Puberty refers to the process of physical changes by which a child's body becomes an adult body capable of reproduction. Puberty is initiated by hormone signals from the brain to the gonads (the ovaries and testes). In response, the gonads produce a variety of hormones that stimulate the growth, function, or transformation of brain, bones, muscle, skin, breasts, and reproductive organs. Growth accelerates in the first half of puberty and stops at the completion of puberty. Before puberty, body differences between boys and girls 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.
Differences between male and female puberty
Two of the most significant differences between puberty in girls and puberty in boys are the age at which it begins, and the major sex steroids involved.
Although there is a wide range of normal ages, on average, girls begin the process of puberty about 1-2 years earlier than boys (with average ages of nine to fourteen for girls and ten to seventeen for boys), and reach completion in a shorter time. Girls attain adult height and reproductive maturity about 4 years after the first physical changes of puberty appear. In contrast, boys accelerate more slowly but continue to grow for about 6 years after the first visible pubertal changes.
The hormone that dominates female development is estradiol, an estrogen. While estradiol promotes growth of breasts and uterus, it is also the principal hormone driving the pubertal growth spurt and epiphyseal maturation and closure. Estradiol levels rise earlier and reach higher levels in women than in men.
In boys, testosterone, an androgen, is the principal sex steroid. While testosterone produces all the male changes characterized as virilization, a substantial product of testosterone metabolism in males is estradiol, though levels rise later and more slowly than in girls. The male growth spurt also begins later, accelerates more slowly, and lasts longer before the epiphyses fuse. Although boys are 2 cm taller than girls before puberty begins, adult men are on average about 13 cm (5.2 inches) taller than women. Most of this sex difference in adult heights is attributable to a later onset of the growth spurt and a slower progression to completion, a direct result of the later rise and lower adult male levels of estradiol.
Physical changes in boys
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 2-3 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 sexual maturation and maintains libido. 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). Potential fertility is reached at about 13 years old in boys, but full fertility will not be gained until 14-16 years of age, although some go through the process faster, reaching it only 1 year later.
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 navel as part of the developing abdominal hair.
Body and facial hair
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.
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 and deepen, sometimes abruptly but rarely "over night," about one octave, because the longer and thicker vocal folds have a lower fundamental frequency. Voices never "break." A typical 12-year old boy's larynx is larger, even before voice change, than an adult woman's. Occasionally, voice change is accompanied by unsteadiness of vocalization in the early stages of untrained voices. Most of the voice change happens during stage 3-4 of male puberty around the time of peak growth. Full adult pitch is attained at an average age of about 15 years. However, it usually precedes the development of significant facial hair by several months to years.
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. Full adult height is usually reached somewhere around 17-18 years of age.
Gigantism: Precocious puberty
The name to a particular growth defect that occurs during childhood, from over-exposure to growth hormone. Precocious puberty and a variety of conditions associated with excessive amounts of testosterone or estrogen in childhood will result in tallness by mid-childhood. People affected by Gigantism grow up in height up to 8ft (approximately 2.40 metres) very rarely. However, the acceleration of bone maturation by the early rise of estradiol results in early completion of growth, and adult heights for these children may actually be below average for genetic potential. The possible symptoms is a Normal genetic variation or Hyperthyroidism, XYY syndrome, Overnutrition, Acromegaly, McCune-Albright syndrome etc.
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. Acne can be prevented by antibacterial face washes and typically diminishes at the end of puberty.
Breast development: 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. Weight loss for overweight teenagers can help reduce the prominence of gynecomastia but not diminish as to pubertal reasons.
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 its causing a lot of stress or anxiety in the boy.
Physical changes in girls
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 10.5 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 six to 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 stages 4 and 5 are not always separately identifiable.
Pubic hair is often the second unequivocal change of puberty noticed, usually within a few months of thelarche. 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 pubic mound 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 navel. 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, and follicles in the ovaries reach larger sizes. The ovaries usually contain small follicular cysts visible by ultrasound.
Menstruation and fertility
The first menstrual bleeding is referred to as menarche, and typically occurs about 2 years after thelarche. The average age of menarche in American girls is about 12.75 years. Menses (menstrual periods) are not always regular and monthly in the first 2 years after menarche. Ovulation is necessary for fertility, but may or may not accompany the earliest menses. In postmenarchal girls, about 80% of the cycles were anovulatory in the first year after menarche, 50% in the third and 10% in the sixth year. 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 is used commonly in the social sciences to designate achievement of fertility.
Body and facial hair
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 hairs along the linea nigra from the pubic hair to the umbilicus. The amount of hair in those areas is less than the male amount. There is a large range in amount of body hair among adult women, and significant differences in timing and quantity of hair growth among different ethnic groups.
