![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
[email protected]Shown: posts 1 to 19 of 19. This is the beginning of the thread.
Posted by JohnL on June 10, 2000, at 5:40:44
Just thought I would share some information from my pdoc meeting a couple days ago.
My pdoc is head of psychiatry at two different institutions. And he has pretty much phased out private practice. As a result he spends most of his time in conferences, meetings, consultations, research, and stuff like that.
He acknowledged that antidepressants are indeed wonder meds. He says 80% of patients who try 2 different antidepressants will improve. But he says recent focus has been on the recognition that of those 80% who improve, a substantial proportion of them do not indeed recover to complete normalcy. Or normal baseline as he called it.
But of course, scientific controlled studies have proven that for a long time. That's because success in controlled studies is usually based on a 50% improvement of symptoms. Fine, but what about the other 50%? Yikes. I like the scientific studies that use stricter criteria. But even with those, success is dependent on each person's unique chemistry.
This is why I believe that there are multiple chemical imbalances that can cause depression, and that low serotonin is just one of them. Obviously if doctors focus on serotonin meds--as evidenced by the universal popularity of SSRIs--then a whole lot of other guilty chemistries are being ignored. And thus considerable--yet incomplete--recovery. Antidepressants as a class only address three of ten possible causes.
In my case for example I experienced substantial improvement on any serotonin antidepressant. Yet I was still left with this crippling anhedonia thing. I never recovered to baseline. As it turns out, the chemistry guilty with me was not low serotonin, NE, or dopamine, but rather malfunction of something in the NE/dopamine relationship. My robust response to Ritalin was the tip-off, as my pdoc phrased it. Or, as I call it, an important clue. All along antidepressants were merely masking the symptoms of depression, but not fixing the cause. Adrafinil ended up being the molecule that hit a bullseye and fixed the problem right at the heart of the source.
Anyway, no real point here. Just wanted to share what we talked about in case anyone's interested.
JohnL
Posted by SLS on June 10, 2000, at 9:39:52
In reply to Incomplete recovery gaining attention, posted by JohnL on June 10, 2000, at 5:40:44
> My pdoc is head of psychiatry at two different institutions. And he has pretty much phased out private practice. As a result he spends most of his time in conferences, meetings, consultations, research, and stuff like that.
Cool. Mine too.
> He acknowledged that antidepressants are indeed wonder meds. He says 80% of patients who try 2 different antidepressants will improve. But he says recent focus has been on the recognition that of those 80% who improve, a substantial proportion of them do not indeed recover to complete normalcy. Or normal baseline as he called it.
Unfortunately, combining drugs early in the course of therapeutic trials still seems to be underutilized. I become extremely frustrated and angered when I read a post here of someone whose doctor has decided to switch them from an SSRI to Wellbutrin when they have already failed to respond to several other drugs monotherapeutically.
> This is why I believe that there are multiple chemical imbalances that can cause depression, and that low serotonin is just one of them. Obviously if doctors focus on serotonin meds--as evidenced by the universal popularity of SSRIs--then a whole lot of other guilty chemistries are being ignored. And thus considerable--yet incomplete--recovery. Antidepressants as a class only address three of ten possible causes.
Three only? Ten only?
It is way more than that - on both accounts.
Perhaps low serotonin is never the cause.
Just because an effective antidepressant works its magic by inhibiting the reuptake of serotonin does not lead to the logical conclusion that it is low serotonin that is responsible for the depression in the first place.
> In my case for example I experienced substantial improvement on any serotonin antidepressant. Yet I was still left with this crippling anhedonia thing. I never recovered to baseline. As it turns out, the chemistry guilty with me was not low serotonin, NE, or dopamine, but rather malfunction of something in the NE/dopamine relationship. My robust response to Ritalin was the tip-off, as my pdoc phrased it. Or, as I call it, an important clue. All along antidepressants were merely masking the symptoms of depression, but not fixing the cause. Adrafinil ended up being the molecule that hit a bullseye and fixed the problem right at the heart of the source.
