Personal experience with enhancing testosterone as treatment of sexual dysfunction
I am sure that a healthy man at any age can elevate his testosterone levels. I am not sure that it will do much for his libido and sexual function.
I have tried a good number of hormonal supplements, and, based on my own experience and the scientific studies of others, I would say that they are not the way to go for sexual enhancement. While the dopamine pathway is not perfect either, medications such as bromocriptine at least have a measurable effect on sexual parameters if hyperprolactinemia is present (when administered correctly).
And then there is always yohimbine (an alpha-2 adrenergic antagonist) and PDE5 inhibitors like sildenafil (Viagra). Both work for their respective indications. Period.
I have not experienced any pro-sexual effects from testosterone undecanoate (Andriol capsules). To the contrary, the supplemental Andriol has probably suppressed my endogenous testosterone production. Testosterone supplementation really only makes sense if the body can no longer be stimulated to produce its own testosterone.
I have taken DHEA for years. Sites that want to sell DHEA will usually include a statement in their sales pitches that DHEA enhances libido or sexual function. I do not think DHEA is counterproductive, but from the perspective of sexual enhancement in healthy men, it is probably just a strong placebo.
Regarding the overall concept, I believe that factors other than merely supplying hormones or precursors should be emphasized. Hormone supplementation, whether with testosterone undecanoate, DHEA, or pregnenolone, has not been shown to enhance the sexuality of basically healthy men. And enhancing sexuality would be my primary aim anyway.
On the other hand, a combination of clomiphene citrate (Clomid) and anastrozole (Arimidex) results in physiological changes that I judge to be testosterone-driven.
Clomiphene citrate stimulates the hypothalamus in a manner that, several steps down the endocrine cascade, results in higher testosterone levels. Anastrozole prevents the conversion of testosterone into estradiol.
I have also experimented with Tribulus terrestris and Tongkat Ali. While often marketed as testosterone boosters, clinical evidence shows Tribulus terrestris does not actually increase testosterone levels in humans, and Tongkat Ali primarily works by influencing sex hormone-binding globulin (SHBG) rather than stimulating the hypothalamus like clomiphene citrate.
Unfortunately, the general enhancement of libido and sexual performance that I had in mind did not occur with any testosterone enhancement regimen.
I, for one, have to make sense of my personal experience with testosterone-enhancing medications, especially when comparing them with scientific information on the same topic.
My current hypothesis (not a theory I invented myself) is that in the endocrine system, circulating testosterone levels alone are not the crucial factor for enhanced libido and sexual performance. One must also possess the appropriate androgen receptor sites, and those receptor sites must be responsive.
Aside from trying to be a knowledgeable layman, I am still just a layman. And like most laymen studying the endocrine system, I initially focused strongly on hormones and neglected the importance of receptors.
However, hormones exert their effects not just on any tissue, but only on tissue that possesses specific receptors responsive to the hormone.
I assume that the effects of testosterone on libido and sexual performance are strongly correlated with androgen receptor density in the brain (for libido) and the reproductive organs (for erectile function). If you want to enhance sexual function, you must optimize both the hormones and the receptor availability.
Let us compare this to an orchestra. To start with, I have four musicians. That is sufficient for playing a few famous Mozart melodies. But if I want to perform a Beethoven symphony, I will have to upgrade. How?
By hiring more musicians? Yes, but if they do not have any instruments to play, they will just stand around.
It is just the same with testosterone.
Sexual function is a concert. The musicians are the testosterone molecules, and the musical instruments are the receptor sites.
Everything is set and running at the concert hall, playing Mozart melodies. If I take away the musicians, there will be silence (if I completely inhibit testosterone, sexual function ceases and my libido disappears).
However, this experiment does not prove that liberally sending more musicians onto the stage will create a full orchestra capable of performing a Beethoven symphony. I would also have to supply the additional violins, drums, and trumpets.
Enhancing testosterone (by supplying it exogenously, stimulating the hypothalamus, or inhibiting aromatase) without increasing receptor availability is like sending empty-handed musicians onto the stage. They cannot accomplish much without the necessary instruments.
Similarly, testosterone can only have a pro-libido and pro-sexual-performance effect if there are specific tissue receptors to which it can bind. In tissues lacking these receptors, testosterone has no effect.
As far as I understand it, I (and probably most other men) do not suffer from a lack of androgen receptor sites mediating aggression that can be influenced by increasing testosterone. Regarding androgen receptor sites for sexual function, however, I seem to possess a number of receptors that largely correlates with my endogenous testosterone production.
For a sexual effect from enhancing testosterone, both would have to be increased: testosterone AND receptor availability. Unfortunately, I have not come across any pharmaceutical that safely claims to increase the number of androgen receptor sites specifically for sexual function.