PSC EXAM 1 Flashcards
(96 cards)
1
Q
Nayeli is pregnant and decides to have a test to identify the fetus’s chromosomes. The results of the test come back and show that the fetus has sex chromosomes XXXY. She does not share the results with her medical team. At birth, what sex is the doctor most likely to assign Nayeli’s infant?
A
MALE
2
Q
Justin was assigned male at birth and has testes, male-typical internal reproductive structures, and male-typical external reproductive structures. In order to begin the developmental cascade that biologically made Justin, what must Justin possess?
A
A functioning SRY gene
3
Q
You are a doctor and a newborn appears male, but has chromosomes XX. What could have caused this?
A
Fetal exposure to steroid hormones in the first 20 weeks of gestation, Crossing over
4
Q
An error has occurred during anaphase and genetic material has been incorrectly separated. What do we call this error?
A
Nondisjunction
5
Q
What is the product of meiosis I?
A
Daughter cells with half the amount of genetic information as the parental cells
6
Q
The bio-social model of sexual and gender differentiation developed by Money & Ehrhardt requires the assumption that gender is binary.
A
false
7
Q
The size of external genitalia (e.g., penis, clitoris) in the human population is best described by which kind of model?
A
Bimodal continuum
8
Q
Willow was assigned female at birth and identifies as a man. What is the difference between Willow’s sex and gender?
A
Willow’s sex is determined by biological factors, but their gender is a psychosocial construct.
9
Q
During the synthesis of steroid hormones, enzymes are ____ in the process of synthesizing a target hormone from cholesterol.
A
Irreplaceable
10
Q
If a pre-cursor hormone is missing during steroid synthesis, is it still possible to make a specific steroid hormone?
A
It depends on our goal/target steroid hormone, pre-cursor hormones are sometimes replaceable
11
Q
Anke Ehrhardt
A
Determinants of sexual
risk behavior
12
Q
John Money
A
Model of sex & gender development
Strengths
* Biological & social determinants
* Applies to exceptions (e.g., intersex)
But understanding of sex & gender is not
complete
13
Q
Biosocial model of sexual differentiation (sex) &
gender development
A
- Chromosomes (Chromosomal sex)
- Gonadal sex
- hormonal sex
- reproductive structures
14
Q
DNA
A
molecule that carries genetic instructions used in
the growth, development, functioning, and
reproduction of all living organisms.
- DNA carries the instructionsfor building proteins, which
carry out all of the body’s
functions - A sequence of DNA makes up
a gene, and different genes
contribute to our traits (e.g.,
eye color, height, etc.)
15
Q
CHROMOSOMES
A
Chromosome: double strand of DNA
Chromosomes are thread-like structures made of DNA that carry our genetic
information
* Chromosomes are made up of long DNA molecules, coiled and condensed, to fit
inside the nucleus
* Humans typically have 46 chromosomes (23 pairs) in most of their cells (except for
sperm and egg cells, which have 23 chromosomes each)
* These chromosomes are inherited from our parents: half from the mother and half
from the father
* Sex chromosomes are a specific pair of chromosomes that determine a person’s
biological sex. The two types of sex chromosomes are X and Y
* In some cases, a person may have more or less than two sex chromosomes (ex: XO
or XXY)
16
Q
KARYOTYPES
A
Cells are collected (usually from a
blood sample or amniotic fluid) and
divided using a technique called cell
culture
- The chromosomes are then stained
and photographed under a
microscope. - The resulting image is organized
into pairs from largest to smallest,
with the sex chromosomes at the
end - Karyotypes are used to identify
extra, missing, or structurally
abnormal chromosomes
17
Q
1, CHROMOSOMAL SEX
A
One gamete (sperm or egg) from the female and the male
* 23 chromosomes from each gamete -> EMBRYO
23 pairs of chromosomes
- one half of a pair =
maternal, other =
paternal)
= 22 pairs = somatic(aka autosomal – include
genes for reproductive structures) ( &
identical)
+ 1 pair of sex
chromosomes ( &
differ)
18
Q
GENES
A
located on the strand of DNA
19
Q
SRY GENE
A
Sex determining chromosome?
= Y chromosome
* requires active SRY*
gene
* “Master switch”
SRY protein gonads
develop into testes
*Sex-determining region of
the Y chromosome/TDF
20
Q
MEIOSIS
A
a type of cell division that reduces
the number of chromosomes by half,
resulting in the formation of gametes
A single cell divides 2x to produce 4
genetically unique cells – containing half
the original amount of genetic information.
