![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 12 to 36 of 45. Go back in thread:
Posted by JGalt on October 25, 2001, at 9:34:59
In reply to Re: Looking for some advice before I see the psydoc » JGalt, posted by JohnX on October 24, 2001, at 22:51:19
Sorry, just saw it somewhere else on this board and figured it meant diagnosis.
Posted by JohnX2 on October 25, 2001, at 12:40:27
In reply to Re: Looking for some advice before I see the psydoc, posted by JGalt on October 25, 2001, at 9:34:59
> Sorry, just saw it somewhere else on this board and figured it meant diagnosis.
I had to register because this server is
all messed up JohnX2 = JohnX.First off, I wouln't mess with dxm and
the potential for olney's lesion. I did post
an interesting patent to a neurologist that was
using dxm in conjunction with a med that inhibited
the liver enzyme cyp-450 2d6 (which breaks in down)
in order to increase its 1/2 life (the time to
escape your body). Check my prior posts with
SLS (JohnX).Ok, Dx = diagnosis. That's what I figured.
Well, lately I have had chronic dysthymia (a lower
than normal mood, but functional) accompanied
with atypical depression symptoms (sleeping to
much, lack of interest, anhedonia).In the past 14 yrs I have had 2 trips into manic-depressive
cycling. My symptoms are closest to bipolar II.
I have been struggling the past 2.5 years with
major depression which persistant ruminations
about suicide, major anhedonia (inability to
experience any pleasure) and physical ailments
such as tension headaches and bruxism (teeth
grinding). A few times I have broken out of the
major depression and held onto a dysthymic state,
or slipped into hypo-mania (just below textbook
manic).I've taken over 23 meds (check the "levity thread").
Part of my problem was not being diagnosed as
bipolar over unipolar depression. With the aid of
anti-convulsants (epilepsy meds that also treat bipolar), I have
stabilized my mood into dysthymia. Lamictal has been
of greatest utility. I recently added Zyprexa to
help with the residual anhedonia.I did get good responses to other anti-depressants
primarily St. John's wort,Zoloft, and Wellbutrin.
Wellbutrin worked best (and btw is good for
treatment of stimulant addiction). But I always
had a problem with the meds driving me a little
hypomanic (slighly manic) followed by pooping out
after a few days. I also tried Adderall which is
basically flavors of d-amphetamine, and it helped
with the depression, but I would grow tolerant in
a few days, and on the 1st days I would be really
manic and do stupid things like make wild trades
in the stock market and lose a lot of wealth.
One time I sent out a hilarious email to a large
number of co-workers asking them to help me watch
out for manic symptoms since I didn't want to make
a fool out of myself. The day I wrote it I was
manic. The next day I read it, saw it was over
*10* full pages of typing filled with outrageous
drivel and overdisclosure about personal issues.
Man, I was so embarrassed.Before the major depression hit me I had a strange
addiction to caffeine (I drank like 1-2 cases of
dietcoke a day), and would chase that with a 6-pack
of beer everynight. Not exactly good for my health.
I also had weird symptoms of severe inability to
sit still, which would go away with walking around
or driving my car (which I typically drive > 30k
miles a year). I don't think it is a compulsive
disorder, but more a slightly ADD symptom which can
be induced by any stimulant abuse.
Anyways, I was a
compulsive overachiever in school and attended
a fairly competitive univerisity where I obtained
a degree in electrical engineering. I currently
am employed by a semi-conductor company as a chip
designer.As part of my compulsive overachieving, I abused
caffeine (since my predisposition to hypomania would
give it a "better than average" boost), to help me
achieve my career and scholastic goals.I've sinces learned that my family has a history
of depression, a cousin has attempted suicide,
sister now takes anti-depressants, lots of
alcoholics.If I could do my life over, I would have gotton
my problem treated a long time ago. I think by
abusing my body for so many years with poor diet,
alcohol, and stimulants that it has made it more
difficult for me to recover. The stimulants will
fry dopamine neurons, and they don't grow back.
My better pdoc was quite schocked that I was never
exposed to stronger stims like d-amphetamine.
This was just because I never hung around anyone
in that type of circle.I hope you can learn from the people on this
groups experiences and save your brain before things
slide any further. Feel free to say whatever you
want about your condition that you may not feel
comfortable confiding in personal acquaintances.
