![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 14 of 14. This is the beginning of the thread.
Posted by JohnX on October 21, 2001, at 16:32:01
A few people on this newsgroup including myself
and SLS have posted issues with getting medication
responses that quickly "poop out".I was wondering if I could put a feeler out for
those who have had this issue. I would be interested
in knowing on what meds this happened and how it
occured, and in particular if this has been an issue
with quick acting meds like Adderall, Dexedrine,
Provigil, and Cylert.Thanks,
John
Posted by Hattree on October 21, 2001, at 18:11:46
In reply to medication poop-out questionaire, posted by JohnX on October 21, 2001, at 16:32:01
The stimulants all poop out on me after a few days at a stretch (if poop out can be described as increased anxiety, depression and exhaustion). I took them at intervals to get myself out of particularly bad spots. However, along with Lamictal I seem to be able to tolerate dexedrine consistently.
>
> A few people on this newsgroup including myself
> and SLS have posted issues with getting medication
> responses that quickly "poop out".
>
> I was wondering if I could put a feeler out for
> those who have had this issue. I would be interested
> in knowing on what meds this happened and how it
> occured, and in particular if this has been an issue
> with quick acting meds like Adderall, Dexedrine,
> Provigil, and Cylert.
>
> Thanks,
> John
Posted by Cindylou on October 21, 2001, at 22:15:52
In reply to medication poop-out questionaire, posted by JohnX on October 21, 2001, at 16:32:01
Hi John,
I am the Queen of Medication Poop-Out.The stimulants Adderall, Ritilin and Provigil all poop out on me after a few days (same as Hattree), to the point where I feel 10 times worse than when I started. (I'll feel really good for those few days, and then WHAM. I'm down.)
Prozac poops out on me after two months. I have tried it 3 times -- I keep thinking it won't happen this time! But it always does.
Wellbutrin seems to help a bit for a week or so, then after that it just kind of supports me a bit -- I don't "crash" on it like the other stimulants. So it kind of "fizzles out" rather than poops out.
I guess that's about it really. I'm currently trying Lamictal + Wellbutrin, but I just started so I don't have feedback on that yet.
I've been on Zoloft and Effexor in the past -- they didn't poop out on me, did help my mood, but I couldn't tolerate the fatigue.
Good luck with your survey -- I am also interested in the responses.cindy
>
> A few people on this newsgroup including myself
> and SLS have posted issues with getting medication
> responses that quickly "poop out".
>
> I was wondering if I could put a feeler out for
> those who have had this issue. I would be interested
> in knowing on what meds this happened and how it
> occured, and in particular if this has been an issue
> with quick acting meds like Adderall, Dexedrine,
> Provigil, and Cylert.
>
> Thanks,
> John
Posted by susan C on October 22, 2001, at 14:54:51
In reply to medication poop-out questionaire, posted by JohnX on October 21, 2001, at 16:32:01
>Well, do you mean, poop out as in elimination or "poop out" as in the medical term (I have heard it is an actual definition)of where a med works for an extended period of time, then stops being effective for no apparent reason.
This happend to me with Prozac after 5 years or so.
Since then, other than a slight improvement with Depakote, no other meds have made it past the one month mark due to side effects, no effects. I have stayed with Depakote out of desperation, tolerating some side effects, which for the most part are small and have tried new AC Keppra with hope over hope that maybe it would work in conjunction with Depakote. But it too is going into the trash bin.
There is also the challenge of things just changing ANYWAY.
mouse in the dark
susan C
Posted by MB on October 22, 2001, at 16:53:41
In reply to medication poop-out questionaire, posted by JohnX on October 21, 2001, at 16:32:01
OK, first off, let me say that all the SSRIs (except Prozac) made me feel 75% better within a few hours. Paxil actually made me feel on top of the world after a single dose. Then, after a period of a few days, the "up" feeling goes away, and I just feel sick: irritable, sweaty, can't sleep very well (toss and turn), restless legs, etc. This lasts about two months, and then the the side effects shift. At the 8 week mark, I become fatigued, tired *all the time*, can't wake up in the morning, can't quit eating sweets, and the weight starts piling on. I have to say that the great mood induced by the first dose NEVER returns. So, contrary to what the literature predicts, I don't feel maximum relief after 8 weeks. I feel maximum relief for the first few days; then anxious, irritable hell for eight weeks; and then I become a zombie with no emotions or motivation or anything. It's totally weird since most people get poop-out after years (or months).
