An end of year update from me. I'm close to 18 months in, and Abilify continues to be effective. I take 0.25mg/daily. The cognitive gains I described a year ago have held and even expanded somewhat. No doubt strict pacing has been a factor in this too.
If I had to quantify it, for me Abilify gave a sustained ~3-5% increase in my capacity to function and quality of life, undiminished over time. I know that doesn't sound like much, but for me it's the difference between being completely zombified around the clock and, with "aggressive" resting and careful pacing, enjoying fleeting spaces of time where I feel close(r) to normal. I never experienced the dramatic improvement that for instance yourself and Martin did; instead it's been a gentle, steady push.
I realize I'm about 3 years late to this thread, but I wanted to respond since I've just been seen at Dr. Bonilla's Stanford clinic. I haven't yet tried Abilify, but the plan (once my psych gets me off Zyprexa, an atypical antipsychotic--prescribed years ago for depression in my case and which I've continued to take because it allows me to sleep at night--of the same class as Abilify) is this: to start at 0.1 mg twice a week, then 0.1 mg per day, then 0.2 mg, 0.4 mg, 0.5 mg, 1 mg, then 2 mg as the upper limit dose. Apparently there are a few compounding pharmacies who will make the drug at subclinical doses for much-reduced fee for Dr. B's patients.
Yes, Trish, they told me immediately that it's experimental--not FDA-approved. My sense was that they try all new patients on this; my PA cited a "cohort study" in which 70% of patients had some degree of benefit from the drug. I don't know the specifics of what a cohort study is--obviously not rigorous like a double-blind study, since it seems no one is doing that for ME treatments?--and how much could be explained by placebo effect.
The problem with the study they did was they tried the drug before "thinking about doing a study". That means that the patients were not enrolled in a clinical trial. The patients were invited to take this medication that the doctors think could help but it is off-label. They may well have told their patients that they felt it could help them reducing brain inflammation and that many of their patients were improved (also known as conditioning).Then they made them come back after a while and assess whether it helped them or not, via a questionnaire. No ethics review. This was also an open-label "trial" which means no placebo, not randomized, the patients were picked and chosen to take the medication, and afterwards, in counting the patient in their review. It is a retrospective study, not a clinical trial.
Milo, I figured it was something like that--i.e., where the placebo effect could've played a big part. Thanks so much for explaining and clarifying, and for the link.
Here's our thread discussing that cohort study. Significant concerns were expressed on the thread, both about whether the data was sufficiently solid to draw any conclusions, and about that particular clinic pushing this treatment for all their ME/CFS patients for several years, but failing to do a proper clinical trial. I think it's well worth reading through the whole thread if someone is prescribed the drug.
I've always thought this too. I remember reading a study about the possible connection between the persistence of toxoplasma gondii in the brain and schizophrenia. The author's claimed that common antipsychotics (might have been olanzapine they referred to but i don't remember exactly) had an anti parasitic effect and that might explain why they treat the illness. I remember thinking, surely if those patients had a brain illness caused by a parasite we would have a drug better suited for that than something like olanzapine?! What's the chance that, of all the drugs we have, the optimal one for treating this infection just so happens to be the psychiatric drug you are already giving to the patients to turn off their dopamine circuits which also shrinks their brains and causes obesity as side effects?
