![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 13 to 37 of 51. Go back in thread:
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
Posted by JohnX2 on March 16, 2002, at 19:58:45
In reply to Re: CRF Antagonists, posted by OldSchool on March 16, 2002, at 12:52:50
Thanks for your reply.
I don't think there is a lot of push to understand medication tolerance because it is not good business (no financial incentive for anyone really; in fact understanding the problem would cost a lot of people a lot of money). This is too bad because a lot of people who are extremely treatement refractory get poopout within days of taking a medicine. Sometimes within hours.John
> To be brutally honest, nobody really knows why SSRIs poop out in some people.
>
> Old School
Posted by Denise528 on March 17, 2002, at 8:49:35
In reply to Re: CRF Antagonists, posted by OldSchool on March 16, 2002, at 12:52:50
Hello,
If this is the case and SSRIs poop out because of dopamine depletion then can someone please explain why Zyprexa seems to be the only drug which is helping me. I thought Zyprexa depleted dopamine even more. Can someone explain please?
Denise
Posted by JohnX2 on March 17, 2002, at 19:46:19
In reply to dopamine depletion and Zyprexa, posted by Denise528 on March 17, 2002, at 8:49:35
Denise,Zyprexa antagonizes (blocks) serotonin receptors that inhibit dopamine release. There are a number of classes of serotonin receptors 5ht-1,5ht-2,5ht-3,etc....
Some of these receptors are known to gate dopamine release in many areas of the brain. Particularly the 5ht-2 variety. So when the SSRI medicines increase serotonin and hit those 5ht-2 receptors with more force, the medicine may reduce dopamine in some areas of the brain. If we can have some medicine that blocks those particular receptors (it just sits on the receptor blocking serotonin and doesn't activate it), then this will increase dopamine release in those areas of the brain.
A more ideal anti-depressant may combine the SSRI quality with the specific serotonin receptor blocking quality in the AP like Zyprexa.Zyprexa also blocks dopamine receptors, so it sort of is a balancing act depending on what part of the brain the medicine is working at.
John
> Hello,
>
> If this is the case and SSRIs poop out because of dopamine depletion then can someone please explain why Zyprexa seems to be the only drug which is helping me. I thought Zyprexa depleted dopamine even more. Can someone explain please?
>
> Denise
Posted by Denise528 on March 18, 2002, at 8:53:36
In reply to Re: dopamine depletion and Zyprexa » Denise528, posted by JohnX2 on March 17, 2002, at 19:46:19
John,
Thanks for the explanation, if serzone acts in a similar way to Zyprexa and Zyprexa seems to be helping me, is there a chance that Serzone would too?
I have already asked you this on another thread but thought I'd sneak the question in again.
Thanks again.....Denise
Posted by JohnX2 on March 18, 2002, at 17:00:20
In reply to Re: dopamine depletion and Zyprexa, posted by Denise528 on March 18, 2002, at 8:53:36
Denise,I'm not sure what you you were taking the Zyprexa for. Serzone is a bit more "intrusive" of a medicine. It takes a bit longer to dose onto and is a coin toss in regards to being as efficacious with anxiety symptoms. It is really good for sleep for those that respond well and less likely to cause sexual complaints than the SSRI medicines.
Since I don't recall what Zyprexa was helping you for, I can't comment on whether or not Serzone may help you. Some things Zyprexa is good for, maybe Serzone won't do as well at.
Regards
John> John,
>
> Thanks for the explanation, if serzone acts in a similar way to Zyprexa and Zyprexa seems to be helping me, is there a chance that Serzone would too?
>
> I have already asked you this on another thread but thought I'd sneak the question in again.
>
> Thanks again.....Denise
Posted by djmmm on March 18, 2002, at 19:19:10
In reply to dopamine depletion and Zyprexa, posted by Denise528 on March 17, 2002, at 8:49:35
because poop-out isn't caused by decreased dopamine, it's caused by an over abundance of serotonin..that's why 5ht1 and 5ht2 antagonists work...zyprexa is a 5ht2 antagonist
http://www.pni.org/psychopharmacology/abstracts/lectures/obesity_antidepressants.html
Posted by Denise528 on March 19, 2002, at 12:33:31
In reply to Re: dopamine depletion and Zyprexa, posted by djmmm on March 18, 2002, at 19:19:10
I seem to be getting conflicting messages. Anyway thanks for the link, I checked the website and it is very informative although not sure I fully understand it.
Denise
Posted by Denise528 on March 19, 2002, at 12:44:49
In reply to Re: dopamine depletion and Zyprexa, posted by djmmm on March 18, 2002, at 19:19:10
Hi,
I've read the web page and excuse me for being thick but I don't really understand it. Is there any chance you can elaborate for me?
Denise
Posted by vanessa on March 20, 2002, at 14:58:39
In reply to Re: dopamine depletion and Zyprexa - djmm, posted by Denise528 on March 19, 2002, at 12:44:49
another question: so if dopamine depletion causes
"poopout" why do MAOIs stop working? My understanding is that MAOIs increase dopamine.
Posted by djmmm on March 20, 2002, at 15:56:44
In reply to Re: dopamine depletion and Zyprexa - djmm, posted by Denise528 on March 19, 2002, at 12:44:49
Dopamine depletion is just a *theory* nothing is proven...just as excess serotonin is a theory...I'm sure there are others. The theory of excess serotonin is not as well known I guess, but I does make sense. Too much serotonin results in a variety of "symptoms" just as too little serotonin does...this is an established fact.
The theory is, medications that agonize/antagonize specific serotonin receptors decrease the stimulation of serotonin into the synapse..meds that have a high affinity for these receptors are always given for "poop-out"
I found this today... I copied it here because I thought that the bit on "reducing medication" supports this theory..
