Vitamin K is found in several forms:
Vitamin K-1 (Phylloquinone), the form occurring naturally in plants; Vitamin
K-2 (Menaquinone), the form produced by intestinal bacteria and also derived
from putrefied fish meal; synthetic vitamin K (Menadione).
Vitamin K is integrally involved in the
clotting mechanism of blood. A deficiency of vitamin K results in decreased
blood levels of prothrombin and clotting factors IV, IX, and X, with subsequent
Humans are unable to synthesize vitamin K.
It must either be acquired from dietary sources, or as metabolic by-products of
intestinal bacteria. Still, the vitamin is so widely distributed in nature that
nutritional deficiencies do not occur under normal circumstances.
Vitamin K is heat-stable and water
soluble; therefore no inactivation or leeching of the vitamin into the water
occurs during cooking. It is destroyed by strong acids or alkalis.
Gamma-irradiation of foods to increase storage life inactivates vitamin K.
Vitamin K requires bile to be absorbed
from the small intestine. It is carried through the bloodstream to the liver by
Vitamin K controls the clotting mechanism
of the blood because its action is directed at the precursor of prothrombin.
Prothrombin is activated to form thrombin, an enzyme which, in turn, converts
fibrinogen to fibrin, the insoluble protein that solidifies the blood clot.
To become active, the glutamate residue on
the inactive prothrombin precursor must acquire a carboxyl group to form a
carboxylglutamate residue. This carboxylation requires the cofactor vitamin K.
The carboxylglutamate group can, in turn, bind a calcium ion to form the enzyme
thrombin. In the absence of vitamin K, no prothrombin is formed, resulting in a
condition called hypoprothrombonemia. A deficiency in circulating prothrombin
decreases the amount of thrombin available for coagulation and increases the
body's tendency to hemorrhage following a blow or injury.
Vitamin K occurs in the liver as inactive
vitamin K epioxide. A reductase (reducing enzyme) is required to change it back
to its active state. There is speculation that coumarin works indirectly by
inhibiting the reductase and, consequently, the vitamin K conversion, rather
than by acting directly on thrombin or fibrin.
Vitamin K supplements are administered by
intravenous or intramuscular injections and, on occasion, can be given orally.
The long-term use of antibiotics destroys
normal intestinal bacteria, in turn decreasing the synthesis and availability
of vitamin K. Supplements of the vitamin should be prescribed to prevent
A decreased level of serum prothrombin
occurs consequent to anticoagulant therapy for thrombosis. To avert potential
life-threatening hemorrhaging, controlled dosages of vitamin K are prescribed,
with phylloquinone, the vitamin K of plant origin, the preferred form.
Hemorrhagic disease due to vitamin K
deficiency can occur during the first few weeks of life. Infants are therefore
routinely injected at birth with one to two milligrams of natural vitamin K per
kilogram body weight as a means of prevention. Menadione, synthetic vitamin K,
is not used because it is fairly toxic to newborns, resulting in hemolytic
anemia, increased serum bilirubin levels, and jaundice (in large dosages).
Hemorrhagic disease of the newborn is
readily treated when it does occur. Natural vitamin K is administered
intramuscularly or by stomach tube at a dosage of one to two milligrams per
kilogram body weight. Recovery occurs within 48 hours of treatment.
An inability to absorb fats and
fat-soluble vitamins can result in bile deficiencies, cystic fibrosis,
diarrhea, ulcerative colitis, or jaundice. Vitamin K supplements of one to two
milligrams per kilogram body weight can be administered in water miscible and
readily absorbed forms.
Symptoms associated with a vitamin K
deficiency include: prolonged blood clotting time, increased bleeding and
hemorrhaging, decreased active prothrombin in the blood, and hemorrhagic
episodes in newborns.
Because vitamin K is common in many foods
and is also synthesized by intestinal bacteria, deficiency in humans is
unlikely to occur under normal conditions.
Several health conditions and therapeutic
regimens can create a vitamin K deficiency and produce overt symptoms of
avitaminosis. And condition which interferes with intestinal absorption of
fats, such as gallbladder disorders, ulcerative colitis, cystic fibrosis,
diarrhea, or obstructive jaundice, will result in a decreased absorption of
A long-term use of antibiotics or
sulfonamides will sterilize the intestines or decrease the activity of gut
bacteria, indirectly causing a decreased availability of endogenous vitamin K.
When dicumarol is prescribed, vitamin K
supplements are given concomitantly to insure against potential
Hemorrhagic diseases due to vitamin K
deficiency can occur in newborns during the first few weeks of life. Newborns
have a very limited supply of the vitamin at birth. Very little is acquired
during fetal life because vitamin K does not readily cross the placenta; the
sterile intestine is not immediately colonized by vitamin K-producing bacteria.
Thus, the infant's stores become low within one week after birth, and bleeding
tendencies may become evident.
Vitamin K deficiencies can also result
from the use of mineral oil as a laxative. The vitamin becomes irreversibly
bound to the oil droplets in the intestine, which cannot be absorbed in that
form, and is ultimately excreted in the feces. Because its use can also result
in deficiencies of the fat-soluble vitamins, mineral oil should not be taken
Unlike the other fat-soluble vitamins,
vitamin K is not stored in any significant quantity in the liver; therefore
toxic levels are rarely achieved.
Synthetic vitamin K (menadione) has double
the potency of natural vitamin K on a per weight basis, resulting in a narrower
margin of therapeutic safety. Because menadione is toxic at excessive dosages,
the Food and Drug Administration has banned is use as an over-the-counter
The possible symptoms of vitamin K
toxicity include: thrombosis, vomiting, kidney tubule degeneration, and
jaundice and hemolytic anemia in newborns.
- RDA for adult males: 80 mcg
- RDA for adult females: 65 mcg
- RDA for children 7 to 10 years: 30 mcg
- RDA for infants: 10 mcg
- RDA for pregnant and lactating women 65 mcg
Intestinal bacteria synthesize vitamin K,
and serve as the only endogenous source of the vitamin for humans.
Vitamin K can be acquired exogenously be
eating a diet composed of the following foods.
Extremely High (650 mcg/100 g)
|· Beef kidney
· Beef liver
| · Cauliflower
Medium (10 - 100 mcg/100 g)
| · Egg yolk
· Whole wheat
Low (0 - 10 mcg/100 g)