Synopsis

Source of validity: Scientific
Rating (out of 5): 2

Vitamin E (specifically alpha-tocopheryl succinate) has been considered for the support and potential treatment of arteriosclerosis (hardening of the arteries) due to its antioxidant properties. The rationale is that oxidative modification of low-density lipoprotein (LDL) plays a significant role in the development of atherosclerosis, and antioxidants like vitamin E might inhibit this process. Some early epidemiological and observational studies suggested an association between higher vitamin E intake and reduced cardiovascular risk. However, large, well-conducted randomized controlled trials (RCTs) and meta-analyses have not demonstrated significant benefit of vitamin E supplementation in reducing the incidence or progression of arteriosclerosis or related cardiovascular events. For example, the HOPE and GISSI-Prevenzione trials found no significant reduction in cardiovascular outcomes with vitamin E supplementation.

Alpha-tocopheryl succinate, an ester form of vitamin E, has been less studied specifically for arteriosclerosis than the more common alpha-tocopherol. Most clinical studies have used alpha-tocopherol. There is some experimental evidence that vitamin E can reduce oxidative stress and inhibit the progression of atherosclerotic plaques in animal models, but these effects have not translated convincingly to human disease. As a result, major guidelines do not recommend vitamin E supplementation for the prevention or treatment of arteriosclerosis. The overall scientific evidence supporting its use is weak (rated 2 out of 5), primarily based on biochemical rationale and limited preclinical data rather than strong clinical outcomes.

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