This is very possible. But it may have nothing to do with a NE/DA relationship. NE alpha-1 agonism may not contribute to either its antidepressant effect or its antinarcoleptic effect. The package insert of Provigil (modafinil) makes no mention of NE and declines to offer a mechanism of action. It describes the ability of it to bind to DA transporter in vitro, but this is probably irrelevant, as so many drugs do at clinically irrelevant high concentrations.
> Anyway, no real point here. Just wanted to share what we talked about in case anyone's interested.
I think all of your points are crucial ones. The tendency for many people to attain only a partial remission from using only one drug is something that has been recognized and addressed by competent psychiatrists for a long time. The NIMH is a good barometer of current putative clinical observations and therapeutic modalities. They tend to be objective and conservative, trying to maintain a consistent level of accuracy. Their research teams have pleaded their case for polypharmacy for many years. They work to discover what treatments work, without necessarily determining with surety the reasons why they work. Of course, one of their ultimate goals is the latter. There is little justification for deeming a partial improvement as being satisfactory. For most people, a nearly complete recovery is possible using the tools that are currently available.
As far as to what extent the underlying physiological perturbations underlying psychiatric disorders are understood, I think it is bit premature to explain them. I imagine that if the brilliant minds in research who are trying to get us all well were willing to express a determination of depression as to its causes, dynamics, and the mechanisms by which successful treatments produce their therapeutic effects, they would have told us by now.
Perhaps dopaminergic drugs make a good bandage to compensate for the underactivity of glutaminergic neurons afferent to the thalamus and hippocampus that have been downregulated due to their chronic overactivity in response to stress. This would allow for a perturbation of the balance between glutaminergic and GABAergic activity there in favor of efferent GABAergic neurons leading to the nucleus accumbens, whereby dopaminergic neurotransmission in this healthy structure is thus inhibited. What do you think? Perhaps adrafinil addresses this by promoting an increase in the neurotransmission of these thalamic and hippocampal glutaminergic neurons. Of course, it could be that modafinil activates cortical function simply by increasing the release of glutamate there. Where's DA, NE, or 5-HT?
I just like to express this sort of caveat every now and then.
- Scott
Posted by NHGRANDMA on June 10, 2000, at 13:42:39
In reply to Re: Incomplete recovery gaining attention, posted by SLS on June 10, 2000, at 9:39:52
JohnL,
How would you technically explain that Ritalin makes me worse when used for depression? After reading of your robust response I decided to try it and ended up crying a couple of hours after taking it. Not just once, but each time. Made depression much worse. Is this a common side effect of Ritalin?
Posted by glenn on June 10, 2000, at 16:38:45
In reply to Incomplete recovery gaining attention, posted by JohnL on June 10, 2000, at 5:40:44
> Just thought I would share some information from my pdoc meeting a couple days ago.
>
> My pdoc is head of psychiatry at two different institutions. And he has pretty much phased out private practice. As a result he spends most of his time in conferences, meetings, consultations, research, and stuff like that.
>
> He acknowledged that antidepressants are indeed wonder meds. He says 80% of patients who try 2 different antidepressants will improve. But he says recent focus has been on the recognition that of those 80% who improve, a substantial proportion of them do not indeed recover to complete normalcy. Or normal baseline as he called it.
>
> But of course, scientific controlled studies have proven that for a long time. That's because success in controlled studies is usually based on a 50% improvement of symptoms. Fine, but what about the other 50%? Yikes. I like the scientific studies that use stricter criteria. But even with those, success is dependent on each person's unique chemistry.
>
> This is why I believe that there are multiple chemical imbalances that can cause depression, and that low serotonin is just one of them. Obviously if doctors focus on serotonin meds--as evidenced by the universal popularity of SSRIs--then a whole lot of other guilty chemistries are being ignored. And thus considerable--yet incomplete--recovery. Antidepressants as a class only address three of ten possible causes.
