Consists of 8 naturally occuring tocopherols. Apparently, a-tocopherol is the most active.
Good sources: Vegetable oils, margarine, wheat germ, nuts, dark green veggies, and whole grains. Liver and eggs contain moderate amounts.
RDA: 10 mg for males and 8 mg for females. However, as your intake of polyunsaturated fatty acids goes up so does the requirement for vitamin E. Remember, the RDA is set to 20% above the level that would cause deficiency symptoms. I think most experts would recommend at least 400 mg/d.
Functions: Vitamin E is an antioxidant (see oxidative damage) that protects cell membranes and other fat-soluble compounds from oxidative damage by free radicals. For example, the oxidative damage to LDL-cholesterol appears to lead to the deposition of cholesterol in the arterial wall leading to atherosclerotic disease. In the past few years many other functions of vitamin E have been clarified. Alpha-tocopherol has direct effect on the control of inflammation, red and white blood cell production, connective tissue growth and genetic control of cell division. Vitamin E acts to reduce free radical damage by converting arachidonic acid is converted to pro-inflammatory (12-HPETE) derivatives. In deficiencies of vitamin E, arachidonic acid is converted to pro-inflammatory leukotrienes and cytokines. In neutralizing free radicals, vitamin E is oxidized to a free radical. Conversion back to the reduced form occurs by reaction with vitamin C (ascorbate).
Deficiency: Almost exclusively limited to premature infants. When it is seen in adults it is usually due to problems with lipid absorption. Symptoms include RBC sensitivity to peroxides and damaged cellular membranes. This is probably due to vitamin E’s antioxidant, protective role.
The principle use of vitamin E is an antioxidant in the protection against heart disease, cancer, stroke and neurodegenerative disease (Alzheimer’s). In addition, alpha-tocopherol supplementation is useful in treating other cardiovascular diseases, diabetes, fibrocystic breast disease, menopause symptoms and tardive dyskinesia. It may also have applications in Parkinson’s Disease and arthritis. Vitamin E is important to immune function, protecting thymic function and white blood cells from oxidative stress.
Symptoms of vitamin E deficiency include nerve damage, muscle weakness, poor coordination, involuntary eye movements, red blood cell fragility, anemia and retrolental fibroplasia (eye disease).
Toxicity: Almost impossible! No toxicity has been noted even at doses 10,000 times the RDA.
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.
