Bioavailability is an important factor affecting requirements. Most dietary vitamin
E is found in food that contains fat. Vitamin E absorption requires micelle formation and
chylomicron secretion by the intestine, although the optimal amount of fat to enhance
vitamin E absorption has not been reported.
Information presently available indicates that vitamin E functions primarily as an
antioxidant in biological systems by trapping peroxyl free radicals (Combs, 1992; IOM,
2000). In this regard, vitamin E is found in cellular membranes associated with PUFA in
phospholipids. In vitamin E deficiency, the oxidation of PUFA is more readily
propagated along the membrane, leading to cell damage and eventually symptoms,
mainly neurological.
V
itamin E requirements have thus been reported to increase when intakes of
polyunsaturated fatty acids (PUFAs) are increased. It has been suggested that a ratio of
at least 0.4 mg (1 µmol)
α-tocopherol per gram of PUFA should be consumed by adults.
However, the method of determining the vitamin E requirement generated by PUFA
intakes is not universally accepted. There are also data to suggest that low-density
lipoprotein (LDL) oxidation susceptibility
in vitr
o
is dependent upon its PUF
A
content.
Although it is clear that the relationship between dietary PUF
A
and vitamin E needs is
not simple, high PUFA intakes should certainly be accompanied by increased vitamin E
intakes.
It is also recognised that the requirements for vitamin E increase with increasing
body weight until adulthood.