know very little about            the rate at which our cells are capable of adding side chains to these            molecules; presumably, if the supply of menadione exceeds the rate at            which the cell can add these side chains, the menadione will exert toxic            effects and cause oxidative damage within the cell. Preliminary evidence            indicates that doses of 1000 micrograms per day of supplemental K₁ may contribute to periodontal disease,³¹ suggesting that            our bodies’ resistance to absorbing this much K₁ from vegetables            may serve an important purpose.

The clearest demonstration that humans require dietary preformed vitamin            K₂ for optimal health is that epidemiological and intervention            studies both show its superiority over K₁. Intake of vitamin            K₂, for example, is inversely associated with heart disease            in humans while intake of vitamin K₁ is not,20 and vitamin            K₂ is at least three times more effective than vitamin K₁ at activating proteins related to skeletal metabolism.³² This nutritional superiority makes it clear why the primitive groups            that Weston Price studied expended so much effort procuring foods rich            in vitamin K₂ like the organs and fats of animals and the            deeply colored orange butter from animals grazing on rich pastures.

The Vitamin K-Dependent Carboxylase

Most known functions of the K vitamins are mediated by the vitamin            K-dependent carboxylase. The carboxylase is an enzyme bound to the membrane            of the endoplasmic reticulum, a cellular organelle involved in the synthesis            and modification of proteins. It uses vitamin K as a cofactor to add            carboxyl groups to the side chains of the amino acid glutamate within            certain vitamin K-dependent proteins (see Figure 3).            This gives them a negative charge, allowing them to bind to calcium,            which carries a positive charge.⁴⁰

Vitamin K-dependent proteins must be carboxylated before they leave            the cell or insert themselves into its membrane. They may contain anywhere            from three to thirteen glutamate residues (amino acids are called “residues”            when they are bound up within proteins) that must be carboxylated; the            carboxylase binds to them only once, however, and carboxylates each            of these before it releases the protein. On the other hand, vitamin            K can only be used for the carboxylation of a single glutamate residue            and the carboxylase must release it after each carboxylation and allow            it to be recycled and returned. A different enzyme, vitamin K oxidoreductase,            recycles the vitamin; this enzyme is the target of the anticoagulant            drug Warfarin and its relatives.⁴⁰ Since Warfarin targets            the recycling of vitamin K rather than the vitamin K-dependent coagulation            proteins themselves, it not only acts as an anticoagulant, but also            causes arterial and aortic valve calcification in both rats²¹ and humans^41,42 and inhibits the mineralization of bone matrix.³⁵

The distribution of the carboxylase among species and among tissues            within an organism can help us understand its significance and that            of its cofactor, vitamin K. With the exception of some microorganisms            that have “stolen” the enzyme by incorporating the genetic            material of other species,⁴³ the carboxylase is present only            in multicellular animals, underscoring its importance to intercellular            communication. In the growing embryo, it is first expressed in skeletal            and nervous tissue; vitamin K is therefore almost certainly essential            to the development of the skeletal and nervous systems from their very            beginnings.⁴⁰

Vitamin K’s activity as a cofactor for the carboxylase may only be            the tip of the iceberg. In osteoblasts, the cells responsible for bone            growth, the greatest concentration of vitamin K₂ exists in            the nucleus where the genetic material is; the second greatest concentration            exists in the mitochondria, the so-called “power house” of            the cell; finally, only the third greatest concentration exists in the            endoplasmic reticulum where the carboxylase is found.⁴⁴ We            do not currently have enough information to understand the role of the            K vitamins in the mitochondria or the nucleus. Osteoblasts possess a            nuclear receptor for vitamin K₂, suggesting it has a role            as a nuclear hormone. Vitamin K₂ has a higher affinity than            vitamin K₁ both for the nuclear receptor⁴⁴ and            for the mitochondrial membrane.⁴⁵ There is also evidence            that vitamin K₂ plays a role as an antioxidant within the            cells that synthesize the myelin sheath, which forms the electrical            insulation of nerves.⁴⁶ Although it took until the 1970s            to define the function of vitamin K as a cofactor for the carboxylase            enzyme, the twenty-first century may well ring in a new revolution in            our understanding of this amazing vitamin with the recognition that            it is, to modify a phrase coined by Tufts University’s Dr. Sarah Booth,            “not just for the carboxylase anymore.”

