![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 51. This is the beginning of the thread.
Posted by Denise528 on March 12, 2002, at 13:08:28
Hello,
Does anyone know when CRF antagonists will be available? Are we talking 5 or even 10 years?
Denise
Posted by OldSchool on March 12, 2002, at 15:04:58
In reply to CRF Antagonists, posted by Denise528 on March 12, 2002, at 13:08:28
> Hello,
>
> Does anyone know when CRF antagonists will be available? Are we talking 5 or even 10 years?
>
> DeniseI wouldnt count on CRF-Antagonists anytime soon. Id say IF they ever come out, it will be ten more years. Furthermore if they ever do come out there is nothing to say they will be anything better than whats already available now.
Old School
Posted by Denise528 on March 13, 2002, at 13:01:48
In reply to Re: CRF Antagonists, posted by OldSchool on March 12, 2002, at 15:04:58
Thanks for the response, I suppose I'm just clutching at straws.
What I really want to know is why SSRIs and tricyclics are no longer working when they used to work so well when I came off them two years ago they were still working so hadn't pooped out at all. Surely there must be a scientific reason for this, am I just not creating any Serotonin in the first place, I really don't understand.The depression is the same as it was before so I still think it is serotonin related. The only reason I knew back then that I was suffering from depression and not some physical disease was that an AD cleared up all my symptoms. Now they don't, does that mean I'm not depressed?
Any ideas?Denise
Posted by OldSchool on March 13, 2002, at 13:21:01
In reply to Re: CRF Antagonists, posted by Denise528 on March 13, 2002, at 13:01:48
> Thanks for the response, I suppose I'm just clutching at straws.
> What I really want to know is why SSRIs and tricyclics are no longer working when they used to work so well when I came off them two years ago they were still working so hadn't pooped out at all. Surely there must be a scientific reason for this, am I just not creating any Serotonin in the first place, I really don't understand.
>
> The depression is the same as it was before so I still think it is serotonin related. The only reason I knew back then that I was suffering from depression and not some physical disease was that an AD cleared up all my symptoms. Now they don't, does that mean I'm not depressed?
>
>
> Any ideas?
>
> DeniseThere is some info on this site regarding "SSRI poopout." Its in the tips and tricks section. Basically, the most common hypothesis as to why ADs poop out over the long haul is dopamine depletion. Many ADs, particularly the serotonergic ones, dampen the dopamine system when taken long term.
Im building a website myself and will have information on this subject at my site.
Old School
Posted by IsoM on March 13, 2002, at 21:52:23
In reply to Re: CRF Antagonists, posted by Denise528 on March 13, 2002, at 13:01:48
I really agree with Old School's idea about dopamine depletion. Dopamine seems to be at the root of the changing face of depression over the years (especially after AD treatment) in depressed people. For me, I find that something that boosts my dopamine levels (or whatever it does to change their expression) works much better in me now than any simple AD.
Posted by Bob on March 13, 2002, at 22:02:18
In reply to Re: Dopamine » Denise528, posted by IsoM on March 13, 2002, at 21:52:23
> I really agree with Old School's idea about dopamine depletion. Dopamine seems to be at the root of the changing face of depression over the years (especially after AD treatment) in depressed people. For me, I find that something that boosts my dopamine levels (or whatever it does to change their expression) works much better in me now than any simple AD.
==================================================
This really begs a big question for me. If this is even remotely possible, then why in the f%#$ aren't the researchers doing studies on this? If they've done studies on this and come to positive conclusions about it, then how come it seems like pdocs in general don't know it? They just keep banging away with SSRIs, and occasionally norepinephrine. Our tools for enhancing dopamine are pathetically limited.
Posted by OldSchool on March 13, 2002, at 22:37:12
In reply to Re: Dopamine » IsoM, posted by Bob on March 13, 2002, at 22:02:18
> > I really agree with Old School's idea about dopamine depletion. Dopamine seems to be at the root of the changing face of depression over the years (especially after AD treatment) in depressed people. For me, I find that something that boosts my dopamine levels (or whatever it does to change their expression) works much better in me now than any simple AD.
>The reason is the war on drugs. Pharmaceutical companies dont want to go there and develop dopaminergic antidepressants for legal/liability reasons. See, the drug companies are afraid that if they create ADs which are heavily dopaminergic, they might become drugs of abuse. Many of the illegal drugs of abuse cause a sudden spike or surge in dopamine, which is extremely pleasureable (cocaine, crack, amphetamines).
