Statins and other lipid lowering drugs have been repeatedly described to decrease blood levels of minor fat soluble components such as vitamin E (as alpha-tocopherol). Clinical consequences of this secondary state of deficiency have not been described so far, but recent biochemical and molecular evidence on homeostatic and molecular responses to vitamin E deficiency in skeletal muscle cells may suggest the hypothesis presented in this paper of a role as risk factor in the development of statin-associated myopathy. This hypothesis that needs to be further investigated, could suggest the need for precautionary measures during lipid lowering therapy, which include timely diagnosis and active prevention of vitamin E deficiency.
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