That is the beuty of this group. We all have problems
and can discuss them openly in an anonymous fashion.Regards,
john
Posted by JGalt on October 26, 2001, at 11:18:45
In reply to Re: Looking for some advice before I see the psydoc » JGalt, posted by JohnX2 on October 25, 2001, at 12:40:27
Interesting, so right now you're basically are same I am diagnosis wise, except I've never had bipolar symptoms. Obviously you've been through an incredible amount more than me, it is amazing how difficult it is to find the right combinations. I imagine with your education and research on antidepressant combo's you're in a better boat than you might otherwise be.
Overachievement through college years, we have that in common, though personally I view that as an asset to my personality (which reminds me, I know it is not the most accurate, but did you ever get into Meyer-Briggs typecasting?). Of course, if it was leading you to abuse drugs, that's not a positive thing, though I did not think that caffeine was capable of damaging the dopamine system? Was there something else you don't mind mentioning that was?
We also both have the family history thing going for both of us. My mom is the only one who was ever diagnosed with depression, but panic/anxiety attacks seem common on my dad's side, and we believe many on both sides do have depression but refuse to seek help.
You mention overdisclose of personal issues during your manic state. I have that as well, though without the manic state. The only information I have on why that may be (I used to be extremely shy) for me is one of my friends from another board in pharmacy school said they were taught that long term ephedrine use wrecks havoc (long lasting) with the GABA system. I don't claim to understand the GABA system very well, but he suggested that people with long term ephedrine use may suffer (in some cases benefit depending upon the extremity) from lack of some (perhaps mostly verbal) inhibitions. I have to wonder, if GHB does affect the gaba system significantly (as opposed to the other theory that it only effects dopamine release), then why am I still the same way. I don't know, it doesn't particularly bother me, and my friends repeatedly telling me that I disclose way too much, especially if on ghb (1,4 butanediol, GHB is illegal and I don't use it), has made me fake a bit of modesty, but still probably more disclosure than average, particularly in the area of drug use (if someone mentions drugs I'm willing to talk for hours about my experiences a theories, its fun on this board, but dangerous and perhaps damaging to ones image by those holding antidrug views in real life).
Hopefully no one minds the fact that my sentences run on. I write papers much better, but am obviously only writing off the top of my head here, and include the full train of thought often without interruption.
Best Regards,
JGalt
Posted by Elizabeth on October 26, 2001, at 11:45:51
In reply to Re: Looking for some advice before I see the psydoc, posted by Gracie2 on October 24, 2001, at 0:39:26
> I disagree about not being totally honest with your psychiatrist. In the first place, doctors
> have no reputation for being stupid.You've probably heard this one before, but...
What do you call the guy who graduated at the bottom of his class in medical school? "Doctor."Yes, they're generally smarter than the average person. That doesn't mean they're perfect or above prejudice. They're human beings; they have weaknesses like the rest of us. And they're not all alike; two doctors can be as different as any two people.
> In the second place, you are there to establish a relationship with him on which he will base your treatment; a dishonest relationship will result in treatment that may be unneccessary for you.
It's sad, but total honesty may result in mistreatment also.
> When you walk into a new doctor's office, you are a blank slate to him; once you tell him about your experience and education, he can talk to you on your own level; otherwise, he must assume you know nothing about psychiatric medication or treatment.
A lot of psychiatrists talk down to patients uniformly. I've even encountered a few who assume that a knowledgeable patient must be a drug addict or otherwise non-trustworthy.
When I was in the hospital for ARDS (adult respiratory distress syndrome -- I was comatose) back in February-March, the doctors in the hospital decided it must have been a benzodiazepine overdose after they heard about my history of depression and since I had tested positive for benzodiazepines. (I had taken Klonopin the night before, *and* the paramedics had given me Ativan at the scene!) My boyfriend (who is a neuropharmacologist by training, and who also, of course, knows me very well) felt that this was not what had happened, since I hadn't been depressed (and I don't hesitate to talk to him when I am feeling depressed). He told them that he thought they should not jump to that conclusion, but instead should do a quantitative tox screen that would show how much of what I had taken. They refused, and the diagnosis of benzodiazepine overdose remained. As a result, when I woke up I was treated as though I was suicidal and could not be trusted (even though I was obviously doing fine emotionally and there was no reason to believe that I was depressed). I wasn't allowed any privacy except when I had to go to the bathroom -- even when my family was visiting me. (And yet they refused to give this supposedly dangerous suicidal patient any sort of antidepressant. As a result, I started getting depressed -- not suicidal, just sad and anergic -- before I was able to go home and start taking my meds again.)