* Purpose:
* Produce genetically diverse
gametes for sexual reproduction
* Maintain the correct chromosome
number in offspring after fertilization
21
Q
GAMETE
A
a reproductive cell
produced during meiosis; female
gametes are ova/egg cells while
male gametes are sperm
22
Q
ZYGOTE
A
fertilization event
between two gametes (egg +
sperm) to make a fertilized egg
23
Q
INTERPHASE
A
Involves cell growth
- DNA replication
occurs, so each
chromosome now has
an additional
chromatid - The number of
chromosomes did not
change (still 46)
24
Q
PROPHASE
A
(“pre”): process of
chromosomes pairing & lining
up
In-between
Cross-over/exchange genetic
information & recombination
25
METAPHASE
chromosomes are now in the
middle of the cell
26
ANAPHASE
chromosomes are pulled away
27
TELOPHASE
we end
up with two DAUGHTER cells!
28
MEIOSIS PMAT 2
END UP W 4 DAUGHTER CELLS
29
NONDISJUNCTION
when a cell receives too many or too few
chromosomes during meiosis typically during anaphase
Because of nondisjunction,
XX and XY are not the only
combination of sex
chromosomes–lots of
diversity
* Can end up with 1 or
more or no sex
chromosomes etc.
30
SEX
Because of nondisjunction,
XX and XY are not the only
combination of sex
chromosomes–lots of
diversity
* Can end up with 1 or
more or no sex
chromosomes etc.
BIMODAL CONTIUUM
31
GENDER
psychological traits
* continuum
* linked to physical/sex
32
KLINEFELTER SYNDROME XXY
Male: 1/650 newborn boys
* Male gender identity
* Often undetected
* Fertility problems?
* little-to-no sperm from reduced testosterone levels
* Other symptoms (often subtle)
* Altered genitalia, decreased muscle mass, increased height,
breast growth; often have learning disabilities
* Varies across individuals
If only 1 sex chromosome is present (i.e., X or Y), viable?
* Fetus is only viable if an X
* If the Y chromosome is present, sex?
* Fetus = male, regardless of number of X chromosomes
* Atypical sex chromosomal combinations
* Common: ~ 1 in 500 births
* Not always visibly obvious +/or with fertility problems
Chromosomal sex is not straightforward
33
Chromosomes: Sex is determined by?
Combination of sex chromosomes
‐ i.e., the presence/absence of Y
2. SRY gene trigger
34
Case: Fetus at 12 weeks
‐ chromosomal sex: XX
(IVF used)
Ultrasound at 14 wks
* Testes, penis present
* Development began at 7 wks
Hormonal influences
* Minimal
How could this happen?
SRY gene on X
chromosome
= TRANSLOCATION
When does translocation occur?
Crossover
Meiosis I
Between Prophase 1 &
Metaphase 1
1/20,000 males/men = XX
* Smaller testes, decreased
testosterone (T), shorter, infertility
* 90% of XX males = SRY translocation
* Prophase I & metaphase
SRY trigger is essential for testes
development
2) Chromosomes other than Y must contain
some of the genes (‘blueprint’) for testes
and male reproductive structures. These
include somatic/ non‐ sex chromosomes
35
HORMONES
chemical messengers produced by
glands in the endocrine system. They travel through
the bloodstream to target organs or tissues to regulate
various physiological processes, including growth,
metabolism, mood, reproduction, and behavior.
Hormones help coordinate and control bodily functions
Hormones bind to specific receptors on or inside
target cells, triggering a response (e.g., growth,
metabolism, or changes in behavior)
36
DIFF TYPES OF HORMONES
Steroid hormones (e.g., cortisol, testosterone, estradiol) — derived from
cholesterol
* Peptide/protein hormones (e.g., insulin, oxytocin) — made of amino acids
* Amine hormones (e.g., adrenaline) — derived from amino acids.
37
GONADAL DIFFERENTIATION
Functional SRY gene
Switch ~ week 7 testes
No switch by week 9 ovaries
* Default pathway of sexual
differentiation?
Default = no activity of SRY or hormones = then differentiates into a female
* (female)
38
MALES
SRY gene
* triggers testes
development
* Testes secrete
Testosterone Wolffian duct
develops (black)
* Critical period for Wolffian
starts at 7-8 weeks
* Testes secrete
Mullerian Inhibiting Substance
(MIS) Müllerian duct
degenerates (grey)
Müllerian duct
degenerates
T4 DHT3 masculinizes
external genitalia
39
FEMALES
No SRY
* gonads develop (name?)
