variety of involuntary movements, especially of the face. It has been reported that the cerebrospinal fluid of patients with TD contains higher-than-normal concentrations of lipid peroxidation products (Lohr et al., 1990), and more recently, plasma also was found to have lipid peroxidation products (Brown et al., 1998). However, a causal relationship between these indicators of oxidative stress and the incidence or severity of tardive dyskinesia has not been established.
Some have reported short-term supplementation of TD patients with vitamin E (Egan et al., 1992; Elkashef et al., 1990; Lohr et al., 1987). The beneficial effects were minor, mostly limited to patients with recent onset of the disease, and the number of subjects was very small. Recently, in 40 patients who were supplemented with 1,600 IU/day of α-tocopherol or placebo for up to 36 weeks, there was a significant difference in mean Abnormal Involuntary Movements Scale scores, in those receiving vitamin E after 10 weeks of treatment (Adler et al., 1998).
A large number of studies have been carried out in the past decade that directly or indirectly concern the relationship between vitamin E intake and chronic disease. Among the effects of vitamin E intakes from supplements are inhibition of LDL oxidation both in vitro and in vivo; inhibition of smooth muscle cell proliferation through inhibition of protein kinase C; inhibition of platelet adhesion, aggregation, and platelet release reactions; and inhibition of plasma generation of thrombin. In addition, supplemental intakes of vitamin E decrease monocyte adhesion to endothelium, decrease monocyte superoxide production, potentiate the synthesis of prostacyclin, upregulate the expression of phospholipase A2 and cyclooxygenase, and inhibit the expression of ICAM-1 and VCAM-1 induced by exposure to ox LDL. Many of these effects have been shown only in tissue culture and have not been studied in vivo. All of these actions could have an influence on health and the development of chronic disease. Some of these effects appear to be independent of the antioxidant properties of vitamin E. Thus, it must be recognized that consumption of large quantities of vitamin E will lead to multiple metabolic and cellular changes in humans. An important question is whether the net result of these changes will be beneficial when large amounts of vitamin E are consumed on a long-term basis.
Clinical trials are currently under way to determine whether high