Appearance
15.9 — Puberty
The average age of the first period in Europe was around 17 in the mid-nineteenth century. Today it is around 12 to 13.
That change is far too fast to be genetic, and the explanation is nutrition and general health — puberty happens when the body can afford it, and for most of history it could not afford it as early.
The trend has largely stopped in well-nourished populations, which supports that explanation, though breast development in girls has continued to start slightly earlier while the age of first period has not — a divergence that is not fully explained.
What starts it
Pulsatile GnRH restarting (Chapter 12.6).
GnRH is active in the fetus and in early infancy — the "mini-puberty" of the first few months, when sex hormones are transiently at near-pubertal levels — and then goes quiet through childhood.
Why it goes quiet, and why it restarts, is not fully understood. This is worth stating plainly, because puberty is one of the most obvious biological processes there is and its trigger remains partly unresolved.
What is established:
Kisspeptin is essential. People lacking kisspeptin or its receptor do not enter puberty, and giving it can initiate the process. It appears to be the direct upstream activator of GnRH neurons.
Body fat contributes, through leptin (Chapter 12.7). Leptin signals adequate energy reserves, and its absence prevents puberty — which fits the observation that girls with very low body fat, from athletic training or eating disorders, have delayed or absent puberty.
Genetics accounts for 50 to 80 percent of the variation in timing, with age of maternal menarche being a reasonable predictor.
And environmental factors including nutrition, chronic illness, and possibly endocrine-disrupting chemicals, where the evidence is suggestive rather than settled.
The sequence in girls
Typical order:
Breast budding (thelarche) — the first sign, typically at 8 to 13, average around 10 to 11.
Pubic hair (pubarche) — usually shortly after, sometimes before.
Growth spurt — peak growth velocity at around 11 to 12, and this is important: in girls the growth spurt comes early in puberty.
First period (menarche) — typically 12 to 13, about 2 to 2.5 years after breast development begins.
And by menarche the growth spurt is largely over. Girls typically grow only a further 5 to 7 centimetres after their first period, because oestrogen has already been closing the growth plates (Chapter 5.1).
Which is a useful thing for a girl worried about her height to know.
Early cycles are frequently irregular and often anovulatory, and it can take 1 to 2 years to settle. Irregularity in the first year or two is normal; absence of any period by 15, or by 3 years after breast development, is not.
Note that pubic and underarm hair is driven by adrenal androgens (adrenarche), which begins around age 6 to 8 and is separate from ovarian activation. So pubic hair alone, without breast development, is not puberty — and distinguishing the two matters when assessing early development.
The sequence in boys
Testicular enlargement — the first sign, typically 9 to 14, average around 11 to 12. A testicular volume above 4 ml marks the onset, and it is measured with a set of graded beads.
And it is frequently missed, because it is not visible in the way breast development is, so boys are often assumed to have started puberty later than they have.
Pubic hair, then penile growth.
Growth spurt — peak velocity at around 13 to 14, which is roughly two years later than in girls.
Voice change — the larynx enlarges under testosterone and the vocal cords lengthen and thicken (Chapter 8.1). The break happens over months and is caused by uneven growth of the structures.
Facial hair — usually last, and continuing to develop into the twenties.
Sperm production begins relatively early in the sequence, typically around 13 to 14, and generally before the growth spurt is complete — so fertility precedes full physical maturity.
Gynaecomastia — breast tissue development — occurs in around 50 to 60 percent of boys during puberty, from the transient imbalance between rising testosterone and its conversion to oestrogen.
It is normal, it is temporary in the large majority — resolving within 6 to 24 months — and it causes considerable distress. Telling a boy that it is common and will pass is a genuinely useful intervention, and it is frequently not said because he does not raise it.
Persistent gynaecomastia beyond two years, or appearing outside puberty, warrants investigation for liver disease, drugs, testicular tumours or Klinefelter syndrome.
Why girls are taller first and shorter later
A frequently asked question with a clean answer.
Girls' growth spurt occurs about two years earlier, so between about 11 and 13 the average girl is taller than the average boy.
Then two things favour boys. They have two additional years of pre-pubertal growth before their spurt begins, adding around 10 centimetres. And their spurt is larger — peak velocity around 10 centimetres a year against 8 to 9 in girls.
Together those account for the adult difference of around 13 centimetres.
And in both sexes, oestrogen closes the growth plates — including in boys, from testosterone converted by aromatase (Chapter 12.6).
The other changes
Body composition diverges sharply.
Girls gain fat, particularly on the hips, thighs and breasts, from oestrogen. Body fat rises from around 16 percent to 25 percent or more.
Boys gain muscle and lose fat, from testosterone. Muscle mass roughly doubles.
And the pelvis widens in girls (Chapter 5.6).
