Aripiprazole - Abilify

Thanks for your thoughts, @5vforest. I do understand that it's sometimes a difficult balance to strike between being supportive of an individual, while at the same time warning them and others about the lack of evidence supporting the treatment, and possibility of worsening and side effects.

It is interesting to observe which discussions of unevidenced treatments provoke disagreement, and which go smoothely and harmoniously.

My impression is that it's fine when individuals simply share their experiences without making exaggerated claims about efficacy and evidence, and without encouraging others to try it too. In those cases people respond to the person's improvement with good wishes, and the person telling their story joins and welcomes the discussion of science and acknowledges that there is no supporting scientific evidence. If that's the sort of discussion you are happy to engage in, then you are welcome to share your experiments.

I think it's important if there are experimental treatments being prescribed by doctors that we discuss them here so there is somewhere online that is searchable where the scientific evidence or lack of it for that treatment is discussed openly. If someone doesn't feel comfortable sharing their own experiences, they can simply report that the treatment is being prescribed and invite discussion about it without revealing their own situation.
 
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Trish said:
Thanks for your thoughts, @5vforest. I do understand that it's sometimes a difficult balance to strike between being supportive of an individual, while at the same time warning them and others about the lack of evidence supporting the treatment, and possibility of worsening and side effects.

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I think it's important if there are experimental treatments being prescribed by doctors that we discuss them here so there is somewhere online that is searchable where the scientific evidence or lack of it for that treatment is discussed openly. If someone doesn't feel comfortable sharing their own experiences, they can simply report that the treatment is being prescribed and invite discussion about it without revealing their own situation.
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I really agree with Trish and Hutan. It is very important to hear the experiences of other people. How else can we learn anything?! I hope that @5vforest, and @leokitten, and @jaybeen and others continue to report their situation. Similarly, we must hear what the scientists here have to say also about lack of evidence, etc. I hope no one backs away from describing what has happened to them with an experimental treatment.
 
Of course there is one unevidenced 'treatment' most members are using, and which we claim is helpful, particularly in reducing frequency and severity of PEM, and which we discuss endlessly, and that's pacing. As @Wilhelmina Jenkins pointed out, a lot of us have decided to stick with that 'treatment', (plus some of us use symptomatic treatments for pain, sleep etc) and have decided not to risk worsening, or the endless roller coaster of trying one experimental treatment after another. I don't criticise those who choose to experiment. That's their personal choice and I wish them well. I've been there, done that and decided not to keep trying.
 
Jonathan Edwards said:
Not an easy one to answer. There are some intelligent people working in closely related fields who might see the value in testing something. After all Fluge and Mella weren't even in the field but were motivated. When IiME wanted to set up a rituximab study in the UK I organised a team who could have done that, none of whom were primarily in the ME field. We didn't follow through because Norway got phase 3 organised and the background immunology was not giving us much to use as a lab tracer.
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Hmmm. Tough situation.

I assume most people tuned into the ME/CFS world would think of Stanford/OMF first. But it seems like there is good reason to doubt their handling of such things.
 
James Morris-Lent said:
Hmmm. Tough situation.
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In some ways it is not particularly unusual. High profile departments are often not very good at doing trials. We did a limited open label study of rituximab in lupus at UCL in 2000 that suggested major efficacy. Formal trials were taken on by high profile lupus units with the result that for 20 years no clear answer came out because the trials were muddled. Finally last year a decent trial was done that showed efficacy.

The oncologists tend to get things right and there is still a culture of doing trials rigorously at meetings so that poor methodology is flagged up. But oncology was always easier to do that in because diagnosis tends to be black and white and there are nice objective outcomes.
 
Perrier said:
How else can we learn anything?
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While I also agree that it is good to hear experiences, as long as they are not pushing doubtful arguments, I don't actually agree with this.

Surely we learn from trials. Sadly so far we have only learnt that things do not work but that is crucially important. We learnt that rituximab does not work. We have learnt that anti-virals do not work. We have also learnt, by members doing the analysis properly, that CBT and GET do not work despite the spin on the papers.

