![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
[email protected]Shown: posts 14 to 38 of 43. Go back in thread:
Posted by Phillipa on January 17, 2006, at 19:16:17
In reply to Re: Which ADs increase DOPAMINE -- Wellbutrin » luca1975, posted by yxibow on January 17, 2006, at 19:11:55
Wellbutrin signigicantly incresed anxiety for me. Fondly, Phillipa
Posted by willyee on January 17, 2006, at 19:49:57
In reply to Re: Which ADs increase DOPAMINE the most?, posted by luca1975 on January 17, 2006, at 17:36:41
Dont think its exgareated.......from reading it seems certain people simply respond to wellburtin postivly.......and for a good number it cause severe anxiety.......who which again shows us were so off with our LOW SEROTIONION excuse my depression......who knows what is really going on,possable the cause of depression varies chemicaly in form from individual to invidual.
Posted by blueberry on January 17, 2006, at 21:32:01
In reply to Re: Which ADs increase DOPAMINE the most?, posted by qbsbrown on January 17, 2006, at 17:11:47
St Johns Wort. I mean, since you asked for the top three, that would be my first choice. But, understand everyone will have a different opinion.
I'm thinking dopamine...st johns wort is strong on that. It affects serotonin, norepinephrine, dopamine, gaba, and glutamate all with about equal affinity. Very balanced. Of the 30 or so meds I've been on over the years, nothing ever came close to being as good as SJW for me.
I'm thinking side effects, especially sexual...st johns wort usually does not have sexual side effects and often increases sex drive due to lowering of prolactin levels. Other side effects such as possible tiredness, restlessness, insomnia, or gastrointestinal discomfort are usually mild and go away within two weeks, and are nothing compared to medications.
Sure I could come up with some med choices too. But why? SJW has everything you are looking for, it is cheap, far easier on side effects, and it has the same likelihood of working as any of the meds.
Posted by shasling on January 17, 2006, at 23:16:54
In reply to Re: Which ADs increase DOPAMINE -- Wellbutrin, posted by Phillipa on January 17, 2006, at 19:16:17
> Wellbutrin signigicantly incresed anxiety for me. Fondly, Phillipa
Made me want to kill people. Other posts as well of people who developed rage in response to it. Wellbutrin.Might want to read up on Pergilode. Purely a dopamine agonist, and I recently read a study that said it tends to work very well at improving dopamine-dependent responses when taken with "another AD". If taken alone, not much response, but with an AD it does. I thought that curious... Seems worth looking into.
Posted by yxibow on January 18, 2006, at 0:24:31
In reply to Re: Which ADs increase DOPAMINE -- Wellbutrin, posted by shasling on January 17, 2006, at 23:16:54
Do remember that Pergolide is an ergot derived anti-Parkinsonism that targets D1 and D2 and anyone who may have the signs of psychosis probably should be precautious of it as it is one the two most common (3:1) side effects. The other is dyskinesia.
Posted by redscarlet on January 18, 2006, at 8:12:15
In reply to Re: Which ADs increase DOPAMINE -- Wellbutrin, posted by shasling on January 17, 2006, at 23:16:54
I too developed rage in response to Wellbutrin (not like me).
It took a long time for me to find out what was causing it but I will not take that stuff again.
Posted by shasling on January 18, 2006, at 11:39:35
In reply to Re: Which ADs increase DOPAMINE -- Wellbutrin » shasling, posted by yxibow on January 18, 2006, at 0:24:31
> Do remember that Pergolide is an ergot derived anti-Parkinsonism that targets D1 and D2 and anyone who may have the signs of psychosis probably should be precautious of it as it is one the two most common (3:1) side effects. The other is dyskinesia.
True, as with any efforts to affect a blanket increase in dopamine...
In fact, even if one has no existing signs of psychosis, tampering with dopamine can precipitate them.
Posted by idolamine on January 18, 2006, at 16:03:59
In reply to Which ADs increase DOPAMINE the most?, posted by qbsbrown on January 16, 2006, at 22:47:22
I read that wellbutrin preferentially blocks the reuptake or norepi, and not dopamine very much. Amineptine would do this. idolamine.
