Vitamin E
The name tocopherol (Vitamin E) was derived from the Greek words of tokos, meaning "offspring" and pherein, meaning "to bear," proving its necessity in the reproduction process. It was formerly known as the "antisterility" vitamin, a deficiency of which has been linked to miscarriages.
As a derivative of chromanol, Vitamin E includes eight naturally occurring forms of the tocopherol and tocotrienol compounds found in plants, with the most potently active and widely known being alpha-tocopherol. Of the two, tocopherols are the most active form, designated alpha, beta, gamma, delta, epsilon, zeta, eta, and theta, with only four having Vitamin E activity (alpha, beta, gamma, and delta). The dl forms are synthetic. Tocopherol is the name used when referring to Vitamin E, and is a generic name for all mono-, di-, and tri-methyl tocols. The beta, gamma, and delta forms of tocopherols differ slightly in chemical structure and generally have lower "Vitamin E" activity. Tocotrienols may have biological activity comparable with that of the tocopherols, but are generally considered of less nutritional importance.
Unlike other fat soluble vitamins, Vitamin E is stored in the body for a relatively short period of time, much like the B and C Vitamins. Since Vitamin E is a fat-soluble compound, it is absorbed in a similar manner as fats. It must be broken down by bile acids secreted from the liver in order to be carried to the absorptive intestinal cells (via the non-carrier mediated passive diffusion process). Any disorder that decreases the surface area of intestinal cells, as celiac disease or the surgical removal of parts of the intestine, will result in the malabsorption of Vitamin E as well as other nutrients.
The liver functions as a rapid turnover store of Vitamin E, never accumulating large amounts, with 60-70% excreted in the feces. Adipose tissue is the long-term storage area, but Vitamin E accumulates slowly there and is released just as slowly. Muscle tissue accounts for much of the stores of Vitamin E.
As an active antioxidant, Vitamin E, along with Vitamin A, Selenium, and Vitamin C, prevent the oxidation of fat compounds. This is very important in blocking the formation of free radicals, known to contribute significantly to the disease process, from forming. Vitamin E appears to block prostaglandins (chemicals that reduce immune responses) and to protect cell membranes from attack by pathogens. It can be destroyed by heat, freezing temperatures, oxygen, processing, iron, chlorine, and mineral oil.
Externally, Vitamin E prevents thick scar formation. Internally, it has been used to prevent cell membrane damage, speed the healing of burns, as a diuretic and an anticoagulant, and to relieve leg cramps. It has also proven to treat successfully fibrocystic diseases of the breast, improving the condition by 70%. Children suffering from epileptic seizures have displayed low levels of Vitamin E, which has proven to help control seizures. For more than half a century, Vitamin E has demonstrated a strengthening effect on the heart, a concept pioneered by the Shute Brothers of Canada. Typically, their theory met with resistance from their medical counterparts. Today, science is finally catching up, validating their claims.
The need for Vitamin E during menopause can increase by ten to fifty times the normal amount required in the premenopausal years. Hot flashes have reportedly diminished in some people when supplements of 1200 mg. were taken along with 1000 mg. of hesperidin (a bioflavonoid).
Vitamin E deficiency rarely occurs because of an inadequate intake. It happens more often when such malabsorption disorders as cystic fibrosis, abetalipoproteinemia, chronic cholestatic liver disease, short bowel syndrome, celiac disease, and chronic diarrhea develop. The most severe malabsorption of Vitamin E occurs when bile flow is impaired or when intestinal lipoprotein synthesis is defective. When malabsorption occurs in adults, it generally takes several years before plasma Vitamin E decreases to a dangerously deficient range. Children, on the other hand, who have malabsorption problems from birth, take a relatively short period of time. If it is left untreated, neurologic and cognitive symptoms develop .
Vitamin E deficiency primarily affects the posterior columns of the spinal cord, the third and fourth cranial nerve nuclei, large caliber myelinated axons of peripheral nerves, the brain stem, and eventually muscles and the retina. Therefore, typical symptoms include loss of deep tendon reflexes, alterations in balance and coordination, impaired movement of the eyes (ophthalmoplegia), muscle weakness, and visual disturbances. If Vitamin E deficiency is corrected during the first few years of life, all symptoms can be reversed or prevented. If not dealt with until symptoms are well advanced, limited improvement can be expected.
