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Posted by not exactly on March 12, 2003, at 5:51:20
In reply to Re: Dopamine agonists (daizy) » Michael Bell, posted by not exactly on March 6, 2003, at 15:02:04
> ... people with SP need to attack the GABA system primarily, then add a little something to increase Dopamine transmission.
Well, I've tried to apply what I've learned from following this thread, and I'm happy to report some dramatic success. I'm now on Klonopin plus Buspar, and I'm finally experiencing virtually complete remission from my long-standing Social Phobia and comorbid treatment-resistant Atypical Depression (anhedonia, mood reactivity, hypersomnia).
Previously, I had been on Desipramine plus Neurontin. After giving the Desipramine a fair trial (5 weeks) and obtaining only slight relief from my depression, I augmented it with Buspar. This yielded a modest improvement, but overall it was still an unsatisfying solution.
Inspired by the enlightening posts in this thread, I decided to make some radical changes. First, I dumped the Neurontin and substituted Klonopin. This gave improved relief from SP and GAD, and eliminated the "dulled" feeling that Neurontin had produced. I then dropped the Desipramine (but kept the "augmenting" Buspar). Wow. Within a few days, I felt much more upbeat, motivated, and "present". This is one of the best states I've ever been in. Not manic, just functional and happy to be alive. And NO SIDE EFFECTS.
I've noticed some amazing changes. Earlier this evening, I attended a meeting with some friends, and there were 3 new members in the group. I had enjoyable conversations with all 3 of them, and I remember their names. Maybe this doesn't seem unusual to you, but it's a BIG change for me. It used to be that the presence of "strangers" would make me so uncomfortable that I wouldn't say anything at all, even to my old friends. It would take me weeks to warm up to new acquaintances enough to make relaxed conversation possible. And months before I had a chance of remembering their names.
I've been feeling this good for several days. I sure hope this state is sustainable. Don't know if this combo would work this well for anyone else, but it's been a miracle cure for me.
- Bob
Posted by Krissy P on March 12, 2003, at 8:59:21
In reply to SUCCESS!, posted by not exactly on March 12, 2003, at 5:51:20
Posted by daizy on March 12, 2003, at 9:04:45
In reply to SUCCESS!, posted by not exactly on March 12, 2003, at 5:51:20
> > ... people with SP need to attack the GABA system primarily, then add a little something to increase Dopamine transmission.
>
> Well, I've tried to apply what I've learned from following this thread, and I'm happy to report some dramatic success. I'm now on Klonopin plus Buspar, and I'm finally experiencing virtually complete remission from my long-standing Social Phobia and comorbid treatment-resistant Atypical Depression (anhedonia, mood reactivity, hypersomnia).
>
> Previously, I had been on Desipramine plus Neurontin. After giving the Desipramine a fair trial (5 weeks) and obtaining only slight relief from my depression, I augmented it with Buspar. This yielded a modest improvement, but overall it was still an unsatisfying solution.
>
> Inspired by the enlightening posts in this thread, I decided to make some radical changes. First, I dumped the Neurontin and substituted Klonopin. This gave improved relief from SP and GAD, and eliminated the "dulled" feeling that Neurontin had produced. I then dropped the Desipramine (but kept the "augmenting" Buspar). Wow. Within a few days, I felt much more upbeat, motivated, and "present". This is one of the best states I've ever been in. Not manic, just functional and happy to be alive. And NO SIDE EFFECTS.
>
> I've noticed some amazing changes. Earlier this evening, I attended a meeting with some friends, and there were 3 new members in the group. I had enjoyable conversations with all 3 of them, and I remember their names. Maybe this doesn't seem unusual to you, but it's a BIG change for me. It used to be that the presence of "strangers" would make me so uncomfortable that I wouldn't say anything at all, even to my old friends. It would take me weeks to warm up to new acquaintances enough to make relaxed conversation possible. And months before I had a chance of remembering their names.
>
> I've been feeling this good for several days. I sure hope this state is sustainable. Don't know if this combo would work this well for anyone else, but it's been a miracle cure for me.
>
> - Bob
>WOW! this is great news. I think Michael's come up with a great theory, with proof it works! I had heard Buspar was good for anxiety. And no side effects you say?... May I ask did you do this with the advise of your doctor? How long has it taken for the effects to kick in? Good Luck........ Daizy
Posted by Ed on March 12, 2003, at 9:36:17
In reply to SUCCESS!, posted by not exactly on March 12, 2003, at 5:51:20
Bob- do you think the Klonopin and the Buspar create a synergistic effect for you? Or do you think each addresses a different symptom cluster?
Posted by Ilene on March 12, 2003, at 9:59:06
In reply to SUCCESS!, posted by not exactly on March 12, 2003, at 5:51:20
>
> Well, I've tried to apply what I've learned from following this thread, and I'm happy to report some dramatic success. I'm now on Klonopin plus Buspar, and I'm finally experiencing virtually complete remission from my long-standing Social Phobia and comorbid treatment-resistant Atypical Depression (anhedonia, mood reactivity, hypersomnia).
>
>
> I've been feeling this good for several days. I sure hope this state is sustainable. Don't know if this combo would work this well for anyone else, but it's been a miracle cure for me.
