lvysaur
Member
- Joined
- Mar 15, 2014
- Messages
- 2,287
Aspirin blocks Arachidonate from entering the COX cascade, which explains a lot of its effects. However, I (and I think some others on here) have noticed a form of aspirin withdrawal, which I attribute to a build up of AA rushing into the COX as the aspirin wears off, producing even more prostaglandins, eicosanoids, etc., than usual.
If instead we blocked the conversion of Linoleic acid to Arachidonic, perhaps it would have better effects? It seems like individual differences in desaturation activity are more prevalent than differences in COX activity.
The two main pathways for AA production are Phospholipase A2 and Phospholipase C.
Phospholipase C - Wikipedia
https://pubs.acs.org/doi/pdf/10.1021/acschemneuro.5b00073
"phytochemical based PLA2inhibitors including curcumin, Ginkgo biloba and Centella asiatica extracts". So we might be able to see some degree of sharing between the effects of aspirin and those of turmeric/ginkgo/gotu kola. I personally never took either of these three so I can't say.
If instead we blocked the conversion of Linoleic acid to Arachidonic, perhaps it would have better effects? It seems like individual differences in desaturation activity are more prevalent than differences in COX activity.
The two main pathways for AA production are Phospholipase A2 and Phospholipase C.
Phospholipase C - Wikipedia
https://pubs.acs.org/doi/pdf/10.1021/acschemneuro.5b00073
"phytochemical based PLA2inhibitors including curcumin, Ginkgo biloba and Centella asiatica extracts". So we might be able to see some degree of sharing between the effects of aspirin and those of turmeric/ginkgo/gotu kola. I personally never took either of these three so I can't say.
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