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What I find interesting about aspirin is that no one really knows how it works (its "mechanism of action"). Its anti-inflamatory effects are a consequence of so
by fasteo 12y ago
What I find interesting about aspirin is that no one really knows how it works (its "mechanism of action"). Its anti-inflamatory effects are a consequence of something else, not the cause.
In the book "Power, Sex, Suicide"[1], Nick Lane states:
"Curiously, aspirin is also a mild respiratory uncoupler; I do wonder how many of its more mysterious benefits may relate to this property"
He is talking about the mitochondrial respitarory chain. In this context, "uncoupled" means that the electron flow does not generate any ATP; instead, all the energy is dissipated as heat. The interesting thing is that uncoupling the electron transport chain reduces electron leakage ("free radicals") and less free radicals has been associatted with ageing and disease.
Will less electron leakage reduce chronic inflamation ? Who knows ...
Once again, the analogy with computer systems is pretty straightforward: If our back-end system is "inflamed" (read, under heavy load) due to incoming HTTP requests, uncoupling it with a message queue system will have anti-inflammatory effects.
[1] http://www.amazon.com/Power-Sex-Suicide-Mitochondria-Meaning/dp/0199205647 http://www.amazon.com/Power-Sex-Suicide-Mitochondria-Meaning...
[2] http://sciencecases.lib.buffalo.edu/cs/files/dinitrophenol.ppt http://sciencecases.lib.buffalo.edu/cs/files/dinitrophenol.p...
- robbiep 12y agoHi there, I think you need to explain yourself a bit better - you have made a statement that is demonstrably false, at least in the sense that you have used it - aspirin is that no one really knows how it works - Aspirin works by a very well understood mechanism of binding irreversibly to the COX enzyme, with a preference for COX1 over COX2. there is no debate about this. Thankyou for pointing me down the rabbit-hole regarding uncoupling and the decrease in free radical production this creates [2], something I was not previously aware of [1] Uncoupling of intestinal mitochondrial oxidative phosphorylation and inhibition of cyclooxygenase are required for the development of NSAID-enteropathy in the rat doi/10.1046/j.1365-2036.2000.00723.x/ [2] Mitochondria and reactive oxygen species 10.1016/j.freeradbiomed.2009.05.004
- fasteo 12y agoIndeed. Wording is important. I meant that the known mechanism that you have mentioned does not explain all its reported benefits. Specifically in the anti-inflammatory effect, it seems like inhibition of prostaglandin synthesis (via COX enzyme binding) is not the reason[1]. As aspirin has so many potential benefits, it seems to me that it has to have some effect in some very basic and common site and the mitochondrial respiratory chain is a good, if not best, candidate. If you are interested in uncoupling and free radical production, Peter[2] has a good amount of info about it. At any rate, aspirin has many knowns unkowns; that´s what I meant in my original post. [1] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2213311/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2213311/ [2] http://high-fat-nutrition.blogspot.com.es/ http://high-fat-nutrition.blogspot.com.es/
- robbiep 12y agoThanks for pointing me to that blog, really interesting stuff. Rob
- atmosx 12y agoAspirin is very well understood, Wikipedia has a very extensive article about how it works. It's a pro-drug, when activated takes a place. Search for Arachidonic Acid pathway if you are interested. Also, By binding free radicals ( a we'll know, side-effect of aspirin and Vitamin C) you get less chances of getting cancer for one.
- fasteo 12y agoI meant that the known mechanisms do not explain all its reported benefits. In the Wikipedia article that you mention this is clearly stated: "However, other effects of aspirin, such as uncoupling oxidative phosphorylation in mitochondria, and the modulation of signaling through NF-κB, are also being investigated."