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Vitamin E (Tocopherol)

  • Heart Health
  • Menopause
  • Menopause
  • Cancer Prevention
  • Lower Cholesterol
  • Alzheimer's

Vitamin E is fat soluble and stored in the liver, fatty tissues, heart, muscles, testes, uterus, blood, adrenal and pituitary glands. Vitamin E is measured in International Units (IU). In regards to Vitamin E, 1 IU is equal to 1 mg.

Vitamin E is composed of compounds called tocopherols. Of the eight tocopherols. - alpha, beta, gamma, delta, epsilon, zeta, eta, and theta- alpha-tocopherol is the most effective.

Vitamin E is an antioxidant that is important in the prevention of cancer and cardiovascular disease. In a study of 2,002 people with heart disease, it was shown that this nutrient, in a dosage of 400 and 800 IU per day, slashed the occurrence of heart attacks by 77 percent and the death rate from heart disease by 47 percent.

Vitamin E has long been recognized as an anticlotting agent, thereby reducing risk of heart attack and stroke. Studies have shown vitamin E's important role in cancer prevention and in the benefits of use during cancer treatment. Animal and human studies have concluded that the nutrient blocks the initiation of carcinogenesis and reduces the incidence of skin, oral, stomach, colon, and breast cancer.

The most recent studies have shown vitamin E supplementation may reduce the incidence of prostate cancer, reverse diabetic neuropathy in Type II diabetics, may increase/improve insulin's effect in Type II diabetes, and significantly improve immune status in aging adults.

Natural sources of vitamin E are better than synthetic vitamin E because natural vitamin E is more available for use by the body than the synthetic form. The natural form of vitamin E is listed as d-alpha-tocopherol; the synthetic form is listed as dl-alpha-tocopherol.

Deficiency: Vitamin E deficiency may result in damage to red blood cells and destruction of nerves. Signs of deficiency can include infertility (in both men and women), menstrual problems, neuromuscular impairment, shortened red blood cell lifespan, spontaneous abortion (miscarriage), and uterine degeneration.

Depleting Agents: Heat, oxygen, freezing temperatures, food processing, iron, chlorine, mineral oil.

Sources: Vitamin E can be found in the following food sources: cold-pressed vegetable oils, dark green leafy vegetables, legumes, nuts, seeds, and whole grains. Brown rice, cornmeal, dulse, eggs, kelp, desiccated liver, milk, oatmeal, organ meats, soybeans, sweet potatoes, watercress, wheat and wheat germ are additional sources.

Herb Sources: Alfalfa, bladderwrack, dandelion, dong quai, flaxseed, nettle, oat straw, raspberry leaf, and rose hips.

Precautions: If you are taking an anticoagulant medication (blood thinner), do not take more than 1,200 IU of vitamin E daily. If you suffer from diabetes, rheumatic heart disease, or an overactive thyroid, do not take more than the recommended dose. If you have high blood pressure, start with a low dose, such as 200 IU and increase slowly.

Dosage Ranges and Duration of Administration: Recommended dietary allowances (RDAs) are as follows:

  • Neonates to 6 months: 4 IU
  • Infants 6 months to 1 year: 6 IU
  • Children 1 to 3 years: 9 IU
  • Children 4 to 10 years: 10 IU
  • Children over 10 years and adults: 12 IU for females, 15 IU for males.

Based on clinical trials, the recommended dose for disease prevention and treatment for adults is 400 to 800 IU/day.

Interactions:

Aspirin
A double-blind, randomized study evaluated the interaction between an antiaggregating agent with vitamin E in 100 patients at risk for transient ischemic attacks (TIAs). Patients were administered either aspirin (325 mg) or aspirin plus vitamin E (400 IU/day) for two years. The group receiving combination therapy had a significant reduction in ischemic events and platelet adhesiveness. However, the incidence of hemorrhagic stroke was not affected by treatment. The combination of vitamin E and aspirin appears to be safe and may benefit patients at risk for TIAs.

Chloroquine Phosphate
Vitamin E inhibits drug uptake in a dose-dependent manner in human cultured fibroblasts exposed to single and repetitive doses of chloroquine and other cationic amphiphilic drugs. Cationic amphiphilic drugs encompass a variety of therapeutic classes of medications including antiarrhythmics, antidepressants, and neuroleptics.

