This is a one page overview of the book “Vitamin K2 and the Calcium Paradox” by Dr. Kate Rheaume-Bleue
I highly advise purchasing a copy – it is well written and the detailed background information is truly fascinating.
Calcium Paradox (Inappropriate calcium metabolism caused by vitamin K2 deficiency)
- Vitamin K2 Mk7 (menaquinone)
- Vitamin K2 Mk4 (menatetrenone)
- Vitamin K1 (phylloquinone)
- Vitamin D3 (cholecalciferol)
- Vitamin A (Retinol) (Beta-Carotene is not vitamin A)
- Osteocalcin (BGP, Bone Gla Protein, BGLAP, Bone Gamma-carboxyglutamate Protein)
- MGP (Matrix Gla Protein)
The paradox: Osteoporosis or arterial calcium plaques? Calcium supplements for osteoporosis increase the risk of heart attack (to the rate of one fracture prevention to two heart attacks). Including a vitamin D supplementation can even worsen this.
The Calcium paradox is just a typical case of failure to separate cause and effect. Minerals are not just lost from bones – they are accumulating in the wrong places instead – which is the main issue. This is due to a deficiency of dietary fat soluble vitamins – K2, D3 and A – not due to a lack of calcium. Adding calcium to the diet under such conditions only adds to the problems.
This apparent paradox is at the centre of several other chronic health problems, including : Diabetes, Varicose veins, Wrinkles (mineralisation in the skin), Kidney disease, Chron’s Disease, Narrow - crowded dental arch, Cancer, Alzheimer’s (Diabetes 3), Infertility, Tooth decay, Joint damage in rheumatoid arthritis.
In women declining estrogen levels after menopause impact bone density in three distinct ways - each counteracted by K2. Estrogen converts vitamin D into its bone building form. Also, declining estrogen levels increases interleukin-6 which stimulates production of osteoclasts (which break down the bones). K2 in the form of Mk7 (menaquinone) counteracts this.
Alzheimer’s is correlated very closely to both heart disease and osteoporosis. (and K2 deficiency and insulin insensitivity in the brain).
Wrinkles – due to decreased kidney filtration - due to increased inactive MGP – due to K2 deficiency. (skin elasticity equates to artery elasticity)
Dietary advice for heart disease prevention has been centred on the “lipid hypothesis” – which stopped people from eating saturated fats and most of the sources of the fat soluble vitamins that actually protect against heart disease (and osteoporosis). Hence today 30% of people die from heart attacks. The so called “French Paradox” of the “Mediterranean diet” is the same “paradox” – the answer is not in the wine! Fatty foods like Foie Gras and fatty cheeses, creamy, buttery sauces and egg yokes are the best sources of K2.
Children who develop in the womb with a K2 deficiency end up with narrow nostrils, crowded dental arch, overlapping teeth – and end up mouth breathing. This is due to the nasal cartilage area being a key site for K2 accumulation in the foetus. The lower 1/3rd of the face is compromised due to premature calcification from the lack of K2. Tooth enamel is also not properly formed – especially for the adult teeth.
The vitamins work together as an interdependent system. Their jobs mainly relate to moving minerals around. In particular vitamins K2, D3 and A work together – influencing each other. (Vitamin E appears to only function as an antioxidant related to polyunsaturated fats)
D3 governs calcium absorption from the intestines. K2 directs the calcium appropriately.
D3 allows for proper parathyroid hormone function to maintain blood calcium levels.
D3 boosts immunity – production of cathelicidins – antimicrobial agents that destroy bacteria, fungi and viruses. Because it is suspected that atherosclerosis is also caused by one of the “cold” bugs – C-pneumoniae – this makes D3 an important line of defence. Restricted D3 limits MGP production for K2 activation and simultaneously limits protection against the bacteria.
D3 protects against all major forms of cancer.
D3 has an inverse relationship with hypertension – combined with K2 the arteries are being cleared.
D3 is required to make MGP (The protein activated by K2 for clearing calcium from blood vessels)
D3 + A are required to make Osteocalcin (The protein activated by K2 for building and strengthening bones) by activating osteoblasts.
K2 Deficiency : D3 + calcium supplementation alone will increase bone density but also can increase arterial plaque due to a relative imbalance (deficiency) of K2. Increased D3 increases the demand for K2. Vitamin A plays a governing role in the relationship and so also needs to be present – but in no specific ratio.
D3 Deficiency : Even with K2 present, if there is not enough D3 then the K2 cannot work – so arterial plaque increases.
D3 has a biphasic effect on vascular calcification – calcification increases if there is effectively too much or too little D3. Excess D3 (for K2 levels) causes uncarboxylated MPG to become excessive and so calcification increases. Insufficient D3 increases the effect of K2 deficiency and so calcification increases.
Calcium supplementation alone does not cause arterial plaque build up. Calcium ratio in plaque is around 20% regardless of calcium intake.
To sum up – deficiency of either D3 or K2 increases arterial plaque. Excess D3 is harmful also because it can induce a relative deficiency of K2.
D3 toxicity is defined as the slow build up of plaque in the soft tissues.
