What I believe PFS is

1h

This give me an complete idea of what PFS could be.

When we when out of drug ( Finasteride ) there was an increase of 5α-reductase activity that was suppressed while in the drug .suggesting that the capacity to produce allopregnanolone is increased see #1
Then read the rest #s

1- 5α-reductase activity is increased in the hypothalamus in late pregnancy (Brunton et al., 2009), suggesting that the capacity to produce allopregnanolone is increased in pregnancy. Allopregnanolone may act locally to enhance GABA

2-Allopregnanolone may act locally to enhance GABA action in the PVN or on inputs to the CRH neurons to attenuate HPA axis responses to stress in late pregnancy.

3- The importance of allopregnanolone to inhibit HPA axis responses to stress in later pregnancy has been tested by blocking its production using a 5αR inhibitor, finasteride (FIN). Blocking allopregnanolone generation with finasteride (FIN) at a dose shown to reduce brain allopregnanolone content by up to 90% (Concas et al., 1998), substantially restores HPA axis responses to systemically administered IL-1β in late pregnant rats.

4- Patients with AD show an increased glucocorticoid production compared to healthy elderly control subjects. In addition, an increased 5α-reduction was seen in patients with AD. Thus an increased glucocorticoid production can be regarded as an early feature of AD since an enhanced production of 5α-reduced metabolites of cortisol was established (Rasmuson et al., 2001). 3α-OH-5α-reduced metabolites of cortisol interact with the GABAA-receptor and enhance the effect of GABA-steroids on the GABAA-receptor.

5- Chronic stress can impair memory (de Quervain et al., 1998). Memory impairment is permanent in persons with a chronically elevated adrenal production of GABA-steroids (Lupien et al., 2005). Memory impairment was also reported in chronic stress syndromes, so called “burn-out syndrome.” “Burn-out syndrome” occurs frequent in patients with AD.

6- The production of cortisol and GABA-steroids increased in parallel during stress (Purdy et al., 1991; Serra et al., 2003; Droogleever Fortuyn et al., 2004). During chronic stress, long-term exposure to GABAA-receptor agonist results in similar changes after prolonged exposure to benzodiazepine and alcohol.

7- Long-term and enhanced activation of the GABAA-receptor is an important factor in of memory impairment during stress. The response of cortisol and GABA-steroids to adrenal stimulation was similar in patients with AD as chronically stressed animals (Nasman et al., 1991, 1996). Patients with mild Alzheimer’s disease have a high and non-suppressible production of cortisol and GABA-steroids (Nasman et al., 1995).

8- After long-term exposure to GABA-steroids, down-regulation of the GABAA-receptor is expected (Yu and Ticku, 1995b; Barnes, 1996). A malfunctioned GABAA-receptor can be an important factor in the pathogenesis of stress-induced depression, “burn-out” syndrome and sex-steroid related depression (Drugan et al., 1989; Wihlback et al., 2006).

9-The down-regulation occurs at different levels in a time dependent manner: (i) desensitization; (ii) receptor internalization; (iii) receptor subunit degradation; (iv) altered expression of receptor mRNA (Barnes, 1996). Exposure to an agonist of the GABAA-receptor may cause changes in receptor mRNA and induce changes of the -receptor subunit composition (Smith et al., 1998.

This is my personal conclusion from what I read
After all seems that the receptor that is fuck is not 5-alpha-reluctance receptor or AR, it is he GABAa receptor the one that is FUCK, this is what I believe that in PFS occurred something similar to a “burn-out” syndrome, in other words a desensitization of GABAA receptors.