Has anybody else noticed that when they withdraw from an antidepressant and then start up again it's like a totally different drug (e.g., different side effects or more/less tolerable)? Now, when I try an SSRI, I go straight to the anxiety/rage/irritible stage. Is this a kindling thing? I mean, can lots of starts and stops kindle a latent bipolar issue?
> A few people on this newsgroup including myself
> and SLS have posted issues with getting medication
> responses that quickly "poop out".
>
> I was wondering if I could put a feeler out for
> those who have had this issue. I would be interested
> in knowing on what meds this happened and how it
> occured, and in particular if this has been an issue
> with quick acting meds like Adderall, Dexedrine,
> Provigil, and Cylert.
>
> Thanks,
> John
Posted by susan C on October 22, 2001, at 17:40:30
In reply to Re: medication poop-out questionaire » JohnX, posted by MB on October 22, 2001, at 16:53:41
kindling, that is what 'they' say happened to me...prozac, ssri s kindled the latent bipolar issue ...I am becoming phobic about meds...
trembling mouse...
susan C> OK, first off, let me say that all the SSRIs (except Prozac) made me feel 75% better within a few hours. Paxil actually made me feel on top of the world after a single dose. Then, after a period of a few days, the "up" feeling goes away, and I just feel sick: irritable, sweaty, can't sleep very well (toss and turn), restless legs, etc. This lasts about two months, and then the the side effects shift. At the 8 week mark, I become fatigued, tired *all the time*, can't wake up in the morning, can't quit eating sweets, and the weight starts piling on. I have to say that the great mood induced by the first dose NEVER returns. So, contrary to what the literature predicts, I don't feel maximum relief after 8 weeks. I feel maximum relief for the first few days; then anxious, irritable hell for eight weeks; and then I become a zombie with no emotions or motivation or anything. It's totally weird since most people get poop-out after years (or months).
>
>
> Has anybody else noticed that when they withdraw from an antidepressant and then start up again it's like a totally different drug (e.g., different side effects or more/less tolerable)? Now, when I try an SSRI, I go straight to the anxiety/rage/irritible stage. Is this a kindling thing? I mean, can lots of starts and stops kindle a latent bipolar issue?
>
>
> > A few people on this newsgroup including myself
> > and SLS have posted issues with getting medication
> > responses that quickly "poop out".
> >
> > I was wondering if I could put a feeler out for
> > those who have had this issue. I would be interested
> > in knowing on what meds this happened and how it
> > occured, and in particular if this has been an issue
> > with quick acting meds like Adderall, Dexedrine,
> > Provigil, and Cylert.
> >
> > Thanks,
> > John
Posted by JohnX on October 22, 2001, at 23:52:39
In reply to Re: medication poop-out questionaire, posted by Hattree on October 21, 2001, at 18:11:46
Its interesting that the Lamictal helps to tolerate
dexedrine. There is mounting evidence that glutamate
stimulated NMDA receptors (which lamictal would
modulate) are important to sensitization to these
types of meds. I have also found that Lamictal helps
with poop-out as well as Klonopin.I'm wondering about the marketability of new meds
in the pipeline like memantine (an NMDA receptor
antagonist) which has potentially unique properties to
prevent medication tolerance build up. There are
a number of companies chasing this route, but
memantine will likely be first out the door.
The people marketing the meds are actually going
for approval for Alzheimers,peripheral neuropathy,
and glaucoma, but physicians can prescribe it
for whatever as long is it is FDA approved.
Provigil for example, a narcolepsy med,
actually gets 80% of its scripts for
things other than narcolepsy.I see many uses in psychiatry for these new
class of meds (nmda antagonists). AndrewB posted
success with memantine to prevent Adderall tolerance.
Interestingly these meds, nmda-antagonists, are
also neuroprotective and would help keep the
other meds from frying neurons. It seems too good
to be true to have a med that is neuroprotective that
also prevents tolerance issues on other meds.Thanks for all the input.
