Also another prime example is people with depression and serotonin. If the neuroinflammatory and monoamine hypothesis of depression is true, then by your account I untreated depressed people should have progressively worse serotonin levels until they basically don’t have much serotonin anymore, but this isn’t the case. People can go decades with chronic lower activity or dysfunction without further neurotransmitter degradation.
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Abilify- Stanford Clinic Patients
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Also another prime example is people with depression and serotonin. If the neuroinflammatory and monoamine hypothesis of depression is true, then by your account I untreated depressed people should have progressively worse serotonin levels until they basically don’t have much serotonin anymore, but this isn’t the case. People can go decades with chronic lower activity or dysfunction without further neurotransmitter degradation.
What evidence do you have to support this?
Abilify has multiple receptor targets where it functions as a partial agonist/functionally selective drug, so where at low doses it will be an agonist compared to higher antipsychotic doses where is is an antagonist.
So it effectively does act as a different drug. It is common knowledge in the psychiatric community that Abilify is a very different drug compared to all the other typical and atypical antipsychotics.
@leokitten the number of drug resident depression is very low. And even then, deep brain stimulation helps a lot of them.
Also i dont like the comparison from Cfs and depression. Because when you postulate a neuroinflammation all the time in Cfs, then there is a progression over time because of undersupply of the tissue. But thats different opinions i guess. I dont believe in a neuroinflammation in Cfs. I think its the downstream effect from the blood undersupply to the whole brain, shown from Systrom. But time will tell i guess.
Also i dont like the comparison from Cfs and depression. Because when you postulate a neuroinflammation all the time in Cfs, then there is a progression over time because of undersupply of the tissue. But thats different opinions i guess. I dont believe in a neuroinflammation in Cfs. I think its the downstream effect from the blood undersupply to the whole brain, shown from Systrom. But time will tell i guess.
Treatment-resistant depression was just an example off the top of my head where research has shown this.
You might be right about neuroinflammation, but multiple ME research groups studying this produced peer-reviewed results that have disagreed with you so far. That being said, none of those papers said that the cause must be in the brain, they just observed it and yes the cause could be coming from outside the brain for sure.
But some of our important symptoms could be coming from neuroinflammation in the basal ganglia, even though the root cause could be somewhere else.
This thread about Abilify is about symptom treatment, not disease modifying treatment in any way.
stefanosstef
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I think it's proven that chronic neuroinflammation downregulates dopamine receptors.This isn't the same as a neurodegenerative disease but all that chronic oxidative stress I belive it predisposes us for any neurodegenerative disease later on.
@Badpack
Read up on neuropsychiatric lupus, or others in the list of proven neurological disorders that also cause significant psychiatric symptoms. No one would say that these are psychiatric disorders, just like ME isn’t either.
But many of these disorders cause neuroinflammation in the brain due to one root cause or another and if there aren’t disease modifying treatments for these disorders then it makes sense to trial symptomatic treatments that might tackle neuroinflammation, etc.
Read up on neuropsychiatric lupus, or others in the list of proven neurological disorders that also cause significant psychiatric symptoms. No one would say that these are psychiatric disorders, just like ME isn’t either.
But many of these disorders cause neuroinflammation in the brain due to one root cause or another and if there aren’t disease modifying treatments for these disorders then it makes sense to trial symptomatic treatments that might tackle neuroinflammation, etc.
Well, tell this to 9/10 colleagues that i talked to haha.
The studies to neuroinflammtion in Cfs just don't impress me. Its a lot of guess work and not really hard evidence in my opinion. Nothing beyond what a mere lowered blood supply cant explain. Maybe because of damaged small fibers in the small arteries. None of those neuropsychiatric symptoms of other autoimmune diseases compares to pem. So there must be key differences.
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THIS THREAD IS BEING RE-OPENED. SEVERAL POSTS HAVE BEEN DELETED BECAUSE THEY WERE ARGUMENTATIVE OR OFF-TOPIC - ESSENTIALLY NOT ADVANCING THE DISCUSSION ABOUT ABILIFY.
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Disruptive threads? Take a deep breath before posting . . .
PLEASE READ THE FOLLOWING POST CAREFULLY BEFORE POSTING HERE - IT EXPLAINS A NEW MODERATOR POLICY REGARDING OFF-TOPIC, ARGUMENTATIVE AND REPETITIVE POSTS, AS WELL AS PERSONAL ATTACKS:
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To add to our discussion regarding combining celecoxib or etoricoxib (COX-2 inhibitors) with Abilify and potential synergistic effects, possibly related to further reducing neuroinflammation.
It’s been known since the 1990s that the COX-2 pathway is intricately involved in peripheral inflammation. But what I didn’t know was how much fairly conclusive research has been done showing how this pathway is also very centrally involved glial activation and neuroinflammation.
