Good sources: Green leafy veggies, fruit (esp. strawberries), spinach, cabbage, egg yolks, fish, liver, and dairy products. A large portion of vitamin K is also produced by flora in the intestines. In fact, prolonged treatment with wide-spectrum antibiotics can decrease blood coagulation. Some 2nd generation cephalosporins (cefoperazone, cefamandole, and moxalactam) can also cause this effect (probably due to a warfarin like mechanism).
RDA: No RDA has been set but 70-40 mg per day appears to be adequate.
Functions: The primary function of vitamin K is to aid in the formation of clotting factors and bone proteins. It serves as a cofactor in the production of six proteins that regulate blood clotting, including prothrombin. In addition, it helps to form osteocalcin, a protein necessary for the mineralization of bone. Vitamin K also aids in the formation of glucose into glycogen for storage in the liver. In addition, it promotes the prevention and reversal of arterial calcification, plague progression and lipid peroxidation. Deficiency may increase the risk of calcification of arterial walls, particularly in individuals on vitamin D supplementation (Vitamin D promotes calcium absorption). Vitamin K exists in three forms: K1, a natural form found in plants (phylloquinone); K2, which is synthesized in the intestine (menaquinone); and K3, a synthetic form that must be activated in the liver (menadione). Vitamin K is absorbed in the upper small intestines and transported throughout the body in chylomicrons.
- Formation of γ-carboxyglutamate- The proteins for prothrombin and the clotting factors VII, IX, and X are formed as inactive precursors. Carboxylation of glutamate residues forms a mature clotting factor that contains γ-carboxyglutamate (Gla). This carboxylation is dependant upon vitamin K. Dicumarol, a naturally occuring anti-coagulant found in spoilt sweet clover, and warfarin, a synthetic analog of vitamin K, both inhibit the formation of Gla.
- Interaction of prothrombin with platelets- The Gla residues contain carboxyl groups (which are negatively charged). These carboxyl groups attract calcium ions (positively charged) which are then able to interact with the phospholipid membranes of platelets.
- Role of γ-carboxyglutamate residues in other proteins- These Gla residues are also present in other proteins but the role of vitamin K in their synthesis is not clear.
Deficiency: Hemorrhage. Infants are given an injection of vitamin K at birth. Their intestines are sterile and they cannot have vitamin K produced (hence the injection). However, deficiency is rare in the adult because of the large amount synthesized by intestinal bacteria.
Excessive bleeding, a history of bruising, appearance of ruptured capillaries or menorrhagia (heavy periods) are the most common clinical symptoms of overt vitamin K deficiency, although subclinical deficiency may not affect clotting mechanisms. Due to its critical role in bone formation, long-term vitamin K deficiency may impair bone integrity and growth, eventually predisposing a person to osteoporosis. Antibiotic usage can induce vitamin K deficiency since it upsets the balance of normal intestinal flora. Anticoagulants such as Coumadin and warfarin can also deplete vitamin K by blocking the activation of prothrombin. However, patients on warfarin or other blood anticoagulants should not supplement with vitamin K unless specifically recommended and approved by their physician. Other causes of deficiency include celiac disease, liver disease, certain medications (i.e. aspirin, Dilantin), very high doses of vitamins A and E (over 600 IU) and gastrointestinal disorders associated with the malabsorption of fats, such as bile duct obstruction, pancreatitis or inflammatory bowel disease.
Toxicity: Toxic to the membrane of RBC’s at high doses. Long-term, high-dose administration can cause jaundice and hemolytic anemia.