Mainstream medicine claims that once cardiovascular disease (CVD) is established, there is no way to reverse it. All one can do is try to inhibit further plaque formation in the hope of delaying the inevitable (vessel blockage/rupture, followed by heart attack and/or stroke). I have already found studies demonstrating that aspirin, in doses of 800mg+ daily can reduce already established atheroma (plaque) and prevent future CVD event. The study below found that vitamin E, in a human-equivalent dose of about 5mg/kg daily, also reduces atherogenesis and improves cardiac function, without displaying antioxidant effects. The role of vitamin E as PUFA antagonist is probably the main mechanism of action, together with its role as an inhibitor of the inflammation producing enzyme COX/LOX, and its inhibitory effects on the release of other inflammatory mediators such as TNF-a, IL-1 and IL-6.
https://doi.org/10.1111/1755-5922.12096
https://pubmed.ncbi.nlm.nih.gov/38717284/
“…The impact of α-tocopherol on atherosclerosis is unclear and controversial. While some studies suggest potential benefits, such as antioxidant properties that may reduce oxidative stress, other studies indicate no significant preventive effects. The intricate interplay of various factors, including dosage, individual differences, and study methodologies, contributes to the ongoing uncertainty surrounding α-tocopherol’s role in atherosclerosis. Further research is needed to clarify its impact and establish clearer guidelines. Therefore, we aimed to evaluate the impact of α-tocopherol on atherogenesis in ApoE−/− fibrillin (Fbn)1C1039G/+ mice, which is a unique mouse model of advanced atherosclerosis with typical features, such as large necrotic cores, high levels of inflammation, and intraplaque neovascularization, that resemble the unstable phenotype of human plaques. ApoE−/− Fbn1C1039G+/− mice were fed a western-type diet (WD) supplemented with a high dose of α-tocopherol (500 mg/kg diet), while control mice were fed a WD containing a low dose of α-tocopherol (50 mg/kg diet). The high dose of α-tocopherol reduced plaque thickness and necrotic core area in the right common carotid artery (RCCA) after 24 weeks WD. Moreover, α-tocopherol decreased plaque formation and intraplaque neovascularization in the RCCA. In addition to its antiatherogenic effect, chronic supplementation of α-tocopherol improved cardiac function in ApoE−/− Fbn1C1039G/+ mice. However, chronic supplementation of α-tocopherol did not decrease lipid peroxidation. On the contrary, α-tocopherol acted as a prooxidant by increasing plasma levels of oxidized LDL and plaque malondialdehyde, an end product of lipid peroxidation. Our data indicate that α-tocopherol inhibits atherogenesis and improves cardiac function independent of its antioxidant properties.”
