![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 21 to 45 of 70. Go back in thread:
Posted by Franz on March 4, 2003, at 21:43:04
In reply to Re: Dopamine agonists » Michael Bell, posted by daizy on March 4, 2003, at 7:44:45
Hi,
I am getting interested in this issue of dopamine and social phobia.
I found there is an European drug (sold OTC in US) called citicholine that increases acetylcholine and dopamine. Wether it increases dopamine in the right place i do not know.
See:
http://lansbury.bwh.harvard.edu/da_reviews_2002.htmciticholine, when administered, undergoes a quick transformation to cytidine and choline, which are believed to enter brain cells separately and provide neuroprotection by enhancing PtdCho synthesis; similar effect may be expected to occur in glaucomatous RGC. Furthermore, citicholine stimulates some brain neurotransmitter systems, including the dopaminergic system
A a side note, with due respect, to prevent Dr Bob aborting this post, I do not understand why importing a product that is sold OTC as a nutritional supplement or whatever in US can be illegal to import (I am referring to the picamilon thread, picamilon is available in the US as a supplement, as well as citicholine also known as CDP-choline).
Posted by Michael Bell on March 4, 2003, at 23:01:38
In reply to Re: Dopamine agonists » Michael Bell, posted by daizy on March 4, 2003, at 7:44:45
Daizy, this is what I think about Social Phobia and neurotransmitters. This theory comes from my own experience, discussions in chat rooms and surfing the net for countless hours. I'll take the transmitter systems one at a time.
Serotonin: High levels: linked with harm avoidance and anxiety, including General Anxiety Disorder. Low levels: linked with some forms of depression, obsessions, deviant thoughts and aggression. I don't believe serotonin is a major player in SP, though it's probably involved on some level (maybe levels are slightly high), uin a complex way we don't know about. My main reason for this belief comes from my own experience as well as what I've encountered regarding SSRIs. One common result that I have found across many chatboards and various studies is that SSRIs do NOT help with SP, and in fact often make the symptoms worse. Those that have noticed an effect often say that they feel emotionally numb as a result of taking these medications. My own feeling is that a medication that removes anxiety through dulling of emotions may be "effective" to some degree, but not in a pleasant way. An interesting things about serotonin - it increases when we "freeze" in frightful situations (similar to mind going blank in social settings)
Norepinephrine -- since this is the fight or flight neurotransmitter, it probably also has a role in SP. Caffeine induces panic attacks in people with SP twice as much as people without SP. Also, beta blockers inhibit norepinephrine from reaching receptors, and are useful for people with performance anxiety. However, studies have shown that people with generalized SP actually have similar NE levels to "normal" people. Also, beta blockers are not very effective for generalized SP. Our receptors are probably hypersensitive to NE, so that we have stronger reactions to situations that should only cause minimal stress.
GABA: I believe most of the evidence points to GABA dysfunction as being the primary culprit in SP. Here's why: The two most effective prescription drugs for SP are Klonopin and Nardil. No other drugs come close. KLONOPIN - works by enabling GABA to bind more easily to its receptors. Klonopin sometimes works so well that it causes disinhibition in some patients, the very opposite of SP. NARDIL - one of the older, irreversible MAOIs, it increases the levels of dopamine, serotonin and norepinephrine in the body and brain. However, other MAOIs, such as Parnate, do the same, and are not nearly as effective as Nardil for SP. The difference is Nardil also a powerful inhibitor of the enzyme that breaks down GABA. I believe it is this action on GABA that makes Nardil such an effective tool. The two other substances that I have heard miraculous results about are ALCOHOL and GHB. In my own experience, alcohol is the single most effective substance I have ever tried for SP, too bad it's dangerous! Most researchers attribute the "wellbeing" effect of alcohol to be due to its potentiation of GABA, however there is also some increased dopamine transmission that takes place as well. The effects of GHB are two-fold. First, it increases the effectiveness of GABA for several hours, causing feelings of wellbeing and disinhibition. Over the course of these hours, it also blocks the transmission of dopamine, causing dopamine levels to build up in the brain. Then the user falls asleep and all the built up dopamine is released, causing the user to wake up refreshed and alert. So here we have four drugs, all which act primarily on GABA, and they are the most effective drugs for SP that we know about. Also, GABA is the most abundant modulator in the brain, around 30% of all transmitters. Low levels have been associated with panic attacks, anxiety disorders, insomnia and a variety of other problems.