In contrast I don't think we have learnt anything from personal experiences, have we? No effective treatments have come from that - except as Trish says pacing, which is a bit different. The UK government may have learnt from Paul Garner's personal experience of positive thinking that it cures LongCovid and set up a huge commercial rehab programme on that basis but for ME so far personal experiences have not got us far and arguably they have led to maybe hundreds of people doing themselves harm with surgery or inappropriate drugs.

It would be good to think that one day a personal experience will trigger the proof of a useful treatment. The personal experiences of Fluge's patients triggered the rituximab trials and it might have proved real.

But I don't think we can say 'how else can we learn anything'? We can learn by stimulating science like DecodeME. More than anything we would learn from members insisting that physicians did proper trials rather than handing out unproven treatments.
 
Moderator note
Moderators are aware that the widening of this discussion has taken the thread off topic, but have decided not to move any posts, since it has relevance here. However we ask now that the thread return to the subject of Abilify.
If you wish to continue discussing how we discuss science and medicine on the forum, please go to this members only thread where some of this discussion has been copied.
 
Seems that my dose is 1,5mg/day.
I would have liked it to be less, but well.
Hopefully this dose will provide me benefits (and no side effects) for a long time.
 
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benji said:
How are you doing, @jonathan_h, has the improvement lasted?
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I just went off it after 4 months on. The benefit I felt initially didn’t get larger with time, and whatever benefit there was was small enough in terms of concrete effects (I wasn’t suddenly not bedbound) that after 4 months on, it was hard to tell what if any effect it was having. I’m hoping this time off it will provide some clarity. I believe I’ve already noticed I’m sweating more again with exertion.

The main reason I stopped though was that I started getting heart palpitations of a new type/severity and wanted to see if abilify was the cause. In a couple weeks off, they’ve gotten less frequent but haven’t disappeared, so we’ll see.
 
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Going back to Abilify and potential pathphysiological mechantistic clues…

Here’s a question, let suppose that the theory that the core pathology of ME causes dopamine and serotonin system dysfunction and this dysfunction then is the direct cause of many important ME symptoms such as PEM, cognitive dysfunction, light and sound sensitivity, fatigue, sleep disturbances, other neurological, etc.

And what is true today and will remain true for a long time is that the only drug class that can treat dopamine and serotonin system dysfunction are dopamine-serotonin system stabilizers (DSSs) which all are antipsychotic drugs that have their well-known side effect profiles and very small but serious risks like TD.

I know the obvious answer is yes we need a phase 3 trial showing efficacy, hopefully a trial on a tight cohort like only very severe pwME. I really believe ME is a heterogeneous disorder and also a subset likely don’t have any form of ME but have something else, so this will ruin trials that are not powered with very large number in the treatment arm, like many hundreds we need when unknown heterogeneous forms of disease are present in a trial.

So what if that trial shows enough efficacy in a subset but not everyone, then what will people do? Those side effects and serious risks will still be there and it will likely take a much, much longer time (if ever) for the small band of ME researchers to figure it out well what is causing the dopamine and serotonin system dysfunction, will people still wait?

EDIT: isn’t this too what people with schizophrenia, major depressive disorder, etc have to deal with when taking such drugs like Abilify? It won’t work well or continue to work in some, and it could also cause serious side effects over the long term in some. Isn’t ME as serious and debilitating if not more than those disorders?
 
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A question for those who know more about clinical trials than I do.
@Jonathan Edwards.

Would it be possible to set up a trial to test whether those who are already using a drug and saying they find it helps their symptoms, to do a double blind crossover trial, or blinded dose response trial to at least determine whether the subgroup who already say it works are getting a real or placebo effect?