>
> - Bob
>I wonder if there is a way to compile the experiences of PBers to correlate symptions/diagnosis with meds that work or don't work.
It would be so valuable to people who are constantly experimenting with all the possible med combinations.
I've read papers that claim X kind of med works best for Y condition, but I don't know rigorous they are. It seems so *obvious* that someone *must* have done it. Although I can see the difficulties,
My database mind is ticking away.
--I.
Posted by not exactly on March 12, 2003, at 19:22:15
In reply to Re: SUCCESS!, posted by daizy on March 12, 2003, at 9:04:45
> WOW! this is great news. I think Michael's come up with a great theory, with proof it works!
If a single datapoint can be considered "proof". YMMV, but I'm a believer now!
> I had heard Buspar was good for anxiety.
Of course, that's its only approved use. The big surprise to me was that it was such an effective antidepressant, at least for my kind of depression.
> And no side effects you say?
None of any significance. Occasional very slight headache, but it's hard to say if it is "caused" by the meds. The wonderful thing is that I don't feel like I'm on medication at all.
> May I ask did you do this with the advise of your doctor?
Yes and no. The meds I'm now taking are current prescriptions from him at the recommended dosages. The choice to stop taking the other 2 prescribed meds was unilateral. He's on vacation now, and I plan to discuss this with him when he returns. In the past, he's never expressed any concern about my choices to discontinue meds when I became convinced that they weren't helping. He knows that I do careful reasearch, understand the chemical/medical implications, and wouldn't do anything rash.
> How long has it taken for the effects to kick in?
The beneficial effects that I'm attributing to the Buspar took about a week to fully manifest. For the first few days, it made me drowsy, foggy, and anxious, but after a while, the effects became just the reverse - I'm now feeling energized, alert, and unstressed.
The Klonopin kicked in almost immediately. The initial sedation disappeared after a day or 2, leaving me feeling self-confident instead of hypersensitive. An instant cure for SP.
Of course, we don't know what (if any) effect the other (now discontinued) meds may have had on the timing or overall result.
- Bob
Posted by not exactly on March 12, 2003, at 19:28:09
In reply to Re: SUCCESS! » not exactly, posted by Ed on March 12, 2003, at 9:36:17
> do you think the Klonopin and the Buspar create a synergistic effect for you? Or do you think each addresses a different symptom cluster?
Hard to say. I'm convinced of the latter, but can't rule out synergy. I've never tried either med as a monotherapy, and I'm not about to try the controlled experiment of discontinuing either of them now.
- Bob
Posted by Ron Hill on March 13, 2003, at 2:57:23
In reply to SUCCESS!, posted by not exactly on March 12, 2003, at 5:51:20
Bob,
Thanks for posting your initial success with Klonopin and Buspar. Because of your post I added Buspar to my list of meds to investigate if my current cocktail poops out.
Thanks, and please keep us informed as to how this trial unfolds.
-- Ron
Posted by not exactly on March 13, 2003, at 4:47:36
In reply to Is the above Dr. BOB?????? (nm), posted by Krissy P on March 12, 2003, at 8:59:21
Posted by not exactly on March 13, 2003, at 5:20:27
In reply to Re: SUCCESS! » not exactly, posted by Ilene on March 12, 2003, at 9:59:06
> I wonder if there is a way to compile the experiences of PBers to correlate symptions/diagnosis with meds that work or don't work.
There are some broad generalities that yield useful guidelines for starting points [e.g. http://www.biopsychiatry.com/depressiontypes.htm] but people's reactions to meds are so ideosyncratic that a simplistic "Rx for every Dx" is unfortunately not possible. If you actually attempted to compile the sort of database you suggest, you'd find so much contradictory evidence that the information would be virtually useless. The most promising approach may be the "flowchart" model [e.g. http://www.mhc.com/Algorithms/Depression/flowchar.htm].
- Bob
Posted by not exactly on March 13, 2003, at 6:24:52
In reply to Re: SUCCESS! » not exactly, posted by Ron Hill on March 13, 2003, at 2:57:23
> I added Buspar to my list of meds to investigate if my current cocktail poops out.
I'm curious - what is your current successful cocktail, and what symptoms does it address?
> please keep us informed as to how this trial unfolds.
Will do.
- Bob
Posted by Ilene on March 13, 2003, at 9:27:35
In reply to Re: SUCCESS! » Ilene, posted by not exactly on March 13, 2003, at 5:20:27
> > I wonder if there is a way to compile the experiences of PBers to correlate symptions/diagnosis with meds that work or don't work.
>
> There are some broad generalities that yield useful guidelines for starting points [e.g. http://www.biopsychiatry.com/depressiontypes.htm] but people's reactions to meds are so ideosyncratic that a simplistic "Rx for every Dx" is unfortunately not possible. If you actually attempted to compile the sort of database you suggest, you'd find so much contradictory evidence that the information would be virtually useless. The most promising approach may be the "flowchart" model [e.g. http://www.mhc.com/Algorithms/Depression/flowchar.htm].
>
> - Bob
>As I said, there would be difficulties...I'm just noodling around. To do it right would be beyond the capacity of a mere mortal. But it's an interesting source of raw data.
(I constructed a little database as a class project that tried to match patients to clinical trials. My biggest problem was the translation of natural language into yes/no criteria. I also discovered that people who were doing this kind of thing at NIH and elsewhere were doing it *wrong*.)
