I have almost completely recovered, this is how I did it

thats quite interesting. i took maca a few days after stopping and a few days before my crash…

Might be worth edging. That is to say, getting an erection and maintaing it for a while without ejaculating.

Bad option I got blue balls doing that, extreme testicle and back/kidney pain with constant precum and reoccurring erections.

My viens in testicle swelled up alot.

Oh, sorry to hear that.

Ok. Cured by masturbation and maybe some exercise.

Exercise is a common theme in stories of cured people. Having sex is a good idea, I mean anything you practice gets better, any muscle or organ you don’t use atrophies. Makes sense.

Next story…

Downregulation of AR via ejaculation

WHAT!?

What do you mean?

:thinking::roll_eyes: What is going on.

I think there are two type of PFS, those that respond to DHT and testosterone and Those with PFS that get worse with the rise of the androgen.

I am planing to take an appointment to the following center, I believe that it is the perfect center to investigate what is really going on with PFS, This center it is probable the only of this type in the world.

https://www.utsouthwestern.edu/education/medical-school/departments/neurology/programs/rare-brain-disorders/clinic.html

https://www.utsouthwestern.edu/education/medical-school/departments/neurology/programs/rare-brain-disorders/

I will like to heard opinions

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I bet they won’t even acknowledge any of this…Who knows but I would print or send all the published research thus far out such as the published Melcangi and the Triash paper on endocrine disruption…How are you gonna proceed when no one knows even what pfs is…No one knows you already talked to the world’s foremost expert on the condition or I would assume he is since he has lead the Baylor study Mohit Khera which appears to atleast have been dragging their feet on this now for 6 years and its not even complete yet…Many symptoms yet to be addressed or explained I always thought it was a brain dis order which Goldstein can show you on a functional MRI what is termed as brain damaged but my understanding its due to androgen receptors increasing in the brain in response to fin lowering dht and being flooded with a chemical type of brain trauma which would be endocrine disruption in of itself…Thus triggering some type of shut down which would be the actual culprit to continuing decline and symptoms such as these gene regulators and if Kheera is correct and androgen dependent genes have been silenced or turned off there is nothing anyone could do about it just as with lowering neurosteriods there is no reversal for this other than your own body’s ability to adapt to these changes over time…But I think your on a wild goose chase here till more is known and more studies are published…

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Here is my opinion. Nothing going to happen, they will just suck money out of you. They cannot know more, than what the current studies are providing.

Everything is an assumption, everything is an hypothesis, there is one thing here for sure, those recoveries and even temporary recovery is telling me that the system is working, irreversible conditions don’t switch like that, sometimes I do not believe that epigenetic will switch the gene on and you get recovered you and tomorrow will going to switch back off again.

2-I consulted a geneticist at Baylor and he told me that it is almost impossible that Finasteride could cause an epigenetic modification, he also told me that epigenetic changes are reversible and not permanents, he told me also that he dosen’t know how Khera will switch those genes.

In my pinion the Baylor study is not speeding the study in my opinion for the following reason:
Khera is a doctor and assistant professor at the university, what time left to dedicate to an study + he is not affected with Fin.

I think that taking the study to at monster center like this one it is different history.

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Neuroactive steroids.

Neuroactive steroids are natural or synthetic steroids that rapidly alter the excitability of neurons by binding to membrane-bound receptors such as those for inhibitory and (or) excitatory neurotransmitters. The best-studied neuroactive steroids are a series of sedative-hypnotic 3 alpha-hydroxy ring A-reduced pregnane steroids that include the major metabolites of progesterone and deoxycorticosterone, 3 alpha-hydroxy-5 alpha-pregnan-20-one (allopregnanolone) and 3 alpha,21-dihydroxy-5 alpha-pregnan-20-one (allotetrahydroDOC), respectively. These 3 alpha-hydroxysteroids do not interact with classical intracellular steroid receptors but bind stereoselectively and with high affinity to receptors for the major inhibitory neurotransmitter in brain, gamma-amino-butyric acid (GABA). Biochemical and electrophysiological studies have shown that these steroids markedly augment GABA-activated chloride ion currents in a manner similar (but not identical) to that of anesthetic barbiturates. Several steroids have also been observed to have convulsant or proconvulsant properties, including the synthetic amidine 3 alpha-hydroxy-16-imino-5 beta-17-azaandrostan-11-one (RU5135) and the natural sulfate esters of pregnenolone and dehydroepiandrosterone. Several of these have been shown to be bicuculline or picrotoxin-like GABAA receptor antagonists. Examples of steroids that alter neuronal excitability rapidly by augmenting or inhibiting excitatory amino acid receptor-mediated responses have also been reported. Recently, allopregnanolone and allotetrahydroDOC have also been measured in brain and plasma where their levels have been shown to fluctuate in response to stress and during the estrous and menstrual cycles of rats and humans, respectively. Although the major fraction of allopregnanolone in tissue, including brain, is of adrenal and/or ovarian origin, appreciable levels of allopregnanolone can still be measured in the brains of adrenalectomized and/or oophorectomized animals. Receptor-active neurosteroids may represent an important class of neuromodulators that can rapidly alter central nervous system excitability via novel nongenomic mechanisms.

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What? I was pointing out that ejaculation downregulates AR in the brain, which could explain this recovery

Never heard this before, thanks.

For me the theory fits perfectly… after ejaculating i get better, if i abstain then my penis shuts down completely. You dont dont experience this?

I am quite willing and happy to test this protocol for August. If I, er, manage to wank the PFS out of me it’d be literally the stupidest cure for any illness ever but I’d take it.

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No i don’t. Nothing changes when i ejaculate or stay abstain for weeks. Im a very mild case of PAS though.

Another very mild case recovered. Haven’t seen any people recover from the full zombie syndrome though. This guy had lower libido that’s it. Hardly inspiring for people in far worse shape

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I tried many things with no improvements on my semen volume. Also they are people who recovered from the “full zombie” thing. You should check out more recovery threads.