Vitamin K2 and the Brain: A Closer            Look

The concentration of vitamin K₂ is higher in myelinated            regions than in non-myelinated regions of the brain (myelin is the sheath            that forms the electrical insulation of neurons) and it is correlated            with the presence of important lipids such as sphingomyelin and sulfatides.            The small amount of K₁, by contrast, is distributed more            randomly,⁷³ suggesting that it may not be as functionally            important. These lipids are part of a broader class of compounds called            sphingolipids that play essential roles in the brain as structural constituents            of membranes, signaling factors, and promoters of cell survival. Vitamin            K₂ supports the activity of the enzyme that catalyzes the            initial reaction for the production of all sphingolipids as well as            the enzyme that catalyzes the final step in the synthesis of sulfatides.            Warfarin or dietary vitamin K deficiency cause marked decreases in the            activities of these enzymes and of the levels of sulfatides in the brains            of rats and mice, while the administration of either vitamin K₁ or K₂ restores them.⁴⁶

In addition to the production of sulfatides and other sphingolipids,            vitamin K₂ plays at least two other important roles in the            brain. The vitamin K-dependent protein gas6 promotes the survival of            brain cells,⁷⁴ and K vitamins, by an unknown mechanism, completely            protect against the free radical-mediated death of the cells that synthesize            myelin. Both an excess of glutamate and a deficiency of cystine can            cause this type of cell death. Although K₁ and K₂ protect against glutamate toxicity equally, K₂ is fifteen            times more effective than K₁ at counteracting the harmful            effects of cystine depletion. Oxidative stress in the vulnerable infant            brain can cause mental retardation, seizures, and cerebral palsy. Adequate            intake of vitamin K₂ during infancy may therefore protect            against these diseases.⁷⁵

Bacterial Production of Vitamin K2

“Vitamin K₂” actually refers to a group of compounds            called menaquinones. While vitamins K₁ and K₂ have different types of side chains, the side chains of the various            menaquinones within the K₂ group are all of the same type            but are of varying lengths. Each of these forms is abbreviated MK-n,            where “n” is a number that denotes the length of the side            chain. Animal tissues exclusively synthesize MK-4, but many anaerobic            bacteria synthesize other menaquinones, which they use for energy production            much in the way that plants use vitamin K₁.⁸⁰ We can therefore obtain vitamin K₂ by absorbing that which            is produced by our intestinal flora or by eating fermented foods, in            addition to eating animal foods which contain vitamin K₂ synthesized from vitamin K₁ found in grass.

Lactic acid bacteria mostly produce MK-7 through MK-10,¹⁸ while MK-10 and MK-11 accumulate in the human liver over time, presumably            originating from bacterial production in the gut.⁸¹ It was            once thought that intestinal bacteria were a major contributor to vitamin            K status: the menaquinone content of stools is high, antibiotics have            been associated with defects in blood clotting that resolve with vitamin            K supplementation, and autopsies show that the great majority of vitamin            K in the liver is present as “higher” menaquinones of bacterial            origin. The balance of the evidence, however, challenges this view.            Most of the menaquinones produced in the intestine are embedded within            bacterial membranes and unavailable for absorption. Antibiotics produce            vitamin K-responsive clotting defects not by reducing the intestinal            production of K vitamins, but by inhibiting the enzyme within the human            body that recycles them. Finally, the liver appears to accumulate higher            menaquinones not because it is supplied with them abundantly but because            it does not use them efficiently. Intestinal production of menaquinones            therefore likely makes some contribution to vitamin K status, but one            that is very small.⁸⁰

Fermented foods such as sauerkraut, cheese, and natto, a soy dish popular            in Eastern Japan, contain substantial amounts of vitamin K₂.            Natto, in fact, contains the highest amount of any food measured; nearly            all of it is present as MK-7.²⁶ MK-7 is highly effective:            one recent study showed that it increased the percentage of activated            osteocalcin in humans three times more powerfully than did vitamin K₁.³² There are no studies available, however, comparing the efficacy of MK-7            to that of the MK-4 found in animal products. MK-9, and presumably MK-7,            stays in the blood for a longer period of time than does MK-4, but this            appears to be because tissues take up MK-4 much more rapidly.³⁰ Whether the rapid uptake of MK-4 or the longer time spent in the blood            by bacterial menaquinones have particular benefits or drawbacks is unclear.            Future research will have to clarify whether the vitamin K₂ synthesized by animal tissues and by bacteria are interchangeable, whether            one is superior to the other, or whether each presents its own unique            value to our health.