* No hormonal activity (T, MIS, DHT)
no T Wolffian duct
degenerates (black)
no MIS Müllerian duct
develops (grey)
no DHT external
genitalia feminized
(vulva)
Critical period starts 9wks
40
DIFFERENTIATION RULE
Activity -> male differentiation
No SRY or hormonal activity -> female
differentiation
SRY action-> testes -> androgens & MIS -> reproductive
structures, including brain & nervous system
41
Organizational effects of hormones
* occur within ‘critical periods’ i.e., windows of development in
which organs are sensitive to hormones
42
FETAL MALE TESTOSTERONE PRODUCTION
Exceptions that prove the rule
‐ Prediction? What happens if
a typically developing female
fetus is exposed to the
hormone testosterone (T)
starting at week 9?
= Critical period for hormonal effects
‐ Wolffian system? = DEVELOPS
‐ Mullerian system? = DEVELOPS
‐ Genitalia? = MASCULINIZED = INTERSEX
43
STEROID HORMONES
Steroid hormones are similar in structure (e.g., estradiol and testosterone)
Precursor hormones can be substituted
* In some (but not all) cases, if a precursor hormone is
missing, the target hormone can still be synthesized
It is inaccurate to
describe hormones as
“male” or ”female”
* For example: Estrogen
must come from an
androgen which must
come from a
progestagen
made in the adrenal glands (corticoids, less of other
steroids), gonads (other steroids) and placenta
* synthesized from cholesterol
* Cholesterol is NOT a hormone
* a type of lipid (fat) derived hormone, which is one class
of hormones.
* important for development, but are also present and
vital throughout the lifespan
44
ENZYMES
Enzymes determine which hormones can be made
* If an enzyme is missing during development, some
hormones cannot be synthesized
* This can lead to many conditions, including some intersex
conditions
* Enzymes cannot be substituted
Rectangular grey‐blue
boxes, red outline
* Enzymes are the same
across horizontal and
vertical lines
* Arrows show direction of
synthesis
45
MONEY-ERHARDT MODEL FACTORS
WHETHER A CHILD IDENTIFIES AS MALE OR FEMALE: HORMONES, CHROMOSOMES, STEROIDS, PRESENCE OF SRY GENE, GONADS, SOCIETY + PARENT INFLUENCE, BRAIN
46
Evolutionary Origins of Sexual Dimorphisms:
Sexual Selection
Competition for mates that occurs within
(intrasexual) and between (intersexual) the sexes
* Males and females have evolved different
behavioral strategies to optimize their chances
47
Evolutionary Origins of Sexual
Dimorphisms: Compensation
Sex differences in brain structure may prevent
differences in behavioral output by
compensating for sex differences in physiology
48
PRARIE VOLES
Highly social, bi-parental
rodents
* Males and females show no
qualitative difference in
parental behavior
* Females- pregnancy changes
response to pups, initiates
maternal behavior
* Males- spontaneously
responsive to pups, no gonadal
involvement
49
VOLE PATERNAL BEHAVIOR
Parental behavior
of males is
dependent upon
activation of
vasopressin (AVP)
system in the
lateral septum
50
IDENTIFYING AS MALE OR FEMALE
CHROMOSOMES - GONADS - HORMONES (DEVELOPS SECONDARY SEXUAL CHARACTERISTICS) - BRAIN - BEHAVIOR
51
SEX DIFFERENCES IN BEHAVIOR
Males
* Scent marking/ vocalization
* Mounting
* Females
* Mate choice
* Receptivity/ lordosis
52
PHOENIX ET AL = HOW DO ANIMALS DEVELOP SEX DIFF IN BEHAVIOR?
Previous work provided extensive evidence that steroid hormones
activated patterns of male and female sexual behavior, but only activated
the behavioral patterns typical of a given sex (in adults).
* It was controversial that steroid hormones at certain times in life (critical
period) could organize the tissues mediating mating behavior (most likely
neural tissues).
* So, this study was designed to establish the developmental effects of
prenatal (in utero) exposure to testosterone in guinea pigs.