The algorithms aren't much help when you've gone through 5 or 6 drug trials and combinations. Some of the recommendations seem like they are based on a show of hands. When you get all excited about a trial of chromium picolinate using 15 people, something is awry.
There's a real difference between physicians who work with patients and those who design research studies. I was astonished when I read that evidence-based medicine was controversial. (That was a few years ago. Maybe it's different now.) What is the practice of medicine supposed to be based on? The Tarot?
When you see your friendly neighborhood psychiatrist, s/he usually bases decisions on personal experience. The "art" of medicine. It's hard to discern patterns when you're not getting a statistically valid sample.
I'm starting to rant. I'd better stop before I feel the need to provide footnotes.
--I.
Posted by jflange on March 13, 2003, at 18:37:29
In reply to SUCCESS!, posted by not exactly on March 12, 2003, at 5:51:20
not exactly:
I am really excited to hear of your success, especially since I too have experienced such a huge remission of social phobic responses since adding Buspar that sometimes I also surprise myself. I too attribute it to B's influence on dopamine but I do not have a real answer for the whys or hows of its mechanism.
You might remember that I take B with Zoloft for their combined dopaminergic and serotonergic effects, but I have been thinking lately that I really do not need the Zoloft (or not as much as I take), since it seems to feel at times like speed.
So I am FASCINATED to hear of your success with Klonopin. K has been in the back of my mind, and I would LOVE to hear you say exactly what you think is going on with this drug combo to make it work for you. I know a good drug combo sometimes feels like magic dust that you'd rather not analyze, but since you say you are a (lay?) med researcher, I would like to hear what your hypothesis is.
congrats!
jflange
Posted by not exactly on March 13, 2003, at 23:48:14
In reply to Re: SUCCESS with K and Buspar, posted by jflange on March 13, 2003, at 18:37:29
> I would LOVE to hear you say exactly what you think is going on with this drug combo to make it work for you. I know a good drug combo sometimes feels like magic dust that you'd rather not analyze, but since you say you are a (lay?) med researcher, I would like to hear what your hypothesis is.
Generally, I'm attributing the SP relief to the Klonopin (GABA transmission enhancement), and the antidepressant action to the Buspar (5-HT1A & D2 effects). But it's also possible that the Klonopin is helping with the depression and the Buspar is helping with the SP. As I've mentioned earlier, I've never tried either of these drugs by themselves, so I'm not sure which one is doing exactly what, or how significant the synergy might be.
I got most of my information /theories on SP/GABA/Klonopin from Michael Bell's previous posts to this thread:
http://www.dr-bob.org/babble/20030301/msgs/206003.html
http://www.dr-bob.org/babble/20030306/msgs/206478.htmlI got most of my information /theories on Buspar from other Psycho-Babble threads:
http://www.dr-bob.org/babble/20010522/msgs/63954.html
http://www.dr-bob.org/babble/20000112/msgs/19512.htmlThe most encouraging part is that the improvement came on slowly, which makes me believe that it was a secondary effect of accomodation/downregulation. In my experience, instant good results tend to fade as my body chemistry manages to compensate for the temporary "imbalance". My hope is that the compensation has already taken place, producing the benefits rather than cancelling them out.
- Bob
Posted by Geoffrey Ruch on April 12, 2004, at 1:39:26
In reply to Re: Dopamine agonists, posted by Michael Bell on March 4, 2003, at 23:01:38
Michael,
I have not read any of the responses to your message, but I have a few questions eating at me and I was hoping you might be able to help me understand.
First of all, I read on the internet, on a site written by a doctor specializing in Social Phobia and Avoidant Personality Disorder, that Parnate is superior to Nardil in treating these disorders. So I'm confused by your assertion that Nardil is superior. Can you tell me where you got this information from. I just started on Parnate a few weeks ago and I'm curious as to why I'm hearing conflicting information.
Next, and most puzzling to me is in regards to Norepinephrine. I am aware that it acts both as a neurotransmitter (in the brain) as well as a hormone from the adrenal cortex. Now, many hypotheses about the cause of depression relate to the belief that Norepinephrine levels are low in the brains of depressives, and thus increasing levels of this neurotransmitter could help in the treatment of depression. Obviously there are numerous drugs out, including Tricyclics, MAO inhibitors, and newer drugs like Effexor, etc. that do just that. Additionally, naturopathic doctors recommend such supplements like the amino acid precursors L-Tyrosine and Phenylalanine (in part) because they can increase Norepinephrine levels in the brain (as well as Dopamine levels). And I've even read that L-Tyrosine has anti-stress qualities (ie. helping people cope with stress). For instance, in a book called "Prescription for Nutritional Healing," Tyrosine is at the top of the list of recommended supplements to deal with stress.
Now with all this said, Norepinephrine as a hormone is involved in the "fight or flight" stress response, and it seems, therefore, that it would increase stress and not HELP with dealing with it; and it would seem that this would impact negatively on depression (ie. increased stress can cause depression). So I'm incredibly confused! I mean, what's the deal? Is Norepinephrine, as a neurotransmitter, a completely different substance from the hormone? Or are some people with depression lacking in this hormone in addition to the neurotransmitter?