>
> In my case for example I experienced substantial improvement on any serotonin antidepressant. Yet I was still left with this crippling anhedonia thing. I never recovered to baseline. As it turns out, the chemistry guilty with me was not low serotonin, NE, or dopamine, but rather malfunction of something in the NE/dopamine relationship. My robust response to Ritalin was the tip-off, as my pdoc phrased it. Or, as I call it, an important clue. All along antidepressants were merely masking the symptoms of depression, but not fixing the cause. Adrafinil ended up being the molecule that hit a bullseye and fixed the problem right at the heart of the source.
>
> Anyway, no real point here. Just wanted to share what we talked about in case anyone's interested.
> JohnL
john, i bought the dr jensen book and found it to ber excellent, much better than the other books i have bought, so thanks for the tip, i may at some point go to see this man if i cant sort myself out, im at about 50-60% better but to me thats not enough, just one question, do you know if serotonin excess can cause depression, its about the only thing dr jensen doesnt mention, i know it can cause the serotonin syndrome but this always appears to me to be being described as a temporary state soon put right, for me serotonin reuptake inhibitors make me much worse very quickly, in zolofts case after 3 hours!
glad to hear the adrafinil is your key
glenn
Posted by JohnL on June 10, 2000, at 18:16:18
In reply to Re: Incomplete recovery gaining attention, posted by SLS on June 10, 2000, at 9:39:52
> I just like to express this sort of caveat every now and then.
>
>
> - ScottExcellent points Scott. Your demonstrated technical knowledge is way over my head, but I think I understood what you were explaining. Very interesting. Makes a lot of sense.
JohnL
Posted by JohnL on June 10, 2000, at 18:26:05
In reply to Re: JohnL Ritalin, posted by NHGRANDMA on June 10, 2000, at 13:42:39
> JohnL,
> How would you technically explain that Ritalin makes me worse when used for depression? After reading of your robust response I decided to try it and ended up crying a couple of hours after taking it. Not just once, but each time. Made depression much worse. Is this a common side effect of Ritalin?Sorry but I don't know why. I'm not well schooled on the technicals of what exactly Ritalin does. But whatever it is, it certainly isn't something your brain chemistry likes.
All the stimulants are quite different. Ritalin for example made me euphoric, almost identical to cocaine. But Adderall, which I assumed was similar yet a bit smoother, made me depressed and I was on the edge of crying.
Hopefully someone else here can help us understand what chemistries are being affected, and what it means that Ritalin made you more depressed. That is a powerful clue, but I can't desipher it.
Posted by JohnL on June 10, 2000, at 19:05:53
In reply to Re: Incomplete recovery gaining attention, posted by glenn on June 10, 2000, at 16:38:45
> john, i bought the dr jensen book and found it to ber excellent, much better than the other books i have bought, so thanks for the tip, i may at some point go to see this man if i cant sort myself out, im at about 50-60% better but to me thats not enough, just one question, do you know if serotonin excess can cause depression, its about the only thing dr jensen doesnt mention, i know it can cause the serotonin syndrome but this always appears to me to be being described as a temporary state soon put right, for me serotonin reuptake inhibitors make me much worse very quickly, in zolofts case after 3 hours!
> glad to hear the adrafinil is your key
> glennCool book, eh? I tell you what, I've spent a lot of money on psychiatric books, some with internationally acclaimed authors. But if I had to choose just one book of them all to keep, it would be this humble unsuspecting $30 book that stirs up so much controversy among those who haven't read it. I agree with you. Excellent book. It fills in all the gaps. I understand he's writing a followup book that goes into more detail.
Well, it almost fills in all the gaps...you're right, I didn't see any mention of too MUCh serotonin in the book. I know I got real depressed when I took just a tiny dose of Moclobemide. While he explains excess NE and excess dopamine, he didn't say the same about serotonin. But like my pdoc always says, anything's possible. He's seen it all.
