Ozeph, do I understand correctly that you intend to take Etifoxine to increase ALLO and Sulforaphane to increase 3a-HSD?
Secondarily, I see that Sulforaphane increases 3a-HSD in the liver, but don’t we need to increase it in the brain instead?
I may try either Etifoxine or Emapunil if it’s available in Thailand, which I doubt. Mirtazapine is also increasing some types of 3A-HSD. But I won’t try it either.
My first choice is to go with a natural supplement that can easily be bought. My regimen is only about diet, exercise and natural supplements. No drugs. I believe drugs are unnatural and harm the body. Most cause liver damage. Maybe Sulforaphane is the same as it may cause liver damage, i don’t know, but at least I know I can get it and try something.
Plus Sulforaphane is also an alternative hair loss treatment that works by increasing 3a-HSD which deactivates DHT and so prevent hair loss. So it’s like going back to what started it all, with a different approach. It’s possible that by decreasing active DHT, the AR won’t be over-expressed and the symptoms of over-expressed AR will decrease. I don’t know.
3a-HSD is the enzyme that transform progesterone into ALLO. I already take some anti-aromatase (Betaine and Choline) to prevent progesterone to be transformed into estrogen and improve my estrogen / testosterone ratio. So i’ll be making the assumption that Sulforaphane will increase 3a-HSD which in turn will increase progesterone transformation into ALLO and decrease DHT. I expect overall changes in the hormones / enzymes / neurotransmitters / neurosteroids all over the body.
As 3a-HSD, DHT and ARs are at the base of many imbalances expressed in pfs symptoms, obviously taking too much Sulforaphane is dangerous. I’ll be very cautious. But I also believe I’ll be starting on the right side of the imbalance: by increasing what is too low and decreasing what is too high. I think the danger lies in overreaching and creating an imbalance on the other side: too much 3a-HSD, too little DHT and messing up the AR again. So taking it slowly and reducing or stopping at first sign of trouble seems to be a reasonable approach.
Sulforaphane is fat based. All fat ends up in the liver, this is why it’s where they test it (in rats anyway as they don’t see a problem in cutting open a rat and taking out it’s liver to check 3a-HSD levels. At some point in the future, if we continue to evolve (which is not that obvious), we’ll see these psychopath scientists as the German doctors who were experimenting on Jews during WW2)
But the point is, rats who were given Sulforaphane did have increased hair growth due to increased 3a-HSD reducing DHT. That suggest that the 3a-HSD had the opportunity to interact with DHT.
There is strong evidence that Sulforaphane promote cognitive functions whereas pfs decreases cognitive functions. If this is so, than Sulforaphane does have an effect on the brain. and may be an antidote to some of the pfs damage.
This is all speculation until tested, which i intend to do in the next month or two. I’m not saying I know it all. I’m like you guys, I’m sick, nobody can help so I’m taking it on myself to find something that can make me feel better.
we can’t get a break from a single thing.
etifoxine might give liver damage
sulforaphane might damage us like finasteride
shit sucks balls lol
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@Ozeph is that hairloss drug you talked about increasing 3a the same as sulforaphane? or is it a different thing that wont mess with our 5a?
There was some guy on this forum claiming recovery from sulforaphane: https://forum.propeciahelp.com/u/NYscientist
…Can’t remember which thread he shared his recovery anecdote in. I tried the same product (Broccoprotect) and all it did was give me a headache, maybe slightly worse mood.
Another had worsening of PFS symptoms with a high-sulfurophane product: A not so crazy idea: reduce DHT binding to AR?
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There is an anti hair loss drug being tested, which raises the 3a-HSD and they actually try to mimic Sulforaphane in a molecule that would act like it. You see, Sulforaphane is created by nature in broccoli sprouts. So pharmaceuticals can’t patent it. So when this happens, they try to construct a similar molecule they can patent. It’s all about money and that’s where the problem lies. If they could produce 3a-HSD, they wouldn’t as they could not get a patent. They have to create something artificial the body will have problem to deal with, so they can patent it and make money.
But back to the topic. 3a-HSD and 5ar are mutual antagonist, like many hormones and enzymes are in our body. This is done so the body can have control and checks on the production of these things.
I believe that by inhibiting the 5ar for a period of time, the body reinforced the 5ar producing mechanism to balance the presence of fin. When we stop fin, 5ar is not inhibited anymore and its production mechanism is still boosted up. We may end up producing more 5ar than we should, which shuts down 3a-HSD as well as overwhelm the Androgen Receptors. The body reacts to the overwhelmed AR with an auto-immune response (by methylating some gene sequences in the AR) but as far as I can tell, does not react to the absence of 3-HSD, which is used in all kinds of transformations all over the body, including changing progesterone into ALLO.
So what I’ll try to test, is introducing Sulforaphane to increase 3a-HSD (depending where I look, Sulforaphane may merely enhance the action of existing 3a-HSD without increasing its volume. Other sources mention a volume increase.)
This should have many effects. It should enable the body to start transforming stuff for which 3a-HSD is a catalyst, like ALLO, and many symptoms related to the lack of 3a-HSD might diminish. It should also lower 5ar which will decrease DHT. At first, the Androgen Receptors should be set too low as they were initially tuned down by the auto immune response. So their response to 5ar and DHT will be lower. I expect possibly increased sexual symptoms. However, lower 5ar also means more testosterone as less is transformed into DHT (normally 10% of testosterone goes into DHT) so the AR response to testosterone will be stronger (so maybe no increased in sexual symptoms). Of course, I also expect an increased production of ALLO and it’s sister neurosteroid, a better regulation of the GABA complex and the elimination of insomnia, anhedonia and anxiety (and maybe other symptoms like dry skin, sex drive and sensitivity) which is the objective of the experiment.
