Vitamin K2: An emerging story
Along with vitamin D, recent studies
put vitamin K2 in the spotlight as a major factor in calcium control in
the body. Long considered a passive accompaniment of atherosclerotic
plaque growth, calcium deposition in coronary arteries, evidenced by
your CT heart scan score, is increasingly looking more like an active
component that may be under your control.
Measuring coronary calcium is the basis for CT heart
scanning. The heart scan score provides a measure of the volume of
calcium in coronary arteries, and thereby yields an indirect index of
total plaque volume. This useful insight originated with the
observations of Dr. John Rumberger and his Mayo Clinic team, who
discovered this relationship in the mid-1990s. Calcium consistently
occupies 20% of total plaque volume. Thus, 2 mm3 of calcium translates
into 10 mm3 of total plaque—hard, soft, and everything in between.
For years, we’ve therefore viewed calcium as just a convenience, a tool
that is easy to visualize, but just a passive marker and not an active
participant in the disease. Some have even argued that calcium is
nothing more than a remnant of prior “rupture,” a scar from the
dangerous activity of a soft plaque. They claim that calcium is, in
fact, a reflection of increased stability of a plaque, since the “hard”
element is not itself prone to rupture. Thus, some believe that, while
it serves a practical purpose, calcium plays no true role in causing
Those arguments are being dashed by new observations into phenomena
behind vitamin K and its role in causing calcium deposition and coronary
For several years since its discovery in 1929, vitamin K has been known
to play a crucial role in maintaining normal blood clotting. Vitamin K
is required by the human liver to manufacture several blood clotting
proteins (clotting factors II, VII, IX, X, and proteins S and C). This
is the basis for administering the vitamin K-blocking drug, Coumadin (warfarin)
to people who have blood clots or risk for blood clot formation, since
clot formation is effectively blocked by the drug.
Determination of the human need for vitamin K was therefore based on the
amount necessary to maintain normal balance between blood clotting and
thinning. We don’t want to have our blood excessively “thinned” and
prone to bleeding, nor do we want “thick” blood prone to clots. Vitamin
K deficiency that disturbs normal clotting is somewhat unusual, often
prompted by antibiotics, since bacteria that normally reside in the
colon are responsible for producing approximately 75% of the vitamin K
needed every day.
Research has uncovered the fact that vitamin K also plays a crucial role
in maintaining bone health. It was found that the amount of vitamin K
required to halt bone absorption leading to osteoporosis requires much
greater intakes than that required for blood clot regulation. Further,
it appears that bone and vascular tissue (like coronary arteries)
maintain a preference for a different form of vitamin K than that
required for blood clotting regulation. Rather than vitamin K1 needed
for clotting, vitamin K2 is the form preferred by bones and arteries (Schurgers
LJ et al 2001). It appears that much of the information generated over
the years for vitamin K focused on the K1 form, ignoring the K2 form
necessary for bone and vascular health.
Normal deposition of calcium occurs only in bone and in teeth. Abnormal
deposition of calcium in the body occurs in three places: the inner
lining of the arteries of the body (the intima) that causes
atherosclerotic plaque; the muscle layer of arteries (“medial
calcification”); and heart valves. K2 appears to be the form of vitamin
K responsible for controlling these phenomena.
How is vitamin K2 involved in coronary atherosclerotic plaque?
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