The other reason has to do with the fact dopaminergic meds might be worse at causing mania or inducing psychosis...again its a liability thing more than anything.
Presently in the USA, if you want a dopaminergic antidepressant you are basically limited to the older MAOIs. Stimulants like Ritalin can be used also as can parkinsons drugs like Mirapex or Amantadine. But these can be troublesome to work with and have bad side effects. Really, all thats available for depression is MAOIs.
There was an antidepressant marketed briefly back in the eighties called Nomifensine. It was extremely dopaminergic and a lot of people really liked it. It was supposed to be great for retarded depression, severe depression, etc. Sadly it was recalled by the FDA. It was the only real true dopaminergic antidepressant ever fielded in the USA besides the MAOIs.
Oh yeah...ECT increases dopamine a lot. ECT has off label anti-parkinsons properties. Its pretty weird that the two best treatments for severe depression...MAOIs and ECT...are both heavily dopaminergic. Kinda tells ya something maybe huh?
Old School
Posted by Bob on March 14, 2002, at 1:25:57
In reply to Re: Dopamine, posted by OldSchool on March 13, 2002, at 22:37:12
Well... all I can say is that if that truly is the case, and dopamine is a promising AD, than that is truly pathetic and sad. It really is.
Posted by OldSchool on March 14, 2002, at 9:57:37
In reply to Re: Dopamine » OldSchool, posted by Bob on March 14, 2002, at 1:25:57
> Well... all I can say is that if that truly is the case, and dopamine is a promising AD, than that is truly pathetic and sad. It really is.
I wouldnt put it quite like that. Pure dopamine antidepressants I dont think is a good idea. However, with many of the current ADs like SSRIs, as you increase serotonin dopamine levels go down gradually and get that poop out of affective "flattening" many complain about on SSRIs.
To solve this problem maybe pharmaceutical companies should try harder to bring a few RIMA MAOIs to the US market, like moclobemide. That would solve the dopamine problem pretty good.
Old School
Posted by Ron Hill on March 14, 2002, at 12:07:11
In reply to Re: CRF Antagonists, posted by OldSchool on March 13, 2002, at 13:21:01
> There is some info on this site regarding "SSRI poopout." Its in the tips and tricks section. Basically, the most common hypothesis as to why ADs poop out over the long haul is dopamine depletion. Many ADs, particularly the serotonergic ones, dampen the dopamine system when taken long term.
-------------------------
Mr. Old School;
I share your belief that SSRI's dampen the dopamine system when taken long term. I do not have hard data to support this belief, but instead it is merely a layman's antidotal self-observation.
For years I was stuck. Without an AD to increase serotonin I was severely depressed. When using an AD to raise serotonin I struggled with what I consider to be low dopamine symptoms (very low motivation, low energy, blunted emotions, etc). At the risk of sounding too overly simplistic, SAM-e has by and large solved this problem for me. I fully realize that we patients are all different and, therefore, what works for me may not work for others. At the same time, however, I have a hunch that there are a lot of people here in Babbleland that could potentially be helped by this over-the-counter (in US) product, albeit an expensive OTC product.
SAM-e is a naturally occurring compound and is manufactured by the human body. However, some people do not produce enough of it and supplementation may be beneficial.
SAM-e is involved in a plethora of various biochemical reactions in the human body. It functions as a very important methyl group donor. With regard to mood and related brain chemistry, SAM-e serves as the methylating agent in the biochemical reaction mechanism whereby various neurotransmitters (serotonin and dopamine in particular) are synthesized from the amino acids in dietary protein.
My layman's opinion regarding the mechanism by which SAM-e helps me is that it raises the serotinin and dopamine levels in my brain in a "balanced" fashion. The following paragraphs give a little more detail regarding my particular situation and the specifics of my SAM-e dosing. Also check out the links at the bottom of this page.
I'm Bipolar II. Lithobid adequately controls my hypomania but does nothing for my depression. Any of the SSRI's will take away my "I want to die" mood but leave me with side effects (loss of ambition, loss of energy, lack of motivation, blunted emotions, etc). I have tried a ton of other ADs over the years, but I will not bore you with the details.
