Online dr gives theory but no solution

Submitted by dr.Richards.MD on .


Yes, this is quite a frequent occurance after using 5-alpha reductase inhibitors. Again this is an example of a modern drug treating the symptoms and not the cause of the problem. Here is what is happening:

Actually during the teen years the body synthesizes high levels of 5-alpha reductase and low levels of Aromatase (for estrogen conversions) and still there is no prostate problems, no hair loss. With much 5-alpha reductase and testosterone our body produces high levels of DHT but one is in the best shape of his life. It is not only the DHT, it is the DHT plus other imbalances and ill processes that will lead to hair loss.

So one has to optimize testosterone-DHT , testosterone-estrogen, and estrogen-DHT ratio. Also it is very importatnt to provide the needed ingredients to prevent excessive binding of testosterone, DHT, and estradiol to hormone receptors that usually takes place after 25-30 years of age and will lead to the ill consequences one may experience.

DHT is a needed for numerous processes, it is very wrong to kill your DHT levels, which will weaken the erection and result in erectile dysfunction. One just needs to regulate it’s activities and prevent excessive binding to androgen receptors on the hair follicle cell membranes, especially if the blood circulation is not so great.

The levels of testosterone won’t matter if there is not sufficient conversion to DHT for proper sexual functioning.


RE: DHT and 3-Adiol G
Submitted by Anonymous on .

Dr. Richard,

First and foremost, thank you for commenting on the above post. Secondly, I wanted your feedback on 3-Androstanediol glucuronide, which is a major metabolite of DHT.

There are over 1600+ individuals on the website. We are starting to notice a trend/pattern of individuals who may have normal or subnormal DHT levels, but very low 3-Androstanediol glucuronide levels(I believe the range is (3.4-22 ng/ml) LINK: viewtopic.php?t=2763…. Most of these individuals are posting #'s between 1.0-5.0 if you look at that link above… THEY ARE in their early to lates 20’s for the most part… These individuals have Erectile Dysfunction, even with normal or high normal testosterone levels.

My question is, how would a doctor go about treating a condition such as this without supressing Testosterone levels too much?

Best Regards,



Submitted by dr.Richards.MD on .

My guess is that the temporary lowered DHT levels and ruined homeostasis may have altered numerous gene expressions for improper Glucuronosyltransferase release, that in turn may have lead to chronically low 3-Androstanediol glucuronide levels. However, this is just an assumption.

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No solution, but his theory (to my knowledge) is not a perspective that’s been adopted by many. It also could explain the age ranges that experience the symptoms, whereas a urologist will always reference older patients who took Proscar and the fact they don’t experience these adverse side effects as a counter argument to PFS. He’s receptive to the fact that this can happen and provides an explanation. Its always positive to read something like this, whether the theory has any legs or not.

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Altered Gene expression. That is part of the investigations in Awor et al’s current work, right?

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9 years later turns out he made a very good assumption.

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Excellent assumption indeed! We really need more doctors like that, and it’s a shame that post went all those years without a comment, but I’m glad it’s still here. How could we go about finding this doctor, to see if he may have developed other assumptions?