What's on Your Mind

[Insertnamehere]

I suspected something like that. But that common pathway is not identical up to the end. It is possible to target different parts of it resulting in a differential modulation of its various components. Someone should work on that, that was my point.




I will never mess with my pain receptors. My pain sensation is excellent (i.e. I have a very high pain tolerance), I don't want to fuck that up.


Lidocaine is a local anesthetic, which wouldn't be suitable to alleviate a headache.






Yeah well, I wasn't asking for my whole ability to sense pain to be abolished. I'm one of the last people on this planet to argue against pain like that.

I had a fever, my airways were clogged up and I couldn't breathe half the time, I had a painful cough and a sore throat, my ears were shut (I don't know what's the term for it in English; it's the same thing that happens when you're on an airplane), and on top of that I had a headache for the second day in a row. It served no beneficial purpose and I would have liked to take away that one thing I could have controlled. As it stood, I didn't do it, because I chose not to lower my fever even though it would have meant getting rid of my headache.

As it is, the choice is either NSIDs or opioids.

Now this next bit comes from a place in which...I don't have enough time on my hands to do a proper bibliographic research for you...

I would venture the guess that having various effects, prostaglandins target different cell types and/or different cell receptors, in turn activating different signaling pathways that lead to these effects. The option would be to develop an antagonist that blocks a specific receptor related to a signaling pathway known to lead to a specific effect without affecting the rest of them.

I'm not currently aware if the entire signaling pathways related to prostaglandins and their effects are known or fully dilucidated. Making up the different components of a signaling pathway can be tricky, especially if the receptors are located in the membrane.

Given that prostaglandins seem structurally quite hydrophobic (to me, when I look at the molecule, at least) I would guess an intracellular receptor, the kind that upon binding the molecule in question turns into a transcription factor directly affecting the expression of target genes.


There is also the fact that OTC medications are mass produced and meant to be usually cheap, so in terms of cost-effectiveness, if you have a medication that can do a number of things targeting just the one effector enzyme, that is, commercially, a good thing.