If, as @leokitten suggest, an experimental treatment only works for some people, then that could at least help determine whether there is a subgroup with a real response, and if testing of relevant biological samples could determine whether there was some factor that could distinguish who would be responders, and who would not, that would enable a full scale double blind trial to be set up for that subgroup.
 
leokitten said:
So what if that trial shows enough efficacy in a subset but not everyone, then what will people do? Those side effects and serious risks will still be there and it will likely take a much, much longer time (if ever) for the small band of ME researchers to figure it out well what is causing the dopamine and serotonin system dysfunction, will people still wait?
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My experience is that his is not realistic assessment of the scenario. Well designed trials tend not to need very large numbers. In general you only need very large numbers of subjects if the drug hardly works. For drugs that really have a significant useful effect five in each group is enough if you design intelligently.

ME is defined in terms of a symptom syndrome. If people fit the syndrome they all have ME as much as each other. If the main pathophysiology of ME is dopamine related then that applies to all of them. If dopamine related pathophysiology is only relevant to a small subset who have an as yet undefined specific disorder there is no particular reason to call that ME. It would be more sensible to call it something else like type 6 dopamine disorder and then we could say that type 6 dopamine disorder was one of the causes of ME.

If there really is such a subset and a drug like aripiprazole has a useful effect it should be possible to demonstrate that effect with a high level of confidence by studying dose requirements and pharmacodynamics.

This relates to Trish's question. Yes, it would make sense to take people who feel they have had a useful effect and to change their dose or treat for specific time windows with gaps in between and gather information on pharmacodynamics - the time profile of the effect. For drugs that work you can get a clear picture of that time profile. The reason why I could be pretty sure rituximab worked for RA after just treating 5 people is that the time profile for all of them was the same and could be repeated with further doses and made biological sense.

I think doing an effectively blinded study on those who feel they have benefited could be very useful. You would probably only need to study 5-10 people.

If I was an ME physician with a genuine interest in benefits of aripiprazole for ME I think I could tease out whether or not the effects were relevant within a year pretty much for certain. And nobody has got anywhere near this despite its use for several years.
 
Responding to a deleted post about a German doctor prescribing larger doses of Abilify.

I would just ignore it. I wouldn't go near an Abilify Facebook page. I don't think I would go near an 'ME/CFS doc' in Germany to be honest. Surely this is all just gossip. We live in a world where important issues have been trivialised to the level of gossip and hearsay.
 
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Well, I wouldn’t feel good taking that much, and I am very sure of my GP would not prescribe it. We are following the Stanford paper, anything else feels very unsafe.

I am not sure I see all the talk about side effects in the FB group, but I don’t follow closely either. However I saw one asking about it, low dose, and nobody answered. Except for one saying that it seemed safe. So both ways are viewed.
 
leokitten said:
Another difference is that Abilify had normalized my sleep! Or maybe the moclobemide with Abilify is the combo making the difference here. But the over two months I was on moclobemide before starting low dose Abilify I didn't have any improvements in sleep.

For the first month or so Abilify made falling asleep more difficult, but once I got through that phase the payback on sleep has been really good. I wake up at a normal early time now and get truly tired, even yawning and watery eyes, at the right time at night. Everything shifted forward back to normal instead of ME falling asleep at 2-4am because of intense wired but tired and other symptoms.

I still need to take my regular sleep meds which I've been cycling and taking for years, but for some reason the Abilify (or together with moclobemide) makes them work much more effectively with a lower dosage, and the important thing is that they never fail to work. And I fall asleep fairly quickly after getting the wave of tiredness..
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interesting that the sleep benefits changed after a month or so.
Hope it is still works that way. I responded also that way to Abilify, in the first month. it was really helping getting tired and go to sleep. It fixed my sleep and sleep cycle (still taking the same amount of sleep aid). But that has now vanished. I still sleep enough hours, so it is ok. But I don’t fall asleep until til 1 a.m, lying awake some hours before that. And sleep until 11 or 12 am, and am tired some hours after also.
All other benefits of Abilify have remained. So strange. I keep experimenting with taking it morning or evening, and with a little lower doses than 1,5mg. Hoping to solve the puzzle.
 
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