Fecundity and Fertility

How can reproduction be measured?

 Fecundity – Potential for reproduction
 Depends on: gamete production, fertilisation, carrying pregnancy to term
 Females are fecund puberty – menopause and only episodically (monthly)
 Males are fecund from puberty (but begins to decline)

 Fertility – a measure of reproduction, the number of children born per person, couple or
population
 Tends to be a population measure e.g. per person/ couple etc.
 Depends on: fecundity, social convention, choice (abstinence, contraception, abortion), sub-
fertility, access to assistive reproductive techniques

 Fertility Rate - The number of births per time period per person, couple or population

Studies measuring fertility/ fecundity

Bar chart shows that the later an individual

is childless, the more likely they are to
remain childless
E.g. 60% of individuals aged 40-44 who are
childless will remain childless, whereas <5%
of individuals aged 15-19 who are childless
will remain so
Fertility rate peaks at 20-24 and then
declines (pink lines)

What causes cessation of fecundity?

In males:
 The declination in sperm production post puberty has been
dubbed ‘andropause’
 Characterised by a loss of libido, erectile dysfunction,
vascular pathology
 Not influenced by testosterone - as illustrated in the graph
(TT production increases)
 Sexual dysfunction accumulates - due to diseases e.g.
vascular disease/ diabetes
 Drugs e.g. Viagra might help solve this?
 Sperm might not remain same quality
 Studies show that some developmental conditions are
linked with paternal age - maybe due to increased
mutagenesis rate

In females:
 Normally occurs after 40s, premature menopause (c.2%) can occur as early as 20s
 Menopause - Hypothalamus ages —> loss of GnRH — > reduced estradiol fluctuation —>
 Like sperm, oocytes decline in quality and this is linked with chromosome abnormalities
 Ovarian decline and failure -- > secondary amenorrhoea
 Donor egg/embryo transfer and hormonal priming can circumvent ovarian failure
 Gametogenesis
 Gametogenesis is the process by which male or female gametes are formed
 Occurs in gonads

Differences between male and female gonads:

v
 Gametogenesis in males
The Testis
Divided into two distinct compartments:
 Tubules - where the spermatozoa develop with
sertoli cells
 Intertubular regions – where androgens are
synthesized in the Leydig cells
 Compartments are separated by the blood/testis
barrier
 Allows communication between vascular + interstitium
 Prevents penetration of tubular wall, basal
component and adluminal compartment
 Prevents sperm leaking into systemic circulation - - > Autoimmune orchitis
 Prevents alteration of the intratubular chemical microenvironment, which is distinct
and necessary for spermatogenesis
 The testis has two functions: gametogenesis and production of sex hormones

What triggers testicular secretions?

Androgens
 Androgen production is controlled by Luteinising hormone (LH) release from the pituitary
 Evidence of this includes:
 Rise in androgens at puberty is preceded by a rise in LH
 Men with low LH levels have low androgen levels

 LH binds to receptors on Leydig cells 

 Hypophysectomy causes Leydig cell regression
 


Spermatogenesis
 Requires LH and follicle stimulating hormone (FSH) (gonadotrophins) as well as the
hormone inhibin (made in the sertoli cells)
 Evidence includes the fact that:
 LH alone does not restore spermatogenesis in hypophysectomised males 

 Spermatogenesis only occurs post puberty

Spermatogenesis
What conditions are necessary for male gametogenesis?
 Temperature must be 4-7 degrees below body temperature
 Which is why testes descend from the body at puberty
 Also why non descent of testes can lead to infertility

The process
Occurs in three phases:
I. Mitosis
 Spermatogonia are pluripotent cells made from stem cells and undergo mitosis ~
5-7 times to produce a committed population of Spermatogonia and eventually
spermatocytes
II. Meiosis
 Spermatocytes undergo meiosis to reduce their chromosome number and
produce early spermatids
 As they divide they they move from the basal to the luminal part of the tubule
III. Cytodifferentiation
 Spermiogenesis - Spermatids transform their phenotype from round spermatids to
elongating spermatids to spermatozoa
 Spermatozoa are released luminally into testicular fluid in a process known as
Spermiation
 Spermatic fluid contains – bicarbonate ions, glycoproteins, cytokines, fructose

 Note: Sertoli cells are closely associated with all spermatogenic phases and regulate it.
 They are also responsible for production of testicular fluid
 Spermatocytes and spermatids attach to sertoli cells and indent into their cytoplasm
 Sertoli cells have FSH receptors and respond to it

How long does spermatogenesis take?

