This deserves much more attention. My main question would be is this…when you stop TRT and try to do PCT, and if you get you’re able to get your body normalized, will the “normal” amount of testosterone be ok, and is the mutation shift back to normal?
I really wish people here would give this MUCH MUCH more attention…My intuition is telling me THIS is the missing link.
It seems we have narrowed down our possibilities to the following:
1.)Try to activate the mutated androgen receptor(if there is a mutation which I think is most likely the CASE here, of course we need testing still) by administering frequent pulses of DHT every 4 hoursas for the length of time, I’m not sure, perhaps 50mg every 4 hours only for 1 DAY a week to see if this will normalize the receptor, adjust dosage if necessary). If this doesn’t work, try doing it 2 days a week and maybe adjusting the dosage…The goal here is to get frequent pulses of DHT in your system.
2 TRT therapy(Supraphysiological doses). May work for some, may not work. Goal would to get Testosterone and DHT levels way up. Frequent pulses of TRT would be beneficial(perhaps 30-50mg per day to start or 5-10 mg every 4 hours for a period of 1 week and then reassess results?)
3.) Synthetic Ligands…This is left up to the clinical researchers, I have no idea which synthetic ligand we would need).
Folks, I’m not doctor, this is just what is what we are going to have to experiment with.
so are you trying this?
this can be good who is on TRT already but what about those who have normal TT and DHT?
sps
I didn’t post extracts from the study I linked to earlier in the thread:
High Dose Androgen Therapy
in Male Pseudohermaphroditism
Due to 5a-Reductase Deficiency
and Disorders of the Androgen Receptor
‘We describe the clinical and biochemical
features of six men with male pseudohermaphroditism
due to androgen resistance. Each of the subjects
had male-gender behavior but incomplete virilization.
The underlying defects in androgen metabolism were
defined by studies of the 5a-reductase enzyme and the
androgen receptor in fibroblasts cultured from biopsies
of genital skin. Four of the six have 5a-reductase deficiency,
and two have defects of the androgen receptor
(the Reifenstein syndrome).’
Seems like the group studied had those skin fibroblast cultures that could be useful to us in
assessing 5AR2 activity, androgen receptor function etc.
Looks like quite a complicated process, but this research was carried out 30 years ago,
surely if we get more awareness and actual real time studies done on us these methods could be deployed?
There’s probably more of us than there are pseudo-hemaphrodites now anyway. 
Selected other stuff:
‘After completion of the nitrogen balance studies the subjects were
given long-term replacement therapy with 500 mg/wk of intramuscular
testosterone esters either in the form of testosterone enanthate or of a
mixture of testosterone propionate, 60 mg; testosterone phenylpropionate,
120 mg; testosterone isohexanoate, 120 mg; and testosterone
decanoate, 200 mg, for 9-36 mo and then were changed to oral
testosterone undecanoate, 80 mg, three times daily.’
‘The androgen receptor defects in the other two subjects
were of two types. One (S.C.) had a diminished amount of
androgen receptor, a finding similar to that observed in other
patients with the Reifenstein phenotype (1, 17, 19-20); the
amount of receptor was too low to be characterized further.
In this patient, 5a-reductase activity was also lower than
average, a finding that has been observed on occasion in
subjects with androgen-receptor defects (25) and in fibroblasts
cultured from the subjects (12). In the other man with an
androgen receptor defect (B.P.), the androgen receptor was
normal in amount but qualitatively abnormal, in that it was
unstable to ultracentrifugation, a phenomenon observed in
some other subjects with androgen resistance (18).’
‘High dose testosterone administration, sufficient to raise
plasma testosterone concentrations to levels above the upper
limit of the normal adult male range, resulted in short-term
positive nitrogen balance and a long-term enhancement of
virilization in all four subjects with 5a-reductase deficiency.’
‘The findings in the present studies indicate that long-term
treatment with supraphysiological doses of testosterone may
be of benefit in partially repairing the incomplete virilization,
and in improving the self-image of masculinity in men with
Sa-reductase deficiency and, in selected instances, of men with
defects of the androgen receptor.’
This seems to bolster Jacobs story about giving a patient huge amounts of thyroid hormone until , over a period of time, became sensitive again to it. Different sex and hormones but same idea.