The second link explain down syndrome, as you can see guys there are different sub-types of GABAA receptors depending of the sub-type that is affected is the clinical pathology.
Seems that is why the androgen receptor wasn’t found as the problem at the Harvard study

Gamma-aminobutyric acid, or GABA , is the brain’s major inhibitory neurotransmitter to prevent overstimulation and therefore promote calm. GABA deficiency symptoms may include depression, anxiety , insomnia, and more…

Selective GABAergic treatment for panic? Investigations in experimental panic induction and panic disorder

Several studies have demonstrated that patients with panic disorder have a dysfunction of the GABA A receptors

Enhancing Orgasm with GABA . Orgasm release is controlled by the body’s levels of gamma-aminobutyric acid ( GABA ). … GABA helps inhibit excitatory neurotransmitters that can cause anxiety if the system is overstimulated. This is important, since chronic anxiety can lead to loss of sexual interest and sexual dysfunction.

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do you think its curable ?

I believe that the trick is fixing the gabaa receptors, stress and anxiety for sure deep the problem.
There also gabab receptors. But so far I believe that it is the gabaa receptors.

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so you argue like this?

fin > lower allopregnenolone > lower action at gabaA receptor(does this receptor then gets more sensitive to the fewer gaba?)

stop fin> suddenly alot allo > sudden spike at gabaA receptor (as if chronic benzo use) > gabaA desensitizes > insomnia,anxiety etc

sounds like the silencing theory of AR aplied to the gabaA receptor. in my particular case it would make a lot of sense, i suffer badly mentals like insmonia,anxiety. after taking a benzo for 1,2 nights and sleeping soundly im like…cured?!

I took gaba supplements and I didn’t feel anything, guess because the gaba receptors are fuck, I Google if it can be fixed and it says that take time.
Also if you can Google : Do gaba affect libido ? And you will get the answer.
When I was without stress I was basically fine, I get anxious to speed the recovery and then it was when I started to experiment with tribulus dopa and creatine then I crashed.

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Intresting that you shared some studies about pregnancy, i have talked to a woman whose PSSD symptoms were gone during pregnancy, unfortunately her PSSD came back after the pregnancy.

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I truly believe that there are two types of PFS

1-those that used the medication for short time ( are producing DHT ) gaba receptors fuck, this group do not tolerate TRT it make worse, they get better sometime with some food that block DHT like tomatoes, they crash because are constantly anxious.

2- ( Do not produce DHT ) adrogens levels are insufficient, and gabaa is not affected, because there are not increase activity of 5-alpha reductase.
This group tolerate TRT, this group crash with chocolate when they are not on TRT.
Note: It use to happen to those that had been using finasteride for long term ( it doesn’t mean that all long term user with PFS are not going to produce DHT)

Type 1 protocol
1- Fix anxiety otherwise nothing going to work and we are going to continuing experiencing crash no matter what protocol do you use, that’s why protocol are no replicated.

2-Normal food and forget that tomatoes have a DHT blocker should no be a problem, this group need to maybe reduced a little bit the DHT levels ( no with fisteride or saw palmetto ) but drink chocolate milk, tomatoes, eat once in a while avocados “not every day” , just to keep in check the DHT ( this group should not be panic or worry about DHT because they are producing it.

3-Avoid stress situation as a top priority.

4-Time is crucial Gaba receptor take long time to desensitize

SSRI’s syndrome and Post Finasteride Syndrome " TWO FACES OF THE SAME COIN "

Type 2 Protocol
2-Fix anxiety too, but most like TRT for life is the solution.

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for the type 1 protocol, would you fix anxiety no matter what or even be cautions. e.g. SSRIs help with anxiety but can mess with androgens too.

I agree if you read above the benzos create the same problem with gaba, that’s why we are fuck, gaba regular pituitary gonada axis PGA giving us low level of testosterone. Also regulate hypothalamus pituitary axis HPA fucking us with the sleep, anxiety and depressive mood.

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I am under a crash now, but after what I believe that I found I never be so relaxed since 2012.