I would also like to know if anyone has found
meds like Lamictal or others help with tolerance.-John
> The stimulants all poop out on me after a few days at a stretch (if poop out can be described as increased anxiety, depression and exhaustion). I took them at intervals to get myself out of particularly bad spots. However, along with Lamictal I seem to be able to tolerate dexedrine consistently.
>
> >
> > A few people on this newsgroup including myself
> > and SLS have posted issues with getting medication
> > responses that quickly "poop out".
> >
> > I was wondering if I could put a feeler out for
> > those who have had this issue. I would be interested
> > in knowing on what meds this happened and how it
> > occured, and in particular if this has been an issue
> > with quick acting meds like Adderall, Dexedrine,
> > Provigil, and Cylert.
> >
> > Thanks,
> > John
Posted by JGalt on October 24, 2001, at 11:34:34
In reply to Re: medication poop-out questionaire, posted by JohnX on October 22, 2001, at 23:52:39
John, very interesting on the Lamictal, hadn't heard of that before. Yes it does sound almost too good to be true, but once in a while we get something like that.
This would obviously be a miracle for many people both depressed and not if 1. You don't eventually develop a tolerance to Lamictal and 2. The NMDA receptors don't eventually peter out. I wonder what higher doses of Lamictal could accomplish, perhaps even less tolerance to the stimulants to a certain point.
This is actually a trick many bodybuilders+ powerlifters take advantage of, perhaps it would also be of some use here. Tolerance to 25mg of ephedrine (an alpha-2 agonist I believe) is generally acheived in a week or less. So when you don't get anything from it anymore, you drop it and use yohimbine (an alpha-2 antagonist) till it drops off, then you repeat the cycle. Also use DLPA everyday to replenish the norepinephrine you're undoubtalby depleting. Logically you can take all of them at once too, just small dosage. This would prevent the dreaded effect of ephedrine (impotence in people with already low sex drives, in fact, yohimbine is considered an aphrodisiac by some) I've been wanting to try the above combo to reduce sleepiness for a while, but haven't gotten bothered getting ahold of any yohimbine yet. Ephedrine is really quite pleasant when you don't have a tolerance, like a weaker adderal (though adderal has that energizing dopamine release), provided you don't have a preexisting heart condition. I guess I'd still opt for the adderal though personally for depression, though ephedrine also has the nice side effect of eliminating many symptoms of the common cold. This will give me another idea on something to ask my doc to try out if he's unwilling on the selegiline since I have absolutely no problem with adderal provided it doesn't have a tolerance.
Well I'll be interested in hearing about it once more people are using Lamictal and we get some idea of what degree it defeats the criteria I set above for it being a perfect drug combo.
They just put my mom on the Lamictal. She responds very poorly to stimulants (she's on the 12hr-Ritalin one right now, but I noticed nothing even when she 1st started, maybe its because they always have her on so many sedative drugs) so maybe they did it to reduce tolerance to the clonozepam (if they even know about this tolerance reducing effect, they didn't reduce her dosages of either drug). Well we'll see if she or I notice any difference in her otherwise lethargic and worn down behavior/mood.
Posted by JohnX on October 24, 2001, at 22:49:05
In reply to Re: medication poop-out questionaire » JohnX, posted by JGalt on October 24, 2001, at 11:34:34
A much more interesting line of meds are
nmda-antagonists. This would include pcp,ketamine,
mk-801, dextromethorphan,and memantine. These meds
directly antagonize stimulation of nmda receptors
as opposed to clamping down on the voltage threshold
required to activate the neuron (as lamictal does).Unfortunately the more "competitive" nmda antagonists
like mk-801,ketamine,pcp can cause hallucinagenic
side effects at high doses and brain damage.
There was originally hope that the research med mk-801
could be used as an epilepsy anti-convulsant/and or
neuroprotective agent, but the clinical trials were abrupty halted
with no explanation. Later a Dr. Olney discovered
that in certain areas of the brain glumate (primarily
a stimulatory chemical) actually stimulates GABA
neurons (inhibitory) via NMDA receptors. These areas
of the brain would become potentially damaged due to
lack of indirect excitation of GABA receptors leading
to something called "Olney's Lesion" in the brain.