DOPAMINE: I believe this to be the second most important neurotransmitter involved in SP, but I actually disagree with people who claim dopamine levels are too low. Quite the opposite, I think we have high levels of dopamine but LOW NUMBER OF RECEPTORS/POOR TRANSMISSION. Here's why: High levels of dopamine linked with paranoia, schizophrenia, stress and panic disorders, all of which have high incidences of SP. Also, in animal studies it has been shown that dopamine levels skyrocket after incidences of social defeat. THis dopamine release leads to reducing binding potential of dopamine to its receptors by decreasing number of dopamine receptors. Finnish studies have shown that people with SP have substantially less number of D2 receptors than normal subjects, and they speculate that this may be a result of downregulation due to chronically high levels of dopamine in the brain. Additionally, although there are some exceptions, almost every post I've read where someone tries a dopamine med on its own to combat SP actually experiences increased anxiety. In my own experience, L-tyrosine and selegiline caused additional anxiety and paranoia. Usually dopamine meds are most helpful as adding an activating effect to drugs such as Klonopin, Valium, Neurontin, etc. This all ties in with low levels of GABA, b/c GABA actually inhibits dopamine production, and low levels of GABA lead to higher levels of dopamine.
So basically: Low GABA = High Dopamine levels = downregulation of Dopamine receptors = reduced sensitivity of receptors = low GABA... and the cycle continues.
So to sum it up, it seems to me that GABA dysfunction is the main reason for SP, with poor dopamine transmission due to chronically excess levels in brain as a result of low GABA. Sorry for writing a novel, but it was clogging up my brain! Good luck.
Posted by KrissyP on March 4, 2003, at 23:43:54
In reply to Re: Dopamine agonists, posted by Michael Bell on March 4, 2003, at 23:01:38
WELL DONE MICHAEL:-)
> Daizy, this is what I think about Social Phobia and neurotransmitters. This theory comes from my own experience, discussions in chat rooms and surfing the net for countless hours. I'll take the transmitter systems one at a time.
>
> Serotonin: High levels: linked with harm avoidance and anxiety, including General Anxiety Disorder. Low levels: linked with some forms of depression, obsessions, deviant thoughts and aggression. I don't believe serotonin is a major player in SP, though it's probably involved on some level (maybe levels are slightly high), uin a complex way we don't know about. My main reason for this belief comes from my own experience as well as what I've encountered regarding SSRIs. One common result that I have found across many chatboards and various studies is that SSRIs do NOT help with SP, and in fact often make the symptoms worse. Those that have noticed an effect often say that they feel emotionally numb as a result of taking these medications. My own feeling is that a medication that removes anxiety through dulling of emotions may be "effective" to some degree, but not in a pleasant way. An interesting things about serotonin - it increases when we "freeze" in frightful situations (similar to mind going blank in social settings)
>
> Norepinephrine -- since this is the fight or flight neurotransmitter, it probably also has a role in SP. Caffeine induces panic attacks in people with SP twice as much as people without SP. Also, beta blockers inhibit norepinephrine from reaching receptors, and are useful for people with performance anxiety. However, studies have shown that people with generalized SP actually have similar NE levels to "normal" people. Also, beta blockers are not very effective for generalized SP. Our receptors are probably hypersensitive to NE, so that we have stronger reactions to situations that should only cause minimal stress.
>
> GABA: I believe most of the evidence points to GABA dysfunction as being the primary culprit in SP. Here's why: The two most effective prescription drugs for SP are Klonopin and Nardil. No other drugs come close. KLONOPIN - works by enabling GABA to bind more easily to its receptors. Klonopin sometimes works so well that it causes disinhibition in some patients, the very opposite of SP. NARDIL - one of the older, irreversible MAOIs, it increases the levels of dopamine, serotonin and norepinephrine in the body and brain. However, other MAOIs, such as Parnate, do the same, and are not nearly as effective as Nardil for SP. The difference is Nardil also a powerful inhibitor of the enzyme that breaks down GABA. I believe it is this action on GABA that makes Nardil such an effective tool. The two other substances that I have heard miraculous results about are ALCOHOL and GHB. In my own experience, alcohol is the single most effective substance I have ever tried for SP, too bad it's dangerous! Most researchers attribute the "wellbeing" effect of alcohol to be due to its potentiation of GABA, however there is also some increased dopamine transmission that takes place as well. The effects of GHB are two-fold. First, it increases the effectiveness of GABA for several hours, causing feelings of wellbeing and disinhibition. Over the course of these hours, it also blocks the transmission of dopamine, causing dopamine levels to build up in the brain. Then the user falls asleep and all the built up dopamine is released, causing the user to wake up refreshed and alert. So here we have four drugs, all which act primarily on GABA, and they are the most effective drugs for SP that we know about. Also, GABA is the most abundant modulator in the brain, around 30% of all transmitters. Low levels have been associated with panic attacks, anxiety disorders, insomnia and a variety of other problems.