Supposed only small percentage that use Finasteride the symptoms are irreversible,
And for some the damage truly are irreversible specially for those that not produce DHT anymore.
For those that produce DHT, and are keeping fighting the symptoms, we are people that are predipose to anxiety and of course Finasteride kill us.
Those people that give a fuck anything and relax are the one that get recovered after stopping Finasteride (For the type 2).
The stubborn one like us never get out the hole, we still in a loop of temporary recovering and crashing.

It all this is true, I believe that the study for those with PFS type 1 it going to be worthless. It is very possible that the found the supposed silent gene that convert T to DHT but only good finding for PFS type 2

Another type of study need to confirm what I posted for sure. But I believe that this finding if this true this is just the beginning of taking a new direction of PFS treatment.

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The book the upward spiral explains about depression and anxiety in the brain and how to fix this using the brains neurotransmitters. It’s science based but clearly written that anyone here could follow. The suggestions do not require supplements/drugs. EMDR therapy is gaining attention for the treatment of anxiety. This program can be done at home https://virtualemdr.com/

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Sorry to get personal but it seems that I fried my androgenreceptors(penis not reacting to existent libido) what would be a possible course of action? Or is it just over and irrepairable?
Aswell as I dont really feel my muscles or muscle soreness from gym anymore. Anything possible to revert that?

Debbie Hampton wrote a book on how to recover from a brain injury, she also has a website. Her brain injury was extremely bad. Maybe you could start there. This condition is so complicated, just do the best you can without making things worse.

Bother, remember this, forget the androgen receptor, Gaba system is interconnect with androgen system, with the neuro-endocrine system ( the whole thing is a machinery), It just take a piece to fail to start a chain of reaction of side effects.

I believe that PFS had been so difficult to treat. because we all have been targeting in the wrong direction.( All this is for what call PFS type 1 ).

That’s the problem we can’t use SSRi because it going worse the situation.
As we see in the pass there all kinds of recovery in this forum example
1-Recoverd after 5 year
2-Recover after vacation and sun exposure.
.
.

And so on…

Note tribulus have also effects on gaba Google it.

[quote=“MOONCHILD, post:14, topic:36222, full:true”]
Bother, rember this and forget the androgen recetor …[/quote]

We have clear evidence that shows overexpression of the androgen receptor in penile tissue of patients with persistent side effects after the use of Finasteride. Pretty much all symptons that are typically described here can be explained by a lack of androgenic action. It’s pretty clear that this is likely the driver of our condition.

You are free to discuss your theories here. But please let me remind you of the terms of use here, which include:

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Yes as I said everything is an hypothesis, but I think that what you said is valid for those that doesn’t have produced DHT.
As so far I know, Harvad study didn’t found overexpression on adrogens receptors.
It depends of the PFS type of the participants in the study, it is my opinion.

If the theory is true, I found something that can help, but I recommend to do a full research before to try it.

Repairing GABA receptors/functionality after Benzodiazepines is Possible

http://www.neurogenesis-inc.com/pdf/battling_thebenzos.pdf

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Supplementation of T. terrestris is regularly incapable of increasing levels of androgenic/estrogenic hormones in blood or urine samples, however, synergic actions over NO synthesis, GABAergic signaling inhibition (through DHEA), dopaminergic signaling and potential for bioconversion to androgens (1875mg doses), indicate a possible application in the treatment of erectile dysfunctions and HSDDA. Protodioscin (PTN), a common saponin from T. terrestris, may stimulate nitric oxide (NO) and other mediators tomodulate central dopaminergic activity and libido. PTN may also be converted to DHEA, which is capable of inhibitingGABA signaling**, therefore promoting improvements in sexual function . B. The relationship between PTN and testosterone (TST), of stimulation or direct conversion, is still unknown, however, in vivo models indicates that T.terrestris may influence concentrations of TST and C. dihydrotestosterone (DHT). PubChem compound database
codes: CID=441891 (PTN); CID=6013 (TST) and CID=10635 (DHT). Adapt

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(Just interjecting. So so very happy you’re here and researching MOON. :slight_smile: )

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