![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 21 to 45 of 45. Go back in thread:
Posted by judy1 on October 27, 2001, at 22:50:33
In reply to Re: Post Traumatic Stress Disorder and etc. » JGalt, posted by JohnX2 on October 27, 2001, at 15:41:06
Just curious- have you been prescribed klonopin? A really decent drug for bp and ptsd too. I am dxed bp1, ddNOS, ptsd (panic) and others almost daily All ad's make me manic, with wellbutrin causing convulsions (I do have a history of bulemia). Re: pdocs- this is my 16th and best, prefers therapy over the 6+ drugs I was on and is willing to treat manic episodes until they resolve with no hospitalization (for that alone I love him). Unfortunately there are a lot of poor pdocs out there and I agree that there is an art to telling them your theories w/o being labeled 'difficult' or neurotic. Unless you're fortunate and find someone secure enough to listen (like I was) Sorry for the rambling, just found this an interesting thread- Judy
Posted by JohnX2 on October 28, 2001, at 0:59:34
In reply to Re: Post Traumatic Stress Disorder and etc. » JohnX2, posted by judy1 on October 27, 2001, at 22:50:33
Klonopin was the 1st med that stablized my condition,
got rid of all pain syndromes, etc. I have been taking
it for on/off almost 2 years and am definately addicted
at this stage. I need 6 mg to get a therapeutic effects.The following meds relieve my jaw tension/bruxism:
-serzone (probably from 5ht-2a antagonism)
-zyprexa (probably from 5ht-2a antagonism)
-adderall (when it works)
-klonopin (always)good klonopin guess on your behalf.
I stumbled onto klonopin by accident to treat
sleaping problems on effexor. Majically it got
rid of all my facial pain. My pdoc was an ideot.
He had a degree in neurology but couldn't understand
my jaw pain and response to meds.Thanks for your interest.
-john> Just curious- have you been prescribed klonopin? A really decent drug for bp and ptsd too. I am dxed bp1, ddNOS, ptsd (panic) and others almost daily All ad's make me manic, with wellbutrin causing convulsions (I do have a history of bulemia). Re: pdocs- this is my 16th and best, prefers therapy over the 6+ drugs I was on and is willing to treat manic episodes until they resolve with no hospitalization (for that alone I love him). Unfortunately there are a lot of poor pdocs out there and I agree that there is an art to telling them your theories w/o being labeled 'difficult' or neurotic. Unless you're fortunate and find someone secure enough to listen (like I was) Sorry for the rambling, just found this an interesting thread- Judy
Posted by JohnX2 on October 28, 2001, at 1:15:56
In reply to Re: Post Traumatic Stress Disorder and etc., posted by JGalt on October 27, 2001, at 21:59:18
> I looked up the DSM-IV for PSTD, clearly is not me. I cannot think of a single event that was extremely traumatic at a young age. I had tons of mild to moderate things, but nothing in particular burned into my memory. No flashbacks or nightmares from my childhood that I remember either. I never have had good long term memory. The DSM-IV stated in such a case the cause was likely simple depression. Still might be worth it to look at the crf antagonists just for curiousity's sake.
>
> The second you said jaw and headache problems, dopamine overload popped in my mind. Here's why. GHB greatly slows down (or perhaps stops) the release of dopamine in the brain. However, dopamine continues to be produced in the brain. After the GHB is metabolized, dopamine release resumes, but guess what, you got more dopamine there. No problem, just a pleasant stimulant effect. But never come all the way down from GHB and the dopamine keeps on building up and up to whatever limit there is. I know this because I've done it, twice. Logically what happens is then all that dopamine is released, you have less hunger, and more noticeably, painful headaches and jaw clamping. Too much dopamine. I'm guessing what is happening with you is you're having too much dopamine, then you take an AD such as wellbutrin, dopamine is released to the point that you have practically none left and you are left with the hypodopaminergic state. This would tend to suggest that you have 1. low dopamine storage capacity or 2. are very sensitive to dopamine agonists. Before you used the wellbutrin, the dopamine kept building up and up. Extreme excess of dopamine is hallmark of schizophrenia and mania. The interim period when taking the AD's that you feel relief is when dopamine is at a reasonable level of storage and being released at the same time, as happens in the theoretical normal person. Make sense or did I miss something? You know, now that I write this it occurs to me, why wasn't ghb ever used to treat bipolar syndrom? Since it prevents dopamine from being released, that gets rid of the mania as far as I understand it, and since during mania I don't believe your body stores more dopamine, it simply releases more. Just come down from it every 6 hours and all would be well, then use AD's while in the depressive state.
>Damn you are smart. It took me a long time to figure
this out. I found most of my interesting information
from an article called "buspirone as an antidote
to SSRI induced bruxism". Here it discussed 2 states
which could cause jaw tension, one is hypo-dompaminergic
and the other is hyper-dopaminergic. Since the
pain is gone with the depression and positive
(and or manic) responses, I have to be lead to
believe that the pain is caused by a hypodopaminergic
state. This also correlates so very well with my
thoughts on the concurrent severe emotional numbing,
and my responses to Serzone,Zyprexa,Adderall,Zoloft,
Wellbutrin. The article was specifically dealing
with SSRI induced bruxism and stated cases of Zoloft
causing this. I had this problem with zoloft quite
severly and zoloft seriously obliterated my emotions
to. I think its pinging of the 5ht-2a receptor causes
the problem. The drug buspar is a 5ht-1a partial
agonist and a slight d2 antagonist. The paper
cited cases where buspar cured the zoloft induced
bruxism and theorized that buspar reduced serotonin
levels, and the 5ht-1a agonism does the opposite
of 5ht-2a agonism (they somehow balance each other).
So anti-anxiety meds often try to antagonize
5ht-2a and or agonize 5ht-1a receptors. Most
SSRIS taken chronically will downregulate the
5ht-2a receptors. But they aren't always all that
efficient and this leads to sexual side effects,
emotinal numbing, muscle tension. The pharmaceutical
companies figured this out and scrambled to find
meds that could antagonize the 5ht-2a receptor.
The 1st new-age anti-depressant that did this
was Serzone and it was touted for its lack of
sexual side effects. But it is a dirty med and
screws with too many other receptors making people
like me crash my car. Anyways, the buspar paper
suggested serzone as another alternative to the
bruxism and it did work for me. But now I'm leaning
towards not beating around the bush and testing
one of these nmda antagonists (memantine). Since
Lamictal is working and zyprexa, it seems like
a logical choice. Sorry for the harangue. But
you come back with great insight. If AndrewB
was still posting to this group he would be having
a field day with you!.Ps. there is a cpc viewer for mac. I get patents
downloaded from a service called www.getthepatent.com.
the images are avaliable at the official us patent
site, put this service has a mirror copy of the full
patent images in this very compressed formats. The
web site has links to the CPC viewer.-john
Posted by judy1 on October 28, 2001, at 10:43:52
In reply to Re: Post Traumatic Stress Disorder and etc. » judy1, posted by JohnX2 on October 28, 2001, at 0:59:34
>
> Klonopin was the 1st med that stablized my condition,
> got rid of all pain syndromes, etc. I have been taking
> it for on/off almost 2 years and am definately addicted
> at this stage. I need 6 mg to get a therapeutic effects.John,
I also take 6mg/day of klonopin (2mg tid) for 4+ years and my pdoc and I certainly don't consider me 'addicted'. He has some patients that have taken more for over a decade. Are you tolerant? How long have you taken 6 mg? Klonopin was something of a miracle drug for me also; I just hope you don't get negative feedback from your pdoc about your dose. Take care- Judy
Posted by JGalt on October 28, 2001, at 15:01:23
In reply to Re: Post Traumatic Stress Disorder and etc. » JGalt, posted by JohnX2 on October 28, 2001, at 1:15:56
Interesting about the hypodopaminergic state also causing teeth grinding. Obviously while on GHB you go to a much lower than normal dopamine release rate, but I've never noticed the bruxism. Probably because at any dosage in which you feel the effects, the drug is also serving as a mild muscle relaxer, inhibits obsessive-compulsive behavior, and recurring thoughts/movements, all postulated to be through the GABA system. Thus it makes sense that teeth grinding would occur.