I wonder, have you tried other serotonin enhancers? It could be that maybe your body just rejects the Zoloft molecule for some reason. As you know from the book, Jensen would like to see how you react to each of several meds in the same class before ruling out that class. If you react poorly to other serotonin meds, then I think the picture becomes clearer and it's definitely time to probe some other likely chemistries. Yeah?
By the way, I did have one phone consultation with Dr Jensen about half a year ago. He's really pleasant to speak with. Not only is his expertise obvious when he speaks or asks a question, but he's very humble, gentlemanly, and mild mannered. Excellent bedside manners. No ego trip with this guy. My one consultation with him was enough to get me pointed in the right direction. He layed out a very clear roadmap for me and my doctor to follow, with enough elbow room to make adjustments to it if we wanted to. And precise explanations of why this and why that. Just in case you ever feel like you're on a deadend road, I thought it might be worth knowing that a lot of people from around the country and the world consult with him by phone about their cases. I'm just one of them. It's not unusual at all for patients to consult with him just once or twice, because he has a knack for getting good results fast. Don't feel weird if you feel like calling his office.
I know it's kind of an awkward and unconventional way of getting help, and thus the obvious hesitation I felt when I was thinking of calling him. It's understandable. It's just so different. But it was actually a very good experience. Keep it in your back pocket just in case you might use it.
JohnL
Posted by shar on June 10, 2000, at 22:07:38
In reply to Re: Incomplete recovery gaining attention, posted by SLS on June 10, 2000, at 9:39:52
I think that when God was handing out Serotonin I was standing behind the door.
Seriously, though, I have this theory that my body will only allow so much Serotonin in my brain (let's say a teaspoon). So, if I take something that inhibits reuptake, my body will eventually catch on, and go about reducing the amount back to a tsp. So, no matter what I do med-wise my body can regulate me back into depression.
I know what ya'll said about 3 and 10, and I guess an infinite number of possible interactions of all neurotransmitters et.al., and I don't know that Serotonin is one of the baddies for me. But, I sort of think my theory could be true (if it were Serotonin). That would at least explain my poop-out experiences.
Are people measuring the amounts of Serotonin, Dopamine, etc. in the brain?
(I know how scientists love theories based on anecdotal evidence with an n=1.)
Shar
Posted by SLS on June 11, 2000, at 8:03:09
In reply to Re: Incomplete recovery gaining attention SLS, posted by JohnL on June 10, 2000, at 18:16:18
Spelling correction:
glutaminergic => glutamatergic
John - You'll find another good explation of some of the glutamate-GABA related effects of Provigil in the thread above:Re: Provigil poop out; klonopin counteracts provigil?
Glutamate and aspartate are two major excitatory neurotransmitters in the brain. Glycine is a major inhibitory neurotransmitter.
I'm sorry that Provigil doesn't seem to be doing the job for you.
- Scott
Posted by Johnturner77 on June 12, 2000, at 13:52:38
In reply to Re: Spelling correction » JohnL , posted by SLS on June 11, 2000, at 8:03:09
SSRI's cause(in me)among other things a kind of mellow sense of well being that is not the same as happiness or certain other senses(sensations) of well being. It is not connected with hope or drive. It is only indirectly connected with pleasure. Rebound causes an irritability that makes me say to myself, hmmm, this must be the depression that SSRI's are designed to treat. Sometimes I wish that I had a vocabulary to describe subjective internal states sufficiently. Perhaps a really wierd set of diagnostic questions might prove illuminating.
Does this medication make you feel like you were surrounded by a wool blanket or warm satin sheets? Do you feel like there is a wall of mud brick surrounding you or glass? Do voices make you feel like you are balancing on a vibrating knife blade or like messages being passed through a key hole?
What sort of metaphors come to mind for you? What new metaphors do your medications bring into your experience? Instead of a pDoc I want a drug experimenting poet! 8>)
What I am looking for is appropriateness and flexibility. I don't want to be limited by my brain or drugs to certain states of being. If I ever end of in a concentration camp(or a job :-) ) I want to be able to control my states sufficiently to be able to find happiness in little things even if the big picture sucks all the courage out of me.
