Anyone understand androgens well?

Has anyone experienced “Reflex-Hyperandrogenicity” before? If so, has there been a recovery.

From what I understand, there is an up regulation in androgen receptors. So does that mean I need to lower my androgen receptors like DHT and T to be back where I was? Also, had my T levels checked and I am at 520 (350-1100 scale). Lower than the normal 25 year old. So little confused. If anyone got any info or knowledge on this would greatly appreciate.

https://newhair.com/baldingblog/propecia-and-reflex-hyperandrogenicity/

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We don’t know the pathophysiology of PFS. Dr. Rassman posts on a Reddit about PFS or hair loss. I find that he is sympathetic to the reality of PFS, but seems to talk about unknown areas as if he has the answers. He doesn’t have the answer, and no doctor has the answer.

It’s also concerning that he quotes an explanation from HairLossHelp (which now redirects back to Rassman’s site), and this does not appear to be a real medical term. It is vague. Maybe it means “immediately increased sensitivity to androgens.” But then what? It’s just a multi-syllabic term that is not really describing or explaining anything new.

There has been plenty of talk here, and some in the research literature, about dysregulation of androgen receptors (maybe upregulation, maybe downregulation). But that’s just a suggestion of where to look, not a description of what’s happening.

If you want to know the state of the science, I would stick to PubMed.gov. If you search “reflex hyperandrogenicity” on pubmed, none of the three results use this term, and none are relevant. So this is apparently a made-up term that has no use for PFS patients.

There is also a bibliography of published research on adverse effects of finasteride here: https://finasteride.network

I believe, forum users around have given it the name ‘‘Reflex-Hyperandogenicity’’. It has use for PFS patients, as I not only deal with this issue, but also ED, EJ, shrinkage, etc. I have a feeling it is all correlated, for my case especially.

@anon22245532

I am definitely not questioning what your experience is, or saying that there is or isn’t dysregulation of androgen receptors (I think it is worth investigating).

What I am saying is that anyone can make up a term, but if it is vague, not recognized by medicine, and/or does not add new knowledge or explanation (and possibly even confuses matters) then I avoid such terms.

There have been members here experience what appears to be “reflex hyperandrogenicity”

https://forum.propeciahelp.com/search?q=reflex

Also evidence that this may occur:

ya, I don’t know what to call the symptoms I am having in that department so that’s why going with what other users have termed it. FIN causes many rare side-effects. But anywho, if you got any info or search ideas how to approach this, would be cool @anon22245532

Yes, done some research under the forum here, but no protocol, or reports of recoveries from it :confused: if you do see one please let me know!

And thanks for posting the article, very interesting

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Importantly, this paper about a “rebound” effect is strictly limited to hair follicles and hair growth parameters. It does not discuss anything related to adverse effects outside of hair growth. There’s no mention of androgens or receptors.

From the Conclusion:

The possibility of a “rebound effect” and hair follicle becoming “drug‐dependent” could not be fully appreciated with previous technologies used in trial protocols. There is some indication however that after 1 year off‐drug and re‐entering “on‐drug” period after drug interruption prevent complete regrowth of hair. Suggestive elements along facts unravelled during this pharmacodynamic study seem to support this “rebound phenomenon” and “drug dependency” hypothesis.

Regarding the use of the term “reflex hyperandrogenicity”: we can find lots of terms on the web or the forum that may or may not be useful, true or valid. For example I can search “flat earth” or “narnia” on the web and get many results, even though these are false or fictional.

If I search the forum for “keto”, “meditation” or “asparagus,” I get more than 50 results in each case. Does that mean each of these is relevant to PFS? I don’t think it’s been shown one way or the other.

I am open to any term, but my questions would be:

  • What is the definition or hypothesis?
  • What is the factual basis or rationale?
  • How could it be verified?

I understand we’re not doing scientific research here on the forum, but if we’re talking hypotheses then I think these guidelines could help.

Have you seen this at the PFS Foundation site? I think it might be too broad, and some of the symptoms seem more common than others, but in case you haven’t seen it:

About PFS
https://www.pfsfoundation.org/about-pfs-post-finasteride-syndrome/

And here are excerpts from two recent articles that give a snapshot of what is known and what isn’t (yet).