Interesting on the 5ht-xx drugs. I've never read deeply on the specific receptors, but from your brief explanation, I agree that an experiment wtih memantidine seems in order. Oh, and I'll warn anyone I know going on Serzone to increase car insurance.
By the way, what did you think about what I said with using GHB for mania? Obviously well under pass out doses, just enough to curtail dopamine release sufficiently for the patient to live normally. From what I understand, mania is almost completely dopamine driven, but I do not know for sure if the body is 1. also producing more dopamine or just releasing what it has and producing at a normal rate or 2. if the body has a definite reachable capacity for dopamine storage which isn't sky high beyond what a normal person is storing. If the body is producing and releasing an incredible amount more of dopamine during mania and if it has a very high amount of storage capacity, and the storage capacity does not greatly lower when they go back to normal or depressive, then my idea wouldn't work very well. Otherwise it would seem like it would, at worst the person might have to go through a simple dopamine reduction program, wherein they take an extra hour or two between doses of GHB, to let those high levels come back to normal, which shouldn't take too long. Of course, finding the right dosage here would be tricky, and the person would have to know how long their eposides generally last and/or allow themselves to come down competely once in a while, so that they aren't taking ghb during the depressive state, which might have the potential to produce another manic state (too much dopamine in storage, can that do it?). It'd just seem like it'd be nicer to the patient to exchange their wild euphoria for something better than having dead emotions as many of the antipsychotics seem to do, provided that not both of the aforementioned conditions were true.
By the way, found this interesting, maybe you've already read it:
Adaptation of N-methyl-D-aspartate (NMDA) receptors following antidepressant treatment: implications for the pharmacotherapy of depression
by
Skolnick P; Layer RT; Popik P; Nowak G; Paul IA; Trullas R
Laboratory of Neuroscience, NIDDK,
National Institutes of Health, Bethesda, USA.
Pharmacopsychiatry, 1996 Jan, 29:1, 23-6ABSTRACT
NMDA antagonists mimic the effects of clinically effective antidepressants in both preclinical tests predictive of antidepressant action and procedures designed to model aspects of depressive symptomatology. These findings led to experiments demonstrating that chronic administration of NMDA antagonists to rodents results in a downregulation of cortical beta-adrenoceptors, a phenomenon also observed following chronic treatment with many antidepressants. These neurochemical and behavioral similarities between antidepressants and NMDA antagonists prompted us to examine the impact of chronic antidepressant treatment on NMDA receptors. Chronic (14 days) but not acute (1 day) administration of seventeen different antidepressants to mice produced adaptive changes in radioligand binding to NMDA receptors. Detailed studies with three antidepressants (imipramine, citalopram, and electroconvulsive shock) show that these changes develop slowly, persist for some time after cessation of treatment, and (for imipramine and citalopram) are dose dependent. Moreover, following chronic treatment with imipramine, these changes in radioligand binding to NMDA receptors appear restricted to the cerebral cortex. Based on the consistency of these effects across antidepressant treatments, we propose that adaptive changes in NMDA receptors may be the final common pathway for antidepressant action. The recent demonstration (Nowak et al., 1995) that radioligand binding to NMDA receptors is altered in frontal cortex of suicide victims (compared to age and post-mortem interval matched controls) is consistent with the hypothesis (Trullas and Skolnick, 1990) that this family of ligand gated ion channels is involved in the pathophysiology of depression.
---------Of course, they find a lot of things low in suicide victims, but the interesting part is the other antidepressants role on NMDA receptor.
Anyway, I found the cpc viewer page, I'll download it later. I'll make up an email later today so that you can send them over.
Best Regards,
JGalt
Posted by JohnX2 on October 29, 2001, at 0:44:48
In reply to Re: Post Traumatic Stress Disorder and etc. » JohnX2, posted by judy1 on October 28, 2001, at 10:43:52
My pdoc is very open about my dosing, although
he tells me that he starts to get nervous around
6 mg. I have tapered up-down on klonopin from between
2-6 mg. 2mg is the minimum to alleviate my facial
pain. The point is that there are better alternatives
to treat my pain. I am not generally taking klonopin
for anxiety or panic attacks, just mainly the pain.
Other meds help with the anxiety.I haven't had a problem with any of my pdocs and klonopin.
I've tried to taper klonopin in the past with
little success, except while on Serzone, where
I almost stopped it cold turkey. The Serzone
alleviated the pain that I was having in my
face and the klonopin was just making me drowsy
on top of it. Zyprexa seems to be helping in a
similiar manner, so the pdoc would like for me
to slowly taper the klonopin if I feel drowsy.I did grow tolerant to klonopin about last year
Oct, ever since then the dose I take is the minimum
to cure most of my pain, but still leave me
a bit anxious.Thanks for your concern.
Sometimes I just say screw it and take a whopper
dose to have an enjoyable few days in my life.
Maybe that isn't helping things any.-john
> >
> > Klonopin was the 1st med that stablized my condition,
> > got rid of all pain syndromes, etc. I have been taking
> > it for on/off almost 2 years and am definately addicted
> > at this stage. I need 6 mg to get a therapeutic effects.
>
> John,
> I also take 6mg/day of klonopin (2mg tid) for 4+ years and my pdoc and I certainly don't consider me 'addicted'. He has some patients that have taken more for over a decade. Are you tolerant? How long have you taken 6 mg? Klonopin was something of a miracle drug for me also; I just hope you don't get negative feedback from your pdoc about your dose. Take care- Judy
Posted by JohnX2 on October 29, 2001, at 0:58:31
In reply to Re: Post Traumatic Stress Disorder and etc., posted by JGalt on October 28, 2001, at 15:01:23
I think I need to understand GHB's workings a bit
better to answer your questions.
From what little I remember about it is was easy to make using supplements
for weight lifting, and people starting taking it recreationally
and the government decided that people should have
this recreational fun, end of story....Usually mania is less thought to be related to dopamine
overproduction/overflow (which is more like a shizophrenic psychosis), and
more related to hyperactive electrical impulses.
Most of the anti-manic agents are indeed epilepsy
meds. They work by inhibiting Na+ and K+
and/or enhancing cl- release. The effect is
to impact the membrane voltage potential so that the
nerve cells fire in a more orderly fashion.
Some of the newer treatments for bipolar do
target dopamine postsynaptic receptors themselves
instead of the electrolytes, zyprexa being a good
example."I'll be back"
-John
> Interesting about the hypodopaminergic state also causing teeth grinding. Obviously while on GHB you go to a much lower than normal dopamine release rate, but I've never noticed the bruxism. Probably because at any dosage in which you feel the effects, the drug is also serving as a mild muscle relaxer, inhibits obsessive-compulsive behavior, and recurring thoughts/movements, all postulated to be through the GABA system. Thus it makes sense that teeth grinding would occur.
>
> Interesting on the 5ht-xx drugs. I've never read deeply on the specific receptors, but from your brief explanation, I agree that an experiment wtih memantidine seems in order. Oh, and I'll warn anyone I know going on Serzone to increase car insurance.