If you-- or anybody else-- could help me understand this (or direct me to where I could find help in understanding it) I would be GREATLY appreciative!!! I mean, if a depressed person under constant inner stress could benefit from increased levels of the NE neurotransmitter but be negatively impacted because of higher NE hormone levels, then what is one to do in such a case??? I'm sure the situation is very complex and it's not as simple as I have laid it out to be. Still, though, there has to be some kind of way to understand it. It's a shame I never asked my psychiatrist to explain it. Now I see a county doctor (in L.A.) who I see for about 20 minutes a session every month and a half, and I really haven't had the time to ask for an explanation.
Anyway, thank you all for allowing me into this discussion!!! I hope it is not too "off-topic." But I think it is relevant nevertheless.
Posted by Michael Bell on April 12, 2004, at 20:20:33
In reply to Re: Dopamine agonists » Michael Bell, posted by Geoffrey Ruch on April 12, 2004, at 1:39:26
> Michael,
> I have not read any of the responses to your message, but I have a few questions eating at me and I was hoping you might be able to help me understand.
> First of all, I read on the internet, on a site written by a doctor specializing in Social Phobia and Avoidant Personality Disorder, that Parnate is superior to Nardil in treating these disorders. So I'm confused by your assertion that Nardil is superior. Can you tell me where you got this information from. I just started on Parnate a few weeks ago and I'm curious as to why I'm hearing conflicting information.
>
> Next, and most puzzling to me is in regards to Norepinephrine. I am aware that it acts both as a neurotransmitter (in the brain) as well as a hormone from the adrenal cortex. Now, many hypotheses about the cause of depression relate to the belief that Norepinephrine levels are low in the brains of depressives, and thus increasing levels of this neurotransmitter could help in the treatment of depression. Obviously there are numerous drugs out, including Tricyclics, MAO inhibitors, and newer drugs like Effexor, etc. that do just that. Additionally, naturopathic doctors recommend such supplements like the amino acid precursors L-Tyrosine and Phenylalanine (in part) because they can increase Norepinephrine levels in the brain (as well as Dopamine levels). And I've even read that L-Tyrosine has anti-stress qualities (ie. helping people cope with stress). For instance, in a book called "Prescription for Nutritional Healing," Tyrosine is at the top of the list of recommended supplements to deal with stress.
> Now with all this said, Norepinephrine as a hormone is involved in the "fight or flight" stress response, and it seems, therefore, that it would increase stress and not HELP with dealing with it; and it would seem that this would impact negatively on depression (ie. increased stress can cause depression). So I'm incredibly confused! I mean, what's the deal? Is Norepinephrine, as a neurotransmitter, a completely different substance from the hormone? Or are some people with depression lacking in this hormone in addition to the neurotransmitter?
> If you-- or anybody else-- could help me understand this (or direct me to where I could find help in understanding it) I would be GREATLY appreciative!!! I mean, if a depressed person under constant inner stress could benefit from increased levels of the NE neurotransmitter but be negatively impacted because of higher NE hormone levels, then what is one to do in such a case??? I'm sure the situation is very complex and it's not as simple as I have laid it out to be. Still, though, there has to be some kind of way to understand it. It's a shame I never asked my psychiatrist to explain it. Now I see a county doctor (in L.A.) who I see for about 20 minutes a session every month and a half, and I really haven't had the time to ask for an explanation.
> Anyway, thank you all for allowing me into this discussion!!! I hope it is not too "off-topic." But I think it is relevant nevertheless.
>The difficult thing about understanding the neurotransmitter systems is that they all seem to modulate each other on some level. Therefore tinkering with one specific transmitter will often have indirect effects on others, or messenger hormones. Making it more complicated is the fact that each transmitter has a variety of pre- and post-synaptic receptors that respectively regulate and are stimulated by the matching neurotransmitter. Furthermore, these receptors will often down or up-regulate in response to increases or decreases in transmission.
Now I'll try to address your question, if I haven't put you to sleep yet.
Norepinephrine is very much implicated in some types of depression, as supported by countless studies on bipolar disorder, selective norepinephrine reuptake inhibitors and unipolar depression. However, there are different types, degrees and causes of depression. Therefore drugs that primarily affect the norepinephrine system may help some who are diagnosed with depression and not others.
Regarding SOCIAL PHOBIA - My conclusion that Nardil is more effective than Parnate for the vast majority of people comes from talking with my P-Doc, a whole lot of internet research, and the makeup of the drug itself.
People with primary social phobia seem to suffer from two major things:1) Fear of social situations (the GABA part)
and
2) Reward deficiency in social situations (the DOPAMINE part)
Regarding #1:
I have no doubt that GABA disfunction is one of the main (if not the main) problems in social phobia. The most effect drugs for social phobia - klonopin, nardil, alcohol and ghb - all have huge effects on the GABA or benzo system. It is the main inhibitory transmitter/hormone in our brains and has been linked to anxiety issues by overwhelming evidence. NARDIL, unlike parnate, is an gaba transanimase inhibitor, meaning it inhibits the enzyme that breaks down GABA (like Sabril, I think). It has been hypothesized that it is this action that makes Nardil so effective for social phobia, on top of its antidepressant effect. But if you find Parnate is working well for you, then definitely stick with it. If you suffer from depression as well, Parnate should definitely alleviate that to some degree. Keep in mind it tends to be an activating drug.Regarding #2: The thing that is so strange about social phobia is that there seems to be a disfunction of two transmitter systems that are polar (well, not quite) opposites: DOPAMINE and GABA. Reward deficiency syndrome as it relates to social anhedonia has been linked to hypofunction of the dopamine system in the mesolimbic portion of the brain. Release of dopamine and binding to postsynaptic receptors is the final pathway in the reward cascade.
