Any updates awor? Thanks for all you are doing.
It’s surprising to most of the doctors, urologists and endos out there. We still haven’t really came close to explaining exactly what is causing this persistent effects (although we all have strong ideas of our own), given that i guess it is surprising that there is a small subcategory of men, i.e. us, who have side effects long after cessation contrary to any MERCK study.
Merck had studies vioxx caused heart attacks the business team just suppressed the results. My bet is the same thing happened here especially because they are and have remained silent on the amount of time the “certain sexual side effects” take to go away in men who discontinued propecia in their studies.
Any status updates? Is it still looking like the results will be ready for disclosure in about a month? Thanks.
Martin, I believe there was never a long term study done though. It’s really hard to trust anything these companies say in terms of studies. Are the medical studies conducted by a third party with no involvement from Merck? If they are involved in any way or shape, how it can it be trusted.
[quote=“bostonusa2009”]
The whole thing wrecks of BULLSHIT. Ive been reading through the data sheet, and first off the whole side effects section contridicts itself by saying “it is important to know all these side effects went away when the medication was stopped or in men who continued treatment.”
The the next line says there have been reports of persistaint ed, gyno, depression, ejaculation disorders post marketing.
And then you have all that crap about how 1.3%of men get ed and .8 get ejaculation dissorders and blah blah.
How the hell can that be true, 5ar2 reduced dht is being blocked, 5ar2 deficiency is a serious medical condition. Merck says 1.8% of men experiance lower libido, when i went to my doctor when i was takin fin, for an unrealated matter, he said hows your libido, i said i dont know and he said losing your libido on fin is almost a given. I didnt really care because i didnt have a girlfriend.
Just re-read this thread. Very encouraging stuff. Let’s hope this is the beginning of the end.
Awor, do you feel that our androgen resistance is due to a mutation? Is it possible for other factors to cause a resistance to androgens besides a mutation?
See screenshot. Possibly AR Post-receptor defect in the DNA binding domain.
Also:
en.wikipedia.org/wiki/Androgen_insensitivity_syndrome
[Size=4]Androgen-Insensitivity Syndrome as a Possible Coactivator Disease[/size]
nejm.org/doi/full/10.1056/NEJM200009213431205
[Size=4]First Detection of Complete Androgen Insensitivity with No Mutation in the Coding Sequence of the Androgen Receptor Gene[/size]
bioscience.org/1996/v1/a/lee1/htmls/lee.pdf
See screenshot. Translational, post-translational or other factors could be a cause of AIS without AR mutation.
Those studies clarify a lot. Are any of the types of AI, besides a mutation, treatable? I read that a mutation is not. Its my opinion that we don’t have a mutation. I feel that its some other type of AI. But that’s just an opinion and opinions mean nothing.
This is my first post. I would like to say that I hope this study goes well. I would be glad to participate but I don’t think I’ll be able to. I am a science researcher and I have been looking at epigenetic changes do to stress factors. 5-AR receptor down regulation makes sense.
You take propecia which lowers DHT, you come off, get the DHT surge which “overwhelms” the receptors/body. Your body compensates by methylating the gene. Thus we have an androgenic insensitivity. The key would be to find out how to reverse this.
I am a recent victim of this horrible poison and I want to get back to normal and I want everyone here to get back to normal. No one deserves to suffer like this because of the greed of a giant pharmaceutical company. However, I think we need to be most efficient in terms of informing doctors.
I think it would be wise of us to list the names of doctors who are receptive to our situation. I have been to 4 doctors, two say its in my head. The other two believe me, one is puzzled, one understands how this can happen and says I just need time to get better. I don’t know what to believe anymore. However, I think it would be wise of us to make sure doctors are reporting the persistent side effects and are communicating to each other in order to shine more light on the situation. This would be more helpful in terms of getting the smartest doctors to start thinking of ways to reverse this.
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When will the results from this study be available?
Welcome to the forum,
If you can find the time you might want to put your story in the members section so others can know your background.
Awor is coordinating the study and said that the results are expected mid to late september.
Is there a specific date on when the results will be out? i apologize if this has been asked before.
You can’t put a date on science.
No specific date. Sometime between mid-end of the month.
Ok, thanks.
While we are all waiting…let me ask the question that has probably been asked 500 times already…just to clarify…
Will the results rule in/out all of the following??
-epigenetic change / over methylation
-5AR type 2 enzyme issues
-androgen insensitivity
-transcription malfunctions
-etc
I apologize if this question has already been answered, but I wasn’t able to find what I was looking for - with the androgen insensitivity theory, and what point is it suspected that androgen insensitivity occurs? Is it a gradual onset? Is it a sudden onset upon discontinuation of the drug when DHT returns to the body?
I also realize that no real answer to this question might exist yet, but after a break from the site and some improvements, I’ve taken a renewed interest in whether the allopregnenolone inhibition issues would potentially be treated separately or as part of the symptomology of androgen insensitivity (i.e. Will treating androgen insensitivity treat all of the finasteride related issues, or must we look at certain symptoms as being part of a separate problem caused by finasteride?).
I think what your getting at is negative autoregulation. Awor explains it a bit here or you can just google scholar it.