Male Typical Behavior
* Inject adult with testosterone
* Expose to receptive female
* Measure mounting
Female Typical Behavior
* Inject adult with estrogen followed by
progesterone
* Expose to male
* Measure lordosis
53
PHOENIX ET AL FINDINGS
Gonadectomy
Hormone treatments
Behavior testing
In Adult Males (no prenatal exposure to
testosterone):
* Adult castration blocks mounting
* Testosterone injection restores mounting
* Estrogen injection does not restore mounting
* In Adult Females (no prenatal exposure to
testosterone):
* Testosterone injection does not increase mounting
Mothers treated with high testosterone throughout pregnancy:
* Daughters: masculinized external genitalia
* Daughters: decreased lordosis, increased mounting when treated
with T as adults
* Sons: male-typical behavior
* Mothers treated with low testosterone throughout pregnancy:
* Daughters: female external genitalia
* Daughters: decreased lordosis, increased mounting when treated
with T as adults
* Sons: male-typical behavior
54
IMPLICATIONS
During development, testosterone acted to
organize tissues so that they respond
differently to gonadal hormones in
adulthood (EFFECTS OF A CRITICAL PERIOD)
55
ORGANIZATIONA-ACTIVATIONAL HYPOTHESIS
Organizational- Effects during development
which set the stage for later responses (IRREVERSIBLE BRAIN DEV)
* Activational- During adulthood, the acute
effect of gonadal hormones (REVERSIBLE TO SEE CHANGES)
56
ORGANIZATIONAL HYPOTHESIS
notion that hormones could permanently alter the
structure of the nervous system.
The notion that hormones could organize non-neural tissue was
uncontroversial, as the sequence and the role of hormones in
genital and reproductive anatomy differentiation was well
known in 1959.
What would have been controversial is the notion that the
nervous system was permanently changed by exposure to
hormones.
57
FEMALE RATS (OVARIECTOMIZED AS ADULTS)
REMOVE GONADS BEFORE DAY 10?
INJECT W T BEFORE DAY 10?
REMOVE GONADS IN ADULTHOOD?
INJECT W T IN ADULT HOOD?
SHOW MALE TYPICAL BEHAVIOR?
- NEEDS T DURING CRITICAL PERIOD + INJECT IN ADULT HOOD FOR ACTIVATIONAL EFFECT
58
MALE RATS
SAME PREMISE AS ABOVE
- NEED BOTH PRENATAL EXPOSURE TO T (REGARDLESS OF REMOVING GONADS), NEEDS IT ALSO IN ADULTHOOD FOR ACTIVATIONAL EFFECTS
59
WHAT ELSE ORGANIZES BEHAVIOR?
Maternal stress reduces fetal androgen
production of males:
* Decreased mounting
* Reduced aggression
* Increased paternal care
* Decrease play behavior
60
Does the Y chromosome contain other factors that could differentially influence a male’s development?
Yes, the Y chromosome carries genes beyond SRY (e.g., genes involved in spermatogenesis, neural function).
Some studies suggest Y-linked genes may influence:
Aggression
Cognitive traits
Brain structure (e.g., vasopressin expression in the lateral septum)
The Four Core Genotypes mouse model shows that XY mice (even without testes) differ behaviorally from XX mice, implying non-SRY Y chromosome effects.
61
Females receive an X chromosome from each
parents, but males only receive an X from their
mothers- does that impact development?
Yes, because:
Females (XX) have two X chromosomes, leading to X-inactivation (random silencing of one X).
Males (XY) have one X, making them more vulnerable to X-linked mutations (e.g., color blindness, Fragile X syndrome).
Some X-linked genes escape inactivation, potentially causing sex differences in gene dosage effects.
62
How can we disentangle the presence or absence
of the Y chromosome in these hormonal studies?
Four Core Genotypes Mouse Model:
SRY is moved to an autosome, allowing comparison of mice with different sex chromosomes (XX vs. XY) but the same gonads (ovaries or testes).
Example comparisons:
XX vs. XY mice with ovaries → Tests sex chromosome effects (no hormonal interference).
XX vs. XY mice with testes → Tests combined effects of chromosomes and hormones.