Supplementing with Vitamin K2

The best sources of vitamin K₂ are fermented foods and grass-fed            animal fats. These foods contain a wide array of nutrients that may            act synergistically with vitamin K₂ in ways we do not yet            understand. Price ‘s vitamin-rich butter and butter oil concentrate            provided not only vitamin K₂ but also vitamin E, vitamin            A, vitamin D, conjugated linoleic acid (CLA) and other nutrients. Nevertheless,            some people may wish to supplement with vitamin K₂ if they            do not have access to high-quality food, wish to use a higher dose to            treat a health condition, or want extra insurance.

Two forms of vitamin K₂ supplements are commercially available:            menaquinone-4 (MK-4), also called menatetrenone, and menaquinone-7 (MK-7).            MK-4 is a synthetic product that is believed to be chemically and physiologically            identical to the vitamin K₂ found in animal fats. This form            has been used in most of the animal experiments and in the Japanese            osteoporosis studies. Although synthetic, it is effective, and there            is no known toxicity. MK-7 is a natural extract of natto, a fermented            soy food popular in Eastern Japan. MK-4 is much less expensive than            MK-7, but no studies have yet compared the efficacy of these two forms.

Menaquinone-4 Supplements: Thorne Research and Carlson            Laboratories both offer cost-effective MK-4 supplements. Thorne’s product            is a liquid supplement. The MK-4 is dissolved in a medium-chain triglyceride            base (the fats found in coconut oil) with mixed tocopherols (vitamin            E). Carlson’s product is less expensive than Thorne’s, but comes in            dry capsules primarily composed of cellulose and other fillers, and            allows the user less control over the dose.

Menaquinone-7 Supplements: Jarrow Formulas and Source            Naturals both offer cost-effective MK-7 supplements. Source Naturals’            product is less expensive, but Jarrow’s contains fewer additives and            certifies that the soy used to make the product is not genetically modified.            Vitamin K₂ supplements interfere with the activity of oral            anticoagulants such as warfarin. Patients who are using warfarin should            only use vitamin K₂ supplements with the knowledge of the            prescribing physician.

REFERENCES

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Follow Up Questions and Answers

Question: How much K₂ is recommended for adults and for            children?

Answer: Unfortunately we do not have any solid numbers on the optimal            or minimum intake of K vitamins, neither from modern scientific analysis            nor from what people consumed in optimal traditional diets. However,            we do know that virtually all adults have some degree of deficiency,            whether this is very small or very substantial, and a recent study suggests            that children are much more likely to be deficient, so children may            actually need more because they are growing. The best thing to do would            be to eat from the foods richest in vitamin K₂: natto, cheese            or goose liver, at least once a week and to eat from the other relatively            rich foods—grass-fed butter, animal fats and fermented foods—on a daily            basis. If you choose to take any of the supplements listed in the article            in addition to this, there is currently no reason to believe that it            is necessary to take more than the minimum dose (one drop of Thorne            or one capsule of Jarrow). In the years ahead, we should see much more            definitive information coming out on this, and hopefully we will also            see some research reopen the questions that Price had raised about the            agricultural practices that lead to the highest levels of Activator            X in foods.

Question: What is the appropriate dose of vitamin K₂ for            maintenance and therapeutic purposes?

Answer: We do not have adequate information on dosage requirements            for vitamin K₂. I would think that for maintenance one should            shoot for 100 mcg minimum, possibly more for children, but we will have            to wait for further research to quantify this. There are unpublished            anecdotes according to which some people have found up to 5-10 milligrams            useful for treating specific conditions, such as autism or spider veins.            At present, this is a matter that the individual must settle through            experimentation.

Question: Do we know the levels of vitamin K₂ in the primitive            societies studied by Dr. Price?

Answer: We have no quantitative information on K₂ as K₂ or as Activator X in primitive societies or in Price’s practice because            Price did not have a means of quantifying the levels by mass—for            example, how many micrograms were contained in a given food sample.            Price could only compare different foods based on the intensity of the            blue color yielded by the test, which he then compared to standards            made from numerous different dilutions of a blue dye. So Price could            say that one food was a richer or poorer source than another, but he            could not determine the precise amount contained within the food.

Question: Is the K₂ found in animal products or fermented            foods affected by cooking?

Answer: I have yet to see any hard data on cooking losses, but everything            I have read indicates that vitamin K is very heat-stable (though it            can apparently incur losses from exposure to light).

