Posted by bleauberry on January 27, 2010, at 17:16:58
In reply to What drugs/agents increase dopamine?, posted by Walfredo on January 26, 2010, at 22:44:11
> Anyways, I'm thinking I want to try to see if low dopamine is what is giving me problems. My most glaring symptoms seem to be low-energy and poor memory which I think may be indicative of a dopamine problem.
There is interplay between NE and DA, and things are different from one part of the brain to another, so pinpointing dopamine is probably too simplistic. Example. According to Stahl, Milnacipran increases dopamine in the frontal cortex because in that part of the brain dopamine is taken up by the NE reuptake sites, there are no dopamine reuptake sites there. Not all NE reuptake inhibitors might have the same effect on that particular part of the brain. Milnacipran hits it strong and thus increases both dopamine and NE. I have seen at pubmed that interplay between NE and DA, similar to this example, exists in various other ways and regions of the brain. So if there is a dopamine problem, my belief is there is also an NE problem. And vica versa. They are partners that work as a team, not entirely separate entities.
>Furthermore, the one drug that basically gave me remission from depression (despite trying all SSRI's) was Paxil and apparently that has a slight affect on dopamine whereas most other SSRI's don't.
I've never heard of Paxil impacting dopamine, but it does have NE reuptake action, and it also shares some similarities of the TCAs.
>Bleauberry has suggested that Norepinephrine might also be an issue with me and I tend to concur but I am already taking Remeron which should help with some of that.
I probably go against the grain here and am not on board with the crowd when I say Remeron does not have significant antidepressant potency. Some readings by Dr Gillman at psychotropical.com go into more detail as to why this is. If anything, Remeron might increase the firing rate of NE, and some indirect action on dopamine, but is basically a potent antihistamine. Gillman can explain its mechanisms and shortfalls a lot better than I can. If I could recall a handful of people here over the years that said how wonderful Remeron was and how its worked for a long time, I would feel differently. I see that with many of the other meds we talk about, but not much with Remeron. For sleep, I am a fan. For depression, I am not. But that's just me, based on the reasons I have shown above. Someone else may feel differently.
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> So, basically, I want to try to boost my dopamine and see if that can help me.For meds, the two best ways to do that are Ritalin or Adderall. They are quite different and so both would need to be tried. Keep in mind, boosting dopamine is overly simplistic. In what region of the brain will it be boosted? By what mechanism?
For naturals, tyrosine. This is problematic too however because the genes will decide how much goes to dopamine and how much goes somewhere else, and it may increase dopamine in places where it works against you instead of for you. The same goes for meds.
Trial and error is needed.
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> I recently quit Abilify and am wondering it's net affect on dopamine.A perfect example of the importance of trial and error. On paper it would appear to be perfect...increases dopamine deficiencies where necessary and decreases excesses where necessary, simultaneously, in various regions of the brain. Dopamine could be too high in Region A and too low in Region B. According to our best theories on how Abilify works, it should fix both.
The brain is too complicated for such rigid simplistic theories. There is a lot more going on. And what we "think" these drugs do, based on indirect inferences on rats or people, is probably just a fraction of what they are really doing.
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> I have also been on Wellbutrin, which I know is supposed to increase dopamine, with little to no therapuetic benefits.It is a weak dopamine reuptake inhibitor and its actual mechanism of action is unknown. My hunch based on a lot of digging is that it probably works through the nitric oxide system and the nicotinic receptors. Its dopamine reuptake is very weak. The fact that it causes seizures at high doses shows it is doing something weird that we haven't yet identified.
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> I came across some posts mentioning Amisulpride (unfortunately not currently available in the US) which was very intriguing to me since it works on dopamine and is used in low doses to treat dysthymia, which is very close to what I have.There is a significant body of scientific evidence supporting amisulpride for dysthymia (low doses 25mg-100mg). It also treats negative symptoms of schizophrenia better than other APs, and negative symptoms look almost identical to dysthymia. It supposedly stimulates dopamine release at low doses without blocking other dopamine receptors, but based on my experience and others it probably does do some AP blockage as well, even at low doses. It was recently discovered it also is a 5ht7 receptor antagonist, and that highlights the whole subject of trying to decide on something based on theoretical mechanism...we are learning new things all the time that change what we commonly assumed.
Amisulpride could be a good test at 25mg for 3 days. The dopamine stimulation at startup is usually feelable. As adaptations take over, that stimulation subsides, and then in a few weeks symptoms overall begin to improve. The first few days, or even the first day, would be a decent test. It can be ordered mailorder from overseas very easily and legally, but due to board rules here we can't share sources. Thank goodness for google searches. It is not likely to cause the emotional numbness/apathy of other ADs. It is better known to specifically increase interest and motivation and socialability.
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> I am curious though what other agents supposedly increase dopamine as I certainly think that giving one a try is worth a shot. My current pdoc is not a fan of the MAOI's, and knowing the side effects, I can't blame her though I am getting desperate to find something that works!Side effects of Parnate are often found to be at least as tolerable as SSRIs/SNRIs, more tolerable than TCAs, and sometimes friendlier than any of them. Side effects are overblown by false hype. Go to revolutionhealth or askapatient.com and see what users have to say...side effects are usually precictable, tolerable with proper titration, and lessen significantly within a couple months. While other ADs score an average of 3.6 on a 1 to 5 scale, Parnate scores a 4.2.
Ritalin. Adderall. Amisulpride. Parnate. Tyrosine. Those are your basic dopamine agents.
Someone might mention a dopamine agonist, but I wouldn't agree with that approach. They will substitute for dopamine with artificial dopamine, but at the same time decrease your own real dopamine.
poster:bleauberry
thread:935098
URL: http://www.dr-bob.org/babble/20100122/msgs/935159.html