Puberty
Puberty refers to the process of physical changes by which a
child's
body becomes an
adult body capable of
reproduction.
Growth accelerates in the first half of puberty and reaches completion by the end. Body differences between boys and girls before puberty are almost entirely restricted to the
genitalia. During puberty major differences of size, shape, composition, and function develop in many body structures and systems. The most obvious of these are referred to as
secondary sex characteristics. In a strict sense, the term
puberty (and this article) refers to the bodily changes of sexual maturation rather than the psychosocial and cultural aspects of adolescent development.
Adolescence is the period of psychological and social transition between childhood and
adulthood. Adolescence largely overlaps the period of puberty but its boundaries are less precisely defined and it refers as much to the psychosocial and cultural characteristics of development during the teen years as to the physical changes of puberty.
Breast development
The first physical sign of puberty in girls is usually a firm, tender lump under the center of the
areola(e) of one or both
breasts, occurring on average at about 11 years of age. This is referred to as
thelarche. By the widely used
Tanner staging of puberty, this is stage 2 of breast development (stage 1 is a flat, prepubertal breast). Within 6-12 months, the swelling has clearly begun in both sides, softened, and can be felt and seen extending beyond the edges of the areolae. This is stage 3 of breast development. By another 12 months (stage 4), the breasts are approaching mature size and shape, with areolae and
papillae forming a secondary mound. In most young women, this mound disappears into the contour of the mature breast (stage 5), although there is so much variation in sizes and shapes of adult breasts that distinguishing advanced stages is of little clinical value.
Pubic hair in girls
Pubic hair is often the second unequivocal change of puberty. It is referred to as
pubarche and the pubic hairs are usually visible first along the
labia. The first few hairs are described as Tanner stage 2. Stage 3 is usually reached within another 6–12 months, when the hairs are too numerous to count and appear on the
mons as well. By stage 4, the pubic hairs densely fill the "pubic triangle." Stage 5 refers to spread of pubic hair to the
thighs and sometimes as
abdominal hair upward towards the
umbilicus. In about 15% of girls, the earliest pubic hair appears before breast development begins.
Vagina, uterus, ovaries
The
mucosal surface of the
vagina also changes in response to increasing levels of
estrogen, becoming thicker and a duller pink in color (in contrast to the brighter red of the prepubertal vaginal mucosa). Whitish secretions (physiologic
leukorrhea) are a normal effect of estrogen as well. In the next 2 years following thelarche, the
uterus and
ovaries increase in size. The ovaries usually contain small
cysts visible by
ultrasound.
Menstruation and fertility
The first
menstrual bleeding is referred to as
menarche. The average age of menarche in American girls is about 12.7 years, usually about 2 years after thelarche. Menses (menstrual periods) are not always regular and monthly in the first 2 years after menarche.
Ovulation is necessary for
fertility, and may or may not accompany the earliest menses. By 2 years after menarche, most girls are ovulating at least several times a year. Over 90% of girls who experience menarche before age 13 years are experiencing very regular, predictable menses accompanied by ovulation within 2 years, and a higher proportion of those with later menarche may not establish regular ovulation for 4 years or more. However, initiation of ovulation after menarche is not inevitable, and a high proportion of girls with continued irregularity several years from menarche will continue to have prolonged irregularity and anovulation, and are at higher risk for reduced fertility.
The word
nubility has been proposed academically to designate achievement of fertility.
Pelvic shape, fat distribution, and body composition
During this period, also in response to rising levels of estrogen, the lower half of the
pelvis widens (providing a larger
birth canal). Fat tissue increases to a greater percentage of the body composition than in males, especially in the typical female distribution of breasts, hips, and thighs. This produces the typical female body shape. Also, the fat goes to the buttocks of a girl, giving their buttocks more shape and curve.
Body and facial hair in girls
In the months and years following the appearance of pubic hair, other areas of skin which respond to androgens develop heavier hair (
androgenic hair) in roughly the following sequence: underarm (axillary) hair, perianal hair, upper lip hair, sideburn (preauricular) hair, and periareolar hair. Arm and leg hair becomes heavier more gradually over 10 years or more. Although in Western culture, hair in some of these areas is unwanted, it rarely indicates a
hormone imbalance unless it occurs elsewhere as well (such as under the chin and in the midline of the chest).
