Cardiovascular and Metabolic Protection by Vitamin E: A Matter of Treatment Strategy?

Abstract

Cardiovascular diseases (CVD) cause about 1/3 of global deaths. Therefore, new strategies for the prevention and treatment of cardiovascular events are highly sought-after. Vitamin E is known for significant antioxidative and anti-inflammatory properties, and has been studied in the prevention of CVD, supported by findings that vitamin E deficiency is associated with increased risk of cardiovascular events. However, randomized controlled trials in humans reveal conflicting and ultimately disappointing results regarding the reduction of cardiovascular events with vitamin E supplementation. As we discuss in detail, this outcome is strongly affected by study design, cohort selection, co-morbidities, genetic variations, age, and gender. For effective chronic primary and secondary prevention by vitamin E, oxidative and inflammatory status might not have been sufficiently antagonized. In contrast, acute administration of vitamin E may be more translatable into positive clinical outcomes. In patients with myocardial infarction (MI), which is associated with severe oxidative and inflammatory reactions, decreased plasma levels of vitamin E have been found. The offsetting of this acute vitamin E deficiency via short-term treatment in MI has shown promising results, and, thus, acute medication, rather than chronic supplementation, with vitamin E might revitalize vitamin E therapy and even provide positive clinical outcomes.

CD36 Signal Transduction in Metabolic Diseases: Novel Insights and Therapeutic Targeting

“…As such, the administration of antioxidant supplements can increase the defense capacity of islet cells to cope with oxidative stress [ 127 ]. Vitamin E is a redox-active natural compound that downregulates levels of ROS under different experimental conditions [ 128 , 129 , 130 , 131 ]. Interestingly, vitamin E reduces the uptake of OX-LDL by inhibiting CD36 expression via the PPARγ signaling pathway [ 132 , 133 , 134 ].…”

Recent Advances in ROS-Sensitive Nano-Formulations for Atherosclerosis Applications

“…After treatment with this nanoparticle, oxLDL uptake and ROS production by human monocyte-derived macrophages were significantly reduced, which is important for preventing the formation of macrophage foam cells [ 72 ]. D -α-Tocopherol, the active form of vitamin E, has multiple protective effects such as reducing oxidative lipids and scavenging ROS in cardiovascular diseases [ 73 , 74 ]. After combination with MnO 2 microparticles, the nano-complex can inhibit progression of atherosclerosis by reducing the ROS levels and inhibiting the oxidation of LDL [ 75 ].…”

Impact of Dietary Lipids on the Reverse Cholesterol Transport: What We Learned from Animal Studies

“…However, long-term supplementation of vitamin E and adverse cardiovascular outcomes has been extensively studied, yielding controversial results [ 145 ]. In contrast, preclinical studies suggest that in particular situations, such as acute myocardial infarction, which leads to an increased vitamin E requirement, vitamin E supplementation could help in preserving cardiac function [ 146 , 147 ].…”