Posted by KarenB on June 13, 2000, at 11:54:05
In reply to Re: Incomplete recovery gaining attention, posted by SLS on June 10, 2000, at 9:39:52
> Perhaps low serotonin is never the cause.You may be right...
> Perhaps dopaminergic drugs make a good bandage to compensate for the underactivity of glutaminergic neurons afferent to the thalamus and hippocampus that have been downregulated due to their chronic overactivity in response to stress. This would allow for a perturbation of the balance between glutaminergic and GABAergic activity there in favor of efferent GABAergic neurons leading to the nucleus accumbens, whereby dopaminergic neurotransmission in this healthy structure is thus inhibited. What do you think?
I think I want a new brain.
By the way, you may remember that Amineptine combined with Sulpiride worked best for me. I'm trying to find alternatives here, stateside. Right now, it's Adderall and Buspar - OK but not totally there yet. I'm going to trial Modafinil starting next week - I have faxed info to doc (he knoweth not the med) and if he won't let me trial it, I go elsewhere. Adderall has me clenching my jaws by afternoon - but, at least I have energy. Like I said, OK but not great...
In your opinion, does the Amineptine/Sulpiride success indicate dopamine depletion? What up with the glutaminergic thing? Is it possible that GABA supplementation could help in a case like this or am I way off base?
Hope you are doing well.
karen
Posted by glenn on June 13, 2000, at 13:08:41
In reply to Re: Incomplete recovery - SLS, posted by KarenB on June 13, 2000, at 11:54:05
>
> > Perhaps low serotonin is never the cause.
>
> You may be right...
>
> > Perhaps dopaminergic drugs make a good bandage to compensate for the underactivity of glutaminergic neurons afferent to the thalamus and hippocampus that have been downregulated due to their chronic overactivity in response to stress. This would allow for a perturbation of the balance between glutaminergic and GABAergic activity there in favor of efferent GABAergic neurons leading to the nucleus accumbens, whereby dopaminergic neurotransmission in this healthy structure is thus inhibited. What do you think?
>
> I think I want a new brain.
>
> By the way, you may remember that Amineptine combined with Sulpiride worked best for me. I'm trying to find alternatives here, stateside. Right now, it's Adderall and Buspar - OK but not totally there yet. I'm going to trial Modafinil starting next week - I have faxed info to doc (he knoweth not the med) and if he won't let me trial it, I go elsewhere. Adderall has me clenching my jaws by afternoon - but, at least I have energy. Like I said, OK but not great...
>
> In your opinion, does the Amineptine/Sulpiride success indicate dopamine depletion? What up with the glutaminergic thing? Is it possible that GABA supplementation could help in a case like this or am I way off base?
>
> Hope you are doing well.
>
> karen
>
>
i have found a shrink who thinks it may be excess serotonin, Robert Cloninger, he calls it serotonin jangling! so how do ssris work? in his opinion by eventually forcing downregulation of serotonin receptors, an interestnig idea
Posted by KarenB on June 13, 2000, at 13:58:57
In reply to Re: Incomplete recovery - SLS, posted by glenn on June 13, 2000, at 13:08:41
> i have found a shrink who thinks it may be excess serotonin, Robert Cloninger, he calls it serotonin jangling! so how do ssris work? in his opinion by eventually forcing downregulation of serotonin receptors, an interestnig idea
According to some literature I read, this is how Buspar controls anxiety - that anxiety is actually caused by overdosing on your own Serotonin, for whatever reasons that may happen. I am sure there are plenty of theories on this as well. I do know that increasing Serotonin levels has never "helped" me in any way.Karen
Posted by AndrewB on June 13, 2000, at 14:21:00
In reply to Re: Incomplete recovery - SLS, posted by KarenB on June 13, 2000, at 11:54:05
Karen,
Sounds like Provigil could work better for you.
