In what way has cerebral spinal fluid been revealing and how do you know this?
Because the previous study by the same department found significant anamolies in the spinal fluid when compared to non-propecia users. Many 5-AR I metabolites were almost undetectable.
Basically, the preliminary findings suggest that the most simple explanation may be the correct one. Our 5AR is impaired (They donāt know which sub-types yet). But they can see that the neurosteroids that are derivative metabolizes of 5AR are depleted in the CSF as compared to control subjects. So 5AR is not doing itās job. We ready suspected this. But the real revelation in all this is the gradual realization by researchers that neurosteroids play a major told in sexual and cognitive function. You can have normal hormonal levels but if your hormones are not being converted into the appropriate neurosteroidal derivative in the central nervous system, you will suffer sexually or cognitively or both.
The good news for us fellas is that their findings have great implications in other fields of medicine. This only gives greater impetus to researchers to forge ahead with the studies.
If their hypothesis is true, one possible treatment would be synthetic 5AR that is capable of crossing the blood brain barrier. We donāt have this something like that at the moment.
Some Italian guy posted the data from two PFS subjects who had their CSF examined and compared to control subjects. I saw it on solvepfs.com. Iāll try to paste it here later. Just by looking at the chart you see that we lack adequate levels of certain key neurosteroids.
Please do, Thanks
The links to that studiesā results were posted many months ago, if you search around I am sure you can find them.
Very low results as compared with the controls among several 5-AR reduced metabolites.
Some even undetectable.
Whatās interesting is these were specifically those from type I rather then type II. The focus has always been on 5-AR II, as Finasteride is listed as strictly a type II inhibitor.
Clearly we know now this isnāt the case, and we really need to measure these 5-AR I metabolites independently.
Unfortunately tests for dihydroprogesterone arenāt very accessible from mainstream labs. But Iād really urge anyone to convince their doctor to ask a private lab to examine these levels.
Did the scientists mention any other way of restoring 5 AR in the nervous system? Did they mention epigenetic modulators or stem cells?
You said earlier that the scientists donāt think this is permanentā¦well if you need synthetic 5 AR that crosses blood brain barrier which doesnāt exist yet - isnāt that permanent?
At least this puts all those other theories to rest.
Thing is, people have recovered from this. Iām wondering if fasting can repair the nervous system or at possibly restore normal epigenetics.
It is part of the reason why although CSF is important to test we very well may find the causation of PFS in any 5-AR producing tissue; perhaps even in the cellular genetics of ANY tissue in the body. As 5 AR is produced several places and PFS is effecting all those tissues.
Yes, but 3-adiol-g is low in PFS patients and Iām wondering if DHT/3-adiol are being metabolized properly. 3-adiol-g, from what I understand, is the hydrophillic form of 3-adiol/DHT that is readily excretable.
I also recently found that the 5ar genes are/are potentially mediated by the androgen receptor. I posted this on solvepfs as well:
glowm.com/section_view/item/349#18791
Oscar posted this in some thread a while back. If this is true, something like androgen insensitivity could presumably lead to 5ar deficiency and low levels of neurosteroids. There are too many possibilities for us to narrow it down at this point.
There is no synthetic 5AR capable of crossing the blood brain barrier YET, mainly because there has never been a need for it. They just have to find something to pair it with to get it through the BBB. They think that this would be possible, and they are probably correct. Nearly all drugs that effect the CNS must cross the BBB, and we have found ways to make that happen before. Itās not unattainable.
If the problem is androgen insensitivity, then why do most of us respond to testosterone initially? Itās more likely that the culprit is 5AR dysfunction which is causing depleted levels of some CNS metabolites. Once our metabolism is fixed the rest of the system should revert back to its natural state.
Whatever happens, it may take several years before we have an official cure. We still have several more studies to go before we can get a drug to treat this.
I love your studies and scientific cure viewpoint and attitude. Everybody needs to do get on board with this, and stop chasing false dreams, like dht therapy.
We need to do the upmost possible to quickly fill out studies with participants and to increase donations by donating monthly.
I canāt speak about that. But androgen insensitivity is another dominating theory and I found that it would affect 5ar. Since my PFS symptoms are the same as my fin sides, Iāve always thought that 5ar must be involved. And I would expect to have additional symptoms if the entire AR signalling was messed up, but who knows.
The other things Iām most curious about are that 1) I got 4 zits on my forehead right before my crash (and I never get acne, let alone 4 zits) and 2) I drank a lot of alcohol beforehand.
awor gave us a story for why AR signalling might down-regulate after the DHT surge, but Iāve yet to hear a story for why the 5ar genes may methylate. I guess it doesnāt matter since I remember reading that other enzyme inhibitors have been documented to cause methylation of its encoding gene.
Could DHT injected into the CSF possibly re-upregulated 5ar? I understand that the DHT surge caused the crash and AR insensitivity and/or 5 ar downreulation, but what if a while after the crash, low doses of DHT into the spine could reactivate 5 ar and AR.
Hey. I also got acne on my face within 10 days of starting fin, pretty much the only acne Iāve gotten in the past 5 or 6 yearsā¦ This was one the reasons I quit taking it.
I didnāt get acne while on fin. I broke out like a teenager (actually, probably worse than I ever did as a teenager) 6 weeks after quitting. That suggests to me that my androgen status at the time was higher than pre-fin.
IF THERE ANY ITALIANS HERE, I STRONGLY ENCOURAGE YOU TO GO QUICKLY TO PARTICIPATE IN THE STUDIES IN MILAN.
They are almost done with the controls, they need PFS patients now. Please go as soon as possible.
Finishing these studies is crucial for fully understanding PFS!!!
If anyone here is in contact with Italians, please urge them to go participate in the studies!!!
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The history of PFS studies shows that participation is often lackluster. It took until spring 2015 to complete studies launched in October 2013.