A diagnosis of low testosterone, known as hypogonadism, and a low sperm count often appear linked, but their relationship is surprisingly complex. The connection is not simply one of cause and effect, especially when considering external hormonal treatments. Understanding how the body naturally regulates these two functions is necessary to grasp why certain interventions can lead to a healthy testosterone level yet a drastically reduced sperm count.
How Testosterone Supports Sperm Production
Testosterone is necessary for the creation and maturation of sperm, a process called spermatogenesis. However, the testosterone level circulating in the bloodstream is distinct from the concentration needed inside the testes, where Leydig cells produce testosterone, maintaining a local concentration often 50 to 100 times greater than blood levels.
This high local concentration of testosterone is delivered to the Sertoli cells, the “nurse” cells supporting the developing sperm. The testosterone binds to receptors on these Sertoli cells, initiating and sustaining the complex process of sperm development and preventing the premature death of germ cells. If a man experiences severe, untreated hypogonadism, the lack of this internal hormonal signal will inevitably lead to a low sperm count. Even so, some degree of spermatogenesis can be maintained with intratesticular testosterone levels as low as 5% to 10% of normal.
The Hormonal System Controlling Both
The production of both testosterone and sperm is coordinated by the Hypothalamic-Pituitary-Gonadal (HPG) axis. This feedback loop involves three organs: the hypothalamus, the pituitary gland, and the testes.
The hypothalamus begins the process by releasing Gonadotropin-Releasing Hormone (GnRH), which signals the pituitary gland. The pituitary then releases two hormones: Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH). LH travels to the testes and stimulates the Leydig cells to produce testosterone, while FSH acts on the Sertoli cells to directly promote spermatogenesis. When circulating testosterone levels become high, the hormone feeds back to the hypothalamus and pituitary, signaling them to reduce the release of GnRH and LH, thereby maintaining hormonal balance.
Why Testosterone Therapy Can Lower Sperm Count
The use of external testosterone, known as Testosterone Replacement Therapy (TRT), can drastically reduce sperm count. When testosterone is introduced into the body, the brain senses the high level in the bloodstream. This triggers the negative feedback loop of the HPG axis.
The hypothalamus and pituitary gland interpret the high circulating testosterone as a sign that the testes are producing enough on their own. Consequently, they halt the release of GnRH, LH, and FSH. The cessation of the LH signal stops the Leydig cells from producing their own testosterone, and the cessation of the FSH signal removes a direct stimulus for sperm production.
This suppression causes the testes to shrink and eliminates the high concentration of testosterone needed inside the testes to support spermatogenesis. Despite having a healthy or even high testosterone level in the blood, the man’s internal testicular environment becomes testosterone-deficient, leading to severe oligospermia or even azoospermia. For a man with fertility concerns, TRT is generally avoided because it acts as a hormonal contraceptive, drastically impairing sperm production.
Treatments to Preserve Fertility
For men who have low testosterone and wish to maintain or restore their fertility, treatment strategies focus on stimulating the HPG axis without introducing external testosterone.
Human Chorionic Gonadotropin (hCG)
One approach uses Human Chorionic Gonadotropin (hCG), an injectable medication that mimics LH. HCG directly stimulates the Leydig cells to produce their own testosterone, thereby maintaining the necessary high intratesticular testosterone levels for sperm production, even while bypassing the suppressed pituitary signals.
Clomiphene Citrate
Another option is Clomiphene Citrate, an oral medication that acts as a Selective Estrogen Receptor Modulator (SERM). Clomiphene blocks estrogen receptors in the hypothalamus and pituitary, preventing the negative feedback signal that would normally suppress GnRH, LH, and FSH release. By stimulating the release of LH and FSH, Clomiphene encourages the testes to naturally increase both testosterone and sperm production. In cases of severe suppression, FSH injection may be added to provide a stronger stimulus to the Sertoli cells. These alternatives allow men to treat low testosterone symptoms while preserving the hormonal signals required for fertility.