by Aftab J. Ahmed, Ph.D.
LIBIDO: Facts and Fantasy
With the exception of prolonging
life, nothing has fascinated,
intrigued and indeed mystified
man more than the fantasy of enhancing
his sexual prowess. Human history is rife
with the symbolisms of sexuality and fecundity
and the list of pills, lotions and potions
to stimulate libido is long and tired. It is
only in the recent past, however, that the
basic mechanisms have been elucidated,
which have allowed us to address the issue
of libido and in fact sexual dysfunction per
se more rationally. Sexual dysfunction is an
umbrella term that encompasses an array of
conditions that afflict both genders. Of these, erectile dysfunction (ED) is the condition
most exhaustively covered by the
mass media—thanks in no small part to the
willingness of the ex-senator Bob Dole to
bring ED out of the closet, as it were. The
“courage” shown by Mr. Dole is largely
responsible for mature emphasis on, and
awareness of, sexual health.
Erectile dysfunction is the dreaded word
that can change lives for good and exact a
heavy emotional price. To the sufferers of
ED, it is most disconcerting that it sneaks
up over the years and is hardly discernible.
Its underlying cause may just as well be psychological
as organic or physical.Conservative estimates are that roughly 150
million men suffer from ED worldwide,
particularly those over the age of 60.
What is ED, or impotence, and how
does it ensue? Essentially ED is the inability
to attain or sustain penile engorgement
necessary for normal coitus and could be
either primary or secondary. Primary ED,
which is quite rare, is indicative of severe
psychopathology; in secondary ED, on the
other hand, the coitus cannot be successfully
completed, despite initial engorgement.
In rare cases, biogenic factors such as low
testosterone and disorders of hypothalamic-
pituitary-gonadal axis complicate the
presentation of primary ED. In secondary
ED, approximately 70 percent of cases are
psychological that include guilt, fear of
intimacy or depression.
The mechanisms that contribute to ED
are numerous and complex (see sidebar)
and may be presented either concurrently
or sequentially.1 A cursory look at the flow
sheet shows that any one of the steps
involved may precipitate and/or aggravate
ED. It also suggests that the erectile process
is so tightly orchestrated that, in turn, is
controlled by a number of biochemical
steps. Thus the ineffable “mind-set” for an
intimate encounter is central to sustained
engorgement of the penile tissue. It is for
this reason that in the early stages of marketing
Viagra, Pfizer’s direct-to-consumer
advertisement blitz forcefully underscored
the importance of romantic context in its
efficacy. The requisite context stimulates
nerves, which begin to fire and, ultimately,
initiate the cascade of reactions that cause
penile tumescence (swelling).
Whereas the hydraulic physiology of the
erectile process was discerned much earlier
than the biochemical steps involved, it is
only recently that the role of blood flow has
been fully understood. This was impelled
by the recognition that the erectile process
is not a result of muscle contractions and
relaxation but is due to blood engorgement.
The more the blood flows through
the male reproductive organ (MRO), the
firmer the penile engorgement. The “gatekeepers”
for the blood flow are smooth
muscle cells in the spongy tissue of MRO.
When smooth muscles are constricted, the
blood flow is restricted to a trickle—not
unlike squeezing a garden hose. When
these same cells relax, however, the blood
flows as if the pressure on the hose were
released. Consequently, as the blood from
the arteries gushes to fill the two expandable
reservoirs inside the MRO, called corpus
cavernosa, rigid and sustained tumescence
results.
What triggers the blood to fill corpus
cavernosa? In the early 1990s it was demonstrated
that in healthy individuals blood
flow is triggered when nerve endings release
nitric oxide (NO), a relatively short-lived
neurotransmitter, which is the same substance
that relaxes smooth muscle cells as
well.2 Quickly thereafter it was found that
NO initiates the cascade of reactions to
engorge the MRO and cause tumescence.
Briefly, nerves in the pelvic area respond to
stimuli from the brain to produce NO,
which dilates the blood vessels throughout
the region to supply blood for engorgement.
Since NO is indispensable in this
process, it was logical to investigate
whether its decreased amounts contributed
to ED. Indeed, it turned out that nitric
oxide synthase, the enzyme that produces
NO, is the culprit in impotence. It should
be noted that aging alone does not necessarily
precipitate impotence. Attendant
organic problems—such as vascular disease,
high blood pressure and damage to the cardiovascular
tree, to name but a few—may suppress the release of NO and contribute to ED.
In light of the foregoing, increase in the
blood flow would be expected to stimulate
libido. Parenthetically, this holds true not
only for men but also for women.
Interestingly, research on sleep has provided
evidence that women undergo similar
changes in blood flow to the pelvic floor
muscle during sleep cycle as do men. Thus a
healthy libidinal response depends on wellfunctioning
vasculature in the urogenital
arteries. It is precisely for this reason that
clinical trials are underway to evaluate the
efficacy of Viagra on female libidinal
response.
While Viagra has become a market
dynamo in amelioration of ED, its mode of
action is inhibitory rather than stimulatory.