Therefore you will often see people with social phobia complaining that, although drugs like Klonopin work wonders for the anxiety part of social phobia, they do not aid with the reward part. In other words, they are not prosocial meds, and do not increase your approach behavior. At the other end of the spectrum, Amisulpride has proven quite effective for dysthimia and anhedonia by binding to dopamine pre-synaptic receptors and increasing transmission.
So the question remains: IF GABA AND DOPAMINE TRANSMISSION/LEVELS ARE INVERSELY RELATED, HOW THE HELL DO PEOPLE WITH SOCIAL PHOBIA INCREASE ONE WITHOUT DECREASING THE OTHER?
Some people have tackled this dilemma by taking Klonopin to kill the anxiety along with adderall/dexedrine to jumpstart the dopamine system. When it works, this combo is very prosocial in nature, though I wouldn't recommend it to anyone who doesn't suffer from adhd.
My feeling all along has been that there is some other transmitter or hormone system that regulates anxiety and reward at the same time, and that it is actually disfunction of this system that is the root cause of social phobia.
My research (which could be way off) has led me to believe that problems with the cholecystokinin (CCK) system is a good candidate for being that mystery system, as it serves as a sort of nexus between gaba and dopamine, and has proven links to anxiety and reward problems. CCK-B antagonists have proven anxiogenic effects, and increase dopamine in certain parts of the brain. Interestingly, high levels of cholecystokinin are linked with anticipatory anxiety, social defeat. CCK also serves as an anti-opiate and lowers the body's natural level of opiods. The opiod system serves as a reward pathway as well.
Hmmm... I think I may import one of these cck antagonists from overseas when I get the chance.
More on this later...
Posted by King Vultan on April 12, 2004, at 20:22:22
In reply to Re: Dopamine agonists » Michael Bell, posted by Geoffrey Ruch on April 12, 2004, at 1:39:26
My understanding is that Nardil is better for social phobia than Parnate for two reasons: 1) Nardil is skewed much more towards serotonin than is Parnate and 2) Nardil also works on GABA, while Parnate does not. Serotonin seems to be the neurotransmitter most identified with social phobia. Paxil, which is FDA approved for social anxiety disorder, is obviously a very powerful SSRI. Nardil's actions on GABA likely have further anti-anxiety effects, which it would have in common with the benzodiazepines.
As for norepinephrine and depression/panic/anxiety, I think this is a complex topic. While it's true that people who suffer from panic attacks are thought to perhaps have overactive norepinephrine systems, this is really a separate issue from that of depression and social anxiety. My own experience (which may be somewhat atypical), and as someone who mainly suffers from depression and social phobia is that I found NE reuptake inhibitors actually quite helpful for both conditions despite moderately increasing my overall anxiety levels. Blocking NE reuptake gave me both an antidepressant lift and an increase in self confidence, self esteem, and assertiveness.
I've also gotten an antidepressant lift from SSRIs and some relief from my social phobia, but for me, anyway, the NE reuptake inhibitors were more effective on the latter. I don't know if I am unique in this respect or if I necessarily have a good explanation for this. As far as Nardil's effects on social phobia, I think it's worth pointing out that if Nardil is highly serotonergic, it follows that it should have a similarly powerful effect on norepinephrine because both neurotransmitters are metabolized by MAO-A. Also, Paxil has the greatest affinity in absolute terms for the NE reuptake transporter of any of the SSRIs (it also has the greatest affinity for the serotonin reuptake transporter). I don't know if these effects on NE actually confer any real ability on social phobia, but I thought I would share the observation.
Todd
Posted by Geoffrey Ruch on April 13, 2004, at 0:47:51
In reply to Re: Dopamine agonists (and CCK) - LONG POST! » Geoffrey Ruch, posted by Michael Bell on April 12, 2004, at 20:20:33
Thank you Michael and "King Vultan" very much for your insights. I appreciate that you responded so quickly.
I don't know why the web site I visited regarding Social Phobia specifically recommended Parnate over Nardil, but it certainly did-- and pretty emphatically. I'll have to look back at that and re-read what it says.
Anyway, I'm hoping that if you, Michael, are correct in that Nardil has the distinct advantage over Parnate of inhibiting the breakdown of GABA, that either adding Klonopin to Parnate (which I have been doing with modest success), and/or adding GABAergic herbs such as Ashwagandha and/or Gotu Kola and/or Valerian and/or others; and/or adding L-Theanine (a GABA "manufacturer" from Green Tea), etc. might make up for the lack of GABAergic properties of Parnate.
With respect to the Klonopin, which I have been taking 2mg of each day, I really don't want to be taking that for very long because of its potential for dependency. The web site I read said not to worry about this, but eventually I think it would be wise of me to cut down and go off of it somewhere down the road-- if not sooner.
