Abilify- Stanford Clinic Patients

[hmnr asg]

Aripiprazole as a candidate treatment of COVID-19 identified through genomic analysis. Crespo-Facorro et al. medRxiv (2020)

Is there anything abilify cant do! lolz

Sadly for me it stopped working. I will stop taking it and resume again in six month, hoping to recreate some of the initial benefits.

Also I read some people on the facebook abilify for ME forum mentioned that inositol is a good candidate for prolonging the duration that abilify helps cfs. Next time around I will take it with inositol.

 

[leokitten]

Also I read some people on the facebook abilify for ME forum mentioned that inositol is a good candidate for prolonging the duration that abilify helps cfs. Next time around I will take it with inositol.

What are people saying is a good inositol daily dosing regimen?

 

[leokitten]

So good to hear that you are doing well on Abilify, it's 7months for me now and it's still working.

@Jessie 107 I’m really glad 😀 it’s working for you such a long time. May I ask, is it still improving symptoms with the same efficacy as early on?

 

[Jessie 107]

@leokitten
Yes it is, I don't have the ill/malaise and flu symptoms that I had before Abilify.
I can also talk more, feed myself and spend more time online.
Fingers crossed it continues!😊

 

[hmnr asg]

What are people saying is a good inositol daily dosing regimen?

So this is apparently due to a Dr Goldstein. Here are some comments related to inositol on the abilify forum:

-" Dr Goldstein sometimes used high doses of inositol which helped from stopping his drugs to work. ".

This is all i found. For ocd I know the dosage is super high, (18 grams per day ). So maybe this is the sort of dosage they refer to. I didnt find anything about the specific dosage.

I have my appointment with Dr Bonilla soon. I will definitely ask if they have any strategy to deal with the abilify poop out.
I was thinking maybe switching to rexulti? or just take the six month break and hope for the best.

 

[leokitten]

I was thinking maybe switching to rexulti?

The new antipsychotics brexipiprazole and cariprazine have significantly different binding profiles, affinities, and intrinsic activities than aripiprazole. Since we don’t know which aspect(s) of aripiprazole’s mechanism of action have a positive effect on ME symptoms, at least in an ME subset, it would take enough pwME guinea pigs to trial brexipiprazole or cariprazine to see if they could hypothetically also work, just like many did with aripiprazole.

For example, both brexipiprazole and cariprazine have significantly less intrinsic activity at the D2 receptor than aripiprazole. So they are far less stimulating, etc. Because of this lower intrinsic activity they will also work differently at low vs high dosages compared to aripiprazole. They could also have different anti-inflammatory effects.

Brexipiprazole has many fold higher 5-HT1A and 2A intrinsic activity than aripiprazole. Cariprazine has very high D3 affinity and intrinsic activity compared to aripiprazole. And so on. So will be trial and error to see if these could work similarly to Abilify.

 

[hmnr asg]

it would take enough pwME guinea pigs to trial brexipiprazole or cariprazine to see if they could hypothetically also work

I think because i got desensitized to abilify perhaps I wouldnt be a good guinea pig. I will just take the six months off and ask Bonilla if theyre doing a trial of the other antipsychotics.

This forum could have been much more useful if more people systematically tried the more promising medications and reported back their experience (like a crowdsourced clinical trial). Instead we see tons of people who just come on threads like this and say things like "my UnCle's frienD's meChaNic took AbiliFy and turnEd inTo a sasQuatch! BE AFRAID! " and just scare everyone away.

I have yet to see one single case of someone having a serious adverse reaction to abilify that wasnt reversed by discontinuation. And at this point so few of us have tried it despite its promise.

 

[leokitten]

Instead we see tons of people who just come on threads like this and say things like "my UnCle's frienD's meChaNic took AbiliFy and turnEd inTo a sasQuatch! BE AFRAID! " and just scare everyone away.

We also need an Abilify RCT which includes a dose-response design. But my serious worry though, and I think many pwME who are laser focused on only having successful phase III RCT treatment results sometimes forget, is I think there are significantly different ME pathophysiological subsets and also many CCC diagnosed pwME who are misdiagnosed. For example, it’s likely many pwME have comorbidities which affect their ME pathophysiology making it quite different from others.

