Recommending high intake of iron is one of the most common dietary recommendations of registered dieticians, as well as many doctors. The fact that lipofuscin – a highly insoluble complex of iron and PUFA peroxides – increases with age is conveniently ignored in those recommendations. The reality is that iron is a heavy metal and there is plenty of evidence implicating it as a causal factor in infections disease, dementia, Parkinson disease (PD), “autoimmunity”, diabetes, CVD, and cancer. The study below now demonstrates that iron, even in physiological concentrations, drives the fattening of the heart after a heart attack, and this ultimately leads to heart failure. Since iron “loves” to interact with PUFA and the latter is preferentially stored in tissues after ingestion, it is likely that most of those fatty acid deposits driving heart failure are made up of PUFA and, consequently, lipofuscin. Conversely, the study claims that iron chelators should be beneficial for both preventing and treating such cases of heart failure. The great news here is that we can go a step further by simply using a natural chemical available in most convenience stores – vitamin E. That humble vitamin is capable of both reducing total body iron stores, as well as preventing/limiting the formation of lipofuscin by reducing the generation of PUFA peroxides (which btw also depend to a great degree on iron availability). In addition, at least one animal study has suggested that vitamin E may be able to dissolve lipofuscin already formed/stored in organs, which further increases the therapeutic potential of this vitamin in heart failure, or aging in general (characterized by increased lipofuscin accumulation). Aspirin is another molecule known to reduce body iron stores, as well as inhibit PUFA peroxidation, though I haven’t seen studies on whether aspirin may help remove lipofuscin.
https://dx.doi.org/10.1038/s41467-022-33776-x
https://medicalxpress.com/news/2022-11-iron-chronic-heart-failure-survivors.html
“…The study, which involved collaborators from institutions in the United States and Canada, followed large animal models over six months. It found that in heart attacks that result in bleeding within the heart muscle—which is about half of them—scar tissue is slowly replaced by fat. Fatty tissue can’t push blood from the heart effectively, and this is what leads to heart failure and eventually to death in many survivors of hemorrhagic heart attacks, Dharmakumar said. “Using noninvasive imaging, histology and molecular biology techniques, and various other technologies, we have shown that iron from red blood cells is what drives this process,” he explained. “When we removed the iron, we reduced the amount of fat in the heart muscle. This finding establishes a pathway for clinical investigations to remedy or mitigate the effects associated with iron in hemorrhagic myocardial infarction patients.” Dharmakumar’s team is currently testing iron chelation therapy to do just that in a just-launched clinical trial.”