Posted by jerrympls on January 18, 2006, at 19:16:38
In reply to Re: Which ADs increase DOPAMINE the most?, posted by blueberry on January 17, 2006, at 5:08:47
The big problem is trying to get a doctor to prescribe something that increases release and/or synthesis of dopamine. Many docs won't do anything with a med if it's off-lable - which is sad because there are so many meds out there that, when used off-lable, could help those with hard to treat depression.
jerry
pharmacy student
Posted by cache-monkey on January 18, 2006, at 19:50:41
In reply to Re: Which ADs increase DOPAMINE the most?, posted by idolamine on January 18, 2006, at 16:03:59
Based on my experience and from what I've read here Wellbutrin can raise anxiety in a large class of people. Particularly those with a pre-existing anxiety condition. My experience parallels yxibow's: I had a huge increase in anxiety, leading to obsessive thinking way beyond my norm. Twas great for the libido and sexual function, though...
I think this has to do with the fact that when you take into account the total effect of Wellbutrin and its metabolizes, the impact is much stronger on NE reuptake than DA.
I would think that low-dose selegiline, with or without precursors, would be more preferential towards DA. At least that's my hope!
Good luck,
cache-monkey
Posted by djmmm on January 18, 2006, at 21:53:50
In reply to Re: Which ADs increase DOPAMINE the most?, posted by jerrympls on January 18, 2006, at 19:16:38
tianeptine (Stablon) can be legally purchased from many "smart-drug" and "antiaging" websites... Im not going to list the specific sites here...but Google will help.
Posted by shasling on January 18, 2006, at 23:21:33
In reply to Re: Which ADs increase DOPAMINE the most?, posted by djmmm on January 18, 2006, at 21:53:50
> tianeptine (Stablon) can be legally purchased from many "smart-drug" and "antiaging" websites... Im not going to list the specific sites here...but Google will help.
Is Stablon good? Have you taken it?Thanks
Posted by SLS on January 20, 2006, at 6:57:53
In reply to Re: Which ADs increase DOPAMINE the most?, posted by linkadge on January 17, 2006, at 12:59:41
Hi Linkadge,
You are right (as usual)
> Thats a good question, and I don't know the answer. Two hypothesis would be the following:
>
> 1. Nardil has an effect on gaba metabolism. Gaba
> asserts an inhibitory controll over
> dopaminergic synapses.
In a normally functioning human brain, this is mostly true. However, it may be that some of us are wired a little differently such that GABA acts, through disinhibition, to increase the synthesis and release of dopamine or even opioids in a way similar to how some people react to alcohol or benzodiazepines. A minority of people become stimulated, aggressive, and hypersexual with these pro-GABAergic drugs.
> 2. Parnate is structurally related to
> amphetamine, (although it is debated as
> to whether parnate posesses any stimulant-like
> effect on dopamine release). There are case
> reports of Parnate abuse, whereas I don't know of any for Nardil.
When I was more vulnerable to self-medication, I tended to abuse Nardil more than Parnate because I found it gave me a reward kick shortly after taking it. Parnate has always left me with a persistent anhedonia which Nardil abolished when it worked.The problem is this: I often see people here advise the choice of Parnate over Nardil when one is concerned about an imagined dopamine deficit syndrome. Yet, there is really nothing to their conceptualization of Parnate as being dopaminergic other than a vague notion of it having stimulant-like properties. As you point out, such properties represent a transient increase in the release and inhibition of reuptake of dopamine (and norepinephrine!). Yet, there is usually no mention of the tendency of this kind of chronic exposure to stimulants to produce depletions of DA stores rather than their replenishment. Another consideration is that a dose of Parnate is in and out of the body in 1-2 hours. (I don't know about its metabolites). If its effectiveness were dependent on the ability of Parnate to release DA, People would have to take it every 2 hours, or the antidepressant effect would not persist. But of course, it does. I believe that any DA release that Parnate might produce is not contributory to its efficacy as an antidepressant. If this were true, adding amphetamine to Nardil should be ubiquitously and immensely effective. To the best of my knowledge, it is not.
How do people know that they need dopamine in the first place?
Is a deficit in dopaminergic neural activity in reward and motivational centers of the brain the result of or the cause of depression? It does seem to be that the final pathways to the expression of depression are dopaminergic, but what has people so convinced that this is the primary site of pathology rather than a secondary downstream consequence of this pathology?
- Scott
Posted by linkadge on January 20, 2006, at 10:19:26
In reply to Re: Which ADs increase DOPAMINE the most? » linkadge, posted by SLS on January 20, 2006, at 6:57:53
All very good points. I think that the rate of MAOI induced psychosis is similar between both Nardil and Parnate, (if that is any indication of the overall increase in dopaminergic neurotransmission)
And yes, if parante is a stimulant, then it might contribute to dopamine depletion.
