Can this difference be caused by the much lower androgenic activity in PFS patients than that in the control group? For example, could this difference be the consequence of the much lower ratio [free T / E2] that PFS patients have compared to the same ratio in healthy patients?
hi awor or anyone else who can answer.
Does this study conclude if nerve damage has occurred in the penis. are the results in your opinion good or bad for our recovery. im sorry but this is all way aboce my head.
Is there some official web site or document or meeting minutes from this event and process that we can point our doctors to, so that they can stay in the loop and perhaps even reach out to professionals investigating the matter? Thanks Awor.
Come on guys, can we get a bit more on what happened at the conference? Was’nt it a full days worth of PFS discussion?
Can we at least know if Irwig or Traish were there? Did the actual full blown conference go off as expected or were things pulled back due to the data?
Is there a thread about this genetic study somewhere that I missed? I’m willing to participate.
Also, did the preliminary findings from the study discover anything about why some of us have consistently low 3-adiol g? Thanks.
“What is clear, though, is that the next step in our investigation will require us to participate in the funding.”
Do you mean us PFS suffers will need to help with the funding?
theoffice.it/itcongressi/story$data=congressi&num=1134&struct=story
Here is the public schedule for the conference (albeit in Italian). Apparently Irwig gave a presentation.
Yes, who else?
Awor wrote
“We currently have a consortium of three scientific research institutes which are working on this problem. We are not doing just one but multiple experiments. They are all funded, and nobody in this forum is being asked to participate in the costs of the studies.”
“These studies are not cheap. You can rest assured that if three institutions are putting money into this, they have a pretty good feeling about what they are doing.”
It seemed as though the institutions were funding the study. Now it is not so clear.
Awor if you would please clarify.
I must admit i haven’t read through all the various literature etc. so i haven’t really grasped the route awor is going down with all this. I’m inclined to think he will be correct with all this as so much of what i have read adds up in my eyes. There seems to be enough literature discussing other receptor and insensitivity issues which we can hopefully utilise to inform us and to support our own theories. Plus awor’s explanation he has suggested - auto-regulation etc. coinciding with a potent hormone, DHT, coming back on to our system is plausible. 2 things are puzzling me about all this however.
The 1st is why i personally was able to get myself back to 100%, albeit for a short period of time and others including myself have made substantial improvements over long periods of time.This makes me doubt whether permanent changes have occurred in our bodies such as genetic changes, methylation, etc. and it is more a signalling problem. This may have been discussed before and structural changes to our bodies and signalling may be inter-related.
The 2nd thing is the recent posting on this thread where people have said they have crashed while on propecia. This suggests a second pathway to acquiring PFS symptoms or another route altogether as the one being proposed by awor. I think this may have been discussed already.
how helpful will the results of this study be in finding treatments soon?
Here is a translation of the same thing from postfinasteridesyndrome.blogspot.com/2011/08/primo-seminario-italiano-sulla-sindrome.html
Translation is a little rough as its from Google Translate but gives us an idea, at least, of what was covered.
First seminar on Italian post syndrome finasteride
SEMINAR ON THE SYNDROME AFTER FINASTERIDE
Great Hall, Hospital Cattinara
Trieste, September 16, 2011
Chairman C. E. Trombetta Moderators Belgrano, B. Fabris
C. Introduction and presentation of the speakers Trombetta
11:00 persistent effects on sexuality in young men who took finasteride hair loss treatment-presentation of the first prospective study
Michael S. Irwig M.D., F.A.C.E. Assistant Professor of Medicine, George Washington University
12.00 Discussion
12.15 Syndrome Post-Finasteride, possible etiology
Worthington A, PhD
13.00 Break
14:00 Syndrome Post-Finasteride-the role of neuro-steroids
Roberto Melcangi, Associate Professor of neuroendocrinology, University of Milan
14:30 Presentation of the research work of the Italian band syndrome Finasteride and post-preliminary data. Presentation of the study group
C. Trombetta
Retrospective clinical study of patients with myelodysplastic syndrome Post-Finasteride
C. Trombetta, G. Mazzon
Evaluation of hypersensitivity of the androgen receptor
Damante, Cauca
assessment of pharmacogenetics in patients with syndrome Post-Finasteride
Toffoli, CRO, Aviano
Finasteride and Semen
G. Ricci
16:00 Conclusion of the work
storage1.evectors.it/files/site000000005/misc/Postfinasteride_ProgrammaPreliminare.pdf
theoffice.it/itcongressi/story$data=&num=1133&congress=structstory
Finally, the Italian medical research can claim a place of honor commitment to sciencevoted to the analysis of potential harmful effects of finasteride.
