Virilization

In the prenatal period, virilization refers to closure of the perineum, thinning and wrinkling (rugation) of the scrotum, growth of the penis, and closure of the urethral groove to the tip of the penis. In this context, masculinization is synonymous with virilization.

Prenatal virilization of genetic females and undervirilization of genetic males are common causes of ambiguous genitalia and intersex conditions.

For many years, it was widely believed that in mammals, the female is the "default" developmental pathway, and the SRY gene on the Y chromosome is responsible for suppressing the development of female characteristics and stimulating males characteristics. In this scenario, an embryo would passively develop female sexual characteristics without intervention by the SRY gene. However, in the early 2000s, other genes, such as WNT4 and RSPO1, were discovered that perform the opposite function – i.e., genes which suppress masculinization and stimulate feminization.[2]

Two processes: defeminization, and masculinization, are involved in producing male typical morphology and behavior.

In common as well as medical usage, virilization often refers to the process of normal male puberty. These effects include growth of the penis and the testes, accelerated growth, development of pubic hair, and other androgenic hair of face, torso, and limbs, deepening of the voice, increased musculature, thickening of the jaw, prominence of the neck cartilage, and broadening of the shoulders.

Virilization can occur in childhood in both males and females due to excessive amounts of androgens. Typical effects of virilization in children are pubic hair, accelerated growth and bone maturation, increased muscle strength, acne, and adult body odor. In males, virilization may signal precocious puberty, while congenital adrenal hyperplasia and androgen producing tumors (usually) of the gonads or adrenals are occasional causes in both sexes.[3]

Virilization in females can manifest as clitoral enlargement, increased muscle strength, acne, hirsutism, frontal hair thinning, deepening of the voice, menstrual disruption due to anovulation, and a strengthened libido.[4] Some of the possible causes of virilization in females are:

• Androgen-producing tumors of the
  • ovaries
  • adrenal glands (see adrenal tumor)
  • pituitary gland (see pituitary adenoma)
• Hyperthecosis
• Hypothyroidism
• Anabolic steroid exposure
• Congenital adrenal hyperplasia due to 21-hydroxylase deficiency (late-onset)
• Conn's syndrome

Transgender people who were medically assigned female at birth sometimes elect to take hormone replacement therapy. This process causes virilization by inducing many of the effects of a typically male puberty. Many of these effects are permanent, but some effects can be reversed if the transgender individual stops or pauses their medical treatment.

Demasculinization refers to the reversal of virilization. Some but not all aspects of virilization are reversible. Demasculinization occurs naturally with andropause, pathologically with hypogonadism, and artificially or medically with antiandrogens, estrogens, and orchiectomy. It is desired by transgender women who have undergone the changes of pubertal masculinization, to restore and induce feminine physical traits that would otherwise be masked or never occur. Some virilized traits remain though (such as body hair, a hard jawline and an enlarged larynx), due to the fashion in which virilization affects a body's physiology.

• Ambiguous genitalia
• Androgen
• Clitoromegaly
• Defeminization
• Feminization (biology)
• Hirsutism
• Secondary sex characteristics
• Sexual differentiation

• Howell, W. M., Black, D. A., & Bortone, S. A. (1980). Abnormal expression of secondary sex characters in a population of mosquitofish, Gambusia affinis holbrooki: evidence for environmentally-induced masculinization. Copeia, 676–681.