Sex differences range from nearly absolute to simply statistical. Sex-dichotomous differences are developments which are wholly characteristic of one sex only. Examples of sex-dichotomous differences include aspects of the sex-specific genital organs such as ovaries, a uterus or a phallic urethra. In contrast, sex-dimorphic differences are matters of degree (e.g., size of phallus). Some of these (e.g., stature, behaviors) are mainly statistical, with much overlap between male and female populations.
Nevertheless, even the sex-dichotomous differences are not absolute in the human population, and there are individuals who are exceptions (e.g., males with a uterus, or females with an XY karyotype), or who exhibit biological and/or behavioral characteristics of both sexes.
Sex differences may be induced by specific genes, by hormones, by anatomy, or by social learning. Some of the differences are entirely physical (e.g., presence of a uterus) and some differences are just as obviously purely a matter of social learning and custom (e.g., relative hair length). Many differences, though, such as gender identity, appear to be influenced by both biological and social factors ("nature" and "nurture").
The early stages of human differentiation appear to be quite similar to the same biological processes in other mammals and the interaction of genes, hormones and body structures is fairly well understood. In the first weeks of life, a fetus has no anatomic or hormonal sex, and only a karyotype distinguishes male from female. Specific genes induce gonadal differences, which produce hormonal differences, which cause anatomic differences, leading to psychological and behavioral differences, some of which are innate and some induced by the social environment.
The various ways that genes, hormones, and upbringing affect different human behaviors and mental traits are difficult to test experimentally and charged with political conflict.
Investigation of other cases of human sex reversal (XX males, XY females) has led to discovery of other genes crucial to testicular differentiation on autosomes (e.g., WT-1, SOX9, SF-1), and the short arm of X (DSS).
|Sex differentiating events|
|0||blastocyst||Inactivation of one X chromosome|
|4||2-3||Development of wolffian ducts|
|5||7||Migration of primordial germ cells in the undifferentiated gonad|
|6||10-15||Development of müllerian ducts|
|7||13-20||Differentiation of seminiferous tubules|
|8||30||Regression of müllerian ducts in male fetus|
|8||32-35||Appearance of Leydig cells. First synthesis of testosterone|
|9||43||Total regression of müllerian ducts. Loss of sensitivity of müllerian ducts in the female fetus|
|9||43||First meiotic prophase in oogonia|
|10||43-45||Beginning of masculinization of external genitalia|
|10||50||Beginning of regression of wolffian ducts in the female fetus|
|12||70||Fetal testis is in the internal inguinal ring|
|12-14||70-90||Male penile urethra is completed|
|14||90||Appearance of first spermatogonia|
|16||100||Appearance of first ovarian follicles|
|17||120||Numerous Leydig cells. Peak of testosterone secretion|
|20||150||Regression of Leydig cells. Diminished testosterone secretion|
|24||200||First multilayered ovarian follicles. Canalisation of the vagina|
|28||230||Cessation of oogonia multiplication|
|28||230||Descent of testis|
In a male, SRY and other genes induce differentiation of supporting cells into Sertoli cells and (indirectly) steroidogenic cells into Leydig cells to form testes, which become microscopically identifiable and begin to produce hormones by week 8. Germ cells become spermatogonia.
Without SRY, ovaries form during months 2-6. Failure of ovarian development in 45,X girls (Turner syndrome) implies that two functional copies of several Xp and Xq genes are needed. Germ cells become ovarian follicles. Supporting and steroidogenic cells become theca cells and granulosa cells, respectively.
In a male fetus, testes produce steroid and protein hormones essential for internal and external anatomic differentiation. Leydig cells begin to make testosterone by the end of month 2 of gestation. From then on, male fetuses have higher levels of androgens in their systemic blood than females. The difference is even greater in pelvic and genital tissues. Antimullerian hormone (AMH) is a protein hormone produced by Sertoli cells from the 8th week on. AMH suppresses development of müllerian ducts in males, preventing development of a uterus.
Fetal ovaries produce estradiol, which supports follicular maturation but plays little part in other aspects of prenatal sexual differentiation, as maternal estrogen floods fetuses of both sexes.
Local testosterone causes each wolffian duct to develop into epididymis, vas deferens, and seminal vesicles. Without male testosterone levels, wolffian ducts degenerate and disappear. Müllerian ducts develop into a uterus, fallopian tubes, and upper vagina unless AMH induces degeneration. The presence of a uterus is stronger evidence of absence of testes than the state of the external genitalia.