And one more thing I wanted to "reveal" is that I have been adding a small dosage of 5-Hydroxy-Tryptophan (5HTP) as well as a small dosage of L-Phenylalanine (LPA). The 5HTP is obviously to enhance Serotonin levels, and the LPA is primarily to enhance the production of 2-Phenylethylamine (PEA, the brain's amphetimine "love molecule")-- DL-Phenylalanine (DLPA) might be a better choice, adding the demention of inhibiting the breakdown of endorphins; and perhaps DLPA is slightly more safe (I don't know). I realize that this could be a risky endeavor (and that these "supplements" usually are pretty strongly contraindicated with MAO inhibitors), but I have not had any problems with them so far. And I have read (from what seem to reputable sources) that these could potentially be helpful if used cautiously/wisely. I'm trying to be very careful (eg. checking my blood pressure regularly), and I wouldn't necessarily recommend it to anybody. I just have been debilitated by depression and anxiety/fear for so long that I feel like I need to take a chance. I kind of feel like I am on a depression/Social Phobia "cocktail," and I guess I'll see how it works out. [Note: I know that 5HTP is contraindicated because of the potential for the "Serotonin Syndrome," but I must say that I am confused about why Phenylalanine and Tyrosine are so contraindicated with MAOi's. I can understand large dosages being a very bad idea, but technically/scientifically I guess I just don't understand what the risk is, especially in small dosages.]
By the way, I just want to add, also, that I understand that healing depression and anxiety disorders, depending on the individual, often must involve much more than changing brain chemistry through medications, herbs, amino acids, etc. Supposedly Interpersonal psychotherapy or Cognitive Behavioral Therapy (and others) can be very effective treatments in their own right-- with severe cases most likely needing both types of treatment synergistically. I have gone the therapy route several times throughout the years (in addition to medication) with little success, but I still believe that at some point it is going to prove very important.
Anyway, I welcome any responses to my post. Thank you.
Posted by zeugma on April 13, 2004, at 8:05:55
In reply to Re: Nardil, Parnate, NE, Social Phobia » Geoffrey Ruch, posted by King Vultan on April 12, 2004, at 20:22:22
> My understanding is that Nardil is better for social phobia than Parnate for two reasons: 1) Nardil is skewed much more towards serotonin than is Parnate and 2) Nardil also works on GABA, while Parnate does not. Serotonin seems to be the neurotransmitter most identified with social phobia. Paxil, which is FDA approved for social anxiety disorder, is obviously a very powerful SSRI. Nardil's actions on GABA likely have further anti-anxiety effects, which it would have in common with the benzodiazepines.
It's my understanding that serotonin is involved in stable bodily self-perception somehow. Social phobia for me is a very visceral feeling of being physically inadequate, and even repulsive. this causes tremendous self-consciousness and anxiety when interacting with others. Clonazepam calms me down, but does not eliminate this feeling (similar effect to a little alcohol). Definitely, GABA is involved, but it's not the whole story, at least for me.
>
> As for norepinephrine and depression/panic/anxiety, I think this is a complex topic. While it's true that people who suffer from panic attacks are thought to perhaps have overactive norepinephrine systems, this is really a separate issue from that of depression and social anxiety. My own experience (which may be somewhat atypical), and as someone who mainly suffers from depression and social phobia is that I found NE reuptake inhibitors actually quite helpful for both conditions despite moderately increasing my overall anxiety levels. Blocking NE reuptake gave me both an antidepressant lift and an increase in self confidence, self esteem, and assertiveness.NE reuptake inhibitors help my ADD, which in itself has caused an increase in confidence, and have alleviated my depression to a great degree. They have done absolutely nothing for social anxiety, although I have only had one panic attack since starting an NE reuptake inhibitor, leading me to believe that panic is noradrenergically mediated, while social anxiety is not (at least in my case).
>
> I've also gotten an antidepressant lift from SSRIs and some relief from my social phobia, but for me, anyway, the NE reuptake inhibitors were more effective on the latter. I don't know if I am unique in this respect or if I necessarily have a good explanation for this. As far as Nardil's effects on social phobia, I think it's worth pointing out that if Nardil is highly serotonergic, it follows that it should have a similarly powerful effect on norepinephrine because both neurotransmitters are metabolized by MAO-A. Also, Paxil has the greatest affinity in absolute terms for the NE reuptake transporter of any of the SSRIs (it also has the greatest affinity for the serotonin reuptake transporter). I don't know if these effects on NE actually confer any real ability on social phobia, but I thought I would share the observation.
>I suspect that my social anxiety is more serotonin- than dopamine-mediated. The thoughts that come to mind when experiencing social anxiety are related to distorted body image (this may not be everyone's experience of course). the way to test this hypothesis would be to try a little clomipramine in lieu of nortriptyline. But given the relative success of Paxil when treating social anxiety, and the fact that SSRI's treat Body Dymorphic Disorder, i would guess that serotonin would be intimately involved in many cases of social anxiety.
Making this all the more complicated is the fact that serotonin and dopamine also seem to be in competitive balance. The consensus I've gotten from people is that SSRi's elicit a 'don't care' attitude in response to imagined flaws, which is consistent with the self-perception hypothesis, but that this attitude generalized causes demotivation and anhedonia. Maybe clomipramine, because of its powerful NE effects (many times more powerful than Paxil) causes less problems with this. And maybe, if you're less preoccupied with imagined flaws, you need less motivation to get by. Anyway, it will be a little clomipramine mixed in with my TCA in a month, if things don't improve.