Height growth in girls
The estrogen-induced pubertal growth spurt in girls begins at the same time the earliest breast changes begin, or even a few months before, making it one of the earliest manifestations of puberty in girls. Growth of the legs and feet accelerates first, so that many girls have longer legs in proportion to their torso in the first year of puberty. The rate of growth tends to reach a peak velocity (as much as 7.5-10 cm or 3-4 inches per year) midway between thelarche and menarche and is already declining by the time menarche occurs. In the 2 years following menarche most girls grow about 5 cm (2 inches) before growth ceases at maximal adult height. This last growth primarily involves the
spine rather than the limbs.
Body odor, skin changes, and acne
Rising levels of
androgens can change the
fatty acid composition of
perspiration, resulting in a more "adult"
body odor. This often precedes thelarche and pubarche by 1 or more years. Another androgen effect is increased secretion of oil (
sebum) from the skin. This change increases the susceptibility to
acne, a characteristic affliction of puberty greatly variable in its severity.
Testicular size, function, and fertility
In boys, testicular enlargement is the first physical manifestation of puberty (and is termed
gonadarche).
Testes in prepubertal boys change little in size from about 1 year of age to the onset of puberty, averaging about
2â€"3 cc in volume and about
1.5-2 cm in length. Testicular size continues to increase throughout puberty, reaching maximal adult size about 6 years later. While
18-20 cc is reportedly an average adult size, there is wide variation in the normal population.
The testes have two primary functions: to produce
hormones and to produce
sperm. The
Leydig cells produce
testosterone (as described below), which in turn produces most of the changes of male puberty. However, most of the increasing bulk of testicular tissue is spermatogenic tissue (primarily
Sertoli and
interstitial cells). The development of sperm production and
fertility in males is not as well documented. Sperm can be detected in the morning urine of most boys after the first year of pubertal changes (and occasionally earlier).
Genitalia
A boy's
penis grows little from the fourth year of life until puberty. Average prepubertal penile length is
4 cm. The prepubertal genitalia are described as stage 1. Within months after growth of the testes begins, rising levels of testosterone promote growth of the penis and
scrotum. This earliest discernible beginning of pubertal growth of the genitalia is referred to as stage 2. The penis continues to grow until about 18 years of age, reaching an average
adult size of about
7-14 cm.
Although
erections and
orgasm occur in prepubertal boys, they become much more common during puberty, accompanied by a markedly increased
libido.
Ejaculation becomes possible early in puberty; prior to this boys may experience
dry orgasms. Emission of seminal fluid may occur due to
masturbation or spontaneously during sleep (commonly termed a
wet dream, and more clinically called a
nocturnal emission). The ability to ejaculate is a fairly early event in puberty compared to the other characteristics. However, in parallel to the irregularity of the first few periods of a girl, for the first one or two years after a boy's first ejaculation, his seminal fluid may contain few active sperm.
If the foreskin of a boy does not become retractable during childhood, it normally begins to retract during puberty. This occurs as a result of the increased production of testosterone and other hormones in the body.
Pubic hair in boys
Pubic hair often appears on a boy shortly after the genitalia begin to grow. As in girls, the first appearance of pubic hair is termed pubarche and the pubic hairs are usually first visible at the dorsal (abdominal) base of the penis. The first few hairs are described as stage 2. Stage 3 is usually reached within another 6–12 months, when the hairs are too numerous to count. By stage 4, the pubic hairs densely fill the "
pubic triangle." Stage 5 refers to spread of pubic hair to the
thighs and upward towards the
umbilicus as part of the developing
abdominal hair.
Body and facial hair in boys
In the months and years following the appearance of pubic hair, other areas of skin which respond to androgens develop heavier
hair (
androgenic hair) in roughly the following sequence:
underarm (axillary) hair,
perianal hair,
upper lip hair,
sideburn (preauricular) hair,
periareolar hair, and the rest of the
beard area. Arm, leg,
chest,
abdominal, and back hair become heavier more gradually. There is a large range in amount of body hair among adult men, and significant differences in timing and quantity of hair growth among different ethnic groups.
Voice change
Under the influence of androgens, the
voice box, or
larynx, grows in both genders. This growth is far more prominent in boys, causing the male voice to drop, rather abruptly, about one
octave, because the larger
vocal folds have a lower
fundamental frequency. Occasionally, this is accompanied by cracking and breaking sounds in the early stages. Most of the voice change happens during stage 4 of male puberty around the time of peak growth. However, it usually precedes the development of significant facial hair by several months to years.