I've been able to get doctors to trust me and to accept that I'm more sophisticated than the average patient, but it often takes a lot of time and effort. As such, I'm cautious about what I say to a new doctor until I get to know him/her better (and until s/he gets to know me better, too).
Just my personal approach (and FWIW, it's always worked for me).
-elizabeth
Posted by Gracie2 on October 26, 2001, at 18:23:55
In reply to Re: Looking for some advice before I see the psydoc » Gracie2, posted by Elizabeth on October 26, 2001, at 11:45:51
Hoo! Got jumped on that time!
In my own defense, I did state in another thread
(about "flakey" patients) that I absolutely believe in "doctor shopping" and have no compunction about doing so with GPs, pdocs, specialists or dentists. Obviously some professionals are more skilled than others, and even many competent docs lack "people skills" (in and out of the exam room in 10 seconds, you practically have to grab them by the coat to ask a question), which nobody appreciates. A lot of patients tolerate it but I figure, with so many doctors around - why put up with that?
So, sure, some doctors are better than others. No argument there.
-Gracie
Posted by JohnX2 on October 27, 2001, at 1:15:47
In reply to Re: Looking for some advice before I see the psydoc, posted by JGalt on October 26, 2001, at 11:18:45
JG,
Don't worry about the rambling. I am the king
and I think that Cam may come in 2nd. ;)
My case history of treatment refractory
depression (now bpii) is not typical for most
people. Most people will find relief from depression after 1 or 2 trials. A lot of times
people can get depression relief but will switch
meds from the side effects.My problem has mainly been misdiagnosis. My
list of meds, which I laugh about now, would be
much shorter had I gotton the right diagnosis. I think if I researched my problem better *before*
seeing the doctor I would have been able to give
him the right symptoms to make an accurate diagnosis. You are in that boat and seem to have
a really good head start on treating your issues.
I think your treatment will be smooth.No-one in my family has symptoms of bp disorder
,but lots of depression and alcoholism.
I believe that my bp is actually a subset
of PTSD (post traumatic stress disorder). PTSD
is tricky to treat, it involves complicated
disruptions to the hpa axis and the "fight-or-flight" feeback mechanisms in the locus coerulus
area of the brain. Anyways, to make an ugly story
short, I had some bad years as a kid with a depressed alcoholic mother, divorce,
family businesss near bankruptcy, blah, blah.
It was after this that i developed non-text book cases symptoms
of bp ii (but text book major depression). The best meds to treat ptsd are actually called crf antagonists,
but these are still experimental and not available. Curiously
nmda antagonists are indirectly crf antagonists and can thus
be anxyiolitic.Anyways, my goal is to reach logical conclusions
as to how to treat my problems in a manner with least side-effects
and most cure. I do not like "dirty" drugs. I
do not like meds who's "mechanism of action are
unknown". I refuse to use this dart-board approach my early physicians had. So I
think if I can nail down why I get AD poop-out and
find a good treatment (crossing my fingers on memantine and a few
others) then I believe I may see a full remission.Anyways, my left-brained,mr.spock, stoic, unemotional thought process
are also symptoms of ptsd (emotions get
blunted). I would like to recapture my emotions
(feelings of well-being and being "attached").
I can experience wild euphoria, but this is
different from feeling "well". I wish I could
describe what I mean. i have had a few full remissions
where my emotions came back and i can not describe the feeling.As far as the brain frying goes, I do believe
that kindled states I experienced on simple
substances like caffeine inducing mania could have
over the long haul bantered noradrenaline and
dopamine neurons. This would definately be analogous
for people abusing strong stims like meth.
I really wish you the best of luck.