Here’s a selection of papers:
https://pubmed.ncbi.nlm.nih.gov/32359360/
https://pubmed.ncbi.nlm.nih.gov/32860157/
https://pubmed.ncbi.nlm.nih.gov/31539536/
https://pubmed.ncbi.nlm.nih.gov/30526621/
https://pubmed.ncbi.nlm.nih.gov/15453089/
It’s been known since the 1990s that the COX-2 pathway is intricately involved in peripheral inflammation. But what I didn’t know was how much fairly conclusive research has been done showing how this pathway is also very centrally involved glial activation and neuroinflammation.
Here’s a selection of papers:
https://pubmed.ncbi.nlm.nih.gov/32359360/
https://pubmed.ncbi.nlm.nih.gov/32860157/
https://pubmed.ncbi.nlm.nih.gov/31539536/
https://pubmed.ncbi.nlm.nih.gov/30526621/
https://pubmed.ncbi.nlm.nih.gov/15453089/
I’m also shamelessly copying @jaybee00’s thread on S4ME here regarding MS fatigue and basal ganglia involvement as it’s relevant, especially because people were looking for additional related evidence of low dopamine and neuroinflammation, of which some was provided earlier in this thread.
Regional microglial activation in the substantia nigra is linked with fatigue in MS, 2020, Singhal et al.
https://nn.neurology.org/content/7/5/e854
Popular article here:
Hunting for a "Hidden Pathology": Why Is Fatigue So Debilitating in Multiple Sclerosis?
https://www.technologynetworks.com/...-so-debilitating-in-multiple-sclerosis-339120
And Cort Johnson’s article on this, which also covers some of the other evidence of basal ganglia involvement in ME mentioned here.
https://www.healthrising.org/blog/2...erosis-fibromyalgia-chronic-fatigue-syndrome/
Thanks @jaybee00 !!
Regional microglial activation in the substantia nigra is linked with fatigue in MS, 2020, Singhal et al.
https://nn.neurology.org/content/7/5/e854
Popular article here:
Hunting for a "Hidden Pathology": Why Is Fatigue So Debilitating in Multiple Sclerosis?
https://www.technologynetworks.com/...-so-debilitating-in-multiple-sclerosis-339120
And Cort Johnson’s article on this, which also covers some of the other evidence of basal ganglia involvement in ME mentioned here.
https://www.healthrising.org/blog/2...erosis-fibromyalgia-chronic-fatigue-syndrome/
Thanks @jaybee00 !!
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Rebeccare
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It's not plagiarism if you cite (and thank) the source!
Neuroprotective effects of the second generation antipsychotics, Chen et al. Schizophr Res, 2019
Systematic review of 24 studies looking at first gen (FGA) and second gen (SGA, atypical) antipsychotics. Multiple studies found evidence of neuroprotection with Abilify and other SGAs, though they were in vitro studies. FGAs either showed no protection or were actually found to be neurotoxic.
Systematic review of 24 studies looking at first gen (FGA) and second gen (SGA, atypical) antipsychotics. Multiple studies found evidence of neuroprotection with Abilify and other SGAs, though they were in vitro studies. FGAs either showed no protection or were actually found to be neurotoxic.
@leokitten so to conclude the last days, you posted a lot of interesting studies. All in favor for Abilify. So then what keeps you from taking it? If there seems no downside for low dose in Cfs ?
The only thing holding me up so far is it won’t be worth for me and my severity level to trial Abilify if it turns out to last only a few months before fading. If it lasts more than a year in some people or with combo cox-2 inhibitors or LDN then that’s a different story, more than a year would be great and I might pull the trigger.
I’m not severe, I fluctuate between moderate and mild-to-moderate, and bedridden during crashes and recovery from crashes, which have been lasting longer and longer over the years as I’ve been slowly deteriorating due to work and constant overexertion. It’s not going to make much difference in my QOL if it only causes improvements for a couple months.
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@leokitten fair enough. Here are some of mine.
This is a case of low dose abilify with severy side effects. Hyperprolactinemia with a chance of Amenorrhea, oligomenorrhea, galactorrhoea, gynecomastia, infertility.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6124876/
Here are Extrapyramidal side-effects of low-dose aripiprazole. No complete recovery.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4750315/
Here are Two Case Reports of rapid onset Akathisia with low dose Aripiprazole
https://www.researchgate.net/public..._with_low_dose_Aripiprazole-_Two_Case_Reports
Other problems that often occure during low dose treatment are Dystonia Symptoms, prolonged abnormal contractions of muscle groups, spasm of the neck muscles, sometimes progressing to tightness of the throat, swallowing difficulty, difficulty breathing, and/or protrusion of the tongue.
and so on. I can understand if they give it to Rons Son. Because he wasnt that much away from death. But everyone who can still visit this forum should be well enough to be very cautious about taking drugs that can be this harmful.
