Male genital development and standards: Popular science on male health regarding size and development

Development of Male Genitalia

During the third week of embryonic development, mesodermal cells migrate to the area around the cloaca, forming a pair of slightly raised folds called cloacal folds. At the head of these folds, close to the cloacal membrane, a genital tubercle forms. At this stage, the embryo may be influenced by internal and external environmental factors, developing in different sex directions. In the sixth week of embryonic development, the differentiation of fetal gonads determines the sex of the fetus. The cloacal membrane is further divided by the rectoseptum into the urogenital sinus membrane and anal membrane, forming the urethral fold and anal fold. A pair of protrusions develop on either side of the urethral fold, forming the scrotal bulge, which later develops into the male scrotum. At this time, the external genitalia are still indistinguishable from males and females in appearance. Between 10 and 12 weeks, under the influence of androgens, the masculinization of the external genitalia becomes increasingly pronounced. The genital tubercle rapidly elongates to form the penis. The skin folds distal to the penis extend beyond the glans, forming the foreskin. The corpora cavernosa and corpora spongiosum originate from the mesenchyme within the genital tubercle, and the two bulges converge to form the scrotum.

Before the 8th week of embryonic development, the external genitalia of both sexes are identical in morphology, and can develop into either male or female forms. In embryos without gonadal function, the vulva develops into a female phenotype. Male development of the vulva depends on the action of dihydrotestosterone (DHT). In early male embryos, the testes can spontaneously secrete testosterone, and later, under the influence of gonadotropins, they secrete testosterone. Testosterone is converted into DHT in the vulvar tissue. This active DHT promotes the development of the urogenital sinus and external genitalia in a male direction. In the absence of androgens, regardless of whether the karyotype is XY or XX, the fetus will exhibit female external characteristics. In cases of insufficient androgen secretion, the fetus will exhibit male hypoplasia. Male sexual differentiation also depends on a substance secreted by the fetal testes that inhibits the paramesonephric duct, causing unilateral paramesonephric duct degeneration and preventing the formation of the uterus and fallopian tubes, thus ensuring the differentiation of male internal reproductive structures. If there is insufficient secretion of substances that inhibit the paramesonephric duct, the newborn male infant may have a fully differentiated uterus and fallopian tubes. If the synthesis, secretion, and conversion of testosterone to dihydrotestosterone in the fetus are impaired, defects in androgen receptor activity and defects in local tissue cells can all cause incomplete sexual development in male embryos.

Before the 12th week of female embryonic development, abnormally high levels of endogenous or exogenous androgens can cause the external genitalia of female fetuses to differentiate into male characteristics, resulting in female pseudohermaphroditism. In embryos with the Y chromosome, the testes, initially called the testicular cords, form in the 8th week. By 4 months, the human embryonic testicular cords are horseshoe-shaped, and the primordial germ cells within differentiate into spermatogonia, which will form sperm in adulthood; the epithelial cells differentiate into Sertoli cells. Subsequently, seminiferous tubules gradually form. Before puberty, the seminiferous tubules are composed entirely of Sertoli cells and spermatogonia. From neonatal to puberty, the Sertoli cells of the testes do not change significantly. In newborns, some spermatogonia degenerate, while others differentiate into adult spermatogonia. Some cells between the seminiferous tubules differentiate into testicular interstitial cells, which secrete testosterone, while others differentiate into fibroblasts, collectively forming the testicular interstitium.

The testes descend to the edge of the pelvis at 18 weeks of embryonic development and descend along the inguinal canal into the scrotum between 28 and 32 weeks. If the testes have not descended into the scrotum after birth, it is considered incomplete testicular descent or cryptorchidism. The human prostate gland is divided into five lobes: left, right, anterior, posterior, and middle. It develops from the prostatic epithelium on the primitive urethra during late embryonic development. It encircles the urethra near the bladder neck in the posterior urethra, and its glandular openings into the seminal colliculus of the posterior urethra. Prostatic fluid can mix with semen through this opening, and it promotes the coagulation and liquefaction of semen.

The size of the penis

The penis is the male external genitalia exposed on the body surface. No two people in the world look exactly alike. The various organs in the human body are not all the same size; they always vary, generally within a range of maximum and minimum. The length of a normal male penis also varies. Experts have conducted research on the length and circumference of the penis in the flaccid state of thousands of Han Chinese young men. The average length of the penis in the flaccid state is 3.7–10.6 cm, with an average of 6.55 cm. The average transverse diameter of the penis is 2.57 cm. The average circumference of the glans penis is 8.50 cm. Therefore, it can be said that the size of the penis of every adult male varies, but as long as it is within the range of 3.7–10.6 cm, it is considered normal.

It is commonly believed that tall men have long penises and short men have short penises, but this is not the case. Although the length of the penis varies considerably in the flaccid state, the difference between a smaller and a larger penis in the erect state is negligible. Clinical studies have shown that, in a normal flaccid state, a penis that appears short and a penis that appears large do not differ significantly in length when stimulated to reach a fully erect state. As long as penile development is normal and there are no congenital malformations, its physiological functions are generally normal and will not affect marriage and fertility. Penises within the normal length range can achieve sexual satisfaction for both partners during erection.

Because a woman's most sensitive areas are located in the outer third of the vagina, a penis within the normal length range, even one that is slightly smaller, can satisfy a woman's sexual needs. There is no need to worry, as this could create psychological burdens and affect marital happiness. If the penis has congenital malformations, it is necessary to consult a specialist. Common malformations fall into two main categories: one is abnormal development of secondary sexual characteristics; the other is various types of hypospadias and epispadias. In cases where the penis is not only shorter than normal but also has varying degrees of penile curvature, it will affect sexual function and fertility, requiring surgical correction. For men whose penis length is slightly smaller than normal, treatment is unnecessary. After puberty, the male reproductive organs are fully developed and will not change further; there is no magic bullet to make the penis larger. As long as the penis is developing normally, even if it is slightly small, it will not affect sexual life.