Testosterone decreases brain 5AR1 and lowers allopregnenolone.

[TubZy]

Wow, you are literally in the same boat as me. Right after the crash my sleep was fucked and wrecked. Now in the last 1 year it's recovered. It's not 100% but I am not longer chronically fatigued and thinking "I got no sleep". So, I know my sleep has improved decently.

I recovered the most when I did a zero-carb diet too. I was doing a raw carnivore diet, all raw meat and raw animal products. Extreme I know, but it worked. I still do it. Perhaps the low carb diet works because it increases stress hormones like cortisol, required to create some glucose via gluconeogensis. At the same time, it's very good for healing in general and lowering inflammation...

Fasting helps. Lowering inflammation helps. Limiting and restricting certain foods definitely help. If you are able to acquire GHB, I would urge you to try it, a dose high enough to induce deep sleep. Helen believes it helps with our cortisol, or lackthereof.

As far as brain fog, that's my main concern. I can get rid of, or trigger brain fog simply from diet. If I go pure animal products, like flesh only, within 3-7 days I am very normal and have a great mood, clarity, control of emotions and general positivity. Adding dairy makes me off balance and very irritable/foggy. However ever since working on digestive health, I can tolerate dairy more, but not 100%.

Also when I came off finasteride, I was hyper sexual, but was also taking creatine too. I was horny and stressed. Tons of fog and anxiety, but uncontrollable sexual desire.

What else do you know about people like us @Boris , what exact symptoms do you have left? What have you done to recover? We should stay in touch.

Yeah dude same. When I first crashed had all symptoms bad (no sleep, low libido, low drive, no muscle anymore, anxiety etc.) and even bad immune system (mono and stuff).

When I came off fin for the first few weeks or so I was hyper sexual than crashed bad which was triggered after taking some stimulants (again cortisol related).

Over time, and experimenting with shit over and over my sex drive got better and libido and everything got better, but still have mental sides and allergies/digestive issues still there. Check out my log as I experimented with some stuff. I am currently trying to figure out if our case is upregulated or downregulated GR. Also my hormones were always high especially test even when crashing and until this day. My test is like 780 I think last time I checked. I never had low hormone issue with PFS and I saw you have the same thing as well maybe that is why our sex drives are still good.

RU486 blocks cortisol/GR and my mental symptoms go away however doesnt fully last once ceasing the drug. I also tried anavar which blocks GR signalling and I felt some beneficial effects from that as well. But I think it has to get across the blood brain barrier in order to work. Meaning just lowering cortisol in general doesnt do anything for me. Needs to block the GR and get into brain. I have not tried GHB though have you tried phenibut? But I'm like 90% sure cortisol is the route of our problem here. Either its too sensitive or cortisol is not working at all. Have you tried taking cortisol directly like prednisone or something?

https://hackstasis.com/threads/tubzy-log-ru-blood-hair-tests-arl-anavar.8/

 

[jacknap]

your experiences is exactly similar to mine. Libido and sex drive etc is all pretty fine its mental stuff that is still remaining. Poor response to stress, some brain fog (at times worse than others etc.) and sleep, but sleep has improved much better over time since crash.

And I get the same exact response as to steroids. Libido goes up crazy and physical effects are there but mental sides increase way worse. The major thing that I tried that completely fixed mental sides temporarily (as in felt normal again) was RU486 but didnt last once stopping it. It is def cortisol related in the brain side for sure at least in my experience

low card diet and fasting also helped with mental sides

couldn't it simply just be adrenal fatigue since having PFS for a few years is really stressful no?

 

[Ocguy]

couldn't it simply just be adrenal fatigue since having PFS for a few years is really stressful no?

My latest hair test I'm totally out of adrenal exhaustion.. took 15 months to get there, was totally wiped out.. I have good energy now, but it hasn't changed the libido dept.

 

[brix]

My latest hair test I'm totally out of adrenal exhaustion.. took 15 months to get there, was totally wiped out.. I have good energy now, but it hasn't changed the libido dept.

