Wambier & Goren (2020). SARS-COV-2 infection is likely to be androgen mediated

Article finds those with higher androgen levels are likely to be more susceptible to SARS-COV-2 viruses.

Wambier CG, Goren A. SARS-COV-2 infection is likely to be androgen mediated [published online ahead of print, 2020 Apr 10]. J Am Acad Dermatol . 2020;S0190-9622(20)30608-3. doi:10.1016/j.jaad.2020.04.032
PubMed: http://pubmed.ncbi.nlm.nih.gov/32283245/

Pre-print: https://www.jaad.org/article/S0190-9622(20)30608-3/pdf


In N.Y.C., the Coronavirus Is Killing Men at Twice the Rate of Women

More men also are infected than women, and they are hospitalized more frequently, new data show. A similar pattern was seen in China.

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@Northern_Star @Dubya_B @axolotl

I think PFS may lower the succebility towards COVID or the rate of bad cases (my flatmate had COVID for 3 weeks and it seems I didn’t get infected or didn’t show symptoms).

Couldn’t we piggypack COVID and it’s relation to AR to generate awareness and interest of researchers for PFS. Of course this wouldn’t be our end target, but any free research and awareness may promote more investigation into PFS.

The androgen receptor (AR) plays a critical role in the innate immune response.

It makes sense that if our AR are not making vital immune end products then we are potentially less likely to suffer from some of the cytokine storm.

There are of course other variables involved that we are likely to be deficient in…

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Acknowledging the importance of androgens during COVID19 pandemic may offer another targeted therapy for trials, with androgen suppression to reduce host vulnerability when infection risk is high.

This could be potentially disastrous if tried on a PFS patient.


Suppression of androgens is what got us there, so it’s very risky I think

Yup. I took ivermectin (anti-parasitic drug) for a parasite I had and it made me worse. Come to find out, it can actually suppress free T levels drastically. Hoping to improve again…

I think one thing working in our favor is that our condition is bloody fascinating. It’s systemic consequences mean that understanding our condition will give insights into how androgenic signaling works in the human body with implications for various diseases, ageing and, of course, also immune response. It’s certainly an angle that we should push and which is highlighted in the Post-Androgen Deprivation Syndrome literature review.

That said, what do you suggest how to spin it into something concrete? There is a race going on to find treatments/vaccines for Covid-19 and I don’t think scientists will make a detour to understand our condition first with the hope to get insights relevant to Covid-19.


Sure, I don’t think we can generate a COVID-spin off research that will solve PFS. But I think we may pitch our syndrome to warmbier and collect together with him epidemiological data on how strong COVID affects the PFS community. It would be data that is relatively easy to generate and if published well it could draw more interest from the research community. PFS is relatively unknown in the research community. Awareness and interest among researchers will benefit us in the long run.

His Co-Author said in a similar article: “To test this hypothesis, it would be informative to study the epidemiology of COVID‐19 patients that are predisposed to either lower or higher AR expression, such as, males suffering from androgenetic alopecia, benign prostatic hyperplasia, or women suffering from polycystic ovary syndrome.”
So this means there is an interest in epidemiological studies of diseases with changes in AR expression and response.

Another paper of them:

“What does androgenetic alopecia have to do with COVID‐19? An insight into a potential new therapy”

We shouldn’t argue against finasteride if it can save life or if it could be used within intensive care. Every study on finasteride can also help us.


I noticed Accutane/isotretinoin was also on this list, along with a few other drugs that have led to people becoming members here:

Other potential drugs that could be studied include: cyproterone acetate, megestrol acetate, chlormadinone acetate, spironolactone, medrogestone, oxendolone, osaterone, bifluranol acetate, flutamide, bicalutamide, nilutamide, topilutamide, enzalutamide, apalutamide, dienogest, drospirenone, medrogestone, nomegestrol acetate, promegestone, trimegestone, ketoconazole, abiraterone acetate, seviteronel, aminoglutethimide, dutasteride, epristeride, alfaestradiol, and isotretinoin. Taken together, the evidence warrants further studies to elucidate the role (if any) of the AR on the severity of COVID‐19 infection.

A potential risk with Accutane is that its major active metabolite (retinoic acid) was found to increase ACE2 in specific organs in a rat study and Accutane appears to inhibit chemotaxis of immune cells by up to 98%. Also a trend of studies finding that retinoids decrease the Th1/Th2 (intracellular vs. extracellular attack) balance of immune response.