Melcangi RC, Casarini L, Marino M, et al. Altered methylation pattern of the SRD5A2 gene in the cerebrospinal fluid of post-finasteride patients: a pilot study. Endocr Connect. 2019;8(8):1118-1125. doi:10.1530/EC-19-0199 | PubMed

Context: Post-finasteride syndrome (PFS) occurs in patients with androgenic alopecia after suspension of the finasteride treatment, leading to a large variety of persistent side effects. Despite the severity of the clinical picture, the mechanism underlying the PFS symptoms onset and persistence is still unclear


Traish AM. Post-finasteride syndrome: a surmountable challenge for clinicians. Fertility and Sterility. 2020 Jan;113(1):21-50. doi:10.1016/j.fertnstert.2019.11.030 | PubMed

Post-finasteride syndrome (PFS) is a constellation of serious adverse side effects manifested in clinical symptoms that develop and persist in patients during and/or after discontinuing finasteride treatment in men with pattern hair loss (androgenetic alopecia) or benign prostatic hyperplasia. These serious adverse side effects include persistent or irreversible sexual, neurological, physical and mental side effects. To date, there are no evidence-based effective treatments for PFS. Although increasing number of men report persistent side effects, the medical community has yet to recognize this syndrome nor are there any specific measures to address this serious and debilitating symptoms. Here we evaluate the scientific and clinical evidence in the contemporary medical literature to address the very fundamental question: Is PFS a real clinical condition caused by finasteride use or are the reported symptoms only incidentally associated with but not caused by finasteride use? One key indisputable clinical evidence noted in all reported studies with finasteride and dutasteride was that use of these drugs is associated with development of sexual dysfunction, which may persist in a subset of men, irrespective of age, drug dose or duration of study. Also, increased depression, anxiety and suicidal ideation in a subset of men treated with these drugs were commonly reported in a number of studies. It is important to note that many clinical studies suffer from incomplete or inadequate assessment of adverse events and often limited or inaccurate data reporting regarding harm. Based on the existing body of evidence in the contemporary clinical literature, the author believes that finasteride and dutasteride induce a constellation of persistent sexual, neurological and physical adverse side effects, in a subset of men. These constellations of symptoms constitute the basis for PFS in individuals predisposed to epigenetic susceptibility. Indeed, delineating the pathophysiological mechanisms underlying PFS will be of paramount importance to the understanding of this syndrome and to development of potential novel therapeutic modalities.

Regarding Reflex Hyper. I am not sure what you are trying to get at, sounds like saying what i am experiencing isn’t real from no factual data? All im doing is sharing my experience and hoping anyone has had success with recovery.
Anyways @anon22245532 , im not sure about factual reserach, but would really like to understand exactly whats going on

It’s common my hair was like Elivis, thick black and straight…With generic it went haywire half shed out, got really kinky and dry…Then the right thin spot got bigger quickly…After stopping in a few months it took another ther huge hit…

So I started brand name and got pfs the second time…Now it still looks like shit but the thin spot grew back and never re balded…

Thanks for sharing. and dude, i feel most people I read about experiencing Hyper-Reflex all had thick Elvis hair (which probably meant we already had low DHT when starting FIN).

So hair thinned out from all areas on the head right? Did you notice an increase in acne, libido, weight gain?

Sorry for all the questions: but after your hair eventually stopped shedding and you recovered some of the lost thinned out hairs? If so, how long did that take?

Nope it never stops…Hetero, dr reddy is notorious for this lots of folks were switched to this from brand name and had to switch back to propecia…

Yeah u need to read my posts folks I switched to propecia and got fucked beyond words…Horrible physical side effects I gained over 100lbs.

Please read my earlier post. I said that I am not questioning your experience. I also explained my concern about the term, “reflex hyperandrogenicity.”

Then I provided some info from recent articles which discuss what is known and what isn’t known from a peer-reviewed research perspective.

These were meant to answer your two concerns. I would like to see more research just as much as anyone else, but this is what we have.

More papers are here: https://finasteride.network

I don’t think androgenetic alopecia is determined by having high or low DHT. There are bodybuilders without genetic male pattern baldness who “blast and cruise” year round on supraphysiological levels of testosterone and other steroids and maintain their hair line and density while another guy on the same steroids will bald even faster than they were genetically determined to.

Sorry to hear that man

Hey dude I too got reflex hyper. How is your sympthoms now?

Still shedding

How about now? Any drop in symptoms?