Assessment of Vitamin E Nutritional Status

Vitamin E deficiency is not a problem, even among people living on relatively poor diets. In depletion studies, very low intakes of vitamin E must be maintained for many months before there is any significant fall in circulating a-tocopherol, because there are relatively large tissue reserves of the vitamin. 

Deficiency develops in patients with severe fat malabsorption, cystic fibrosis, chronic cholestatic hepatobiliary disease, and in two rare groups of patients with genetic diseases  

Patients who lack the hepatic tocopherol transfer protein (Section 4.2) and suffer from what has been called AVED (ataxia with vitamin E deficiency) are unable to export a-tocopherol from the liver in VLDL. 

In both groups of patients, the only source of vitamin E for peripheral tissues will be recently ingested vitamin E in chylomicrons. They develop cerebellar ataxia, axonal degeneration of sensory neurons, skeletal myopatby, and pigmented retinopatby similar to those seen in experimental animals. 

In premature infants, whose reserves of the vitamin are inadequate, vitamin E deficiency causes a shortened half-life of erythrocytes, which can progress to increased intravascular hemolysis, and hence hemolytic anemia. In infants treated with hyperbaric oxygen, there is a risk of damage to the retina (retro-lental fibroplasia), and vitamin E supplements may be protective, although this is not firmly established (Phelps, 1987). 

The most commonly used index of vitamin E nutritional status is the plasma concentration of a-tocopherol because it is transported in plasma lipoproteins, it is best expressed per mole of cholesterol or per milligram of total plasma lipids (Horwitt et al, 1972 Winbauer et al., 1999). The reference range is 

Sources From data reported by Horwitt et at. 1972 Sauberlich et at. 1974 Mor- 

12 to 37 /Mmol per L ranges associated with inadequate and desirable status are shown in Table 4.3 an optimum concentration for protection against cm-diovascular disease and cancer is 30 /Mmol per L (Morrissey emd Sheehy, 1999). 

Overall emtioxidant status, as opposed to specificedly vitamin E status, can be assessed by a variety of measures of Upid peroxidation, including measurement of  

Plasma total thiobarbituric acid-reacting substances (TEARS)  

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