Libido: what IS it? (a serious question, honest)

Pete Wilson pwilson at
Fri Aug 16 15:28:42 EST 1996

[ The following is all from the point of view of a prostate-cancer
survivor and biology amateur. Please accept my apologies if my
understanding of the picture is in great and laughable error. ]

QUESTION: When I go to the medical library and look in physiology texts
or dictionaries for "effects of testosterone" or "libido" definitions,
I'm disappointed to find that the exact mechanics of libido are nowhere 
explained. Therefore, I ask what, precisely, is the chain of biological 
events (though not necessarily excluding psychological events) by which 
sexual desire (apart from physical sexual arousal) appears? Is this
chain of events known, or mostly known? Has anyone on this group an
answer or, much better yet, a REFERENCE that has an answer?

BACKGROUND: There are several side-effects in therapies for adenocarcinoma
of the prostate gland (PCa). A common therapy, excision of the prostate
gland (called "radical prostatectomy") often results in impotence, the
loss of erectile function. This loss of erectile function is *not* the
concern of this post. This loss of function is well understood and has a
purely mechanical basis: the neurovascular bundles upon which the function 
depends (Demonvilliers fascicles, I *think*) lie close alongside (sometimes 
embedded in) the prostate gland and are very often removed with the gland.

Another common therapy, often called "Combined Hormonal Therapy" or
"CHT," uses two chemical agents. One agent of this CHT acts to 
suppress the production of testosterone by the testes; the second agent
acts to block uptake of testosterone (from other sources) by the prostate 
gland. This suppression and blockade of testosterone (and therefore of 
dihydrotestosterone) can act to halt or reverse tumor cell growth.

As patients, we should not be surprised to discover that CHT also acts to
utterly and completely suppress the libido. During the several (3-12)
months of the usual course of CHT, patients report a complete absence
of interest in sex. Erotic fantasies and dreams also disappear, and one
is left with dim memories and profound puzzlement as to just what all the 
fuss was about. It's all very strange and curious, I can tell you.

But if a patient undergoes monotherapy, i.e., just the suppression of 
testosterone production by the testes; but declines to use the blockading 
agent (the "second agent," above), then libido often is only minimally 
affected. Adrenal testosterone seems to be sufficient to maintain near-
normal libido under monotherapy. (The production of T by the adrenals is
the reason that monotherapy is a very unwise treatment for PCa.)

A few oncologists have advised their patients to opt for the shortest
reasonable period of CHT because, these oncologists say, a longer
period of CHT will permanently damage the structures underlying libido,
leaving the patient with total and lifelong disinterest in sex. Not too
many patients are warmed by this prospect, yet the dangers of too
short a course ( <= 3 months) of CHT are well documented.

I am trying to research the issue of the mechanical, chemical, molecular
basis of libido so as to try either to confirm or to refute the claims of 
the few oncologists who advise against the usual (6-8month) course of CHT, 
perhaps ("certainly," IMO) against their patients' interests.

Thanks very much, and sorry for the longish post.
Regards, Pete Wilson (pwilson at

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