Castration is defined as the surgical removal of the testes, a procedure medically known as bilateral orchiectomy. This intervention directly eliminates the body’s main source of androgen hormones, particularly testosterone. The testes are responsible for producing the vast majority of circulating testosterone, a hormone that regulates male physical development, metabolism, and reproductive function.
The Immediate Hormonal Shift
The most immediate consequence of the procedure is the near-total cessation of testosterone production. The testes produce approximately 95% of the body’s testosterone, with only a small residual amount coming from the adrenal glands. Following bilateral orchiectomy, testosterone concentration declines, reaching “castrate levels”—defined as below 50 nanograms per deciliter—within hours.
This dramatic drop disrupts the hypothalamic-pituitary-gonadal (HPG) axis. Normally, testosterone provides negative feedback to the pituitary gland and the hypothalamus, regulating the release of Luteinizing Hormone (LH) and Follicle-Stimulating Hormone (FSH). Without the primary hormone source, this feedback loop is broken. The pituitary gland increases its output of LH and FSH in an attempt to stimulate the now-absent testicular tissue. The resulting hormonal state is profound hypogonadism, which drives all subsequent long-term physical and psychological changes.
Alterations to Body Composition and Secondary Characteristics
Chronic testosterone deprivation fundamentally changes the body’s metabolic and physical landscape. A visible change is a significant alteration in body composition, characterized by a loss of lean muscle mass, known as sarcopenia. This muscle atrophy occurs because testosterone is an anabolic hormone; its absence increases muscle protein breakdown while impairing the muscle’s ability to synthesize new protein.
The loss of muscle mass is coupled with an increase in total body fat, particularly a redistribution of adipose tissue to a central and abdominal pattern. Testosterone normally inhibits the expansion of fat, so its removal promotes a shift toward a higher percentage of body fat. The resulting decrease in muscle strength and frailty can manifest within weeks to months following the procedure.
Skeletal health also suffers under this androgen-deficient state, leading to a rapid loss of bone mineral density (BMD). Testosterone contributes to bone health directly by signaling through androgen receptors on osteoblasts, and indirectly by converting into estrogen, which maintains bone mass. The loss of both mechanisms impairs the formation of new bone, particularly the spongy inner structure known as trabecular bone. This accelerated bone loss increases the long-term risk of developing osteoporosis and fragility fractures, especially in the lumbar spine and femoral neck.
Physical changes in secondary sex characteristics also become apparent over time. Body and facial hair often thin out, and the progression of male-pattern baldness, which is androgen-dependent, ceases. If the procedure occurs before puberty, the larynx never fully develops, resulting in a permanent high-pitched voice. If performed after puberty, the voice pitch remains the same, though volume may slightly decrease.
Impacts on Sexual Function and Psychological Well-being
The hormonal shift affects sexual function, with a loss of libido, or sexual desire, being a common and early symptom. Testosterone is the primary driver of male sexual interest, and its deficiency leads to a reduction in sexual thoughts and fantasies. While the body can no longer produce sperm, leading to sterility, the impact on erectile function is more complex.
The low androgen state compromises the structural integrity of the erectile tissue in the penis by reducing the smooth muscle content in the corpus cavernosum. This change impairs the tissue’s ability to trap blood and achieve full rigidity, resulting in erectile dysfunction. A small percentage of men may still achieve a functional erection, often psychologically triggered, especially if their residual free testosterone levels are slightly higher.
The lack of testosterone alters brain chemistry, leading to changes in mood and cognitive function. Men frequently report psychological symptoms such as low mood, dysphoria, irritability, and fatigue. These symptoms often overlap with clinical depression, and hormonal deprivation is associated with an increased risk of developing a depressive disorder.
The neuroprotective effects of testosterone are also lost, negatively impacting cognitive performance. Individuals may experience impaired memory, reduced concentration, and slower processing speed following the procedure. These psychological and cognitive changes compound the physical alterations, often leading to issues with self-identity and reduced quality of life.
Medical Context and Therapeutic Applications
Surgical castration is primarily used as a form of Androgen Deprivation Therapy (ADT) to treat advanced prostate cancer. Since prostate cancer cells often rely on androgens for growth, eliminating the main source of testosterone can effectively slow the progression of the disease. This is achieved either through bilateral orchiectomy or via chemical castration using medications that block the HPG axis.
For patients undergoing castration for reasons other than prostate cancer, hormone replacement therapy (HRT) is initiated. HRT is necessary to mitigate the severe long-term health risks associated with chronic hypogonadism, such as osteoporosis, muscle wasting, and cardiovascular issues. If the procedure is performed to halt the growth of an androgen-sensitive tumor, HRT is avoided to maintain the therapeutic effect of androgen suppression.