K2 activated MGP reverses atherosclerosis. (37% in 6 weeks in animal studies - 50% in people – totally due to K2)
A therapeutic dose of K2 alone is considered to be 120 mcg of Mk7. Double that during and after menopause. (There is no toxicity with K2 at high levels)
Balancing D3 and K2 for a minimal therapeutic dosage requires supplementation in the order of 1000 iu D3 to 100 to 200 mcg of K2 Mk7(most potent and long lasting version) 8000 iu of D3 is a good therapeutic dose level.
Calcium supplementation may not be necessary when sufficient K2 is available – though for those with osteoporosis it may still be needed.
K2 deficiency can develop in less that 7 days as it is not recycled in the body.Humans also depend on the food chain for supplies as we don’t readily convert K1 to K2 by ourselves.
K2 partners with D3 to inhibit the production of osteoclast cells that break down bone – and causes existing osteoclasts to die. This helps to tilt the bones towards building instead of breaking down.
Vitamin A regulates (lowers) the production of MGP.
Vitamins A and D regulate the activity of genes that cause cells to produce the proteins to which minerals and water soluble vitamins will bind.This is why the fat-soluble vitamins are the true foundation of health – they are required to make use of all other nutrients. A and D are the base – K2 is added for optimum health.
Vitamin A is necessary for night vision – it boosts the immune system and is considered the “anti-infective vitamin”. It increases the number of osteoclast cells (breaking down bone) necessary for bone remodelling. This removes old weak bone to be replaced with new, stronger tissue and is necessary in fracture repair. A also stimulates osteobalsts (producing osteaocalcin). In women A is necessary for estrogen, progesterone and other hormone production and in men for sperm production. A ensures cell differentiation – which protects against cancer by inhibiting tumour development. Lack of A causes dry skin and dry eyes, thinning hair, brittle nails, anemia and susceptibility to colds and flu. A is required for protein utilisation. It’s takes a lot of overdosing to make A toxic – however several symptoms are shared with A deficiency – because they are actually caused by induced D and K2 deficiency and vice versa. When you take more of one fat-soluble vitamin you create a greater need for the others. If those others are lacking then toxicity symptoms result. However…
When D3 and A are supplemented together you never see toxicity symptoms of either vitamin – no matter how high the intake of either vitamin.
D3 stimulates production of K2 dependent Gla proteins – increasing demand for K2. This enhances all bone/artery repair and building functions. Isolated – on it’s own A inhibits MGP production – minimizing demand for K2. A allows the body to get by when K2 is scarce – temporarily. Calcium excretion from the body is highest in summer (plaque cleansing) due to blood levels of retinol – vitamin A – which peaks in August – despite no increase in intake. During winter calcium loss is minimal as it goes into the arterial plaque. In summer the A vitamin causes excretion of calcium in the urine – after it is removed by K2 from the arteries. Summer grass fed food has higher levels of both A and K2.
A and D do not operate together in a ratio – instead they operate in a “switch model” whereby a minimum amount of one switches off the toxic effects of the other.
K2 activates a protein called osteocalcin (bone gla protein or BGP – created from osteblasts in bone) – which attracts calcium to the bones and teeth. K2 also activates another protein called MGP (matrix gla protein) which removes calcium from soft tissues.When K2 levels are inadequate those proteins are useless – calcium then just embeds itself in soft tissues instead. Vitamins A and D together cause bone osteoblasts to create osteocalcin. Vitamin D also stimulates MGP production.
Osteocalcin acts as a hormone causing insulin producing beta cells in the pancreas to release more insulin. At the same time it directs fat cells to release the hormone adiponectin, which increased sensitivity to insulin. (Hence the connection to diabetes, obesity, insulin resistance health issues) This demonstrates that the skeleton is an endocrine gland – with K2 being a critical nutrient.
Osteocalcin (K2 activated) also affects male fertility by enhancing the synthesis of testosterone.
K2 – through an enzyme called vitamin K-dependent carboxylase alters the structure of the osteocalcin and MGP proteins – hence activating them to bind calcium. When there is a K2 deficiency the proteins are “under-carboxylated".
Men’s bones – via ostecalcin production regulates testosterone production. Osteocalcin is mainly confined to the bones.
K2 activates proteins responsible for the deposition of calcium and phosphorous salts in the bones and teeth.
MGP is found throughout the body, in bones, blood vessels, heart, lungs, kidneys and cartilage. Uncarboxylated K2 deficient MGP is associated with disease in each of these areas. Many types of malignant tumours produce MGP – K2 deficiency fosters cancer growth.
K2 plays a role in infant growth by preventing premature calcification of the cartilaginous growth zones of the bones.
K2 increases mineral content and decreases bacterial count in saliva.
K2 increases learning capacity – the brain contains one of the highest concentrations of K2 where it is involved in the synthesis of the myelin sheath of the nerve.
K2 supplementation prevents and repairs dental caries.
K2 (menaquinone) supplementation reverses atherosclerosis.
Other K2 dependent proteins also protect against atherosclerosis. Growth arrest-specific gene 6 (Gas6) promotes rapid clearance of dead smooth muscle cells that can act as an anchor for circulating fats. K2 dependent protein S encourages the immune system to take out gently arterial garbage rather than launch an inflammatory attack – which would encourage plaque formation.