Height growth in boys
Compared to girls' early growth spurt,
growth accelerates more slowly in boys and lasts longer, resulting in a taller adult stature among males than females (on average about
10 cm or 4 inches). The difference is attributed to the much greater potency of
estradiol compared to testosterone in promoting bone growth, maturation, and
epiphyseal closure. In boys, growth begins to accelerate about 9 months after the first signs of testicular enlargement and the peak year of the growth spurt occurs about 2 years after the onset of puberty, reaching a peak velocity of about 8.5–12 cm or 3.5–5 inches per year. The feet and hands experience their growth spurt first, followed by the limbs, and finally ending in the trunk. Epiphyseal closure and adult height are reached more slowly, at an average age of about 17.5 years. As in girls, this last growth primarily involves the
spine rather than the limbs.
Male musculature and body shape
By the end of puberty, adult men have heavier
bones and nearly twice as much skeletal
muscle. Some of the bone growth (e.g., shoulder width and jaw) is disproportionately greater, resulting in noticeably different male and female skeletal shapes. The average adult male has about 150% of the lean body mass of an average female, and about 50% of the body fat.
This muscle develops mainly during the later stages of puberty, and muscle growth can continue even after a male is biologically adult. The peak of the so-called "strength spurt," the rate of muscle growth, is attained about one year after a male experiences his peak growth rate.
Body odor, skin changes, acne
Rising levels of androgens can change the fatty acid composition of perspiration, resulting in a more "adult" body odor. As in girls, another androgen effect is increased secretion of oil (sebum) from the skin and the resultant variable amounts of acne.
Breast development in boys: pubertal gynecomastia
Estradiol is produced from testosterone in male puberty as well as female, and male
breasts often respond to the rising estradiol levels. This is termed
gynecomastia. In most boys, the breast development is minimal, similar to what would be termed a "breast bud" in a girl, but in many boys, breast growth is substantial. It usually occurs after puberty is underway, may increase for a year or two, and usually diminishes by the end of puberty. It is increased by extra adipose tissue if the boy is
overweight.
Although this is a normal part of male puberty for perhaps half of boys, breast development is usually as unwelcome as upper lip hair in girls, and can be removed surgically if the boy's distress is substantial.
Typical puberty is described above, but many children vary with respect to timing of onset, tempo, steadiness of continuation, and sequence of events.
Timing of onset
Puberty is a process with a gradual onset beginning with changes of neuronal function in the
hypothalamus, resulting in rising
hormonal signals between
brain and
gonads, proceeding to gonadal growth and production of
sex steroids, which in turn induce changes in responsive parts of the body. The definition of onset, therefore, depends on the perspective (e.g., hormonal versus physical) and purpose (establishing population normal standards, clinical care of early or late children, or a variety of other social purposes). The most commonly used definition of onset for both social and medical purposes is the appearance of the first physical changes described in this section of this article, but it should be understood that these physical changes are the first outward signs of preceding neural, hormonal, and gonadal function changes that are usually impossible or impractical to detect.
The age at which puberty begins can vary widely between individuals and between populations. Age of puberty is affected by both genetic factors and by environmental factors such as nutritional state or social circumstances. Timing may also be affected by environmental factors (exogenous hormones and environmental substances with hormone-like effects) and there is even evidence that life experiences may play a role as well.
Ethnic/racial differences have been recognized for centuries. For example, the average age of
menarche in various populations surveyed in the last several decades has ranged from 12.0 to 18.5 years. The earliest mean is reported for African-American girls and the oldest for high altitude subsistence populations in Asia. However, it is clear that much of the higher age averages reflect nutritional limitations more than genetic differences and can change within a few generations with a substantial change in diet. The median age of menarche for a population may be an index of the proportion of undernourished girls in the population, and the width of the spread may reflect unevenness of wealth and food distribution in a population.
Genetic influence on pubertal timing
Various studies have found direct genetic effects to account for at least 50% of the variation of timing of puberty in well-nourished populations. The genetic association of timing is strongest between mothers and daughters. The specific
genes affecting timing are not defined yet. Among the candidates are the
androgen and LH receptor genes.