Since then researches have tried to develop meds
that are "non-competitive" nmda antagonists. They
primarily antagonize glutamate release only during
pathological activation, and allow normal glutamate
flow during regular activation. Memantine, a medication
prescribed in Germany for about a decade, is being
studied for clinical trials in the US. Primarily
they are going for therapeutic treatment of
neurodegenerative diseases like Alzheimers, glaucoma,
and peripheral neuropathy, but the med could also
treat muscle spasticity, development of tolerance,
parkinson's and possibly other disorders.If you are interested in learning more, you can
review a website www.memantine.com and also do
searches on medline at :http://psychiatry.medscape.com/Home/Topics/psychiatry/directories/dir-PSY.JournalRoom.html
BTW, my interest is not in having a medication to
help people cosmetically, but rather help people in
serious need of adjuctive medication to help prevent
"poop-out" of psychiatric meds (where ADD meds
like dextroamphetamine would fit in).Thanks for your interesting "real world" information.
-john
> John, very interesting on the Lamictal, hadn't heard of that before. Yes it does sound almost too good to be true, but once in a while we get something like that.
>
> This would obviously be a miracle for many people both depressed and not if 1. You don't eventually develop a tolerance to Lamictal and 2. The NMDA receptors don't eventually peter out. I wonder what higher doses of Lamictal could accomplish, perhaps even less tolerance to the stimulants to a certain point.
>
> This is actually a trick many bodybuilders+ powerlifters take advantage of, perhaps it would also be of some use here. Tolerance to 25mg of ephedrine (an alpha-2 agonist I believe) is generally acheived in a week or less. So when you don't get anything from it anymore, you drop it and use yohimbine (an alpha-2 antagonist) till it drops off, then you repeat the cycle. Also use DLPA everyday to replenish the norepinephrine you're undoubtalby depleting. Logically you can take all of them at once too, just small dosage. This would prevent the dreaded effect of ephedrine (impotence in people with already low sex drives, in fact, yohimbine is considered an aphrodisiac by some) I've been wanting to try the above combo to reduce sleepiness for a while, but haven't gotten bothered getting ahold of any yohimbine yet. Ephedrine is really quite pleasant when you don't have a tolerance, like a weaker adderal (though adderal has that energizing dopamine release), provided you don't have a preexisting heart condition. I guess I'd still opt for the adderal though personally for depression, though ephedrine also has the nice side effect of eliminating many symptoms of the common cold. This will give me another idea on something to ask my doc to try out if he's unwilling on the selegiline since I have absolutely no problem with adderal provided it doesn't have a tolerance.
>
> Well I'll be interested in hearing about it once more people are using Lamictal and we get some idea of what degree it defeats the criteria I set above for it being a perfect drug combo.
>
> They just put my mom on the Lamictal. She responds very poorly to stimulants (she's on the 12hr-Ritalin one right now, but I noticed nothing even when she 1st started, maybe its because they always have her on so many sedative drugs) so maybe they did it to reduce tolerance to the clonozepam (if they even know about this tolerance reducing effect, they didn't reduce her dosages of either drug). Well we'll see if she or I notice any difference in her otherwise lethargic and worn down behavior/mood.
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
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
Posted by JohnX2 on October 26, 2001, at 0:59:38
In reply to Re: medication poop-out questionaire » JGalt, posted by JohnX2 on October 26, 2001, at 0:50:45
From medline, beware of drug interactions.
Effect of venlafaxine versus fluoxetine on metabolism of dextromethorphan, a CYP2D6 probe.
J Clin Pharmacol 2001 Apr;41(4):443-51 (ISSN: 0091-2700)Amchin J; Ereshefsky L; Zarycranski W; Taylor K; Albano D; Klockowski PM [Find other articles with these Authors]
Wyeth-Ayerst Laboratories, 240 North Radnor-Chester Road, St. Davids, PA 19087, USA.Two antidepressants, venlafaxine and fluoxetine, were evaluated in vivo for their effect on cytochrome P450 2D6 (CYP2D6) activity, measured by the ratio of
dextromethorphan, a sensitive CYP2D6 marker, to its metabolite dextrorphan (i.e., DM:DT) excreted in urine after DM coadministration. Twenty-eight healthy extensive
metabolizers of CYP2D6 received either venlafaxine (37.5 mg bid for 7 days, then 75 mg bid until Day 28) or fluoxetine (20 mg daily for 28 days); 26 completed the study.