> Todd
Posted by Iansf on April 13, 2004, at 19:12:42
In reply to Re: Nardil, Parnate, NE, Social Phobia, posted by zeugma on April 13, 2004, at 8:05:55
> > My understanding is that Nardil is better for social phobia than Parnate for two reasons: 1) Nardil is skewed much more towards serotonin than is Parnate and 2) Nardil also works on GABA, while Parnate does not. Serotonin seems to be the neurotransmitter most identified with social phobia. Paxil, which is FDA approved for social anxiety disorder, is obviously a very powerful SSRI. Nardil's actions on GABA likely have further anti-anxiety effects, which it would have in common with the benzodiazepines.
>
> It's my understanding that serotonin is involved in stable bodily self-perception somehow. Social phobia for me is a very visceral feeling of being physically inadequate, and even repulsive. this causes tremendous self-consciousness and anxiety when interacting with others. Clonazepam calms me down, but does not eliminate this feeling (similar effect to a little alcohol). Definitely, GABA is involved, but it's not the whole story, at least for me.
> >I would have to agree that serotonin seems to be the main neurotransmitter involved with social phobia. I had the most success dealing with it when I took Prozac and Luvox, both of which work primarily on serotonin. if the side effects hadn't been so problematic, I'd be on one of them now. Life was SO much easier and more fulfilling when I was on them. In contrast, I'm now taking Wellbutrin, which acts on norepinephrine and dopamine, and it is virturally useless in terms of reducing social phobia.
Wellburtin helps with depression, but the continued presence of social phobia limits its effectiveness even in this regard. Because I can't do what I want to do, because I'm alone so much and because I struggle financially - all due to social phobia - it's very difficult to keep my spirits up.
So for me at least, what's needed is an SSRI that doesn't destroy my sex life, make me too uncaring and make me sleep either too much or too little. How I wish a med like that were available.
Posted by Geoffrey Ruch on April 14, 2004, at 0:30:53
In reply to Re: Nardil, Parnate, NE, Social Phobia » zeugma, posted by Iansf on April 13, 2004, at 19:12:42
I just wanted to give the web site of "The Anxiety Network International," and specifically the pages which talk about how Parnate is superior to Nardil in treating Social Phobia and Avoidant Personality. I'm incredibly confused as to why one source says one thing and another says something different. But anyway, if anybody cares to read about it, the address is: www.anxietynetwork.com/spmed.html
Posted by Michael Bell on May 5, 2004, at 0:38:42
In reply to Re: Dopamine agonists (and CCK) - LONG POST! » Michael Bell, posted by Geoffrey Ruch on April 13, 2004, at 0:47:51
Sorry it took so long to reply. I'd like to address a couple issues you raised. My responses are in CAPS under your statements
> Thank you Michael and "King Vultan" very much for your insights. I appreciate that you responded so quickly.
>
> I don't know why the web site I visited regarding Social Phobia specifically recommended Parnate over Nardil, but it certainly did-- and pretty emphatically. I'll have to look back at that and re-read what it says.DEFINITELY DO AS MUCH RESEARCH AS POSSIBLE. THE MORE INFORMED YOU ARE, THE MORE CONFIDENT YOU'LL BE WHEN TALKING TO P-DOCS. LIKE I SAID, IF PARNATE WORKS FOR YOU, STICK WITH IT, BUT I CAN TELL YOU IN MY OWN EXPERIENCE NARDIL DESTROYED SOCIAL PHOBIA.
>
> Anyway, I'm hoping that if you, Michael, are correct in that Nardil has the distinct advantage over Parnate of inhibiting the breakdown of GABA, that either adding Klonopin to Parnate (which I have been doing with modest success), and/or adding GABAergic herbs such as Ashwagandha and/or Gotu Kola and/or Valerian and/or others; and/or adding L-Theanine (a GABA "manufacturer" from Green Tea), etc. might make up for the lack of GABAergic properties of Parnate.
>
ALSO CHECK OUT PICAMILON, WHICH IS GABA COMBINED WITH NIACIN. L-THEANINE WORKED OKAY FOR ANXIETY. NEVER TRIED VALERIAN OR ASHWAGANDHA.> With respect to the Klonopin, which I have been taking 2mg of each day, I really don't want to be taking that for very long because of its potential for dependency. The web site I read said not to worry about this, but eventually I think it would be wise of me to cut down and go off of it somewhere down the road-- if not sooner.
>
THIS IS A HOTLY DEBATED TOPIC. BENZOS CAN BE HABIT FORMING, BUT MANY DOCTORS CLAIM THAT THIS IS NOT THE CASE FOR THOSE WITH TRUE PHYSIOLOGICAL ANXIETY DISORDERS. I'VE BEEN TAKING ABOUT 1MG A DAY OF KLONOPIN FOR A WHILE, AND DO NOTICE SOME REBOUND ANXIETY IF I SKIP A FEW DAYS. EITHER WAY, ASK YOURSELF THIS: WOULD YOU RATHER BE MED-FREE BUT COMPLETELY OWNED BY YOUR SOCIAL ANXIETY, OR RISK POSSIBLE DEPENDENCY ON A DRUG THAT DOES WONDERS FOR THE ANXIETY? REMEBER, YOU CAN ALWAYS TAPER OFF WHEN A BETTER MED COMES ALONG IN THE FUTURE.
