To the Editor: Tardive dyskinesia (TD) is a disorder characterized by various abnormal involuntary movements of the face, neck, trunk, and extremities that is precipitated by the use of antipsychotic medications.1 In general, the incidence of TD has been reported to be 5% per year for typical antipsychotics and 1% per year for atypical antipsychotics.2 This disorder is a devastating condition that until only recently had no US Food and Drug Administration—approved treatments. While prevention remains the best treatment option, several off-label medications, such as antioxidants, have demonstrated a therapeutic benefit in treating and preventing the progression of TD.3 There are several hypotheses for the etiopathology of TD. We will focus on the neurodegenerative hypothesis, which suggests antipsychotics increase dopamine metabolism and turnover, leading to the formation of free radicals.4 The neuronal damage caused by oxidative stress and free radicals may lead to the development of TD.5 Antioxidants are reducing agents that have the capability to accept electrons from free radicals, therefore neutralizing and preventing them from causing damage.6
Vitamin E is one of many antioxidants used for the treatment of TD; however, there is insufficient evidence to either prove or disprove its efficacy.4 Daily doses of up to 1,600 mg of vitamin E have been studied in patients with TD.6 Vitamin E therapy is not without consequence, as its use may lead to significant harm. Two trials7,8 concluded that treatment with vitamin E increased the risk of hemorrhagic stroke. Findings from another study9 suggested that patients with vascular diseases or diabetes who took vitamin E 400 IU daily for 7 years had a 13% increased risk of heart failure. Furthermore, the Selenium and Vitamin E Cancer Prevention Trial (SELECT)10 found a 17% relative increase in the incidence of prostate cancer in men taking only vitamin E supplementation, which started to emerge around year 3 of the study.
https://www.psychiatrist.com/PCC/article/Pages/2018/v20n02/17l02170.aspx
