SEX HORMONES

1. SEX HORMONES • Endocrine glands: • glands that secrete internally (into bloodstream) • Exocrine glands: • secrete externally (i.e. sweat glands) • Endocrine glands secrete hormones • Hormone: • complex chemical with specific actions for specific organs only

2. SEX HORMONES(CONT’D) • Pituitary gland: • called master gland but • Hypothalamus controls pituitary: • Dual function: as a gland, and as a part of the CNS. • As a gland, it reacts to hormonal levels in the bloodstream. As CNS, it reacts to higher brain functions (perceptions, thoughts, feelings, moods). • The pituitary stimulates the gonads: ovaries and testes

3. SEX HORMONES (CONT’D) • Pituitary produces: • FSH • LH • oxytocin (orgasm, birth, milk release) • prolactin • Testes produce: • testosterone • estrogen • inhibin

4. SEX HORMONES (CONT’D) • Ovaries produce: • estrogen • progesterone • testosterone • inhibin • Inhibin • regulates levels of FSH • LH is regulated by levels of either testosterone (males) or estrogen (females)

6. SEX HORMONES (CONT’D) • Follicle-Stimulating Hormone (FSH) – pituitary • In Women: • stimulates the ovary to activate a follicle, maturing an egg • In Men: • stimulates spermatogenesis

7. SEX HORMONES (CONT’D) • Luteinizing Hormone (LH) – pituitary: • In Men: • stimulates Leydig cells in testes to produce testosterone • In Women: • stimulates rupture of follicle, releasing egg, and creating corpus luteus to produce progesterone.

8. SEX HORMONES (CONT’D) • Gonadotropin-Releasing Hormone (GnRH): • released by the hypothalamus in response to sensory receptors or thoughts. • stimulates the pituitary to release its hormones • Estrogen: • hormone produced by the ovaries. Thickens endometrium, starting a week after menstruation

9. SEX HORMONES (CONT’D) • Progesterone: • hormone produced by the corpus luteum of the ovaries after ovulation • Both estrogen and progesterone drop to lowest levels at the end of menstrual cycle. • The low levels of estrogen stimulate the beginning of another cycle.

10. SEX HORMONES (CONT’D) • Testosterone: • produced by gonads and adrenals in both sexes. • Responsible for male characteristics, and for sex drive in both sexes.

11. SEX HORMONES (CONT’D) • Hormonal Output Regulation: • Homeostasis: • state of perfect equilibrium of all physiological states. It’s constantly being broken and restored. E.g. thirst. Hypothalamus central role in homeostasis.

12. SEX HORMONES (CONT’D) • Hormonal Output Regulation (Cont’d): • Negative feedback loops: • When something is low (sodium, estrogen, glucose, etc. etc.) hypothalamus gets signal via bloodstream and activates mechanisms to increase substance. • When something is too high, another negative feedback loop signals to stop production or ingestion. • The hypothalamus signals all other endocrine glands to either step up or decrease production.

13. SEX HORMONES (CONT’D) • THE ROLE OF TESTOSTERONE IN SEX • Testosterone mediates sexual response in both sexes. • It comes in two forms: • bound and free • Men: 95% bound, not active for sexual desire 5% free • Women: 97-99% bound 1-3% free

14. SEX HORMONES (CONT’D) • THE ROLE OF TESTOSTERONE IN SEX (Cont’d) • Amount needed varies in individuals of both sexes. Women more sensitive. • More testosterone does not produce more sexual desire

15. SEX HORMONES (CONT’D) • THE ROLE OF TESTOSTERONE IN SEX (CONT’D) • Additional testosterone has adverse effects: • Men: • hair loss, salt and fluid retention, possible testicular cancer, acne, digestive problems, irritability, aggression • Women: • facial and body hair, muscle mass, smaller breasts, larger clitoris, voice deeper

17. SEXUAL DIFFERENTIATION • Gestational Development of Genitals: • First seven weeks: undifferentiated • two gonads • two sets of ducts (Mullerian and Wolffian) • genital tubercles • genital folds • genital swelling • 7th week: • Y chromosome, if present, turns gonad into testicle.

