Very interesting. Could you please update?
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Interesting, I did not take Finasteride but the substance that I hired I block 3a-hydroxysteroid.
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Damn I totally forgot about this thread. Pretty much everything I tried in 2017 failed to do anything. I used peptides in 2018 (like BPC-157 and TB-500). BPC caused noticeable improvements in orgasm and affect but I’m pretty sure that was due to its indirect effect on dopamine. Semax helped a little cognitively. I still had watery ejaculate, sleep problems, and some anhedonia so its clear BPC didn’t address the core problem. All of these improvements failed to stick. None of the other peptides that I tried (Epitalon, TB, IGF, Melanotan II, PT-141) did anything.
Early this year I tried a month of saw palmetto extract and topical SP, which improved my sleep from about 4.5 hours at a time to averaging 6 hours, and improved my affect and libido quite a bit (still had orgasm issues and watery ejaculate though). So far I can say that directly antagonizing 5AR has helped me the most. I will probably cycle Fin at some point, but only because I’m assuming everything else is going to fail. I recognize the risks with using Fin again, even for only a few days, so don’t bother convincing me not to do it. I don’t consider this condition worth living with, and if I’m going to die anyway then I might as well throw everything and the kitchen sink at it.
As far as 3a-hydroxysteroid is concerned? I have no idea anymore. It is clear that our 3a-diol-g is low though, so I still think the problem is less from 5AR and more from things downstream of it. I think this finding is shared by people with Post-Accutane Syndrome.
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I also ordered 1000mg broccoli sprout extract to try.
5ar and 3a-HSD are mutual antagonists and both are needed to create ALLO which would improve sleep.
If your 5ar was too high, it would make your 3a-HSD too low and then you cannot produce ALLO.
That’s my theory for myself as my DHT levels are normal, which may mean normal 5ar but low 3a-HSD.
I’ll try to boost both together, 3a-HSD using sulforaphane and Glycine, and 5ar using creatine and Tribulus Terrestris. Of course, I’ll try boosting 3a-HSD first and will boost 5ar only if sleeps gets better and sexual symptoms worst.
Your sleep improvement using saw palmetto only encourages me to try and find something that boosts 3a-HSD without touching 5ar (other than by antagonizing it with 3a-HSD). Saw palmetto is a 5ar antagonist as we all know. It’s akin to fin and dunasteride. One effect inhibiting 5ar would do is to increase 3a-HSD.
It also shows it’s not your body’s blueprint that has changed, but only your hormone balance which has stabilized in an uncomfortable way.
I think @Burt_Kocain is right with his assessment that after the crash, there’s a fluctuation period and the first thing to address is to stabilize the body. I did this with a ketogenic / carnivore diet with lots of protein, saturated fat, and no carbs. I pretty soon added no carbs protein shake and when I stabilized, added some aminos like 5-HTP, Tyrosine and L-Dopa.
Now I’m stable, with insomnia well in-bedded in me. I will try Sulforaphane as it has shown to increase 3a-HSD without touching 5ar. It’s a broccoli sprout extract as I’m not too fond of drugs.
I will not take the dose indicated. those guys are maniacs. But I’ll have all the details on Amino Acid For neurological symptoms
@Burt_Kocain, you’re on a suicidal path. Just give me a few weeks and I’ll come up with results from boosting 3-a-HSD and lowering 5ar. I’ve written a regimen that, for me, eliminated all symptoms except insomnia. Brain fog, anhedonia, anxiety were the first to go.
Try some of those below, you can always try saw palmetto and finasteride later if you really must. (And I think you shouldn’t, it’s been done before: people get better, than worst and stay worst, but as you say it’s useless to try and change your mind)
Check those threads:
1- Success Stories Compilation
2-Please share results with a ketogenic or high fat intake diet
3-The use of Collagen (to fix the guts and inflammation caused by food)
4-Amino Acid For neurological symptoms
5-Amino Acids for Sexual Symptoms
6-Ozeph Regimen and Supplement
And the one that started it all: My regimen, and it's working
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Well, I don’t intend on trying Fin again for at least a month anyway. I thought I’d try a 2 week water fast and a month-long NoFap period just to see if they help at all. If you get positive results then of course I’ll try sulforaphane instead.
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EDIT: I cancelled my previous order of sulforaphane capsules in favor of buying broccoli sprouts, as there’s no evidence of bioavailable sulforaphane in capsule or pill form that I’ve seen. Apparently an enzyme called myrosinase that’s required to convert glucoraphanan into sulforaphane, which is released only by chewing the actual sprout.
I also came across a study comparing the levels of DHT in people eating alfalfa vs broccoli sprouts, and comparing both to baseline.
