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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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Open exchange of input and ideas is how hypotheses are constructed, then tested, then matured into actual theses which could definitely help a whole lot of patients in this forum.But once people start listing, non-objective reasons for it while putting them forward like they are objective reasons then this is fully open to critique.
I'd be interested too.@stefanosstef everyone seems to always say low dose works in an opposite way than full dose. Do you have a study at hand for this ? Would like to read into this some more.
Could you cite your sources for that significant evidence?One significant positive thing about pramipexole (and I believe also with ropinirole) is that there’s significant scientific evidence that it exhibits strong mitochondrial protective effects in the brain.
@YippeeKi YOW !!@stefanosstef everyone seems to always say low dose works in an opposite way than full dose. Do you have a study at hand for this ? Would like to read into this some more.
Low-dose systemic aripiprazole (<1 mg/kg) also increased extracellular dopamine levels in the cortex [62, 63]. On the other hand, high-dose systemic aripiprazole (10–40 mg/kg) reduced dopamine levels [64–66]. This biphasic effect may depend on the prevalence of agonistic 5-HT1AR-mediated effects at low doses, and the prevalence of inhibition of mesocortical dopaminergic neurons activity at high doses [65].
@choochoo and which study implies that cfs patients have low dopamine ?
Could you cite your sources for that significant evidence?
And I thought that any mitochondrial involvement in ME had been negated by either you or another poster in this thread a little ways back.
So how about using the same scanning techniques on patients in an Abilify trial. Scans before and after a course of treatment?And a few other well known studies which found neuroinflammation in CFS in certain areas of the basal ganglia, as well as other areas. Neuroinflammation we discussed will cause neurotransmitter dysfunction in those brain areas.
@stefanosstef thanks. Will look into this some more.
@leokitten decreased activity in these regions doesn't automatically means less dopamine activity though. Otherwise Cfs ppl would show significant symptoms of other diseases with low dopamine in these regions. Like Huntingtons diseases or Parkinson.
In what way, and exactly how. And to what new effect?Please take into account that the low dose regimen discussed here effectively change antipsychotics into totally different drugs.
In what way, and exactly how. And to what new effect?
This seems to fly in the face of all laws of physics. Would be interested in knowing more, could you cite your sources?
@leokitten sure, but Cfs ppl even after +20 years of sickness dont show any sign of progression in this way. No dyskinesia or other sign that would show a progression in lowering dopamine over time. So the theory here would be it gets lowered once and then stays there forever ? without any progression or worsening in dopamine levels ever again ? Doesnt sound very plausible to me.
I truly hope that's not the case .... I know how grim this illness gets, but even that can be turned around, and it could be that Abilify is exactly what will do that for you ....Believe me there is not much to lose on my end at this point.
I hope more than that. Maybe a shining success story? Yeah, that's the ticketAnd maybe at least I can be a data point on this forum for others to use in forming some kind of hypothesis.
Agreed, and thank you for your very civil postEdit:Actually that is what partial agonism means.Receptor agonism at low doses and antagonism at full doses.