What does that look like on a hair test?

 

[MCurtone]

Yeah dude same. When I first crashed had all symptoms bad (no sleep, low libido, low drive, no muscle anymore, anxiety etc.) and even bad immune system (mono and stuff).

When I came off fin for the first few weeks or so I was hyper sexual than crashed bad which was triggered after taking some stimulants (again cortisol related).

Over time, and experimenting with shit over and over my sex drive got better and libido and everything got better, but still have mental sides and allergies/digestive issues still there. Check out my log as I experimented with some stuff. I am currently trying to figure out if our case is upregulated or downregulated GR. Also my hormones were always high especially test even when crashing and until this day. My test is like 780 I think last time I checked. I never had low hormone issue with PFS and I saw you have the same thing as well maybe that is why our sex drives are still good.

RU486 blocks cortisol/GR and my mental symptoms go away however doesnt fully last once ceasing the drug. I also tried anavar which blocks GR signalling and I felt some beneficial effects from that as well. But I think it has to get across the blood brain barrier in order to work. Meaning just lowering cortisol in general doesnt do anything for me. Needs to block the GR and get into brain. I have not tried GHB though have you tried phenibut? But I'm like 90% sure cortisol is the route of our problem here. Either its too sensitive or cortisol is not working at all. Have you tried taking cortisol directly like prednisone or something?

https://hackstasis.com/threads/tubzy-log-ru-blood-hair-tests-arl-anavar.8/

I never took cortisol or prednisone. To be honest I was a daily coffee consumer. It wasn't until I stopped coffee completely that I began to recover. However I had cortisol tests and I had normal cortisol levels, maybe slightly elevated but nothing extreme.

I have not tried phenibut. I want to stay away from those things. Only GHB is okay with me, as our body actually produces it, albeit in small amounts.

What is GR? Glucocortisoid receptor? I'm not as advanced in that area. We have cortisol but its not getting into the brain and activating?

 

[Ocguy]

What does that look like on a hair test?

When ca/mg is in perfect ratio.. 6.67. I was always low now it finally balanced out. Still more work to do, but hopefully the adrenals will be able to handle it better and quicker.. I'll post it up in my log soon

 

[TubZy]

I never took cortisol or prednisone. To be honest I was a daily coffee consumer. It wasn't until I stopped coffee completely that I began to recover. However I had cortisol tests and I had normal cortisol levels, maybe slightly elevated but nothing extreme.

I have not tried phenibut. I want to stay away from those things. Only GHB is okay with me, as our body actually produces it, albeit in small amounts.

What is GR? Glucocortisoid receptor? I'm not as advanced in that area. We have cortisol but its not getting into the brain and activating?

Yeah, I crashed from a hardcore preworkout post fin. Like a few weeks after which really crashed me very hard prior to that sides were no that bad. I stopped all stims too and slowly recovered sleep which took about a year.

Yes, that is GR. Yeah either the receptors are upregulated or downregulated since fin is a progestin but can't convert to cortisol like normal progesterone does in the brain and this alters GR expression. I'm not 100% sure of this theory as a few of us are trying to further clarify it more.

GHB is interesting but I'm hesitant since anything that really increases neurosteroids tends to act as a bandaid rather than force body to upregulate neurosteroids naturally if you get what I'm saying (either if its produced naturally by the body or not, taking testosterone is an easy example of what I'm saying). Otherwise I would just take nicotine religiously since it also increase neurosteroids but when you come off it you are usually worse for a few days to a week before you bounce back to baseline again.
Never tried GHB though although someone posted a thread of someone getting cured by it.

 

[hairsuit]

5[alpha]-reductase is a regulator of glucocorticoid action and metabolic phenotype in human liver | SFEBES2014 @Helen according to this 5ar inactivates cortisol, so any 5ar inhibitors would increase cortisol and then coupled up with a stressful event while on fin for eg would downregulate GR receptors ? And is why some crash on fin

Hmmmmm...... fellas, have we explored this? @Helen ? The combo of Fin AND a stressful event. Both times I crashed were during the two most stressful events of my adult life. Anyone else have this experience? Could stress and Fin coupled effect with causing the crash?