>
> By the way, what did you think about what I said with using GHB for mania? Obviously well under pass out doses, just enough to curtail dopamine release sufficiently for the patient to live normally. From what I understand, mania is almost completely dopamine driven, but I do not know for sure if the body is 1. also producing more dopamine or just releasing what it has and producing at a normal rate or 2. if the body has a definite reachable capacity for dopamine storage which isn't sky high beyond what a normal person is storing. If the body is producing and releasing an incredible amount more of dopamine during mania and if it has a very high amount of storage capacity, and the storage capacity does not greatly lower when they go back to normal or depressive, then my idea wouldn't work very well. Otherwise it would seem like it would, at worst the person might have to go through a simple dopamine reduction program, wherein they take an extra hour or two between doses of GHB, to let those high levels come back to normal, which shouldn't take too long. Of course, finding the right dosage here would be tricky, and the person would have to know how long their eposides generally last and/or allow themselves to come down competely once in a while, so that they aren't taking ghb during the depressive state, which might have the potential to produce another manic state (too much dopamine in storage, can that do it?). It'd just seem like it'd be nicer to the patient to exchange their wild euphoria for something better than having dead emotions as many of the antipsychotics seem to do, provided that not both of the aforementioned conditions were true.
>
> By the way, found this interesting, maybe you've already read it:
>
>
> Adaptation of N-methyl-D-aspartate (NMDA) receptors following antidepressant treatment: implications for the pharmacotherapy of depression
> by
> Skolnick P; Layer RT; Popik P; Nowak G; Paul IA; Trullas R
> Laboratory of Neuroscience, NIDDK,
> National Institutes of Health, Bethesda, USA.
> Pharmacopsychiatry, 1996 Jan, 29:1, 23-6
>
> ABSTRACT
>
> NMDA antagonists mimic the effects of clinically effective antidepressants in both preclinical tests predictive of antidepressant action and procedures designed to model aspects of depressive symptomatology. These findings led to experiments demonstrating that chronic administration of NMDA antagonists to rodents results in a downregulation of cortical beta-adrenoceptors, a phenomenon also observed following chronic treatment with many antidepressants. These neurochemical and behavioral similarities between antidepressants and NMDA antagonists prompted us to examine the impact of chronic antidepressant treatment on NMDA receptors. Chronic (14 days) but not acute (1 day) administration of seventeen different antidepressants to mice produced adaptive changes in radioligand binding to NMDA receptors. Detailed studies with three antidepressants (imipramine, citalopram, and electroconvulsive shock) show that these changes develop slowly, persist for some time after cessation of treatment, and (for imipramine and citalopram) are dose dependent. Moreover, following chronic treatment with imipramine, these changes in radioligand binding to NMDA receptors appear restricted to the cerebral cortex. Based on the consistency of these effects across antidepressant treatments, we propose that adaptive changes in NMDA receptors may be the final common pathway for antidepressant action. The recent demonstration (Nowak et al., 1995) that radioligand binding to NMDA receptors is altered in frontal cortex of suicide victims (compared to age and post-mortem interval matched controls) is consistent with the hypothesis (Trullas and Skolnick, 1990) that this family of ligand gated ion channels is involved in the pathophysiology of depression.
> ---------
>
> Of course, they find a lot of things low in suicide victims, but the interesting part is the other antidepressants role on NMDA receptor.
>
> Anyway, I found the cpc viewer page, I'll download it later. I'll make up an email later today so that you can send them over.
>
> Best Regards,
> JGalt
Posted by JGalt on October 29, 2001, at 2:09:42
In reply to Re: Post Traumatic Stress Disorder and etc. » JGalt, posted by JohnX2 on October 29, 2001, at 0:58:31
Well actually the stated reason it was banned was because some girls died off of it after some guys slipped it in their drinks and raped them. Never mind that alcohol is used to rape hundreds of women each year, no where near the level of the very isolated incidences of GHB rapes, and the fact that GHB is not harmful if used without other depressants (all the deaths occurred when it was combined with alcohol, rophyenol or other hard depressants, particular those involving the alchol reducing enzymes). The actual number of deaths was extremely low, but it was banned anyway. There is some speculation that the real reason is because it induces Stage 4 sleep (in pass out doses), which is very much needed in nacrolepsy, and it is a potent anti-suicidal and antidepressant amongst other things in non-passout doses. Of course, being a natural chemical present in small amounts even in food, it couldn't be patented. So, the feds made it illegal, and thus opened the way for the pharmaceutical companies to come in and make the drug at several hundred times profit under the brand name Xyrem. Its supposed to inhibit dopamine release but not production and storage, and cause said stored dopamine to be released upon coming down off the drug (thus causing a user to suddenly wake up 4 hrs after a dose if they take a knock out dose and their body didn't really want to be asleep). The bodybuilding aspect is due to the fact that it raises growth hormone levels (in response to the stored dopamine), however, it also raises prolactin levels, thus indirectly lowering testosterone and raising estrogen (very mildly) thus cancelling out any benefits from the growth hormone. It's also supposed to be an agonist to certain (unknown) parts of the GABA system. Its used in other countries as an antisuicidal, an antidepressant, an antianxiety, an antidysthymic, and to treat nacrolepsy by helping users reach the deeper but yet non-rem stages of sleep. I don't think you'll find too much more if you research it. LD-50 in humans is supposed to be about 300 grams. Anything over 4 grams is a knockout dose in almost everyone. Between 2-4 is the therapuetic range for the other disorders I mentioned. Pretty large safety factor in there. Roughly 36mg's I believe in an average sized steak. It was originally legal and sold well. Then it was made illegal, GBL became popular since it converts to GHB in the body, or you can convert it yourself with only NaCl. That was made illegal too, so 1,4 Butanediol is enjoying its day in the sun until more/all the states ban it. Then who knows where. Well enough about that. I don't have mania so I guess I don't get to test it.
I downloaded the cpc viewer and made up an email account. Email the file to JhnGalt@hotmail.com. Thanks a lot!
Best Regards,
JGalt
Posted by JGalt on October 29, 2001, at 23:26:27
In reply to Re: Post Traumatic Stress Disorder and etc., posted by JGalt on October 29, 2001, at 2:09:42
I started using modafinil today a little bit. I only got 4 hours of sleep last night (not because of insomnia) and too much noise to stay asleep around here so I thought that it would be an appropriate time to give it a test run on something it was designed for (keeping a tired person awake and alert but not wired). Woke up 8am. At 10am, after my usual 9am 200mg's caffeine and 50mg's ephedrine (doc said I could take it for my typically clogged up sinuses), 500mg's of N-Acetyl Tyrosine and B-vitamins I was still feeling like I could go back to bed any minute and didn't really feel like staying up (I typically sleep 10+hrs). Took 200mg's of modafinil and was feeling pleasantly awake, far from wired, but very functional until about 4 or so, so then I took another 100mg's and I'm still awake at 12, though I could go to sleep if I wanted too. Really quite a nice drug.
By the way, just to see if there was any difference, I took some of the legal ghb-like drug around 5pm (hour after 2nd low dose of modafinil). A normal dose hit me quite a lot harder than I expected as far as sedation goes, but didn't really change the pleasant antianxiety, friendliness feel of it (the sedation felt like the sedation that is present at higher, in love with life type doses, but without that feeling). The sedation was not very long lasting though, I believe the modafinil eventually dominated. If the believed pharmacology of both the drugs are correct, this kinda makes sense. It would be the sudden switch from modafinil induced glutamate dominance to ghb and sleep deprivation induced gaba dominance. The antianxiety effects of ghb are likely from a specific gaba receptor that modafinil wouldn't counteract. This stuff does seem to be wearing off a little bit though. Usually if I only got 4 hrs of sleep I'd have been napping all day so I gotta give it some good credit. I may go for selegiline+modafinil, that would seem quite appropriate for my condition, barring deciding to do the self research required to determine the correct dosage of DXM in that other motivational/in touch with life coctail that I discussed earlier in this thread. Insurance wouldn't cover either drugs very well but I only need a prescription to make it legal, so I can order overseas if I please then, and just keep the prescription here for legal purposes I would imagine. Wish I had enough to do an honest week long test run to see if I form a tolerance to it or check on actual rebound sleep with me but I can't...judging from the posts on this and other boards though, it seems like quite a useful drug as long as you aren't using things that are more sedative than it can counteract.