So without knowing much about ME pathophysiology, I think most if not all drug trials for drugs that really could work are doomed. I thought the same about the RituxME trial. There really could be a subset that have a real disease modifying or symptomatic response to rituximab that isn’t placebo effect. But it would never be found with different subsets or other unknown confounders in the same trial.

So it seems we have to have major pathophysiology discoveries before we can really even attempt trials, it doesn’t make sense to me otherwise. When I hear, “ME clinicians need to trial these treatments”, they forget the huge potential flaw going this route that ME clinicians likely already know and a reason why they aren’t yet spending the resources to do so. We don’t know nothing about this illness and it likely will screw up trials clumping CCC diagnosed patients blindly in the same trial.

 

[jaybee00]

Brex also works, even better, according to someone on the FB group. Caripraz might be hard to get an RX for because in doesn’t have an indication for depression— only schizophrenia.

 

[leokitten]

This forum could have been much more useful if more people systematically tried the more promising medications and reported back their experience (like a crowdsourced clinical trial). Instead we see tons of people who just come on threads like this and say things like "my UnCle's frienD's meChaNic took AbiliFy and turnEd inTo a sasQuatch! BE AFRAID! " and just scare everyone away.

I have yet to see one single case of someone having a serious adverse reaction to abilify that wasnt reversed by discontinuation. And at this point so few of us have tried it despite its promise.

I’m also really afraid of even posting my experience on S4ME. Like many of you, I’m having a major and significant response to Abilify and I was moderate-severe to severe, bedridden 22 hours a day or so for 5 months straight. Before that I was moderate housebound and only left the house once every 2-3 weeks for all of 2020. I’ve been in a steady decline for years and NEVER had fluctuations like others have which would explain this.

I also had an expectation bias for it to work much faster than it did if it was going to work at all, and after reading the Stanford paper I was seriously expecting it to likely not work very well at all. It took a much longer time to work and what happened was totally different than my expectation.

Yesterday I did an exertion experiment. I decided to do a short but very exertive event well beyond what would totally destroy me with 150% certainty before Abilify. Guess what no PEM, no worsening. I don’t feel any negative effects from it.

I guess that it’s placebo effect? I won’t do it again but I needed to see once. I will keep people posted if I get any really delayed PEM.

 

[jaybee00]

https://forums.phoenixrising.me/threads/abilify-tolerance.82726/page-3

This page has the chapter from Jay Goldstein’s book.

Dosage is 4g

 

[jaybee00]

inositol is reported to reverse desensitization of serotonin receptors,

https://www.sciencedirect.com/science/article/abs/pii/S0924977X97004094

 

[jaybee00]

I’m also really afraid of even posting my experience on S4ME.

Because your experience is an obvious placebo!! Nothing will ever work unless it has 5 consecutive RCT studies all conducted in the UK. And all 5 trials must show a 1000% improvement or else it’s an obvious placebo!

 

[jaybee00]

https://www.sciencedirect.com/science/article/abs/pii/0006899393915579

Myo-inositol reduces serotonin (5-HT2) receptor induced homologous and heterologous desensitization

 

[hmnr asg]

And many shoot down the idea of abilify (or any other experimental treatment) because they claim the "science" behind why it works is not fully known and so its a sham (or at best, not worth a try).

So many people are on antidepressants and as I recall the science behind that is changing. The explanation of why it works was purely post-hoc.

 

[leokitten]

Brex also works, even better, according to someone on the FB group.

What Rexulti dose are they taking? pwME reporting significant benefit from Rexulti can help shed some clues as to what common Abilify and Rexulti mechanisms of action contribute to improved ME symptoms.

For example, if Wikipedia is correct, Rexulti has an opposite dose related D2 mechanism of action compared to Abilify.