K2 completely blocks free radical accumulation and brain cell death. It also protects the brain cells from depletion of glutathione, a key antioxidant in the body.
Calcium Cycle osteoporosis – atherosclerosis connection
Interplay between fat soluble vitamins, calcium metabolism and the seasons.
Arterial plaque builds up in winter and diminishes in summer. Bone density lowers only in the winter – stays constant in summer but doesn’t regain density.
K2 content and vitamin A (retinol) content of dairy increases in the warm months during periods of rapid grass growth and plummet in the winter. During rapid grass growth vitamin K1 is abundant in the membrane of the chloroplast – where photosynthesis takes place. When cows, chickens or pigs consume green chlorophyll containing plants they ingest phylloquinone (K1), which is then converted to K2 in direct proportion to the amount of K1 in their diet. This doesn’t happen in grain fed animals. K1 rich food is also rich in beta-carotene. This imparts the yellow colour associated with subsequent K2 rich food.
Rates of death from heart attacks decreases in the summer and increases in the winter (Northern Hemisphere). Blood vessel calcification increases in the winter and deceases in the summer – with a 3% seasonal variation in calcification which mirrors mortality rates. This cardiac mortality pattern is not determined by only vitamin D levels – which it follows roughly – but by K2 levels, which it follows precisely.
Triage Theory of Ageing
Long term degeneration takes place at minimum nutritional levels – the body being designed to privilege immediate requirements for survival at the expense of long term function – including DNA repair and decay of mitochondria (cell’s energy production). Chronic illness associated with K2 deficiency falls into this category. With the K vitamins the body privileges blood clotting function before bone protein activation. This is why RDA nutrient levels are usually dramatically low – as they relate to immediate survival mode only.
Dietary K2 Sources
Animal fats give K2 Mk4 which has a half life of only 2 hours. Fermented foods give K2 Mk7 from bacteria – which lasts for days in the body and is far more effective in general with far smaller supplements (1/10th dosage required). In cheese and yoghurt it’s mainly K2 Mk7 that’s present from fermentation.
Wild game – duck, pheasant, rabbit, venison, elk, boar etc. (naturally thrive on green vegetation)
Goose liver (foie gras)
Butterfat of mammalian milk, eggs of fish, organs and fats of animals.
Synthesized in animal tissue and mammary glands from Vitamin K1 in rapidly growing green grass. Vitamin K1 is found in association with the chlorophyll of green plants in proportion to their photosynthetic activity. The content of this vitamin in butterfat is proportional to the richness of its yellow of orange colour, directly associated with beta-carotene.
Natto (fermented soya beans), Goose liver, Certain cheeses, Animal fat such as egg yoke, butter and lard of grass fed animals.
Dietary Fat Soluble Nutrient Dense Foods
Fish, Seafood, Cod Liver Oil (careful with pollution!) – Grass fed milk and dairy products. Veal liver is very high in vitamin A.
Cooked vegetables (not raw).
Minerals and other key nutrients
Magnesium, zinc, boron and B vitamins all cooperate to enhance bone density. Green leafy vegetables.
To work to improving the strength of blood vessel walls – flavonoids. Those are plant based compounds especially cherries, blackberries, onions,garlic and the white membrane in citrus fruits.
Food to Avoid
Trans Fats – they contain a mutant version of the K vitamin (DHP). There is even less conversion of K1 to K2 – and higher atherosclerosis and osteoporosis.
Vitamin D is damaged by the antinutrient phytic acid – found in whole grains, bran, raw seeds and raw nuts. The trick is in the detailed preparation where soaking and cooking disable the phytic acid.
Supplement dosage information is from a Mercola article:
"While the ideal or optimal ratios between vitamin D and vitamin K2 have yet to be elucidated, Rheume-Bleue suggests that for every 1,000 IU’s of vitamin D you take, you may benefit from about 100 micrograms of K2, and perhaps as much as 150-200 micrograms (mcg).
The latest vitamin D dosing recommendations, which call for about 8,000 IU’s of vitamin D3 per day if you’re an adult, means you’d need in the neighborhood of 800 to 1,000 micrograms (0.8 to 1 milligram/mg) of vitamin K2."
Researchers are also looking into other health benefits. For example, one recent study published in the journal Modern Rheumatology1 found that vitamin K2 has the potential to improve disease activity besides osteoporosis in those with rheumatoid arthritis (RA). Another, published in the journal Science2, found that vitamin K2 serves as a mitochondrial electron carrier, thereby helping maintain normal ATP production in mitochondrial dysfunction, such as that found in Parkinson’s Disease.
According to the authors:
“We identified Drosophila UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson’s disease that affects mitochondrial function. We found that vitamin K(2) was necessary and sufficient to transfer electrons in Drosophila mitochondria. Heix mutants showed severe mitochondrial defects that were rescued by vitamin K(2), and, similar to ubiquinone, vitamin K(2) transferred electrons in Drosophila mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K(2) that serves as a mitochondrial electron carrier, helping to maintain normal ATP production.