 

[TubZy]

Hmmmmm...... fellas, have we explored this? @Helen ? The combo of Fin AND a stressful event. Both times I crashed were during the two most stressful events of my adult life. Anyone else have this experience? Could stress and Fin coupled effect with causing the crash?

possibly if cortisol is not working properly it could alter GR expression. So stressful event demands even more cortisol and since fin is synthetic progesterone it cant convert normally into cortisol like bio-identical progesterone can which could alter GR expression. My stress tolerance was horrible on fin and even worse with PFS. @Helen already showed the study of androgen deprivation on the GR

 

[MCurtone]

This makes sense. If fin is a progestin which mimics progesterone...it could shut down natural progesterone production. Then this fake progesterone (fin) also cannot convert to cortisol.

Stressful events = death. In addition, with 5ar inhibition, it prevents what small amounts of cortisol that are there, from reaching its final metabolite, THDOC.

Refer to this flow chart. Not only allopreg is affected, but also THDOC.

 

[TubZy]

This makes sense. If fin is a progestin which mimics progesterone...it could shut down natural progesterone production. Then this fake progesterone (fin) also cannot convert to cortisol.

Stressful events = death. In addition, with 5ar inhibition, it prevents what small amounts of cortisol that are there, from reaching its final metabolite, THDOC.

Refer to this flow chart. Not only allopreg is affected, but also THDOC.

View attachment 1706

Right, I posted that full chart in the studies section of the forum as well before.

Also, I found this.

Brain Steroidogenesis Mediates Ethanol Modulation of GABAA Receptor Activity in Rat Hippocampus
jneurosci.org/cgi/content/fu … 521?ck=nck

“Ethanol, progesterone, CB34, and GHB stimulate 3,5-THP production in isolated hippocampal tissue.”

"…pretreatment of animals with the 5-reductase inhibitor finasteride, which inhibits the biosynthesis of 3,5-THP (see Fig. 1), reduced the extent of the ethanol-induced increase in the cerebrocortical concentration of 3,5-THP and prevented certain neurochemical, electrophysiological, and behavioral effects of ethanol. "

"The effects of ethanol, progesterone, CB34, and GHB were prevented by pretreatment of the tissue with 1 µM finasteride for 10 min (data not shown). "

"Finally, we tested the effect of GHB on GABAA receptor function. The systemic administration of this compound, like that of ethanol, increases the plasma and brain concentrations of neuroactive steroids in rats (Barbaccia et al., 2002). "

"Progesterone, CB34, and GHB also each increased the amplitude and the decay time of GABAA receptor-mediated mIPSCs. Because these latter drugs also increase 3,5-THP biosynthesis, these results further support the role of brain steroid metabolism in shaping GABAA receptor-mediated inhibition in a discrete brain area (Belelli and Herd, 2003). "

"Progesterone is metabolized by neurons and glial cells to 3,5-THP (Hu et al., 1987; Bitran et al., 1995; Follesa et al., 2000), whereas CB34 is a selective agonist of the PBR and stimulates steroidogenesis in the brain and peripheral organs (Serra et al., 1999).

The capacity of GHB to increase both plasma and brain levels of 3,5-THP as well as other neurosteroids after systemic administration has been proposed to involve GABAB receptors (Barbaccia et al., 2002). "

"Furthermore, prolongation of current decay time byethanol, progesterone, CB34, and GHB was abolished by finasteride, again supporting the role of 3,5-THP in the modulatory action of these drugs in hippocampal pyramidal cells. "

 

[TubZy]

So it seems GHB has a modulating affect on GABA A. This is interesting and maybe that is why you are improving in baseline despite feeling better while taking it @MCurtone since it modulates the receptor rather than act like a pure agonist like for example phenibut, Xanax etc.

