Low dose Naltrexone - How might it work biologically in ME/CFS?

Mister Person said:
About narcan vs naltrexone I had the same thought, wondering what the difference was. There are 3 opioid receptors, mu kappa beta or something like that, narcan binds strongly to all 3 I was told, while naltrexone strongly binds 2 weakly binds the third

The metabolism study u link states :By these data we can hypothesise a complex regulatory role of opioids in metabolic balance in obesity.
So it's still related to opioids. Also I wanna mention tak242 the drug earlier it's said to be highly selective, with little off target activity but they say there is always off target activity, and due to the presence of some chemical structure it causes methemoglobinemia

Interesting that you bring up naltrexone having other properties elsewhere, I guess there's always a lot going on with any drug isn't there. I didn't look deeply into it but there are links to hgh and fertility too somehow.

Re antidepressants, depression is related to inflammation too somehow, panadol apparently can relieve depression. I am not sure I believe in the lack of neurotransmitter theory for depression, even though I know nothing about it, because if it was true why are we not measuring it to diagnose?
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It is interesting isn't it. My note re: the antidepressants analogy was really to note that the 'spiel' tends to always infer specific, where there are a lot of antidepressants these days that are used off-label or for other purposes. So I'm intrigued to be open-minded to the potential that given we are talking 'low dose' (so not blocking 'all' or 'nearly all' receptors which would be the purpose used for the Narcan type use) could there be the likelihood that it isn't necessarily opioid-receptor in brain effects only that are leading to the effects for those it is working well for.

I just wondered whether turning method on its head and looking at those who it genuinely does seem to work well with (rather than the usual 'representative sample' jump in with a trial before narrowing down with exploratory research [method often used in research areas outside of medicine]) and seeing 'how' for those might give us more clues. Particularly given the individualised dosage issue and - I don't know enough whether there is half-life or anything like that - there might be some clues there in seeing 'the effect' and finding out more qualitatively about 'in who' and 'how'.
 
Mister Person said:
Do most CFS with pain find it beneficial in the same way fibromyalgia patients do? Ie at least does it help as a pain killer?
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I had a thought, are we going to attribute pain in cfs due to fibromyalgia or pain in cfs due to cfs? And, if we attribute to fibromyalgia does that mean cfs experiences fatigue both from fibromyalgia and from cfs?
 
Wait sorry if this is wrong place for me to ask, but who the heck should I target to see if I were to try to obtain tak 242? I'm a fibro patient with PEM, which complicates things because when doctors see me they think I'm another chronic pain patient. I asked a rheumatologist I was seeing but he said he'd look into it after consulting the literature. He never got back to me and doesn't wanna see me cuz he thinks his only job was checking if I had autoimmunity, and left me to an anesthesiologist chronic pain doctor now who, like most other doctors struggle to understand what I'm trying to communicate. I like to think that I'll break through with this anesthesiologist, because they know about neuroinflammation surely. The paper I read about neuroinflammation and chronic widespread pain was in a journal for anesthesiology.

What kind of doctor would have the knowledge? About neuroinflammation and stuff? Pre sure rheum or anesthesiology be the way to go but would like to hear a 2nd brain

I thought a me doctor would be most understanding, but the one me doctor in nz quit just as covid started and there don't seem to be any in Australia.
 
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RedFox said:
Tak-242 or Resatorvid is an experimental drug that, as far as I can tell, hasn't been approved anywhere.
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Yes but, you can ask to try it, in a similar way that ampligen is available I think. It's a matter of convincing a doctor and then convincing somebody at the Pharma comoany. Given that a phase 3 trial has been done, although failed, it seems reasonable to say it's safe to try once, though long term is unknown I think
 
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