If you want, next time I order from India, I can order you some sulpiride. It will save you shipping charges. I think they sell it dirt cheap.
AndrewB
Posted by KarenB on June 13, 2000, at 23:34:15
In reply to Re: Karen, posted by AndrewB on June 13, 2000, at 14:21:00
> Karen,
>
> Sounds like Provigil could work better for you.
>
> If you want, next time I order from India, I can order you some sulpiride. It will save you shipping charges. I think they sell it dirt cheap.
>
> AndrewBHey, that's really thoughtful, Andrew. Let me think about it, though, and I'll let you know. Those extra 5-10lbs added previously by the Sulpiride are certainly not being missed:)
I'll try the Provigil first and see what happens. Thanks for the offer - I may take you up on that.
Karen
Posted by SLS on June 14, 2000, at 7:46:02
In reply to Re: Incomplete recovery - SLS, posted by glenn on June 13, 2000, at 13:08:41
> >
> i have found a shrink who thinks it may be excess serotonin, Robert Cloninger, he calls it serotonin jangling! so how do ssris work? in his opinion by eventually forcing downregulation of serotonin receptors, an interestnig ideaYes. Yes. Yes.
- Scott
Posted by SLS on June 14, 2000, at 8:56:47
In reply to Re: Incomplete recovery - SLS, posted by KarenB on June 13, 2000, at 11:54:05
Dear Karen,
Hi.
> > Perhaps low serotonin is never the cause.> You may be right...
> > Perhaps dopaminergic drugs make a good bandage to compensate for the underactivity of GLUTAMATERGIC neurons afferent to the thalamus and hippocampus that have been downregulated due to their chronic overactivity in response to stress. This would allow for a perturbation of the balance between GLUTAMATERGIC and GABAergic activity there in favor of efferent GABAergic neurons leading to the nucleus accumbens, whereby dopaminergic neurotransmission in this healthy structure is thus inhibited. What do you think?
> I think I want a new brain.
Take a number.
> By the way, you may remember that Amineptine combined with Sulpiride worked best for me. I'm trying to find alternatives here, stateside. Right now, it's Adderall and Buspar - OK but not totally there yet. I'm going to trial Modafinil starting next week - I have faxed info to doc (he knoweth not the med) and if he won't let me trial it, I go elsewhere. Adderall has me clenching my jaws by afternoon - but, at least I have energy. Like I said, OK but not great...
Again, I consider the combination of sulpiride/amisulpride with amineptine to be one of the most well conceived strategies I have come across. As far as what to use as a replacement for amineptine, I have given it some thought, but haven't come up with much. I have mentioned to a few doctors a drug called mazindol (Mazinor, Sanorex) as a candidate to fill this role. to a few doctors, but it I did not receive any feedback. I doubt it has been considered as a potential augmenting agent, at least not in the last 15 years. Like amineptine, it is a reuptake inhibitor of both dopamine and norepinephrine without promoting the release of either.
I am beginning to wonder if combining Serzone with a dopaminergic drug may be particularly effective. I may consider trying it before heading back to Parnate. Have you ever tried Serzone alone or in combination with anything? It might go well with sulpiride - sort of like a more selective Zyprexa. Anyway, it looks good to me on paper (or a webpage).
Modafinil (Provigil) or Adrafinil (Olmifon) look to be interesting drugs that might provide utility as adjunctive or augmenting drugs. As can be seen from JohnL's experience it seems to go quite well with amisulpride.
This evening, I hope to be able to send a FAX to London and place an order for sulpiride. My doctor consulted with a colleague in NYC who has had a great deal of experience with sulpiride. It is his opinion that sulpiride is superior to amisulpride for treating depression. I'm not happy to hear about the weigh-gain thing, but 10 pounds is not an unreasonable price to pay for my resurrection. Interestingly, this doctor stated that one either responds early or doesn't respond at all. From what I can see here, that seems to hold true, as some people experience little more than profound sedation with no antidepressant response to be later obtained.
