Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively. The amount of testosterone synthesized is regulated by the hypothalamic–pituitary–testicular axis (Figure 2). In addition, the amount of testosterone produced by existing Leydig cells is under the control of LH, which regulates the expression of 17β-hydroxysteroid dehydrogenase. This additional information could suggest, contrarily, that testosterone may encourage greed or selfishness. In humans, testosterone appears more to promote status-seeking and social dominance than simply increasing physical aggression. Thus the link between testosterone and aggression and violence is due to these being rewarded with social status. For individuals raised as females, bilateral gonadectomy is recommended in childhood to avoid virilization and to eliminate the risk of testicular tumors (36). Final height in CAIS is above normal mean female height, probably due to the action of the growth-controlling gene (GCY) located at the Y chromosome (15). Patients with AIS developed breasts with estradiol levels in normal male range suggesting that the lack of androgen action is the main driver of breast development in these patients, rather than an increased estrogen secretion. Androgenic insensitivity syndrome is the most common cause of disorders of sexual differentiation in 46,XY individuals. Nearly all studies of juvenile delinquency and testosterone are not significant. Testosterone levels play a major role in risk-taking during financial decisions. In humans and other species that utilize allomaternal care, paternal investment in offspring is beneficial to said offspring's survival because it allows the two parents to raise multiple children simultaneously. The number of Leydig cells in turn is regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Testosterone is also synthesized in far smaller total quantities in women by the adrenal glands, thecal cells of the ovaries, and, during pregnancy, by the placenta. In the final and rate limiting step, the C17 keto group androstenedione is reduced by 17β-hydroxysteroid dehydrogenase to yield testosterone. Testosterone, via its active metabolite 3α-androstanediol, is a potent positive allosteric modulator of the GABAA receptor. In the bones, estradiol accelerates ossification of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. It’s crucial to understand that this is a generalization, and significant individual variation exists within every ethnic group. Puberty initiates the process, but full maturation of the androgenic system can take years. Thirdly, the thickness and coarseness of the hairs can be an indicator. Does hair appear relatively uniformly across your cheeks, chin, and neck, or are there significant sparse patches from the outset? It requires patience, proper care, and an understanding of what your beard needs. As has been also found for other steroid hormone receptors such as estrogen receptors, androgen receptors can have actions that are independent of their interactions with DNA. Thus, changes in levels of specific proteins in cells is one way that androgen receptors control cell behavior. One of the known target genes of androgen receptor activation is the insulin-like growth factor 1 receptor (IGF-1R). Testosterone is therefore responsible primarily for the development of male primary sexual characteristics, whilst dihydrotestosterone is responsible for secondary male characteristics. Androgen-regulated genes are critical for the development and maintenance of the male sexual phenotype. That’s where androgen sensitivity comes in—and at the center of it is the androgen receptor (AR). We lose sight of the complex interplay among sex hormones—including both androgenic and estrogenic hormones—stress hormones like cortisol, and the critical role of hormone receptor sensitivity. If we narrow our focus on male sex hormone health to specific levels of free, bound, and total testosterone, we risk losing the bigger picture. Typically in AIS, basal testosterone and LH levels are elevated demonstrating the impairment of androgen negative feedback on the anterior pituitary (22). In MAIS, hormone concentrations are usually normal, but elevated serum LH and testosterone levels could be found in these patients (19). In our cohort, the final height of CAIS individuals (165.7 ± 8.9 cm) was taller than described for Brazilian females, but lower than expected for Brazilian males (15). Impairment of androgen secretion and defects in the androgen receptor will compromise the virilization process. In humans, the critical period for genitalia virilization occurs between 8 and 14 weeks of gestation and depends on the presence of androgens and of a functioning androgen receptor (9). AIS was first described by Morris, in 1953, with the clinical description of 82 female patients with testes but female phenotype and for this reason Morris named the syndrome as testicular feminization (4).