Body shape, fat distribution, and body composition
During this period, also in response to rising levels of estrogen, the lower half of the pelvis and thus hips widen (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, buttocks, thighs, upper arms, and pubis. Progressive differences in fat distribution as well as sex differences in local skeletal growth contribute to the typical female body shape by the end of puberty. At age 10 years, the average girl has 6% more body fat than the average boy, but by the end of puberty the average difference is nearly 50%.
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.
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.
Various studies have found direct genetic effects to account for at least 46% 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 is an androgen receptor gene.
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 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 requirements) 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 increased consumption of animal protein, other changes 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 menstruation 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.
Physical activity and exercise
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.
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.
Environmental chemicals and hormones
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 cattle farming but have been banned in chicken meat production for 40 years. 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.
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 are 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 11.1 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, based on NCHS data collected in the 1970s and reported in 1985 (Tanner et al., 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 10 m||10y 11 m||13y 0 m|
|B3||9y 10 m||11y 11 m||14y 0 m|
|B4||10y 6 m||12y 11 m||14y 5 m|
|PH2||9y 0 m||11y 3 m||13y 6 m|
|PH3||9y 8 m||11y 11 m||14y 3 m|
|PH4||10y 5 m||12y 7 m||14y 7 m|
|Menarche||10y 10 m||12y 9 m||14y 7 m|
|Peak height velocity||9y 0 m||11y 6 m||14y 0 m|
However, a later survey performed in the mid-1990s by a group of American primary pediatric practices with slightly different methods reported both a mildly earlier average onset, greater range, and more importantly, a significant difference between white and African-American girls in the early stages (Table 2) (Herman-Giddens et al.).
|Stages||3rd percentile||50th percentile||97th percentile|
|B2||6y 5 m||10y 0 m||13y 7 m|
|B3||8y 7 m||11y 4 m||14y 1 m|
|B4||10y 4 m||12y 9 m||15y 3 m|
|B5||11y 4 m||14y 6 m||17y 9 m|
|PH2||7y 2 m||10y 5 m||13y 8 m|
|PH3||8y 8 m||11y 5 m||14y 2 m|
|PH4||10y 5 m||12y 2 m||14y 7 m|
|PH5||10y 10 m||12y 2 m||16y 8 m|
|Menarche||10y 6 m||12y 6 m||15y 3 m|
|Peak height velocity||10y 0 m||12y 0 m||14y 0 m|
|Stages||3rd percentile||50th percentile||97th percentile|
|B2||5y 0 m||8y 11 m||12y 10 m|
|B3||7y 7 m||10y 2 m||12y 11 m|
|PH2||4y 9 m||8y 9 m||12y 9 m|
|PH3||7y 6 m||10y 3 m||13y 0 m|
|Menarche||9y 10 m||12y 2 m||14y 6 m|
|Stages||3rd percentile||50th percentile||97th percentile|
|PH2||9y 11 m||12y 0 m||14y 1 m|
|PH3||11y 3 m||13y 1 m||14y 11 m|
|PH4||12y 0 m||13y 10 m||15y 9 m|
|G2||9y 3 m||11y 2 m||13y 9 m|
|G3||10y 2 m||12y 4 m||14y 8 m|
|G4||11y 3 m||14y 0 m||15y 5 m|
|Stages||3rd percentile||50th percentile||97th percentile|
|4 cc or 2.5 cm||9y 6 m||11y 0 m||13y 6 m|
|6 cc or 3.5 cm||12y 0 m|
|12 cc or 3.6 cm||11y 6 m||13y 8 m||16y 6 m|
|15 cc or 3.8 cm||14y 6 m|
|Peak height velocity||11y 0 m||13y 3 m||15y 8 m|
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.
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 14-15 years for American girls and 16 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 adrenal glands are a second source for steroid hormones. Adrenal maturation, termed adrenarche, typically precedes gonadarche in mid-childhood.
- 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 testosterone.
- 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 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" increases 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 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 mid cycle 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 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.
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. Boys who develop mild gynecomastia or even developing swellings under nipples during puberty are told the effects are temporary in some male teenagers due to high levels of Estradiol.
Another hormonal change in males takes place during the teenage years for most young men. At this point in a males life the testosterone levels slowly rise, and most of the effects are mediated through the androgen receptors by way of conversion [dehydrotestosterone] in target organs (especially that of the bowels). Consequently, there is a transformation that takes place and the processes in which human waste and urine are released by the body are reversed.
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.
- Gordon, Catharine M.; Laufer, MR (2005). "Chapter 4: Physiology of puberty", in Emans SJH, Goldstein DP, Laufer, MR, eds.: Pediatric and Adolescent Gynecology, 5th ed., Philadelphia: Lippincott, Williams & Wilkins, pp. 120-155. ISBN 0781744938.
- Gungor, Neslihan; Arslanian SA (2002). "Chapter 21: Nutritional disorders: integration of energy metabolism and its disorders in childhood", in Sperling, MA ed.: Pediatric Endocrinology, 2nd ed., Philadelphia: Saunders, pp. 689-724. ISBN 0721695396.