Four months ago I went to my regularly scheduled visit with my pdoc. At the time, I was only taking Li because of the AD side effects and, therefore, depression was a problem. My pdoc had recently reviewed several studies showing success in treating depression using SAM-e in conjunction with an AD and success using SAM-e alone. He suggested that I take two 200 mg SAM-e tablets daily in conjunction with 25 mg of Zoloft. (I am hypersensitive to most medication so I take small doses). Initially, I was skeptical because over the years I have taken a lot of over-the-counter supplements, most of which did very little to ease my depression. But I told my pdoc that I would give it a try.
Initially I could only take one 200 mg tablet of SAM-e every other day. If I took more, I would experience side effects (flush, nausea, confused thinking, general ill feeling, "skin crawling"). However,within about five days, my depression began to lift and I now have my life back. Yeah!!! Currently, I take one 200 mg tablet daily without any adverse side effects. In total I daily take 600 mg Lithobid, 12.5 mg Zoloft, and 200 mg SAM-e. Eventually, I plan to discontinue the small amount of Zoloft.
Bottom line: 200 mg SAM-e daily has helped me more than any of the many ADs I've tried over the years. For me personally, SAM-e has turned out to be a lifesaver! I have waited to post on this topic until I gave it some time to make sure it did not poop out right away. So far I have four months of excellent results and absolutely no hint of poop out.
It is very important to take plenty of B-6, B-12 (use sublingual form) and folate with the SAM-e to prevent the build up of homocystiene. Also, SAM-e is absorbed more efficiently by the small intestines when it is taken on an empty stomach. However, I usually eat a small bite ot food to reduce nausea. SAM-e, like many perscription ADs, can induce mania in bipolar patients if the patient is not taking an adequate amount of a mood stablizer.
Here are some links to articles on the topic. Do some research (use "SAM-e" in search engine). Buy a good name brand to ensure product quality.
http://www.biopsychiatry.com/sameart.html
http://more.abcnews.go.com/sections/living/inyourhead/allinyourhead_36.html
http://www.psycom.net/depression.central.same.html
http://www.mhsource.com/expert/exp1041299b.html
http://www.arthritissupport.com/track/goto/rtgoto30l.cfm
-- Ron
Posted by Ritch on March 14, 2002, at 12:38:29
In reply to Re: SAM-e May Increase Dopamine Production » OldSchool, posted by Ron Hill on March 14, 2002, at 12:07:11
>.... Initially I could only take one 200 mg tablet of SAM-e every other day. If I took more, I would experience side effects (flush, nausea, confused thinking, general ill feeling, "skin crawling"). However,within about five days, my depression began to lift and I now have my life back. Yeah!!! Currently, I take one 200 mg tablet daily without any adverse side effects. In total I daily take 600 mg Lithobid, 12.5 mg Zoloft, and 200 mg SAM-e. Eventually, I plan to discontinue the small amount of Zoloft.
>
> Bottom line: 200 mg SAM-e daily has helped me more than any of the many ADs I've tried over the years. For me personally, SAM-e has turned out to be a lifesaver! I have waited to post on this topic until I gave it some time to make sure it did not poop out right away. So far I have four months of excellent results and absolutely no hint of poop out.
>
> It is very important to take plenty of B-6, B-12 (use sublingual form) and folate with the SAM-e to prevent the build up of homocystiene. Also, SAM-e is absorbed more efficiently by the small intestines when it is taken on an empty stomach. However, I usually eat a small bite ot food to reduce nausea. SAM-e, like many perscription ADs, can induce mania in bipolar patients if the patient is not taking an adequate amount of a mood stablizer.>
> -- RonRon,
Thanks for sharing that experience. I have a question though- Have you noticed any improvement in your attentional/focusing abilities? Improvement that you feel goes beyond just lifting depression? I have got ADHD problems really bad and wonder if that would be helpful for adults. I have read somewhere that a lot of parents give SAM-e to their ADHD kids who have problems with standard psychostimulants-such as tics and anxiety (with mixed results). Just wondering.