I don't know if any direct tests have been done to compare nardil and parnate in their ability to affect dopaminergic neurotransmission.
>How do people know that they need dopamine in >the first place?That is a good question. I don't mean to cause any disrespect, but I don't understand how people come to the conclusion. I suppose it is usually because SSRI's don't work for them. Anhedonia is not strictly indicitive of abnormal dopamine signalling. It would not be a problem if it were a benign assumption.
Anhedonia is generally a symptom of all types of depression, and has been effectively treated by antidepressants of many different classes.
The MSS4 gene has been implicated in anhedonia. When rats are stressed, they become anhedonic, and MSS4 drops. Both SSRI's and TCAs increase the MSS4 gene in the hippocampus.
MSS4 is thought to controll the excitability of limbic circutry.
I personally think that anhedonia is a sign of atrophy to certain hippocampal regions, people who are anhedonic can't even remember what is/was pleasurable.
But you are very right. We tend to assume things based on the *presumed* biochemical actions of a drug.
Linkadge
Posted by shasling on January 20, 2006, at 11:09:45
In reply to Re: Which ADs increase DOPAMINE the most? » SLS, posted by linkadge on January 20, 2006, at 10:19:26
> All very good points. I think that the rate of MAOI induced psychosis is similar between both Nardil and Parnate, (if that is any indication of the overall increase in dopaminergic neurotransmission)
>
> And yes, if parante is a stimulant, then it might contribute to dopamine depletion.
>
> I don't know if any direct tests have been done to compare nardil and parnate in their ability to affect dopaminergic neurotransmission.
>
>
> >How do people know that they need dopamine in >the first place?
>
> That is a good question. I don't mean to cause any disrespect, but I don't understand how people come to the conclusion. I suppose it is usually because SSRI's don't work for them. Anhedonia is not strictly indicitive of abnormal dopamine signalling. It would not be a problem if it were a benign assumption.
>
> Anhedonia is generally a symptom of all types of depression, and has been effectively treated by antidepressants of many different classes.
>
> The MSS4 gene has been implicated in anhedonia. When rats are stressed, they become anhedonic, and MSS4 drops. Both SSRI's and TCAs increase the MSS4 gene in the hippocampus.
>
> MSS4 is thought to controll the excitability of limbic circutry.
>
> I personally think that anhedonia is a sign of atrophy to certain hippocampal regions, people who are anhedonic can't even remember what is/was pleasurable.
>
> But you are very right. We tend to assume things based on the *presumed* biochemical actions of a drug.
>
>
> Linkadge
>
>
> Guys, the short answer for me is that it is a complete lack of volition that causes me to lean in that direction. As well as the fact that serotonin tx does absolutely nothing, noradren/norepi tx makes my body go and causes me to run around, electrically, almost frantically just doing things, but there's still something very much missing; and I'm doing things sort of because I have to at the mercy of the adrenaline. On the correct dopaminergic, however, I have more energy, but it isn't based simply on my body being driven. I have energy because I find interest in things. The change feels very much like what I imagine 'normal' must be, rather than electric, and I have a reasonable amount of volition, initiative and reward. During the small window when Abilify (which only affects dopamine) was working for me, I finally felt absolutely normal, calm, productive and capable of doing everyday things; and I took care of everyday things because I *wanted* to, not because I *had* to, as is the feeling on noradr/norepi. Unfortunately, it later made me crazy and I had to stop taking it but that is beside the point...That having been said, and really with all due respect because you all do some really informed and helpful posts, I am disappointed that anyone who doesn't know those of us who have identified dopamine as our probable issue (and really who knows us better than us?) would question and/or discount that. I mean, we've all had enough of that from doctors and family members, etc. and it is never helpful and always degrading to be discounted in that way. That was one thing I immediately noticed about this site was that one's credibility about one's own condition was assumed, and that was such a gift. I am surprised and disappointed to find that kind of thing here, which had previously seemed like an unconditionally safe place where my knowledge of me would not be discounted by someone who 'knew' better.
>
>Suzie
>
>
>
>
>
>
>
>
Posted by Declan on January 20, 2006, at 11:37:30
In reply to Re: Which ADs increase DOPAMINE -- Wellbutrin » luca1975, posted by yxibow on January 17, 2006, at 19:11:55
Hi Yxibow
In my experience Khat is a LOT less awful than Tenuate. Khat is actually nice. I chewed the leaves.
Declan
Posted by linkadge on January 20, 2006, at 11:50:12
In reply to Re: Which ADs increase DOPAMINE the most?, posted by shasling on January 20, 2006, at 11:09:45
I'm not trying to degrade your intuition. I too fared poorly on SSRI's.