> And one more thing I wanted to "reveal" is that I have been adding a small dosage of 5-Hydroxy-Tryptophan (5HTP) as well as a small dosage of L-Phenylalanine (LPA). The 5HTP is obviously to enhance Serotonin levels, and the LPA is primarily to enhance the production of 2-Phenylethylamine (PEA, the brain's amphetimine "love molecule")-- DL-Phenylalanine (DLPA) might be a better choice, adding the demention of inhibiting the breakdown of endorphins; and perhaps DLPA is slightly more safe (I don't know). I realize that this could be a risky endeavor (and that these "supplements" usually are pretty strongly contraindicated with MAO inhibitors), but I have not had any problems with them so far. And I have read (from what seem to reputable sources) that these could potentially be helpful if used cautiously/wisely. I'm trying to be very careful (eg. checking my blood pressure regularly), and I wouldn't necessarily recommend it to anybody. I just have been debilitated by depression and anxiety/fear for so long that I feel like I need to take a chance. I kind of feel like I am on a depression/Social Phobia "cocktail," and I guess I'll see how it works out. [Note: I know that 5HTP is contraindicated because of the potential for the "Serotonin Syndrome," but I must say that I am confused about why Phenylalanine and Tyrosine are so contraindicated with MAOi's. I can understand large dosages being a very bad idea, but technically/scientifically I guess I just don't understand what the risk is, especially in small dosages.]
>
PHENYLALANINE AND TYROSINE ARE (GENERALLY) CONVERTED INTO DOPAMINE, WHICH CONVERTS INTO NORADRENALINE. YOU DON'T WANT TO INCREASE NORADRENALINE RELEASE WHEN TAKING AN MAOI. BY THE WAY, RECENT STUDIES OF DPLA HAVE CONTRADICTED THE EARLIER CLAIMS THAT DPLA INHIBITS THE BREAKDOWN OF ENDORPHINS.> By the way, I just want to add, also, that I understand that healing depression and anxiety disorders, depending on the individual, often must involve much more than changing brain chemistry through medications, herbs, amino acids, etc. Supposedly Interpersonal psychotherapy or Cognitive Behavioral Therapy (and others) can be very effective treatments in their own right-- with severe cases most likely needing both types of treatment synergistically. I have gone the therapy route several times throughout the years (in addition to medication) with little success, but I still believe that at some point it is going to prove very important.
>
I'M SURE THAT CBT CAN HELP WITH CHANGING CERTAIN THOUGHT PATTERNS AND HOW YOU PERCEIVE SITUATIONS. BUT I HAVE NO DOUBT THAT MANY CASES OF GENERALIZED SOCIAL PHOBIA ARE STRICTLY PHYSIOLOGICALLY BASED. THERE IS A BRAIN CHEMICAL DISFUNCTION AT WORK, AND MEDS ARE IMPORTANT IN REMEDYING THAT.
> Anyway, I welcome any responses to my post. Thank you.I WISH YOU THE BEST.
Posted by kenny7 on November 12, 2008, at 20:58:03
In reply to Re: Dopamine agonists » Stan, posted by not exactly on March 6, 2003, at 4:48:01
If you were a scientist (pharmacist,) you'd have noticed by now Buspar only looks good on paper. It is not for Social Anxiety. It makes you extrememly dizzy, and then thats it. I was on 45 within a couple of weeks. Neurontin, Mr. Scientist, should only be a poor part of an augmentation strategy. Michael, that "theory" is wrong on many counts. The brain doesn't just work that way. If dopamine were left alone in the brain it would adapt as if it does with multiple other receptors in the brain. "Gaba" is the key? It shouldn't be your first line treatment but benzos are best for GABA. The pills don't work...they are different. Who was asking about an AD+benzo combo? If your anxiety weren't made up...You'd realize anxiety increases at the initiation of treatment with an AD. Not my girl Nardil though. I'm lucky enough to be pumping 90mg of that into my body. Still, I have seen specialists in Boston and at major Universities and my Social Anxiety is refractory (treatment resistant.) So next time one of you people nlush...Think of people with twitching faces as they simply enter a room. Nardil is the greatest drug for SP; hands down! It is not a culprit...Haha.
Posted by kenny7 on November 12, 2008, at 21:05:19
In reply to Re: Dopamine agonists » Michael Bell, posted by Ilene on March 9, 2003, at 21:28:29
I've read this too much! EPINEPHRINE is adrenaline. Stop reading WIKIpedia and go to school. You learn mad sh*t.
Posted by kenny7 on November 12, 2008, at 21:09:18
In reply to SUCCESS!, posted by not exactly on March 12, 2003, at 5:51:20
Neurontin sedating? Just wait...I've been on Clonazepam for over 9 months at 3 mg. I cannot possibly get off. Your "remission" has nothing to do with the buspar.Solely, the kpin. It WILL make your depression worse if taken daily (if you have real SP, you will take it daily) I guarantee it.
This is the end of the thread.
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