Open Letter to the Advocates of 5AR2 Deficiency and Adiol-G

This post is to the address of the increasingly loud advocates of the 5AR2 deficiency theory and Adiol-G

This whole 5AR deficiency theory is really neat. After all, we all know that finasteride permanently inhibits the 5AR type 2 enzyme. It just got blown away and never came back. Real easy for everyone to understand, no complicated science involved here. We just need to come up with lots of good research about what symptoms occur when 5AR is inhibited and we’ve got the explanation to (almost) everything. With low Adiol-G we’ve even got a smoking gun. The fix to this mess is real easy too: all we need to do is to raise Adiol-G (??). This, of course, we can easily do by supplementing DHT. And anything that comes up that doesn’t fit the picture will just get ignored. Or even better, we’ll make up some pseudo-scientific reason why things are the way they are (we can, for example, blame estrogen or other hormones). After all, we don’t want to poop this party. It’s just too good to be true. One of the most puzzling medical phenomenons in the last decade got solved by a bunch of laymen armed with nothing more than google and an internet forum.

Do you guys seriously believe it’s that easy? Come on, get real.

Of particular note is that the most prominent voices of this theory have no personal experience whatsoever in supplementing androgens, particularly not DHT. Otherwise, they would have instantly realized from the reaction of their bodies, that their theory can impossibly be true. You actually don’t need to do any complicated testing to verify this, you can just plain and simply get yourself a tube of Andractim and rub it in. To those addressed: You can’t replace experience with google (or with testing for that matter). This whole thing reminds me a little of sex in early junior high school. Everybody is talking about it, everybody thinks they know what they are talking about, and practically nobody is actually doing it. Most guys back then thought they knew what sex was all about just by reading the magazines.

If 5ar were damaged, supplementing DHT should have a massive positive effect. This is not the case, not even in combination with TRT and aromatase inhibitors. To the 5AR deficiency crowd: Why are you ignoring this fact and making up excuses to justify this? My guess is because you are either in denial mode and/or haven’t tried any of this yourself.

All those who have read my posts may recall that I am dead set against supplementing DHT. But maybe it will take a couple of guys to try it out, to really understand what they’ve been talking about. Hopefully these guys will then truthfully report their experience back to the forum. Once they do that, I guarantee you that this 5AR deficiency theory will be buried for good. To facility this, I am prepared to give away my stock of Andractim DHT gel for free. Alternatively, I can provide you with a secure, cheap, legal and reliable source to buy the stuff mail order. Just send me a pm if you are so inclined. And to stay safe, don’t take it longer than a week (unless you get a really good reaction to it).

But why is it such a problem to get a little high on Adiol-G? The main issue I have with the increasingly loud 5AR deficiency voices in this place is that it is distracting my efforts to get a scientist interested in researching the most LIKELY TRUE cause of our problem, namely some form of androgen insensitivity (receptor, gene expression, whatever). The current state of this forum hurts my credibility when I’m talking with these people. Right now, if I point them to this place they’ll think we’re a bunch of nut cases. Everybody seems to have their own pet theory. Everybody is diagnosing everyone and too many people around here seem to think that they are world class endocrinologists.

To make things worse, the 5AR deficiency theory even makes sense at first sight. But from personal experience with supplementing DHT and reflecting the questions below, I know it’s way off the mark (no matter what Adiol-G says). Accordingly, I DO NOT want potential scientist candidates to get the wrong idea and start pursuing a dead end route. It would also be REAL helpful if we could get a little more focused, all get our act together and stand behind ONE theory. That would make it so much easier to get some funds together to pay for some initial science involvement and get things going. Just do the maths: Everytime a new guy hits this forum a collective voice advises him to get hundereds of dollars worth of blood testing done. This is COMPLETELY USELESS. Has blood testing ever uncovered and solved anyone’s problem around here? No? Why can’t we seem to learn in that respect? Imagine if this money would instead have been invested in a fund. We could easily have USD 500K worth of money together by now and you can be sure that we would all be a lot further than we are now.

Despite my slightly aggressive and sarcastic tone (sorry, but it seems like a normal one doesn’t seem to have any effect on you guys), I fully understand where you’re coming from because I’ve been there myself. When I first came to this forum, I initially used to think exactly like the 5AR deficiency guys: Finasteride killed my 5AR because that’s what it does. It’s a no-brainer. The logical consequence was to supplement DHT (Andractim, Proviron). So that’s what I did. I even considered Masteron. But the negative reaction I got from Proviron and Andractim eventually convinced me not to do it. Fair enough, but once everybody has been through their own 5AR deficiency loop it is now high time to move on.