>
> DOPAMINE: I believe this to be the second most important neurotransmitter involved in SP, but I actually disagree with people who claim dopamine levels are too low. Quite the opposite, I think we have high levels of dopamine but LOW NUMBER OF RECEPTORS/POOR TRANSMISSION. Here's why: High levels of dopamine linked with paranoia, schizophrenia, stress and panic disorders, all of which have high incidences of SP. Also, in animal studies it has been shown that dopamine levels skyrocket after incidences of social defeat. THis dopamine release leads to reducing binding potential of dopamine to its receptors by decreasing number of dopamine receptors. Finnish studies have shown that people with SP have substantially less number of D2 receptors than normal subjects, and they speculate that this may be a result of downregulation due to chronically high levels of dopamine in the brain. Additionally, although there are some exceptions, almost every post I've read where someone tries a dopamine med on its own to combat SP actually experiences increased anxiety. In my own experience, L-tyrosine and selegiline caused additional anxiety and paranoia. Usually dopamine meds are most helpful as adding an activating effect to drugs such as Klonopin, Valium, Neurontin, etc. This all ties in with low levels of GABA, b/c GABA actually inhibits dopamine production, and low levels of GABA lead to higher levels of dopamine.
>
> So basically: Low GABA = High Dopamine levels = downregulation of Dopamine receptors = reduced sensitivity of receptors = low GABA... and the cycle continues.
>
> So to sum it up, it seems to me that GABA dysfunction is the main reason for SP, with poor dopamine transmission due to chronically excess levels in brain as a result of low GABA. Sorry for writing a novel, but it was clogging up my brain! Good luck.
Posted by KrissyP on March 5, 2003, at 0:16:44
In reply to Re: Dopamine agonists » KrissyP, posted by not exactly on March 4, 2003, at 16:24:14
Thanks:-) FWIW, thank you FYI, I find your site very helpful PRN what a smart guy to have done this:-) BTW, I know most of the icons-but being new and all, there are way easier ways to put words in a post other than spelling them out-your point exactly! And.... I say this:
IDBTD! Meaning I don't beg to differ that your site has been a helpful, educational, and supportive thing in my life the past few days-
THX-Kristen:-)
Thanks for this site Kristen,
>
> > Please? what does FWIW mean LOL:-)
>
> FWIW = "for what it's worth"
>
> BTW, FYI see:
> http://www.dr-bob.org/babble/20010122/msgs/52652.html
> very handy, IMHO
>
> HTH,
> Bob
>
>
Posted by not exactly on March 5, 2003, at 1:57:34
In reply to Re: Dopamine agonists » not exactly, posted by noa on March 4, 2003, at 19:39:11
> I don't see HTH on the list
DYJHIWTH? :-)
HTH = "hope this helps"
see also:
http://www.netlingo.com/emailsh.cfm- Bob
Posted by not exactly on March 5, 2003, at 2:56:34
In reply to Re: Dopamine agonists, posted by Michael Bell on March 4, 2003, at 23:01:38
> ... I actually disagree with people who claim dopamine levels are too low. Quite the opposite, I think we have high levels of dopamine but LOW NUMBER OF RECEPTORS/POOR TRANSMISSION.
