Posted by JohnX2 on October 26, 2001, at 0:50:45
In reply to Re: medication poop-out questionaire, posted by JGalt on October 25, 2001, at 9:57:04
Interesting stuff.He is my advice about dxm, *DO NOT* take it
with any MAOI inhibitor. Also taking things
like yohimbine with an MAOI inhibotor is bad.
Also yohimbine will substantially potentiate
dxm because it interferes with its metabolism.I speak from experience. I was experiencing
a caugh while taking
a weird combo of remeron,manerix,selegiline,
reboxetine and klonopin. I took a swig of
robitussin as it helps to relieve the caugh,
and my heart felt like it was about to
stop beating. Scary .hit.I did find an unconventional approach to
using dxm as a therapeutic agent described
by a neurologist in a patent disclosure(s). The
idea was to co-prescribe dxm with a medicine
that inhibits its breakdown. This substantially
increases the 1/2 life (the time for the body
to break it down), and made it easier to use
as a therapeutic agent for things he was treating,
tinnitus, peripheral neuropathy, withdrawal fom
addictive drugs.check out www.uspto.gov
look up patents 5,863,927
also 6,207,674.I'm not sure why he has patented this. Would
one need to send him a royalty if they used it? ;)He suggests quinidine (a heart med) as the adjunct
to inhibit the liver enzyme, but Prozac would work
too (do a search on Medline for fluoxetine and
dextromethorphan and you will get a hit on the
drug interactions). dextromethorphan is often used
to test wheather or not another drug inhibits
cyp450-2d6. When this happens the ratio of
dxm:dextrophan (the metabolite) goes up substantaily.-john
> 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:JohnX2
thread:81909
URL: http://www.dr-bob.org/babble/20011025/msgs/82322.html