Technische Universität München

The Entrepreneurial University

The functions of the male and female reproductive systems are regulated by hypothalamic-pituitary-gonadal axis. The artificially increasing level of androgens by administration of AAS leads to profound changes in this axis.
In male AAS users is observed the clinical syndrome of hypogonadotrophic hypogonadism (decreased serum FSH and LH, low endogenous testosterone production, impaired spermatogenesis, and testicular atrophy). AAS inhibit LH secretion by acting directly on the anterior pituitary and by inhibiting the secretion of GnRH from the hypothalamus. This in turn causes a corresponding decrease in secretion of both LH and FSH and the decrease in LH reduces the production of endogenous testosterone. A dual action of both FSH and high levels of intratesticular testosterone is necessary for complete quantitative and qualitative spermatogenesis. Oral or parenteral administration of AAS does not raise the androgen level in the testes to as great a degree, but inhibits LH and FSH secretion. Consequently, the net effect is impaired spermatogenesis. Semen quality decreases, and infertility, manifested as oligospermia or azoospermia, along with abnormalities of sperm motility and morphology, often results. Due to these changes testicular atrophy is observed in male AAS users. This state is usually reversible after steroid withdrawal, but some case reports indicate that the problems may persist for up to 3 years and that recovery does not always occur.
Serum concentrations of estradiol, androstenedione and DHT increase because of peripheral conversion of AAS. Gynaecomastia is associated with the peripheral conversion of AAS to estrogens, due to the huge amounts of administered aromatizable androgens. Once gynaecomastia is diagnosed cosmetic surgery is often needed to correct the problem. Enhanced sexual desire, higher incidence of erectile difficulties and priapism are reported in male athletes during AAS cycle. Towards the end of a cycle some men may experience loss of libido. Case reports indicate that AAS abuse can induce enlargement and even adenocarcinoma of the prostate gland. Androgenetic alopecia is accelerated in male AAS users who have inherited a tendency for baldness.
In women AAS use can result in inhibition of follicle growth and ovulation, irregularities of menstrual cycle and infertility. The observed menstrual abnormalities include dysmenorrhea, oligomenorrhea or amenorrhea. Breast atrophy, ovarian cyst formation (polycystic ovarian syndrome) with recurrent inflammation and atrophy of the uterus are reported as frequent damaging effects of AAS administration in female athletes. Menopause also may be reached sooner in women with a long history of steroid use. In women the misuse of AAS leads in all cases to masculinisation, to a greater or lesser degree (enlargement of the clitoris, lowering of the voice, hair loss and hirsutism. Most of these side effects are irreversible. In addition changes in libido are also observed after steroid abuse. The decision to undergo a sex transformation taken by a former East German female athlete suggests that long lasting AAS intake during puberty could lead to sexual identity disturbances in women.
The other endocrine effects of anabolic steroids include changes in serum concentrations of some hormones, impairment of the thyroid function (decreased T3, T4), and insulin resistance and diminished glucose tolerance.