Environmental factors affecting pubertal timing
If genetic factors account for half of the variation of pubertal timing, environment factors are clearly important as well. One of the earliest observed environmental effects is that puberty occurs later in children raised at higher altitudes. The most important of the environmental influences is clearly nutrition, but a number of others have been identified, all which affect timing of female puberty and menarche more clearly than male puberty.
Nutritional influence on pubertal timing
Nutritional factors are the strongest and most obvious environmental factors affecting timing of puberty. Girls are especially sensitive to nutritional regulation because they must contribute all of the nutritional support to a growing fetus. Surplus
calories (beyond growth and activity requiriements) are reflected in the amount of
body fat, which signals to the brain the availability of resources for initiation of puberty and fertility.
Much evidence suggests that for most of the last few centuries, nutritional differences accounted for majority of variation of pubertal timing in different populations, and even among social classes in the same population. Recent worldwide improvements in nutrition and increases in childhood fatness have resulted in falling ages of puberty, mainly in those populations with the higher previous ages. In many populations the amount of variation attributable to nutrition is shrinking.
Although available dietary energy (simple calories) is the most important dietary influence on timing of puberty, quality of the diet plays a role as well. Lower
protein intakes and higher
plant fiber intakes, as occur with typical
vegetarian diets, are associated with later onset and slower progression of female puberty.
Studies have shown that calcium deficiency is a cause of late puberty, irregular and painful, cramping during menstration with excessive blood loss, and lowered immune response to infections in young girls. This could be from a deficient diet or lack of vitamin D from too little sun exposure. This lack of calcium could predispose them to osteoporosis later in life.
Effect of physical activity and exercise on pubertal timing
The average level of daily physical activity has also been shown to affect timing of puberty, especially female. A high level of exercise, whether for athletic or body image purposes, or for daily subsistence, reduces energy calories available for reproduction and slows puberty. The exercise effect is often amplified by a lower body fat mass.
Effect of physical illness on pubertal timing
Many chronic diseases can delay puberty in both boys and girls. Those that involve chronic inflammation or interfere with nutrition have the strongest effect. In the western world,
inflammatory bowel disease and
tuberculosis have been notorious for such an effect in the last century, while in areas of the underdeveloped world, chronic
parasite infections are widespread.
Effect of environmental chemicals and hormones on pubertal timing
There is theoretical concern, and animal evidence, that environmental hormones and
chemicals may affect aspects of prenatal or postnatal sexual development in humans. Large amounts of incompletely metabolized estrogens and
progestagens from pharmaceutical products are excreted into the sewage systems of large cities, and are sometimes detectable in the environment.
Sex steroids are sometimes used in poultry or cattle farming. Although agricultural laws regulate use to minimize accidental human consumption, the rules are largely self-enforced in the United States. Significant exposure of a child to hormones or other substances that activate estrogen or androgen
receptors could produce some or all of the changes of puberty.
Harder to detect as an influence on puberty are the more diffusely distributed environmental chemicals like PCBs (
polychlorinated biphenyl), which can bind and trigger estrogen receptors.
More obvious degrees of partial puberty from direct exposure of young children to small but significant amounts of pharmaceutical sex steroids from exposure at home may be detected during medical evaluation for
precocious puberty, but mild effects and the other potential exposures outlined above would not.
Effect of stress and social factors on pubertal timing
Some of the least understood environmental influences on timing of puberty are social and psychological. In comparison with the effects of genetics, nutrition, and general health, social influences are small, shifting timing by a few months rather than years. Mechanisms of these social effects are unknown, though a variety of physiological processes, including
pheromones, have been suggested based on animal research.
The most important part of a child's psychosocial environment is the family, and most of the social influence research has investigated features of family structure and function in relation to earlier or later female puberty. Most of the studies have reported that menarche may occur a few months earlier in girls in high-stress households, whose fathers are absent during their early childhood, who have a stepfather in the home, who are subjected to prolonged
sexual abuse in childhood, or who are
adopted from a developing country at a young age. Conversely, menarche may be slightly later when a girl grows up in a large family with a biological father present.
More extreme degrees of environmental stress, such as wartime refugee status with threat to physical survival, have been found to be associated with delay of maturation, an effect that may be compounded by dietary inadequacy.
Most of these reported social effects are small and our understanding is incomplete. Most of these "effects" are statistical associations revealed by
epidemiologic surveys. Statistical associations are not necessarily causal, and a variety of covariables and alternative explanations can be imagined. Effects of such small size can never be confirmed or refuted for any individual child. Furthermore, interpretations of the data are politically controversial because of the ease with which this type of research can be used for political advocacy. Accusations of bias based on political agenda sometimes accompany scientific criticism.