Posted by JohnX2 on October 30, 2001, at 23:39:43
In reply to Re: Modafinil test day, posted by JGalt on October 29, 2001, at 23:26:27
I'm saying **** it and *I am going* to be doing
a memantine trial. I'm putting together a proposal
for my pdoc, and he'll probably be blown away by
the amount of technical information that I include,
and he may be a little angry that I took some
meds on the sly, but the solution to my problem
is too clear, in my view. Anyways, he'll want me to
take lithhium otherwise, which I refuse to take. Memantine has
few side effects at least from what is reported here
and my case is compelling. I just wonder if Chris
(my pdoc) will freak out over insurance reasons.
He is old school and is incredulous over anything
that doesn't have the full clinical data to support
it.I tried adding wellbutrin again at a stronger
dose while taking otc rxxxxxxxn-dm when the
Wellbutrin caused tinnitus or any pain in my head.
This fairly quickly alleviates the pain and
I have gotton another breakout from dysthymia.
But the dm poops out rather fast because of
its half life, and my mood goes back to that
numb state. which I can duplicate by taking
a mother-load of coffee or modafinil. Modafinil
had a short lived anti-depressant effect (like
2 hours), and then it pooped out, gave me severe
headache and a little tinnitus. It was a dead
ringer for what happens if I drink a bunch of
coffee.If I can't do the memantine trial, then I might
just say the hell with it and try the prozac
enzyme inhibition trick with otc rxxxxxxn-dm.Good luck with your meds, keep us posted.
-john
> I started using modafinil today a little bit. I only got 4 hours of sleep last night (not because of insomnia) and too much noise to stay asleep around here so I thought that it would be an appropriate time to give it a test run on something it was designed for (keeping a tired person awake and alert but not wired). Woke up 8am. At 10am, after my usual 9am 200mg's caffeine and 50mg's ephedrine (doc said I could take it for my typically clogged up sinuses), 500mg's of N-Acetyl Tyrosine and B-vitamins I was still feeling like I could go back to bed any minute and didn't really feel like staying up (I typically sleep 10+hrs). Took 200mg's of modafinil and was feeling pleasantly awake, far from wired, but very functional until about 4 or so, so then I took another 100mg's and I'm still awake at 12, though I could go to sleep if I wanted too. Really quite a nice drug.
>
> By the way, just to see if there was any difference, I took some of the legal ghb-like drug around 5pm (hour after 2nd low dose of modafinil). A normal dose hit me quite a lot harder than I expected as far as sedation goes, but didn't really change the pleasant antianxiety, friendliness feel of it (the sedation felt like the sedation that is present at higher, in love with life type doses, but without that feeling). The sedation was not very long lasting though, I believe the modafinil eventually dominated. If the believed pharmacology of both the drugs are correct, this kinda makes sense. It would be the sudden switch from modafinil induced glutamate dominance to ghb and sleep deprivation induced gaba dominance. The antianxiety effects of ghb are likely from a specific gaba receptor that modafinil wouldn't counteract. This stuff does seem to be wearing off a little bit though. Usually if I only got 4 hrs of sleep I'd have been napping all day so I gotta give it some good credit. I may go for selegiline+modafinil, that would seem quite appropriate for my condition, barring deciding to do the self research required to determine the correct dosage of DXM in that other motivational/in touch with life coctail that I discussed earlier in this thread. Insurance wouldn't cover either drugs very well but I only need a prescription to make it legal, so I can order overseas if I please then, and just keep the prescription here for legal purposes I would imagine. Wish I had enough to do an honest week long test run to see if I form a tolerance to it or check on actual rebound sleep with me but I can't...judging from the posts on this and other boards though, it seems like quite a useful drug as long as you aren't using things that are more sedative than it can counteract.
Posted by JGalt on October 31, 2001, at 0:41:48
In reply to Re: Modafinil test day, posted by JohnX2 on October 30, 2001, at 23:39:43
Best of luck with the pdoc and memantine. I can certainly understand not wanting to take lithium (I never will either) from what I've read about it and seen it do to people. I did some more reading in the archives today about what you, andrewb, and several other members of this board said about the memantine and stimulant tolerance. Interesting stuff, it does seem like you're taking the right course of action here. If that and/or the prozac+r-dm doesn't work then its back to the lamictal I assume?
Also, don't you think that there's probably better/cheaper ways to get dxm w/o the cough syrup? I seem to remember seeing some 30mg dxm only pills someplace. Actually I've seen raw dxm powder advertised too but it was sold as a "non-consummable" (thus removing the company from any liability should you decide to consume it anyway). Honestly I probably would have tried a tiny amount (like 3mg) and then slowly edged my way up to the final dose...but it seems that that company is no longer able to legally sell it even with the non-consummable label. Bummer.
A final thought on the Modafinil. Perhaps you were taking too high of a dose? It would seem to be possible for too much glutamate to produce a headache and tinnitus. I have trouble believing that what you are getting is an effect usually seen at the right dosage for you. I was using it merely for fatigue, not antidepressant effects. I would think it would require a significantly higher dose to get antidepressant effects.
btw, I go to the pdoc tomorrow. We'll see how it works out. Not to hound you for them, but did you ever send those cpc files you mentioned? If you already have sent them, great! (that just means hotmail is slow)...if not, I still am interested in them if you have some time to send them over.
Best Regards,
JGalt
Posted by JohnX2 on October 31, 2001, at 2:38:02
In reply to Re: Modafinil test day JohnX2, posted by JGalt on October 31, 2001, at 0:41:48
Excuse me if this gets posted twice, my
prior attempt didn't show up.Check your email. I sent 2 docs on stimulant
sensitization, and 1 on bruxism. I also sent
a number of patents. 1 is for a nover
anti-depressant and I think you will find it very
"amusing".Regarding modafinil, I tried it at a low dose and
it worked for like a couple hrs then pooped out,
almost identical to coffee. I wonder what causes
the poop out. I get a huge headache and tinnitus.
The tinnitus is treatable with lamictal and nmda
antagonists (see the patent disclosures).Lamictal is difficult to get onto because of the possibilit
of a rash. It took me 1.5 months to get to 150mg
which was the thereapeutic dose to life Major Depression.
I won't drop it, but will continue to try augmenting
it.Regards,
john
> Best of luck with the pdoc and memantine. I can certainly understand not wanting to take lithium (I never will either) from what I've read about it and seen it do to people. I did some more reading in the archives today about what you, andrewb, and several other members of this board said about the memantine and stimulant tolerance. Interesting stuff, it does seem like you're taking the right course of action here. If that and/or the prozac+r-dm doesn't work then its back to the lamictal I assume?
>
> Also, don't you think that there's probably better/cheaper ways to get dxm w/o the cough syrup? I seem to remember seeing some 30mg dxm only pills someplace. Actually I've seen raw dxm powder advertised too but it was sold as a "non-consummable" (thus removing the company from any liability should you decide to consume it anyway). Honestly I probably would have tried a tiny amount (like 3mg) and then slowly edged my way up to the final dose...but it seems that that company is no longer able to legally sell it even with the non-consummable label. Bummer.
>
> A final thought on the Modafinil. Perhaps you were taking too high of a dose? It would seem to be possible for too much glutamate to produce a headache and tinnitus. I have trouble believing that what you are getting is an effect usually seen at the right dosage for you. I was using it merely for fatigue, not antidepressant effects. I would think it would require a significantly higher dose to get antidepressant effects.