For all those that are convinced that the root cause of our problem is 5AR type 2 deficiency, take a minute to think about following questions:

  1. Why does the problem start becoming really serious only after roughly 2-3 weeks OFF of finasteride? Finasteride has substantially cleared out of our system by then and could not have massively killed more 5AR at that point! So why did we crash only weeks later?

  2. Our body regenerates enzymes to replace what gets eliminated. If you believe that we have become permanently 5AR2 deficient, you are basically saying that the regeneration of 5AR2 enzyme has permanently failed. By what mechanism do you propose that finasteride is supposed to suppress the regeneration of this enzyme for good? Why would this permanent suppression only happen after years in some cases?

There is no documented scientific rationale behind a chemical like finasteride permanently inhibiting the reproduction of an enzyme. This is in sharp contrast with the receptor desensitization theory, which has scientific backing for the basic fact that:

sciencedirect.com/science?_o … 2ffe570e2f

Doesn’t this statement ring any bells?

  1. Finasteride inhibited DHT production by over 70% while on it. Why do many men, even in this forum, have no problem with this level of inhibition for years and then all of the sudden crash? Do you seriously think that even more 5AR gets inhibited while off the drug? Do you have any idea how low your Adiol-G must have been while on fin and you were still feeling great?

  2. Some guys are in this mess after taking only 3 pills. I only took around 30. If you believe that prostate shrinkage is a main mechanism behind this, do you really think it’s realistic that such a small number of pills shrunk our prostates beyond repair?

  3. How do you explain the variability in symptoms that many of us are experiencing if the assumption is that 5AR is permanently damaged?

  4. If our 5AR is presumably dead, why does supplementation of DHT either get no response or even makes things worse? No, it is NOT estrogen! Before you claim this, get your estrogens tested before and after supplementing DHT. Don’t fool yourself. And I am not talking about short term improvements, I am talking continuous supplementation at normal doses for at least 2 months.

  5. Why is everybody so sure that Adiol-G needs to be in the highest range in order to be able to get an errection? Finsucks asked this question once in the Adio-G thread. Since this thought doesn’t fit in the picture he just got ignored.

  6. Why are some guys going around this forum, relentlessly claiming that everyone’s Adiol-G tests are low, despite the fact that this is not true.

  • What about maracatu with his 76.6% of reference range result?
  • What about finsucks with his 51.6% of reference range result?

Why are some people ignoring this? Does repeating the same BS over and over again make it any more true?

  1. Why aren’t the Adiol-G figures in the “Database” correlated with Testosterone values (from same date)? Since Adiol-G is metabolized from DHT and DHT from Testosterone, don’t you think that this is relevant? A lot of guys around here seem to have low T. That means they should also have low DHT. How then can you expect to find high Adiol-G figures??

Low testosterone is likely to result in low Adiol-G. So getting all excited about low Adiol-G figures without matching testosterone values is useless. I posted about this too. It doesn’t fit, so it got ignored.

  1. If 5AR2 is supposed to be dead, how can you justify that jairus increased his Adiol-G by over 23% with testogel supplementation??

  2. Why is 3a-Adiol-G supposed to be the gold standard to measure 5AR type 2 activity when its formation depends on the throughput of another enzyme - 3a-HSD - which is variable by nature, subject to gene regulation and also depends on other genetic traits?

Have you ever considered that enzymes actually have a regulatory function and are not just processing substrate A to substrate B at a constant rate? What if the body actually thinks that there is too little DHT around because it has become insensitive to androgens and has therefore downregulated 3a-HSD? This is just to illustrate that there can be slightly more sophisticated reasons as to why many have low 3a-Adiol-G than just simply because of low DHT / 5AR2 deficiency.

Additionally, DHT seems to get mainly metabolized to Adiol 17-G. What do you say about that? (finsucks found this one out, of course his post on the subject just got ignored)

Preferential Metabolism of Dihydrotestosterone to Androstanediol 17-Glucuronide in Rat Prostate
endo.endojournals.org/cgi/conten … 123/6/2788

  1. Why do some members experience massive hair loss after quitting Finasteride? Isn’t hair loss supposed to be mediated by DHT? Isn’t that why we took a DHT inhibiting drug in the first place? I am loosing hair at a rate you can’t imagine. I’ve lost more hair in the past 18 months than I have in the previous 18 years. I am growing thicker body hair all over like never before. What is the hormone that mediates body hair growth? You got it.

