Psychology 3533 Understanding Human Sexuality

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Transcript Psychology 3533 Understanding Human Sexuality

SEX HORMONES
 Endocrine

glands that secrete internally (into
bloodstream)
 Exocrine

glands:
glands:
secrete externally (i.e. sweat glands)
 Endocrine
glands secrete hormones
 Hormone:

complex chemical with specific actions for
specific organs only
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
SEX HORMONES (CONT’D)
 Pituitary




FSH
LH
oxytocin (orgasm, birth, milk release)
prolactin
 Testes



produces:
produce:
testosterone
estrogen
inhibin
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)
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
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.
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
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.
SEX HORMONES (CONT’D)
 Testosterone:


produced by gonads and adrenals in both
sexes.
Responsible for male characteristics, and for
sex drive in both sexes.
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.
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.
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
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
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
SEXUAL DIFFERENTIATION
 Gestational

First seven weeks: undifferentiated
•
•
•
•
•

Development of Genitals:
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.
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.)
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.)
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.

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.
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)
 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.

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.

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.

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.
 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).