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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.

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