Argument #1: Unless you are on chemotherapy or have another serious illness, it is highly unlikely to have hair loss if 5AR2 is supposed to be dead. Just because not everybody is experiencing hair loss post fin, the pro 5AR deficiency folks have decided to just ignore this one.

  1. Are you sure that a “simple” 5AR2 deficiency alone can cause such a massive health damage like some of us are experiencing? Don’t you think you are dismissing the role of testosterone and 5AR type 1 a little too quick?

Argument #2: The 5AR deficiency folks are talking like DHT produced by 5AR2 is the only androgen hormone that counts. What about testosterone? testosterone actives the androgen receptors just like DHT does, only at a lower rate. It has a number of positive effects, that are just simply being ignored (see below). And what about 5AR type 1 or circulating DHT for that matter? Are you sure all this has no importance? Read this:

eje-online.org/cgi/content/full/152/6/875

  1. Finally, the most important argument to arrest the 5AR deficiency theory, and this one CANNOT BE IGNORED: Why do some members have muscle wasting even though DHT is not necessary for muscle development? Don’t believe it? Read this:
  • Anabolic effects of testosterone are preserved during inhibition of 5alpha-reductase.
    ncbi.nlm.nih.gov/pubmed/1748 … inalpos=13

  • Inhibition of 5alpha-reductase blocks prostate effects of testosterone without blocking anabolic effects.
    T caused a significant 16% decrease in subcutaneous fat that was not blocked by MK-434 (another 5AR type 2 inhibitor).

Testosterone alone reduces fat? Does that ring any bells? Why then are some guys on TRT (like me) still putting on midsection fat (despite top class diet)?

To summarize

I can fully appreciate that everyone in this place is desperate to find a solution. I can also understand that the whole androgen receptor desensitization theory is complex and not everyone has the patience and interest to try and understand it. But I increasingly do not have any understanding for people that sit around theoretizing all day, without having tried any of this stuff themselves, specially if they are ignoring important facts. If we are not reacting to androgens in the way that we should be, we have become androgen insensitive. Period. There is no need or benefit to invent other reasons like 5AR deficiency, however neat the theory might seem. And repeating the same rubbish day in day out is not going to make it any more true, even if everyone starts believing it because it is repeated so often.

It is going to take our full and undivided energy to get ahead with this problem. We are not going to make it if we are all pulling in different directions. I can guarantee you that we will all still be sitting here in the same place in ten years if we don’t start getting coordinated. It may seem tempting at first sight to follow a path that seems easy to understand and quick to travel. But if it leads to a dead end, like the 5AR deficiency/Adiol-G story, then it’s just a waste of time.

Let me make an analogy for you. You’re afoot on a road in the middle of a desert and arrive at an intersection. If you turn right, you only need to travel one mile. Unfortunately, the short road will only lead you to a sand pit. If you turn left, you will have to walk a hundred miles and might not make it. But the reward is a hotel with food and drink. You maybe will still be in the desert, but at least you’ll be one step further.

We need to start traveling that long road TOGETHER. If we’re together on this and one falls, we can help him to keep on going. Maybe we can all chip in and buy a car in order to travel the road faster. This will only work if we all want to go in the same direction. So the first thing we have to achieve is consensus. No testing or googling in this world is going to show us the way. We need more people like JN with the balls to actually try this stuff. Get yourself a tube of Andractim and try it for 2 or max. 3 days. Send me a pm to get the source. Talk this over with your doctor. A quick test won’t kill you and I guarantee that it will make you see clearer in this matter. I am not endorsing long term use or telling you to start a therapy with this stuff. Just give it a quick try. Accept what your body is telling you and report it back to THIS THREAD:

propeciahelp.com/forum/viewt … 8718#18718

If you think that you’re going to come up with some hormonal excuse if doesn’t work, get those hormones that you have in mind assayed before, during and after taking Andractim.

Let’s make 2010 a more successful year for everyone. This time hopefully TOGETHER and heading in the same direction.

Thank you for the time you have taken to read this post.

