unsaturation than by their mass (Draper, 1993). Moreover, PUFAs are not deposited in the tissues in the same proportions that they occur in the diet. Finally, dietary PUFAs are modified by elongation and desaturation and are catabolized to various degrees depending on energy status (Jones and Kubow, 1999).

There are also data to suggest that low-density lipoprotein (LDL) oxidation susceptibility in vitro is dependent upon its PUFA content. A 10 percent PUFA diet with 34 percent of calories from fat increased LDL oxidation susceptibility compared to a 19 percent monosaturated fatty acid (MUFA) diet with 40 percent of the calories from fat, without changing the α-tocopherol content of the LDL (Schwab et al., 1998a). In a double-blind crossover trial in 48 postmenopausal women, supplementation with fish oil increased LDL oxidation susceptibility, while supplementation with both fish oil and α-tocopheryl acetate significantly decreased it (Wander et al., 1996).

The effect of the fatty acid composition of reduced-fat diets on the in vitro oxidation of LDL was also examined in 14 moderately hypercholesterolemic (LDL greater than 3.36 mmol/L) female and male subjects (aged 44 to 78 years). Each subject consumed each of five reduced-fat diets (30 percent of energy from total fat, 17 percent from protein, and 53 percent from carbohydrate) which included 20 percent of energy from beef tallow, canola oil, corn oil, olive oil, or rice bran oil for a period of 32 days. When the data from all dietary phases were pooled, LDL α-tocopherol levels and plasma 18:1/18:2 ratios were positively related to LDL oxidation resistance (Schwab et al., 1998b).

Although it is clear that the relationship between dietary PUFA and vitamin E needs is not simple, high PUFA intakes should certainly be accompanied by increased vitamin E intakes.


Infants Ages 0 through 12 Months
Method Used to Set the Adequate Intake

No functional criteria of vitamin E status have been demonstrated which reflect response to dietary intake in infants. Thus recommended intakes of vitamin E are based on an Adequate Intake (AI) that reflects a calculated mean vitamin E intake of infants fed principally with human milk.

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