Posted by anonymoose on December 1, 2007, at 11:52:18
In reply to Re: On Trivastal Again. Feeling soooooooo goood.., posted by clipper40 on November 29, 2007, at 23:55:49
Us dopaminergic depressives have been so ill-served by current clinical psychiatry and its hard-on for SSRIs. I think it's scandalous how unwilling to acknowledge they are (or ignorant of the fact that) there is a significant subset of us out there that neither need or want increased serotonergic transmission.
I haven't been posting much lately, because I've been too busy getting out and living life, starting to rebuild over the rubble of 10 years of SSRI-worsened anhedonia...and having a ball of a time doing it.
Been on .75mg/day of Mirapex, and the difference has been remarkable. Nothing like my experience with SSRIs and SNRIs, which turned out to be no better than placebo (I hope it works...I think it's working...Maybe it's working...D***, this ain't doing jack s***.) By the fourth day, the effect was like a lightbulb turning on. The anergia slowly melted away, and I could finally get off the couch and do simple things around the house if I wanted to, like vacuum the nasty carpet. The terrible dementia-like symptoms, which I had been fearing would be permanent, also melted away, with my severely damaged cognition and verbal fluency steadily returning to normal levels.
I'm currently at about a ~70% level of symptomatic remission, with my healthy pre-depression mental state of age 17 serving as the baseline. .75mg/day is a relatively low dosage, and I probably could have asked the doc to increase it already, but I've been holding off to see if I can kickstart my own natural dopamine synthesis into action with basic supplementation (B Complex, DLPA, Omega-3s).
Side effects have been minor, and included some initial nausea and decreased appetite. My biggest complaint was the whacked-out sleep caused I think by the increased D2-stimulation at night, but I fixed that by taking the Mirapex earlier in the day.
I'm guessing that dopamine agonists don't directly increase dopaminergic vesicular stores, because the agonist isn't subject to the reuptake pump like natural dopamine is? If that's the case, would it be preferable in the long run to shoot for increased natural dopamine synthesis (via supplementation or MAO-B inhibition, etc.) instead of relying on "synthetic dopamine" like the agonists?
If you were to increase dopamine in the synaptic cleft via MAO-B inhibition, for example, would the DAT (dopamine transporter) eventually upregulate in response? If my logic serves me correctly, this upregulation would be a good thing over the long run, right? Since it will help to replenish vesicular stores?