This is a case of low dose abilify with severy side effects. Hyperprolactinemia with a chance of Amenorrhea, oligomenorrhea, galactorrhoea, gynecomastia, infertility.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6124876/
Here are Extrapyramidal side-effects of low-dose aripiprazole. No complete recovery.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4750315/
Here are Two Case Reports of rapid onset Akathisia with low dose Aripiprazole
https://www.researchgate.net/public..._with_low_dose_Aripiprazole-_Two_Case_Reports
Other problems that often occure during low dose treatment are Dystonia Symptoms, prolonged abnormal contractions of muscle groups, spasm of the neck muscles, sometimes progressing to tightness of the throat, swallowing difficulty, difficulty breathing, and/or protrusion of the tongue.
and so on. I can understand if they give it to Rons Son. Because he wasnt that much away from death. But everyone who can still visit this forum should be well enough to be very cautious about taking drugs that can be this harmful.
I’m personally looking for a treatment that can get me back to work again on a more consistent basis without bad PEM, crashes, and deterioration to bedridden disability. More than the very minimum work I can do now, and any new treatment can’t just work for a relatively short time.
I know for people of worse severity levels more minor improvements can be huge for QOL. But for me, fluctuating between moderate and mild-to-moderate, I can do basic things at home, go out for short trips for things or even restaurants occasionally, and even take short walks without severe problems.
But when I start ramping up the fairly constant exertion and activity required to work and meet work deadlines, even part time, that’s a great deal more exertion, and within a week my ME symptom severity starts exploding and becoming unbearable and unmanageable. Then follows the full blown PEM and crashes over and over again and further permanent deterioration. Sleep for me becomes impossible after overexertion, even with polypharmacy, it feels like there is so much inflammation in my head that I’m so wired and exhausted my body won’t be able to sleep for days until I collapse. Just that ONE symptom would make work impossible for a healthy person!
So I’m at this weird severity level where when I can fully adaptive pace, rest, and not exert when I shouldn’t then I’m not in ME hell. But when I ramp up exertion via part-time work or physical activity then that is too much. So for me a treatment needs to be that good so I’m basically mild ME again and it needs to last.
I know for people of worse severity levels more minor improvements can be huge for QOL. But for me, fluctuating between moderate and mild-to-moderate, I can do basic things at home, go out for short trips for things or even restaurants occasionally, and even take short walks without severe problems.
But when I start ramping up the fairly constant exertion and activity required to work and meet work deadlines, even part time, that’s a great deal more exertion, and within a week my ME symptom severity starts exploding and becoming unbearable and unmanageable. Then follows the full blown PEM and crashes over and over again and further permanent deterioration. Sleep for me becomes impossible after overexertion, even with polypharmacy, it feels like there is so much inflammation in my head that I’m so wired and exhausted my body won’t be able to sleep for days until I collapse. Just that ONE symptom would make work impossible for a healthy person!
So I’m at this weird severity level where when I can fully adaptive pace, rest, and not exert when I shouldn’t then I’m not in ME hell. But when I ramp up exertion via part-time work or physical activity then that is too much. So for me a treatment needs to be that good so I’m basically mild ME again and it needs to last.
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Yep there are always risks, everyone is different in how they will react and what they are willing to risk given their ME situation.
Think about this, suppose if they found rituximab consistently helped 15% pwME for a couple years or more, and rituximab has these insane and dangerous side effects and can cause such immunosuppression that can cause death (e.g. COVID, bacteria, etc), it’s really up to people if they want to risk taking it.
Think about this, suppose if they found rituximab consistently helped 15% pwME for a couple years or more, and rituximab has these insane and dangerous side effects and can cause such immunosuppression that can cause death (e.g. COVID, bacteria, etc), it’s really up to people if they want to risk taking it.
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I am 23h bed bound, sometimes my brain fog gets so bad that i nearly forget my own name. But still, i wouldnt take a drug that can destroy my cerebellum. What if a good medication comes around in some months/years and i cant walk anymore because i bought 1-2 months of relieve in exchange for Akathisia or other Extrapyramidal damages that make me disabled for live.
And in this 6 years sickness i tried a lot, Plasma exchange, rituximab, high dose prednisolone, MTX, rapamune, SS31 and sooo much more. And still, i wouldnt touch abilify.
And in this 6 years sickness i tried a lot, Plasma exchange, rituximab, high dose prednisolone, MTX, rapamune, SS31 and sooo much more. And still, i wouldnt touch abilify.