Yes, interesting. Probably when listing they had in mind that it may modulate AR expression or androgene levels?

Well, it makes complete sense as to why - for the same reason they are suggesting them in line with their theory. These drugs are all antiandrogenic by various mechanisms:

Image taken from the monograph by awor and I, Post-Finasteride Syndrome as an Epigenetic Post-Androgen Deprivation Syndrome, in which we outline the significant antiandrogenic effects of the substances bringing users here:


While this large range of pharmaceutical and natural substances may seem broad and mechanistically distinct, the notable commonality is dramatic antiandrogenic endocrine disruption. Any treatments targeting the AR or suppressing androgens are known to have adverse effects on other critical physiological functions ​(Bourke et al., 2011)​. Narrow mechanistic perspectives often inform substance grouping for analysis of the risk of permanent male reproductive malformations and irreversible sexual disorders in the developing foetus. Through analysis of adverse outcome pathway networks, Kortenkamp illustrated that independent mechanistic effects from a very broad range of substances meet at nodal points in the network to result in common down-stream antiandrogenic effects and adverse outcomes. Kortenkamp suggested that – in addition to phthalates – substances capable of AR antagonism, cholesterol transporter down-regulation, and interruption or inhibition of steroidogenic or cholesterol synthesising enzymes should be included in an expanded consideration of substances capable of inducing male reproductive malformation. (Kortenkamp, 2020).


Yes, the study on CAG repeats is interesting. But it doesn’t explain why also people with short and medium repeats get PFS. Probably those with longer CA-repeats are the ones who get symptoms after just a few pills of Finasteride and yes, I think it turns them from hyperandrogenic to hyperandrogenic. But what is the mechanism behind?

As far as I know CAG repeats are hard-coded on the DNA and either you are born with it or not. Epigenetic changes or more like a cap that sits on top or like a locker that could be removed. So I think it is not possible to gain CAG repeats.

As CAG repeats are associated with hair loss and people with hair loss are more likely to use finasteride there may be a selection bias that CAG repeats are overrepresented among PFS patients when it actually not necessarily would be the case.

Still I think the there may be something to the AR although it does not explain changes in neurosteroids and 5AR2 methylation among many patients.

Don’t know if there are any studies on CAG and prostate cancer. Would make sense. It would also mean bold guys may have more or more aggressive prostate cancer.

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It would make sense if we have in the community a higher or lower succeptibility to viral infections associated with colds. Of course without diagnostics the forum members it will not indicate if the common cold was a viral or a bacterial infection. Therefore and for social desirability we may have some screwed data in the survey.

Still I think there is something to it that PFS patients in general may be less succptible to viral colds:
TMPRSS2 is one gene involved in the androgene signaling:

Official Symbol
TMPRSS2provided by HGNC
Official Full Name
transmembrane serine protease 2provided by HGNC
Primary source
See related
Ensembl:ENSG00000184012 MIM:602060
Gene type
protein coding
RefSeq status
Homo sapiens
Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo
Also known as
PP9284; PRSS10
This gene encodes a protein that belongs to the serine protease family. The encoded protein contains a type II transmembrane domain, a receptor class A domain, a scavenger receptor cysteine-rich domain and a protease domain. Serine proteases are known to be involved in many physiological and pathological processes. This gene was demonstrated to be up-regulated by androgenic hormones in prostate cancer cells and down-regulated in androgen-independent prostate cancer tissue. The protease domain of this protein is thought to be cleaved and secreted into cell media after autocleavage. This protein also facilitates entry of viruses into host cells by proteolytically cleaving and activating viral envelope glycoproteins. Viruses found to use this protein for cell entry include Influenza virus and the human coronaviruses HCoV-229E, MERS-CoV, SARS-CoV and SARS-CoV-2 (COVID-19 virus). Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Apr 2020]

Identification of TMPRSS2 as a Susceptibility Gene for Severe 2009 Pandemic A(H1N1) Influenza and A(H7N9) Influenza


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This is an older post but did your T levels go back up after taking Ivermectin, with the side effects from the vaccines I’m looking for alternatives.

Thank you!

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Just a note Ivermectin is horrible causes a bunch of side effects, I wouldn’t recommend anyone try this. I didn’t experience any side effects but I’ve read forums of others dealing with side effects from it