 Production of spermatozoa from a human spermatogonial stem cell takes about 64 days
o Each step in the process takes a defined & characteristic amount of time

 Groups of stem cells initiate development at approximately 16 day intervals

 Locally groups of stem cells coordinate their time of entry into spermatogenesis
 In different localities development of stem cells is not synchronized
o Therefore, the overall output of sperm is continuous not pulsatile. 


Production of sex hormones – Androgens

What are the functions of androgens?
 Stimulate accessory sex gland growth and secretions in men e.g. seminal vesicle, prostate,
epididymis 

 Stimulate secondary sex body hair patterns in both men and women 

 Exert anabolic and myotrophic effects to affect body shape 

 Metabolised in target tissues to forms with differential activity. 

 Female Gametogenesis

Preparing for gametogenesis

 Stromal tissue contains primordial follicles
 Female germ cells are present in follicles of the ovary and are
known as primordial oocytes
 Follicles ~ Tubules
 Like male cells they undergo mitosis to increase the number of
cells but not to the same extent
 Because females only release one or two eggs a month
unlike males and their millions of sperm
 During fetal life the germ cells enter their first meiotic division
 They arrest in meiosis during prophase I and enter the dictyate
phase
 Thereafter most germ cells die around the time of birth

The Process of gametogenesis

 Oocyte develops within a follicle –
oocyte-follicular unit
 Before ovulation, many follicles
undergo atresia (apoptosis, death)
 Therefore only a small
percentage make it to pre-
ovulatory follicle stage

Primordial to Preantral
 Occurs spontaneously rather than because of hormones
 A few of these will undergo this process each month
 Major growth phase of oocyte: from 10- >120 μm diameter and lots of RNA and protein
synthesis
 Zona pellucida secreted by oocyte containing glycoproteins
 Granulosa cells proliferate and develop several layers outside the ZP
 Loads of gap junctions form between granulosa cells which is important because it’s
avascular
 Stromal cells condense to form thecal cells “case”

Hormones required:
 Does not depend on exogenous hormones
 Does not produce hormones
Antral
 By early antral stage, fluid begins to accumulate
containing substances such as serum,
glycoproteins - analogous to testicular fluid - how
oocytes are transmitted
 Interna (theca) develops some blood vessels
 Required to deliver nutrients and hormones to the
unit since pituitary input is required for
subsequent stages
 Little further oocyte growth occurs but RNA levels
continues to rise
 Granulosa cells proliferate to many layers and
commence follicular fluid secretion and formation of an antrum
o The mass of granulosa cells surrounding the oocyte is known as the cumulus oophorus
‘heaped egg-carrier’
 Thecal cells develop LH receptors and require LH
 Thecal cells are like Leydig cells in the males
o Make androgens under influence of LH
 Only a little of these androgens are secreted into the blood stream
 Majority are converted into oestrogens by granulosa cells under the influence of
FSH
 Granulosa cells develop FSH receptors and require FSH
 Oestrogens bind and stimulate the granulosa
cells that made them
 Oestrogen production is increased by inhibin,
made by granulosa cells under FSH
 Inhibin production is slow during preantral
phases but starts to rise as the antrum develops
 Rising inhibin levels stimulate androgen output
by the thecal cells and its conversion to
oestrogens by the granulosa cells
 So inhibin generates a positive feedback loop on
granulosa cells
 Inhibin also selectively depresses FSH output so its levels remain lower than LH

Preovulatory follicle
 Positive feedback effects of oestrogen lead to a rapid increase in oestrogen output
 The thecal layer becomes hyperaemic (high blood flow) and its output of androgens
rises, further increasing oestrogen output
 Follicular fluid secretion increases rapidly and the follicular antrum swells
 The granulosa cells also develop LH receptors and start synthesizing progesterone under
LH stimulation

Hormones required:
 High levels of LH

Ovulation
 Follicle surface thins and ruptures at the stigma
o Under influence of LH and prostaglandins
 The oocyte is released to the surface of the ovary in its cumulus oophorus carried in
follicular fluid
 The antrum collapses and is invaded by blood vessels
 The granulosa cells transform into large lutein cells
 Some of the thecal cells mingle with them as small luteal cells
 Lead to the formation of the corpus luteum

What’s happening to the oocyte during follicular changes?

