I rarely get that pyloric spasm anymore, and its been years since it was persistent enough to need NO2-Glycerin. Maybe because I ingest nic now by vaping, or maybe because I tend to be more chill than I was back then.
Cyrus, are you an MD? You mentioned med school, and clearly know a lot about medicine. If so, thanks for your input in this forum! Even if you are not, your input is most appreciated and useful information. I have learned much from your excellent posts.
OT comment: I have used nic for about 17 years now to combat residual peripheral nerve pain from damage from Guillain-Barre Syndrome, which I had back in '95. First it was with smoking, but now primarily from vaping. Typing long hours was the killer, with fine motor wrist nerves getting all up in a dander. Many a miserable day in grad school (my PhD is in computational chemistry), but since I started vaping in fall of '09, I have found it works much better than smoking, and have found some literature support for using nic for nerve pain wrt other degenerative nerve illnesses.
Are you aware of this? And if so, could you explain the theory behind why nic works in a way a non-medical person could understand?
Hey kurt!
I'm finishing the last leg of medical school now, in April or so I'll be an M.D.
I have an awareness of nicotine being a potent anti inflammatory, though admittedly I never searched for the mechanism at play, and don't know much about its use in the treatment of peripheral neuropathic pain
I should throw up disclaimer I suppose:
I'm merely presenting my understanding of these things for my buddies, and am not in anyway trying to diagnose, treat or cure a disease. Please consult your own physician if you have questions, and if you have an erection lasting more than 6 hours go to the ER, and pray lol
Off the top of my head, sometimes merely reducing blood flow to an area that is inflamed will result in an anti inflammatory effect.
Simple example, those with arthritis or tendonitis, the area swells, fluid collects, which essentially represents dilated blood vessels which facilitate transport of various signaling molecules, the net effect of which is pain, heat, sensitivity, itching, burning, etc. Inflammation = rubor (redness/increased blood flow) dolor (pain) and calor (heat).
As such, cold packs, ice, etc, in a very real sense have an anti inflammatory effect in these situations, because they cause vasoconstriction, cooling, and blunting of pain signals. Ibuprofen essentially does the same, though through biochemical signaling.
EDIT: And hence nicotine via its vasoconstrictive properties may effect this in part
Now if nerve pain has a componenent of 'ordinary' inflammation as above, than a vasoconstrictor could indirectly relieve some symptoms, so perhaps nic could give some kind of relief in this scenario
But Neuropathic pain all in all is a bit of a different animal and our understanding of it, and ability to treat it, is limited. Roughly speaking, chronic damage of any sort will eventually lead to a scenario where the nervous system, or the are of nervous system in question, is constantly 'seeing' pain, often out of proportion to what is happening (see "peripheral sensitization or central sensitization" for more info). What basically happens is there is a 'wind up' over time, and the nerves in question are now over sensitive to traffic, and they say ouch when they shouldn't
This is one of the reasons that pain specialists believe pain should be stopped before it starts, or pre-empted, if possible, to prevent the neural remodeling and changes that will eventually lead to this situation. And of course in vivo, a bit of this situation, along with the picture above of swelling, redness, pain, etc, all can co exist to varying degrees and feed each other
An example: There is a condition called "post herpetic neuralgia," where after a flare up of a herpes virus (often unbeknownst to the patient) the patient can be left with explosive pain every time their cheek, for example, is so much as stroked gently.
How does the body modulate pain, including neurologic pain?
There are areas of the brain that fire off 'pain modulatory signals' down into the spinal cord and what not. Noradrenaline, dopamine and serotonin are known to play a role, as are the opioid receptors (morphine anyone?). In fact these pathways cross and interact in many ways.
In a nut shell, the neurotransmitters in question have multiple points of contact where they can essentially 'talk' to a pain pathway and tell it to calm down, shielding the subjective awareness of said pain from the patient. The example I love to use is, think of a lunatic all jacked up on the illegal white powder drug that is insufflated typically. Why do you they feel so little pain? Because they're firing off Noradrenaline, dopamine etc at supra-physiologic levels. The pain is "still there" and the signal is traveling back from the bullet he just took to the gut, but it hits the spinal cord and gets a big
from the neurotransmitter brigade that's been released due to the drug. They roll out from the brain and say "sorry man, you're not invited."
EDIT: BTW this is why serotonin/noradrenaline re uptake inhibitors (cymbalta/effexor), dopamine/noradrenaline re uptake inhibitors (wellbutrin) and serotonin/noradrenaline/dopamine re uptake inhibitors (tricyclc antidepressants) work so wel for some patient with chronic neuropathic pain. There is a new class of drugs being developed called "triple re uptake inhibitors" based off of the ....... chemical skeleton, ....... being a prototypical triple re uptake inhibitor itself.
wow, that word was censored. insert benzoylmethylecgonine
Note also that wellbutrin is chemically similar to amphetamine, really nothing but a substituted amphetamine, and also a triple re uptake inhibitor in essence
Now directly with respect to nicotine
There is something called the cholinergic anti inflammatory pathway
cholinergic means 'mediated by acetylcholine. Acetylcholine is a neurotransmitter that can act on any cholinergic neuron, by definition. There different types of cholinergic receptors, but the one we're interested in is the
nicotinic-cholinergic receptor
our friend nicotine can act upon, and activate, the nicotinic cholinergic receptor. Hence its a nicotinic-cholinergic
agonist. (Agonist = goes to a receptor and activates it)
There are again areas of the brain from which efflux nicotinic-cholinergic signals that effectively suppress inflammation: levels of TNF Alpha notably, and various signaling molecules (cytokines) are inhibited from being released. Roughly, acetylcholine/nicotine can jump on the receptor of the white blood cell in question (the macrophage) and tell it to stop spraying napalm all over the place.
Acetylcholine/nic can also reduce the 'wind up' and 'hypersensitivity' I touched on above in the context of neuropathic pain proper. That mechanism I'm fuzzy on.
So all in all I wouldn't be shocked to discover that you're getting relief for a neuropathic condition via nic. Using nic and nic analogues to modulate such pathways is a bit of a hot topic right now, check out google scholar, loads of great papers most new. Seems like you're getting some mix of a general anti inflammatory effect and a specifically neuropathic analgesia. And not surprised that vaping worked better for you than smoking, because nicotine is not primarily pro inflammatory, but smoke is.
I'm going to keep reading up on this, I find pharmacology fascinating. Sorry if there was too much gobley ...., i'll clean it up if need me just ask.
