Acute Corticotropin-Releasing Factor Receptor Type 2 Agonism Results in Sustained Symptom Improvement in Myalgic Encephalomyelitis

[Reading_Steiner]

This company / experiment was actually mentioned in that article I found from 2019 in New Zealand.
This theory actually makes the the most sense out of all theories so far if you think about the CCI cases whereby their CFS appeared to be caused by physical pressure on areas of the brain, I've been wondering for a while how that could be possible. I also found out recently that multiple chemical sensitivity is caused by the brain, not the immune system. My panic attack experience was caused by overreacting to a random pain in my chest,
I had general anxiety disorder for months after, I think it could be an indication that something wasn't right, a precursor to the same neurological mechanisms that cause CFS and MCS. I had other psychological problems in the 5 years prior to all that, in the paper it says that other health problems or life problems, at a young age especially, correspond with increased rates of developing CFS.

 

[roller]

its again like:
a) elephant in the room
b) they are pondering on how to glue the tea cup

 

[seamyb]

This talk of panic attacks is messed up. I had mad ones out of nowhere about 5 years ago, thought I was dying each time. Had about 3 of these per day. Went on the sertraline and they eventually went away over a few months. Not long after I came off sertraline a year ago I came down with CFS.

Did an SSRI pause my descent into chaos?

 

[Irat]

This talk of panic attacks is messed up. I had mad ones out of nowhere about 5 years ago, thought I was dying each time. Had about 3 of these per day. Went on the sertraline and they eventually went away over a few months. Not long after I came off sertraline a year ago I came down with CFS.

Did an SSRI pause my descent into chaos?

Yes psychiatric drugs are basicially a neurotoxin and i have been destroyed by one .but if you first came down with cfs a year later,this did not happen to you.but it could have been a trigger added to your bucket.....
https://www.madinamerica.com/2018/01/what-really-call-psychiatric-drugs/

 

[godlovesatrier]

I never had any issues around anxiety. Hpa did feel off for years. If I got stressed a few years ago my muscles would literally crash. It's better now probably because I'm in a stable relationship and less anxious about life but it's much better than it used to be. My body doesn't over react anymore. Not really sure what worked to help that but having a partner who you can rely on does help a lot.

So I can see why this might be dead useful for some of us. I remember my early symptoms were just terrible fatigue totally unrelenting all day every day, sore throat, severe dizziness which was just awful which went on for about 16 months before improving and night sweats where I'd just wake up soaking wet. Be interesting one day to know what subsets well fit into based around things like our symptoms.

 

[bensmith]

I read on s4me or whatever that they all think this trial is not promising at all. Kind of a bummer reading that. Really could use some help.

 

[gregh286]

Unfortunately again, this is 100% bs.

Yep
Downstream horseshit
Of course hpa is over activated. Body thinks it's under continual attack. Rats in a trap.

 

[Diwi9]

I'm not seeing the results in the physical exertion section of the results. The main improvements were on patient self-reporting. The results of this study, especially being unblinded, are underwhelming. Cortene might be a tool in the toolbox, but it is no cure.

 

[DrUniverse]

Yep
Downstream horseshit
Of course hpa is over activated. Body thinks it's under continual attack. Rats in a trap.

Well the Body IS under continual Attack.

 

[gregh286]

Well the Body IS under continual Attack.

Yep or it perceives it is.
One or other.
Cell danger response. Backed that horse since long time.

 

[Oliver3]

Mabey his bucket is not full yet.just a few more triggers and the ship could sink.depends on how big ones bucket is (resilience) and how many triggers thrown at

This is my point . Its allostatic load. What creates the difference. He has a different frame, different spine. He's smaller than me.
Everyone has a breaking point no matter how hard and strong they are but he works extremely long hours as a photographer and then runs, all with an anxiety disorder.
So there's obviously another element.
I call him the terminator cos nothing stops him

 

[Oliver3]

This company / experiment was actually mentioned in that article I found from 2019 in New Zealand.
This theory actually makes the the most sense out of all theories so far if you think about the CCI cases whereby their CFS appeared to be caused by physical pressure on areas of the brain, I've been wondering for a while how that could be possible. I also found out recently that multiple chemical sensitivity is caused by the brain, not the immune system. My panic attack experience was caused by overreacting to a random pain in my chest,
I had general anxiety disorder for months after, I think it could be an indication that something wasn't right, a precursor to the same neurological mechanisms that cause CFS and MCS. I had other psychological problems in the 5 years prior to all that, in the paper it says that other health problems or life problems, at a young age especially, correspond with increased rates of developing CFS.