- Marshall, William A.; Tanner, JM (1986). "Chapter 8: Puberty", in Falkner F, Tanner JM, eds.: Human Growth: A Comprehensive Treatise, 2nd ed., New York: Plenum Press, pp. 171-209. ISBN 0-306-41952-1.
- Rosenfield, Robert L. (2002). "Chapter 16: Female puberty and its disorders", in Sperling, MA ed.: Pediatric Endocrinology, 2nd ed., Philadelphia: Saunders, pp. 455-518. ISBN 0721695396.
- Styne, Dennis M. (2002). "Chapter 18: The testes: disorders of sexual differentiation and puberty in the male", in Sperling, MA ed.: Pediatric Endocrinology, 2nd ed., Philadelphia: Saunders, pp. 565-628. ISBN 0721695396.
- Marshall (1986), p. 176-7
- MacGillivray MH, Morishima A, Conte F, Grumbach M, Smith EP (1998). "Pediatric endocrinology update: an overview. The essential roles of estrogens in pubertal growth, epiphyseal fusion and bone turnover: lessons from mutations in the genes for aromatase and the estrogen receptor". Horm. Res. 49 Suppl 1: 2-8. PMID 9554463.
- Abbassi V (1998). "Growth and normal puberty". Pediatrics 102 (2 Pt 3): 507-11. PMID 9685454.
- Styne (2002), p. 598
- Jones, Kenneth W. (2006). Smith's Recognizable Patterns of Human Malformation. St. Louis, Mo: Elsevier Saunders. ISBN 0-7216-0615-6.
- Marshall (1986), p. 180
- Marshall (1986), p. 187
- Marshall (1986), p. 188
- Tanner JM, Davies PS (1985). "Clinical longitudinal standards for height and height velocity for North American children". J. Pediatr. 107 (3): 317-29. PMID 3875704.
- Gordon (2005), p. 151
- Marshall (1986), p. 186-7
- Rosenfield (2002), p. 462
- Siegel MJ, Surratt JT (1992). "Pediatric gynecologic imaging". Obstet. Gynecol. Clin. North Am. 19 (1): 103-27. PMID 1584537.
- Apter D (1980). "Serum steroids and pituitary hormones in female puberty: a partly longitudinal study". Clin. Endocrinol. (Oxf) 12 (2): 107-20. PMID 6249519.
- Marshall (1986), p. 196-7
- Southam AL, Richart RM (1966). "The prognosis for adolescents with menstrual abnormalities". Am. J. Obstet. Gynecol. 94 (5): 637-45. PMID 5906589.
- Hips widen during female puberty coulmbia.edu
- Gungor (2002), p. 699-700
- Rosenfield (2002), p. ?
- Xiaojia Ge, Misaki N. Natsuaki, Jenae M. Neiderhiser, David Reiss (2007). "Genetic and Environmental Influences on Pubertal Timing: Results From Two National Sibling Studies," Journal of Research on Adolescence, 17(4), 767-788
- Mustanski, B. S., Viken, R. J., Kaprio, J., Pulkkinen, L., & Rose, R. J. (2004). "Genetic and environmental influences on pubertal development: Longitudinal data from finnish twins at ages 11 and 14," Developmental Psychology, 40, 1188-1198.
- Treloar, S. A., & Martin, N. G. (1990). "Age at menarche as a fitness trait: Nonadditive genetic variance detected in a large twin sample," American Journal of Human Genetics, 47, 137-148.
- Kaprio, J., Rimpela, A., Winter, T., Viken, R. J., Rimpela, M., & Rose, R. J. (1995). "Common genetic influences on BMI and age at menarche," Human Biology, 67, 739-753.
- Comings, D. E., Muhleman, D., Johnson, J. P., & MacMurray, J. P. (2002). "Parent-daughter transmission of the androgen receptor gene as an explanation of the effects of father absence on age of menarche," Child Development, 73, 1046-1051.
- Finley, Harry. "Average age at menarche in various cultures", Museum of Menstruation and Women's Health. Retrieved on 2007-08-02.
- Whincup, P H; J A Gilg, K Odoki, S J C Taylor, D G Cook (2001-05-05). "Age of menarche in contemporary British teenagers: survey of girls born between 1982 and 1986". BMJ 322: 1095-1096. Retrieved on 2007-08-02.
- "Girls maturing slightly earlier", BBC News, 2001-05-03. Retrieved on 2007-08-02.
- Ducros, A. and Pasquet, P. "Evolution de l'âge d'apparition des premières règles (ménarche) en France". Biométrie Humaine (1978), 13, 35-43.
- 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.
- NIH guide to puberty and adolescence
- Teen Puberty
- Growing Up Sexually: A World Atlas
- Pictures and detailed information about breast development during puberty
- 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.
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