 Oocyte meiosis reactivates in the pre-ovulatory oocyte due to the high levels of LH
o The prophase nuclear membrane breaks down
o The oocyte enters first meiotic metaphase, then anaphase then telophase as a
primary oocyte
 The first meiotic division is unequal
o The chromosomes are divided equally but almost all the cytoplasm ends up in one
of the cells (the oocyte)
o Produces a small first polar body and a large oocyte
o Means that the oocyte contains loads of material synthesized from the earlier
stages
 The oocyte then immediately enters the second meiotic division as a secondary oocyte
o It gets as far as second meiotic metaphase but then arrests a second time
o It reenters meiosis when it’s fertilizes
 Thought to prevent the egg from creating a fetus on its own
(parthenogenesis) because the ovary is a conducive environment for egg
growth

The corpus luteum

 The Corpus Luteum is “the post-ovulatory follicle”

Contains:
 Large luteal cells derived from the granulosa
o Expand and increase the production of
progesterone
 Small luteal cells derived from the theca interna cells
o Continue to produce androgens which pass to the
large luteal cells which then convert them to
oestrogen
 Inhibin is secreted in large amounts
 The corpus luteum ---- > corpus albicans (dies) unless
woman becomes pregnant

Timing of female gametogenesis

 Activity of the ovary is cyclic

Why does only one egg make it to ovulation?

 Eggs want to enter the antral phase all the time, they are suppressed by eggs which are
further along in the cycle
 When that egg is ovulated than it in turn supresses eggs before it
 Progesterone mediated

Changes in the uterine lining over the ovarian cycle

Over the course of the cycle, the uterine lining grows and develops
Red = oestrogen, blue = progesterone, thickness = strength of action
Early development is heavily dependent on oestrogen, whilst later requires progesterone

Other cyclic changes

 Mucus secretion – supports the passage of sperm
o Allows the sperm to penetrate further to allow fertilisation
 Body temperature rises with ovulation and luteal phase

What is the endocrine basis of the ovarian cycle?

 Hypothalamus has a portal circulation which allows nuclei to release hormones that can
act on the anterior pituitary but not on the systemic circulation
 These releasing hormones act on various cells of the anterior pituitary including:
o Gonadotrophs: LH and FSH o Lactotrophs: Prolactin
o Somatotrophs: GH o Corticotrophs: ACTH
o Thyrotrophs: TSH

How does the hypothalamus cause gonadotrophin release?

 Medial pre-optic arcuate nucleus of the hypothalamus projects to the portal plexus
 The hypothalamus releases GnRH causing FSH and LH secretion from the anterior
pituitary
 GnRH secretion is in turn controlled by gonadal hormones 

o Generates positive or negative feedback loops 


Feedback loops in males

 Only negative feedback is seen 

 Rising testosterone depresses LH and FSH output 

 Rising inhibin selectively depresses FSH output

Feedback loops in females

Oestrogen
 Slowly rising oestrogen depresses LH and FSH output 

 Rapidly rising oestrogen stimulates LH and FSH output

Progesterone 

 Progesterone has a direct negative feedback effect 
 on gonadotrophin release
 Also inhibits the positive feedback effect of oestrogen 

o Therefore, high progesterone -- LH & FSH reduced output 


Inhibin 

 Made during late antral phase by Granulosa cells in response to FSH
 Selectively depresses FSH output so levels (and surge) remain lower than LH
 Ensures you don’t make new eggs when one is developing

The hormone cycle in females

 At beginning of cycle pituitary release FSH
and LH
 As follicles grow they secrete oestrogen,
which has a negative feedback effect on
gonadotrophins
 At day 12 there’s a rapid increase in
oestrogen levels which promotes
gronadotrophin release
 LH peaks at day 14 causing ovulation
 Rest of LH stimulates production of corpus
luteum
 CL secretes progesterone in the last part of the cycle
o Has a negative feedback effect on the gonadotrophs, so they decrease
gonadotrophin release which prevents further follicle development

How do female and male gametogenesis differ?

Differences between gametes:

 Puberty

What are the stages that one goes through life?

 Embryonic and fetal existence  Puberty and adolescence
 Infancy and childhood
  Early and middle adulthood
 Late adulthood and old age

What is puberty?
 Derived from the Latin pubes, meaning “hair”
 Psychological, morphological and behavioral changes that transition an individual from
being a sexually immature child to a sexually mature, reproductively fertile adult.
 Children going through puberty are described as being pubescent
 Occurs in all animals but only mammals have it for so long
o Might be because their brain needs longer to develop or because there’s some
beneficial state of childhood
 Human females – 12 to 14 years of age 

 Cow – 12 months 

 Pig – 7 months 

 Ewe – 6 to 7 months
 Mouse – 30 to 35 days 

 Variable in both male and females in terms of how fast it’s onset

What are the signs of puberty occurring?