Another limitation of the social research is that nearly all of it has concerned girls, partly because female puberty requires greater physiologic resources and partly because it involves a unique event (menarche) that makes survey research into female puberty much simpler than male. More detail is provided in the
menarche article.
Average timing for American children
Some of the most complete reference data are available for American children and is included here. Average age for first signs of breast development in girls is about 10.5 years. Average age for first signs of testicular enlargement in boys is 11.5 years. See Tables below for approximate average ages and ranges for other milestones of physical development of North American children.
Duration of puberty (time from onset to completion) varies less between children than does the age of onset. Duration of puberty in girls from onset of breast development to cessation of growth is roughly 5 years. Duration of puberty in boys from first testicular enlargement to cessation of growth is about 6 years.
Table 1 provides 3rd, 50th, and 97th
percentiles for attainment of selected stages by American girls as reported in 1985. In these tables,
B, PH, and
G refer to the
Tanner stages of physical puberty:
B is breast,
PH is pubic hair, and
G is genitalia (penis and testes).
B1, PH1, and
G1 are the prepubertal stages of each of these, while
B2,
PH2, and
G2 are the earliest signs of puberty.
B5,
PH5, and
G5 are adult stages at the end of puberty. The
Tanner stage article contains links to fuller explanations of the specific stages. All three tables below express ages as years and months (y and m).
| Stages | 3rd percentile | 50th percentile | 97th percentile | | B2 | 8y 10m | 10y 11m | 13y 0m |
|---|
| B3 | 9y 10m | 11y 11m | 14y 0m |
|---|
| B4 | 10y 6m | 12y 11m | 14y 5m |
|---|
| PH2 | 9y 0 m | 11y 3m | 13y 6m |
|---|
| PH3 | 9y 8m | 11y 11m | 14y 3m |
|---|
| PH4 | 10y 5m | 12y 7m | 14y 7m |
|---|
| Menarche | 10y 10m | 12y 9m | 14y 7m |
|---|
| Peak height velocity | 9y 0m | 11y 6m | 14y 0m |
|---|
|
However, a later survey from a group of American primary pediatric practices reported both a slightly earlier average onset, greater range, and more importantly, a significant difference between Caucasian and African-American girls at some stages (
Table 2).
| Stages | 3rd percentile | 50th percentile | 97th percentile | | B2 | 6y 5m | 10y 0m | 13y 7m |
|---|
| B3 | 8y 7m | 11y 4m | 14y 1m |
|---|
| B4 | 10y 4m | 12y 9m | 15y 3m |
|---|
| B5 | 11y 4m | 14y 6m | 17y 9m |
|---|
| PH2 | 7y 2m | 10y 5m | 13y 8m |
|---|
| PH3 | 8y 8m | 11y 5m | 14y 2m |
|---|
| PH4 | 10y 5m | 14y 7m | 14y 7m |
|---|
| PH5 | 10y 10m | 12y 2m | 16y 8m |
|---|
| Menarche | 10y 6m | 12y 10m | 15y 3m |
|---|
| Peak height velocity | 10y 0m | 12y 6m | 14y 0m |
|---|
|
| Stages | 3rd percentile | 50th percentile | 97th percentile | | B2 | 5y 0m | 8y 11m | 12y 10m |
|---|
| B3 | 7y 7m | 10y 2m | 12y 11m |
|---|
| PH2 | 4y 9m | 8y 9m | 12y 9m |
|---|
| PH3 | 7y 6m | 10y 3m | 13y 0m |
|---|
| Menarche | 9y 10m | 12y 2m | 14y 6m |
|---|
|
--| Stages | 3rd percentile | 50th percentile | 97th percentile | | PH2 | 9y 11m | 12y 0m | 14y 1m |
|---|
| PH3 | 11y 3m | 13y 1m | 14y 11m |
|---|
| PH4 | 12y 0m | 13y 10m | 15y 9m |
|---|
| G2 | 9y 3m | 11y 6m | 13y 9m |
|---|
| G3 | 10y 2m | 12y 4m | 14y 8m |
|---|
| G4 | 11y 3m | 13y 3m | 15y 5m |
|---|
|
| Stages | 3rd percentile | 50th percentile | 97th percentile | | 4 cc or 2.5 cm | 9y 6m | 11y 6m | 13y 6m |
|---|
| 6 cc or 3.5 cm | | 10y 2m | - | 12 cc or 3.6 cm | 11y 6m | 14y 0m | 16y 6m |
|---|
| 15 cc or 3.8 cm | | 16y 6m | - | Peak height velocity | 11y 0m | 13y 6m | 15y 8m |
|---|
|
Variations of tempo and progression
Tempo is the speed at which the process of pubertal changes progresses from beginning to end. The duration of puberty generally varies less than timing of onset, and approximates 4 years for girls and 6 for boys (from first physical changes to attainment of adult height). Nevertheless, some healthy children can proceed through puberty at a faster or slower tempo than most.