Collagen and connective tissue is a huge factor in anxiety disorders CCI and cfs etcetc

 

[junkcrap50]

First promising... But open-label study again. We have to wait.

Thank you for somebody finally getting it's a open label study. It's a open-label, phase 1 study. It's only meant to test for safety and see if the drug is probable or promising enough for more studies. That's it. Everyone's dumping all over it because, "Oh well it's not blinded, there's no control, study size is too small, etc. etc." So, yes, we have to wait for more studies, which hopefully there will be as this study is promising.

I read on s4me or whatever that they all think this trial is not promising at all. Kind of a bummer reading that. Really could use some help.

Well... I can't really say what I'd like to on s4me. But one critism of the study I do think is valid is that the study used poor measures for symptom change/improvement. It could have been better and wouldn't have been much harder. But, I don't think it's reason enough to not do a second, larger phase 2 study.

 

[Martin aka paused||M.E.]

But, I don't think it's reason enough to not do a second, larger phase 2 study.

Not at all. If they include the excluded CPET... For example...

 

[godlovesatrier]

I just tried explaining the quality of study problem with someone on twitter the other day who had put out an article about immune drugs helping ME patients. Based on PR threads the drugs and indeed the studies haven't really proven out there original assumptions.

It's annoying to see it raise people's hope falsely. At least at the very very early stages where they've only done the basics in the study for a particular compound or drug.

 

[Reading_Steiner]

I assumed the study description was being honest, it can take a lot of effort to get through the statistics and people can't do that for every one they read. We need some kind of genuine lead, some clue that stands up to scrutiny that can't just be dismissed as a downstream effect, its so frustrating, the only good thing lately is the long covid lobby putting us on the map.

 

[Rebeccare]

It's a open-label, phase 1 study. It's only meant to test for safety and see if the drug is probable or promising enough for more studies. That's it. Everyone's dumping all over it because, "Oh well it's not blinded, there's no control, study size is too small, etc. etc." So, yes, we have to wait for more studies, which hopefully there will be as this study is promising.

I was recently reading another thread about Cortene in which someone actually contacted the company, and this was part of the reply:

As to a timeline, getting a new drug approved is a long process. We will need to run at least two more trials before we can apply for FDA approval. Best case, these will each take a couple of years.”

I'll look forward to reading Cort's take on it (which is always helpful for people like me who aren't science-brained), as he's written about this drug in the past: https://www.healthrising.org/blog/2...new-drug-for-chronic-fatigue-syndrome-me-cfs/

 

[Wishful]

I did check further, and found lots of discussion about the paper, mostly dismissing it as not providing adequate proof that the drug works for ME. However, I didn't find any dismissal of the hypothesis for the core cause of ME. That's important to me. The drug might fail to match the theoretical reaction for a number of reasons (not getting to the right place, an unknown countereffect, etc). They haven't proven that their hypothesis is correct, but it hasn't been proven incorrect either.

I've always believed that my glial cells were involved in my ME. Perhaps the cells producing or responding to CRF2 are affected by the glial cells around them, and perhaps there is a feedback loop locking both types of cells into that abnormal state.

Cortisol drugs have triggered temporary remission in myself and several other people. Perhaps it 'jiggles' the CRF2 mechanism enough to switch it out of the abnormal state, but longer term cortisol supplementation causes alterations which then make this state switching less likely.

Despite the dismissals of the trial, I still feel optimistic that they might be on the right track.

 

[Martin aka paused||M.E.]

However, I didn't find any dismissal of the hypothesis for the core cause of ME.

Then you have to check what VanElzakker said on Twitter.

 

[Wishful]

Then you have to check what VanElzakker said on Twitter.

No, I've never checked Twitter. Never plan to.