>
> btw, I go to the pdoc tomorrow. We'll see how it works out. Not to hound you for them, but did you ever send those cpc files you mentioned? If you already have sent them, great! (that just means hotmail is slow)...if not, I still am interested in them if you have some time to send them over.
>
> Best Regards,
> JGalt
Posted by SLS on October 31, 2001, at 7:17:22
In reply to Re: Modafinil test day, posted by JohnX2 on October 30, 2001, at 23:39:43
Hi John.
Could you summarize why you think memantine would be effective for you, how you would use it, and what you expect from it?
Thanks.
Also, what is "otc rxxxxxxxn-dm"?
I have mentioned memantine to my doctor. He seems genuinely inquisitive. Perhaps you should call a few different doctors to see if they would be receptive to such things. I have never canvassed for doctors on the phone, and don't know how often you can get one to interview on the phone, but some people here have described success going about things this way.
Take care.
- Scott
Posted by JohnX2 on October 31, 2001, at 8:31:31
In reply to Re: Modafinil test day » JohnX2, posted by SLS on October 31, 2001, at 7:17:22
Hi Scott,Ok. Here's where I'm at.
xxxxxxx-dm is just generic robitussin-dm.
If you look at the ingredients 1 tsp is
equivalent to 10mg of dextromethorphan hydrobromide.
Theoretically, if you read those patents, and
I can email the docs to you as I did to JG
(they include all the images), I could pull
a prozac or nortryptyline trick to mimick
memantine (i.e. increase the 1/2 life substantially
of dxm to allow a small 30mg once or twice a
day dosing). Dextromethorphan is a well studied
medication and has the "similar" properties as memantine.
It just has a crummy half-life and can cause
dissacciative effects and potentially Olney's
lesion (which is discussed in detail in one of
those patents). So, I would really prefer to
test memantine.So basically, I have found that if instead of
using the shotgun approach of testing meds, which
I did at first, and instead tried to find meds
that treated my physical ailments that could also
by coincidence treat my depression/hypo-mania, then
I have had more luck.I have discussed in many of my
threads my logical conclusion regarding my
facial pain and bizarre anti-depressant responses.
I have studied and found a clear trend between
the anti-depressants that help with the anhedonia
and pain *without* poop-out and have also looked
carefully at the better anti-depressants for
my anhedonia, specifically wellbutrin. I have
also looked extensively to try to understand why
I experience this damn medication poop out.Here is the most common demonitor:
NMDA receptor activity. Activity in the
Ventral Tegmental Area and how the dopamine
is sensitized and dispersed to the frontal
cortex or limbic system (nucleus accumbens).
The med that pulled me out of depression
was Lamictal a glutamate stabilizer via
electrolyte balancing. The nmda antagonists
are different as they can "tame" pathological
nmda activation and calcium release that is
not supposed to be there and which I believe
is causing some sort of down stream adjustment
that causes the med poop out.So where to go from here.
Meds that worked for pain:Serzone,Zyprexa 5ht-2a,alpha-1 antagonists
these receptors are somehow coupled to glutamate
relese and hence nmda activations. Ergo, stimulation
activates the nmda receptors. A dysfunctional
chronic stimulation could lead to some exhaustion,
sensitization,who nows what. The antagonists
of the 5ht-2a receptors I believe are taming
the nmda receptors to give a more "repeatable"
firing pattern and better "tone" in my brain's
complecated feedback system.Adderall is a sympathomemetic dopamine and sertonin releaser
and a potent dopamine reptake inhibitor. It works
for me *wildy* for a day and slowly craps out over
3 days. Modafinil, caffeine work for a few hours
before they quit (assuming a interim med vacation).Where is my dysfunction? I have no clue. I just
see a trend. I think my dysfunction is in the LC,
and I believe meds like Tenex and Clonidine may
also help to resychronize my brain. I have exhausted
the anti-convulsants and need to think outside the
box. So my brain is telling me to go after the source.
Why do I get poop-out from stims in a short span
of time? I don't know, but it is probably glutamate
related. So, what if I interrupt the sensitization
process using well backed up statistical data on
nmda antagonists and my own tinkering with robitussin
to try to attack the most common chemical in the
brain directly?Will it work. I don't friggin know. But I am
forever an optimist and trying my damndest not
to give up. Maybe I won't hit paydirt. But I
would prefer to use some deductive reasoning
to pick my meds since this is my nature as
a human being, left-brained, engineering geek
instead of continuing this assinine shot-gun
approach. "we don't know how the medicine works"
is no longer acceptable to me.So that's about it.
What do you think? I hope you are having good
luck. I mean if you can't sustain a buzz on
amphetamines then some fundamental feedback
loop in your body is dysfunctional and needs
to be addressed. This is my opinion. I am very
opinionated. I think there is a good reason why
you also did well on Lamictal and the anti-psychotics.
I was looking into correlations on the other meds
you took and started to find some, but it just
seemed you should try the most novel approach
(and with few side effects to boot).PS. I can email all my relavant documents
related to the amphetamine sensitization
theories and also the bruxism paper. They
seem to jive. I also have the patents which are
interesing to read. You just need to download
the cpc viewer (a special viewer for these compressed
documents) from cartesian (there is a link at
getthepatent.com). As a bonus I send a hilarious
patent on a "very different" type of anti-depressant.So what are you thinking?
regards
john> Hi John.
>
> Could you summarize why you think memantine would be effective for you, how you would use it, and what you expect from it?
>
> Thanks.
>
> Also, what is "otc rxxxxxxxn-dm"?
>
> I have mentioned memantine to my doctor. He seems genuinely inquisitive. Perhaps you should call a few different doctors to see if they would be receptive to such things. I have never canvassed for doctors on the phone, and don't know how often you can get one to interview on the phone, but some people here have described success going about things this way.
>
> Take care.
>
>
> - Scott
Posted by JohnX2 on October 31, 2001, at 11:18:07
In reply to Re: Modafinil test day » SLS, posted by JohnX2 on October 31, 2001, at 8:31:31
Oh yeah,Here is my main concern about the memanine
pitch. If I approach the doctor with my experience
on Adderall and is I explain how dxm is like
memantine, then he might start to get suspicious
that I am abusing street drugs or dxm on the
side, WHICH I AM NOT. I would prefer to get
a robust anti-depressant response from something
that worked before like Zoloft or Wellbutrin and
without the weirdism and poopout. Anyways the
neurologist he referred me to suggest a muscle
relaxant baclofen, and memantine is actually
listed as a skeletal muscle relaxant in the
Merck Index of chemical/meds. So the to recommendations
coincide. I also think it may be worthwhile to
compine acamprosate with memantine. There could
be synergistic action. PS. Forest Labs of
celexa fame (soon to be off patent) is
acquiring the rights for both acamprosate and
memantine in the US; I wonder where they'll go with it?-john
>
> Hi Scott,
>
> Ok. Here's where I'm at.
>
> xxxxxxx-dm is just generic robitussin-dm.
> If you look at the ingredients 1 tsp is
> equivalent to 10mg of dextromethorphan hydrobromide.
> Theoretically, if you read those patents, and
> I can email the docs to you as I did to JG
> (they include all the images), I could pull
> a prozac or nortryptyline trick to mimick
> memantine (i.e. increase the 1/2 life substantially
> of dxm to allow a small 30mg once or twice a
> day dosing). Dextromethorphan is a well studied
> medication and has the "similar" properties as memantine.
> It just has a crummy half-life and can cause
> dissacciative effects and potentially Olney's
> lesion (which is discussed in detail in one of
> those patents). So, I would really prefer to
> test memantine.
>
> So basically, I have found that if instead of
> using the shotgun approach of testing meds, which
> I did at first, and instead tried to find meds
> that treated my physical ailments that could also
> by coincidence treat my depression/hypo-mania, then
> I have had more luck.
