Naltrexone restores impaired transient receptor potential melastatin 3 ion channel function in NK cells from ME/CFS patients, Cabanas et al, 2019

Cheesus said:
Naltrexone works fantastically for me. I went from being almost as sick as Whitney Dafoe to using my laptop several hours a day, listening to audiobooks, sitting in bright rooms, and holding prolonged conversations in a matter of weeks.
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Awesome! As an aside, I also experienced some benefits from it in the past, though far milder than what you are describing, but could not continue taking it due to side effects. But just because a drug helps some people, it doesn't make it effective in general as a treatment for a condition. Some people with a diagnosis of ME/CFS also improved while on rituximab and we know for a fact from a double-blind trial that it does not work. This research team is suggesting that naltrexone targets what they claim is THE pathway in this illness. If that were the case, given how many people have tried it, you'd expect many more recoveries I think. I know at least a couple dozen people who have tried this and they still have ME.
 
There are studies that indicate that LDN is also a mixed bag for ppl with MS. Some benefit while others don't. Some have experienced insomnia and nightmares which was a side effect in my case.
 
I've not read the paper, only the abstract. I find it really hard to believe that one drug affecting one receptor on one ion channel is the mechanism for improvement in responders to LDN.

If you watched Alain Moreaus presentation at the recent OMF symposium you might remember he noticed cellular impedance changes in Jurkat cells soaked in patient plasma when different compounds were added. Patch clamp used by NCED measures voltage, which has a relationship to impedance, and impedance is measured by Moreau.

What is noticeable to me is that other Australian researchers are forming collaborative relationships either amongst themselves, or with other international groups, but not these guys. I wonder why....... if they really have discovered the core mechanism and a biomarker surely they'd be urging other groups to replicate........
 
I think I have worse pain if I don’t take LDN but having said that, it doesn’t make a huge difference to me. I have tried a variety of doses and currently am back down to 4.5mg because more didn’t seem to add benefit. Initially I had some improvement that I would put down to the medication but that wore off....
 
I'm curious as to how click-baity they are prepared to get with their communications, "You won't believe this one simple cure for CFS/ME that doctors don't want you to know about!"?

Or perhaps "Read all about the research that NCNED could do and the Kardashians couldn't!"??
 
There was an initial TRPM3 measurement study with 6 patients and 6 controls recruited and patch clamp measurements reported in August 2018
Paper : Loss of Transient Receptor Potential Melastatin 3 ion channel function in natural killer cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients
Link : https://molmed.biomedcentral.com/articles/10.1186/s10020-018-0046-1
Thread : https://www.s4me.info/threads/loss-...om-cfs-me-2018-marshall-gradisnik-et-al.5468/

The initial study was followed up with a replication/validation study with 6 patients and 6 controls recruited Oct-Dec 2018 and published Apr 2019
Paper : Validation of impaired Transient Receptor Potential Melastatin 3 ion channel activity in natural killer cells from Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis patients
Link : https://molmed.biomedcentral.com/articles/10.1186/s10020-019-0083-4
Thread : https://www.s4me.info/threads/valid...er-cells-from-cfs-me-2019-cabanas-et-al.9231/

From what I can tell there is overlap in results between patients and controls ...... and to be truthful I don't understand (understatement) what the plots and tables are showing. If this was a significant result, why are some healthy controls also getting the same measurements? e.g. this plot and table from the Validation study. All very confusing to me...
upload_2019-10-21_13-25-53.png

I took a quick look at the other threads linked above, and unfortunately there is no discussion on the interpretation of actual results. Is everyone else as confused as me??????

I believe that the study on this thread uses the same measurements techniques as the previous two papers with the addition of Naltrexone as a "treatment" for the stimulated cells.
 
It all looks fairly straightforward to me.

You can easily tell the difference between controls and pwME using the dat on those plots using the following method.

pwME are on the right in the column marked CFS/ME and healthy controls are not.

What the different coloured lines mean I don't know, but the charts are so organised that the results are obvious without needing to know that.

To be, slightly, more serious, it looks like the control group is much more (or less) sensitive to the thingies they added that pwME.

It's difficult to be sure on those plots but it looks like there may be little or no overlap between groups. If so that would be the 3rd or 4th 'project' that looks like that in the last several months.

As such I would be strongly tempted to dismiss it as conceptual/experimental error or artifact.

But I am not a scientist, and barely know some numbers, so possibly not the best knowing things person .
 
Sid said:
Naltrexone is one of the few things that we can be 100% sure doesn't work for ME/CFS given how many clinicians prescribe it to our patient population in the States and how many of us have tried it on our own without any major benefit. It's so widely available and cheap compared to something like RTX which needed a huge trial to debunk it.
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LDN has been a godsend for me: improved sleep, reduced pain, reduced hyperacusis, reduced numbness/tingling, some increased stamina/reduced PEM and, most significantly, improved cognitive functioning (I wouldn’t be able to do any advocacy work without it).

Having said that, I’m still mostly bedbound, so it’s definitely not a cure nor has it improved my energy levels vastly.
 
Is this really talking about LDN which is used for a rebound effect (as I understand it) of brief, mild inhibition of the receptor, or naltrexone to actually block the opiod agonist's inhibition of trpm3 channel?
 
dreampop said:
Is this really talking about LDN which is used for a rebound effect (as I understand it) of brief, mild inhibition of the receptor, or naltrexone to actually block the opiod agonist's inhibition of trpm3 channel?
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Yep, you are correct LDN is nowhere mentioned. The test they did was to block opioid receptors for 24 hours, which restored TRPM3 function. So it seems to me like one would want to use regular dose naltrexone, not LDN, if the idea is to restore TRPM3. This is all even more confusing when you consider that naltrexone as originally developed for alcoholism is used in 25/50 mg doses, but nobody in the autoimmune or ME/CFS communities seem to be using it at that dosage.
 
This world-first discovery suggests new potential pharmaco-therapeutic interventions in ME/CFS,” co-author and Stafford Fox Medical Research Professorial Fellow, Professor Sonya Marshall-Gradisnik said.
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Since some people are already using LDN, and I think Jarred Younger (?) is planning or has started a clinical trial, it's hardly a world first discovery. They do like to overblow their small research findings.
 
Trish said:
Since some people are already using LDN, and I think Jarred Younger (?) is planning or has started a clinical trial, it's hardly a world first discovery. They do like to overblow their small research findings.
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Sadly, Jarred Younger’s trial has been suspended, though I’m not sure why. It was suspended without having started. No participants had been deemed eligible or had started on the protocol.
https://clinicaltrials.gov/ct2/show...e+syndrome&cntry=US&state=US:AL&draw=2&rank=1
 
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