Crazy CFS 'protocol' - random idea

[happy_to_fight]

I have seen this excerpt from doctor M article, it was commented here that it could mean that 5ar(2?) is not working properly in spinal cord or brain? Also it seems like testosterone is much higher in PFS CFS and dht is very low. Then there are reports that dht compounds applied on the skin make people worse after working for some time. Could brain or spinal cord detect that the small 5ar activity it has causes big 5ar activity(or dht ‘production’ because of dht cream application) in the body and it shuts down itself even more? So perhaps in the past the hormonal therapies by means of intramuscular injections or subdermal applications were the wrong approach and we should try to inject dht straight into the CFS fluid(just to saturate brain and spinal cord, nothing more)? Or do something that centers around CFS and not plasma. Perhaps rats could help us testing this ‘protocol’ if they have similar changes, so if rat pfs~human pfs?

I know it is crazy, but I would like to hear your input as I am ignorant about many facts about this condition.

I am here making the assumption that external hormones cross BBB and spinal cord blood barrier such that CFS concentrations< plasma and that CFS hormone injection would increase mostly csf levels and not plasma.
I am also assuming that malfunctioning 5ar in brain or spinal cord and messed up hormone levels are responsible for a lot of PFS symptoms.
Also obviously I am assuming that there is a mechanism of feedback between body 5ar2/AR and CFS 5ar2/AR.
And I am assuming that higher DHT levels would increase 5ar activity in CSF, brain, spinal cord or perhaps there is another way to do it if increasing dhr won’t cut it.
And I am totally ignoring the concept of ar overexpression here.
And probably even more assumptions are made because of the lack of knowledge(my or existing scientific understanding). (Those are a lot of assumptions actually)
If it is too crazy then I have no problem with this thread being deleted
Also I don’t want anybody to even think about trying it on himself ofc.

[Cbrandel]

Lots of stuff doesn’t make sense in PFS.

Like we have a lot of T in CSF right? And DHT is low yes.

But if 5AR were broken why is the no progesterone or estradiol?

Progesterone is upstream of 5AR and estradiol is downstream of T but doesn’t interact with 5AR.

I like to think about PFS like a river, when we blocked 5AR it’s like putting a blockade on a river. What happens is the river will change flow direction.

In PFS that would mean when we block 5AR other enzymes will start to up/downregulate to compensate. Only because you withdraw the blockade there’s no guarantee the original flow will be restored.

[happy_to_fight]

I see now that BoySuffers has only exclusively mental sides without drop in libido(edit, he had testicle pain). I don’t know how that would work with not functioning 5ar. Perhaps the drop in dht in not enough to give sexual sides, but the drop in neurosteroids is just right to wreak havoc? Perhaps it is in some way related to androgen receptors that can work with lower ammounts of dht or be ‘satisfied’ with mostly testosterone.
When it comes to Prog and E perhaps there is some unknown mechanism which makes malfunctioning 5ar drop Prog, Preg and E (but only in the brain or spinal cord). Nobody knows I guess. There are so many puzzles to this like receptors, gene expression, enzymes, hormones and even perhaps places where the hormones are produced.
I am speculating all this 5ar stuff, because I would really like for the mechanism to be simple and the same for all of us (and preferably fixable). And not working 5ar seems ‘logical’ as fin blocked it in the first place and just the crux like where it is blocked could be the real heart of the pfs problem. But then ofc it doesn’t explain other symptoms in easy way(or any way whatsoever) like muscle wastage unless some unknown mechanism or some interactions between tissues with working and nonworking 5ar blah blah blah
We could benefit from House MD alike on our case. Or more like medical equivalent of Albert Einstein.

[happy_to_fight]

Btw, I think melcangi showed that rats have some PFS like problems after stopping fin. Would giving rats fin+dht give us possibly any more knowledge about this condition? (I don’t want to resurrect the idea of underground rat lab)
Edit. Could this check whether dht and androgen receptor is driving this condition solely? Could this check which role of this condition dht metabolites have and which metabolites of other hormones?

[happy_to_fight]

I feel like I will get some heat for this, but if PFS was on to be solved then it is going to be done thanks to rat studies provided we would establish that they get PFS that is very similar to humans. Because in rats one would be able to analyse all tissues when it comes to gene expression, which is not really possible in humans and a lot of PFS probably does lie in brain/spinal cord and there might be other organs that are very overlooked, but play major role in this condition. We won’t probably get much answers on why does shit hit the fan while quitting from rats(they are not really talkative and don’t know what the crash is, also rat fin dosages differ from humans), but if we would establish similar gene expression changes in rats male parts to those seen in Baylor, then we could infer that the PFS is similar(I think it is similar as rats got same ‘depressive’ symptoms after quitting fin in doc M study) and go from there perhaps. Maybe if we find what PFS is then we could start testing some treatements or ‘protocols’ on rats. What do you think?

[happy_to_fight]

Just as a curiosity M gives rats 3mg fin per kilo, I wonder if everyone would get pfs after 250mg per day treatment. Is the answer to this an obvious no or the answer isn’t so obvious?