Learn something new every day!
Althought I must admit I am still trying to figure out what some of you have said, so I will pick everything apart and hopefully you will both respond in the most "dumbed down" terms possible:
Sexual functioning is influenced by androgens
For the users, what exactly *is* an androgen? My half tongue in cheek guess is that its similar to a nerve. Maybe a little dangly thing that, when activated, transmits erotic sensations resulting in what we call libido.
The wood-inhibiting property of finasteride is a direct consequence of its interference with the metabolism of testosterone to its more potent metabolite, DHT.
It was an interesting sensation to go on Finasteride. As Bryan knows, I was an extremely hypersensitive responder to everything it did in my body. I could tell you without a minute of study in a library, exactly what tissues had 5-ar present, as their sensitivity and function changed very noticeably. I could have marked them with a crayola marker on my skin. Additionally, the difference in the "sweetness" of the libido I felt prior to Propecia
(when it was dominated by the more potent DHT)... to the way sex drive felt while ON propecia and experiencing a testosterone
(versus DHT) jolt .... to the way sex drive felt after I discontinued Propecia
(again being run by the more potent DHT) ... was extremely noticeable. I remember making a mental note of how it actually felt "Different". Still there. Still true. But somehow ... less "sweet" for lack of a better term.
The reason that finasteride produces fewer side-effects than classical antiandrogens (at a comparable clinical effect) is that androgen activity is selectively reduced in tissues where 5aR is present
Translation: Finasteride only affects certain parts of the body, whereas an "Antiandrogen" globally affects all androgen containing tissues.
The spillover effect from circulating androgens is probably relatively small.
Please clarify this. Assumption: You're saying that the effect from the resulting increase in free Testosterone is not usually too noticeable. You probably wont see much increase in libido from that time period soon after starting finasteride when testosterone increases. Yes?
There is an upper limit... androgen activity can be reduced by 5aR inhibitors, because other androgens (e.g., testosterone) aren't prevented from activating the androgen receptor
"androgen activity" again in this case means effect on libido? Meaning, though ye inhibit DHT, thine Testosterone may still arouse Thee?
Once you have a reasonable understanding of androgen metabolism and 5aR distribution in various tissues, the idea of using systemic 5aR inhibitors such as finasteride will become much less attractive.
Amen to that one. Put another way, you're basically pouring paint into an Olympic Sized pool when all you really wanted to do was give a few tiles some color.
If peak mental and physical performance is of importance to you, you'd be much better served by a topical antiandrogen such as spironolactone.
On a scale of 1 to 100 ..... 1 being ineffective and 100 being completely effective .... and for the sake of argument Propecia being ... say ... 83 on that scale :lol: .... honestly where would you rate the effectiveness of topical spironolactone 5% lotion in actually working?
Theory is all well and good but it doesn't explain how after 6 months of finasteride I have seen no effect on my libido, mental or physical performance.
Is it correct to say that sensitivity, awareness, and even possibly tissue distribution of androgen receptors that are compatible with DHT may differ from person to person? The theory has been raised that some guys live a life of libido powered by testosterone versus DHT ....
Natural estrogens in physiological doses do actually increase the libido
Translation for the tards (of which I am one) ... This means naturally produced estrogen in your body does contribute to libido. That "Physiological doses" thing threw me for a minute there
DHT itself is antiestrogenic, which is probably the most important factor in explaining estrogenic related side-effects.
Please rephrase this. This, rephrased, will answer the initial guy's question in the first post, and simultaneously correct any misinformation I may have spewed. My statement was excess T gets converted to E in the brain, liver, etc. Clearly I was wrong. Your answer to his question then is "DHT is an anti-estrogen". What does DHT do that reduces estrogen? Does it then follow that lack of DHT formation equals increased ability for estrogen to form and "pile up" ?
DHEA which eventually finds it's way over 17ß-HSD to androstendiole. Androstentiole immediately attaches to the estrogen receptors and is metabolized via testosterone (circumventing free endoplasmatic 5ar) to E2 (=> gyno). <----- Do you have any references to support this outlandish claim?
Id like you two to resolve this so I can know what the hell is being disagreed on here
Estrogen is important for maintaining libido in both sexes, but that doesn't contradict what anyone else has said in this thread. Kevin mentioned estrogen specifically in connection with gyno, not libido.
I was mainly referring to the statement that "excess T gets converted to E". Go to a well equipped library to verify these outlandish claims.
Wait, so I was right, or I was wrong? Since this question gets asked at least 43 times a day, I need to know the accurate response.
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