Vitamin K

• Method of Action
• Consequences of Deficiency
• Recommended Dietary Allowances

• Properties and Uses
• Toxicity Levels
• Food Sources

Description

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 hemorrhagic tendencies.

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.

Method of Action

Vitamin K requires bile to be absorbed from the small intestine. It is carried through the bloodstream to the liver by lipoproteins.

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.

Properties and Uses

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 hemorrhaging.

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.

Consequences of Deficiency

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 vitamin K.

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 life-threatening hemorrhage.

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 for constipation.

Toxicity Levels

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 supplement.

The possible symptoms of vitamin K toxicity include: thrombosis, vomiting, kidney tubule degeneration, and jaundice and hemolytic anemia in newborns.

Recommended Dietary Allowances

• 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

Food Sources

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)

Medium (10 - 100 mcg/100 g)

Low (0 - 10 mcg/100 g)