An interruption of progression of puberty is usually, but not always, due to abnormal causes such as
malnutrition or
anorexia nervosa. Perhaps the most common apparently healthy variation is apparent interruption for a couple of years just after attainment of an early sign of initiation. For instance, some girls may seem to develop stage 2 breast buds at 6 or 7 years of age with no other signs of puberty, and nothing may happen for 2 or 3 years. Physicians refer to this as "unsustained puberty."
Variations of sequence
The sequence of events of pubertal development can occasionally vary. For example, in about 15% of boys and girls,
pubarche (the first pubic hairs) can precede, respectively,
gonadarche and
thelarche by a few months. Rarely,
menarche can occur before other signs of puberty in a few girls. These variations deserve medical evaluation because they can occasionally signal a disease.
Conclusion of puberty
In a general sense, the conclusion of puberty is reproductive maturity. Criteria for defining the conclusion may differ for different purposes: attainment of the ability to reproduce, achievement of maximal adult height, maximal gonadal size, or adult sex hormone levels. Maximal adult height is achieved at an average age of 14.5 years for American girls and 17.5 years for American boys. Potential fertility (sometimes termed
nubility) usually precedes completion of growth by 1-2 years in girls and 3-4 years in boys. Stage 5 in the tables above typically represents maximal gonadal growth and attainment of adult hormone levels.
The endocrine
reproductive system consists of the
hypothalamus, the
pituitary, the
gonads, and the
adrenal glands, with input and regulation from many other body systems. True puberty is often termed "central puberty" because it begins as a process of the
central nervous system. A simple description of hormonal puberty is as follows:
#The brain's
hypothalamus begins to release pulses of
GnRH. #Cells in the anterior
pituitary respond by secreting
LH and
FSH into the circulation.#The
ovaries or
testes respond to the rising amounts of LH and FSH by growing and beginning to produce
estradiol and
testosterone.#Rising levels of estradiol and testosterone produce the body changes of female and male puberty.
The onset of this neurohormonal process may precede the first visible body changes by 1-2 years.
Components of the endocrine reproductive system
The
arcuate nucleus of the
hypothalamus is the driver of the reproductive system. It has
neurons which generate and release pulses of GnRH into the portal venous system of the
pituitary gland. The arcuate nucleus is affected and controlled by neuronal input from other areas of the brain and hormonal input from the
gonads,
adipose tissue and a variety of other systems.
The
pituitary gland responds to the pulsed GnRH signals by releasing LH and FSH into the blood of the general circulation, also in a pulsatile pattern.
The
gonads (
testes and
ovaries) respond to rising levels of LH and FSH by producing the
steroid sex hormones,
testosterone and
estradiol.
The
adrenal glands are a second source for steroid hormones. Adrenal maturation, termed
adrenarche, typically precedes gonadarche in mid-childhood.
Major hormones of puberty
*GnRH (
gonadotropin-releasing hormone) is a
peptide hormone released from the
hypothalamus which stimulates
gonadotrope cells of the anterior
pituitary.
*LH (
luteinizing hormone) is a larger protein hormone secreted into the general circulation by gonadotrope cells of the anterior pituitary gland. The main target cells of LH are the
Leydig cells of testes and the
theca cells of the ovaries. LH secretion changes more dramatically with the initiation of puberty than FSH, as LH levels increase about 25-fold with the onset of puberty, compared with the 2.5-fold increase of FSH.
*FSH (
follicle stimulating hormone) is another protein hormone secreted into the general circulation by the gonadotrope cells of the anterior pituitary. The main target cells of FSH are the ovarian
follicles and the
Sertoli cells and
spermatogenic tissue of the testes.
