Nelson Vergel
Founder, ExcelMale.com
Anabolic Steroid Side Effects- Part 3
By Dr Mauro Di Pasquale
For Part 1
For Part 2
There are also several other hormones and compounds, such as inhibin and the endogenous opioids, involved in the regulation of testosterone secretion. For example inhibin, a hormone produced by certain testicular cells (Sertoli cells) in response to FSH, regulates androgen production by other testicular cells (Leydig cells); and beta-endorphin, synthesized by Leydig cells under LH control is known to regulate Sertoli function, and thus to affect inhibin production (19.) One recent study showed evidence for a direct effect of naloxone on testicular steroidogenesis in the male rats. Thus the endogenous opioids may have an effect on not only the release of GnRHJLH, but may also have a direct testicular effect on steroidogenesis.
The use of exogenous hormones disrupts the HPTA, with the degree of disruption dependant on several factors including the type of anabolic steroid used, the dosage used, the duration of treatment, and the presence of any underlying pathology. All male athletes using anabolic steroids experience some testicular dysfunction, resulting in decreased serum testosterone levels, testicular atrophy, azoospermia and sometimes the development of a female habitus including gynecomastia. On discontinuation of the anabolic steroids there is normally a variable time period over which the HPTA remains depressed. In most cases the serum hormones soon return to normal.
However, with high doses of anabolic steroids used for extended periods oftime, there is often a prolonged impairment of testicular endocrine function, secondary to hypothalamic-pituitary dysfunction, and in many cases primary testicular dysfunction. It appears from the athletes I have followed, that the long term suppression of testicular steroidogenesis results in not only hypothalamic-pituitary dysfunction but also gonadal impairment that may not be as reversible as is generally thought. Thus testosterone and the anabolic steroids seem to have direct effects on all components of the HPTA, and possibly even on suprahypothalamic mechanisms.
In many cases of chronic suppression of the HPTA there appears to be a resetting of the serum testosterone - with LH and FSH levels returning to normal values after the anabolic steroids are discontinued, but with a markedly decreased serum testosterone. Ordinarily one would expect elevated LH and FSH values in light of the low serum testosterone. Such is not usually the case. I've found a low serum testosterone associated with elevated gonadotrophin levels in only a minority of HPTA suppressed patients. In these patients the hypothalamic/pituitary function was intact; the primary problem was one of testicular dysfunction. In a few of these patients, testicular dysfunction was irreversible.
19 Morris PL, Vue WW, Bardin CW. Beta-endorphin regulation of FSH stimulated inhibin production is a component of a short loop system in testis. Biochem Biophys Res Comman 1987; 148(3):1513-1519.
By Dr Mauro Di Pasquale
For Part 1
For Part 2
There are also several other hormones and compounds, such as inhibin and the endogenous opioids, involved in the regulation of testosterone secretion. For example inhibin, a hormone produced by certain testicular cells (Sertoli cells) in response to FSH, regulates androgen production by other testicular cells (Leydig cells); and beta-endorphin, synthesized by Leydig cells under LH control is known to regulate Sertoli function, and thus to affect inhibin production (19.) One recent study showed evidence for a direct effect of naloxone on testicular steroidogenesis in the male rats. Thus the endogenous opioids may have an effect on not only the release of GnRHJLH, but may also have a direct testicular effect on steroidogenesis.
The use of exogenous hormones disrupts the HPTA, with the degree of disruption dependant on several factors including the type of anabolic steroid used, the dosage used, the duration of treatment, and the presence of any underlying pathology. All male athletes using anabolic steroids experience some testicular dysfunction, resulting in decreased serum testosterone levels, testicular atrophy, azoospermia and sometimes the development of a female habitus including gynecomastia. On discontinuation of the anabolic steroids there is normally a variable time period over which the HPTA remains depressed. In most cases the serum hormones soon return to normal.
However, with high doses of anabolic steroids used for extended periods oftime, there is often a prolonged impairment of testicular endocrine function, secondary to hypothalamic-pituitary dysfunction, and in many cases primary testicular dysfunction. It appears from the athletes I have followed, that the long term suppression of testicular steroidogenesis results in not only hypothalamic-pituitary dysfunction but also gonadal impairment that may not be as reversible as is generally thought. Thus testosterone and the anabolic steroids seem to have direct effects on all components of the HPTA, and possibly even on suprahypothalamic mechanisms.
In many cases of chronic suppression of the HPTA there appears to be a resetting of the serum testosterone - with LH and FSH levels returning to normal values after the anabolic steroids are discontinued, but with a markedly decreased serum testosterone. Ordinarily one would expect elevated LH and FSH values in light of the low serum testosterone. Such is not usually the case. I've found a low serum testosterone associated with elevated gonadotrophin levels in only a minority of HPTA suppressed patients. In these patients the hypothalamic/pituitary function was intact; the primary problem was one of testicular dysfunction. In a few of these patients, testicular dysfunction was irreversible.
19 Morris PL, Vue WW, Bardin CW. Beta-endorphin regulation of FSH stimulated inhibin production is a component of a short loop system in testis. Biochem Biophys Res Comman 1987; 148(3):1513-1519.