Effects of GHB on GABAA receptor-mediated synaptically evoked IPSCs recorded from CA1 neurons
Finally, we tested the effect of GHB on GABAA receptor function. The systemic administration of this compound, like that of ethanol, increases the plasma and brain concentrations of neuroactive steroids in rats (Barbaccia et al., 2002). Bath application of GHB (0.1-10 mm) induced a time- and concentration-dependent increase in mIPSC amplitude (Fig. 9A,C,E,I). In contrast to ethanol, but consistent with its lack of direct activity at the GABAA receptor (Serra et al., 1991), GHB failed to affect mIPSC amplitude during the first 3 min of bath application. The modulatory effect of GHB became evident, however, after perfusion for ∼10 min. At a concentration of 300 μm, GHB increased mean mIPSC amplitude by 32 ± 4% after perfusion for 30 min (Fig. 9E). The effect of 300 μm GHB was completely reversed after drug washout for 10 min (Fig. 9A,C,E,I). GHB (300 μm) did not affect mIPSC frequency (Fig. 9F) but significantly increased the decay time constant τw (Fig. 9G,H). Pretreatment of hippocampal slices with 1 μmfinasteride also prevented the GHB-induced increase in mIPSC amplitude and decay time constant (Fig. 9B,D,E,G,H).

 

[Helen]

So it seems GHB has a modulating affect on GABA A. This is interesting and maybe that is why you are improving in baseline despite feeling better while taking it @MCurtone since it modulates the receptor rather than act like a pure agonist like for example phenibut, Xanax etc.

Effects of GHB on GABAA receptor-mediated synaptically evoked IPSCs recorded from CA1 neurons
Finally, we tested the effect of GHB on GABAA receptor function. The systemic administration of this compound, like that of ethanol, increases the plasma and brain concentrations of neuroactive steroids in rats (Barbaccia et al., 2002). Bath application of GHB (0.1-10 mm) induced a time- and concentration-dependent increase in mIPSC amplitude (Fig. 9A,C,E,I). In contrast to ethanol, but consistent with its lack of direct activity at the GABAA receptor (Serra et al., 1991), GHB failed to affect mIPSC amplitude during the first 3 min of bath application. The modulatory effect of GHB became evident, however, after perfusion for ∼10 min. At a concentration of 300 μm, GHB increased mean mIPSC amplitude by 32 ± 4% after perfusion for 30 min (Fig. 9E). The effect of 300 μm GHB was completely reversed after drug washout for 10 min (Fig. 9A,C,E,I). GHB (300 μm) did not affect mIPSC frequency (Fig. 9F) but significantly increased the decay time constant τw (Fig. 9G,H). Pretreatment of hippocampal slices with 1 μmfinasteride also prevented the GHB-induced increase in mIPSC amplitude and decay time constant (Fig. 9B,D,E,G,H).

GABA and Glutamate: Their Transmitter Role in the CNS and Pancreatic Islets | IntechOpen

 

[MCurtone]

@Boris Its difficult for me to understand your 2 latest posts here, in a nutshell, what's the summary? What is GHB doing that could be helping us?

 

[TubZy]

@Boris Its difficult for me to understand your 2 latest posts here, in a nutshell, what's the summary? What is GHB doing that could be helping us?

Read post #72 I summarized it a it better. The study shows that GHB has a modulation affect on the receptor rather than strictly just an agonist. Meaning it can adjust up or down depending on the body rather than just say an GABA receptor agonist like Xanax where it will just act on the receptor directly and activate it, which in turn means when you come off the Xanax you have withdrawals type symptoms. I'm not saying you can't get withdrawals from GHB but given its naturally produced by the body it seems to act differently than taking a traditional agonist like xanax, phenibut etc. Which is why your baseline is increasing instead of decreasing when you cease GHB. Maybe dosage and frequency is key too.

I know GHB keeps getting compared to baclofen but even though it technically looks like it act similar people don't react the same at all.

Baclofen - who's tried it?