Together with pioneers Traish Irwig and joins a young group of all-Italian study The Urology Clinic of Trieste, in collaboration with the Department of Biological Sciences, Faculty of
Medicine, University of Udine and the Center for Experimental and Clinical Pharmacology CRO Aviano, has started a complex research project to deepen the knowledge about the syndrome Post-Finasteride.
The purpose of this conference is to disseminate knowledge in the medical possibility of taking finasteride adverse effect in the short and long term, illustrating the results of preliminary studies Italian group.
Obviously the meeting between the researchers will be achieved with a fruitful exchange of information, laying the groundwork for future collaborations between different disciplines involved in the study of this new disease.
The conference brochure states:
There is extensive evidence in the scientific literature as the intake of this drug result in about 5-6% of cases on sexual reversible side effects, especially loss of libido, erectile deficiency, disorders of ejaculation. In some patients, these side effects persist even after discontinuation of treatment could be even worse with the onset of symptoms such as depression, anxiety, fatigue and severe alteration of secondary sexual characteristics leading to a noticeable deterioration in the overall quality of life.
We look forward to the results so that there will be certain to “give a shock” to the community medical, in particular the uro-andrological, often deaf to reports of patients “victims” of the molecule.
The thing with epigenetics and post translational modifications is that they are in state of potential change. The theory does not suggest that there is a genetic mutation (this would be more permanent) but more like a changing of switches in what genes are turned on and off. These switches under the right conditions can go back to the way they were but our bodies have accustomed themselves to this bad state so will think this is normal. So we may improve a bit under the right conditions and then deteriorate as the body attempts to make us “normal” again. Ideally what we need is something to make them stick and stay that way. This is not out of the realm of reason. I personally have had improvements and then slipped back again. The sun and lots of walking and rest and for some reason doxycycline promote a better environment for my genes to be in. Unfortunately the U.K. doesn’t have all that much sun.
As for the problem whilst on finasteride - the crash as it were. Think about it. The half life of finasteride is 6hours. If one takes a dose in the morning one day and perhaps misses a day or takes it late the next day the action of finasteride will lessen potentially leading to a rise in DHT. This would assume one is taking it at poor time intervals. Also as finasteride is metabolised in the liver to inactive metabolites if for some reason the person metabolises quickly this could lead to normalisation of DHT levels.
as awor said, better abstain fron speculate, but i know is hard task
however,being realist, will be great thing if studies proof undoubtebly the root cause of our condition.
in this case we r lucky
19 when u improved did u see improvement in sensativity. i have days where im better than others but i dont see this as an improvement. i am genetally getting worse with a bit of imprivement for a day and then slightly more worse than ever. its a downward slope. i fear any improvements specifically with sensativity are just neves have a last go before death. i think all side effects are curable over time but i have not seen penis sensativity improve for anyone. i feel this is permenant. after 1.5 years of suffering my libido is up so im sure for most this side along with brain fog etc will improve. the numbess wont - any comments
i’mstill convinced that numbness come from prostate area.
well i can’t predict if prostate is damaged or only works bad for some genetic/hormonal whatever insensitivity but lot of time i saw improvements in sensitivity when prostate tension was low
did u take any transrect echo?
I think a few of you are going to be asked to stay on topic…
sorry man, u have right
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Crashing on the drug can be explained rather easily, inhibition of dht, and vital neurosteroids, some bodies just cant handle it.
The real brain drainer is why dont we get better when dht and 5ar2 return, and why is this when some people crash. -
Why a persistiantly low 3a-diol-g?