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Thanks for posting this.
Do you have any feedback from your doctor on these values?
I’m no doctor, but it appears ALL of your lab values are camping at the LOW end of all ranges. But considering they ARE within the ranges, I would expect a doctor to say they are fine.
Having said this, I think there is a HUGE difference between “within range” and “Optimal”.
The lower values of 3bdiol and 3adiol support the similar findings in the Italian study imo. But they don’t appear to be dangerously low in your case.
We need more labs from members to build a common theme. And helpful to know: Age, Which 5ar inhibitor you took, Duration taken, How long since quit, What treatments tried and how long.
These factors my help explain differences in values, and possibly narrow down specific criteria given commonly shared profiles. Ideally, this stuff should be in your PH profile, or signature.
Maybe vincentv can chime in on this?
Not they don’t. It’s the complete opposite.
The Italian study indicated significantly higher levels of 3B-diol in subjects then controls.
Spstriken’s level are just reflective of his low-end testosterone and DHT. All proportionate.
So far we have no evidence of anyone independently finding high levels of 3b-diol. It’s a nice theory but seems like a dead-end.
Thank you for the alpha hard link. I will need to research this product to come to my own conclusion as to how close to androhard it is.
I am deff interested in seeing your version of cdnutd methods.
So in general how long have you been cycling straight Dht and DHT prohormones for?
Would you be willing to type up a time line of your experiences with DHT/DHT prohormones cycling experiences to include exactly what you did and what improvements it any you experienced?
Cycling of DHT and or DHT prohirmones seems to be the most logical thing to do but yet we have such a small amount of members who actually tried it one being cdnuts who claims recovery.
Yea exactly, They would have needed to have been high to confirm Vincents study
Danny fc and 5alpha are correct. I mistakenly commented low levels confirm study finding but should have said HIGH levels would confirm it. Sorry bout that.
Ok, so my eagerness to find some reason to investigate this theory further is deflating.
What say Vincentv about all this? I’m still open minded, but not convinced yet.
Well do you guys have the same symptoms and hormonal profile as the guys in the study? Probably not…
People around here have different sets of hormonal profiles so you cant jus pyt everyone in the same bag and say we all have one condition, which is the same for everyone and has one common reason.
This pfs thing is prpbably a multitude of factors.
.
It will be one underlying factor that causes sexual dysfunction in PFS patients.
That is the primary symptom, and I don’t believe it can be derived from different reactions to the same drug. There has to be a common denominator.
The problem is it goes deeper then any layman can understand - hence why long-term members lose interest despite no recovery. It’s an unsolvable riddle without deep research supported by huge financial resource.
Our only hope is that there’s well directed and focused research that goes beyond the obvious. Any studies on the primary hormones is just a waste of time. We need intensive experiments into the androgenic activity of PFS patients, and an understanding of why it’s impaired compared to controls.
Doctors don’t really understand the CNS and brain. At least for me, this seems to have caused a disconnect in my CNS/brain. I don’t feel my body the same. Emotionally flat ect. Hormones all check out fine but my body probably isn’t using them. I sleep but I don’t feel rested. If I workout my body gets sore but I don’t perceive it.
In my opinion people with pfs fit into different categories and there is no common denominator for everyone. The proof is not everyone experiences the same sides and the sides dont go by severity of the disease.
Not everyone has sexual disfunction from finasteride and we also have people with very strong neurological and no sexual sides, and pepple with strong sexual sides but no neurological dysfunction…
The 5-AR enzymes have a role in the production of neurosteroids. While finasteride isn’t only supposed to be a type II inhibitor, there’s enough evidence to suggest it also impairs type I.
Personally I was a complete zombie the first 10-14 months following discontinuation.
A lot of long-term members have found this is one symptom that improves with time. About 12 months in I felt I began to recover from the mental side-effects. Just not the physical ones.
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Ageed.
Only thing is I have not completely ruled out an obvious cause. I really think it could still be something simple as reduced 5AR activity as far as the cause of the common sexual sides that we all get. We all get them straight out even if it’s 2 diff degrees. Also in my opinion if you don’t get them you don’t have PFS. You may deff be suffering from sides from the drug but once PFS blows up in the medical community I believe being diagnosed will be contigent upon having sexual sides that remain.
Ohh and I still think Vincents theory could be right, but we are just not looking at the right meabolities.
Vincent hope you are still around these days.
Wanted you to take a look at this info I copied off of Wikipedia:
Inhibition of 5α-reductase results in decreased conversion of testosterone to DHT, leading to increased testosterone and estradiol. Other enzymes compensate to a degree for the absent conversion, spec voifically with local expression at the skin of reductive 17b-hydroxysteroid dehydrogenase, oxidative 3a-hydroxysteroid dehydrogenase, and 3b-hydroxysteroid dehydrogenase enzymes.
Ok so the first sentence about how takibg DHT inhibitets stopping the conversion blah blah blah blah resulting in higher T and estradiol levels we all know about… Ok so cool.
Well what about this other stuff about how inhibiting these enzymes resulting in “other enzymes” compensation…
Could these other enzymes that are now “being produced more of” be your metabolite that’s acting as an estrogen somewhere?
Should we start looking into what ever the hell any of that stuff is and how to test for it?
Yeah that’s the point of this thread. The “3b-hydroxysteroid dehydrogenase enzyme” in particular is what we’re discussing, as the Italian study found high levels of 3b-diol. (A substrate of the enzyme)
Unfortunately no member on here has found they have higher levels of this hormone.
If it was the case, it would be difficult to treat. Inhibitors of this enzymes do exist (Trilostane), but also have other functions that are important for the body. I tested 50mg doses regardless of this risk, and found it had no improvements on our condition.
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Hmmm guess you and Vincent where one step ahead of me with my understanding of what exactly it was that we were looking for. To bad my 3b-Diol did not come Back high. I would gladly get any blood work done in the future to help confirm or deny any theory you or Vincent are looking into to.
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Depressed guy,
Did you take Fin, dut or Saw P?
Have you ever had your cortisol levels tested.
Did you take Saw p, Fin or dut?
Did you ever have your cortisol levels tested?
Which lab did 3a-diol testing for you in India?
did you have testing done