Vegetable oils and lipid-rich plant products (e.g. nuts, seeds, grains) are the main dietary sources of vitamin E (10,11). In Western diets, vitamin E intake derives mainly from fats and oils contained in margarine, mayonnaise, salad dressing, and desserts, and increasingly also from fortified food (e.g., breakfast cereals, milk, fruit juices) (12-14). It is noteworthy that the U.S. diet contains large amounts of y-tocopherol compared with populations in other Western countries, which is a result of the high consumption of soybean and corn oils containing more y- than a-tocopherol (15). Vitamin E used for food fortification or dietary supplements consists mainly of a-tocopherol, derived either from natural sources (i.e., methylated y-tocopherol from vegetable oil) or from synthetic production; it is usually esterified to increase stability.
The most recent data available on vitamin E intake in the United States were reported in 1999 from the Third National Health and Nutrition Examination Survey (NHANES III, 1988-1994) among >16,000 U.S. adults showing a mean vitamin E intake of 10.4 a-TE in men and 8.0 a-TE in women (16). With the new definition of vitamin E activity from the FNB (6) distinguishing among a-tocopherol stereoisomers, these intake values of vitamin E are likely not as high. New studies are required to update these data on vitamin E intake because dietary patterns have changed during recent years and the consumption of fortified food and vitamin E supplements has increased.
The FNB indicates a recommended daily allowance (RDA) for adults of 15 mg vitamin E including food, fortified food, and supplements (6). This RDA refers to a-tocopherol because it is the only form of vitamin E that has been shown to reverse deficiency symptoms in humans. The recommendations are based largely on in vitro studies of M. Horwitt dating back to 1960; these studies are still considered to offer the most adequate data for defining the physiologic status and health benefits of vitamin E in humans. In these studies, prevention of H2O2-induced erythrocyte hemolysis was used as test system (17). However, except when vitamin E is clearly deficient the erythrocyte hemolysis test is not a useful indicator of vitamin E functional status. Thus, the guidelines of the FNB were discussed critically in the literature and it was strongly agreed that other assays and new biomarkers were required in the future to define the physiologic role and beneficial potential of vitamin E in humans (18,19).
The recommended daily intake of 15 mg vitamin E is considered rather unlikely to be achieved by North Americans and other Western countries through diet alone.
Although universal dietary supplementation has not been not recommended, a dose of 200 mg/d vitamin E (RRR-a-tocopherol) has been suggested to saturate plasma levels and elevate tissue levels; this may have possible health effects in the long term (20). In the future, subpopulations at risk for vitamin E deficiency in well-nourished populations such as the United States and other Western countries have to be defined. These specific groups, e.g., the elderly or individuals suffering from chronic diseases, may benefit in particular from regular intake of vitamin E supplements.
As an upper limit for supplemental vitamin E intake, the FNB published a dose for adults of 1 g/d a-tocopherol (i.e., 1500 iu RRR- or 1100 iu all-rac-a-tocopherol); this dose is considered safe, showing no apparent side effects (6). In human intervention studies, various doses of vitamin E up to 3600 iu/d have been used (21). Nevertheless, conclusive evidence from long-term studies regarding biological effects and safety of chronic intake of pharmacologic doses of vitamin E are lacking. In the Alpha-Tocopherol, Beta Carotene (ATBC) Cancer Prevention Study (22) with Finnish smokers consuming 50 iu/d vitamin E for 6 y, an increase in mortality from hemorrhagic stroke was observed; however, other intervention studies did not report such an adverse effect (23,24). It was suggested that pharmacologic doses of vitamin E are contraindicated in persons with blood coagulation disorders because vitamin E might exacerbate defects in the blood coagulation system due to its inhibitory effects on platelet aggregation (19,25).
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