All the best to everyone.

awor

Links
You can check out my experience with supplementing androgens here: propeciahelp.com/forum/viewt … 3250#18792

Here is my member story: propeciahelp.com/forum/viewtopic.php?t=757

Find out more about androgen insensitivity: propeciahelp.com/forum/viewtopic.php?t=2216

6 Likes

Hey chaps, firstly thanks Awor for this excellent post. Secondly, i just want to say that i have noticed very good results with masteron. I am currently in the desert of Australia and on a little phone with v poor reception. Please note i am reducing my weekly T from 250 to 60, and am also reducing e2. So a few variables. I Felt better after 10 mins of injecting. The only thing i’m going to commit myself to saying is that i have noticed very good results with masteron. I will update and contribute to this excellent thread when i am back in civilisation. JN.

JN,

You are a warrior my friend…Truely are…Get back to us when you are home…

-Anonnn

Hi awor,

Thanks for the inciteful post, this has certainly grabbed my attention.

I myself am guilty of jumping on the 5ar2 deficiency bandwagon because as you say, it is the most logical idea.

I have a keen interest in your theory of receptor desensitization, i had posted in the original thread a while ago to see how the theory was going but didn’t hear back so i assumed that it had died off for some reason.

I have recently been looking at selective androgen receptor modulators (SARMs) as a possible course of treatment if it was to turn out our receptors are down-regulated. I’m not sure how familiar you are with these, i am still trying to find out about them myself, mostly from bodybuilding forums where it is currently being used.

Ostarine is a SARM that is currently in Phase 3 trials, from what i understand it works by stimulating the androgen receptor resulting in increased muscle and bone density but without negative effects on the HPTA.

I realise that i may be drastically oversimplifying a complex issue but not many other members of the forum have shown an interest in SARMs so i was hoping to get some thoughts.

Also, in order to further pursue this theory of androgen insensitivity, what is the next step? what tests need to be done, people need to be contacted, protocols need to be tried etc.

Right, I think i have to be candidly honest. A day after posting i have noticed ‘very good’ effects, i have to explaing this. I’m still on a little phone. I noticed ‘a feeling of goodness’ come over me and stay within 10 mins of injecting. I feel better. Acne has returned to R side neck. Perhaps increased sweating, more ejaculate, erections slightly better with regular semi morning woods. Perhaps a few more hairs falling out. But i’m a long long way from ‘normality’ and i must admit to being a bit scared that ‘replacement of DHT’ won’t sort me out. I will do a good screen of hormones when i get back to work. I need a break. I’m tired of this. JN.

Right chaps,

I just made a big post but I lost it. This is the slimmed down version.
I have been thinking a lot.

I have noticed the following 2 weeks on masteron

  1. Within 10 mins I FELT BETTER. Markedly so. Zero anxiety. Much happier. No argument.
  2. Increased sweating
  3. Increased acne R side neck (a third of what it was pre fin)
  4. Increased body hair (difficult to assess but I think so)
  5. Increased vascularity arms and legs, hands, feet
  6. Loss of central abdo fat, much more ‘cut’
  7. Increased beard density
  8. Increased nasal bogies ( I used to pick my nose a lot, this is a good sign, and I wasn’t looking for it)
  9. Improved erections, semi morning woods regularly, nearly full boner when fully stiumlated, more ejaculate (but still stringy), fuller scrotum, larger testes. Libido difficult to assess as I’ve been messing around with Arimidex
  10. Noticeably deeper sleep (wasn;t looking out for this, but feeling more refreshed).
  11. possibly deeper voice.

Clearly have responded to DHT addition. Shame it’s not a total cure but I need to do full hormone profile (I am VERY interested in my Prolactin level).

Need to give it more time.
Hopefully this is all Adiol G related, but we need to be open minded.
This is my avenue of exploration for the next few weeks to months. Please don’t expect too much from me, please leave me in peace. Do not pm me, do not text me, do not contact me apart from AWOR who I want to chat to on skype. Awor, you have my skype details. I’m about to email you my email address.

Please contribute to the healthy debate Awor has set before us,

JN

That is great news JN!

So how would one test for androgen insensitivity?

From what i understand the test for androgen insensitivity syndrome (AIS), is to examine the response of SHBG to stanozolol as outlined in the link below:

springerlink.com/content/5xke760vmwl9xf47/

Is this a helpful test for post-fin sufferers?

