I don’t disagree with your take on solonjk’s approach, however this experience isn’t unique, it was just the first and most obvious that popped into my head. I think most guys cannot exert the same level of energy and recover quickly like they would pre-finasteride regardless of how hard they push it. Think extended refractory period. Masturbation and pushing sexual activity often rationalized as the best way to recover, similar to training, ends up digging the person suffering from PFS into a deeper hole resulting in exhaustion, more shrinkage, bottomed out libido, more fatigue, etc.
This thread is quite long, so I was unable to read it all. I really hope the exact same penis skin tests have been preformed on men that completely recovered from PFS symptoms to compare with long term sufferers and normal men.
If we are funding the next round of research, will we be getting more frequent updates (say, every 2 weeks)?
I am sure if Awor could update everyday, he would. But as he said, he has to respect the scientists time frame, which is completely understandable. He does drop us an awful lot of information though, as much as he can I think. I feel you though, this research is very exciting and very interesting. It is so important we all support it. It could help a lot of people, maybe even beyond just Propecia. Thank you Awor, Mew and the rest of the gang. You give me hope.
Well said… thanks mew and awor for all the work you do.
Awor, I’m just curious. But you said you are in contact with Dr. Traish? Does that mean that he is actually doing research on this problem or just that you talk with him about the science behind it?
Awor, is the T-cell regulatory gene CTLA4 something you guys are looking at?
Awor, does this statement still hold true?
“The mechanism we are looking at is, by itself, capable of explaining every single symptom that we know about (including most hormonal abnormalities). In other words, if we can find a way to counter-act it, we can theoretically solve the whole problem.”
I’m a bit confused at some of the generalizations and assumptions that are often perpetuated on this forum:
“DHT came back.” – How do we know this? How do we know there was a surge of DHT upon discontinuation of finasteride? There was no testing done during that precise phase to support this assumption that DHT production necessarily went back to high or “normal” or pre-fin levels. And once measured, aren’t DHT values all over the place in PFS patients? So some are able to produce “normal” levels of DHT, others (like myself) are on the low end of the range. And the vast majority of us have no “before” snapshot to even know what is normal for us.
“…making many of us feel better…” – What % of people felt better after quitting fin? I certainly didn’t. I just kept sliding down in health.
“…and then we crashed.” – My impression is that the timeline for most PFS patients is: experiencing symptoms --> quitting finasteride. Did most people just randomly quit finasteride for shits and giggles and then there was this monumental crash? Didn’t we quit fin BECAUSE we had awful side effects?
Regarding supplements that helped or hurt: there is no standard response to any of these (Zinc, juicing, milk thistle). How can a conclusion be made from inconsistent anecdotal reporting?
Regarding TRT: Again, there is no standard response to TRT. Some DO feel better on TRT, some feel worse, many have ups and downs. There is such a vast degree of variability in TRT protocols and individual hormonal balancing that we can’t completely control for these confounding factors.
Regarding Exercise (as an androgen booster): There is no standard response to exercise. Some feel better when pushing themselves, some have diminished stamina and greater recovery time. Furthermore, some complain of muscle wastage, while others are fit.
Don’t get me wrong, I’m very interested in know what in the hell was tested in this experiment, what the outcome was, etc. And I wholeheartedly applaud the initiative. I’m all for as much scientific exploration and testing of hypotheses as possible. But I am perplexed at the way a WIDE variety of reactions to various substances are being manipulated to explain a theory. There seem to be many gross, unsubstantiated conclusions.
I realize that a lot of people are eagerly awaiting the results of this study and clinging on to hope that it provides a magic bullet. And perhaps the testing committee is sitting on a major breakthrough, some universal marker of PFS, some discovery of permanent genetic change, some black and white causative finding, and perhaps I am totally ignorant and will eat my words once the findings are published. But am I wrong to suggest that we’re stretching the data here to fit a preconceived conclusion?
anything new here?
Maybe I can get some thoughts on this, my Endocrinologist is starting to think that there is something messed up with my/maybe our P450 cytochrome. He wants me to have this mapped/tested, my question has this been looked at or is this a waste of time?
Do you have any caffeine intolerance? Cyt P450 is responsible for caffeine metabolism, when impaired a cup of coffea will impact you for a much longer time than usual, usually with anxiety, excitability, insomnia…
Shortly after my fluoroquinolones intoxication I had this, but it resolved in a few weeks. So I doubt it’s a significant issue in my case, although I do have highish E2 (CYT P450 also take care of E2 metabolism, but my problem could be in phase II process, where glucuronidation takes care of E2 nanaymiriam.files.wordpress.com/2011/05/liver-detox-pathway.jpg)
This thread might be of interest to you
viewtopic.php?f=1&t=6173
Its not a waste of time whatsoever, in fact it could provide additional clues since Cytochrome P450 is involved in the metabolism of Finasteride:
Identification of human cytochrome P450 isozymes responsible for the in vitro oxidative metabolism of finasteride.
ncbi.nlm.nih.gov/pubmed/8654202
propecia.com/propecia/shared/documents/pi.pdf
I would urge you to proceed with your Endo’s suggestion to have genetic mapping done on your Cytochrome p450 enzyme, especially CYP3A4 subfamily and gene cluster on chromosome 7q21.1. To my knowledge, nobody else has had this done yet.
Pls report back any results.
We should talk about this on a liver thread. I am thinking something along these lines now.
Sounds like a very good endo to even put thought into it like that. Are there other PFS victims seeing him/ her?
CYP3A4 is one of the genes that will be examined in genetics study with 63 patients (saliva). I don’t quite see the point of doing the same investigation in parallel with a single patient, specially if he has to pay for it. A sample size of 1 will not be very significant from a statistical point of view.
If he doesn’t need to pay for it, then I don’t see why not, especially as he is not one of the 63 genetics patients (saliva). 
Either way, it would be interesting to know the results.
This study can’t find out if there are epigenetic changes in the brain right? Or are there markers that may reveal neurological changes?
Ok, first off I dont have to pay for it so my doctor is checking into it. Hopefully I can get it approved, if so I am going to do it. I am the first PFS patient my doctor has seen and he really is trying to help me get out of this whole mess. These past 5 months have been a living nightmare I am typically a really positive person but when I got home and started to research this subject, the magnatude really hit home and now makes it hard to stay positive. I by no means am a doctor but this looks to me to be a permanent thing (I hope to God I’m wrong). Awor my doctor said there were like 52 genes that fall under the P450 cytochrome, my question to you is the multiple genes you are looking at fall under this??? The more eyes we can get on this the faster we can get some answers, if I had to put all my money towards reseach this is where I would be putting it. Thanks for the imput. OUT
It’s about time someone with some authority looked at this. The pragmatist in me has impelled me to conduct some experiments. I am an Accutane afflictee, and I recently started taking some Isotretinoin. I began with micro doses and ramped up to 100mgs a day; and surprise, surprise (not really) it wasn’t even capable enough to crack my lips. In the past, I have always been extremely sensitive. It also had no effect on nocturnal erections (not impaired).
What sort of timeline are we looking at now on this experiment?