I believe if the dose of Sulporaphane is initially low, and then slowly increased over a sufficiently long period of time, it will give time for the 5ar and the AR to adapt to the new levels of hormones and enzymes. 3a-HSD is the natural antagonist of 5ar. Both are produced by the body and the body is made to deal with that pair. Fin is not. The body is not made to deal with the presence of fin in the balance of 5ar and 3a-HSD and that’s why taking fin damages 3a-HSD even more than it does 5ar. It looks like fin inhibits both as I started having severe insomnia while still on fin.
As I said before, taking Sulforaphane is an action that mingles in the same configuration panel as fin did. So yes, it can make us worst. But if it’s that configuration panel that is messed up, this is where an action needs to be taken to re-balance things.
I think a very slow approach is advised, to give time for the body to adapt. I also believe this could be instrumental in helping those whose AR have completely been shut down, but will not cure this aspect of pfs. If some specific gene sequences of the AR have been methylated to be neutralized by an auto immune response, when the AR cells reproduce, they may reproduce the methylated gene along with the methyl molecule attached to it. However, if new AR are created (instead of old ones reproducing) and the condition that caused the genes to be methylated is no longer present, it is possible the new ones won’t be methylated. 5-azacytidine can also be used to de-methylate genes (but I won’t get there now, this is beyond me)
All of this is very speculative. Here’s what I think: If you had a severe reactions to pfs and you’re plagued with multiple symptoms, especially the shrinkage of reproductive organs suggesting a complete shut down of the AR, don’t try this. As a matter of fact, I suggest nobody tries this. there’s no point risking more than one person to test this thing.
I will try it because I have very little sexual, physical and neurological symptoms. What I have is a lack of calming neurosteroids (like Allopregnanolone (Also called 3a,5a-THP) and tetrahydrodeoxycorticosterone (also called 5a-THDOC)) which are GABAergic regulators. So my remaining symptoms have to do with the GABA (A) receptors and that’s where the drug I’m taking (Clonazepam) is acting. This is why I can’t take Taurine or GABA to try and fix it. ALLO is the main GABA complex regulator. Taurine to a lesser degree, but Clonazepam gets in the way. I will obviously have to decrease Clonazepam as I increase Sulforaphane so that I don’t get both ALLO and Clonazepam over-acting on my GABA (A) receptors.
I have insomnia, I wake up frequently, I have occasional mild anxiety and the only thing I have to counter the 3 stress hormones (Cortisol, Adrenaline and Nor-Adrenaline) which are normally counter balanced by the two calming neurosteroid (ALLO and 5a-THDOC) is the confidence and calm brought by Serotonin and the good mood brought by Dopamine. I still have mild anhedonia and lower than normal sex drive, although it’s not at zero. Dry skin is very slowly disappearing and at this point is not bothering me.
So let me give this a shot and I will keep you posted. Then if I just mess myself up, it will avoid you unnecessary complications. If I get better, we will have one more element to add to the puzzle and my regimen could be a possible cure or at least be helpful to people having had a similar initial response to pfs to what I had.
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Good luck soldier, may you see victory.
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Thank you for your efforts ozeph, this is an angle I have not seen approached on this forum
I was reading another thread and one guy mentions having tried etifoxine Deciphering progesterone and post translational mechanisms.
Very interesting.
Sage is now conducting clinical trials with the oral formulation of Allopregnanolone.
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Now I understand why some sources mention 5-ar as the enzyme that produces ALLO, while some other mention 3a-HSD: it takes both !
https://www.sciencedirect.com/topics/neuroscience/allopregnanolone
I have DHT therefore I have 5-ar. As I mentioned, 5-ar and 3a-HSD are mutual antagonist. So I’m probably missing 3a-HSD.
Anyway we’ll see soon enough
Ganaxolone is another one. It seems many Allopregnanolone boosting drugs are being developed.
Allopregnanolone is now available if you enroll in a clinical trial conducted by sage for 217.
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Good point. Are they only in the US? It would be great if a couple people from here could try it. Would save a couple years of anticipatory speculation.
Ganaxolone has been around since the 90s and yet still isn’t on market. I’m not holding my breath. Sage does seem like it might only be a couple years away. It would save us a lot of speculation about what role Allo has in our problems if someone could find a way to try it. I’d even go so far as to say that if Sage 217 doesn’t provide relief then Allo isn’t our problem.
I don’t think we have a single problem.
Leaky guts have to be fix as food intolerance becomes more acute, the guts flora has to be adjusted, the vagus nerve have to be addressed, the testosterone / estrogen ratio has to be kept in check, the thyroid functions too, Many appears to have low serotonin and low dopamine levels, many have low testosterone / DHT levels, vitamin D is definitely something to address for lots of us.
I’ve always been saying a global approach needs to be taken. As an example, I stopped taking protein shakes (once or twice a day) for a week, and it was hard to keep the exercise and just to stay on track. I re-introduced it and things are fine again. Protein shakes gives you all essential and a few non-essential amino acids. I think the body needs to have an abundance of amino acids, as well as saturated fat so that when it attempts to fix something, at least its got the ingredients to do so.
Sage 217 is fine. But better than a drug is the ability to produce our own ALLO. Most drugs that provide something we need make the body’s natural production mechanism lazy. On the long run, we just become addicted to the drug. (Again I would point out this is not a problem for pharmaceuticals)
I would have to look at it again more carefully but I think part of the idea behind Sage and allo analogues in general is that they do not influence body’s own production. Just mentioning my rough recollection of this in case anyone wants to look into it more deeply. I seem to recall that that is the basic problem with exogenous allopregnanolone, which the analogs are designed to address.
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