> ... people with SP have substantially less number of D2 receptors than normal subjects, and they speculate that this may be a result of downregulation due to chronically high levels of dopamine in the brain.Fascinating! I really like this theory, because it finally explains some things that never made sense before. For example, it would explain why I responded so well to Mirapex (a dopamine agonist) but after a while it completely "pooped out". Perhaps at first it improved the stimulation of the too-sparse dopamine receptors, but eventually there was a compensatory further downregulation. MAOIs would probably have the same limitation. What sort of drug would enhance dopamine transmission without causing this compensation? A dopamine reuptake inhibitor? A pre-synaptic antagonist? Seems like what is really needed is a med that interferes with the downregulation compensation process.
And how could one reverse the downregulation that had already taken place? Would REDUCING the dopamine levels cause the receptors to become more sensitive? Maybe an antipsychotic/neuroleptic would, in the long term, induce an UPregulation? What do you think?
- Bob
Posted by daizy on March 5, 2003, at 7:47:36
In reply to Re: Dopamine agonists, posted by Michael Bell on March 4, 2003, at 23:01:38
Well Thanx for telling your theory, Its very interesting, you know it seems to make a lot of sense, and explains why some drugs work and others just make it worse!
>"Most researchers attribute the "wellbeing" effect of alcohol to be due to its potentiation of GABA, however there is also some increased dopamine transmission that takes place as well. The effects of GHB are two-fold. First, it increases the effectiveness of GABA for several hours, causing feelings of wellbeing and disinhibition. Over the course of these hours, it also blocks the transmission of dopamine, causing dopamine levels to build up in the brain"
Yes michael, this is true with my experience of taking GHB. I believe this is what happens when taking MDMA also, correct me if Im wrong.
>"Also, GABA is the most abundant modulator in the brain, around 30% of all transmitters. Low levels have been associated with panic attacks, anxiety disorders, insomnia and a variety of other problems"
> "DOPAMINE: I actually disagree with people who claim dopamine levels are too low. Quite the opposite, I think we have high levels of dopamine but LOW NUMBER OF RECEPTORS/POOR TRANSMISSION. Here's why: High levels of dopamine linked with paranoia, schizophrenia, stress and panic disorders, all of which have high incidences of SP. Also, in animal studies it has been shown that dopamine levels skyrocket after incidences of social defeat. THis dopamine release leads to reducing binding potential of dopamine to its receptors by decreasing number of dopamine receptors. Finnish studies have shown that people with SP have substantially less number of D2 receptors than normal subjects, and they speculate that this may be a result of downregulation due to chronically high levels of dopamine in the brain" Or could this also be because of, in my instance, taking drugs that then increased dopamine?>"So basically: Low GABA = High Dopamine levels = downregulation of Dopamine receptors = reduced sensitivity of receptors = low GABA... and the cycle continues.
>
> So to sum it up, it seems to me that GABA dysfunction is the main reason for SP, with poor dopamine transmission due to chronically excess levels in brain as a result of low GABA"
So does this mean that to combat SP and anxiety, you need a drug that primarily increases GABA, and then adding an SSRI or SNRI to increase the levels of others?I think I have understood!
Posted by Michael Bell on March 5, 2003, at 10:59:53
In reply to Re: Dopamine agonists » Michael Bell, posted by not exactly on March 5, 2003, at 2:56:34
> > ... I actually disagree with people who claim dopamine levels are too low. Quite the opposite, I think we have high levels of dopamine but LOW NUMBER OF RECEPTORS/POOR TRANSMISSION.
> > ... people with SP have substantially less number of D2 receptors than normal subjects, and they speculate that this may be a result of downregulation due to chronically high levels of dopamine in the brain.
>
> Fascinating! I really like this theory, because it finally explains some things that never made sense before. For example, it would explain why I responded so well to Mirapex (a dopamine agonist) but after a while it completely "pooped out". Perhaps at first it improved the stimulation of the too-sparse dopamine receptors, but eventually there was a compensatory further downregulation. MAOIs would probably have the same limitation. What sort of drug would enhance dopamine transmission without causing this compensation? A dopamine reuptake inhibitor? A pre-synaptic antagonist? Seems like what is really needed is a med that interferes with the downregulation compensation process.
>
> And how could one reverse the downregulation that had already taken place? Would REDUCING the dopamine levels cause the receptors to become more sensitive? Maybe an antipsychotic/neuroleptic would, in the long term, induce an UPregulation? What do you think?
