Post Finasteride Syndrome clinical review

I’m not sure if this clinical review was ever published here but it’s worth a read. “This is why it is hypothesized that post-finasteride syndrome patients could carry an expansion mutation of the CAG and/or GGN triplet of exon 1 of the androgen receptor gene, although lower than 40 repetitions, resulting in a silent mutation, becoming evident after the inhibition of the 5AR.”

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do CAG and GGN indicate possible target areas for demethylation agents?

never seen this in my life btw thanks for sharing

4 years later and we’ve made no progress.

That paper could have just as well been submitted in 2020.

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I believe that a cag repeat disorder is unfixable right now as Huntington’s and Kennedy’s both have no real therapies; it would fit into why we’re unresponsive to androgens and why there is a overexpression of androgen receptors. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2084330/

So, this is bad news ?

At some point people will stop running self experiments, coming up with theories and band together to support efforts to boost awareness and appropriate research.

Any day now.

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right

but knowing that CAG and GGN repeat disorder might be the case

would that give us gene targets?

Ppl have been tested for this and it’s normal, at least that’s what I remember reading and my interpretation

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I have been visiting this forum for a few months and recently decided to create an account. I created this account just to complete the survey.
this is a message for you who have not yet completed the survey: people took the time to do it. we need real science!
I realized that the administrators are tired of the lack of collaboration. these guys know a lot about this condition but they can’t do anything alone.
every effort is necessary. take your herbs, do your own treatment, seek a cure, but please contribute to the work of those who are trying to find out what is happening. Many have understood this, but many have not.

this condition is still denied by most doctors. understand: currently almost nobody is interested in researching this! it is necessary for the patients themselves to stimulate studies on this condition. union is needed. 15 years ago, no one would have imagined that in 2020 there would be so little about it.
PLEASE, UNDERSTAND IT:
doctors and scientists will only be interested in this when there are enough studies on it.
Ps.: sorry for my english.

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Your English is great! Don’t worry :slight_smile:

Thank you, @Brasileiro. :+1:

Why would this make us incurable? We had this genotype before PFS and we all responded well to androgens. Now if our genotype resulted in a protein receptor that was messed up regardless of propecia then I would say it’s incurable but we were once normal

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Idk if I have to say this again but someone can correct me if I’m wrong, PEOPLE HAVE BEEN TESTED FOR THIS AND ITS NORMAL.

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It’s not just me who has proposed this it was in @awor and @axolotl latest paper.

If it’s a cag repeat disorder of the androgen receptor then there is no technology currently available that can reverse this apart from gene therapy which lets be honest won’t be available until 20 plus years that’s just the reality of it.

My point is that we wouldn’t have to fix this CAG repeat because we all had this genotype prior to pfs and functioned normally. It would be something else that we would have to fix

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Just to clarify on this, the admins’ hypothesis is not that CAG repeat polymorphism is an issue in PFS.

They reviewed literature and experiments demonstrating that overexpression of the normal AR can cause a similar toxicity to polyglutamine expansion and that overexpression is a consequence of androgen deprivation. Overexpression has been confirmed in PFS patient tissue in the Di Loreto study. The admins also reviewed a paper that shows that, while the CAG repeat has been correlated to symptoms in PFS - suggesting relevance of the AR - there is not a pathologically expanded CAG repeat.

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Thank you for clarifying this @Tzinkman I may have misinterpreted what their paper was stipulating. So can we rule out that a cag repeat disorder isn’t an issue with PFS or do you know of anyone here that has got this tested?

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I think this is the relevant study about PFS symptoms and CAG repeats in the AR.

I’m having a hard time interpreting this paper is it saying there’s a distinguishable difference in cat repeat and symptoms of PFS patients? Can anyone answer this please