Mitch
Posted by johnj on March 14, 2002, at 13:02:59
In reply to Re: CRF Antagonists, posted by Denise528 on March 13, 2002, at 13:01:48
Doesn't this help with the dopamine system? What about eating foods to help with dopamine production? What about vitamins? Just some thoughts I hope people can respond to. Thanks
Posted by IsoM on March 14, 2002, at 13:15:08
In reply to Dopamine from Wellburtin??, posted by johnj on March 14, 2002, at 13:02:59
Denise, the only thing I've found that has helped with the dopamine problem is adrafinil (Provigil would do the same), nothing else has for me. I'd sure like to know if anything else would work too aside from SAMe. It's riduclulously expensive! How do they justify the expensive? I can't imagine the cost of manufacture is that high!
Posted by Geezer on March 14, 2002, at 14:00:14
In reply to Re: Dopamine, posted by OldSchool on March 13, 2002, at 22:37:12
> > > I really agree with Old School's idea about dopamine depletion. Dopamine seems to be at the root of the changing face of depression over the years (especially after AD treatment) in depressed people. For me, I find that something that boosts my dopamine levels (or whatever it does to change their expression) works much better in me now than any simple AD.
> >
>
> The reason is the war on drugs. Pharmaceutical companies dont want to go there and develop dopaminergic antidepressants for legal/liability reasons. See, the drug companies are afraid that if they create ADs which are heavily dopaminergic, they might become drugs of abuse. Many of the illegal drugs of abuse cause a sudden spike or surge in dopamine, which is extremely pleasureable (cocaine, crack, amphetamines).
>
> The other reason has to do with the fact dopaminergic meds might be worse at causing mania or inducing psychosis...again its a liability thing more than anything.
>
> Presently in the USA, if you want a dopaminergic antidepressant you are basically limited to the older MAOIs. Stimulants like Ritalin can be used also as can parkinsons drugs like Mirapex or Amantadine. But these can be troublesome to work with and have bad side effects. Really, all thats available for depression is MAOIs.
>
> There was an antidepressant marketed briefly back in the eighties called Nomifensine. It was extremely dopaminergic and a lot of people really liked it. It was supposed to be great for retarded depression, severe depression, etc. Sadly it was recalled by the FDA. It was the only real true dopaminergic antidepressant ever fielded in the USA besides the MAOIs.
>
> Oh yeah...ECT increases dopamine a lot. ECT has off label anti-parkinsons properties. Its pretty weird that the two best treatments for severe depression...MAOIs and ECT...are both heavily dopaminergic. Kinda tells ya something maybe huh?
>
> Old SchoolYes it does tell you something and I completely agree with this assessment. I took Merital (nomifensine) on a clinical trial basis in the 80s. At this point I can't give an honest report of effecacy - can't remember. My recall on the drug would not be meaningful, in any case, since I was always treated for Unipolar Depression and not DXed Bipolar until 2001.
Merital was manufactured by Hoechst and removed from the market due a small number of cases of haemolytic anaemia.
http://www.nomifensine.com/haemtwo.htm
Geezer
Posted by OldSchool on March 14, 2002, at 14:13:17
In reply to Re: Dopamine, posted by Geezer on March 14, 2002, at 14:00:14
Here is some info on ECT increasing dopamine levels:
http://www.mhsource.com/expert/exp1033098g.html
ECT and the Brain
Q. My mother receives ECT treatment for chronic depression episodes. I would like to know more about how ECT works on the brain. Can you also recommend some literature?
A. The precise mechanism of ECT (electroconvulsive therapy) is not known, despite a good deal of research. What is known is that it is extremely effective for severe depression and a number of other serious psychiatric conditions, and that it is a very safe procedure for the vast majority of patients. The memory disturbance that has alarmed the general public is relatively minor and temporary; in fact, IQ test scores have been found to improve after ECT, probably because the depression has been successfully treated. There is no credible evidence that ECT causes brain damage.In general, it is thought that ECT stimulates deep brain structures that are involved in the regulation of mood. Major changes also occur in numerous chemicals that normally govern the communication between nerve cells in the brain-- the so-called neurotransmitters. These chemicals, such as serotonin, dopamine, and norepinephrine, are altered in complex ways by ECT. Dopamine is a brain chemical that tends to boost mood and energy. Increased dopamine levels may be linked to ECT's effects on depression. But since ECT also works well in mania, something else must be going on. ECT also increases the activity of certain brain receptors for serotonin, a chemical that plays an important part in depression. (Medications like Prozac also work on serotonin, but in different ways than ECT).