>
> - Bob
>Bob, it's so interesting what you've added to the thread regarding your experiences. I also believe that when we take drugs that increase dopamine, this allows the reduced number of receptors to be stimulated by the increased dopamine - for a while. Then the brain registers this excess dopamine, and further downregulates the number of receptors, hence the poop-out effect. I too am trying to find out about drugs that effect dopamine transmission itself and not just increase overall dopamine levels.
Regarding upregulation - interestingly, in people with Parkinson's disease, studies have shown that as the number of dopamine cells gets lower, the brain upregulates the number of receptors to compensate. However, eventually the number of cells get so low (80% reduction) that even having a higher number of receptors doesn't help. So there is probably a way to increase the number of dopamine receptors, but safety is a big issue.
Posted by jumpy on March 5, 2003, at 11:38:17
In reply to Re: Dopamine agonists, posted by Michael Bell on March 5, 2003, at 10:59:53
> Bob, it's so interesting what you've added to the thread regarding your experiences. I also believe that when we take drugs that increase dopamine, this allows the reduced number of receptors to be stimulated by the increased dopamine - for a while. Then the brain registers this excess dopamine, and further downregulates the number of receptors, hence the poop-out effect. I too am trying to find out about drugs that effect dopamine transmission itself and not just increase overall dopamine levels.
>
> Regarding upregulation - interestingly, in people with Parkinson's disease, studies have shown that as the number of dopamine cells gets lower, the brain upregulates the number of receptors to compensate. However, eventually the number of cells get so low (80% reduction) that even having a higher number of receptors doesn't help. So there is probably a way to increase the number of dopamine receptors, but safety is a big issue.Hey Michael,
Very interesting. So with nardil, is the benefits solely in the increase in GABA levels and the increases in dopamine/serotonin/norepi are actually detrimental? I am on nardil and klonopin ... should I just taper off the nardil and increase the klonopin if increasing GABA is the sole goal (and nardil might be hurting with the serotonin/dopamine/norepi effects)?
Thanks.
Jumpy
Posted by not exactly on March 5, 2003, at 13:44:19
In reply to Re: Dopamine agonists, posted by Michael Bell on March 5, 2003, at 10:59:53
> Regarding upregulation - interestingly, in people with Parkinson's disease, studies have shown that as the number of dopamine cells gets lower, the brain upregulates the number of receptors to compensate. However, eventually the number of cells get so low (80% reduction) that even having a higher number of receptors doesn't help. So there is probably a way to increase the number of dopamine receptors, but safety is a big issue.
I sometimes worry about Parkinson's. I have no symptoms of the disease yet, but it concerns me that most of the meds that have dramatically helped me are in fact primarily for Parkinson's rather than depression or SP. Do I have the so-called "Parkinson personality" (the description fits like a glove, see http://www.parkinson.org/pr24.htm and http://www.geocities.com/parkinsonforum/hypothesis/overview.htm), and am I therefore at risk for an early onset of the disease itself? I wonder if drugs that are neuroprotective and reputedly slow the advance of Parkinson's, such as selegiline (low dosage), might have a long-term benefit.
The up/down regulation issue also reminds me of the triumphs and tragedies in the famous "Awakenings" story.
BTW, I responded well to Klonopin, but never tried it very long, or as a monotherapy. My pdoc switched me from Klonopin to Neurontin because he was concerned about the addiction potential of benzo's. Neurontin helped in much the same ways as Klonopin, but never as well, and with some subtle but worrisome long-tem effects. I've reported on my reaction to Neurontin in another thread [http://www.dr-bob.org/babble/20030125/msgs/137900.html].
- Bob
Posted by daizy on March 5, 2003, at 15:47:35
In reply to Re: Dopamine agonists » Michael Bell, posted by not exactly on March 5, 2003, at 13:44:19
I did a search on GABA, and found you can get capsules, Is this something totally different to the GABA we are talking about?
Posted by noa on March 5, 2003, at 16:52:43
In reply to Re: Dopamine agonists » Michael Bell, posted by not exactly on March 5, 2003, at 13:44:19
The second site you linked is very interesting! I like the way the info is organized, too.
But when I read the first link, I was somewhat skeptical of a Parkinsons personality, because there, it is described as:
"...appear to be highly intelligent, successful, responsible, conscientious, hard-working, less likely to smoke or drink, law abiding individuals."