For staters, abilify is a multaple monoaminergic agonist and antagonist. You've got some pretty potenet serotonin receptor 5-ht1a agonism with this drug. Serotonin 1a agonists are usually active in most lines of depression, but they are not dopaminergics per-se. You've also got some strong 5-ht2a receptor antagonism. Serotonin 2a antagonists can reduce stress' effect on BDNF.
So, in my oppinion, the combination of these two non-dopaminergic effects could account for a good majority of the antidepressant effects of this drug.Abilify is also a very strong dopamine antagonist, at certain receptors.
>I am disappointed that anyone who doesn't know >those of us who have identified dopamine as our >probable issue (and really who knows us better >than us?)Just because a drug works doesn't mean thats what the deficiancy was. Stimulants can improve a subset of depressions very rapidly, if only temporarily. But not everybody who has mood improvement on a stimulant was dopamine deficiant.
>would question and/or discount that. I mean, >we've all had enough of that from doctors and >family members, etc. and it is never helpful and >always degrading to be discounted in that way.
Its nice to fit things into boxes, but I just don't think the brain works that way. I would say the same thing to somebody with schitsophrenia. The dopamine theory of schitsophrenia is just one theory. Just because an antipsychotic works doesn't mean it is getting to the root of the problem. There are other theories of schitohprenia too.
>That was one thing I immediately noticed about >this site was that one's credibility about one's >own condition was assumed, and that was such a >gift. I am surprised and disappointed to find >that kind of thing here, which had previously >seemed like an unconditionally safe place where >my knowledge of me would not be discounted by >someone who 'knew' better.I am not trying to discount or discretit anyones condition by any means. All I am saying is that the most brilliant researchers on this earth have not yet been able to pinpoint what exactly dysfunctional in mood disorders. So while experience with a certain drug might be indicitive of something, it does not conclude anything.
The problem with dopaminergics is that they can activate the pleasure centeres of the brain directly. That prompt relief can lead people to make incorrect conclusions. To anyone with chronic pain, an opiate seems to fix a deficiancy in something, but we know it is not getting to the root of the problem by any means.
Linkadge
Posted by shasling on January 20, 2006, at 13:36:12
In reply to Re: Which ADs increase DOPAMINE the most?, posted by linkadge on January 20, 2006, at 11:50:12
Just so that I understand the position, there is no such thing as dopamine deficiency, or just no such thing as it having an effect on one's sense of volition, reward, etc.?
For the record,I am aware that Abilify acts as an antagonist on one set of receptors and an agonist on another. Although I am not a chemist nor a doctor, what do I have - and no one else does - is the totality of my experience, spanning 25 years and close to as many meds, struggling for relief. And other circumstances not necessary to go into here in that it is unnecessary to convince anyone of what my opinion is, it being an opinion, and being mine. What you have is an opinion as well, and you are certainly entitled to it. I'm just saying it seems unnecessary and perhaps destructive to issue blanket opinions that certain theories that others may have here are invalid. Now, you may be right, of course, but don't we deserve to come to that on our own? I mean, we are all here trying to figure out why we are depressed/whatever and it won't get better. I don't know what your particular condition is, but if a discussion ensued wherein your condition was alleged to be invalid - thus implying you may think you know what is going on with your own condition, but you are really clueless - might it not invalidate you and thus sort of hurt?
The beliefs I have come to are not impacted by the statements that were made, and I feel no need to convince anyone else of them; I just said I was disappointed by blanket opinions of the invalidity of things that others here are trying to work through.
Again, with all due respect...
Posted by linkadge on January 20, 2006, at 14:51:20
In reply to Re: Which ADs increase DOPAMINE the most? » linkadge, posted by shasling on January 20, 2006, at 13:36:12
>Just so that I understand the position, there is >no such thing as dopamine deficiency, or just no >such thing as it having an effect on one's sense >of volition, reward, etc.?
I never said either. I just questioned under what pretenses one is able to discern what exactly the problem is. For instance, if you are basing your assumption that you have a dopamine deficancy based on sucess with abilify, then that would not be correct in my oppinion.
Additionally, I am arguing that mood responce to stimulants is by no means indicitive of a dopamine deficancy.