For more information about ECT, contact the National Depressive and Manic Depressive Association at 800-82-NDMDA. The booklet Electroconvulsive Therapy: A Guide, by Dries & Barklage (Lithium Information Center, Dean Foundation, 8000 Excelsior Drive, Suite 302, Madison WI 53717-1914), is a bit dated (1989) but may still be useful. A more technical view is provided by H. Sackheim in Psychopharmacology Bulletin, 30:281-308, 1994.
March 1998
Since ECT is used sometimes off label for parkinsons and neuroleptic induced movement disorders, it must have some major dopaminergic activity.
Old School
Posted by Bob on March 14, 2002, at 14:16:34
In reply to Re: Dopamine, posted by OldSchool on March 14, 2002, at 9:57:37
> > Well... all I can say is that if that truly is the case, and dopamine is a promising AD, than that is truly pathetic and sad. It really is.
>
> I wouldnt put it quite like that. Pure dopamine antidepressants I dont think is a good idea. However, with many of the current ADs like SSRIs, as you increase serotonin dopamine levels go down gradually and get that poop out of affective "flattening" many complain about on SSRIs.
>
> To solve this problem maybe pharmaceutical companies should try harder to bring a few RIMA MAOIs to the US market, like moclobemide. That would solve the dopamine problem pretty good.
>
> Old School==================================================
Well, what I meant was that if the pure domapamine ADs were a good idea, then it was pathetic. From what you're saying, though, they are not. I figured that was probably the case, since we have dopamine agonists, and they are not treatments for depression, per se.
Posted by Ron Hill on March 14, 2002, at 14:43:08
In reply to Re: SAM-e May Increase Dopamine Production » Ron Hill, posted by Ritch on March 14, 2002, at 12:38:29
Have you noticed any improvement in your attentional/focusing abilities? Improvement that you feel goes beyond just lifting depression? I have got ADHD problems really bad and wonder if that would be helpful for adults. I have read somewhere that a lot of parents give SAM-e to their ADHD kids who have problems with standard psychostimulants-such as tics and anxiety (with mixed results). Just wondering.
>
> Mitch
-----------------------Mitch,
Yes, SAM-e somewhat improves my focus/attention and the improvement occurs immediately upon taking the dose. I (layman) think that the effect is attributable to an increase in dopamine but I'm not sure that my assessment of the mechanism is consistent with the rapid onset of the improved attention.
Mitch, I read your posts frequently so I know that your dx is bipolar II with co-morbid ADHD. As you know, I am bipolar II but initially I was misdiagnosed as ADHD and prescribed ritalin. (I am currently 49 and started taking meds for the first time six years ago). Within a couple of months, ritalin pushed me into a full blown mania but, initially, ritalin provided a wonderful focus/attention enhancement. I say this only to let you know that I know what you mean by your question. SAM-e, of course, does not dial-in my attention like ritalin once did but, instead, SAM-e provides a "softer" effect that may (unlike ritalin) prove sustainable over the long haul.
My (layman) hunch is that rarely would SAM-e be very useful as an ADHD mono-therapy. In my opinion, SAM-e is much more effective as a "mood brightener" than an ADHD medication. With all that being said, SAM-e may function well as an add-on to ADHD medication.
Just to reiterate what SAM-e does for me: SAM-e takes away the side effects (lack of motivation, blunted emotions, lack of energy, and etc) caused by SSRI's.
Mitch, if you decide to give SAM-e a try, remember those B's especially B-6, SUBLINGUAL B-12, and folate. Based on what I know about you via reading you posts, I suspect you already take your B's. Are you taking a bioactive SUBLINGUAL B-12 (methylcobalamin)? If not, why not?
-- Ron
Posted by Ritch on March 14, 2002, at 22:33:23
In reply to Re: SAM-e May Increase Dopamine Production » Ritch, posted by Ron Hill on March 14, 2002, at 14:43:08
> Have you noticed any improvement in your attentional/focusing abilities? Improvement that you feel goes beyond just lifting depression? I have got ADHD problems really bad and wonder if that would be helpful for adults. I have read somewhere that a lot of parents give SAM-e to their ADHD kids who have problems with standard psychostimulants-such as tics and anxiety (with mixed results). Just wondering.