Keep us posted on your progress.Oh yeah, forgot to mention that you are correct
about gaba agonists being neuroprotective agains
nmda hypoactivity. Anaesthesiologists are well aware
of this as are their insurance carriers.-john
> Interesting, so right now you're basically are same I am diagnosis wise, except I've never had bipolar symptoms. Obviously you've been through an incredible amount more than me, it is amazing how difficult it is to find the right combinations. I imagine with your education and research on antidepressant combo's you're in a better boat than you might otherwise be.
>
> Overachievement through college years, we have that in common, though personally I view that as an asset to my personality (which reminds me, I know it is not the most accurate, but did you ever get into Meyer-Briggs typecasting?). Of course, if it was leading you to abuse drugs, that's not a positive thing, though I did not think that caffeine was capable of damaging the dopamine system? Was there something else you don't mind mentioning that was?
>
> We also both have the family history thing going for both of us. My mom is the only one who was ever diagnosed with depression, but panic/anxiety attacks seem common on my dad's side, and we believe many on both sides do have depression but refuse to seek help.
>
> You mention overdisclose of personal issues during your manic state. I have that as well, though without the manic state. The only information I have on why that may be (I used to be extremely shy) for me is one of my friends from another board in pharmacy school said they were taught that long term ephedrine use wrecks havoc (long lasting) with the GABA system. I don't claim to understand the GABA system very well, but he suggested that people with long term ephedrine use may suffer (in some cases benefit depending upon the extremity) from lack of some (perhaps mostly verbal) inhibitions. I have to wonder, if GHB does affect the gaba system significantly (as opposed to the other theory that it only effects dopamine release), then why am I still the same way. I don't know, it doesn't particularly bother me, and my friends repeatedly telling me that I disclose way too much, especially if on ghb (1,4 butanediol, GHB is illegal and I don't use it), has made me fake a bit of modesty, but still probably more disclosure than average, particularly in the area of drug use (if someone mentions drugs I'm willing to talk for hours about my experiences a theories, its fun on this board, but dangerous and perhaps damaging to ones image by those holding antidrug views in real life).
>
> Hopefully no one minds the fact that my sentences run on. I write papers much better, but am obviously only writing off the top of my head here, and include the full train of thought often without interruption.
>
> Best Regards,
> JGalt
Posted by JGalt on October 27, 2001, at 13:14:50
In reply to Re: Looking for some advice before I see the psydoc » JGalt, posted by JohnX2 on October 27, 2001, at 1:15:47
Post Traumatic Stress Disorder, your brief discussion on it will probably lead me to research it some later. I have heard it before in reference to police brutality, but never anywhere else. So basically it can apply to any situation that your body stays in the fight-flight response much longer than it should and no amount of "thinking yourself down" from the event will help. I've had that a lot at times, in fact, I believe part of my problem is that when I need to get something done, I not only have some lack of motivation do it, there's also a certain fear response that my body produces. Like fear of getting started and then fear of continuing. I don't know why, I succeed at most things I try at, but I never even thought about it until reading your post, that that, in combination with low energy, is why I have trouble setting out on projects that would probably provide me with pleasure, and perhaps increased energy. At times this feeling of fear can also lead me to decide to not do something I know I should do that would help to ensure the success of something I'm trying at.
Adderal, the 6 total times I've tried it, helps wonderfully, but even though I never have taken it on consecutive days, the next day I will always be low on energy and motivation, which is why I know it is addictive and has a high tolerance building potential. But Adderal, in addition to providing me with motivation, seems to completely eliminate this, whatever the heck it is.
GHB (or things that convert to GHB) is the only other drug that does so, but of course it also has some negative things about it too. While it does NOT produce tolerance, if you have ever used it several weeks in a row without break, and to help get to sleep at times too (resulting in no REM sleep), you know its effects on memory and causing ADD like behavior...it does need to be stopped every once in a while or else you will have trouble focusing on tasks, and short+long term memory will be reduced, and connections between things in your mind are reduced too. This is of course if you abuse it, which I now know where the line between abuse and use is. It produces a feeling of love+trust towards everything, which can sometimes be a negative aspect. Enough about that, the fact is, it, and Adderal, both are able to eliminate this fear of doing, though adderal obviously has many more positive things about it until you develop complete tolerance. Still, GHB is a very theraputic chemical (it is present in your body and food too) when used properly, and its lack of tolerance is very nice.