>
> In your opinion, does the Amineptine/Sulpiride success indicate dopamine depletion?It sure sounds like a logical possibility. It may be that there is a reduced rate of synthesis of dopamine within the presynaptic neuron. The gas tank is always near empty. Sulpiride and amisulpride tell the neuron to assemble more dopamine molecules. It also tells it to release more of them when it is asked to. MAO inhibitors tell the neuron not to waste any dopamine molecules by preventing it from disassembling them. Amineptine tells the neuron to leave the released molecules outside and not let them back in. This allows the released dopamine to accumulate near the postsynaptic neuron and stimulates it to fire, sending the message on the the next one.
> What up with the glutaminergic thing?
I'm not sure. I was just guessing about the stress thing.
I'm sorry that I misspelled the word. It should be "glutamatergic" derived from the name of the excitatory neurotransmitter, glutamate.
Scientists seem pretty confident that Provigil causes the levels of glutamate outside the cell to increase, possibly by promoting its release. This seems to turn-off the GABA neurons. GABA neurons tell dopamine neurons to "shut-up". Now these dopaminergic neurons are allowed to talk more.
Provigil => More glutamate => Less GABA => More talkative dopamine neurons.
It is unclear whether or not Provigil affects norepinephrine directly.
Lamictal may do just the opposite. It may decrease the release of glutamate, allowing GABA neurons to tell overly-talkative dopamine neurons to quiet down. Perhaps this is why Lamictal can quiet overly-talkative people who are in a manic state.
Lamictal => Less glutamate => More GABA => Less talkative dopamine neurons. (possibly)
Some of the other anticonvulsant mood stabilizers also seem to increase GABA activity, although through other mechanisms.
GABA is a neurotransmitter that generally helps to prevent areas of the brain from getting overly excited. It helps quiet many different types of neurons in addition to dopaminergic ones.
> Is it possible that GABA supplementation could help in a case like this or am I way off base?
I didn't know there were GABA supplements. I don't know enough about it to comment.
Good thinking, though.
> Hope you are doing well.
I'm not, but thank you so much for asking.
- Scott
Posted by AndrewB on June 14, 2000, at 11:12:28
In reply to Re: Incomplete recovery - SLS » KarenB, posted by SLS on June 14, 2000, at 8:56:47
Bowl me over Scott. That information on sulpiride is so interesting. It sounds like you have a great psychiatrist working with you. Do you have any other information on sulpiride that he passed along to you. I'd like to know more. more, more.
Scott, clutch your lucky rabbit’s foot and hope that you are in the group that responds to sulpiride. I'm, as always, am hoping that the gods stop their conspiracy against you and, instead, let a shaft of ‘positive response to pharmacological therapy’ shine down upon you.
Scott, on another topic, I think it is clear that some of the positive action of dopaminergic drugs is due to upregulation of portions of the dopamine system and nothing more. A person apathetic from a stroke that damaged his frontl lobe is helped by the dopaminergic amantadine. The person with fatigue and poor concentration due to a strain of viral encephalitis that produced lesions upon his dopaminergic system is helped by bromcriptine. Isn’t it clear that certain aspects of anxiety, reward, motivation and mood lie within the limbic system and are modulated, at least in part, by D2/D3 receptors, and that damage to those parts of the brain or dysfunction of those receptors are the ultimate physiological cause of some mood and anxiety (and other) symptoms. We don’t have to always looks farther afield and say that the positive effect of a dopaminergic drug is due ultimately to modification of the HPA axis or some kind of masking effect upon that axis. Stress doesn’t just modify and damage the HPA axis. The effects of stress are global. For a better understanding of how stress in our lives can modify the dopaminergic system read the paper entitled, The role of stress in the pathophysiology of the dopaminergic system.’
