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:
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?
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:
Doesn’t this statement ring any bells?
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?
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?
How do you explain the variability in symptoms that many of us are experiencing if the assumption is that 5AR is permanently damaged?
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.
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.
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?
- 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.
If 5AR2 is supposed to be dead, how can you justify that jairus increased his Adiol-G by over 23% with testogel supplementation??
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
- 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.
- 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:
- 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)?
This study demonstrates that 5alpha-reductase inhibitors may block the undesirable effects of T on the prostate, without blocking the desirable anabolic effects of T on muscle, bone, and fat.
ncbi.nlm.nih.gov/pubmed/1536 … inalpos=23
Testosterone increases lean body mass and decreases fat mass in a dose- and concentration-dependent fashion.
ncbi.nlm.nih.gov/pubmed/1535 … inalpos=24
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:
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.
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