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Testosterone: the Good, the Bad, and the Ugly |
E-Newsletter No. 37
Testosterone and testosterone analogues
have long been used in the athletic community for improving lean muscle tissue and
strength. Although this action of testosterone was denied over the years, the scientific
proof of the link between testosterone and muscle was shown in 1996. Since that time there
has been a virtual explosion in the use of testosterone and testosterone analogues. The
term commonly employed to refer to this class of compounds has been anabolic-androgenic
steroids. Lest there be any confusion testosterone is an anabolic-androgenic
steroid.
Other new terms to describe medical conditions or states with a direct relation to
testosterone are andropause and sarcopenia. Andropause is the age-related decline of the
level of testosterone in males. This level has been found to decrease approximately 1% per
year beginning at age 25. The level of bioavailable testosterone may decline to a level
whereby symptoms are produced. These symptoms may include the following: decrease in
libido, energy, strength or endurance; height loss; a decrease in the enjoyment of life;
unexplained depression or sadness; increased fatigue or sleepiness; and erection
dysfunction. In both males and females aging is associated with marked changes in body
composition, the principle element being a decrease in skeletal muscle mass. This
involuntary decline in lean body mass is referred to as sarcopenia. The determinants of
sarcopenia are poorly understood but studies have shown an improvement of lean body mass,
muscle, and strength with androgens.
The impact of low testosterone may have additional effects of a much more harmful nature.
Other long-term consequences include increased cardiovascular risk and osteoporosis. The
preceding statements are an excellent case for the use of androgens. However, the use of
androgens is not restricted to only those individuals with abnormally low levels of
testosterone. And it is exactly due to this reason that the use of androgens be undertaken
with due diligence and thought. The physiology of testosterone production is a complex
interplay between multiple organ systems. This system is termed the
hypothalamic-pituitary-gonadal axis or better known by the acronym HPGA. The production of
testosterone is totally dependent upon a hormone produced by the hypothalamus, GnRH or
gonadotropin releasing hormone, which in turn causes the secretion of a hormone, LH or
luteinizing hormone, by the pituitary gland. It is this hormone, LH, which is directly
responsible for the testicular production of testosterone. The system is in a dynamic
state of equilibrium which is a simple way of stating that any change of one component
will necessarily cause a change in the remaining components of the system.
Androgen Induced Hypogonadism
The use of exogenous androgen, testosterone, will result in a decrease and possible
cessation in the body's production of GnRH, LH and testosterone. After an individual stops
or halts the use of testosterone, or other androgen, the body does not immediately resume
the production of these hormones. A period of androgen induced hypogonadism, AIH, begins
of an unknown duration and severity. This period is related and proportional to the type,
dose and duration of the androgen(s) used during treatment. While the clinical
presentation of androgen induced hypogonadism may differ considerably from one individual
to another one of the most common variants is termed hypogonadotropic hypogonadism. The
adverse effects and consequences of hypogonadism have been previously mentioned. For the
individual beginning testosterone treatment with normal levels the period after androgen
cessation deserves important consideration.
While some research suggests that the hormonal axis will spontaneously return to normal
shortly after cessation of testosterone administration, birth control studies utilizing
testosterone have taken over 6 months for HPGA normalization. Now that the many positive
effects of androgens are being widely publicized, this single known fact of hypogonadism
after androgen cessation receives barely a mention or footnote. Although there are
anecdotal reports concerning medical treatment for androgen induced hypogonadism,
well-controlled studies establishing such protocols have yet to be established or
performed. Testosterone therapy, once begun, may become a life-long commitment. In the
individual who has mild or moderate benign prostatic hyperplasia, BPH, or latent prostate
cancer, CaP, androgen treatment may be potentially problematic. Additionally, since many
of the more serious side-effects of hypogonadism, cardiovascular, osteoporosis, and
depression; are insidious in nature one may not become aware or seek help for androgen
induced hypogonadism until it is too late for optimal treatment. Research and
investigations into the development, duration, and medical treatment of androgen induced
hypogonadism will greatly benefit the assessment of the risk: benefit ratio of androgen
therapy.