Still, Selegiline does not eliminate this problem really, it simply provides some more motivation to do things, and also is stimulating. This allows one to use GHB effectively, as it helps to keep one more alert while on it, and reduces the effective dosage quite nicely.
Well after all that ranting, can you give me any insight or advice into my problem? Since you mentioned the NMDA antagonists being helpful in this regard, I think I may eventually try a combination of lamictal+adderal. I would think that if lamictal reduces NMDA receptor sensitivity, that it would work roughly the same, do you think I am correct?
I personally would love to try my idea mentioned before of adderal+low dose dxm+prozac+1,4 butanediol (GHB precursor), but I know that no psych doctor is going to go for a such a combination. Of course, then again, if I were to do such a combination, I would obviously not mention the rationale behind it or either of the two non-mainstream chemicals.
Your approach seems like a logical one to the problem. I cannot understand why someone would not research a drug or drug combination that some person had given them or the disease for which they are taking it. Even GHB can't make me that trusting!
I can understand why wild euphoria is not what you're looking for. One should desire their emotional state to have connection with real life events. Having wild euphoria while washing off an apple would not be particularly pleasurable because one knows that one's pleasure is not stemming from what one is doing. That is why I would question a drug that kept a person very happy all the time, or a person who would want to be. While I would certainly have no qualms about a majority of the people being on a drug that increased the capacity of their pleasure, or perhaps simply multiplied all positive emotions by 2 and divided all negative emotions by 2, I would have a problem with a drug that made all emotions more positive by a factor of 2 being used for anyone that wasn't truly depressed.
I see what you mean about true mania being induced by caffeine having the potential to damage dopamine receptors.
Also interesting that my thoughts about gaba agonists working to protect from NMDA hypoactivity have already been proven. I'll have to do some research to find out just what the gaba agonists are, and whether ghb or precursors are amongst them. If that is unknown, perhaps I'll also have to find out if drugs which are specific gaba antagonists exist outside of a chemical lab, evaluate their safety, and see if they prevent GHB's effects. This could take a while, but it might pay off. Sometimes I wonder why the same people that prescribe the drugs aren't the ones that go through pharmacy school to learn how drugs work and how to make interesting combinations of them.
JGalt
Posted by JohnX2 on October 27, 2001, at 15:41:06
In reply to Re: Post Traumatic Stress Disorder and etc., posted by JGalt on October 27, 2001, at 13:14:50
This is long, but you are such a good listener
and have interesting retorts, so here I go
again:I'll try to get you some more info on ptsd
later. basically it can occur if one is under
substantial oncontrolled and unpredictable duress
for prolonged periods of time. But usually this
has to be *quite severe*. What happens is 1 of 2
things, A) the body maintains toxic level of
cortisol, which can goof up the hippocampus
B) the body is habitually releasing
adrenaline, and this causes neuroadaptive changes
(feeback breakdown) in the locus coerulus.The meds to treat ptsd are usually clonodine,
tenex,inderal, but the crf antagonists are most
likely to help the most (and I see utility in the
nmda antagonists). The ADs generally give
spotty results . I'll
let you do the rest of the research. Usually
after the trauma there may be nightmares and flashbacks,
which there was for me, but this was like 15 years
ago. So I don't have that now, but my brain has
adapted to the situation in a way that blunts my
emotions, makes me sensitive to stimulants (which
could most definately be related to the breakdown
in the locus coerulus). I'm leaning towards an LC
breakdown theory for me. It could explain manic
responses too.Also I have this jaw and tension
headache problem and I get a weird response on
the AD's that worked well. I'll give Wellbutrin
as an example (it is similar in structure to
ephedrine,amphetamine..). After taking WB at
a therapeutic dose for about 1 week, I usually
get a depression lift, sometimes into severe mania.
Then, it very quickly fades at the drop of a coin,
and all of a sudden my emotions go *DEAD NUMB*, I can't
even feel a deep breath and I get this excrucitating
pain in my jaw and head which is directly proportional
to the emotional numbing. It is like I am ping
ponging from positive to negative psychosis (read
up about schizophrenia), the negative psychosis
(complete lack of emotions), occurs with too little
dopamine in the frontal cortex.