Human studies: Examine rare conditions like:
Swyer Syndrome (XY females, SRY mutation)
de la Chapelle Syndrome (XX males, SRY translocation)
Turner Syndrome (XO) vs. Klinefelter Syndrome (XXY)
63
Four Core Genotypes:
Mouse model
SRY gene was removed from the Y
and inserted onto an autosome, so
it is inherited independently of the
sex chromosomes
Relevance to humans:
* Loss of function mutation in SRY:
Swyer’s Syndrome
* “XY Females”
* Recombination of SRY to X: de la
Chapelle Syndrome
* “XX Males”
* Note: this is the same as the
XX Male condition described
in Lecture 3 (with abnormal
SRY gene translocation)
64
EFFECT OF SEX CHROMOSOMES
REGARDLESS OF GONADS
habit formation [XX(ovaries or testes) > XY(ovaries or
testes)]
* aggression [XY(ovaries or testes) > XX(ovaries or testes)]
* pain perception [XX(ovaries or testes) > XY(ovaries or
testes)]
* vasopressin in the lateral septum [XY(ovaries or testes) > XX
(ovaries or testes)]
* neural tube closure errors in dev [XX(ovaries or testes) > XY
(ovaries or testes)]
* parenting [XX(ovaries) > all others]
65
EFFECT OF GONADS
sexual behavior & sexual differentiation of the body
* thickness of cerebral cortex [M(testes) > F(ovaries)]
* expression of progesterone receptors in the brain [M(testes) > F(ovaries)]
66
How can we have
differences in brain
development? More
specifically, how might these
differences in developmental
processes result in sexual
dimorphisms within the brain?
SYNAPTIC PRUNING = USE IT OR LOSE IT
Neurons communicate through
the use of chemical and
electrical signals
* Network activity gives rise to
behavioral output
67
How can gonadal hormones
influence brain development?
Amount of apoptosis = SELECTIVE PRUNING
* Regulate the number and
type of synapses a cell
makes
* Outgrowth of axons and
dendrites W TESTES
68
HYPOTHALAMUS
OXYTOCIN AND VASOPRESIN PRODUCE
FLEEING, FEEDING, FIGHTING
HYPOTHALAMIC NUCLEI
- REGULATE PAIR BONDING, REGULATION, BLOOD PRESSURE
- CAN RELEASE HORMONES
SEXUAL DIMOPHISM = SIZE OF NUCLEI DIFFERENT
MPOA = FOR SEXUAL BEHAVIOR, EFFECTS OF TESTOSTERONE PRENATALLY
69
POSTERODORSAL MEDIAL AMYGDALA
1.2 – 2x larger in males than females
* Important for male sexual arousal
* Sensitive to testosterone throughout life
70
What about the brains of men and
women of trans* experience?
LARGER BNST IN MALE THAN FEMALE
MTF = LOOKS CLOSELY MATCHING HETEROSEXUAL FEMAL, EXPERIENCING HORMONE REPLACEMENT THERAPY
71
Sexual dimorphism in brain
activation
FMRI: Greater activation of hypothalamus in girls (and women)
compared to boys (and men)
72
Does brain activation reflect a
child’s gender identity?
Hypothalamic
activation does
reflect ADOLESCENT
gender identity
Greater activation of hypothalamus in pre-
pubescent girls compared to pre-
pubescent boys
No statistically significant difference
between boys with gender dysphoria and
control boys
Statistically significant difference between
boys with gender dysphoria and control
girls
73
How would you distinguish organizational and activational effects of hormones?
Organizational effects typically involve changes to physiological structures, while activational effects typically do not
Organizational effects are typically irreversible, while activational effects are typically reversible
Organizational effects typically occur in utero, while activational effects typically occur in adulthood
74
According to studies in guinea pigs, how does prenatal hormonal exposure affect an individual?
Prenatal hormone exposure has organizational effects on brain tissue
75
Researchers decide to make a new mouse model. They remove the SRY gene from the Y chromosome and create a mouse with XY chromosomes. We would expect this mouse to have what kind of gonads?
ovaries
76
Mark is a typically-developing, male-bodied person going through puberty. What effects should he expect to experience from activity of the HPA axis?
Growth of pubic hair, oily skin
77
During puberty, what kinds of effects should we expect hormones to have on the body?
Both organizational and activational
78
Maria is a typically-developing, female-bodied person. During puberty, she experienced a number of changes to her body. Which of these changes is a secondary sex characteristic?
Widening of the hips
79
You are a pediatrician and a blood test indicates that your pre-pubescent patient has unusually high levels of circulating androgen. What symptoms led you to run this blood test?
Your patient has axillary hair growth
Your patient has acne
Your patient is tall for their age
80
In the HPG axis, the hypothalamus produces
[ Select ]
, which signals the pituitary gland to produce Gonadotropins , which causes the gonads to produce
[ Select ]
.
GnRH, gonadotropins, sex hormones
81
In considering the pathway from cholesterol to a target hormone, if an enzyme is missing, an alterative pathway is _____ . If a pre-cursor hormone is missing, an alternative pathway is ___.
not avail, usually avail
82
organizational hypothesis
developmental effects of hormones that set the stage and
enable later responses
* When?
