As I mentioned in Part III of this series, there is an inverse association between decreased bone calcification and increased vascular calcification, neither of which is a good thing. In other words, those who shrink and crumble into the osteopenia/osteoporosis thing are also those most likely to deposit unwanted calcium in their aging blood vessels. The heart of this supplemental calcium controversy (do I take it or not?) lands squarely here: how does our body calcify that which holds us upright while also preventing calcium build-up where it does not belong? What matters here is not just the necessity of incoming calcium to balance calcium loss but also an ongoing incoming supply of the known co-factors needed for proper calcium use.
Back, once again, to an evolutionary perspective. In Part II I mentioned our Ice Age ancestors who ate a high-calcium diet of plants and insects and little or no grain--a food source both low in calcium and high in phytates (substances that bind calcium thus preventing effective absorption). Now let's go back even further to our remote water-based relatives who spent their lives swimming about in calcium-rich seas. Early evolutionary pressure, therefore, required the development of mechanisms to prevent widespread calcification through their soft, fishy tissues. The ability to survive and thrive depended--still depends!--on the limitation of calcium deposition solely to skeletons be they external shells or, much later, internal bones. Elaborate regulatory mechanisms developed over eons that promote calcium phosphate crystallization in the right place and prevent it elsewhere.
The central actors in strong bone production are cells that package mineral matrix--a mixture of calcium, phosphate, enzymes, and proteins--and then deposit it along collagen fibers also produced by these cells. This can happen in the right place (in bones that are growing as in children or repairing as in adults) or the wrong place as in aging aortas or arteries. Cells that can turn into osteoblasts (bonemakers) are not only found within the skeleton but also in the walls of blood vessels. The most important protein responsible for bone mineralization is osteocalcin which is dependent on vitamin K2 for proper function. The most important protein responsible for the prevention of mineralization outside of bones is matrix gamma-carboxy glutamic acid which is also dependent on vitamin K2 for proper function. Do you see where this is going?
I am here to tell you that I had no idea why I've been taking vitamin K2 regularly for the past year except for a vague notion that it was good for bone health. I'm certain that I learned nothing about this in medical school decades ago when the importance of vitamin K to proper blood clotting was emphasized but no one mentioned its importance to mineralization. For those of you who haven't spent hours studying the literature on vitamin K as I have while writing this series, there are two main forms of K: K1 important to normal blood clotting function, and K2 which is integral to the deposition of calcium in the body. More on that in Part V.
Recent studies abound on the benefits of K2 with respect to cardiovascular health. The Rotterdam Study, published in 2004, found that persons with the highest levels of K2 were less than half as likely to die of coronary heart disease or develop severe aortic calcification over a seven year period than those with the lowest levels, and almost 75% less likely to die of anything in that same time period.
Wow, if you haven't got K2, get some!
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1) Geleijnse, J et al. Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study. J. Nutr. November 1, 2004 vol. 134 no. 11 3100-3105.
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