I have tracked the bruxism down
to an area of the brain called the prefrontal
cortex. A hypodopaminergic state of dopamine projected
from the VTA to the medial prefrontal cortex would
cause disinhibition of the muscles of the face.
The prefrontal cortex is where dopamine stops
acetylcholine from sending muscle spasm signals to
the jaw/face.
Those dopamine neurons have no feedback receptors,
which makes them unique. They are gated directly
by 5ht-2a receptors and the dopaminergic firing
from the VTA (the center for sensitization to
medications like stimulants and opiods). The
dopaminergic firing (whether it is pacemaker or
burst) is also linked by gaba and nmda innervations
in the VTA. The nmda innervations in the VTA are
linked to 5ht-2a receptors. Scientists have found that
by directly antagonizing nmda receptors in the vta
(i.e. by taming them to be more pace-maker), the
sensitization to amphetamine is reduced. I have
an interesting article on amphetamine sensitization,
search through my old posts for summaries.I have found before my depression experience, that
when I was in college if I stayed up for very long
and drank gobs of caffeine, the caffeine would wear
off and i would get a tension headache similar to
the one I describe. But back then, a good night
of sleep would make it go away. So I have lots of
correlations, I also found a lot of data recently
regarding 5ht2a antagonists treating tension headaches
and attenuating the locomotor effects of prolonged
amphetamine stimulation.Regarding your potential cocktail, I don't know
much about anything related to ghb or precursors,
except that ghb is illegal, so I'll stop short
of there. The idea behind the dxm enzyme inhibition
if you read the patent disclosures was to
increase its 1/2 life so that a low dose can be
taken and with fewer dosing.
It could be done with xxx-dm from the local
pharmacy without a prescription.
Again, the drug level of dxm would probably need
to be monitored, not a good idea to mess with getting
a leasion. Anyways, the meds that would prevent
nmda hypoactive toxicitiy (and you probably would
have to be having dissaciative effects to reach
the level to be honest), are alpha-2 agonists,
potential 5ht-2a agonists, and primarily GABAa
agonists. Do a patent search on the subject of
nmda antagonists and you will get a lot of interesting
information. memantine is probably the safest
nmda antagonist, but dxm is well studied and
older. There are some patent write ups by Olney
describing the biological underpinnings of
nmda hypoactivity lesions (he suggests anti-cholinergics
as a post condition treatment). I also found
some patents by someone showing how alpha-2 agonists
could prevent the hypoactivity.I have most of these patents with all the diagrams
in a nice compressed format called cpc. If you
download the cpc viewer I'd be happy to mail them
to you.good luck,
john> Post Traumatic Stress Disorder, your brief discussion on it will probably lead me to research it some later. I have heard it before in reference to police brutality, but never anywhere else. So basically it can apply to any situation that your body stays in the fight-flight response much longer than it should and no amount of "thinking yourself down" from the event will help. I've had that a lot at times, in fact, I believe part of my problem is that when I need to get something done, I not only have some lack of motivation do it, there's also a certain fear response that my body produces. Like fear of getting started and then fear of continuing. I don't know why, I succeed at most things I try at, but I never even thought about it until reading your post, that that, in combination with low energy, is why I have trouble setting out on projects that would probably provide me with pleasure, and perhaps increased energy. At times this feeling of fear can also lead me to decide to not do something I know I should do that would help to ensure the success of something I'm trying at.
>
> Adderal, the 6 total times I've tried it, helps wonderfully, but even though I never have taken it on consecutive days, the next day I will always be low on energy and motivation, which is why I know it is addictive and has a high tolerance building potential. But Adderal, in addition to providing me with motivation, seems to completely eliminate this, whatever the heck it is.
>
> GHB (or things that convert to GHB) is the only other drug that does so, but of course it also has some negative things about it too. While it does NOT produce tolerance, if you have ever used it several weeks in a row without break, and to help get to sleep at times too (resulting in no REM sleep), you know its effects on memory and causing ADD like behavior...it does need to be stopped every once in a while or else you will have trouble focusing on tasks, and short+long term memory will be reduced, and connections between things in your mind are reduced too. This is of course if you abuse it, which I now know where the line between abuse and use is. It produces a feeling of love+trust towards everything, which can sometimes be a negative aspect. Enough about that, the fact is, it, and Adderal, both are able to eliminate this fear of doing, though adderal obviously has many more positive things about it until you develop complete tolerance. Still, GHB is a very theraputic chemical (it is present in your body and food too) when used properly, and its lack of tolerance is very nice.