> >
> > Mitch
> -----------------------
>
> Mitch,
>
> Yes, SAM-e somewhat improves my focus/attention and the improvement occurs immediately upon taking the dose. I (layman) think that the effect is attributable to an increase in dopamine but I'm not sure that my assessment of the mechanism is consistent with the rapid onset of the improved attention.
>
> Mitch, I read your posts frequently so I know that your dx is bipolar II with co-morbid ADHD. As you know, I am bipolar II but initially I was misdiagnosed as ADHD and prescribed ritalin. (I am currently 49 and started taking meds for the first time six years ago). Within a couple of months, ritalin pushed me into a full blown mania but, initially, ritalin provided a wonderful focus/attention enhancement. I say this only to let you know that I know what you mean by your question. SAM-e, of course, does not dial-in my attention like ritalin once did but, instead, SAM-e provides a "softer" effect that may (unlike ritalin) prove sustainable over the long haul.
>
> My (layman) hunch is that rarely would SAM-e be very useful as an ADHD mono-therapy. In my opinion, SAM-e is much more effective as a "mood brightener" than an ADHD medication. With all that being said, SAM-e may function well as an add-on to ADHD medication.
>
> Just to reiterate what SAM-e does for me: SAM-e takes away the side effects (lack of motivation, blunted emotions, lack of energy, and etc) caused by SSRI's.
>
> Mitch, if you decide to give SAM-e a try, remember those B's especially B-6, SUBLINGUAL B-12, and folate. Based on what I know about you via reading you posts, I suspect you already take your B's. Are you taking a bioactive SUBLINGUAL B-12 (methylcobalamin)? If not, why not?
>
> -- Ron
Thanks Ron,Yes, I got some sublingual B-complex stuff about a month ago and take it every day with lunch. I am also taking approx. 1G of flax oil with that as well. I know I need to take a little extra Vitamin E with the flax (and I do that too). I am thinking about increasing the flax oil to 2G daily and trying to eliminate nearly all unwanted fat in my diet at the same time. Thanks for "reiterating" why you take the SAM-e (to counter sfx of SSRI). I get similar probs with the little bit of Celexa I take, but it is a can't live without it can't shoot it situation with low-dose SSRI. I will break out the cash and get some SAM-e.
Thanks Mitch
Posted by Ron Hill on March 15, 2002, at 12:04:59
In reply to Re: SAM-e May Increase Dopamine Production » Ron Hill, posted by Ritch on March 14, 2002, at 22:33:23
> Yes, I got some sublingual B-complex stuff about a month ago and take it every day with lunch. I am also taking approx. 1G of flax oil with that as well. I know I need to take a little extra Vitamin E with the flax (and I do that too). I am thinking about increasing the flax oil to 2G daily and trying to eliminate nearly all unwanted fat in my diet at the same time. Thanks for "reiterating" why you take the SAM-e (to counter sfx of SSRI). I get similar probs with the little bit of Celexa I take, but it is a can't live without it can't shoot it situation with low-dose SSRI. I will break out the cash and get some SAM-e.
>
> Thanks Mitch
-------------------------Mitch, please post regarding the effectiveness/ineffectiveness of SAM-e as you take it over the next few weeks. I have a hunch it may be of some benefit to you. I hope so!
-- Ron
Posted by Ritch on March 15, 2002, at 20:38:43
In reply to Re: SAM-e May Increase Dopamine Production » Ritch, posted by Ron Hill on March 15, 2002, at 12:04:59
Posted by Anna Laura on March 16, 2002, at 0:13:06
In reply to I will be sure to post about it (nm) » Ron Hill, posted by Ritch on March 15, 2002, at 20:38:43
http://www.macalester.edu/~psych/whathap/UBNRP/parkinsons/COMT%20inhibitor.html
Posted by JohnX2 on March 16, 2002, at 4:11:26
In reply to Re: CRF Antagonists, posted by OldSchool on March 13, 2002, at 13:21:01
> There is some info on this site regarding "SSRI poopout." Its in the tips and tricks section. Basically, the most common hypothesis as to why ADs poop out over the long haul is dopamine depletion. Many ADs, particularly the serotonergic ones, dampen the dopamine system when taken long term.
>
> Im building a website myself and will have information on this subject at my site.