Question: Is the Wulzen anti-arthritis factor in butter a separate            compound from K₂?

Answer: I do not know whether the Wulzen factor is a separate compound;            however, others have suggested that they are separate because Wulzen            found this factor to be destroyed by pasteurization, whereas Price and            maybe others found activator X to be heat-stable.

Question: Fermented foods are said to be good sources of K₂ but in your article you say that most of the vitamin K₂ produced            by bacteria in the gut is now believed to be embedded in the bacterial            membranes and unavailable for absorption. One might think therefore            that the vitamin K₂ produced in fermented foods is similarly            unavailable. Are the bacteria in fermented foods different? Does stomach            digestion free up the K₂?

Answer: Whether it is because some bacteria secrete the K₂ or because the acidic digestion of the stomach ruptures the membranes            I do not know, but the absorption of K₂ from natto is near            complete.

Question: Does yogurt contain vitamin K₂?

Answer: Yogurt has roughly the same amount of K₂ as milk,            with just a tiny bit produced. This is probably because commercial yogurt            is only fermented for four hours, whereas hard cheese is fermented for            at least two months.

Question: Can you calculate how much K₂ is in commercial            versus grass-fed butter?

Answer: I do not think this can be calculated. The primary confounder            is that commercial butter comes from cows in confinement operations            fed massive amounts of menadione, a portion of which can be converted            into K₂. We have no idea at what rate this is turned into            K₂ and how it compares to K1 from grass as a precursor to            K₂, so we have no baseline from which to calculate.

Question: I’d like to use natto as a source of K₂, but I            have an allergy to yeast. Do you know which microorganisms ferment soy            to create natto, and whether yeast is used in other parts of the process?

Answer: Natto is fermented with Bacillus subtilus, subspecies natto.            Yeast is not essential to the process as far as I know, but I do not            know whether the cultures tend to pick up yeast or whether for some            reason some products may also deliberately use yeast. You may want to            inquire with a specific manufacturer or from whomever you buy the culture            if you choose to make your own.

Editor’s note: Natto is definitely an acquired taste, one usually not            acceptable to westerners.

This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Spring 2007.

About the Author

[authorbio:masterjohn-chris]

 www.westonaprice.org

Conclusion: A combination of dietary and non-dietary lifestyle modifications, begun in midlife or later in relatively healthy women, could have prevented at least half of the cases of type 2 diabetes in this cohort study of U.S. women.

Results: The 24-year risk of diabetes was 9.6% under no intervention and 4.3% when all interventions were imposed (55% lower risk [95% confidence interval = 47 to 63%]).
The most effective interventions were:
• weight loss (24% lower risk)
• physical activity (19%)
• moderate alcohol use (19%)
Overweight/obese women would benefit the most, with 10.8% point reduction in 24-year risk of diabetes. The validity of these estimates relies on the absence of unmeasured confounding, measurement error, and model misspecification.

Methods: Using data from the Nurses’ Health Study, we followed 76,402 women from 1984 to 2008.
We estimated the risk of type 2 diabetes under eight hypothetical interventions:
• quitting smoking
• losing weight by 5% every 2 years if overweight/obese
• exercising at least 30 minutes a day
• eating less than three servings a week of red meat
• eating at least two servings a day of whole grain
• drinking two or more cups of coffee a day
• drinking five or more grams of alcohol a day
• drinking less than one serving of soda a week

Background: Randomized trials have examined short-term effects of lifestyle interventions for diabetes prevention only among high-risk individuals. Prospective studies have examined the associations between lifestyle factors and diabetes in healthy populations but have not characterized the intervention. We estimated the long-term effects of hypothetical lifestyle interventions on diabetes in a prospective study of healthy women, using the parametric g-formula.

Ref: Danaei, Goodarz; Pan, An; Hu, Frank B.; Hernán, Miguel A. EPIDEMIOLOGY, 20131044-3983

Antibodies tell us the state of health of our cells in the presence of invading pathogens and infections/viruses. We must ensure a healthy immune system and lymphatic system (cleans our blood from toxins).

Pathologies of antibodies

Anti-thyroid peroxidase antibodies are associated with the absence of distant metastases in patients with newly diagnosed breast cancer.

The production of antibodies in Graves’ Disease is thought to arise by activation of CD4+ T-cells, followed by B-cell recruitment into the thyroid. These B-cells produce antibodies specific to the thyroid antigens.  In Hashimoto’s Thyroiditis, activated CD4+ T-cells produce interferon-γ, causing the thyroid cells to display MHC class II molecules.  This expands the autoreactive T-cell repertoire and prolongs the inflammatory response.