For illustrations, see the External links section.
Males become externally distinct between 8 and 12 weeks, as androgens enlarge the phallus and cause the urogenital groove and sinus to fuse in the midline, producing an unambiguous penis with a phallic urethra, and a thinned, rugated scrotum.
A sufficient amount of any androgen can cause external masculinization. The most potent is dihydrotestosterone (DHT), generated from testosterone in skin and genital tissue by the action of 5α-reductase. A male fetus may be incompletely masculinized if this enzyme is deficient. In some diseases and circumstances, other androgens may be present in high enough concentrations to cause partial or (rarely) complete masculinization of the external genitalia of a genetically female fetus.
Further sex differentiation of the external genitalia occurs at puberty, when androgen levels again become disparate. Male levels of testosterone directly induce growth of the penis, and indirectly (via DHT) the prostate.
Visible differentiation occurs at puberty, when estradiol and other hormones cause breasts to develop in girls. However, fetal or neonatal androgens may modulate later breast development by reducing the capacity of breast tissue to respond to later estrogen.
General habitus and shape of body and face, as well as sex hormone levels, are similar in prepubertal boys and girls. As puberty progresses and sex hormone levels rise, obvious differences appear.
In males, testosterone directly increases size and mass of muscles, vocal cords, and bones, enhancing strength, deepening the voice, and changing the shape of the face and skeleton. Converted into DHT in the skin, it accelerates growth of androgen-responsive facial and body hair. Taller stature is largely a result of later puberty and slower epiphyseal fusion.
In females, in addition to breast differentiation, estrogen also widens the pelvis and increases the amount of body fat in hips, thighs, buttocks, and breasts. Estrogen also induces growth of the uterus, proliferation of the endometrium, and menses.
The difference in adult masculine and feminine faces is largely a result of heavier jaw and jaw muscle development induced by testosterone in late adolescence. Masculine features on average are slightly thicker and coarser. Androgen-induced recession of the male hairline accentuates these differences by middle adult life.
Sexual dimorphism of skeletal structure develops during childhood, and becomes more pronounced at adolescence. Sexual orientation has been demonstrated to correlate with skeletal characters that become dimorphic during early childhood (such as arm length to stature ratio) but not with characters that become dimorphic during puberty (such as shoulder width) (Martin & Nguyen, 2004).
In most animals, differences of exposure of a fetal or infant brain to sex hormones produce significant and irreversible differences of brain structure and function which correlate with adult reproductive behavior. This seems to be the case in humans as well; sex hormone levels in male and female fetuses and infants differ, and both androgen receptors and estrogen receptors have been identified in brains. Several sex-specific genes not dependent on sex steroids are expressed differently in male and female human brains. Structural sex differences begin to be recognizable by 2 years of age, and in adult men and women include size and shape of corpus callosum and certain hypothalamic nuclei, and the gonadotropin feedback response to estradiol.
Human adults and children show many psychological and behavioral sex differences, both dichotomous and dimorphic. Some (e.g., dress) are learned and obviously cultural. Others are demonstrable across cultures and may have both biological and learned determinants. For example, girls are, on average, more verbally fluent than boys, but males, on average, are better at spatial calculation. Because we cannot explore hormonal influences on human behavior experimentally, and because potential political implications are so unwelcome to many factions of society, the relative contributions of biological factors and learning to human psychological and behavioral sex differences (especially gender identity, role, and orientation) remain unsettled and controversial.
Current theories of mechanisms of sexual differentiation of brain and behaviors in humans are based primarily on three sources of evidence: animal research involving manipulation of hormones in early life, observation of outcomes of small numbers of individuals with disorders of sexual development (intersex conditions or cases of early sex reassignment), and statistical distribution of traits in populations (e.g., rates of homosexuality in twins). Many of these cases suggest some genetic or hormonal effect on sex differentiation of behavior and mental traits; others do not.
In addition to affecting development, changing hormone levels affect certain behaviors or traits that are gender dimorphic, such as superior verbal fluency among women..
In most mammalian species females are more oriented toward child rearing and males toward competition with other males.
Biologically, this perspective is supported by the fact that there are neither female genes nor female hormones that correspond to the hormones active in males only. Estrogen, for instance, is present in both the male and female fetus.
‘translation’ to the human situation possible? (2007)Hormones and Behavior 50:579–88.
Hughes IA, Houk C, Ahmed SF, Lee PA, LWPES/ESPE Consensus Group. (2006) Consensus statement on management of intersex disorders. Arch Dis Childhood.
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