Obviously, this is too broad to be useful. And,possibly spurious. One could easily imagine several ways that one could get the impression that patients diagnosed with Parkinsons have these traits vs. their opposites: some possibilities, imho: poor people get less discerning health care and therefore are diagnosed way less, or diagnosed with alternative illnesses thought to be more prevalent in the poor; more economically successful people tend to live longer and are able to function in their jobs longer becuase jobs tend to be white collar, not physical labor; stress and strains and injuries from long years of labor could be mistaken for the causes of some Parkinsons symptoms, or of earlier aging, which can seem to mask P. symptoms; Drug and alcohol use can mask P. symtpoms, or get in the way of access to good health care, or prejudice health care professionals from diagnosing properly, etc. etc. etc.
The second link talks more about compulsive tendencies. I will have to go back and look at the research they based this on, but that sounds more promising to me than the above characteristics.
I sometimes think about Parkinsons. My grandmother essentially died of it. It was not diagnosed that readily. In fact, my dad and his siblings actually suspected my grandfather of abusing her becuase she had been falling a lot and getting bruised. He had developed a drinking problem in later years to self-medicate his depression. But abuse did not fit his m.o., in that he tended to be a quiet, withdrawn drunk, very depressed, and had more of a tendency to wander aimlessly than to have any kind of angry outbursts. After a while, they realized that my GM was falling because of something neurological and then she saw a specialist who diagnosed her. This was back in the 60's.
I don't even have a clue if P. is hereditary, but of course, I think about it from time to time.
Posted by Ed on March 5, 2003, at 16:59:43
In reply to Re: Dopamine agonists » Michael Bell, posted by not exactly on March 5, 2003, at 13:44:19
> BTW, I responded well to Klonopin, but never tried it very long, or as a monotherapy. . . . >
> - BobBob- have you tried/did you respond to, Nardil. You and I have very similar symptoms and I responded well to Nardil but couldn't bear the weight gain. I think dopamine is the culprit. --Ed
PS-- I had concluded that these symptoms we share are not so different from the negative symptoms of schizophrenia. I don't know if that has any relevance-- maybe it means nothing-- maybe there are only so many symptoms that can manifest from brain dysregulation, and entirely different problems can manifest entirely similar symptomology.
>
>
Posted by not exactly on March 5, 2003, at 18:18:54
In reply to Re: Dopamine agonists » not exactly, posted by Ed on March 5, 2003, at 16:59:43
Ed,
> have you tried/did you respond to, Nardil.
Not yet, but it's high on my list of things to try if/when my current AD (Desipramine augmented w/ Buspar) proves disappointing. The only MAOI I've ever tried was the Selegiline Patch, which was very effective for me.
> I had concluded that these symptoms we share are not so different from the negative symptoms of schizophrenia.
Atypical antipyschotics (which I haven't tried yet either) might help also, especially in low dosage as an adjunct to an AD.
- Bob
Posted by zeugma on March 5, 2003, at 20:19:09
In reply to Re: Dopamine agonists, posted by Michael Bell on March 4, 2003, at 23:01:38
This is a very interesting discussion. I definitely have Social Phobia, but I have only become aware of it as a result of taking an AD for depression and overall dysfunction and malaise. The fear I used to feel was too constant to put a finger on what was causing it and why. Now I am aware that I am terribly uncomfortable interacting with others, and I mentally try to prepare myself, while waiting for the elevator, for the dreaded possibility that there might actually be someone in that elevator with whom I might have to interact. At least now I can try to prepare myself, but it's exhausting and extremely demoralizing when my preparations fail, which is often.
I used to drink alcohol to deal with this, and it worked but took a toll on my body. I basically dropped out of graduate school for a couple of years because I found I couldn't write papers without getting very drunk in the process. I suppose writing for me is too much of an
'interaction.' Also I have noticed a kind of 'cognitive stiffness' that alcohol, in particular, seemed to remedy. People said I seemed much more natural and normal when drunk than when sober. I do know that something happens in my brain when I drink that magnifies my problem-solving and creative capacities, and helps me pass for 'normal.' GABA release and dopamine transmission sound like likely reasons for this, especially the dopamine transmission. Dopamine governs movement, right? A lot of times I feel that life is a series of incredibly complicated movements, and I can only manage a few at a time until I trip myself up. It's that 'fluidity' that I value so much in alcohol. I'm wondering if I should think about taking Nardil. Right now I'm on 40 mg nortriptyline and 30 mg Buspar. I'm thinking I should push the dosages of these meds as much as possible- they've both helped a lot but have also made me aware of how far I still have to go. If I didn't practically live on soy products, curiousity, as well as a desire to solve these long-standing problems, would have asking for Nardil next time I see my doc.
