Anabolic steroids making musclemen infertile. Growing numbers of men are becoming infertile because they take anabolic steroids in their quest for a muscular body, doctors have warned. Urologists are seeing more and more men whose difficulty in becoming a father is linked to consumption of the muscle-boosting drugs. Steve Payne, a consultant urologist at the Manchester Royal Infirmary and a council member of the British Association of Urological Surgeons, said: “Many fit young men who believe they are at the peak of physical perfection don’t believe it could be their fault when their wives or girlfriends find it difficult to become pregnant. “They are insulted when it is suggested that they undergo a sperm test, and horrified when the results of those tests show an absence of sperm in the sample.”
Such men are then referred to a urologist, and undergo a blood test. If they have been using steroids, they often have what Payne calls deranged levels of sex hormones. Men who regularly go to the gym should avoid taking steroids to bulk up, Payne added. Acne, aggression and an unexplained, orangey skin tone akin to a tan are also associated with use of steroids.
Dr Allan Pacey, a senior lecturer in andrology at Sheffield University, warned: “It is a very real risk that men who take anabolic steroids will become infertile. It’s almost certain that they [the steroids] will have an effect of some sort on their fertility and, in the worst-case scenario, that sperm production will stop altogether. Some men who stop taking steroids never regain their reproductive capacity and for others it takes years for normal sperm production to resume, Pacey added.
Clomiphene citrate is an orally administered, nonsteroidal ovulatory drug typically used in female infertility management. It has both estrogenic and antiestrogenic properties. Clomiphene citrate initiates a series of endocrinologic events that cause a gonadotropin surge, which in turn causes an increase in steroidogenesis. Clomiphene citrate is thought not to have any inherent androgenic or anti-androgenic effect. In this case, we were challenging the pituitary gland to produce a surge of gonadotropins to help restore function to the Leydig cells to produce T.
Clomiphene citrate has been shown to increase T levels in both normal and impotent hypogonadal men probably reflecting the primacy of estrogen over T in the feedback regulation of male gonadal function. In a small, doubleblind, placebo-controlled, crossover study of clomiphene against placebo in impotent men with secondary hypogonadism, there was a significant rise of LH, FSH, and T with clomiphene. However, the study in these 17 men did not reveal any improvement of sexual function as measured with questionnaires and penile tumescence and rigidity testing.
Another study investigated the hormonal response to clomiphene in alcoholics with hypogonadism and found that
clomiphene can increase androgens and estrogens. The rise in estrogens was thought to be due to peripheral conversion of androgens to estrogens. Paradoxically, one study failed to show that clomiphene could restore pituitary testicular responsiveness in hypogonadotrophic hypogonadism but succeeded with human chorionic gonadotropin .
Clomiphene citrate has been used successfully in the treatment of idiopathic hypogonadotrophic hypogonadism induced by excessive exercise such as marathon running.
In that case report, reestablishment of the physiologic hypothalamic-pituitary-gonadal axis with the return of normal T and gonadal function was achieved with clomiphene citrate (50 mg, 2 times per day) over 5 months. In our case, the reestablishment of eugonadal status was achieved with just a short challenge of clomiphene citrate 100 mg over 2 weeks,but the patient relapsed. He needed a longer course of 2 months of clomiphene citrate to maintain eugonadal status.
Both cases, including ours, suggest that early intervention with clomiphene can restore the hypothalamic-pituitary-gonadal axis. We are still continuing to follow up our patient to establish long-term effects. The patient did not suffer from
any hot flashes or other side effects from clomiphene citrate. There have been no previously documented cases of clomiphene citrate improving exogenous steroid-induced testicular failure. The mechanism of initial testicular failure could be due to the suppression of LH due to the use of exogenous steroids, which in turn leads to decreased T levels. We postulate that clomiphene citrate can reestablish the axis even after steroid abuse has initially shut down the axis. It can induce the gonadotropin surge, initiate T levels to increase, and improve gonadal function and reverse symptoms. This was possible in this case as the patient was relatively young and presumably had a more elastic axis.