Menarche / Wet Dream
Girls
 Menarche = first ovulation – definitive sign
o First ovulation some months (or up to 2 years) after menarche
o Slight risk of pregnancy after menarche and even some cases of pregnancy before
menarche 

o For several months after menarche, a female may miss some periods 

 First ovulation is not fertile – doesn’t contain an egg because not fully complete
Boys
 Wet dream = first ejaculation - similar level of maturity to menarche
o Spontaneous erections become more frequent during puberty
 Response to stressful or emotionally-charged stimuli – often not sexual
matters 

o Spontaneous erections and nocturnal emissions tend to decrease after puberty
 ‘Wet dream’ doesn’t contain much sperm - largely contains spermatic fluid

 These are not the first events of puberty – preceded by 2-4 years of other changes
dependent on steroid hormones from gonads (gonadarche) and from the adrenal gland
(adrenarche) 


Growth Spurt
 Describes an acceleration followed by deceleration of growth
 The later the age of take off, the higher the peak height
 Which is why boys end up being ~10cm taller than girls
(because they take off 2 years later)
 Growth occurs in multiple dimensions – i.e. there’s both
muscle and skeleton growth
 Sexual dimorphism – shoulders widen in boys, hips widen in
girls
o Driven by sex hormones
 Patients with hypopituitarism need growth hormone and
steroid supplementation for it to occur

Changes in body composition

 Males are 1.5 times lean mass (because of muscle and bone)
 Driven by androgens, accounts for why males are stronger than females
 But women have twice as much body fat (concentrated around hips/ breasts)
 Supposed to be a way to prepare for childbirth

Secondary sexual characteristics

Girls
 Growth and widening of pelvis
 Appearance of pubic and axillary hair
 Breasts grow and mature

 Sweat and sebaceous glands become more active (can result in acne)

 Slight lowering of voice 


Boys
 Pubic and axillary hair, plus hair on face, chest and extremities 

 Sweat glands in axilla (may produce odour) 

 Sebaceous glands active in skin of scrotum, face, back, chest with some acne 

 Nipple pigmented and areola darkens and widens 

 Vocal cords in larynx lengthen – voice deepens (“breaks”) such that the pitch of the adult
male voice is an octave lower than that of females 


Gonadal changes
Females
 Ovaries, oviducts, uterus, vagina grow and mature 

 Ovulation doesn’t occur because the pituitary is yet to release hormones to drive it
 Newborn ovaries are ~2 cm in length, each contains 500,000 follicles

 No follicles ovulate during childhood, but many growing follicles become cystic or atretic
 At puberty, about 83,000 follicles remain
 Ovaries of pubescent females weigh more than those of a child because some remaining
follicles have enlarged

Males
 Growth and maturation of the testes, vas deferens, seminal vesicles, prostate gland 

 Scrotum and penis grow markedly 

 Testes descend from abdominal cavity during 7th or 8th month of fetal life
o Under control of mullerian-inhibiting substance (MIS) and testosterone – pulled
down by a gubernaculum attached to testes and scrotum
 In newborn – seminiferous tubules contain spermatogonia and Sertoli cells
 Some Leydig cells are present at birth but are invisible by 6 months of age
 9 years – spermatogenesis begins, Leydig cells are visible
 14/15 years – mature spermatozoa produced, testes increase in size 24-fold(!) due to
enlarged diameter of seminiferous tubules (tubules fill with testicular fluid)

Failure of testicular descent – Cryptorchid testes

 In 3 - 4% of males, testes fail to descend by birth - 0.8% by 1 year of age and 0.3% by
onset of spermatogenesis
 Spermatogenesis requires temperature 3.1°C lower than abdominal cavity, and if it
begins inside cavity then damage ensues – only Sertoli and Leydig cells remain, resulting
in sterility
 Cryptorchidism treated early in childhood – surgery or treatment with gonadotropins or
GnRH which can cause descent before damage is done

Other changes
 Metabolic rate, blood pressure and heart rate increase 


Acne
 Caused by androgens in both sexes which increase secretions of sebum from sebaceous
glands
 Glands can become clogged and infected producing acne – pimples, blackheads, cysts on
 face, chest and back
 NOT caused by poor hygiene
 Can be treated with antibiotics, salicylic acid, benzoyl peroxide or female
hormones/androgen antagonists
Sequence of events

How is puberty classified clinically?