Plasma concentrations of both drugs and their active metabolites were determined. DM:DTs were evaluated at baseline (Day 0), on Days 7 and 28 of dosing, and 2 weeks after
drug discontinuation (Day 42). Steady-state drug and metabolite levels were achieved in both groups by Day 28. Mean DM:DTs for venlafaxine and fluoxetine differed statistically
significantly (p < 0.001) on Days 7, 28, and 42. Comparisons of DM:DT as a percentage of baseline values showed that DM:DT increased 1.2-fold for venlafaxine and 9.1-fold for
fluoxetine on Day 7 (p < 0.001) and increased 2.1-fold for venlafaxine and 17.1-fold for fluoxetine on Day 28 (p < 0.001). Inhibition of CYP2D6 metabolism persisted for 2
weeks after discontinuation of fluoxetine, unlike the case with venlafaxine. These in vivo results confirm in vitro data demonstrating significantly weaker inhibition of CYP2D6 with
venlafaxine than with fluoxetine. This suggests that clinically significant interactions involving CYP2D6 inhibition could occur between fluoxetine and drugs metabolized by
CYP2D6 but may be less likely to occur with venlafaxine.
>
> 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
Posted by JGalt on October 26, 2001, at 10:51:12
In reply to Re: medication poop-out questionaire » JGalt, posted by JohnX2 on October 26, 2001, at 0:50:45
Very interesting on the dxm, that could take care of that problem if one were to try to use the approach I mentioned of using a long lasting form of ghb. BTW, I wouldn't even want to try dxm w/ an MAOi, if I said that in my post I certainly would never try it. I can picture myself getting out the selegiline, and the dxm, and then a big red warning light going off in my brain. Yohimbe, the bark, I won't use myself. I have some here, thought it would help with ephedrine induced impotence. Even at a normal dosage, the stuff makes my heart rate go through the roof and I start feeling sweaty and anxious. Half normal dosages still have roughly the same effect. Yohimbine is supposed to be better in this regard, but still should not be thrown in with an MAOi inhibitor of course. Actually yohimbine is supposedly a weak MAOi inhibitor (at the dosages your heart can handle the stimulant effects from) from what I've read. Perhaps that is also a reason it should not be combined w/ DXM.
Anyway, thanks for the info. One sure way to get the doc to think I'm a neurotic...suggest a combo of:
Adderal+DXM+longer lasting GHB+low dose Klonopin+Prozac
on my 1st visit.
Posted by Joey on October 29, 2001, at 19:45:28
In reply to medication poop-out questionaire, posted by JohnX on October 21, 2001, at 16:32:01
> After just being diagnosed with ADD, I was taken off of Effexor two weeks ago. I tried Wellbutrin for two days and just felt like I was going to die. So now I've been taking 20 mg of Adderall (10mg doses twice a day), and my poop-out periods are quite literal: just a bit down and tired. I want to try Ritalin SR, Dexidrine, or something else that lasts longer, but my doctor is being silly about giving me stimulants period because she's really not a psychatrist. I meet my new one in a month, and I hope he does give me something that lasts longer because I don't really know what to do sometimes when the Adderall wears off. Should I take more? Should I sneak in some leftover antidepressants (this does NOT help), or do I just do something that doesn't require a lot of attention? The latter seems to be the best solution. But I want something that lasts longer--definitely. That's my story, JohnX.
> A few people on this newsgroup including myself
> and SLS have posted issues with getting medication
> responses that quickly "poop out".
>
> I was wondering if I could put a feeler out for
> those who have had this issue. I would be interested
> in knowing on what meds this happened and how it
> occured, and in particular if this has been an issue
> with quick acting meds like Adderall, Dexedrine,
> Provigil, and Cylert.
>
> Thanks,
> John
This is the end of the thread.
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