Off label use of Aripiprazole shows promise as a treatment for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Crosby et al. 2021

@leokitten

Prescribing this medication might even jeopardize your diagnosis if your disability insurance reviews your case in the future? There is no biomarker for ME, it's based on your medical history, onset and the expertise/experience of your ME doctor.

Personally, I would feel very uncomfortable having Abilify on my records.
 
I am glad for anyone who is experiencing symptom improvement as a result of taking abilify.


I do have a couple of concerns though.

I have read many comments that suggest that the dose being used for me/cfs is uniquely low and side effects will only occur at high doses.

Actually low dose abilify (1-2 mg) has been used for depression and anxiety for years.


I was prescribed it at that dose for those reasons in 2009.

I experienced a side effect of intrusive repetitive suicidal thoughts which went away when I stopped taking abilify.

To be clear, I was not suicidal.

Fortunately, I recognized that I was experiencing a side effect of abilify and stopped the medication.


My concern is that if someone else doesn’t make the connection—or doesn’t make it quickly enough, this side effect could exacerbate already existing depression and suicidal ideation (secondary to me/cfs), which could result in suicide.

It did take me several days to realize what I was experiencing was a medication side effect.


Secondly, I don’t think that the retrospective study by Dr. Bonilla can be relied upon to be accurate (even for the kind of study it is). I have heard numerous accounts from Stanford patients who say that their reports of abilify side effects were ignored by Dr. Bonilla, and were not necessarily recorded in their medical charts. They were not informed they were part of a study. And they were pressured to take abilify or to give it another try when they stopped taking it.


If Dr. Bonilla is having difficulty obtaining funding for a study of abilify I question if this background might be a factor.


It concerns me that patients worldwide are relying on the expertise of the Stanford me/cfs clinic regarding abilify as a treatment for me/cfs, and that expertise is questionable and it appears that the research that is being done there is being done in a very sloppy way.
 
This has been the most successful treatment I have tried since I got cfs ten years ago. With this paper hopefully patients can try and convince their doctors to prescribe abilify and try it out for themselves. I would just print it and bring it to their office.

Edit: having said that, the benefits can disappear after a few months. The best solution I have found has been to to take a few months off and start again (4-6 months).
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This first comment on that Reddit thread points out the problem of tolerance and how s/he overcame it.
 
vsou said:
I was prescribed it at that dose for those reasons in 2009.

I experienced a side effect of intrusive repetitive suicidal thoughts which went away when I stopped taking abilify.

To be clear, I was not suicidal.

Fortunately, I recognized that I was experiencing a side effect of abilify and stopped the medication.


My concern is that if someone else doesn’t make the connection—or doesn’t make it quickly enough, this side effect could exacerbate already existing depression and suicidal ideation (secondary to me/cfs), which could result in suicide.

It did take me several days to realize what I was experiencing was a medication side effect.
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I share your concern. In 2016 the French national drug authority (ANSM) issued a safety warning to healthcare professionals against the off-label prescription of Abilify for autistic youth. They mention the increased risk of suicide that requires close monitoring. https://translate.google.com/transl...e-Point-d-Information-actualise-le-05-04-2016
 
Also https://www.s4me.info/threads/open‐...c-fatigue-syndrome-haghighi-et-al-2021.18971/
https://onlinelibrary.wiley.com/doi/full/10.1002/brb3.2040
published 2 Feb 2021
Dopamine stabiliser trial for ME.

I don't know what to think of all this stuff. Ages ago ME doctors were loading up patients with Hydro Cortisone and Klonopin. That caused havoc for many--and some are still unable to get off these drugs. Then there was GcMaf, which made some sick. You'd read here and there that so and so got better, and many tried this stuff with long term consequences. Now there are trials of brain drugs. Oh yes, low doses. I recall that's what was said about the hydrocortisone, nothing bad will happen, just low doses. But things did not pan out that way.

I am not saying not to do trials, but it's so hard when the core problem of ME is not even in close sight.
 
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Mij said:
@leokitten

Prescribing this medication might even jeopardize your diagnosis if your disability insurance reviews your case in the future? There is no biomarker for ME, it's based on your medical history, onset and the expertise/experience of your ME doctor.

Personally, I would feel very uncomfortable having Abilify on my records.
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Really so taking an antidepressant would jeopardize your ME disability claim too? Or taking LDN would jeopardize it because it’s a drug used to treat alcohol abuse in higher doses?

Remember the most widely used indication for Abilify (5–10mg per day) is as an add-on med to antidepressants. Abilify isn’t used as much as an antipsychotic (15-30mg per day) anymore as it wasn’t found to be as effective as other drugs on the market.
 
leokitten said:
Really so taking an antidepressant would jeopardize your ME disability claim too? Or taking LDN would jeopardize it because it’s a drug used to treat alcohol abuse in higher doses?
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No, my CFS diagnosis might be reversed to a diagnosis of depression/anxiety instead. Did you forget the stigma attached to CFS? Mental illness is treatable and might require that I be an active participant in treatment? If the insurance company doesn’t see evidence of best practices of medical care and active engagement by me, then my might be reversed- quickly.
 
lunarainbows said:
anecdotally I was told by my autism counsellor (edit: and assessor) that some people with autism (who already have differences in brain functioning), have been permanently harmed by psychiatric and anti psychotic medications and so doctors need to be aware of possible harm even at lower doses if I am ever offered something as an impatient at hospital
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"permanently harmed" - and even worse :(

Mij said:
This has nothing to do with being 'adult'. Come on now. Your ME doctor would have to truly understand what is occurring in your own particular case in order to even consider it.
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And then consider whether they want to take the professional and medical risk of prescribing off-list?
 