Anti-thyroid autoantibodies (or simply anti-thyroid antibodies) are autoantibodies targeted against one or more components of the thyroid. The most clinically relevant anti-thyroid autoantibodies are anti-thyroid peroxidase antibodies (anti-TPO antibodies), thyrotropin receptor antibodies (TRAbs) and thyroglobulin antibodies. TRAbs are subdivided into activating, blocking and neutral antibodies, depending on their effect on the TSH receptor.

Anti-sodium/Iodide (Anti–Na⁺/I⁻) symporter antibodies are a more recent discovery and their clinical relevance is still unknown. Graves’ Disease and Hashimoto’s Thyroiditis are commonly associated with the presence of anti-thyroid autoantibodies.

Although there is overlap, anti-TPO antibodies are most commonly associated with Hashimoto’s Thyroiditis and activating TRAbs are most commonly associated with Graves’ Disease. Thyroid microsomal antibodies were a group of anti-thyroid antibodies, they were renamed after the identification of their target antigen.

Connie’s comments: Being happy, strong immune system, proper hygiene and healthy pregnancy ensures a strong immune system.

CLINICAL NEUROPHYSIOLOGY, 20131388-2457Available online 27 March 2013 Publication year: 2013 Source:Clinical Neurophysiology
Listening to Mozart K.448 has been demonstrated to improve spatial task scores, leading to what is known as the Mozart effect. Previous study revealed the positive effects of Mozart K.448 in reducing epileptiform discharges in children with epilepsy. However, the mechanism remains unclear. Parasympathetic activation has been shown to help seizure control in many studies. The recent study investigated the effect of Mozart music on epileptiform discharges and autonomic activity with the following results:
• Listening to Mozart music decreased epileptiform discharges in children with epilepsy.
• The majority of these patients showed an increase in parasympathetic tone during music exposure.

Connie’s Comments: All babies should be rocked to sleep with Mozart music as the background music. I have used this method with my two homebirth babies now teens excelling in art, music, reasoning/logic and academics. This music is in contrast with the excitotoxic effects of EMF, radiation, cell phones, electric lines and other electric appliances.

The immune-suppression caused by acute stress can be reduced by a regular practice of moderate exercise which is known to modulate the expression of secretory-IgA. This antibody is essential for protection against infections and maintenance of homeostasis at the mucosal level.
In comparison with sedentary mice, moderate exercised mice displayed an up-regulating effect on the production of secretory-IgA and IgA-plasma cells, on the expression of all mRNA transcripts from secretory-IgA associated proteins, and on all cytokines tested.
However, serum (blood) levels of adrenal hormones (for dealing with stress, maintaining sodium, steroids and masculinizing effects) were not altered. Future studies on secretory-IgA production are necessary to support the substantive effect of moderate exercise on protection and homeostasis at the intestinal level.

DRAGO-SERRANO, M.-E.
INTERNATIONAL JOURNAL OF SPORTS MEDICINE(EFIRST):, 20120172-4622

All of the reports support the role for fiber-rich foods and dietary fiber (DF) as an important part of a healthy diet. All of the five identified Nordic papers found protective associations between high intake of DF and health outcomes; lower risk of cardiovascular disease, type 2 diabetes, colorectal and breast cancer.

None of the reports and few of the Nordic papers found clear evidence for the Glycemix Index (GI) in the prevention of risk factors or diseases in healthy populations, although association was found in subgroups, e.g., overweight and obese individuals and suggestive for prevention of type 2 diabetes.

It was concluded that DF is associated with decreased risk of different chronic diseases and metabolic conditions. There is not enough evidence that choosing foods with low GI will decrease the risk of chronic diseases in the population overall.

However, there is suggestive evidence that ranking food based on their GI might be of use for overweight and obese individuals. Issues regarding methodology, validity and practicality of the GI remain to be clarified.

Keywords: dietary fiber; glycemic index; Nordic Nutrition Recommendations
(Published: 25 March 2013)
Citation: Food & Nutrition Research 2013. 57: 20709 – http://dx.doi.org/10.3402/fnr.v57i0.20709

Reported by Connie Dello Buono for Motherhealth, in home caregiving for homebound bayarea seniors 4088541883 ; motherhealth@gmail.com