>
> Still, Selegiline does not eliminate this problem really, it simply provides some more motivation to do things, and also is stimulating. This allows one to use GHB effectively, as it helps to keep one more alert while on it, and reduces the effective dosage quite nicely.
>
> Well after all that ranting, can you give me any insight or advice into my problem? Since you mentioned the NMDA antagonists being helpful in this regard, I think I may eventually try a combination of lamictal+adderal. I would think that if lamictal reduces NMDA receptor sensitivity, that it would work roughly the same, do you think I am correct?
>
> I personally would love to try my idea mentioned before of adderal+low dose dxm+prozac+1,4 butanediol (GHB precursor), but I know that no psych doctor is going to go for a such a combination. Of course, then again, if I were to do such a combination, I would obviously not mention the rationale behind it or either of the two non-mainstream chemicals.
>
> Your approach seems like a logical one to the problem. I cannot understand why someone would not research a drug or drug combination that some person had given them or the disease for which they are taking it. Even GHB can't make me that trusting!
>
> I can understand why wild euphoria is not what you're looking for. One should desire their emotional state to have connection with real life events. Having wild euphoria while washing off an apple would not be particularly pleasurable because one knows that one's pleasure is not stemming from what one is doing. That is why I would question a drug that kept a person very happy all the time, or a person who would want to be. While I would certainly have no qualms about a majority of the people being on a drug that increased the capacity of their pleasure, or perhaps simply multiplied all positive emotions by 2 and divided all negative emotions by 2, I would have a problem with a drug that made all emotions more positive by a factor of 2 being used for anyone that wasn't truly depressed.
>
> I see what you mean about true mania being induced by caffeine having the potential to damage dopamine receptors.
>
> Also interesting that my thoughts about gaba agonists working to protect from NMDA hypoactivity have already been proven. I'll have to do some research to find out just what the gaba agonists are, and whether ghb or precursors are amongst them. If that is unknown, perhaps I'll also have to find out if drugs which are specific gaba antagonists exist outside of a chemical lab, evaluate their safety, and see if they prevent GHB's effects. This could take a while, but it might pay off. Sometimes I wonder why the same people that prescribe the drugs aren't the ones that go through pharmacy school to learn how drugs work and how to make interesting combinations of them.
>
> JGalt
Posted by JGalt on October 27, 2001, at 21:59:18
In reply to Re: Post Traumatic Stress Disorder and etc. » JGalt, posted by JohnX2 on October 27, 2001, at 15:41:06
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.
By the way, I did my research on GABA antagonists. It turns out that all the GABA antagonists we currently have are either non-specific, or carry a rather high risk of seizures, or they are not incredibly easy to purchase or store. All of them except for two. Adrafinil and Modafinil, though both of those are not complete antagonists except at inhuman dosages, I think 500-700mg would be sufficient as that is their believed method of action. So I guess my next theoretical mission if I were to want to pursue that regimine would be to take a 500-700mg dose of modafinil , then take some 1,4 butanediol. That much modafinil would easily be able to give me a headache due. If the 1,4 butanediol prevents this headache then 1,4 butanediol is a gaba agonist. Simple enough if I were to want to find out. I don't think I'd bother unless the curiousity strikes me hard enough someday. Really after I wrote out what I did above about GHB and dopamine, it would probably be a bad redundant to combine it with a dopamine agonist I would imagine if the uncompletely tested pharmacodynamics of ghb are correct.
I understand the idea behind lengthening DXM's effects. A drug with such powerful effects needs something to lengthen its halflife to be useful theraputically.
Hmm, if alpha-2 agonists were to help prevent onley's lesions, then logically beta-2 agonists would exacerbate them. Guess I have to throw out the ephedrine if I were to try it using a different gaba agonist such as one of the benzodiazapines.
I'll check up on that cpc reader and see if it works on a mac and get back to you.
Thanks again,
JGalt
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
Go forward in thread:
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.