(www.stockton-press.co.uk/server-java/Propub/stockton/spmp_v5_n1_p14_o1.fulltext)
Your serve Scott!Karen, I wanted to let you know about a paper on the net that talks about ADHD and drug treatment for it. It is very interesting. The author believes that ADHD is of dopaminergic origin as evidenced by his findings that selegiline and tyrosine, which both act solely on the dopamine system, were as effective as amphetamines on ADHD. This certainly would explain amineptine’s effectiveness for you. (BTW, I disagree with Scott that amineptine is a reuptake inhibtor of NE. It only is a reuptake inhibitor of dopamine. I think Peter J made it clear that there is an NE effect from amineptine but it is from some other mechanism than reuptake.......and how significant is it anyway?) You can find this paper at www.mhsource.com/pt/p960741.html
I wonder how a COMT inhibitor combined with selegiline would work for ADHD?
One final note. There is case reported where a women lost her menses due to sulpiride. When given bromocriptine, the menses returned. I presume this is due to bromocriptine’s ability to reverse the elavated prolactin level that sulpiride causes in women. From what I’ve read, the weight gain is also due to elevated prolactin levels and, thus, should be prevented by the tandem use of bromocriptine with one’s sulpiride. Bromocriptine is also available from that Indian pharmacy.
Scott, I tried l-dopa with entacapone and selegiline. Seemed to give me a very good arousal, but it’s just one day and my first impressions are often way of base. Problem is that l-dopa does, as the amisulpride’s label instructions warned, contradict (or take away) the action of amisulpride and thus cause the return of depression and related symptoms. I don’t know what I’ll do next. Probably I’ll take the l-dopa combo again and see if the same thing happens. Considering Tasmar, the other, stronger COMT.
AndrewB
Posted by SLS on June 14, 2000, at 14:43:38
In reply to Scott and Karen: Sulpiride, ADHD, etc., posted by AndrewB on June 14, 2000, at 11:12:28
> Karen, I wanted to let you know about a paper on the net that talks about ADHD and drug treatment for it. It is very interesting. The author believes that ADHD is of dopaminergic origin as evidenced by his findings that selegiline and tyrosine, which both act solely on the dopamine system, were as effective as amphetamines on ADHD. This certainly would explain amineptine’s effectiveness for you. (BTW, I disagree with Scott that amineptine is a reuptake inhibtor of NE. It only is a reuptake inhibitor of dopamine. I think Peter J made it clear that there is an NE effect from amineptine but it is from some other mechanism than reuptake.......and how significant is it anyway?) You can find this paper at www.mhsource.com/pt/p960741.html
Thanks for the citations, Andrew. I smiled when I read the comments regarding glutamate and stress. That was one hell of a lucky guess. Perhaps I have something here. It will take me some time to review the whole article. I'm feeling like crap.It's ashame that amineptine had to go away. It may not have been the best antidepressant in the world, but it was a good tool. I hope it makes a reappearance. Ritalin is also a potent DA reuptake inhibitor. Have you ever tried combining it with amisulpride?
> Scott, I tried l-dopa with entacapone and selegiline. Seemed to give me a very good arousal, but it’s just one day and my first impressions are often way of base. Problem is that l-dopa does, as the amisulpride’s label instructions warned, contradict (or take away) the action of amisulpride and thus cause the return of depression and related symptoms.
I have a hard time imagining that l-dopa can displace amisulpride from PREsynaptic receptors, thereby reducing its antidepressant effects. Perhaps they were referring to amisulpride's antipsychotic effects. I would guess that this is the case.
I think amisulpride is sold under the trade name Deniban in Italy. I'm pretty sure its official indication is for depression, and it is sold in 50mg doses. Trivia.
> I don’t know what I’ll do next. Probably I’ll take the l-dopa combo again and see if the same thing happens. Considering Tasmar, the other, stronger COMT.
Is Tasmar due to be withdrawn from the US market? I know it has been withdrawn in several countries. How are you supposed to go about monitoring liver function?
- Scott
This is the end of the thread.
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