>
> I have discussed in many of my
> threads my logical conclusion regarding my
> facial pain and bizarre anti-depressant responses.
> I have studied and found a clear trend between
> the anti-depressants that help with the anhedonia
> and pain *without* poop-out and have also looked
> carefully at the better anti-depressants for
> my anhedonia, specifically wellbutrin. I have
> also looked extensively to try to understand why
> I experience this damn medication poop out.
>
> Here is the most common demonitor:
> NMDA receptor activity. Activity in the
> Ventral Tegmental Area and how the dopamine
> is sensitized and dispersed to the frontal
> cortex or limbic system (nucleus accumbens).
> The med that pulled me out of depression
> was Lamictal a glutamate stabilizer via
> electrolyte balancing. The nmda antagonists
> are different as they can "tame" pathological
> nmda activation and calcium release that is
> not supposed to be there and which I believe
> is causing some sort of down stream adjustment
> that causes the med poop out.
>
> So where to go from here.
> Meds that worked for pain:
>
> Serzone,Zyprexa 5ht-2a,alpha-1 antagonists
> these receptors are somehow coupled to glutamate
> relese and hence nmda activations. Ergo, stimulation
> activates the nmda receptors. A dysfunctional
> chronic stimulation could lead to some exhaustion,
> sensitization,who nows what. The antagonists
> of the 5ht-2a receptors I believe are taming
> the nmda receptors to give a more "repeatable"
> firing pattern and better "tone" in my brain's
> complecated feedback system.
>
> Adderall is a sympathomemetic dopamine and sertonin releaser
> and a potent dopamine reptake inhibitor. It works
> for me *wildy* for a day and slowly craps out over
> 3 days. Modafinil, caffeine work for a few hours
> before they quit (assuming a interim med vacation).
>
> Where is my dysfunction? I have no clue. I just
> see a trend. I think my dysfunction is in the LC,
> and I believe meds like Tenex and Clonidine may
> also help to resychronize my brain. I have exhausted
> the anti-convulsants and need to think outside the
> box. So my brain is telling me to go after the source.
> Why do I get poop-out from stims in a short span
> of time? I don't know, but it is probably glutamate
> related. So, what if I interrupt the sensitization
> process using well backed up statistical data on
> nmda antagonists and my own tinkering with robitussin
> to try to attack the most common chemical in the
> brain directly?
>
> Will it work. I don't friggin know. But I am
> forever an optimist and trying my damndest not
> to give up. Maybe I won't hit paydirt. But I
> would prefer to use some deductive reasoning
> to pick my meds since this is my nature as
> a human being, left-brained, engineering geek
> instead of continuing this assinine shot-gun
> approach. "we don't know how the medicine works"
> is no longer acceptable to me.
>
> So that's about it.
>
> What do you think? I hope you are having good
> luck. I mean if you can't sustain a buzz on
> amphetamines then some fundamental feedback
> loop in your body is dysfunctional and needs
> to be addressed. This is my opinion. I am very
> opinionated. I think there is a good reason why
> you also did well on Lamictal and the anti-psychotics.
> I was looking into correlations on the other meds
> you took and started to find some, but it just
> seemed you should try the most novel approach
> (and with few side effects to boot).
>
> PS. I can email all my relavant documents
> related to the amphetamine sensitization
> theories and also the bruxism paper. They
> seem to jive. I also have the patents which are
> interesing to read. You just need to download
> the cpc viewer (a special viewer for these compressed
> documents) from cartesian (there is a link at
> getthepatent.com). As a bonus I send a hilarious
> patent on a "very different" type of anti-depressant.
>
> So what are you thinking?
>
> regards
> john
>
>
>
> > Hi John.
> >
> > Could you summarize why you think memantine would be effective for you, how you would use it, and what you expect from it?
> >
> > Thanks.
> >
> > Also, what is "otc rxxxxxxxn-dm"?
> >
> > I have mentioned memantine to my doctor. He seems genuinely inquisitive. Perhaps you should call a few different doctors to see if they would be receptive to such things. I have never canvassed for doctors on the phone, and don't know how often you can get one to interview on the phone, but some people here have described success going about things this way.
> >
> > Take care.
> >
> >
> > - Scott
Posted by JohnX2 on October 31, 2001, at 11:41:36
In reply to Re: Modafinil test day, posted by JohnX2 on October 31, 2001, at 11:18:07
man, my grammar/spelling is atrocious when I read
my posts after the fact. Good thing
I didn't major in english. I hope this doesn't
ding me for reliability of information. I type
really fast, that is my excuse. ;)-john
>
> Oh yeah,
>
> Here is my main concern about the memanine
> pitch. If I approach the doctor with my experience
> on Adderall and is I explain how dxm is like
> memantine, then he might start to get suspicious
> that I am abusing street drugs or dxm on the
> side, WHICH I AM NOT. I would prefer to get
> a robust anti-depressant response from something
> that worked before like Zoloft or Wellbutrin and
> without the weirdism and poopout. Anyways the
> neurologist he referred me to suggest a muscle
> relaxant baclofen, and memantine is actually
> listed as a skeletal muscle relaxant in the
> Merck Index of chemical/meds. So the to recommendations
> coincide. I also think it may be worthwhile to
> compine acamprosate with memantine. There could
> be synergistic action. PS. Forest Labs of
> celexa fame (soon to be off patent) is
> acquiring the rights for both acamprosate and
> memantine in the US; I wonder where they'll go with it?
>
> -john
>
>
>
>
> >
> > Hi Scott,
> >
> > Ok. Here's where I'm at.
> >
> > xxxxxxx-dm is just generic robitussin-dm.
> > If you look at the ingredients 1 tsp is
> > equivalent to 10mg of dextromethorphan hydrobromide.
> > Theoretically, if you read those patents, and
> > I can email the docs to you as I did to JG
> > (they include all the images), I could pull
> > a prozac or nortryptyline trick to mimick
> > memantine (i.e. increase the 1/2 life substantially
> > of dxm to allow a small 30mg once or twice a
> > day dosing). Dextromethorphan is a well studied
> > medication and has the "similar" properties as memantine.
> > It just has a crummy half-life and can cause
> > dissacciative effects and potentially Olney's
> > lesion (which is discussed in detail in one of
> > those patents). So, I would really prefer to
> > test memantine.
> >
> > So basically, I have found that if instead of
> > using the shotgun approach of testing meds, which
> > I did at first, and instead tried to find meds
> > that treated my physical ailments that could also
> > by coincidence treat my depression/hypo-mania, then
> > I have had more luck.
> >
> > I have discussed in many of my
> > threads my logical conclusion regarding my
> > facial pain and bizarre anti-depressant responses.
> > I have studied and found a clear trend between
> > the anti-depressants that help with the anhedonia
> > and pain *without* poop-out and have also looked
> > carefully at the better anti-depressants for
> > my anhedonia, specifically wellbutrin. I have
> > also looked extensively to try to understand why
> > I experience this damn medication poop out.
> >
> > Here is the most common demonitor:
> > NMDA receptor activity. Activity in the
> > Ventral Tegmental Area and how the dopamine
> > is sensitized and dispersed to the frontal
> > cortex or limbic system (nucleus accumbens).
> > The med that pulled me out of depression
> > was Lamictal a glutamate stabilizer via
> > electrolyte balancing. The nmda antagonists
> > are different as they can "tame" pathological
> > nmda activation and calcium release that is
> > not supposed to be there and which I believe
> > is causing some sort of down stream adjustment
> > that causes the med poop out.
> >
> > So where to go from here.
