Have any of you tested Allopregnanolone or 5 alpha reductase?

  1. I am wondering if 5 alpha reductase stays low after you stop with propecia. I couldn’t find if there are any tests done. This would be really good to know so we know if side effects we are getting are from screwing 5 alpha reductase or something else. I am surprised there are no articles or posts about post propecia 5 alpha reductase levels. Or maybe I just didn’t find it?

  2. Has anybody tested allopregnanolone levels? Allopregnanolone is neuro steroid that is lowered by the highest degree, after 4 months of propecia it is lowered for 600%. But these are lowering levels while still on propecia, I couldn’t find any article how are levels after propecia is discontinued. Also very surprised, this should be one of the first thing to check I guess. Unfortunately I couldn’t find any lab in my country that could test this, I am looking now for any lab within Europe.

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There is no reason to think that 5 alpha reductase is at the root of this problem. Any problem with it, would be a downstream effect. Otherwise we would profit from DHT supplementation. Unfortunately, we typically don’t and many even become worse.

There are no custom Allo tests and no established reference ranges, as far as I know. It’s also not necessary to test this. In this study, neurosteroid levels of “PFS” patients was compared to healthy controls showing signficant alterations:

Thank you for that publication. But why do you think there is no reason to think that 5 alpha reductase it at the root of this problem? The study you published showed decreased levels of DHT and neuroactive steroids which is exact result of 5 alpha reductase blockage, so it seems 5 alpha reductase remains inhibited also after finasteride discontinuation.

You also wrote: “Otherwise we would profit from DHT supplementation.”. Because DHT is not the only hormone impacted by 5 alpha reductase, there are many others. And by fixing just one hormone you don’t resolve others which are as much important. Also by adding DHT you need to closely monitor also T. Some people get much better by adding DHT anyway.

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Hey @newbie, welcome back.

I can’t help with your question but could you fill out a member story? As you’ve been dealing with this so long, it would be helpful to you and everyone here for you to fill out our symptom survey too.

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Any effect on neurosteroids is more likely a downstream effect of improper induction of 3α-HSD which is dependent on AR gene Expression.

A deficiency in 5 alpha reductase does not explain key symptoms like muscle wastage. And deficiency in 5 alpha reductase would result in low DHT, which would normally mean that DHT supplementation would be beneficial with regard to some symptoms. But many of us don’t feel anything or get even worse when supplementing DHT, which points towards some kind of “insensitivity” to androgens.

If you are interested in the science of all this, please read this: https://www.google.de/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&cad=rja&uact=8&ved=2ahUKEwietOur0NrjAhWDi1wKHTZnCCMQFjAAegQIAhAC&url=https%3A%2F%2Fpost-finasterid-syndrom.de%2Fwp-content%2Fuploads%2F2017%2F03%2FDas-5ARI-Absetzsyndrom.pdf&usg=AOvVaw2Li9E_ei-B4YlROjDuCsRV

It’s nine years old and some parts are a bit dated, but it still explains quite well, what we here think is probably wrong with us. Please also read these two papers:

  1. Endocrine Disruptors: The bigger picture
  2. Post-finasteride Syndrome: A Review of Current Literature (Mohit Khera, Baylor College)
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Ha, I just realized he had not posted in eight years. :smiley:

@newbie Welcome back. Your username is not appropriate anymore :wink:. Please listen to Greek and take the survey.

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I am wondering whether lack of response to DHT is not in fact as a result of an adaptation of the body to shut down HPTA axis - i.e. reduce Testosterone as a way of compensating for the increased DHT. Evidence for this may be found when people initially react positively to DHT but then the effect quickly wears off.

Has anyone ever tried supplementing both DHT and a combination of other hormones (whatever those need to be - T, LH, etc?) in order to oppose any such adaptation so as to force the adaptation to happen at the level of the AR?

I just literary wrote the same thing in two different threads, sorry.

P.S. This needs to be tested. We need to produce some PFS mice STAT! Funding an animal study, anyone? :slight_smile:

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Interesting thought, @Sibelio.