Tanner system
In women largely based on hair and breasts

In males largely based on pubic hair, penis and testes

Endocrine basis of puberty changes
Secondary sexual characteristics are driven by sex hormones
Sex hormones release is the consequence of gonadal activation

In females
 Ovarian oestrogens cause growth of breast and female genitalia
o Estradiol is released from growing follicles in ovary and oestrone from body fat
 Androgens from ovary and adrenal gland cause growth of female pubic and axillary hair,
voice lowering, sebaceous gland development and long bone growth
o May also increase sex drive in pubescent girls
o Released in large quantities from adrenal gland, as well and the thecal cells

In males
 Testicular androgens cause development of genitalia and body hair
 and enlarging of
larynx and laryngeal muscles

Endocrine changes in puberty

What are the hormonal levels in neonates?
 LH and FSH pulses occur during first 20 weeks of life
and plasma levels are at the adult level 

 Thereafter secretion ceases and levels are low or
undetectable through childhood and juvenile stages


 First change in puberty is a rise in FSH, followed by
increasingly pulsatile LH 

 Note – changes occur whether or not testosterone is
present – evidence of altered hypothalamic GnRH
output independent of any negative feedback 

 In both sexes – rise in dehydroepiandrosterone
(DHEA) is first endocrine change in puberty – adrenarche

Changes in females
 LH, FSH and estradiol levels rise
 Sudden surge of LH (and FSH), sufficient to cause
menstruation, causes menarche though not
necessarily ovulation 

 Eventually endocrine system and brain mature so
that LH surge can cause ovulation 

 Development of gonads leads to release of
oestrogens which drives secondary sexual
characteristics
 Hormonal fluctuations are more pronounced in puberty because gonads aren’t
developed enough to exert feedback effects on the pituitary
 Levels are high in adults but feedback prevents the massive fluctuations

Changes in males
 Rise in FSH and LH (~ 10 years) causes onset of
spermatogenesis and rise in androgen secretion
(testosterone) from testes
 Androgen release from testes drives secondary
sexual characteristics as well as an increase in the
touch sensitivity of the penis and sex drive
 Oestrogens also rise slightly in males – released
from the Sertoli cells
o Might explain why some males exhibit
gynecomastia
o Goes away within 2 years

 Because both males and females release both major

sex hormones, it’s the balance of androgens vs oestrogens in both males and females
determines secondary sexual characteristics

Non gender specific hormones

Growth hormone (GH)

 Secreted from anterior pituitary in greater amounts near to puberty
 Responsible (along with androgens) for growth of long bones and tissues
 Major effect on protein synthesis and glucose homeostasis

 GH deficiency => short stature, delayed sexual maturation

Thyroid hormones
 Increase in secretion from thyroid gland, secondary to increased thyroid stimulating
hormone (TSH) from anterior pituitary 

 May account for rise in metabolic rate in both sexes
 Also essential for body growth 


What triggers puberty?

 All driven by pulsatile GnRH
 GnRH pulses precede rises in LH, FSH and sex steroids

Why don’t puberty changes occur in children?

Brain “gonadostat”
 Androgens/oestrogens exert negative feedback on GnRH production 

 Steroids in children exercise this negative feedback – low GnRH and low 
 LH/FSH 

 Hypothalamus thought to be VERY sensitive to steroidal inhibition during childhood (6 –
15 times more than in adults), thus even low steroid concentrations exert inhibition 

 As puberty approaches – sensitivity of hypothalamus to negative feedback decreases 

 Evidence comes from the fact that smaller amount of oestrogen required to lower LH/
FSH levels in girls than in women

Central inhibition of GnRH pulse generator

 GnRH pulse generator inhibited by other brain areas during childhood
 Inhibition lifted at puberty => adult patterns of pulsing
 Evidence? Specific lesions/tumours in rat brain cause early puberty, suggesting these
regions inhibit GnRH secretion
 Evidence? Children born without gonads (no steroids for negative feedback) still have
low LH/FSH levels throughout childhood and GnRH release occurs at normal age

In girls only

 Oestrogens can exert positive feedback on gonadotropin secretion
 High blood levels cause surge of LH (and FSH) in adult women but this does not happen
in younger females
 Late in puberty an LH/FSH surge results and is responsible for first ovulation
 May result from maturation of hypothalamic GnRH surge centre or ability of pituitary to
synthesise and store adequate gonadotropins