This seems like a low evidence paper ...I agree with others that this needs better evidence before making claims of any drugs efficacy.

Makes me wonder about methodology ...subjective measures with drugs that have mind altering side effects? Seems like mostly garbage to me. We deserve better than this but at least they published something to show it was garbage and how flawed experimental design can be. Good to flag these authors for future scrutiny.

im not going to comment on Twitter postings ...other than to add to comments by others ...it’s disappointing
 
Hutan said:
They seem to have taken out the 25% of participants with the worst results, and then shown that the remaining 75% averaged pretty minor improvements on subjective outcomes in an open label trial.
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Yes it's frustrating that they don't simply report the change for the whole group. They report data for 66 responders and 20 responders but that is still less than the 101 patients who took Aripiprazole. Is that due to missing values?

Jaybee00 said:
~50% reduction in fatigue and brain fog is pretty significant...
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The 50% reduction was seen only in the group that got better and their improvement might be due to regression to the mean, natural improvement, response bias etc.
 
Does Abilify increase alertness or reduce (physical) fatigue by 50%?

I have taken low dose (25mg) trazodone for sleep. I've asked pharmacists, ME doctor and other specialists why a low dose antidepressant works so well for sleep, but no one knows the answer. They no longer rx higher dose trazodone for depression because it's more effective as a sleep aid. I once increased the dose to 50mg (for one night) and became very dizzy for one week, the pharmacist told me that this was rare and had never heard of anyone experiencing this.
 
Mij said:
I have taken low dose (25mg) trazodone for sleep. I've asked pharmacists, ME doctor and other specialists why a low dose antidepressant works so well for sleep, but no one knows the answer.
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Trazodone - StatPearls - NCBI Bookshelf
The unique property of trazodone, where it simultaneously inhibits SERT, 5-HT2A, and 5-HT2C receptors, is that it avoids the issue of sexual dysfunction, insomnia, and anxiety that commonly presents with SSRIs and SNRIs therapy. Trazodone reduces levels of neurotransmitters associated with arousal effects, such as serotonin, noradrenaline, dopamine, acetylcholine, and histamine. Low dose trazodone use exerts a sedative effect for sleep through antagonism of 5-HT-2A receptor, H1 receptor, and alpha-1-adrenergic receptors.
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arewenearlythereyet said:
This seems like a low evidence paper ...I agree with others that this needs better evidence before making claims of any drugs efficacy.

Makes me wonder about methodology ...subjective measures with drugs that have mind altering side effects? Seems like mostly garbage to me. We deserve better than this but at least they published something to show it was garbage and how flawed experimental design can be. Good to flag these authors for future scrutiny.

im not going to comment on Twitter postings ...other than to add to comments by others ...it’s disappointing
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This is something I've been wondering about. Initially with old SSRI trials for various "functional" conditions, but also with Mestinon for me/cfs. The concern is it goes beyond subjective outcomes and into things like steps walked. I found Mestinon modestly stimulating. Not a stimulant stimulant, but certainly in that direction. Yes, there is the CPET, but it might do 2 things at once and overstate it's outcomes.

With Abilify you'd think you'd have similar problems. I've read enough on it since this study was released to know it's stimulating for a good portion of people that take it, and in various manifestations.

The only idea I have is that you'd have to use something arbitrarily long until overdoing it spirals out. I could push through PEM for a long time at points in my illness, particularly when I was quite young.
 
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That isn't to say things that can be stimulating shouldn't be studied. It just seems daunting. I have been taken reading some of the comments on Abilify. It's not something I've read with regularity and acknowledging the severe limitations of anecdotes coupled with publicity, a single clinic etc...
 
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dreampop said:
With Abilify you'd think you'd have similar problems. I've read enough on it since this study was released to know it's stimulating for a good portion of people that take it, and in various manifestations.

The only idea I have is that you'd have to use something arbitrarily long until overdoing it spirals out. I could push through PEM for a long time at points in my illness, particularly when I was quite young.
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That's been happening to me with midodrine and Mestinon over the last year. I find them a bit perverse because they reduce the symptoms of orthostatic intolerance, which are draining, but they don't prevent PEM.

They enabled me to exert myself more at first, so I pushed, and now my physical and mental abilities while being on these treatments are back to where they were before I got on them. When I forget to take them or have to skip them (e.g. for a medical exam), I feel worse than pre-treatment with significant brain fog, dyspnea/tachypnea and postural tachycardia.

Pacing and rest as needed remain the only answers until we have a treatment that prevents PEM, not drugs with stimulating effects, whether they are stimulants or not.
 
leokitten said:
OMG but why are you taking drugs with potentially nasty side effects that haven’t been proven in any RCTs to work in ME/CFS? :nailbiting:

Isn’t it funny how I read all over S4ME posts of users doing this with various drugs etc, yet it’s interesting to see very little blowback or dire warnings from other members, if at all, compared to what I’ve seen on Abilify threads.
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There have been RCTs of midodrine and Mestinon for POTS, and midodrine is officially indicated for the treatment of orthostatic hypertension.

In my case, there were no side effects from the drugs, only from overexertion because I am not in a position where I can stop working. That would have happened regardless of the treatment. Ideally, people with ME who have OH and/or POTS and have been prescribed midodrine and/or Mestinon should be able to pace themselves, so that they can benefit from the "boost" while avoiding overexertion.

If it needs to be said, I don't have an opinion for or against Abilify at the moment because there is no evidence that it might or might not work in ME/CFS. It would be great if it does.

With the current absence of evidence, I don't think it is responsible to tell people with ME to go to their doctor and ask for a prescription for Abilify, especially given the known side effects. Janet Dafoe shouldn't have tweeted this.

ETA: only midodrine is approved for orthostatic hypotension, not Mestinon.
 
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