>For the record,I am aware that Abilify acts as >an antagonist on one set of receptors and an >agonist on another. Although I am not a chemist >nor a doctor, what do I have - and no one else >does - is the totality of my experience, >spanning 25 years and close to as many meds, >struggling for relief. And other circumstances ?>not necessary to go into here in that it is >unnecessary to convince anyone of what my opinion is, it being an opinion, and being mine.You don't need to convince me. I never asked that.
>What you have is an opinion as well, and you are >certainly entitled to it. I'm just saying it >seems unnecessary and perhaps destructive to >issue blanket opinions that certain theories >that others may have here are invalid.
I am not saying that your experiences may not lead you to more appropriate treatment. I am just saying that we don't really have enough diagnostic tools to make that exact conclusion.
For instance, if somebody said to me that they must be dopamine deficiant because wellbutrin worked, then that too may be misuided due to that fact that wellbutrin may have more effect on norepinephrine than dopamine.
We only really had one pure dopaminergic antidepressant which was amineptine. So I am just wondering what leads people to this conclusion, thats all.
>Now, you may be right, of course, but don't we >deserve to come to that on our own? I mean, we >are all here trying to figure out why we are >depressed/whatever and it won't get better. I >don't know what your particular condition is, >but if a discussion ensued wherein your >condition was alleged to be invalid - thus >implying you may think you know what is going on >with your own condition, but you are really >clueless - might it not invalidate you and thus >sort of hurt?I restate that I never claimed that your condition was invalid. I was simply wondering how you reached the conclusion that your condition was solely due to a deficiancy in dopamine. Allong the same lines, I might argue that a responce to SSRI's is not necessarily indicitive of serotonin deficiancy. (All the currently available SSRI's have other targets such as SIG-1R, Allopregnalone etc) If somebody was deficiant in serotonin, we would expect them to respond to any SSRI, but we know that is not the case. There are many reasons why I would question people's conclusions. I am not saying they are wrong, I am just questioning their conclusions.
>The beliefs I have come to are not impacted by >the statements that were made, and I feel no >need to convince anyone else of them; I just >said I was disappointed by blanket opinions of >the invalidity of things that others here are >trying to work through.I did not intend you to stop doing what helps you the most. This board is full of many different opinions.
Linkadge
Posted by SLS on January 20, 2006, at 15:10:33
In reply to Re: Which ADs increase DOPAMINE the most? » SLS, posted by linkadge on January 20, 2006, at 10:19:26
Hi Link.
> The MSS4 gene has been implicated in anhedonia.
What is MSS4?
Thanks.
- Scott
Posted by shasling on January 20, 2006, at 15:14:49
In reply to Re: Which ADs increase DOPAMINE the most?, posted by linkadge on January 20, 2006, at 14:51:20
Okay, fair enough. Thanks for the debate.
And with respect to:
"I am just saying that we don't really have enough diagnostic tools to make that exact conclusion."
I agree completely, and therein lies the problem. It leaves us in the dark, grasping at straws and adopting various methods in the struggle to unlock just what is the mystery that causes us to suffer; working through anything we can think of to find relief. In a better world we wouldn't have to do that.
We can still find things to agree on : )
Suzie
Posted by linkadge on January 20, 2006, at 15:36:14
In reply to Re: Which ADs increase DOPAMINE the most? » linkadge, posted by SLS on January 20, 2006, at 15:10:33
Don't know a whole lot about it. Have just read a few abstacts. It seemed like another interesting target.
http://molpharm.aspetjournals.org/cgi/content/full/62/6/1332
Linkadge
Posted by SLS on January 20, 2006, at 15:40:32
In reply to Re: Which ADs increase DOPAMINE the most?, posted by shasling on January 20, 2006, at 11:09:45
Hi Suzie.
I came to believe that dopamine was the key to all of my problems in 1983 once my first tribe of doctors at Columbia Presbyterian gave up on treating me pharmacologically. I have been through the self-education and brainstorming theorization process for over 20 years without any formal education. Big deal. I have been employed by two psychopharmacologists as a research assistant. Big deal. I have been a research patient at the NIMH and was one of the first people whose brains were imaged using positron emission tomography. Big deal. While there, I encountered a few more MD and PhD brains to pick. I remain in contact with them today. Big deal.
I first began chasing bupropion and nomifensine in 1983. Both were touted as being dopamine reuptake inhibitors, and it was hypothesized that this was the mechanism that bestowed upon them their antidepressant properties. As of today, these drugs are more poorly understood than they were 20 years ago. The same goes for lithium after 60 years. The more we learn, the more we realize how little we understand. What I have learned, I thought I might share with others: We don't know sh*t. We certainly don't know enough about the biology of psychiatric disorders to deduce an exclusionary role of one neurotransmitter over another, whether it be to explain the etiology of the pathology or the treatment of the disorder. To realize this is, I believe, enhances our chances of getting well. It demands that we keep open minds to the many treatments that are emerging in the nursery of neuroscience and prevents our uneducated pretension of understanding from becoming our own impediment to success. This is as true for doctors as it is for patients.
