Differential Gene Expression in Post-Finasteride Syndrome Patients - Dr. Khera - Baylor

Yeah, you’re correct. There is a lot of studies done which shows just that.

However after X amount of hours these genes mostly go back to baseline.

But if you keep working out often the genes will either chronically express themself more, or have a greater respond to stimuli (eg express themself more after workout).

I would assume that it’s right, however the body doesn’t want to change at all. That is why even though working out is very healthy, it’s also very exhausting.

Basically for your gene expression to change chronically you need stress and couple it with time. How much stress and time is individual.

From the data we have on fin it’s basically putting tremendous amount on stress on the (male) body when you lower DHT. But this still doesn’t explain why some people get PFS and some won’t.

And yeah I read the Baylor study and they saw that AR was over expressed in penile tissue. Pretty much confirming the other study we had some years ago.

It’s not surprising though as any anti androgen would probably do this. What’s interesting is why it won’t down regulate when off fin, as excess androgens should down regulate the AR expression.

But since we don’t have data on either people on fin without symtoms or people who has been on fin before and quit but didn’t get PFS, it’s really hard to draw any conclusion how big of an impact the AR expression have on us.

Edit: Just posting this because they show gene expression post workout pretty good.

Most expression 4-8 h post workout, and back to baseline after 24 h.


I feel the same way . Self experimentation is very dangerous and anyone saying this is correct . I have worsened my self through through self experimentation. But self experimentation is also the reason why I’m currently sleeping 7 hrs straight at a time a lot of nights and the reason why I’m not always constipated now . If I could bring my current sexual function up to a reasonable level through more self experimentation then I could just move on from this while I still have some led left in my pencil . It’s gambling though and unfortunately most who gamble don’t come up on top in the long run.

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I dont know. Im a little surprised no one has touched on this or brought up this observation.
After paging through the study it seems the author(s) are not so convinced this is an androgen mediated disease.


Together, overexpression combined with less functional activity may be responsible for certain PFS symptoms, possible through effects on neurosteroid levels but also through ARinduced tissue toxicity

Also noticed this…All those funky symptoms reported here by some like, changes in hair quality, hair becoming dry, brittle even notice mine grows completely different and in a different pattern now and is more curly frizzy rather straight is probably due change in gene expression of the follicles…

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I didnt think thats what was stated though, that the data didnt support this.
Do we still have this full study?
The link expired.

I just looked at it again the link here works now…its at the very top of the study…

This is what I was talking about @holyhead. The full study is available elsewhere without having to pay?
I read this and now this link is expired.
Also what you just posted was a guess before the data I believe.
A Hypothesis.

Yea I just clicked on it and asked if I wanted to download the pdf again? So I assumed it is still working

This is what I got.
URL signature expired

You’re right a guess!

I click it and it downloads again…clear your cache and try it

Anyone confused :confused: about how to interpret Baylor this guy lays it all out in easy to understand eloquent passages :laughing::rofl:

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No thats weird. Can everyone else still access the full study?
Anyways there was a statement in there towards the end about possible ar overexpression to compensate for diminished ar signaling, but the author stated that didnt seem to be the case based on the data.

I got this from Accutane.

I was confused about this part as well reading through. They seemed to measure two hormones or metabolites(I forget the name) as a measure of androgen receptor activity. I was unaware you could measure the activity of the androgen receptor. It made it seem like you could measure emissions from a gas engine except apply this to the androgen receptor. The authors also said that the AR is highly complex and that no definitive conclusions can be drawn

It interacts with over 200 proteins if I remember correctly…the AR

Yes, but my point would maybe be you are not looking to reinstate some sort of loss of androgen function.
There was another line in there as well, they thought of diminished ar signaling (or compensate for the loss of) but they said the data showed quite the opposite as to why they thought the ar gene might be overexpressed.