As many of my readers know, DVT is a rather serious condition that can be lethal by causing pulmonary or brain embolism. Any patient diagnosed with such a condition is typically put on blood thinners for life. Not only do those blood thinners have variety of nasty side effects, they often cause death by the opposite mechanism – excessive bleeding in GI tract or brain. Aspirin has been shown to be superior to pharma drugs for managing DVT, but mainstream medicine seems to have “ganged up” on aspirin and is now recommending against its use in any but the most limited of circumstances. The study below may present an alternative to aspirin (and especially the pharma drugs for DVT), while also explaining the mechanism behind DVT formation/progression. Namely, vitamin E seems to act similarly to aspirin in ameliorating DVT and its complications, and the mechanism of action seems to be related to iron, or more specifically iron overload. Just like aspirin, the study below found that vitamin E inhibits iron overload in the cell and thus prevents something called ferroptosis – i.e. a type of cell death caused by said iron overload. Just a few minutes ago, I did a post showing that the toxicity of the amino acid cysteine can be eliminated by blocking the cellular uptake of iron (and thus ferroptosis). So, it seems that aspirin and vitamin E can also block the toxic effects of cysteine, which may explain their life-extending effects, mimicking dietary cysteine restriction. The human equivalent dosage (HED) of vitamin E was 15mg/kg daily, orally and the type of vitamin E used was alpha-tocopherol. The protective effects of vitamin E on DVT were already visible on day 7 after administration started. Now, at such HED, doctors will scream that vitamin E would also massively increase bleeding risk, just like aspirin. However, the study found no such effects.
“…Vitamin E treatment significantly reduced thrombus size, decreased neutrophil count, neutrophil percentage, platelet count, interleukin-6, and interferon-γ levels, and increased the number of live births and placental efficiency, with no effect on coagulation. It promoted thrombus dissolution and recanalization. Furthermore, vitamin E significantly decreased ferroptosis levels. In vitro, Erastin successfully induced endothelial cell ferroptosis. Vitamin E treatment significantly promoted the proliferation, migration, invasion, and tube formation of injured endothelial cells. It also markedly reduced the levels of reactive oxygen species and malondialdehyde, decreased the number of damaged mitochondria, and substantially alleviated ferroptosis in the injured endothelial cells.
Conclusion: Vitamin E significantly promoted the dissolution and recanalization of DVT during pregnancy, potentially by reducing endothelial cell ferroptosis. This study provides a new therapeutic strategy and insights into the mechanism for managing pregnancy-associated DVT.”