- Scott> > Guys, the short answer for me is that it is a complete lack of volition that causes me to lean in that direction. As well as the fact that serotonin tx does absolutely nothing, noradren/norepi tx makes my body go and causes me to run around, electrically, almost frantically just doing things, but there's still something very much missing; and I'm doing things sort of because I have to at the mercy of the adrenaline. On the correct dopaminergic, however, I have more energy, but it isn't based simply on my body being driven. I have energy because I find interest in things. The change feels very much like what I imagine 'normal' must be, rather than electric, and I have a reasonable amount of volition, initiative and reward. During the small window when Abilify (which only affects dopamine) was working for me, I finally felt absolutely normal, calm, productive and capable of doing everyday things; and I took care of everyday things because I *wanted* to, not because I *had* to, as is the feeling on noradr/norepi. Unfortunately, it later made me crazy and I had to stop taking it but that is beside the point...
>
> That having been said, and really with all due respect because you all do some really informed and helpful posts, I am disappointed that anyone who doesn't know those of us who have identified dopamine as our probable issue (and really who knows us better than us?) would question and/or discount that. I mean, we've all had enough of that from doctors and family members, etc. and it is never helpful and always degrading to be discounted in that way. That was one thing I immediately noticed about this site was that one's credibility about one's own condition was assumed, and that was such a gift. I am surprised and disappointed to find that kind of thing here, which had previously seemed like an unconditionally safe place where my knowledge of me would not be discounted by someone who 'knew' better.
Posted by shasling on January 20, 2006, at 16:13:58
In reply to Re: Which ADs increase DOPAMINE the most? » shasling, posted by SLS on January 20, 2006, at 15:40:32
Hi Scott,
Actually, I don't think that I ever really lobbied for a strictly dopaminergic basis of my condition. Nor did I write the original post... I actually suspect (have to suspect *something*, because I agree - we really don't know sh*t, and the alternative is random medication taking which seems REALLY unlikely to help...) that I've got some HPA and/or adrenal thing going on as well, and who knows what else. If I knew the answer I'd be better. My point about the dopamine was that I've kinda ruled out the other two of the big three and am going with that for now, seeing if it fits. Again, my experience with Abilify seemed to confirm/reinforce it. Parhaps I misunderstood Abilify to only affect dopamine and I'm wrong - that would be okay, I'm not trying to know everything, I just want to be able to get out of bed and clean the cat box.
I guess my point in the exchange with Link, and maybe I'm not very good at expressing myself, is that suspecting any given neurotransmitter is simply a framework from which to make decisions about what to try next. If my issue isn't dopamine, I'd find that out myself in due time.
My point in my initial post had nothing to do with dopamine; it was that I was disappointed to see anybody's theory of the moment discounted, people who may be just hanging on to that in order to have some hope or whatever, or just to have some sense of (even if false) mastery of what is going on with them. That ain't me right now, but there are a lot of people out there just hanging on who probably don't need to be invalidated. I was really psyched to have found a place that was so affirming and where my credibility about me seemed to be assumed and respected that I was disappointed in references to 'imagined dopamine deficiency' etc. This board had always seemed to be a safe and affirming place for people in pain, and I was disappointed in that. That's all. Not telling you what to do or say, just food for thought. No intention of being confrontational.
Thanks,
Suzie
Posted by linkadge on January 20, 2006, at 16:49:34
In reply to Re: Which ADs increase DOPAMINE the most?, posted by shasling on January 20, 2006, at 16:13:58
It's not so much that I want people to loose hope.
In my mind, I've been deficiant in just about every chemical at one point or another, and while it gave me some hope and a new way to frame my thinking, it really has not led to a whole lot.
I guess the main reason that I kind of urge not to go down that path is because can close doors.
For example, after trying effexor, I figured that I had "basically" tried the TCA's, which were SNRI's too. But clomipramine worked when effexor didn't. I put it off, thinking it was a dead end.
So I guess I'm saying that self educaton is good, but don't let it close doors, cause you never know what might help, sometimes the treatments can surprise you.
Linkadge
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Dr. Bob is Robert Hsiung, MD,
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