This may explain, at least partially, the side
effects of Viagra, even though it works
almost immediately. For obvious reasons,
two pharmaceutical houses have Viagra-like
drugs in preparation. Quite plausibly,
Viagra’s side effects will be recapitulated in
these new remedies as well. It is for concerns
such as these that the so-called “Viagra
refugees” are clamoring for natural alternatives
to boost libido.
There are “natural solutions” galore that
claim to restore sexual function overnight as
if by magic. In fact, in the fray of the cluttered
market place of Viagra alternatives, it is
difficult not to be taken by the unabashed
enthusiasm and indeed, unqualified promises
of a carnal Shangri-la. Thus it is difficult to
differentiate products that have a fighting
chance to alleviate the symptoms of ED from
those with non-validated claims. For example,
inasmuch as testosterone replenishment
may help resolve sexual dysfunction, it is a
viable option only under competent clinical
supervision. Likewise, numerous herbs have
been positioned to mitigate, if not outright
reverse, ED symptoms. While circumstantial
evidence does suggest that some of the herbs
could help attenuate the severity of ED over
extended periods of time, it should be noted
that these are “preventive” modalities at best.
That is, they are likely to be effective only if
used over the long haul as part of a disciplined
nutritional regimen. In other words,
contrary to the received opinion, there are no
quick fixes unless, of course, the underlying
problem is adequately addressed.
Erectile dysfunction is a chronic condition which takes
decades to develop.
As such, a systemic
approach in its management
is a more
realistic alternative.
Since blood flow to
the erectile tissue is
the critical factor,
substances that
enhance circulation
should mitigate ED.
Citrulline, a relatively
specialized amino
acid in the body, is
the precursor that
optimizes blood flow
by “pacing” the vasculature.3 Mechanistically, citrulline is converted
to L-arginine, which is a known
inducer of NO. Thus by inducing the
body’s own vasodilator, citrulline ensures
blood flow in sufficient amounts to the
pelvic floor to engorge the erectile tissue.
Since citrulline increases NO levels via
arginine, the question is forced whether arginine
might not be a more obvious alternative.
Not so, for arginine is less prone to be
absorbed efficiently to induce NO. After all,
it has to compete with a surfeit of amino
acids for the same transporters in the intestinal
wall to enter the bloodstream. In contrast,
the relative rarity of citrulline facilitates
its more ready transport across the intestinal
wall. Importantly, oral intake of citrulline
more effectively produces arginine in situ to
generate NO.4 Put differently, citrulline
increases the plasma levels of
induced arginine better than orally
ingested arginine. How so?
Arginine is assimilated over the
digestive tract and upon entering
hepatic circulation, the bulk of it
is degraded. In contrast, citrulline
is not cleared by the liver, rather,
it is taken up by the kidney and
other tissues where it is converted
to arginine. Specifically, oral
intake of citrulline results in 60
percent increase in the plasma
levels of arginine. It is significant
that citrulline sustains
plasma arginine levels much
longer than intake of a
similar dose of arginine
supplementation.5
By increasing the
blood flow, citrulline
tweaks the body’s
repair kit to reduce the
severity of ED presentation,
which should
recharge the libido for
a revitalized life.
Hence, citrulline provides
a more rational
approach toward sexual
dysfunction, which
stands in stark relief to
much-touted aphrodisiacs
with exaggerated
claims. Named after
Aphrodite, the Greek
goddess of beauty and physical love, these
supposed stimulants range from anchovies to
adrenalin, licorice to lard, scallops to Spanish
fly and everything in between. Aphrodisiacs
fan the fantasy of unlimited, even insatiable,
libido. Such fantasy, however enticing, militates
against not only human physiology but
also the alleged functions of a multitude of
aphrodisiacs. Therefore, a systemic modality
that helps correct the underlying problem is
a more meaningful means to restore vitality
and robustness. In that regard, citrulline is
not an aphrodisiac but is much more that
over time could potentially rejuvenate the
zest for life. Equally, by promoting circulation
through the highways and byways of the
cardiovascular tree, citrulline fosters better
health, which is indispensable for a healthy
libido.
Aftab J. Ahmed, Ph.D. is director
research and development and business development.
Marlyn Nutraceuticals, Inc.
E-mail:
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References
1) McConnell, J. and Wilson, J. “Impotence,” In Harrison’s Principles of Internal Medicine, Isselbacher et al., Eds. McGraw-Hill, Inc., New York, New York, 1998, p. 263 ff.
2) Burnett, A. “Nitric Oxide in the Penis: Physiology and Pathology,” J. Urology: 157, 320, 1997.
3) Waugh, W., Daeschner, W., Files, B, McConnel, M. and Strandjord, S. “Oral Citrulline as Arginine Precursor,” J. Nat. Med. Assoc., in press, 2001.
4) Windmueller, H. and Spaeth, A. “Source and Fate of Circulating Citrulline,” Am. J. Physiol.: 241, E473, 1981.
5) Waugh, W. “Orthomolecular Medical Use of L-Citrulline for Vasoprotection, Relaxative Smooth Muscle Tone and Cell Protection,” United States Patent No. 5 874 471, 1999.
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