In both inherited and acquired deficiency states, vitamin E deficiency can contribute to cerebellar dysfunction and central cognitive effects because α‑tocopherol protects vulnerable neurons, including cerebellar Purkinje cells, from ongoing oxidative damage across the lifespan. In AVED, where an α‑TTP defect prevents normal vitamin E transport, deficiency is associated with spinocerebellar ataxia, Purkinje cell loss, degeneration of sensory neurons, and a characteristic “dying back” neuropathy, yet long‑term α‑tocopherol supplementation over many years can slow or even prevent further neurologic progression when started early. Experimental and clinical data also show that even brief interruptions in vitamin E supplementation can measurably lower plasma total radical‑trapping antioxidant capacity before obvious symptom worsening, highlighting renewed oxidative vulnerability of nervous tissue and reinforcing the importance of consistent repletion to support normal neurogenesis and central nervous system function. This medication is commonly used for High Cholesterol.
Thapa S, Shah S, Chand S, Sah SK, Gyawali P, Paudel S, Khanal P. Ataxia due to vitamin E deficiency: A case report and updated review. Clin Case Rep. 2022 Sep 6;10(9):e6303. Schuelke M, Finckh B, Sistermans EA, Ausems MG, Hübner C, von Moers A. Ataxia with vitamin E deficiency: biochemical effects of malcompliance with vitamin E therapy. Neurology. 2000 Nov 28;55(10):1584-6. N. Stojiljkovic, S. Redko, F. Gupta, S. Kathiresu Nageshwaran, W. Tse. Cerebellar ataxia due to vitamin E deficiency [abstract]. Mov Disord. 2023; 38 (suppl 1). Traber MG. Vitamin E: necessary nutrient for neural development and cognitive function. Proc Nutr Soc. 2021 Aug;80(3):319-326.
Some side effects may be linked to nutrient depletion caused by this medication.
Research demonstrates that fibrates, particularly fenofibrate, are known to increase homocysteine levels. Elevated levels of homocysteine is associated with increased risk of a range of health problems including atherosclerosis, stroke, and neurological diseases, and vitamin Bs including vitamin B6 helps facilitate the breakdown of homocysteine and may be helpful in reducing homocysteine levels.
Fenofibrate has been shown in studies to increase the toxic effect of ultraviolet (UV) radiation that may lead to side effects such as hives, itching, and skin rash. Taking vitamin E before UV exposure is found in research to significantly help block UV-fenofibrate effects on the skin. Vitamin E supplementation should be considered when taking this drug therapy.
Fenofibrate has been shown in studies to increase the toxic effect of ultraviolet (UV) radiation that may lead to side effects such as hives, itching, and skin rash. Taking vitamin C before UV exposure is found in research to significantly help block UV-fenofibrate effects on the skin. Vitamin C supplementation should be considered when taking this drug therapy.