2 replies to this topic

[j03]

For some reason my jaw tension/bruxism, gastric reflux, and migraines are cured on Nortriptyline and Mirtazapine.

I tried every drug and supplement therapy for GERD and was going to even have surgery before I realized the only time I didn't have reflux in the last 10 years was on these two drugs.

I am also taking Adderal, which is working amazingly for my ADD, so I don't want to stop it.

Remeron makes me way too fatigued, to the point I cannot function the next day regardless of dose.

Nortrptyline induces a sort of dyslexia in combination with stimulants (too much norepinephrine probably) and obliterates my short-term memory.


They both effect the H1, a1-adrenergic, mACh, receptors. So, what receptor is probably involved in ameliorating the jaw tension/GERD?

If I had to take one of the above, it would be Nortipyline, as it's side-effect profile is more tolerable than the extreme fatigue of Mirtazepine, but I'm wondering if there's something else out there, probably of the tricyclic class, that would have more synergy with Adderal?

[Tubemode]

The agonism of adrenergic receptors can ameliorate the release of gastric acid. This is one of the main reasons why digestion comes to a halt during a sympathomimetic (fight or flight) crisis.

Everything seems to point towards acetylcholine though. The said neurotransmitter is often associated with bruxism and intestinal discomfort. With this in mind, I do think Nortriptyline is responsible, largely because it is anticholinergic.

Might want to look into Wellbutrin.

The agonism of adrenergic receptors can ameliorate the release of gastric acid. This is one of the main reasons why digestion comes to a halt during a sympathomimetic (fight or flight) crisis.

Everything seems to point towards acetylcholine though. The said neurotransmitter is often associated with bruxism and intestinal discomfort. With this in mind, I do think Nortriptyline is responsible, largely because it is anticholinergic.

Might want to look into Wellbutrin.

[jadamgo]

Mirtazapine's biggest problem is its collosal half-life, which causes you to remain sedated into the next day. This problem goes away at the higher doses, upwards of 30mg, as alpha-2 antagonism begins overpowering the 5HT2 and H1 antagonism. (Speaking of histamine antagonism, it's possible that mirtazapine antagonizes the H2 receptor, which would make it work like common OTC acid reducers.)

If you tried those higher doses, you'd have to take them in the morning instead of at night because it would be waking you up instead of sedating you. Hopefully, you wouldn't just end up in a combined sedative/stimulant fog -- some people do, some people don't. It's impossible to predict.