I wonder if any of us have tried huge amounts of TRT over a long period of time. And, what are the risks? I am considering trying this if Jacobs agrees. I really dont want to be on TRT so long though that my native production is gone forever.
Solonjk, that’s a great idea, or maybe email Dr. Irwig, the physician conducting the study…perhaps he would have useful insight on how to go about it.
Solonkj, an afterthought…do you have a spokesperson? Someone who can draft letters and can represent the group in this endeavor? If not, perhaps collectively you can appoint someone to assume this role. It’s a great idea to start contacting universities/medical centers as you mentioned. If I can be of any help, let me know. In case you’re wondering who I am. I am a friend of a PFS sufferer and I am trying to help. I still cannot believe that Merck has let this happen. It’s obscene. But, I do believe there are answers and a cure, hopefully it will be found very, very soon.
Solonjk, you mean Professor ‘Ieuan’ Hughes at Cambridge?
Ive also sent off a few emails to these academics and doctors, I got no response, and looking back these emails must of made me seem crazy. HOW can we get their attention??? WHY should they care??? (…why did this illness catch the attention of Dr Irwig I wonder?)
My current plan is to get reffered to some of these experts that work as consultants on the NHS and grab their attention that way. For example Professor Hughes works as a consultant, but only in paediatrics as I understand. I know of a few other good people to get reffered to - some are so good they also work for Merck!! 
Solonjk, You certainly have put in a lot of work and effort. It’s very discouraging (to say the least) not to hear back from all your inquiries with regard to your solicitation to the research centers/universities. I wonder if it would be helpful to try to raise money in order to pay a specialist for their time? Even if this person could read over the very many possible etiologies proposed by the members. It would be so beneficial to have theories either “ruled in” or “ruled out”, this way if one is not plausible, other members can move on from them. Maybe there could be a PO Box (address) set up where we all can contribute funds/raise money for this purpose. Also, perhaps applying for government funding for research…if an interested research center/university can be brought on board, maybe that would be a way to entice them (with the research grant). From their point of view, I would think there would be accolades and recognition from their peers if they were to be able to understand and thereby treat this drug-induced syndrome. Also, it would be great to get this drug off the market (for hair loss) before another innocent kid puts it in their mouth. I hope you don’t mind my suggestions. I’m just trying to think of whatever I can to do.
why this thread has died?Am I missing something?
Yes, mutation of the AR gene has been more or less ruled out as a cause.
Why?
Because a handful of guys have already tested negative for a mutation of the androgen receptor and were also shown to have normally functioning receptors, which implies that there is no mutation. There is a discussion about it in this thread: http://www.propeciahelp.com/forum/viewtopic.php?f=27&t=2216
I believe moonman1 also tested negative for AR gene mutation: http://www.propeciahelp.com/forum/viewtopic.php?f=5&t=3901&start=400
(towards bottom of page).
Moonman1 did not take Finasteride, he took Saw Palmetto.
I did not test negative nor positive. I do have much of my genome mapped…and can read most of my SNPs, but I have no idea how to tell if they are mutated or not. And if it is epigenetical, then its not possible to tell.
I recently contacted the doctor, through email, in this study that was researching High Content Analysis ( HCA ) as a means to determine what type of Androgen Insensitivity a person may have…along with the possible solution based on the type. I told him about PFS and if it was possible to get HCA testing done.
He told me that he was not able to get Government funding to continue the research. He said Androgen Insensitivity ( AI ) is a relatively new disease and it is hard to get funding for.
That sucks, although thanks for trying. Did he have any thoughts on PFS?
What I don’t understand is when I spoke to the doctor he said people with androgen insensitivity have normal or high levels of testosterone, not low. My last blood test showed that my testosterone and dht levels were low. I don’t understand this. If Ai is marked by normal or high testosterone levels why would mine and others be low, if AI is the supposed cause of are problems? I would like to hear opinions on this.
this question in Mew’s words is million dollar question. But we do have who normal or above normal level of DHT and Total T yet are suffering. What about people who were already on TRT before taking fin like Awor and Whalen72. I think this doctor is wrong. I have read few posts on messo and musclechatroom where people were doing fine on TRT used fin or betasitosterol and got all sides.Even they increased their T injections but not success.
why you guys are so much biased against Saw Palmetto. Various studies have shown it to be comparable with finasteride/dutasteride. It does the same job.