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

Cock is kicked for all of us.

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Guys, I came back to post and give you hope, my total testosterone level initially was in low 300 in 2012, recently my last blood work this year 2021 came back in 600, My sexual performant is perfectly good, I am no even think about PSF anymore, Lost in Austin, a member of this forum text me yesterday and came back just for curiosity.
Like a month ago, studently I have a panicky attack that last for more than a week. but after it passed, I came back even better of what I was. I think that most those genes slowly over the time got regulated by themselves and the patient start to recovered at some point. also is possible that for some individuals the time of recovery is longer that others and for some never recover.


thanks for coming back.

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It appears the moderators deleted the comments of the most virulent PFS-denying weirdo. This could be a sign that things are changing. In the past, the moderators have tried to put on a veneer of objectivity with an obvious and undeniable favoritism towards pro-fin, PFS denying crowd. Not saying they don’t have an agenda but this was in part due to their inability to understand the science involved.


Baylor study hopefully can be foundation stone for causal study… A study that proves a theory that can explain how if fin is consumed then a happens causing b causing c causing d causing symptoms.


Forget about my post, do not try GHK, seem that also block DHT…

Forget about my post, do not try GHK , seem that also block DHT…
Reduce DHT formation in the hair follicles – 5-alpha reductase exists in 2 forms; type 1 which function in hair follicles and type 2 which acts in prostate tissue. Follicle damaging DHT is produced in the hair follicles. Pro- pecia (finasteride) inhibits 5-AR throughout the body and improves hair growth. But it works best on the type 2 form, and is best suited for for controlling prostate enlargement. It also must be administered by pills that spread the drug throughout the body. However, increased copper ions in the skin is better at inhibiting the type 1 5-AR that damages hair growth. Sugimoto et al (Sugimoto 1995) found that copper (II) ions could give up to a 90% inhibition of type 1 5-AR. at At 0.12 micrograms copper ion per milliliter, there was a 50% reduction in activity of type 1 alpha reductase but copper (II) ions were 10-fold less active on inhibiting the type 2 prostate type. Thus, copper ions are more specific inhibitors of 5-AR than finasteride." (6)

# GHK and DNA: Resetting the Human Genome to Health

I was also a patient and was 45.


Wow, great to see this released.

None of us are able to undo our past decisions. But we can control the decisions we make now and in the future. I think we all have cause to be slightly more optimistic about the future - we know more than we did previously, and others can build on this study. This is a good development.

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I have not read the study or this thread carefully and have nothing useful to contribute. So I’m just rambling like most in this thread.

When I think of altered gene expression why do I think of things like greater chance of getting specific types of cancer and diseases and not so much like a specific symptom such as ED or poor orgasm or poor ejaculation quality and quantity. Does anyone know anything about gene expression as it relates to how fast a certain gene can become alerted ? Because for a lot of people including my self the sexual sides happened overnight while on the fin, dut or saw P. So that leads me wonder ok if a gene becoming altered can cause these sexual sides then that probable means that a gene can become altered very quickly. If generally speaking genes becoming altered takes place over an extended period of time then in my opinion genes becoming altered is probable not the explanation for these sides . If I’m right it still can’t be a good thing but I am speaking in terms of “ok this thing caused this side specifically”. I don’t currently know enough about the subject to answer my own question


What exactly do we know so far about what this study is saying about the AR receptors specifically? Anything or did I misread that ?

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I heard next step is genetic predisposition study?

Would be interesting if awor could comment on this study. After all it seems to align with his thesis.

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Gene expression can change rather quick.

For example working out will change gene expression in a few thousand genes post exercise.



I’m assuming you have read studies confirming that working out can change gene expression very quickly ? You are usually on point with everything you say so that’s why I’m assuming this .

Now if something as “simple” as working out can change gene expression very quickly then I’m assuming pretty much anything we do could change gene expression very quickly ? Such as let’s say not working out could cause changes in gene expression? And thinking along those lines is it surprising to hear that living in an altered state of extremely reduced sexual function, constipation and low sleep quality and the stress that comes along with living like this would cause changes in gene expression?

I ask my self these questions while trying to make the best educated guess that I can make when determining if fin, dut or saw P cause the changes in gene expression or are the changes in gene expression a consequence of living in a PFS like state. From an actual mechanism responsible for specific sides point of view this question feels important…

Also do you know what the Baylor study said about the Androgen receptors ?


The idea of 3000 genes being over/under expressed, caused by a cascade effect from several primary genes seems to fit with how my PFS developed. My PFS was like a slow burn that lasted 3 years, initially just ED, then insomnia, depression, eye and ear problems, shrinkage, etc. all developing slowly until I finally bottomed out. It seemed like one thing would lead to another and that would lead to another. Glad to see we are finally making progress again. Will be happy to contribute when new studies are finalized.


What do you guys think we are looking at here? Abnormal methylation, pro inflammatory genes predicting the state, increased myostatin signalling, mutagenesis?

Does anyone realistically think that they are able to develop a cure in the next 10-20 years? I doubt it. Maybe in 20 years we will know what pfs ist excatly. This is like long meta game, but doesnt not help any individuals currently.

What I suggest is that you get a team of scientist to experiment with certain substances and develop theories on what can be improved just symptomatically.

If I could improve my baseline by a certain amount and avoid crashes I wouldnt give a fuck about pfs anymore. There are a good amount of people who recovered and live a normal life.


Which is your current situation after all these years?
Could you tell us what has improved or not?

Without an understanding of what PFS is, we cannot create animal models. Without animal models, we cannot test substances safely. Testing them on patients doesn’t seem very ethical considering the way people’s bodies seem to respond to “therapies”.

FWIW I personally think within 10 years is very realistic if everyone in the community gets together and gets behind the same approach. I don’t know if expecting everyone in the community to do that is realistic though.


We got nothing from self experimentation. We got something from the foundation. This will continue to be this way imo. Set up monthly donation schedule guys. We need to understand the causal mechanisms behind pfs to be able to take advantage of medical tech advances that are happening independently of our problem.