Tocopherols dietary intake

In a large trial (37) conducted in eight European countries— European Antioxidant Miocardial Infarction and Breast Cancer (EURAMIC) trial—the fatty acid composition, a-tocopherol, and /3-carotene levels were determined in adipose tissue of patients with acute Ml. The study supported the hypothesis that /3-carotene protects against Ml because it reduces the oxidation of PUFA. The concentration on adipose tissue was considered due to the dietary intake. 

Based on the plasma concentration of a-tocopherol to prevent significant hemolysis in vitro (14 to 16 /xmol per L), the U.S./Canadian estimated average requirement is 12 mg per day, giving a Recommended Dietary Amount (RDA) of 15 mg per day (Institute of Medicine, 2000) - a 50% increase on the previous RDA (National Research Council, 1989). This increase arose partly as a result of considering only the 2R isomers in dietary intake (Section 4.1). Average intakes are of the order of 8 to 12 mg of a -tocopherol equivalent per day it would be difficult meet this reference intake without significant changes in diet or use of supplements. 

Vitamin K is a fat-soluble vitamin. The RDA for the adult man is 10 mg of a-loeophenol, or its biological equivalent. The RDA for infants should also be mentioned, as vitamin E deficiency, when it occurs, tends to strike this population. The RDA for the newborn is 5 mg of a-tocopherol, or its equivalent. The vitamin needs of the infant have been expressed in terms of the amount of polyunsaturated faltj acids (as fats and oils) in the diet, for example, 0,7 mg of a-tocopherol per gram of linoleic acid. A common level of dietary intake is about 10 mg per day. A deficiency iit the vitamin is quite rare. 

Freeman VL, Meydani M, Yong S, Pyle J, Wan Y, Arvizu-Durazo R, Liao Y. Prostatic levels of tocopherols, carotenoids, and retinol in relation to plasma levels and self-reported usual dietary intake. Am J Epidemiol 2000 151 109-118. 

Skin of hairless mice subjected to chronic low levels of UV displayed increased epoxide at 4 weeks and maximum levels at 10 weeks (69>70). Subsequently, it was shown a-epoxide hydrase increased starting at 8 and peaking at 15 weeks and that its elevation coincided with a decline in epoxide but also a rapid increase in tumor incidence (70,71). Dietary intake of ascorbate, butylated hydroxytoluene (BUT), dl-a-tocopherol and reduced glutathione decreased levels of a-epoxide by 50% and suppressed tumor formation induced by UV light (72,73). 

In the presence of low body stores of vitamin E, one might expect that marginal dietary intakes could more easily lead to the deficiency state. In various mammalian species, including man, the placenta has a limited capacity to transfer tocopherol to the fetus (Abderhalden, 1945 Dju et al.,... 

Since the tocopherol content of feeds varies with the season and since the amount of tocopherol in milk is a reflection of the dietary intake, it is to be expected that the tocopherol content of butter will vary throughout the year. Anglin, Mahon, and Chapman (1955) estimated the tocopherol content of 329 butter samples collected throughout the year from 28 towns in 8 provinces in Canada. The average values by months are presented in Kg. 5. Highest values were noted during the late summer months and lowest values during the late winter months. A 100% variation occurred,... 

The levels of ascorbic acid, a-tocopherol, folic acid, carotenoids, and flavonoids within the body are maintained by dietary intake. While the role and importance of dietary antioxidants are currently unclear, antioxidant defense can be modulated by increasing or decreasing the intake of foods containing these antioxidants. There are a number of reasons for recommending dietary changes in preference to supplementation for achieving increased antioxidant status, as follows. 

Table 6.4 summarizes the concentrations of a range of endogenous (i.e., nondietary) simple phenols, including a-tocopherol, and ascorbate in plasma from healthy individuals. The total simple phenol and ascorbate concentration is between 159 and 380 pM. The maximum additional concentration that is likely to be achieved from dietary sources, 3 to 22 pM, is marginal by comparison adding only between 0.3 and 5% if it is assumed, quite reasonably, that the typical mean intake is taken over three equal meals. Many people consume a much smaller quantity of dietary PPT and even those consuming double the... 

Research Council defined 1 mg of a-tocopherol as 1 unit of a-TE (mg x 1). The activities as a-TE of other vitamers were (3-tocopherol, mg x 0.5 y-tocopherol, mg xO. 1 8-tocopherol, mg x 0.03 a-tocotrienol, mg x 0.3 and (3-to-cotrienol, mg x 0.05. The activities of y- and 8-tocotrienol were undetectable. The Recommended Dietary Allowances (RDAs) are only based on intake of the 2R-stereoisomeric forms of a-tocopherol (RRR-, RSR-, RRS-, and RSS-tocopherol) from food, fortified food, and vitamin supplements (Food and Nutrition Board, 2000). The 2S-stereoisomeric forms of a-tocopherol and the other tocopherols ((3-, y-, and 5-tocopherol) and tocotrienols are not used to estimate the RDAs. 

I 90 Pietinen P Rimm EB, Korkonen R et al, Intake of dietary fiber and risk of coronary heart disease in a cohort of Finnish men. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Circulation 1996 94 2720-2727,... 

Kritchevsky and Kritchevsky (2000) provided a summary of the evidence linking dietary cholesterol to the risk of CHD in 10 cohorts from eight large, well-conducted prospective studies that were reported since 1980, which included the Nurses Health Study, the Health Professionals Followup Study and the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. In eight of the cohorts there was no statistical association between cholesterol intake and the risk of CHD. In one of the positive studies the association was established by simple univariate analysis and was not adjusted for other dietary variables. The other study adjusted only for fat intake. There is no compelling evidence from these epidemiological studies that dietary cholesterol is associated with the risk of CHD. 

The U.S./Canadian Dietary Reference intakes report (Institute of Medicine, 2000) departed from tradition by considering only the contribution of the 2R isomers to vitamin E intake, and proposed an equivalence of 0.45 iu per mg for synthetic all-rac-a-tocopherol, although in consideration of upper tolerable levels of intake (Section 4.6.1), they considered the contribution of aU isomers equally However, although the 2S isomers have a shorter half-life than -tocopherol in the circulation, and hence a lower apparent biological availability, they are active in animal biological assays (Hoppe and Krennrich, 2000). 

Regardless of the mechanisms involved, these results provide additional evidence for the concept that the intake of dietary flavonoids can be associated with improvements in the oxidant defense system that are physiologically relevant. This concept is further supported by the finding by Actis-Goretta et al. (unpublished), that 2 hours after the consumption of 105 g of chocolate, the depletion of a-tocopherol in plasma oxidized with AAPH was slower than in the same subjects before, and 6 hours after, chocolate consumption. 

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