ever, the evidence is strong enough to warrant continued investigation.
There is a sound biochemical basis for the notion that the accumulation of damaged proteins in the lens leads to cataract formation and that free-radical damage contributes to this protein damage (Taylor, 1993). Studies in experimental animals show that antioxidant vitamins, including vitamin E, can protect against lens damage (Jacques et al., 1994).
At the epidemiological level, there have been nine studies relating vitamin E status to risk of at least one type of cataract. Five reported a protective association (Jacques and Chylack, 1991; Knekt et al., 1992; Leske et al., 1991; Robertson et al., 1989; Vitale et al., 1993), while four reported no association (Hankinson et al., 1992; Mares-Perlman et al, 1994a,b; Mohan et al., 1989).
Only one intervention study has been carried out to test the effects of α-tocopherol alone on the prevalence of cataracts (Teikari et al., 1998). A subgroup of men participating in the Finnish ATBC study were examined at the end of that study for cataracts. There were no differences in the prevalence of nuclear, cortical, or posterior subcapsular cataracts between control subjects and those taking 50 mg/day of α-tocopherol.
The most characteristic manifestation of vitamin E deficiency in humans is neuropathy affecting both the central and the peripheral nervous systems, particularly sensory axons (Sokol, 1988). The neuropathology associated with frank vitamin E deficiency has been discussed above. The discussion that follows focuses on neurological diseases in which free-radical damage has been proposed to play a role and in which vitamin E might therefore play a protective role.
Parkinson's Disease. Parkinson's disease is characterized by dopaminergic cell death in the substantia nigra. Reported local changes in the substantia nigra compatible with a role for oxidative stress in Parkinson's disease include signs of increases in lipid peroxidation, increases in iron concentration, and decreases in some of the antioxidant defense mechanisms (Muller, 1994). However, a placebo-controlled, double-blind study of 800 patients given 2,000 IU/day of all rac-α-tocopherol failed to show any beneficial effect (Parkin-