Skin — sebaceous glands enlarge under androgens, and acne affects up to 85 percent (Chapter 14.5). Apocrine sweat glands activate, producing adult body odour (Chapter 14.1).
Brain — and this is the change that matters most for behaviour.
The limbic and reward systems mature earlier than the prefrontal cortex, which continues myelinating into the mid-twenties (Chapter 11.5).
So there is a period of several years in which drive, sensitivity to reward and emotional reactivity are at adult or above-adult levels while the system that restrains them is not.
This is not an excuse and it is a genuine explanation for increased risk-taking, sensitivity to peer influence and emotional volatility in adolescence. And risk-taking in adolescence is not merely a defect — it is plausibly adaptive, since leaving the family group and establishing independence requires taking risks.
Sleep timing shifts later — the circadian rhythm genuinely delays by 1 to 3 hours during adolescence, which is biological rather than behavioural.
Which is why early school start times are a documented problem. Trials of later start times show improved sleep duration, attendance, academic performance and mental health, and reduced adolescent car crashes. It is one of the better-evidenced and least-implemented interventions in adolescent health.
When puberty comes early
Precocious puberty — before 8 in girls or 9 in boys.
Central (true) precocious puberty — early activation of the normal axis. In girls, around 80 to 90 percent have no identifiable cause. In boys, a cause is found far more often, which is why boys are investigated more aggressively — brain imaging is standard.
Peripheral precocious puberty — sex hormones from elsewhere: adrenal, gonadal or exogenous. Distinguished because it does not follow the normal sequence and because gonadotropins are suppressed rather than raised.
Why treat it:
Final adult height is reduced. Early sex hormones close the growth plates early, so a child who is initially the tallest in the class ends up shorter than they would have been. This is counter-intuitive and it is the main physical reason for treatment.
And there is a psychosocial reason — a child in a body years ahead of their peers and their own emotional development, with the associated risks.
Treatment is a GnRH agonist, exploiting the continuous-exposure paradox to switch the axis off until an appropriate age (Chapter 12.1). It is fully reversible on stopping.
And two benign variants that need recognising rather than treating:
Premature thelarche — isolated breast development in a young girl, with no other pubertal signs and no growth acceleration. Usually resolves.
Premature adrenarche — isolated pubic hair and body odour from early adrenal androgens, without gonadal activation.
Distinguishing these from true precocious puberty avoids unnecessary investigation and treatment, and the key features are the absence of other signs and normal growth velocity.
When puberty is late
Delayed puberty — no signs by 13 in girls or 14 in boys.
Constitutional delay of growth and puberty — much the commonest cause, particularly in boys, and it is a normal variant. Often a family history of a late-developing parent. The child is short for age but has a bone age that is correspondingly delayed, and they eventually reach normal adult height.
Reassurance is usually sufficient, and it is frequently inadequate as a response. The psychological effect of being the last to develop is real, and a short course of low-dose testosterone in boys to start the process is a reasonable and commonly used option that does not compromise final height.
Functional causes — chronic illness, malnutrition, inflammatory bowel disease, coeliac disease, excessive exercise, or eating disorders. Puberty is energetically expensive and the body defers it when resources are short.
And delayed puberty is sometimes the presenting feature of coeliac disease or Crohn's disease, which is why those are considered.
Hypogonadotropic hypogonadism — the hypothalamus or pituitary is not signalling. Kallmann syndrome combines it with an absent sense of smell, because the GnRH neurons and the olfactory neurons migrate together during development and fail together.
Hypergonadotropic hypogonadism — the gonads have failed. Turner syndrome (45,X) in girls and Klinefelter syndrome (47,XXY) in boys (Chapter 1.7).
Turner syndrome deserves specific mention because it is frequently diagnosed late. Short stature is present from childhood, and the absence of puberty is often what prompts the diagnosis at 13 to 15 — by which time growth hormone treatment, which improves final height, has lost much of its window.
Any girl with short stature and no other explanation should have a karyotype, and that is the practical lesson.
Talking about puberty
A short section, because the medical content has a practical counterpart.
Children who know what is coming cope far better than those who do not.
Girls who reach menarche without having been told what it is find it distressing, and this remains common in some settings.
Boys are told less than girls, and typically receive no equivalent preparation for their own changes — nocturnal emissions, voice change, gynaecomastia — which is a documented gap.
The specific facts that reduce distress: that the sequence and timing vary enormously and normally; that breast asymmetry is common and usually settles; that gynaecomastia in boys is normal and temporary; that early periods are often irregular; that acne is treatable; and that comparing yourself with peers is uninformative because the timing differs by years.
What the next page fixes
Puberty starts the reproductive years. Chapter 15.10 covers how they end — menopause in women, the more gradual changes in men, and what is treatable in both.