Posted by Stan on March 6, 2003, at 1:37:19
In reply to Re: Dopamine agonists » Ed, posted by not exactly on March 5, 2003, at 18:18:54
> Ed,
>
> > have you tried/did you respond to, Nardil.
>
> Not yet, but it's high on my list of things to try if/when my current AD (Desipramine augmented w/ Buspar) proves disappointing. The only MAOI I've ever tried was the Selegiline Patch, which was very effective for me.
>
> > I had concluded that these symptoms we share are not so different from the negative symptoms of schizophrenia.
>
> Atypical antipyschotics (which I haven't tried yet either) might help also, especially in low dosage as an adjunct to an AD.
>
> - Bob>>>>>>>>>>>>>>>>>>>>>>>>>>>
hi bob -- last i heard, you were in the process of phasing out neurontin -- have you reduced that to zero now and replaced it with buspar? if so, what do you think of the change? thanks
Stan
Posted by not exactly on March 6, 2003, at 4:48:01
In reply to Re: Dopamine agonists » not exactly, posted by Stan on March 6, 2003, at 1:37:19
> last i heard, you were in the process of phasing out neurontin -- have you reduced that to zero now and replaced it with buspar? if so, what do you think of the change?
Stan,
It's only been a week since I started the Buspar, and the effect is still ramping up. I'm going to wait until the Buspar benefits plateau out before trying to wean myself off the Neurontin completely. Being a scientist at heart, I like to control my variables - change only one thing at a time. Otherwise, I won't know what med change is responsible for what symptom change. Of course, there are so many subtle variables that I can't control (or even be aware of) so I may never really be sure. For now, the Buspar is helping with anxiety, but it's too soon to tell if it will provide the same benefits that Neurontin has.
- Bob
Posted by Michael Bell on March 6, 2003, at 12:24:45
In reply to Re: Dopamine agonists » Michael Bell, posted by daizy on March 5, 2003, at 7:47:36
> >
> > So to sum it up, it seems to me that GABA dysfunction is the main reason for SP, with poor dopamine transmission due to chronically excess levels in brain as a result of low GABA"
>
>
> So does this mean that to combat SP and anxiety, you need a drug that primarily increases GABA, and then adding an SSRI or SNRI to increase the levels of others?
>
> I think I have understood!
>
Since Klonopin and a few others seem to be very effective for SP with little or no direct effect on serotonin or norepinephrine, I guess what I was saying is people with SP need to attack the GABA system primarily, then add a little something to increase Dopamine transmission.
>
Posted by Michael Bell on March 6, 2003, at 12:35:26
In reply to Re: Dopamine agonists » Michael Bell, posted by jumpy on March 5, 2003, at 11:38:17
>
> Hey Michael,
>
> Very interesting. So with nardil, is the benefits solely in the increase in GABA levels and the increases in dopamine/serotonin/norepi are actually detrimental? I am on nardil and klonopin ... should I just taper off the nardil and increase the klonopin if increasing GABA is the sole goal (and nardil might be hurting with the serotonin/dopamine/norepi effects)?
>
> Thanks.
>
> JumpyJumpy, I think the creators of Nardil "stumbled" on a highly effective med for Social Phobia when they came up with Nardil. I'm not sure of the exact date, but Nardil has been around for at least a couple decades. Social Phobia wasn't even recognized as a separate illness until very recently, long after Nardil was on the market. What probably happened (and I'm guessing here" is that it was intended primarily as an antidepressant, but over the years they started getting reports that it worked really well for agoraphobia/SP. So now its marketed as a SP med as well. I don't know if the effects on DA, NE and SE are detrimental, but I'm positive that GABA is the reason for its supreme effectiveness. Parnate, Selegiline (high doses), Moclobemide, etc. don't work nearly as well for SP.
