If iron chelators work in Parkinson’s there should be some positive effect with supplemental quercetin. I very much doubt there will be. See the page on Parkinson’s disease. If quercetin does not work in the treatment of Parkinson’s disease then the narrative that treatment of Parkinson’s disease requires iron chelation has to be re-thought. I would avoid supplementing with quercetin until there are definite clinical studies to the effect that quercetin in the real world ameliorates symptoms of Parkinson’s disease which I think will be never.
Quercetin is found in fruits and vegetables. Querectin found in foods could have benefcial effects. Like other antioxidants, when obtained from food, quercetin could have beneficial effects.
A search for “iron chelation” and “Parkinson’s” pulls up 460 cites inPubMed. Given iron chelators worked in Parkinson’s disease that would be outstanding. Iron chelation in Parkinson’s disease, however, always seems to be full of promise but there have been no payoffs in terms of treatment. There are many, many ways available to chelate iron. Quercetin is for example a quite effective iron chelator. Polyphenols are quite effective iron chelators. Deferiprone, which an iron chelator, has been tried in Parkinson’s disease. Deferirone is not significantly effective in the treatment of Parkinson’s disease.
Why haven’t iron chelators worked by now in Parkinson’s disease? Perhaps because iron chelators can’t work in Parkinson’s disease. There could be difficulties with iron in Parkinson’s disease but those difficulties could be due dysregulations of iron metabolism rather than due to iron being toxic per se.
A major focus of this blog has been on aconitase 1, which is an enzyme in the citric acid cycle, which is regulated by iron. With low levels of iron in the gut activity of aconitase 1 in the gut will be low which will dysregulate the citric acid cycle. The citric acid cycle is a major energy producing cycle. With under activity/ fluctuations in the citric acid cycle there could be on-off effects.
Levodopa is an iron chelator. Aconitase 1 is regulated by iron. Increasing iron levels increases activity of aconitase 1. On-off effects associated with levodopa could at least partly be due to the iron chelating properties of levodopa. If this idea is correct all attempts to gradually release levodopa are misguided. Gradually releasing levodopa would only prolong the iron chelating effects of levodopa turning on-off effects into off effects.
Iron chelators are being clinically tested in a number of neurodegenerative illnesses such as Alzheimer’s and Parkinson’s disease . I do not think iron chelation is going to work. In fact I think iron chelators will make Alzheimer’s and Parkinson’s worse. I very much hope I am mistaken. The difficulty isn’t iron per se but rather dysregulation of iron regulated biological processes. Sensible ideas are wrong all the time. Iron chelation is a very sensible approach to treatment of Alzheimer’s and Parkinson’s which I think is going to be disastrous.