*
Testosterone is a steroid hormone produced primarily by the Leydig cells of the testes, and in lesser amounts by the
theca cells of the ovaries and the adrenal cortex. Testosterone is the primary mammalian
androgen and the "original"
anabolic steroid. It acts on
androgen receptors in responsive tissue throughout the body.
*
Estradiol is a
steroid hormone produced by
aromatization of testosterone. Estradiol is the principal human
estrogen and acts on
estrogen receptors throughout the body. The largest amounts of estradiol are produced by the
granulosa cells of the ovaries, but lesser amounts are derived from testicular and adrenal testoterone.
*Adrenal
androgens are steroids produced by the
zona reticulosa of the
adrenal cortex in both sexes. The major adrenal androgens are
dehydroepiandrosterone,
androstenedione (which are precursors of testosterone), and
dehydroepiandrosterone sulfate which is present in large amounts in the blood. Adrenal androgens contribute to the androgenic events of early puberty in girls.
*IGF1 (
insulin-like growth factor 1) rises substantially during puberty in response to rising levels of
growth hormone and may be the principal mediator of the pubertal growth spurt.
*
Leptin is a protein hormone produced by
adipose tissue. Its primary target organ is the hypothalamus. The leptin level seems to provide the brain a rough indicator of adipose mass for purposes of regulation of
appetite and
energy metabolism. It also plays a permissive role in female puberty, which usually will not proceed until an adequate body mass has been achieved.
The process of puberty from an endocrine perspective
The
endocrine reproductive system becomes functional by the end of the first
trimester of fetal life. The testes and ovaries become briefly inactive around the time of birth but resume hormonal activity until several months after birth, when incompletely understood mechanisms in the brain begin to suppress the activity of the arcuate nucleus. This has been referred to as maturation of the prepubertal "gonadostat," which becomes sensitive to negative feedback by
sex steroids.
Gonadotropin and sex steroid levels fall to low levels (nearly undetectable by current
clinical assays) for approximately another 8 to 10 years of childhood. Evidence is accumulating that the reproductive system is not totally inactive during the childhood years. Subtle increases in gonadotropin pulses occur, and ovarian follicles surrounding
germ cells (future
eggs) double in number.
Normal puberty is initiated in the hypothalamus, with de-inhibition of the pulse generator in the arcuate nucleus. This inhibition of the arcuate nucleus is an ongoing active suppression by other areas of the brain. The signal and mechanism releasing the arcuate nucleus from inhibition have been the subject of investigation for decades and remain incompletely understood.
Leptin levels rise throughout childhood and play a part in allowing the arcuate nucleus to resume operation. If the childhood inhibition of the arcuate nucleus is interrupted prematurely by injury to the brain, it may resume pulsatile gonadotropin release and puberty will begin at an early age.
Neurons of the arcuate nucleus secrete gonadotropin releasing hormone (GnRH) into the blood of the pituitary portal system. These GnRH signals from the hypothalamus induce pulsed secretion of LH (and to a lesser degree, FSH) at roughly 1-2 hour intervals. In the years preceding physical puberty, these gonadotropin pulses occur primarily at night and are of very low amplitude, but as puberty approaches they can be detected during the day. By the end of puberty, there is little day-night difference in the amplitude and frequency of gonadotropin pulses.
An array of "autoamplification processes" increase the production of all of the pubertal hormones of the hypothalamus, pituitary, and gonads.
Regulation of
adrenarche and its relationship to maturation of the hypothalamic-gonadal axis is not fully understood, and some evidence suggests it is a parallel but largely independent process coincident with or even preceding central puberty. Rising levels of adrenal
androgens (termed adrenarche) can usually be detected between 6 and 11 years of age, even before the increasing gonadotropin pulses of hypothalamic puberty. Adrenal androgens contribute to the development of pubic hair (
pubarche), adult
body odor, and other androgenic changes in both sexes. The primary clinical significance of the distinction between adrenarche and gonadarche is that pubic hair and body odor changes by themselves do not prove that central puberty is underway for an individual child.
Hormonal changes of puberty in girls
As the amplitude of LH pulses increases, the theca cells of the ovaries begin to produce testosterone and smaller amounts of
progesterone. Much of the testosterone moves into nearby cells called
granulosa cells. Smaller increases of FSH induce an increase in the
aromatase activity of these granulosa cells, which converts most of the testosterone to estradiol for secretion into the circulation.