1 Like

awor

i would be glad to take you up on your offer but im with a doctor in treatment now:

10% testogel 100 mg per day
1.5 grain armour thyroid
20 mg hydrocortisone

i am on the gel now for 4 weeks and currently at 1 grain armour, raising tomorrow to 1.5

i went in for the blooddraw today of adiol g, total t, e2 and dht

will keep you updated, 26th of february getting results

i would take andractim but i will not skew my treatment results… thanks for the offer though

im starting to agree with awor. i have taken androgel and andractim with no results. i was on for 2 years and it’s been 3 years off and i don’t lose hair at all. im only 25 years old and things are not looking optimistic.

Bruins,

I don’t understand what you are saying. I’ve read your posts from october and you said you got good results including improved ejaculate and better erections. Maybe your hormones got a little out of whack?

You may want to monitor your hormones more closely. Testosterone:Estrogen ratio should be 50:1 from what I heard.

For someone who has 800 testosterone, you should be at around 16 Estradial.

You could also try 5-alpha androstane 3, 17 beta diol
which is a naturally occuring compound for DHT.

I wish you best luck, I’m struggling just like you are…

We will get better though and I’m not gonna stop pursuing a lawsuit, even if it takes me 50 years.

Check out the main thread on this subject, we’ve been through that extensively: propeciahelp.com/forum/viewt … 2216#16025

It would be fantastic if you could post your experience in this thread: propeciahelp.com/forum/viewtopic.php?p=18718

Please post your experience here: propeciahelp.com/forum/viewtopic.php?p=18718

1 Like

awor,
I agree that we need to focus our efforts. I think a lot of us have been subconciously hoping for a solution coming from the scientific community. I have been to more doctors and spent more cash over the years and have come up with little. I think one of the problems is the anonymity of the internet. On one hand it gives us the ability to vent our frustrations and express fears, but ultimately it leaves the problem in the ether. I think we need to meet with other members of the forum in our local areas. Perhaps some of you have already done this. I live in New York, and would be willing to meet with anyone who was interested, if only to discuss face to face what can be done.
As for andractim, I’ve taken it, and did not feel a benefit. I mistakenly took a way too high dosage the first few times, and almost bit the head off a few unfortunate people, but no increase in sex drive.
As far as organizing goes, I think it would do to specalize and use our particular strengths. I for one have no aptitude for understanding the fine points of what is going on scientifically (what is commonly accpeted I mean not what baffles the doctors.)
It might make sense to get an idea of what people here do. ie do we have any lawyers any doctors, public advocates, people in the media. One of our main obstacles I think in really organizing is the private and embarassing nature of our problems, I mean god bless anyone who can and will generate intrest, but I for one cannot see myself sitting with oprah and talking about how my libido’s been in the tank for eight years. Call me prideful.
In any event I agree with the jist of your post.

Meeting in person is fine, but it doesn’t really change much. I’m just throwing this out here but a number of us use Google Talk (GTalk) to discuss this outside of the forum, and I deeply encourage anyone who is serious about making waves to use GTalk and meet with us there.

1 Like

"If 5ar were damaged, supplementing DHT should have a massive positive effect. "

Awor, I sincerely appreciate your efforts on raising awareness regarding AR receptor downregulation. So please don’t take this the wrong way - you b need to consider that BOTH mechanisms are at work here[/b]. Some evidence that both are involved are subjective, but consider the following:

1.) JN had medium term success supplementing with Human Growth Hormone (GH), and I have had some success using arginine based GH secretagogue (symptoms decreased espcially erectile, and IGF-1 doubled). Why is this significant? Because GH acts to upregulate androgen sensitivity. AND higher IGF-1 levels boost 5AR2 activity (higher GH triggers higher IGF-1). I have bloodwork to prove this, although it is not a pure experiment, as I raised total serum T by ~ 100% using low dose clomiphene, and at the end of an 8 week cycle of secretagogue, with both effects combined my Adiol-G was raised around 50% (still subnormal even by Quests wide open range, but up nonetheless along with symptom relief). Yes increased serum T means greater substrate for 5AR2 to react upon. If I get a chance I will test Adiol G again with T adjusted up a little over 100% from baseline, but no secretagogue, to seperate out the secretagogue effect from the increased substrate effect.

2.) Have been reading, on and off, a book on androgen receptors, prepared by one of the top world experts in the field… Funny thing here - an entire chapter is devoted to discussing 5AR2. And sections of 2 or 3 other chapters also discuss 5AR2 at some length. If AR and Adiol-G (5AR2 activity marker/metabolite) are completely unrelated then why would a world renowned AR expert include this information?