 

[Helen]

Read post #72 I summarized it a it better. The study shows that GHB has a modulation affect on the receptor rather than strictly just an agonist. Meaning it can adjust up or down depending on the body rather than just say an GABA receptor agonist like Xanax where it will just act on the receptor directly and activate it, which in turn means when you come off the Xanax you have withdrawals type symptoms. I'm not saying you can't get withdrawals from GHB but given its naturally produced by the body it seems to act differently than taking a traditional agonist like xanax, phenibut etc. Which is why your baseline is increasing instead of decreasing when you cease GHB.

I know GHB keeps getting compared to baclofen but even though it technically looks like it act similar people don't react the same at all.

Baclofen - who's tried it?

tons of people react to baclofen the same. just go on propecia forum.

tons of people tried it and I would say it is 50/50 same as with GHB

GABA-B Agonists

 

[MCurtone]

I just find that people who have success from the phenibut, bacolfen etc, it stops working after some time.

Yes you can definitely become addicted and have withdrawals from GHB, but only if you are dosing multiple times per day, every day. Users who use it to sleep, a few times a week, don't become addicted. Even myself, I only used it 2-3 times in 6-8 months and the results lasted.

@Boris If this is true and its modulating rather than being an agonist...It's almost the way adaptogenic herbs work. Brings up what needs to come up, and down what needs to come down. My theory is that using GHB is somewhat like jumping a car. When the battery dies, you just need a kick. Then you are functioning again. I can definitely say without question, that using GHB changed and bettered my baseline tolerance to stress. It increased my cognitive functions too. I think cycling it could be key. However I used large doses to induce deep wave sleep.

Getting deep, restful sleep alone in itself is incredibly restorative. We all know PFS people have utter, shit sleep. All makes sense. Stuck in fight or flight mode, depleted neurosteroids which are responsible for calming oneself, and in addition, cortisol cannot be deactivated due to inhibited 5ar (THDOC).

 

[joekool]

If you're looking at a gaba b antagonist, i would say check on fasoracetam. It'll upreg those receptors

 

[Helen]

If you're looking at a gaba b antagonist, i would say check on fasoracetam. It'll upreg those receptors

Joe, this one makes sense, are you going to try it?

 

[TubZy]

I just find that people who have success from the phenibut, bacolfen etc, it stops working after some time.

Yes you can definitely become addicted and have withdrawals from GHB, but only if you are dosing multiple times per day, every day. Users who use it to sleep, a few times a week, don't become addicted. Even myself, I only used it 2-3 times in 6-8 months and the results lasted.

@Boris If this is true and its modulating rather than being an agonist...It's almost the way adaptogenic herbs work. Brings up what needs to come up, and down what needs to come down. My theory is that using GHB is somewhat like jumping a car. When the battery dies, you just need a kick. Then you are functioning again. I can definitely say without question, that using GHB changed and bettered my baseline tolerance to stress. It increased my cognitive functions too. I think cycling it could be key. However I used large doses to induce deep wave sleep.

Getting deep, restful sleep alone in itself is incredibly restorative. We all know PFS people have utter, shit sleep. All makes sense. Stuck in fight or flight mode, depleted neurosteroids which are responsible for calming oneself, and in addition, cortisol cannot be deactivated due to inhibited 5ar (THDOC).

Yes, I agree. I have tried a million GABA type drugs when I first crashed esepcially when I had bad sleep issues (Xanax, Ambien, phenibut etc) and every single one of them I would get a horrible rebound effect the day (even after one dose).

I think the fact that GHB is natural to the body and dosing plays a much bigger role. On top of that it was studies as an anti Alzheimer type drug too versus say benzos increasing the chances of mental diseases so it does have some merit. I agree it is not an overnight cure, but could have potential in the long run. I wonder what would happen if you eats ton of food that contains GHB, lol doesn't passion fruit contain it?

5a-dhp which also weakly increases neusteroids gave me some luck initially but then just stopped working altogether even until this day.