3 ms·
Hi 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 i
by robbiep 12y ago
Hi 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