While the final results suggested broccoli sprouts didn’t significantly lower DHT, in the Discussion section the authors state "… we could not exclude the influence of alcohol. Based on our hypothesis, SFN induces 3α-HSDs in the liver, and these enzymes subsequently decompose DHT. These enzymes are also induced by alcohol via the Nrf2 pathway [20]; therefore, participants who habitually drink alcohol might have limited ability to induce these enzymes. In fact, plasma levels of DHT tended to decrease with broccoli sprouts intake, with the exception of participants who appeared to show alcohol-associated impacts on liver function (γ-GTP < 50 IU/L and ALP < 260 IU/L) (S1 Table)."
While Ozeph tries the liposomal form, which I’d still consider a worthwhile trial, I’ll buy a few boxes of broccoli sprouts and begin by eating the same amount (50 g) that the participants in this study did. At some point I intend to eat an entire container a day. What’s great about this is that I can buy these at the supermarket down the street, and I can begin tomorrow.
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sulfurophane boosts 3a without touching 5a?
can you give source on this? sounds interesting, and reduces the risks of trying it
I’ve read that it promotes the digestion of DHT without affecting 5ar.
Just for the record, early on I took brocomax, and didn’t see any improvement from it. Didn’t hurt me either tho
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Boosting 3a-HSD will reduce 5ar as they are mutual antagonists. This is how the body is meant to work. From what I understand, fin destroys both.
But I got Tribulus Terrestris and Creatine: to boost 5ar in case it drops too low.
To my knowledge, Sulforaphane does not directly touch 5ar, only through 3a-HSD.
Here’s something on the subject: https://www.ncbi.nlm.nih.gov/pubmed/26923074
More: https://perfecthairhealth.com/part-4-of-4-attacking-dht-by-increasing-dht-metabolism/
It does however affect DHT and serum testosterone, and the increased 3a-HSD does decrease 5ar.
So boosting androgens might be a good idea, while taking Sulforaphane. I’ll test that as well.
Here’s something on boosting androgen through alfalfa sprouts: https://www.oatext.com/daily-intake-of-alfalfa-sprouts-but-not-broccoli-sprouts-influence-plasma-levels-of-androgen-in-middle-aged-males.php
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Finasteride doesn’t have any appreciable affinity for 3a-HSD. It simply lowers 3a-reduced steroids by drastically reducing the substrates that 3a-HSD acts upon. Just want to clear this up.
Not quite sure what is meant by 3a-HSD and 5ar being mutual antagonists. They work synergistically when everything is in order. Could you please explain?
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That seems right, they work at different steps of the process.
I’ve read somewhere that they were mutual antagonists, I don’t have time to check my sources again today, too much work, but even if I’m wrong I’m right in assuming that I need to raise both 3a-HSD and 5ar to transform progesterone into ALLO.
I may have to do a progesterone blood test if I don’t get the results I expect.
But I have a question to you. If my DHT levels are normal, doesn’t that mean my 5ar is at least within range, even if on the lower side ?
Yes, probably overall 5ar activity is in range. There does appear to be a lack of 5-ar activity in the brain/CNS according to the Melcagni neurosteroid study though.
I think one of the original propositions made in the 5ari-withdrawal paper is that 3a-HSD is lowered due to lack of induction by AR signalling, without an appreciable deficiency of DHT. This was shown to be the case in one form of genetic androgen insensitivity syndrome. Those patients had normal DHT, but very low A-diol-G.
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Well, than, let’s hope Sulforaphane does the job the AR are not doing. We’ll know soon enough.
my hair stopped falling out and i have a full head of hair even after discontinuation. what’s likely the cause of that?
From what I’ve seen on this forum, there are people who seem to display symptoms of low androgens like yourself, and people who display symptoms of androgen hypersensitivity, like me. My hair loss, for example, returned to where it was before Fin. I still have oily skin (albeit not as much) and my facial and body hair are growing at the same rate they did before.
Your DHT levels may have just stayed low after discontinuation, possibly because your 5AR activity never returned to baseline. For me, I imagine my DHT levels and 5AR activity DID resume, BUT everything downstream got fried due to DHT overload. Of course, this is all theory. It may be possible that my 5AR and DHT are also fried but my hair just so happens to be more sensitive to DHT than yours. However, I respond very poorly to androgen-boosting activities and substances, and improved after using things that inhibit 5AR like zinc and saw palmetto. I imagine those things would probably make you feel worse.
Have you ever attempted activities or taken substances to increase T and DHT? If so, did they help you feel better? I remember there was one guy on this forum who recovered a while back by starting to work out all the time and taking things that boosted his androgens, but he was one of the guys that never had a formal crash - he just didn’t get back to baseline after stopping Fin. If you’re in the same boat as him, then I doubt 3a-HSD is problematic for you. You probably just need to increase your 5AR activity.
I’ve seen some theories on other forums that believe there may be a “Type 1” and “Type 2” PFS, basically the same as you mentioned. One type has high DHT, one has low. One responds well to TRT/DHT/etc. and the other gets worse. I don’t understand or remember all the details, but it sure does seem to line up with the stories I’ve seen on here and other places.