Also, I wouldn't want to recommend any changes in your med cocktail. I'm just working on theory here, with no medical background. Try and figure out how you felt with each med, and the effects that adding them to your regimen had. Then talk to your psych and see what he thinks. Good luck!
Posted by not exactly on March 6, 2003, at 15:02:04
In reply to Re: Dopamine agonists (daizy), posted by Michael Bell on March 6, 2003, at 12:24:45
> ... people with SP need to attack the GABA system primarily, then add a little something to increase Dopamine transmission.
This sounds like a good plan, but what do you think that "little something" should be? What med (or class of meds) might have a long-term beneficial effect on Dopamine transmission? I would think that anything which increases the amount of DA present (or otherwise stimulates DA receptors, such as a direct DA agonist) runs the risk of eventual dowregulation (a.k.a. "poop-out").
- Bob
Posted by jumpy on March 6, 2003, at 16:09:14
In reply to Re: Dopamine agonists jumpy, posted by Michael Bell on March 6, 2003, at 12:35:26
Posted by daizy on March 6, 2003, at 16:34:11
In reply to Thanks a million Michael! (nm) » Michael Bell, posted by jumpy on March 6, 2003, at 16:09:14
Yes I should also say THANK YOU! ;-)
Posted by djmmm on March 6, 2003, at 17:56:47
In reply to Re: Dopamine agonists (daizy) » Michael Bell, posted by not exactly on March 6, 2003, at 15:02:04
Nardil, Zonegran and GHB are the only meds that I know of that specifically target GABA and Dopamine...
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8991786&dopt=Abstract
Posted by Ilene on March 9, 2003, at 21:28:29
In reply to Re: Dopamine agonists, posted by Michael Bell on March 3, 2003, at 19:26:29
> Daizy, an agonist potentiates increases dopamine/effects of dopamine, whereas antagonist would inhibit dopamine. In my situation, and in most situations I've read about (this board included), drugs that primarily increase dopamine (or effectiveness of dopamine) make anxiety symptoms worse in people with SP. The reason I'm trying to get an idea of the effectiveneness of these types of drugs on SP is because I'm convinced dopamine levels/transmission has a role in SP, but I can't put my finger on it. By the way, If you're looking to for calmness, try a drug that works on GABA, if your doc is cool with it.
>
> Also, I have a theory on neurochemical cause of Social Phobia, but it's quite long. Let me know if you want to hear it, and I'll post it. Thanks.*I'm* interested. I don't know if I have SP. I don't know if it matters; depression and inability to socialize go hand in hand for me.
I've been wondering--are there any drugs that amp up dopamine (or keep it from being taken up) that don't affect other neurotransmitters? Would Parkinson's drugs do it? If so, why aren't they prescribed more often for people w/ mood disorders? Is it because of side effects or some other deeply biochemical reason? Should I palm some Sinemet the next time I see my dad?
How much of the pleasure of "drugs of abuse" is due to dopamine? Is part of it from the adrenalin boost?
Life is *full* of mysteries.
--I.
Posted by Ilene on March 9, 2003, at 23:47:01
In reply to Re: Parkinsons, posted by noa on March 5, 2003, at 16:52:43
> The second site you linked is very interesting! I like the way the info is organized, too.
>
> But when I read the first link, I was somewhat skeptical of a Parkinsons personality, because there, it is described as:
>
> "...appear to be highly intelligent, successful, responsible, conscientious, hard-working, less likely to smoke or drink, law abiding individuals."
>
> Obviously, this is too broad to be useful. And,possibly spurious. One could easily imagine several ways that one could get the impression that patients diagnosed with Parkinsons have these traits vs. their opposites:
>
> The second link talks more about compulsive tendencies. I will have to go back and look at the research they based this on, but that sounds more promising to me than the above characteristics.
>I wonder how useful it is to evaluate personality *after* someone has been diagnosed, and I wonder if the disease affects personality long before other symptoms become apparent. Or is it supposed to be the other way around? Uptight folks get Parkinson's? Assuming it affects personality at all. There are a zillion hard-working, conscientious, non-smokers who *don't* get Parkinson's.
> I sometimes think about Parkinsons. My grandmother essentially died of it. It was not diagnosed that readily.
>
> I don't even have a clue if P. is hereditary, but of course, I think about it from time to time.Supposed to be *not* hereditary. My dad has it.
--I.
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