3.) Have been studying, since I got my first piss poor adiol-G serum level back, all the food and food substances that inhibit 5AR2. Amazing, the AR book has a Chapter 6 that talks about foods that downregulate AR. Ready for this? Green tea polyphenols, quercetin, Resveratrol, DHA, all downregulate AR in the prostate (resveratol lowers levels of AR related proteins in all areas). And all these substances are ALSO 5AR2 inhibitors.

4.) The 5AR2 gene SRD5A2, the AR receptor genes, and the vitamin D receptor gene VDR are all part of the same superfamily. While not yet grasping the entire significance of this, consider that just about every single member of this forum, that has had vitamin D tested, turns out to be deficient, and, even for those that have supplemented with very high doses, remain somewhat deficient. Please refer to the vitamin D thread and my comments in a couple places there. It would appear that the connection here is more than casual . . .

I totally agree with you that the AR receptor theory is hard to grasp, even for those of us that have a scientific background. The mechanics of 5AR2->Adiol-G and finasteride effects are much easier for all of us to begin to understand. Please keep an open mind, and BTW, if you happen to know how the androgen receptor interacts with inhibin I am all ears. And your quote above - oversimplifies in that what appears to be important is where we make DHT, not just how much we have of it. If we aren’t converting it in the prostate, pituatary, and testis via 5AR2, the normal DHT levels resulting from 5AR1 activity in the skin may not in fact result in much progesterone to allopregnanolone conversion. .Does AR downregulation effect allopregnanolone (or other neurotransmitter) synthesis? If not how to explain those on this forum with brain fog?

The future may in fact prove that AR downregulation is causative to 5AR2 suppresion. If and when that is proven I will owe you a beer or three. In the mean time I find that both theories overlap and support one another, more than compete with one another. Sorry if my tone sounds harsh, do not intend for it to be. And yes, I’ve been remiss in posting some of my own results.

Respectfully - kazman

1 Like
  1. By what specific mechanism(s) would androgen insensitivity cause lower levels of testosterone and DHT and raised levels of estradiol?

  2. If the main culprit of our problems is in fact epigenetic changes resulting in androgen insensitivity, then would raising testosterone to supraphysiological levels ameliorate our symptoms? According to Dr. Crisler, this is often what is necessary when treating men who have Post-Propecia Syndrome with TRT. Or is it the case that with androgen insensitivity higher levels of testosterone would have no effect?

I have no idea what to believe, but thank you, Awor for posting this.

Unlike some of you, I believe I would be willing to go on Oprah and even (if it were possible) to show my anatomy before and after to the public. The problem is, Merck would have “experts” go on other programs to either discredit or belittle our concerns and assure everyone that the risks are low compared to success rates.

Funny (not so funny) thing about the whole situation for me is that I care, but then I don’t care because at a fundamental level, my being has stopped caring about life the way a normal functioning person (not depressed or pharmaceutically altered) SHOULD be concerned about life and society. Memories of how life used to be and thoughts of “things I might one day enjoy” usually only serve to cause frustration.

The problem we find ourselves in seems even worse to me than the sordid state of politics, the middle class of the developed world, and the world economy (however many ways you want to circumscribe the ‘state of things in the world’). I say this not necessarily because we’re dealing with this on a very fundamental, physical, and personal level, but because it seems inevitable that history will move forward or mankind will self-destruct. ATM, I see no solution, but I have a small bit of hope that sunshine and exercise could one day get the recovery ball rolling.

JN, I will be interested to hear about what happens with you assuming that you are doing DHT on then off again… a cycle, I suppose you would call it.

Updated my previous post to list known food constituents that downregulate AR activity and are also 5AR2 inhibitors.

So you’re telling that you became insensitive to T only and not DHT? Considering that you still lose your hair, everything is okay there. How’s your body hair and beard?
Or are we talking about low T symptoms like muscle wastage and stress and stuff like that?
Please give an explanation to a low-IQ-ed simple peasant like me also! I as well need help :slight_smile:.

I think this theory is the simplest answer: it can easily be associated with every side effect no matter what the hormones are (because the hormones just don’t matter, if your body is insensitive to them). I will certainly ask my doctor about it and see how he rules it out.
I have quite high T levels, but am still infertile. Why? Because my body doesn’t respond to T.
I have quite high T levels, but my scrotum skin is still stretched and my testicles hang low. Why? Because my body doesn’t respond to T.
The same with no morning woods and weak erections.

Fanjeera, infertilitiy is also a symptoms of zinc deficiency. Have you tried a zinc taste test from the chemist/pharmacy?