Vitamin K2 Deficiency is COMMON
References: Cranenberg 2007 in Thrombosis and Haemostais Beulens in Diabetes Care 2010
We spent the first 60 years of Vitamin K2 thinking it was a subtype of K1 and all about blood clotting. We also thought it was plentiful in our gut, and that its deficiency was rare. It wasn’t until the late 1990s that information started to trickle out. Then, Cranenberg put it all together in 2007.
It had become apparent that two critical proteins involved with calcium metabolism were activated by K2. Osteocalcin is the protein that grabs calcium and cements it into bone. The other, Matrix Gla Protein, or MGP for short, is the protein that pulls calcium out of your arteries. When you have a lack of MGP, your arteries “harden” and become bone-like. When you lack activated osteocalcin, your bones cannot incorporate calcium and you develop osteoporosis. Both of these two proteins are activated by K2. That means K2 is sitting astride two of the major epidemics of our modern era; coronary artery disease and osteoporosis.
What Cranenberg describes in the review article is: “In healthy individuals, substantial fractions of osteocalcin and MGP circulate as incompletely carboxylated species, indicating that the majority of these individuals is subclinically vitamin K-deficient.” Did you get that? Most of our MGP and osteocalcin is circulating in our bodies and not activated. And we have substantial risks for the diseases that lack of activation is responsible for.
What begs the question is “What are we waiting for?” and “Is there any toxicity to starting supplementation?” and “How did we get in this mess?” We’ve now known this in little pieces for the last 5 years.
Our traditional medical model is to insist that you have to have a randomized placebo controlled trial of therapy to see if it addresses an issue. That model takes many millions to conduct a study. K2 is not patentable. There will be no studies. There is no money in it. So don’t wait. All we will find are small, convincing physiology studies showing the mechanisms.
The question then arises, how did we get here? Easy. A hundred years ago all our cows moved of the pasture (the source of green grass and K1) and onto the feedlot. Our diets became K2 deficient. Other things happened too. We moved indoors and lost Vit D. Vit D helps you absorb the calcium you need for your bones, but without K2, you can’t activate the osteocalcin to cement it into your bones. Hence we have the terrible conundrum: you eat calcium to make your bones denser, and take D to make stronger bones, andyour calcium ends up in your arteries.
WWW. What will work for me. We don’t have a measure of K2 as a blood test. We can only measure “uncarboxylated osteocalcin”, and that test is still hard to find. But you are deficient. We all are. It’s widespread. And K2 is utterly non-toxic. (So far as we know so far.) If you are on coumadin, it may interfere at very high doses, but we aren’t sure of that yet. More studies to follow. In the meantime, I’ve got a few more K2 stories to tell you. Next week. So, stop by the office, order it on line, but start on K2 – 200 mcg a day of MK7. Or buy grass raised butter from Denmark at Whole Foods. If you want a surrogate measure of how K2 deficient you are, get your coronary arteries tested for calcium content with a CT scan. Or a DEXA scan of your bones to see if you have too little calcium there. Then you’ll know your risks.
1. Vit K2 deficiency is rare and unusual to find? T or F
Answer: False. That’s what we thought for the last 70 years, but we now know its widespread.
2. The only way to detect the lack of K2, for the present is to measure the level of “un activated” protein called osteocalcin in our blood. T or F.
Answer. True but a trick question. You can find if you are deficient in sneaky ways such as checking to see if you have calcium in your coronary arteries. If you do, you get a snapshot that you never activated MGP protein that sucks calcium out of your arteries. Same logic with osteoporosis.