When taking Vitamin E for the first time, it is best to begin with a small dose, increasing gradually. A sudden large dose can produce headaches or aggravate a rheumatic heart condition. Vitamin E can be destroyed by the inorganic iron form of ferrous sulphate. If this form be taken, it should be done so at least eight hours away from any Vitamin E supplement. The problem arises from taking extra amounts, and not with preparations that contain both Vitamin E and iron together. The inorganic forms of ferrous gluconate, peptonate, citrate, or fumerate do not destroy Vitamin E. Vitamin E is available in oil-base or water-soluble forms and works best when taken with B Complex, inositol, and Vitamin C. Another factor that affects Vitamin E intake is the amount of polyunsaturated fatty acids in the diet. As the consumption of polyunsaturated fatty acids increase, so does the Vitamin E requirement.
Note: Cautious Vitamin E intake should accompany those who have overactive thyroids, diabetes, high blood pressure, or rheumatic fever. It can elevate blood pressure in hypertensives, but can lower blood pressure if dosages start small and are slowly increased. This method has also proven effective with diabetics to reduce their insulin levels -- but must be done with professional supervision. Large intakes of Vitamin E (1200 mg. or more) can interfere with the metabolism of Vitamin K and, to a certain extent, that of Vitamin A absorption and, because of that, it is advisable not to exceed 800 mg. for 2 weeks before or after surgery. Although Vitamin E is considered non-toxic, a child with a Vitamin K deficiency should not be taking large doses of the vitamin as it can impair normal blood clotting and aggravate any existing disorder. People with a history of rheumatic heart disease may not be able to tolerate more than 150-200 IU of Vitamin E per day.
Summary:
Names include: Vitamin E, vitamin E1, antisterility factor/vitamin, factor X, Eprolin-S, Epsilan, Ephynal, Syntopherol, E-Vimin, Eviphero, Etavit, Phytogermine, Profecundin, Tokopharm, Viteolin, Escorb, Vacuals, Covitol, Envion.
Forms include: alpha tocopherol, beta tocopherol, delta tocopherol, gamma tocopherol, alpha-tocopherol acetate, alpha-tocopheryl acetate concentrate, alpha-tocopheryl acid succinate, epsilon-tocopherol, zetal-toc, zeta2-tocopherol, eta-tocopherol, Vitamin E2(50)/tocoquinone-10/tocopherylquinone.
Deficiency symptoms include: (rebound symptoms, if large doses are halted abruptly), anemia, degenerating muscles, muscular weakness, sore muscles, charley horse, ceroid deposits in muscles, degenerating endocrine glands, sterility, degenerating peripheral vascular system, deterioration of nervous system, angina, decreased survival time of red blood cells, RBC rupture, increased creatinine in urine, acne, increased need for oxygen, slow healing, scars/stretch marks remain, wrinkled skin, decreased ozone/radiation/cancer resistance.
Toxicity symptoms include: headaches, nausea, dizziness, decreased basal metabolic rate, fatigue, muscle weakness, decreased thyroid hormone levels, increased blood triglycerides in women, slightly increased blood fats, thinner blood, increased bleeding, decreased blood sugar, blurred vision, chapped lips, inflammed mouth, deterioration of digestion, decreased sexual organ function, and a decreased ability to convert Provitamin A to vitamin A.
Inhibitors include: ferrous sulfate, vitamin Bp, heat, O2, freezing temperatures, food processing, chlorine, mineral oil, laxatives, estrogen, thyroid hormones, and contraceptive pills.
Helpers include: Vitamins A, B Complex, B1, BH, C, F, manganese, selenium, phosphorus.
Alpha-vitamin E is a specific form of Vitamin E, also known as alpha-tocopherol. Its forms are: alpha-tocopherol, alpha-tocopherol acetate, alpha-tocopherol acid succinate.
Alpha-Vitamin E acetate is a specific form of alpha-Vitamin E, also known as: Vitamin E acetate, and alpha-tocopherol acetate.
Alpha-Vitamin E acid succinate is a specific form of alpha-Vitamin E, also known as vitamin E acid succinate, alpha-tocopherol acid succinate, and d-tocopherol acid succinate.
Beta-Vitamin E is a specific form of Vitamin E, also known as beta-tocopherol, cumotocopherol, neotocopherol, and p-xylotocopherol.
Gamma-Vitamin E is a specific form of Vitamin E, also known as gamma-tocopherol and o-xylotocopherol.
Delta-Vitamin E is a specific form of Vitamin E, also known as delta-tocopherol.
Epsilon-Vitamin E is a specific form of Vitamin , also known as epsilon-tocopherol.
Zeta 1-Vitamin E is a specific form of Vitamin E, also known as zeta 1-tocopheral.
Zeta 2-Vitamin E is a specific form of Vitamin E ,also known as zeta 2-tocopherol.
Eta-Vitamin E is a specific form of Vitamin E, also known as eta-tocopherol.
Vitamin E2(50) is a specific form of Vitamin E, also known as Vitamin E2, tocoquinone, and 10/tocopheryl quinone.