18. SEXUAL DIFFERENTIATION (CONT’D) • 10th-11th week: • in absence of Y chromosome, ovaries develop. • Both types of gonads start producing their respective hormones. • Female: • absence of testosterone causes degeneration of Wolffian ducts. Mullerian ducts form internal sex organs (uterus, etc.)

19. Sexual Differentiation (Cont’d) • Gestational Development of Genitals (Cont’d): • Female: • absence of testosterone causes degeneration of Wolffian ducts. Mullerian ducts form internal sex organs (uterus, etc.) • Male: • testes produce anti-Mullerian hormone, so they disappear. Wolffian ducts become internal sex organs (epididymis, etc.)

20. SEXUAL DIFFERENTIATION (CONT’D) • Gestational Development of Genitals (Cont’d): • Tubercle, folds and swelling develop into external genitals for each sex. • The default model is female. In the absence of any step to go to the male model, the child will be female.

22. EFFECTS ON BRAIN DEVELOPMENT • While sex hormones are directing gonadal differentiation, they also affect brain differentiation, particularly in the hyothalamus. • The hypothalamus has neurons that are estrogen sensitive, they bind to estrogen. • If testosterone is present, these cells become insensitive to estrogen. • Conversely, if estrogen is present, these cells become sensitive to estrogen. • This difference is crucial for the hormonal feedback loops in the hypothalamus - pituitary - gonads circuit. • Hormone disruptors (chemicals in the environment) could significantly alter this plan of development.

23. Some Variations of the Usual Sex Differentiation Path • Hermaphrodite, pseudohermaphrodite • Congenital adrenal hyperplasia (CAH) • Progestin-induced pseudohermaphroditism • Androgen insensitivity: • genetic male with female phenotype • 5-alpha reductase syndrome (girls that turn into boys at puberty)

24. Hermaphrodite: • Someone with both male and female reproductive organs, both internal and external. • The majority (60%) are XX. • 33% are XX but with SRY (sex determining region on the Y) present. • 7% are XY. • Where SRY not present, mutation is suspected, but not known yet.

25. Pseudohermaphrodite: • Only the external sex organs are either ambiguous or do not correspond with the chromosomal profile of XX or XY. Various causes, e.g. CAH (see below). • Congenital Adrenal Hyperplasia (CAH) or Adrenogenital Syndrome: • XX (girls) whose adrenal glands secrete too much testosterone during gestation, which causes masculinization of the external genitals and, it is suspected, of certain regions of the brain, resulting in more masculine behaviour (“tomboys”). Normal female development and fertility.

26. Progestin Induced Pseudohermaphroditism: • Iatrogenic effect of progestin given to pregnant women to prevent miscarriage. In XX fetuses, effects similar to CAH. Progestin seemed to have an androgenic effect, in varying degrees. No longer used. • Androgen insensitivity: • XY (genetic male) with female phenotype. During gestation, fetal tissues are insensitive to testosterone, so they develop with female external genitals, but have no female internal organs because the Mullerian ducts have been eliminated. Testicles are initially formed but don’t descend. Reared as girls, female gender identity.

28. 5-Alpha Reductase Syndrome (5-ARD): • 5-alpha reductase is an enzyme that catalyzes conversion of testosterone to dihydrotestosterone during fetal development, necessary for normal development of external and internal genitals. When absent, feminized external genitals are present at birth and the internal genitals have varying degrees of abnormality. The cause of the absence of 5-ARD is a recessive gene. At puberty, the large amounts of testosterone produced promote a masculine phenotype, but the individual is infertile. Generally, male gender identity.

29. These variations highlight the complex nature of masculinity and femininity, both biological and social. • According to John Money, eight variables interplay to arrive at an individual’s gender (see text).