Men facing prostate cancer treatment often worry about resulting hormonal changes, particularly the effect on testosterone levels. Prostate cancer cells rely on male hormones, or androgens, to grow, making treatments that target these hormones highly effective. It is important to distinguish between the physical removal of the prostate gland and the systemic medical therapies designed to alter the body’s hormonal environment. This article clarifies the specific relationship between prostate removal and testosterone production, while detailing treatments that intentionally cause significant hormonal shifts.
Where Testosterone is Produced
The prostate gland is hormone-responsive, using androgens like testosterone for growth and function, but it is not the source of these hormones. The vast majority of circulating testosterone (90% to 95%) is produced by the Leydig cells located within the testes.
A smaller amount (5% to 10%) is synthesized by the adrenal glands, which sit on top of the kidneys. The brain controls this production through the hypothalamic-pituitary-gonadal axis. The hypothalamus releases gonadotropin-releasing hormone (GnRH), which signals the pituitary gland to release luteinizing hormone (LH). LH then travels to the testes to stimulate testosterone production.
Direct Impact of Radical Prostatectomy
Radical prostatectomy, the surgical procedure to remove the entire prostate gland and seminal vesicles, does not typically result in a long-term reduction of serum testosterone levels. The surgery is performed in the pelvic region and intentionally leaves the testes, the primary testosterone-producing organs, completely intact.
A temporary decline in testosterone may be observed in the first month following the procedure. This short-term dip is generally attributed to the physiological stress and trauma associated with major surgery. Studies show that testosterone levels usually recover and return to their pre-operative baseline values within about three months.
In some cases, testosterone levels may even show a slight, long-term increase, along with an increase in Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH). This suggests the prostate might have mildly suppressed the body’s hormone control system, a suppression that is lifted after removal. The surgery itself does not cause the severe, long-term testosterone deficiency often associated with prostate cancer treatment.
Other Treatments Causing Hormonal Changes
The primary reason many prostate cancer patients experience low testosterone is the use of Androgen Deprivation Therapy (ADT), also known as hormone therapy. ADT is a systemic medical treatment designed to intentionally reduce androgen levels to inhibit the growth of hormone-sensitive prostate cancer cells. The goal is to achieve “castrate levels” of testosterone, typically defined as below 50 nanograms per deciliter (ng/dL).
One common method involves drugs called Luteinizing Hormone-Releasing Hormone (LHRH) agonists or antagonists. LHRH agonists (e.g., leuprolide or goserelin) initially overstimulate the pituitary gland’s receptors, causing them to shut down. This stops the release of LH, halting the signal for testosterone production in the testes. LHRH antagonists (e.g., degarelix) achieve the same result more quickly by directly blocking the pituitary receptors without the initial temporary surge in testosterone known as a “flare.”
Another approach is the use of anti-androgen medications. These do not stop testosterone production but instead block the androgen receptors on the surface of cancer cells. By preventing testosterone and dihydrotestosterone (DHT) from binding, the drugs stop the cancer cells from receiving the growth signal. Surgical castration, known as bilateral orchiectomy, is sometimes performed as an alternative to drug therapy to permanently stop the primary source of testosterone production.
Post-Treatment Monitoring and Management
Monitoring hormone levels is an important part of post-treatment care, regardless of whether a patient underwent radical prostatectomy or received ADT. Low testosterone levels, whether from ADT or pre-existing conditions, can cause common symptoms. These include fatigue, decreased sex drive, hot flashes, and a loss of muscle mass and bone density.
For patients who received ADT, testosterone recovery time is highly variable. It depends significantly on the duration of the therapy, the patient’s age, and their baseline testosterone level before treatment. While about 75% of men may see their testosterone levels rise above 300 ng/dL within two years of stopping ADT, only about half will return to their exact pre-treatment level. Monitoring is necessary to manage persistent symptoms and determine if hormone levels are returning to a functional range.
Testosterone Replacement Therapy (TRT) is an option for men with persistently low testosterone after treatment, but it requires careful consideration. Historically, TRT was avoided due to the belief that testosterone would fuel cancer recurrence. Modern clinical data suggest that for select patients definitively treated for localized prostate cancer, such as with a successful radical prostatectomy, TRT can be safely administered. The goal is often to raise the total testosterone level to a range between 450 and 700 ng/dL.
Patients who start TRT must be closely followed with regular blood tests, including monitoring their Prostate-Specific Antigen (PSA) levels, to watch for any sign of cancer recurrence. If an undetectable PSA level rises after starting TRT, it can signal a recurrence that was previously masked by the low hormone environment. The decision to start TRT is a shared one between the patient and their urologist or oncologist, balancing quality of life improvement against the theoretical risk of stimulating any remaining cancer cells.