The phrase “Do men’s balls drop?” suggests a singular, sudden event, but the reality is a complex, multi-stage biological process called testicular descent. This mechanism involves intricate hormonal signaling and anatomical changes essential for the formation of the male reproductive system.
The Initial Location of the Testes
The testes do not originate in the scrotum but begin their development high within the body. In the early male fetus, the gonads form on the posterior abdominal wall, near the developing kidneys, in a region known as the urogenital ridge. This initial, high placement is similar in both male and female embryos before sexual differentiation is complete.
The movement away from this warm, internal environment is biologically necessary for future reproductive function. Sperm production (spermatogenesis) requires a temperature several degrees lower than the core body temperature. The final location in the external scrotum provides this cooler environment. This journey is an active, hormonally-driven relocation controlled by a sequence of genetic and endocrine signals that unfold over several months of gestation.
The Two-Phase Mechanism of Descent
Testicular descent is described as a two-stage model, with each phase regulated by distinct hormones and anatomical movements.
The Transabdominal Phase
This first stage occurs relatively early in gestation, between the 8th and 15th weeks. This initial movement is largely controlled by Insulin-like factor 3 (InsL3), a hormone produced by the Leydig cells in the fetal testes. InsL3 acts on the gubernaculum, a ligament-like structure connecting the caudal end of the testis to the future scrotal area.
Under the influence of InsL3, the gubernaculum swells, thickening and expanding. This swelling anchors the testis near the entrance to the inguinal canal, preventing the gonad from moving higher as the fetus grows. Simultaneously, the cranial suspensory ligament, which attaches the gonad to the upper abdominal wall, regresses, positioning the testis for the next major leg of its journey.
The Inguinoscrotal Phase
The second stage takes place later in the pregnancy, typically between the 25th and 35th weeks of gestation. This phase involves the testis moving through the inguinal canal, a passage in the abdominal wall, and into the scrotum.
This final migration is primarily dependent on androgens, specifically testosterone, also secreted by the fetal Leydig cells. Testosterone promotes the outward migration of the gubernaculum, which actively guides the testis along the pathway and into the scrotal sac. The genitofemoral nerve, which releases a neuropeptide called CGRP, also plays an important role in controlling the direction of this complex migration.
Timing and Completion of the Process
After the transabdominal phase is complete by the 15th week, the testis pauses near the inguinal canal until the third trimester. The inguinoscrotal movement begins around the 7th month of pregnancy, with the majority of testes fully descending into the scrotum by the 33rd gestational week. Most male infants are born with their testes already in the correct, final position.
For a small percentage of newborns, the descent completes in the first few months after birth. This postnatal movement is linked to a natural surge in the infant’s gonadotropin and testosterone levels. If the testis has not reached the scrotum by about six months of age, spontaneous descent becomes highly unlikely.
Clinical Implications of Failed Descent
When the two-phase process of descent is interrupted, the condition is known as cryptorchidism, or undescended testes. This is the most prevalent congenital anomaly of the male reproductive system, affecting up to 3% of full-term male infants.
Leaving the testes in an undescended position, such as the inguinal canal or abdomen, exposes them to the body’s core temperature. This excessive heat exposure can cause irreversible damage to the sperm-producing cells, leading to fertility impairment later in life. The risk of infertility is significantly higher in bilateral cases compared to unilateral cryptorchidism.
The condition also carries a heightened risk of developing testicular cancer, which is four to ten times greater than in the general population. Furthermore, it increases the risk of testicular torsion, a painful twisting of the spermatic cord.
The standard medical intervention for cryptorchidism is a surgical procedure called orchiopexy. Current guidelines recommend performing this operation between 6 and 18 months of age to reposition the testis into the scrotum. Early surgical correction minimizes the duration of heat-related damage and reduces the long-term risk of germ cell malignancy.