Posted by JGalt on October 25, 2001, at 9:57:04
In reply to Re: medication poop-out questionaire » JGalt, posted by JohnX on October 24, 2001, at 22:49:05
Well I went and typed out a big long response to this, then had to confirm my registration to post, and wouldn't you know, AOL decides to quit on me during the registration. Argghh...thankfully I got something to calm me down.
Anyway, my mom is on Lamictal and klonopin, but not the 12-hr ritalin. She is only on the startup dose (25mg eod) but says she does notice significantly more energy throughout the day. The doctor apparantly knows nothing about its NMDA properties, simply put her on it to replace topamax which was causing some ridiculous weight loss. I told her to lobby for some adderal (she's tired all the time, rather unmotivated, similiar to my own symptoms, only more severe and she doesn't care too much about the lack of energy).
About the DXM and likewise drugs. Turns out that those Onley lesions aren't really all that bad even at the dissociative doses (well, the level 3 and 4 stages is where they seem to show up the most). Anyway, my theory is, what if these NMDA antagonists would work at non-dissociative doses. I'm thinking somewhere around 50mg of DXM, since acc. to the FAQ, 100mg seems to be the threshold dose. At this dosage, brain damage should be so small as to be inconsequential I would imagine. If you really wanted to go all out on preventing brain damage, it would seem logical that you could take something that would occupy the GABA receptors prior to taking the DXM, thus preventing the cause of the Onley's lesions, assumably selective production? of only glutamate. I believe GHB is capable of this, or perhaps 1,4 butanediol, which would be more time released (still every 4-6 hrs or so, this could present a problem if DXM completely inhibits other things from binding to the GABA). Actually there is a patent out for a GHB derivative that lasts 8-12 hrs, I could see someone making some money off that if they wanted to pursue this. That is of course, if the method of action of GHB is how I remember it (GABA agonist amongst other things)...but I'm not sure, I only remember the doc who discovered it was looking for a way to make GABA cross the blood brain barrier.
So lamictal increases NDMA receptor sensitivity. Interesting. In some ways that may be better than DXM since it might be possible, through extended use of DXM, to decrease receptor sensitivity. I don't know. For one, I would be very interested in a drug that could increase dopamine and perhaps norepinephrine sensitivity. Perhaps this is what tricyclics are supposed to do, I don't know, I never studied them too much due to their supposed dumbing down effects. In any case, I'm sure something more effective could be found for them. Combining something like that with selegiline and lamictal and low dose adderal would seem like it would be the ultimate antidepressant in theory.
Of course, then again, maybe it will happen with extended use that glutamate will 1. become depleted in the brain or 2. have its receptors decreased in number or sensitivity. If that is the case, our body's chemistry is really against us, and our only hope for indefinite long term freedom from depression/melancholy, etc. will be the genetic engineering as described in the Hedonistic Imperitive.
Best Regards,
John Galt
poster:JGalt
thread:81909
URL: http://www.dr-bob.org/babble/20011025/msgs/82267.html