What is the evidence that shows GnRH is responsible for onset of puberty?
 GnRH pulses precede rises in LH, FSH and sex steroids
 Exogenous GnRH pulses in pre-puberty initiate puberty
 Brain tumours which activate premature GnRH production lead to premature puberty
 Brain tumours/damage which prevent GnRH production lead to delayed puberty
 Removal of GnRH pulses returns the pubertal individual to ‘pre-puberty’

Other hormones involved in onset of puberty

Neurokinin B and Kisspeptin
• Genetic defects in families in Turkey in which more than one member did not go through
puberty
• Severe congenital gonadotropin deficiency

Arises due to mutation in two genes: TAC3 (one family) and TACR3 (three families).
• TAC3 gene codes for Neurokinin B while TACR3 produces its receptor 

• Neurokinin B, a member of the substance P–related tachykinin family, is highly expressed
in hypothalamic neurons that also express kisspeptin, a recently identified regulator
of gonadotropin-releasing hormone secretion 

• Cause of rise in GnRH

Historical changes in menarche

Was around 15.5 in 1875 and now it’s about 13.5

Why is onset of menarche getting earlier?

Nutrition
 Hypothesis arises because puberty begins consistently at 47 kg for girls and 55 kg for boys
 May be body fat rather than weight
 o 11kg for girls
 Leptin, which sense adipose stores may be responsible – has receptors in the
hypothalamus
o Makes sense because you couldn’t carry a baby successfully if you were
underweight
 Some human genetic disorders in Leptin pathway result in failure of puberty 

 Overweight children tend to enter puberty earlier than lean peers 

 Anorexics don’t have periods
 Levels peak before stage 5 of puberty then reduce to adult levels 

 But not necessarily causal – maybe early puberty causes obesity?

Day length
 Melatonin (makes you sleepy) and other pineal secretions may inhibit reproductive
function 

 Lesions of pineal gland => precocious puberty 

 Secretory tumours of pineal gland => delayed puberty 

 Artificial lighting? Does this increase day length? ---- > less melanotonin release ---- >
puberty 

 Blind children undergo early puberty (as do deaf children) – paradoxical – they're in
constant darkness 

 Sensory deprivation? Seems to accelerate sexual maturity 

 Seasonality – some evidence to suggest females reach menarche at a certain time of year,
which varies geographically

Stress
 In lab animals, certain stressors can delay sexual maturity 

 Some stressors (emotional or physical) can delay 
 puberty in humans 

 May be a role played by adrenal glands
o May become enlarged leading to increased secretion of cortisol? 


 Opposite also proposed – stress during infancy and childhood can accelerate puberty (e.g.
family stress) 

 Girls who grow up in the absence of biological father, especially with stepfather present,
tend to enter puberty earlier 

 Young girls with excess parental conflict, parent-child conflict, or no biological father and
presence of stepfather:
o Passed through puberty more rapidly 

o Reached menarche about 5 months earlier, on average 

o Had first sexual intercourse at an earlier age 

 o Had children at an earlier age 

o Spent less effort and time with their children 

o Formed less stable bonds with their partners 


Pollutants

 Some chemicals in industrial synthesis of plastics act as weak oestrogens.
 Controversial, but exposure to some of these “xenoestrogens” may accelerate puberty 

 Some pollutants (dioxins, polychlorinated biphenyls) may delay male puberty 


Altitude/climate
 For every 100 m increase in altitude, puberty delayed by 3 months 


Genetic Factors
 Thought to explain 15% of variation 

 In USA – black girls reach puberty ~ 1 year earlier than white girls 

 Menarche tends to be similar in mothers and daughters (and within 2 months in identical
twin girls) 

 Variant of CYP3A4 gene influences production of liver enzyme that degrades testosterone
– high activity form => high oestrogen/ testosterone ratio 

 Two copies – 90% of girls begin breast development by age 9.5 One copy – 56%

 No copies – 40% 

 Is the reverse true in boys? 


Psychosocial changes in puberty

 Adolescence is a very challenging time – socially as well as biologically 

 Sexual awakening can lead to concerns about sexuality, sexual 
 adequacy, confusion
about love, fear of sexually transmitted disease 

 Young people must adjust to physiological, anatomical, psychological and emotional
changes 

 Increased feelings of body consciousness

 Low self esteem, if they don’t feel “normal” compared with peers at a time of 
 great
inter-individual variation 

 All of this occurs in a society that expects adult behaviour, yet still treats them like
children
 True precocious or delayed puberty should be treated