>
> Old SchoolIn 100 words or less ;)
What is your insight regarding the degenerative mechanism by which SSRI's poop out?Also do you think this phenomina can be baggaged into the same mechanisms responsible for the development of tolerance to simulants, and if so why?
How is this dopamine depletion "maintained"?
As an anology, if your car is consistently running low on oil (dopamine) would throwing more oil at it directly be the right fix for the problem? (playing devils advocate)
Thanks for your insight.
John
Posted by Ritch on March 16, 2002, at 10:12:17
In reply to What about COMT inhibitors?, posted by Anna Laura on March 16, 2002, at 0:13:06
Anna,
Thanks for those links. I bookmarked the wemove.org website for alter reference. I am going to stick with tinkering with OTC supplements for a while and see how that goes first. I wasn't aware of the existence of the newer COMT inhibitors. I don't have a diagnosis of any movement disorder at this time. I believe it is just SSRI induced, and would like to find a way to continue taking a low-dose of SSRI with the motor side effects ameliorated somehow,
thanks,
Mitch
Posted by OldSchool on March 16, 2002, at 12:39:06
In reply to What about COMT inhibitors?, posted by Anna Laura on March 16, 2002, at 0:13:06
> http://www.macalester.edu/~psych/whathap/UBNRP/parkinsons/COMT%20inhibitor.html
>
>
> http://www.wemove.org/kidsmove/tre_med_dopamine.html
Since I developed EPS Ive gotten all familiar with these parkinsons meds and Ive wondered if the COMT Inhibitors are any good for TRD. I know one of them I read is rather toxic to the liver so would probably not be a good idea to mess with unless you had parkinsons.Im wondering if the COMT Inhibitors creates the same somnolence and confusion and low blood pressure the dopamine agonists can cause.
Posted by OldSchool on March 16, 2002, at 12:52:50
In reply to Re: CRF Antagonists » OldSchool, posted by JohnX2 on March 16, 2002, at 4:11:26
>
> > There is some info on this site regarding "SSRI poopout." Its in the tips and tricks section. Basically, the most common hypothesis as to why ADs poop out over the long haul is dopamine depletion. Many ADs, particularly the serotonergic ones, dampen the dopamine system when taken long term.
> >
> > Im building a website myself and will have information on this subject at my site.
> >
> > Old School
>
> In 100 words or less ;)
> What is your insight regarding the degenerative mechanism by which SSRI's poop out?
>
> Also do you think this phenomina can be baggaged into the same mechanisms responsible for the development of tolerance to simulants, and if so why?
>
> How is this dopamine depletion "maintained"?
>
> As an anology, if your car is consistently running low on oil (dopamine) would throwing more oil at it directly be the right fix for the problem? (playing devils advocate)
>
> Thanks for your insight.
> JohnJohn, Im just an average guy with severe refractory depression. Im not up on all the super duper technical stuff behind these drugs. Ive taken a lot of them and read a lot about them but many of the questions above I simply dont have the knowledge to answer.
As far as "SSRI poopout" goes Ive already posted one leading theory behind it...gradual dopamine depletion. Another theory behing AD poop out is subclinical hypothyroidism. Still another is missing mild, not so noticeable bipolar traits which can be fixed by lithium augmentation or lamictal. Still another is too much alcohol usage...some people drink a lot of booze on meds and your meds wont work as good if you drink alcohol regularly.
Another idea could be that you really have psychotic depression but its been missed and you need to have ECT or add anti-psychotics to your antidepressant. Another idea is that depression doesnt involve just the monoamine system but also the opiate system. Opium was used for treatment of melancholia as far back as the 19th century. There are some who believe the opiate system needs to be targeted in some cases of depression. There is that opiate drug buprenorphine which is used for refractory depression rarely, most Pdocs wont prescribe it no matter how bad off you are though.
All I can tell you is that after youve had your thyroid tested by your psychiatrist and it checked out OK, and youve maybe tried lithium augmentation there are basically two major treatments for refractory depression. One is ECT. The second is MAOIs. Basically thats it. Thats all there is. ECT has very broad, across the board effects on your brain and nervous system. MAOIs are also very broad and increase a wide range of brain neurotransmitters, unlike SSRIs.
SSRIs increase specific brain chemicals, mainly serotonin. While ECT and MAOIs do a whole bunch of stuff at the same time.
To be brutally honest, nobody really knows why SSRIs poop out in some people.
Old School
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