Vitamin K: Bones & Blood

Vitamin K: Bones & Blood

In 1935, danish scientist Henrik Dam identified
a fat soluble compound that was necessary for blood to clot. He called this compound vitamin K, K for Koagulation,
clotting. We know today that there are actually several
compounds, similar in structure, that have vitamin K activity, and we refer to them collectively
with the name vitamin K. Without these compounds, our liver cannot build or activate many of
the key proteins, including prothrombin, that are involved in the blood clotting cascade,
the sequence of events that allows your blood to turn from liquid to solid at wound sites
to prevent infections and hemorrhages. Without vitamin K, a little cut in your finger
could turn into a deadly threat, because that little wound would never heal, and drop after
drop you would eventually bleed to death. Luckily for us, vitamin K deficiency is extremely
rare and unlikely in healthy individuals, because bacteria in our gut are able to build
some vitamin K which can be subsequently be absorbed and at least partially cover our
needs. In food, vitamin K is mostly found in green
leafy vegetables, such as spinach, kale, cabbage, turnip greens, dark green lettuce, and then
also broccoli, Brussels sprouts, asparagus, peas, soybeans and green beans. Vegetable oils, and particularly soybean oil,
also provide some vitamin K. All foods of animal origin provide some vitamin
K, although the only rich source of it is liver. Vitamin K is resistant to heat, so cooking
doesn’t damage it. The adequate intake for vitamin K is set at
90 micrograms for adult women and 120 micrograms for adult men. Although it’s a fat soluble vitamin, our
body is not very good at storing it, but we easily get all we need and deficiencies are
rare. The most frequent cases of vitamin K deficiency
are due to fat malabsorption or extended use of antibiotics that kill the intestinal bacteria,
although older adults eating little vegetables are more at risk. Excess vitamin K has no known toxicity symptoms,
thus no upper level has been set. Indeed, although vitamin K deficiency prevents
adequate blood clotting, the reverse is not true, in other words, high levels of vitamin
K do not promote blood clotting or cause exaggerated clotting responses. This is rather a consequence of atherosclerosis,
and it increases the risk for heart attacks or strokes. These individuals often need to take blood
thinning medications, such as warfarin (coumadin), which acts precisely by inhibiting vitamin
K clot-promoting action. People taking this medication must therefore
control their vitamin K intake and make sure to keep it stable, because sudden variations
would dangerously increase or decrease the effect of the drug. It is mostly for this reason, and because
deficiencies are extremely rare, that most multivitamin supplements contain little or
no vitamin K. Vitamin K is not only necessary for clotting. It plays at least one other equally important
role, and it involves bone health. Indeed, vitamin K is a necessary coenzyme
in the synthesis of key bone proteins, including osteocalcin which binds calcium, thus strengthening
the bone structure. For this reason, vitamin K deficiency may
independently lead to osteoporosis and bone fracture risk. There are no early deficiency symptoms of
vitamin K. The only visible signs are blood hemorrhages,
and osteoporosis or bone fractures, both of which occur with prolonged and substantial
deficiencies of this vitamin.



  • jarrad2000

    Thank you very much! I learned a few things 🙂

  • Pakalini

    Excellent! What books have you read and which ones you could recommend?

  • Fernando Crociani

    Bel video!

  • Dazzletoad

    Lengthy intro, and weird bird noises.

    Get on with it.

    *Edit: Great video when it started. Although warfarin doesn't inhibit vitamin k coagulability. It inhibits the recycling of vitamin K and thus the ability of the compound to modify factors II, VII, IX, and X (as erll as proteins C, S, and Z).

    Vitamin K gammacarboxylates glutamic acid residues on these factors so that they are able to adhere to phospholipid membranes and thus activate each other.

    This utimately results in the cleavage of fibrinogen by thrombin, which produces the resultant fibrin mesh, and thronbin's activation of factor 13 for the crosslinking of fibrin.

    Informative nonetheless.

  • Your email address will not be published. Required fields are marked *