Brexpiprazole has more blocking and less stimulating activity at the dopamine receptors than its predecessor, aripiprazole, which may decrease its risk for agitation and restlessness.[11] Specifically, where aripiprazole has an intrinsic activity or agonist effect at the D2 receptor of 60%+, brexpiprazole has an intrinsic activity at the same receptor of about 45%. For aripiprazole, this means more dopamine receptor activation at lower doses, with blockade being reached at higher doses, whereas brexpiprazole is the opposite.

 

[Hutan]

I’m also really afraid of even posting my experience on S4ME.

Because your experience is an obvious placebo!! Nothing will ever work unless it has 5 consecutive RCT studies all conducted in the UK. And all 5 trials must show a 1000% improvement or else it’s an obvious placebo!

Personally, I'm very happy for patients and clinicians to think creatively, consider the risks versus the possible benefits, and try things. But, as soon as a drug looks likely to be part of a clinician's tool kit and as soon as those clinicians start thinking about telling other clinicians to use it, they should also be thinking about doing a robust trial that ensures that the placebo response can be discounted. Because, there are plenty of examples in medicine generally and ME/CFS particularly, where an expectation bias and natural illness fluctuations has suggested something works, when a blinded placebo-controlled trial of that same something shows it doesn't. (Check out the Mendus trial of CoQ10 with its blinded and open treatment arms, for example.)

Saying that isn't a criticism of patients trying a drug that isn't proven yet. But it is a criticism of clinicians who don't get on to do good blinded trials, or don't at least keep very careful records of all the people that they give an experimental treatment to. The Ablify report had problems, including an inadequate accounting for dropouts that created a selection bias. We need ME/CFS research to be better than that.

It's not an excuse for clinicians to say that they don't have time, or that time getting a trial underway means that they have less time to treat patients. If a good trial is done and it suggests that a drug really can make a meaningful difference, then clinicians and researchers around the world would pick that up, and many patients would benefit. It might even result in an understanding of the cause of the illness. And, if a good trial is done and it suggests that the drug doesn't help, then everyone can focus their energy on other possibilities and patients aren't being exposed to side effects for no benefit. A useful blinded crossover trial for Ablify could have been done by now if everyone understood that that is important.

What I'm seeing happening on the Science for ME forum is people pushing for a systematic approach to evaluation of proposed new treatments, so that there are helpful treatments for everyone with ME/CFS sooner.

 

[leokitten]

But, as soon as a drug looks likely to be part of a clinician's tool kit and as soon as those clinicians start thinking about telling other clinicians to use it, they should also be thinking about doing a robust trial that ensures that the placebo response can be discounted.

What I'm seeing happening on the Science for ME forum is people pushing for a systematic approach to evaluation of proposed new treatments, so that there are helpful treatments for everyone with ME/CFS sooner.

The problem is, and I feel ME clinicians know this, is the likelihood of multiple ME subsets, misdiagnosed ME patients, and other unknown confounding factors, that without some knowledge of pathophysiology in at least one subset then drug trials for drugs that really could work for a subset are doomed.

I currently think we need to understand more than near zero about ME and have more accurate diagnostic capabilities before RCTs are really worth spending the resources to do. So in that sense I disagree with many from S4ME and understand much more why patients and doctors experiment with off-label treatments.

 

[leokitten]

Saying that isn't a criticism of patients trying a drug that isn't proven yet. But it is a criticism of clinicians who don't get on to do good blinded trials, or don't at least keep very careful records of all the people that they give an experimental treatment to. The Ablify report had problems, including an inadequate accounting for dropouts that created a selection bias. We need ME/CFS research to be better than that.

Yep this is true, we do need better than that.

 

[mitoMAN]

Just reporting back. Raised to 1mg on Wednesday last week. Noticing some improvements now, more wired, but also up a bit earlier (usually I am passed out for like 17 hours without being able to hold phone, now maybe jus 14 hours!)
After my passing out phase I was able to leave the bed for 2-4 hours per day already before Abilify.
My health status is really weird, I have some very bad 17-20 hours then I get much much better each day at 2am after midnight.
Can organize lots of stuff etc. in those "up times"

Sidenote: I am also taking ITPP containing Myo-Inositol Trispyrophosphate