Chlorpromzine
Vitamin E inhibits drug uptake in a dose-dependent manner in human cultured fibroblasts exposed to single and repetitive doses of chlorpromazine and other cationic amphiphilic drugs. Cationic amphiphilic drugs encompass a variety of therapeutic classes of medications including antiarrhythmics, antidepressants, and neuroleptics.

Cyclosporine
A study with ten healthy subjects evaluated the interaction between water-soluble vitamin E and cyclosporine. After two doses of cyclosporine (10 mg/kg po), oral vitamin E was randomly administered with the drug. Concomitant administration of vitamin E and cyclosporine significantly decreased the clearance and steady-state volume of distribution for the drug. The combination therapy increased the area under the curve (AUC) for cyclosporine. The increased AUC may be the result of enhanced bioavailability. However, a subsequent in vitro study suggested that vitamin E and cyclosporine antagonize one another.

Desipramine
Vitamin E inhibits drug uptake in a dose-dependent manner in human cultured fibroblasts exposed to single and repetitive doses of desipramine and other cationic amphiphilic drugs. Cationic amphiphilic drugs encompass a variety of therapeutic classes of medications including antiarrhythmics, antidepressants, and neuroleptics.

Estradiol
Preliminary findings indicate that hormone replacement therapy (HRT) may preserve the content of vitamin E in LDL particles that, in turn, reduce the amount of oxidized LDL. Concomitant administration of vitamin E with transdermal estradiol was shown to improve LDL, HDL, and total cholesterol status in postmenopausal women. Most studies showing a benefit from vitamin E on heart disease risk have used quantities of vitamin E (400 to 800 IU/day) that are much higher than RDA values.

Gemfibrozil
There are conflicting reports regarding the effect of gemfibrozil on vitamin E status in hyperlipidemic patients. In one study, gemfibrozil treatment in men with combined hyperlipidemia reduced serum ubiquinone-10 and gamma- and alpha-tocopherol levels. In another study, gemfibrozil had no effect on vitamin E status and increased the LDL vitamin E/lipid peroxide ratio concentrations.

HMG-CoA Reductase Inhibitors
HMG-CoA reductase therapy may decrease the antioxidant capacity of vitamin E on LDL cholesterol. However, coadministration of vitamin E (300 IU) with simvastatin (20 mg) improved markers of blood vessel elasticity in hypercholesterolemic patients more than simvastatin monotherapy. Similar benefits may be observed with fluvastatin and other HMG-CoA reductase inhibitors.

Oral Contraceptives
Oral contraceptives reduce some of the vitamins and enzymes involved in the oxidative defense system. Impaired antioxidant status can increase the susceptibility to lipid peroxidation and possibly thrombosis in women. Some of these effects can be counteracted by vitamin E supplements.

Propranolol
Vitamin E inhibits drug uptake in a dose-dependent manner in human cultured fibroblasts exposed to single and repetitive doses of propranolol and other cationic amphiphilic drugs. Cationic amphiphilic drugs encompass a variety of therapeutic classes of medications including antiarrhythmics, antidepressants, and neuroleptics.

Verapamil
An in vitro study suggested that vitamin E antagonized the chemosensitizing effects of verapamil. Tests performed using the human small cell lung cancer line demonstrated that the inclusion of alpha-tocopherol (25 mcg/mL) prevented the ability of verapamil (2 mcg/mL) to sensitize the cells to the effects of doxorubicin and vinblastine.

Warfarin
Vitamin E does not appear to enhance the pharmacologic effects of warfarin. However, the administration of high doses of vitamin E to individuals with reduced levels of vitamin K may potentiate a vitamin K deficiency and increase the anticoagulant effect of warfarin. Although the mechanism of this interaction is unclear, vitamin E may affect the carboxylation of prothrombin, a vitamin-K-dependent step in the production of coagulation factors.

Zidoyudine
Antiviral activity and bone marrow toxicity of zidovudine (AZT) were evaluated in the presence of water-soluble vitamin E (alpha-D-tocopherol acid succinate (ATS)) in two cell test systems. In the MT4 cell line, ATS displayed a dose-dependent increase in anti-HIV activity that was six times greater than when AZT was also administered. In addition, vitamin E showed significant protection against AZT-induced toxicity in murine bone marrow cells.

 

 

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