Rising levels of estradiol produce the characteristic estrogenic body changes of female puberty: growth spurt, acceleration of bone maturation and closure, breast growth, increased fat composition, growth of the uterus, increased thickness of the
endometrium and the vaginal mucosa, and widening of the lower pelvis.
As the estradiol levels gradually rise and the other autoamplification processes occur, a point of maturation is reached when the feedback sensitivity of the hypothalamic "gonadostat" becomes positive. This attainment of positive feedback is the hallmark of female sexual maturity, as it allows the midcycle LH surge necessary for
ovulation.
Levels of adrenal androgens and testosterone also increase during puberty, producing the typical androgenic changes of female puberty: pubic hair, other androgenic hair as outlined above, body odor, acne.
Growth hormone levels rise steadily throughout puberty.
IGF1 levels rise and then decline as puberty ends. Growth finishes and adult height is attained as the estradiol levels complete closure of the
epiphyses.
Hormonal changes of puberty in boys
Early stages of male hypothalamic maturation seem to be very similar to the early stages of female puberty, though occurring about 1-2 years later.
LH stimulates the Leydig cells of the testes to make testosterone and blood levels begin to rise. For much of puberty, nighttime levels of testosterone are higher than daytime. Regularity of frequency and amplitude of gonadotropin pulses seems to be less necessary for progression of male than female puberty.
As the testosterone levels slowly rise, most of the effects are mediated through the androgen receptors by way of conversion to
dihydrotestosterone in the target tissues (especially of the skin).
However, a significant portion of testosterone in adolescent boys is converted to estradiol. Estradiol mediates the growth spurt, bone maturation, and epiphyseal closure in boys just as in girls. Estradiol also induces at least modest development of breast tissue (
gynecomastia) in a large proportion of boys.
The age at which puberty occurs has dropped significantly since the
1840s. Researchers refer to this drop as the 'secular trend'. From
1840 through
1950, in each decade there was a drop of four months in the average age of menarche among Western European female samples. In
Norway, girls born in 1840 had their first menarche at average 17 years. In France in 1840 the average was 15.3 years. In
England the 1840 average was 16.5 years for girls. In
Japan the decline happened later and was then more rapid: from 1945 to 1975 in Japan there was a drop of 11 months per decade.
The most likely cause, as is generally accepted, is the increase of weight gain in the world's youth. Some scientists and researches hypothesize it may be caused by hormones and other additions in processed milk and meats.
* See
Precocious puberty* See
Delayed puberty* See
Menarche,
gonadarche,
pubarche,
thelarche,
adrenarche.
*
Child sexuality*
Adolescence* Herman-Giddens ME, Slora EJ, Wasserman RC, et al. Secondary sexual characteristics and menses in young girls seen in office practice: a study from the pediatric research in office settings network.
Pediatrics, 1997; 99:501-12.
Newer data suggesting we should be using lower age thresholds for evaluation.* Plant TM, Lee PA, eds.
The Neurobiology of Puberty. Bristol: Society for Endocrinology, 1995.
Proceedings of the latest (4th) International Conference on the Control of the Onset of Puberty, containing summaries of current theories of physiological control, as well as GnRH analog treatment.* Tanner JM, Davies PS. Clinical longitudinal standards for height and weight velocity for North American children.
J Pediatr 1985; 107:317-29.
Highly useful growth charts with integrated standards for stages of puberty.* Ducros, A. and Pasquet, P. Evolution de l'âge d'apparition des premières règles (ménarche) en France. Biométrie Humaine (1978), 13, 35â€"43.
*
Guide to Growing Up Wikibook - A wikibook covering ways to cope with many of the challenges that teens face.
*
Teen Puberty*
NIH guide to puberty and adolescence*
Growing Up Sexually: A World Atlas*
Love and sex section - youthinformation.com*
Family Practice Notebook: Sexual Development*
Research shows how evolution explains age of puberty,
ScienceDaily, December 1, 2005.
* Mark Hanson, P. Gluckman.
Evolution, development and timing of puberty,
Trends in Endocrinology & Metabolism, January 2006.
*
Neurobiological Mechanisms of the Onset of Puberty in Primates,
Endocrine Reviews, 2001 Feb;22(1):111-51.