* Irreversible
* Involve major changes to anatomy/physiology
* Prenatal (critical period)
* Puberty (sensitive period)
83
activational hypothesis
Activational refers to later, acute effects of gonadal
hormones
* Reversible
* Can occur at any point in life, even adulthood
* Modulate (regulate) activity of existing physiology
84
puberty
A physiological event
* Childhood -> Adulthood...in a sense
© Joanna Scheib 2023. This content is protected and may not be shared, uploaded, or distributed.
* Characterized by changes in physical appearance
* Involves:
* Attaining reproductive capability
* Completing sexual and physical organ
development
* Gradual transition to adulthood, puberty is
only part of it
85
steps of pubertal changes
Physical
2. Behavioral
Reproductive
3. Reproductive organs (primary sex traits)
4. Secondary sex characteristics
86
physical and behavioral changes for both sexes
Growth spurt
* Growth of pubic and underarm hair (axillary hair)
* Increased sebaceous gland production (i.e., oily
skin)
* Starts earlier
Hormonal effects begin several
years before
* Testosterone increases sex
drive and interest
87
HPA axis
hypothalamus --> anterior pituitary --> adrenal gland -->target cells
Adrenal glands secrete androgens → pubic
and axillary (body) hair
88
secondary sex traits HPG axis
hypothalamus --> anterior pituitary --> gonads --> primary reproductive organs target cells (secondary sex traits) --> further develop reproductive organs, secondary sex traits
Physical traits that distinguish mature
males from mature females
* Not required for reproduction
* Hypothalamus-pituitary-gonadal (HPG) axis
* Ovaries secrete estrogens → female 2° sex
traits
* Testes secrete androgens → male 2° sex traits
89
secondary sex traits MF
Females
* Breast development
* Widening of hips
* Softening of skin
* Body fat increases (2x)
* Body fat distributes
to breasts and hips
Males
Development of facial hair
* Deepening of voice
* Growth of upper body muscles
* Increased bone mass
* Increased muscle mass
90
sex steroid production
hypothalamus (GnRH) -> pituitary (gonadotropins = LH, FSH), --> ovary and testes (sex hormones = estrogen/testosterone) -> feminization or masculization -> sexual and physical maturation/cessation (with androgens added from adrenal gland)
91
reproductive organs
Testes increase 10x in size (organizational)
* Spermarche: onset of sperm production
* Sperm production is testosterone dependent
(activational)
* Short period of subfertility surrounding spermarche
* Vas deferens also increases in size
* Uterus and vagina mature (organizational)
* Menarche: onset of menstrual/ovulatory cycles
* Cycles are estrogen- and progesterone-dependent
(activational)
* Subfertility for several years following onset
92
typical pubertal timelines
Females
* 8-13 years old
* Males
* 9-14 years old
* Begins with ovary growth followed by increases in estradiol
* Progresses to physical growth, then breast growth (thelarche), menarche
* Physical growth, then testicular growth, then increases in testosterone, then
spermarche
93
permanent physical changes = require no continued hormonal maintenance
Altered before or in puberty, require no continued hormonal
maintenance
* Voice pitch (larynx physiology) – for males
* Adam’s apple – for males
* Breast growth – for females
* Bone structure
* Height
* Primary reproductive structures (i.e., gonads, internal
reproductive structures, genitalia)
94
impermanent pubertal changes = requires hormonal upkeep
Sperm production – for males
* Ovulation and menstruation – for females
* Facial hair – for males
* Body hair – for males
* Fat and muscle distribution
95
feminizing
Androgen blocker
* Slows facial and body hair
growth
* Reduces sex drive
* Reduces ability to make sperm and ejaculate --> Dependent on how long you take androgen blockers (up to 2 years
for these effects to kick in)
* Slight breast growth --> These can be irreversible even after stopping androgen blockers
Supplemental estrogen
* Slows facial and body hair growth
* Reduces testicular size
* Softening of skin
* Reduces muscle mass, increases fat mass
* Nipple and breast growth
* Reduces ability to make sperm and ejaculate
96
masculinizing
Supplemental testosterone
* Body hair growth
* Gradually lowers voice
* Increased muscle mass (especially in the upper body)
* More oily skin
* Cessation of menstruation
* Lowers ability to become pregnant
* Increased sex drive, but also vaginal dryness
