I am contacting a researcher who is interested in the association of hormomal withdrawl and it's effects on the brain, mitochondria and metabolics

Dear fellow sufferers and science enthusiasts,

I coincidentally found a researcher whose primary research interest is the effects of hormonal withdrawal and its effects on the brain, mitochondria, metabolism.

“My primary research interest is to assess the impact of hormonal withdraw on the brain during life span, and how this might be a risk factor for development of mitochondrial-related diseases. Reduced hormonal levels in the brain are associated with a dysregulation in lipid metabolism, and this pathophysiology may account for an increased neuroimmune response in the brain of Alzheimer’s and Parkinson’s patients, and this response is dependent on the sex. More importantly, sex differences on glial cells have been also observed, and these cells might be as important as neurons for brain homeostasis. My interests also include addressing neuroprotection by androgens/estrogens in brain diseases”

As far as I can see he was so far looking mostly into post-menopausal changes. PFS, PSSD could be a good model for a male equivalent.
When approaching this scientist I would like to add some PFS, PSSD related studies on how changes in neurosteroids and sex hormones may change the brain, mitochondria, lead to metabolic diseases and brain disorders.

If you have any study references that would be of interest to him, please feel free to add them here, so that I can integrate them.

@anon22245532 @axolotl @Dubya_B @slavoushka @Sibelio @silentpain89 @whathaveidone4669 @Northern_Star


Axolotl’s recently-posted PFS literature review contains a section of mitochondrial discussion with citations:

There are several sections throughout containing discussion of metabolic effects of androgens.

Our blog page on post-Lupron/post-GnRHa cites a few studies regarding the effects of sex-hormone deprivation on mitochondrial function, including a good one from Prof. Traish.

A few studies that describe androgens and other steroids in relation to glial cells:






  1. https://onlinelibrary.wiley.com/doi/full/10.1111/cns.12781 - inhibition of brain dopaminergic system by fin (rat model)

  2. https://www.karger.com/Article/Abstract/442982 - Effects of Subchronic Finasteride Treatment and Withdrawal on Neuroactive Steroid Levels and Their Receptors in the Male Rat Brain.

  3. https://www.sciencedirect.com/science/article/abs/pii/S0028390811000165?via%3Dihub - Isolation rearing-induced reduction of brain 5α-reductase expression: relevance to dopaminergic impairments.

  4. https://www.ncbi.nlm.nih.gov/pubmed/21361868 - Steroid 5α-reductase as a novel therapeutic target for schizophrenia and other neuropsychiatric disorders.

  5. https://www.sciencedirect.com/science/article/pii/S0091302220300273?via%3Dihub

  • Physiopathological role of the enzymatic complex 5α-reductase and 3α/β-hydroxysteroid oxidoreductase in the generation of progesterone and testosterone neuroactive metabolites
  1. https://www.sciencedirect.com/science/article/abs/pii/S0960076017301024?via%3Dihub - Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients
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Would be nice if you passed along his info to the Foundation. Perhaps they can work together

Hey @PastUser, welcome back!

Could you please find some time to participate in our survey. Would be great to have data from some veterans :wink:

Post-Drug Syndrome Survey FAQ. Survey NOW LIVE - Please Participate

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This one is one of the scarriest ones:

Treatment of male rats with finasteride, an inhibitor of 5alpha-reductase enzyme, induces long-lasting effects on depressive-like behavior, hippocampal neurogenesis, neuroinflammation and gut microbiota composition

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So a talked to him. He is a friend of melcangi and has an indepth knowledge about the changes of mitochondria after hormone withdrawl. He thinks the changes in the lipid profile, glucose metabolism, the course of the illness and the differences in symptoms between young and old people exposed to finasteride may point towards mitochondrial changes through finasteride. If we want to do any research into that area he will be open to do that.

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We don’t have unlimited resources as a community, so don’t you think it would be more prudent to continue focusing resources on the hypothesis (overexpressed AR) that has a study to back it?

Melcangi for example has done research into PFS with the assumption that a lack of neurosteroids is the cause of our condition. This does not appear to be the case because there are numerous symptoms in some patients (such as penile tissue loss), that cannot be explained by a deficit in neurosteroids. While I appreciate all the research he has done into our condition that has allowed us to establish that some things aren’t functioning as they should in our bodies, this has not given us anymore insight into what specifically (on a genetic/epigenetic level) is driving our condition. Figuring out what’s driving this at the root is our best bet moving forward.


Yes exactly, that’s why we have to put all puzzle pieces together and find a theory that explains everything. Melcangi’s work brought new insight that shouldn’t be ignored, but rather be seen as one of the puzzle pieces that needs to be explained. I think AR research is imptortant allthough it seems to me that AR overexpression is not cause, but cosenquence. I don’t think that is the right time for a study that looks at mitochondrial changes, but that is something we should keep in mind and that we can all check ourselves. If we have private data from a handful of people who analyzed their mitochondrial function, we know whether it is worth or not to pursue that path or not in the future


Are there any relatively simple, cost effective tests to look at mitochondrial function further?


What is troublesome is that it sounds as if he ranks changes in physiology after hormone withdrawal in possibly asymptomatic organisms as being equivalent to PFS. Does he have any interest in actual symptomatic post-drug patients?

It would be great if he did.

there is mitochondrial dysfunction of the AR and, in some people, 5AR2 which is what is causing our issues


Yes, I think he is open towards working with us as. He is a neuroscientist. So far he worked mostly with postmenopausal women. I think he is good in what he is doing. He knows about finasteride and PFS but is not an expert in that field. In case reaseach should one day go more towards the questions what role the mitochondria play in this disease, he seems to be a good adress.

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What do you mean by mitochondrial dysfunction on the AR?

I will talk to him what preclinical data will require. He says we could put together with hom a proposal to access preclinical data.

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The researcher may already know about this study that links low T, insulin sensitivity and impaired mitochondrial function.

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Yes, that is probably why he asked me a lot whether the lipid profile like triglycerides is altered in PFS.

Were you guys able to make any headway bro? @simonsayss

He is open for a clinical study.
Would costs around 10k irish pounds to get data from 10 patients + control groups. He says that would be enough to see whether that path is worth pursuing. Invitro and animal studies would be achievable with less than 10k.

Although cheap mitochondrial dysfunction probably shouldn’t be the first thing we should look at. I first want to learn more about the possible association between mitochondrial damage and PFS. But of course, I will stay in touch.

I will attach some studies, that he send me. Maybe you also want to learn more about the topic.

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