Suppressed 3a-hydroxysteroid may be the cause?

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.

the thing is, my DHT levels are normal, total T levels are low, and Free T levels are elevated out of range (extremely High)

I dont even know whats going on anymore LMAO. and yes I’ve tried to increase 5AR activity via CDSnuts protocol. I didn’t get a single benefit from it. I still take various herbs due to placebo of mild feelings of “well being” and “relaxation”. but its not like im super stressed out or anything unless i think about my diminished cognitive ability.

My lab results are the exact opposite. So strange.

Wow, that sounds really messed up. What are your E levels?

Any DHT that is formed within your muscles or finds its way into your muscles is quickly deactivated by an enzyme known as 3 alpha-hydroxysteroid reductase (3a-HSD)

I will have to increase 5ar by using Creatine and Tribulus Terrestris.

Hi, I’m new here, I’ve been reading for several days and I got to this thread. The information they share is very good, it is incredible how far finasteride can go. But there are things that leave me a little confused. I took only one pill, a single dose of finasteride, but I had my accident 2 weeks later. No libido and sexual impotence. then I got better through the days around February 15 and on, but this Monday I crashed again. I had a big drop in my libido and nothing of morning or night erections. In the afternoon or midday I get erections if I stimulate a lot with porn or mentally, but they are weak and the ejaculation is small. The truth is I am very afraid of what may happen to me, it generates a lot of uncertainty if I am going to crash again, or if I will improve. What do you think you should do? My blood tests are:

Normal T4L

Normal TSH

Prolactin 12.90 (reference 4 - 15.20)

Serum testosterone 4.15 (reference 2.18 - 9.06)

Free testosterone 425 (reference 198-619)

I would greatly appreciate your opinions or answers about it

Can you give me any recommendations or protocols to follow?

Thank you very much for the information and for the post that you do, I really want to move forward
@Ozeph @Burt_Kocain @ncsugrad thanks

Do you know who or where this recovery story is ? Pretty important because it sounds like me … no formal crash

moderate. Total T Levels are low but it could be way worse. I don’t have any low T symptoms like low energy, sexual sides, oranything, unless my neuro sides are impacted by them rather than the low neurosteroids.