> > Meds that worked for pain:
> >
> > Serzone,Zyprexa 5ht-2a,alpha-1 antagonists
> > these receptors are somehow coupled to glutamate
> > relese and hence nmda activations. Ergo, stimulation
> > activates the nmda receptors. A dysfunctional
> > chronic stimulation could lead to some exhaustion,
> > sensitization,who nows what. The antagonists
> > of the 5ht-2a receptors I believe are taming
> > the nmda receptors to give a more "repeatable"
> > firing pattern and better "tone" in my brain's
> > complecated feedback system.
> >
> > Adderall is a sympathomemetic dopamine and sertonin releaser
> > and a potent dopamine reptake inhibitor. It works
> > for me *wildy* for a day and slowly craps out over
> > 3 days. Modafinil, caffeine work for a few hours
> > before they quit (assuming a interim med vacation).
> >
> > Where is my dysfunction? I have no clue. I just
> > see a trend. I think my dysfunction is in the LC,
> > and I believe meds like Tenex and Clonidine may
> > also help to resychronize my brain. I have exhausted
> > the anti-convulsants and need to think outside the
> > box. So my brain is telling me to go after the source.
> > Why do I get poop-out from stims in a short span
> > of time? I don't know, but it is probably glutamate
> > related. So, what if I interrupt the sensitization
> > process using well backed up statistical data on
> > nmda antagonists and my own tinkering with robitussin
> > to try to attack the most common chemical in the
> > brain directly?
> >
> > Will it work. I don't friggin know. But I am
> > forever an optimist and trying my damndest not
> > to give up. Maybe I won't hit paydirt. But I
> > would prefer to use some deductive reasoning
> > to pick my meds since this is my nature as
> > a human being, left-brained, engineering geek
> > instead of continuing this assinine shot-gun
> > approach. "we don't know how the medicine works"
> > is no longer acceptable to me.
> >
> > So that's about it.
> >
> > What do you think? I hope you are having good
> > luck. I mean if you can't sustain a buzz on
> > amphetamines then some fundamental feedback
> > loop in your body is dysfunctional and needs
> > to be addressed. This is my opinion. I am very
> > opinionated. I think there is a good reason why
> > you also did well on Lamictal and the anti-psychotics.
> > I was looking into correlations on the other meds
> > you took and started to find some, but it just
> > seemed you should try the most novel approach
> > (and with few side effects to boot).
> >
> > PS. I can email all my relavant documents
> > related to the amphetamine sensitization
> > theories and also the bruxism paper. They
> > seem to jive. I also have the patents which are
> > interesing to read. You just need to download
> > the cpc viewer (a special viewer for these compressed
> > documents) from cartesian (there is a link at
> > getthepatent.com). As a bonus I send a hilarious
> > patent on a "very different" type of anti-depressant.
> >
> > So what are you thinking?
> >
> > regards
> > john
> >
> >
> >
> > > Hi John.
> > >
> > > Could you summarize why you think memantine would be effective for you, how you would use it, and what you expect from it?
> > >
> > > Thanks.
> > >
> > > Also, what is "otc rxxxxxxxn-dm"?
> > >
> > > I have mentioned memantine to my doctor. He seems genuinely inquisitive. Perhaps you should call a few different doctors to see if they would be receptive to such things. I have never canvassed for doctors on the phone, and don't know how often you can get one to interview on the phone, but some people here have described success going about things this way.
> > >
> > > Take care.
> > >
> > >
> > > - Scott
Posted by JGalt on October 31, 2001, at 12:30:52
In reply to Re: Modafinil test day, posted by JohnX2 on October 31, 2001, at 11:41:36
Memantine going to be coming into the US...wow, that'd be great! On one hand I almost wish it had some sort of abuse potential. Isn't it pitiful, you could buy bulk viagra, steroids, rophynol, sleeping pills, ritalin, phen-fen for cheaper than can be bought in a pharmacy, because they all have recreational and/or common use purposes. Even something as expensive and rare as modafinil exists on the black market, and the prices are dirt cheap compared to any pharmacies in existance. Yet I can't buy something that doesn't have much abuse/commune use potential because the the underground market is far too small to warrant black market labs to produce it...arrgghhh. Sorry, I was just looking at the prices of memantine sans insurance and it fired up a little aggression in me.
Anyway, John, I was just curious, how did you come up with the 30mg once or twice a day dosage (obviously with the prozac trick) for dxm? Is that just a guess as my guess of 50mg was or is it based on some data.
Lol, abusing DXM...from what I've read about it online, a great number of people hate using it in "recreational" doses, and those that do like, only a very small percentage continue to use it on a regular basis. Kind of like lsd, a person uses it out of curiousity or to gain some insight, and once they've gained that (or realized that it can't be gained by the drug) they aren't interested in it much anymore. Neither drug has any euphoriant or addictive capacity, and as such, very little abuse potential. Of course I would not expect the average mediahyped doc to realize this.
Sorry to hear about the modafinil...like everything, it apparantly doesn't work for everyone. Although I really have yet to hear from anyone who tried ghb for "depressive ideation and/or anxiety" that it did not work for. Read up on this article some time, it fails to mention the memory effects, but then again at nonabusive dosages memory effects would be nonexistant (which this author states is anything less than or equal to 2.5mls or grams per 6 hrs, I would tend to agree, and that dosage is effective for our purposes, and no tolerance or dopamine buildup either): http://www.biopsychiatry.com/ghb/authentic.html
John, I got those articles but my computer crashes when I try to download them...I suspect a problem with hotmail. I'll email you a different address soon.
JGalt
Posted by JGalt on October 31, 2001, at 15:32:21
In reply to Re: Modafinil test day, posted by JGalt on October 31, 2001, at 12:30:52
Just got back from the doc...with a script for selegiline and lorazepam. He seemed receptive and seemed to understand that I knew what I was talking about (I decided to go into detail about somethings that would show I knew what I was talking about, and try to stay away from talking much about all the other lesser important things that I take and etc.). He said he would prefer I be on Wellbutrin, but he said he'd give me a month back on selegiline to decide if I thought I should switch, and agreed that parnate and effexor would also be proper choices if I wanted to try one of them first. Seems to be the kind of guy I was looking for...willing to listen to what his patient wants and consider it w/o having much experience with it himself. I'm quite surprised. Hope it continues.
JGalt
Posted by JohnX2 on November 1, 2001, at 0:07:02
In reply to Re: Modafinil test day, posted by JGalt on October 31, 2001, at 12:30:52
I'm glad to here about your pdoc success.
I think Wellbutrin is a good med to try if
you want to stay away from the MAO inhibitors
and the food restrictions. I would recommend
a Wellbutrin trial over effexor. Effexor would
be the last resort (for me).The dosing on the dxm was based off the patent
disclosure made by the neurologist. He was
typically using a heart med, but anything that
inhibits the liver enzyme cyp 450-2d6 would work.
He mentioned one patient taking 20 mg of Prozac.
He also listed a number of other meds, some of
which were anti-depressants.Keep us posted on your progress. Sound like
you got hooked up to a good pdoc.Regards,
john> Memantine going to be coming into the US...wow, that'd be great! On one hand I almost wish it had some sort of abuse potential. Isn't it pitiful, you could buy bulk viagra, steroids, rophynol, sleeping pills, ritalin, phen-fen for cheaper than can be bought in a pharmacy, because they all have recreational and/or common use purposes. Even something as expensive and rare as modafinil exists on the black market, and the prices are dirt cheap compared to any pharmacies in existance. Yet I can't buy something that doesn't have much abuse/commune use potential because the the underground market is far too small to warrant black market labs to produce it...arrgghhh. Sorry, I was just looking at the prices of memantine sans insurance and it fired up a little aggression in me.
>
> Anyway, John, I was just curious, how did you come up with the 30mg once or twice a day dosage (obviously with the prozac trick) for dxm? Is that just a guess as my guess of 50mg was or is it based on some data.