Psychology Today
March, 1999Another unknown is what's behind poop-out--whether it is true pharmacologic failure or a worsening of the disease, a relapse that overrides medication. Other factors that can dent a medication's apparent effectiveness are aging (which tends to worsen or change depressive symptoms), substance abuse, a coexisting medical illness and noncompliance, a big problem.
Rajinder Judge, M.D., clinical research physician for Prozac at Eli Lilly, estimates that just 50% of patients actually take antidepressants properly. "They miss doses or just stop on their own," she says. It is not uncommon for patients to drop their medications after four months, although prevention of relapse is believed to warrant longer treatment. Some find the side effects too pesky. Others become overconfident because they feel so much better. "Once you recover," Judge explains, "you don't want to be reminded of those dark days and the only thing reminding you is this little pill."
Whatever the cause of poop-out, it can almost always be remedied by upping (or sometimes even reducing) the dose, or changing or adding medications. Whereas older medications--so-called tricyclic antidepressants and monoamine oxidase (MAO) inhibitors--can be dangerous at high doses, amounts of the SSRIs can be doubled and then doubled again without harm, according to Peter Kramer. "Sometimes the patient ends up on a more complicated regimen to get the same effect," he says. "Or sometimes it's a matter of taking a person off one drug and reintroducing it later. One way or another, it is mostly possible to get people back to where they were."
http://www.findarticles.com/cf_0/m1175/2_32/53985476/print.jhtml
Posted by Denise528 on March 24, 2002, at 10:25:49
In reply to Re: dopamine depletion and Zyprexa » Denise528, posted by JohnX2 on March 17, 2002, at 19:46:19
JohnX2,
How do serotonin receptors inhibit dopamine release?
Denise
Posted by House_DJs on December 22, 2003, at 23:01:01
In reply to Re: Dopamine » OldSchool, posted by Bob on March 14, 2002, at 1:25:57
Speaking as if there are only ‘a few’ neurotransmitters in the brain that are involved with Clinical Depression/Anxiety Disorders. When there are a vast number that work in conjunction w/eachother to control one’s mood.
Just because you no longer respond to SSRI’s doesn’t eliminate Serotonin as a possible problem. Remember, we all have enough Serotonin in our bodies, it’s just how our brain’s are using it where the problem lies. We must remember that there are several areas of the brain that are ‘chemically imbalanced’ in sufferers. Those that respond to SSRI’s - balancing out Serotonin has positive effects on the rest of the faulty neurotransmitters, lifting them out of their malfunctioning state.
I don’t know why we’re focusing in on Dopamine? Why not the several other branches of Serotonin like Serotonin 1A or Serotonin 3? Why not focus in on imbalanced Noradrenaline levels? Substance P levels? BDNF levels? & Last but definitely not least – CRF levels? When people on the board start talking like they’re ‘so sure’ of what they’re saying is when you know you’re being mislead. The Psychiatrists/Psychologists themselves haven’t mastered this illness, so how could any of us?
CRF antagonists by the way should be out in about 5-6yrs. if the Clinical Trial phases go as successfully well as they have bin. I’m lucky enough to have a Doctor that works @ a Psych. Facility who will be involved w/the Clinical Trials in a year & a half. He promised me a reserved spot to try the drug(s). We’ll see what comes of it. My doc. Believes it’s the Amygdala that is the root of all the other malfunctioning neurotransmitters in the brain. i.e. Serotonin & other neurotransmitters being imbalanced is just an effect of the Amygdala malfunctioning. The Amygdala plays an incredible role in Mood Disorders. It stores emotional memories of past experiences & controls fear response, etc. CRF antagonists will work to bring the Amygdala back to normal, thus alleviating Anxiety Disorders & Clinical Depression, without having to try & tweak the malfunctioning brain from the 2ndary effects, 3rd, 4th & 5th – all in hopes of truly correcting the neurotransmitter at the root that’s behind this all.
Yes it’s bin known that long-term SSRI use results in imbalanced levels of Dopamine & Noradrenaline. But beyond this, the most successful AntiDepressants always have bin the least used ones… MAOI’s & ECT as OldSchool stated. MAOI’s come w/no harm so long as you obey the diet that comes with it. ECT, 6months of short-term memory loss w/o any permanent damage.
If you’re still hooked on OldSchool’s Dopamine theory, let me inform you about Wellbutrin – it’s an AntiDepressant that strictly works on Dopamine. It’s bin proven to be NO MORE EFFECTIVE than any other AntiDepressant. So the answer to all our problems doesn’t lie in Wellbutrin. Beyond that, Effexor taken close to the maximum dose works on Serotonin, Noradrenaline & Dopamine – again, Effexor hasn’t bin shown to be more effective than any other AntiDepressant. & Then there’s all those methamphetamines (ADD medications) to try that strictly boost your Dopamine levels. NONE of which have been shown to be significantly effective in cases of Clinical Depression – I myself have tried Ritalin & Dexedrine with 0% relief. So yes they have studied the impacts of Dopamine in Depression, & the fact of the matter is – it plays little of a role in the grand scheme of things.
Lastly I’ve heard of no studies (my Doctor confimed this) of ECT specifically improving the flow of Dopamine from cell to cell in Depressed patients. For those that are truly familiar w/ECT, it’s like a reboot/restart for your brain. For those that find an alleviated Depression w/it, it balances out any neurological malfunction – ALL of it, not just Dopamine. & for those that don’t, well needless to say…
Let me inform you that the information i’ve provided above was all given to me by my Psychiatrist Dr.Martin Katzman @ the Centre For Addiction & Mental Health. He’s is the chief Anxiety Disorder & Clinical Depression specialist. He’s done vast research w/numerous drug companies & consults with the top medical professionals of the world.
Hope you found this as informative as I did writing it.
Amer Q.
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