>
> Lol, abusing DXM...from what I've read about it online, a great number of people hate using it in "recreational" doses, and those that do like, only a very small percentage continue to use it on a regular basis. Kind of like lsd, a person uses it out of curiousity or to gain some insight, and once they've gained that (or realized that it can't be gained by the drug) they aren't interested in it much anymore. Neither drug has any euphoriant or addictive capacity, and as such, very little abuse potential. Of course I would not expect the average mediahyped doc to realize this.
>
> Sorry to hear about the modafinil...like everything, it apparantly doesn't work for everyone. Although I really have yet to hear from anyone who tried ghb for "depressive ideation and/or anxiety" that it did not work for. Read up on this article some time, it fails to mention the memory effects, but then again at nonabusive dosages memory effects would be nonexistant (which this author states is anything less than or equal to 2.5mls or grams per 6 hrs, I would tend to agree, and that dosage is effective for our purposes, and no tolerance or dopamine buildup either): http://www.biopsychiatry.com/ghb/authentic.html
>
> John, I got those articles but my computer crashes when I try to download them...I suspect a problem with hotmail. I'll email you a different address soon.
>
> JGalt
Posted by JohnX2 on November 1, 2001, at 0:22:01
In reply to Re: Modafinil test day » JGalt, posted by JohnX2 on November 1, 2001, at 0:07:02
BTW, I have much better luck with email
accounts at yahoo. For some reason, I
get tons of SPAM on hotmail, and i have set
up many account there.-john
>
> I'm glad to here about your pdoc success.
> I think Wellbutrin is a good med to try if
> you want to stay away from the MAO inhibitors
> and the food restrictions. I would recommend
> a Wellbutrin trial over effexor. Effexor would
> be the last resort (for me).
>
> The dosing on the dxm was based off the patent
> disclosure made by the neurologist. He was
> typically using a heart med, but anything that
> inhibits the liver enzyme cyp 450-2d6 would work.
> He mentioned one patient taking 20 mg of Prozac.
> He also listed a number of other meds, some of
> which were anti-depressants.
>
> Keep us posted on your progress. Sound like
> you got hooked up to a good pdoc.
>
> Regards,
> john
>
> > Memantine going to be coming into the US...wow, that'd be great! On one hand I almost wish it had some sort of abuse potential. Isn't it pitiful, you could buy bulk viagra, steroids, rophynol, sleeping pills, ritalin, phen-fen for cheaper than can be bought in a pharmacy, because they all have recreational and/or common use purposes. Even something as expensive and rare as modafinil exists on the black market, and the prices are dirt cheap compared to any pharmacies in existance. Yet I can't buy something that doesn't have much abuse/commune use potential because the the underground market is far too small to warrant black market labs to produce it...arrgghhh. Sorry, I was just looking at the prices of memantine sans insurance and it fired up a little aggression in me.
> >
> > Anyway, John, I was just curious, how did you come up with the 30mg once or twice a day dosage (obviously with the prozac trick) for dxm? Is that just a guess as my guess of 50mg was or is it based on some data.
> >
> > Lol, abusing DXM...from what I've read about it online, a great number of people hate using it in "recreational" doses, and those that do like, only a very small percentage continue to use it on a regular basis. Kind of like lsd, a person uses it out of curiousity or to gain some insight, and once they've gained that (or realized that it can't be gained by the drug) they aren't interested in it much anymore. Neither drug has any euphoriant or addictive capacity, and as such, very little abuse potential. Of course I would not expect the average mediahyped doc to realize this.
> >
> > Sorry to hear about the modafinil...like everything, it apparantly doesn't work for everyone. Although I really have yet to hear from anyone who tried ghb for "depressive ideation and/or anxiety" that it did not work for. Read up on this article some time, it fails to mention the memory effects, but then again at nonabusive dosages memory effects would be nonexistant (which this author states is anything less than or equal to 2.5mls or grams per 6 hrs, I would tend to agree, and that dosage is effective for our purposes, and no tolerance or dopamine buildup either): http://www.biopsychiatry.com/ghb/authentic.html
> >
> > John, I got those articles but my computer crashes when I try to download them...I suspect a problem with hotmail. I'll email you a different address soon.
> >
> > JGalt
Posted by Cam W. on November 1, 2001, at 1:04:10
In reply to Re: Modafinil test day » SLS, posted by JohnX2 on October 31, 2001, at 8:31:31
John - FWIW - In Canada, Novartis Consumer Health makes a product called Delsym™. It is a sustained-release dextromethorphan syrup (dextromethorphan polistirex). A single 60mg dose (2 teaspoonfuls) provides plasma concentrations of dextromethorphan simialr to those obtained with two 30mg doses of dextromethorphan HBr given at six hour intervals. After repeated doses at steady state, equivalent plasma concentrations are maintained when Delsym is taken every 12 hours as compared to dextromethorphan HBr every six hours. - Cam
Posted by JohnX2 on November 1, 2001, at 12:21:59
In reply to Re: Modafinil test day » JohnX2, posted by Cam W. on November 1, 2001, at 1:04:10
Cool, thanks a lot!!! Maybe usefull in
psychiatry? What do you think?BTW, what is it used for in Canada, strictly
as an antitussive, or its it used to treat any
other disorders?-john
> John - FWIW - In Canada, Novartis Consumer Health makes a product called Delsym™. It is a sustained-release dextromethorphan syrup (dextromethorphan polistirex). A single 60mg dose (2 teaspoonfuls) provides plasma concentrations of dextromethorphan simialr to those obtained with two 30mg doses of dextromethorphan HBr given at six hour intervals. After repeated doses at steady state, equivalent plasma concentrations are maintained when Delsym is taken every 12 hours as compared to dextromethorphan HBr every six hours. - Cam
Posted by Cam W. on November 1, 2001, at 13:18:06
In reply to Re: Modafinil test day » Cam W., posted by JohnX2 on November 1, 2001, at 12:21:59
John - The Delsym is strictly an antitussive. I did read of a study done at a University in British Columbia (either UBC or the University of Victoria) where they were using high doses in refractory neuropathic pain. They found that there might me some analgesic activity in refractory pain cases, but the dose they were able to give was limited by side effects, especially of the CNS variety. This preliminary study had a very high drop out rate.
- Cam
Posted by JohnX2 on November 1, 2001, at 16:17:09
In reply to Re: Modafinil test day » JohnX2, posted by Cam W. on November 1, 2001, at 13:18:06
I wonder what the impact is of the metabolic
ratio of dextromethorphan:dextrophan?
In the enzyme tricks I looked at the
ratio would go from like 1.5:1 to 20:1,
leaving the dextrophan out of the ball
game. Would the dextrophan cause the crummy
side effects?thnx,
john
> John - The Delsym is strictly an antitussive. I did read of a study done at a University in British Columbia (either UBC or the University of Victoria) where they were using high doses in refractory neuropathic pain. They found that there might me some analgesic activity in refractory pain cases, but the dose they were able to give was limited by side effects, especially of the CNS variety. This preliminary study had a very high drop out rate.
>
> - Cam
Posted by Cam W. on November 1, 2001, at 17:41:01
In reply to Re: Modafinil test day » Cam W., posted by JohnX2 on November 1, 2001, at 16:17:09
John - The side effects that were experienced were excessive sedation and ataxia. Both of these would be centrally induced. Since dextrophan doesn't cross the blood brain barrier as readily as dextromethorphan, one would suspect the the parent compound as the culpert. The enzyme they use to slow the metabolism of DM is to allow more complete penetration of the BBB, thus higher brain levels of DM.
Also, dextromethorphan tablets have been sold as MDMA in Europe. One would think that the ataxia, sedation and the reported emotional lability may pass for MDMA effects in drug-naive ravers.
- Cam
Would the dextrophan cause the crummy
> side effects?
>
> thnx,
> john
This is the end of the thread.
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