In humans, puberty is 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 (derived from the Latin word puberatum (age of maturity, manhood)) 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.
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, girls typically begin the process of puberty at age 10, boys at age 12. Girls usually complete puberty by ages 15-17, while boys usually complete puberty by ages 17 or 18. Any increase in height beyond these ages is uncommon. Girls attain 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.
In males, testosterone, an androgen, is the principal sex hormone. 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 on average 2 cm shorter 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.
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.
The onset of puberty is associated with high GnRH pulsing, which precedes the rise in sex hormones, LH and FSH. Exogenous GnRH pulses cause the onset of puberty. Brain tumors which increase GnRH output may also lead to premature puberty
The cause of the GnRH rise is unknown. Leptin might be the cause of the GnRH rise. Leptin has receptors in the hypothalamus which synthesizes GnRH. Individuals who are deficient in leptin fail to initiate puberty. The levels of leptin increase with the onset of puberty, and then decline to adult levels when puberty is completed. The rise in GnRH might also be caused by genetics. A study discovered that a mutation in genes encoding both Neurokinin B as well as the Neurokinin B receptor can alter the timing of puberty. The researchers hypothesized that Neurokinin B might play a role in regulating the secretion of Kisspeptin, a compound responsible for triggering direct release of GnRH as well as indirect release of LH and FSH.
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 cm in length and about 1.5–2 cm in width. Testicular size continues to increase throughout puberty, reaching maximal adult size about 6 years after the onset of puberty. After the boy's testicles have enlarged and developed for about one year, the length and then the breadth of the shaft of the penis will increase and the glans penis and corpora cavernosa will also start to enlarge to adult proportions. While 18–20 cc is an average adult size, there is wide variation in testicular size in the normal population
The testes have two primary functions: to produce hormones and to produce sperm. The Leydig cells produce testosterone, which in turn produces most of the male pubertal changes. Most of the increasing bulk of testicular tissue is spermatogenic tissue (primarily Sertoli and Leydig cells). Sperm can be detected in the morning urine of most boys after the first year of pubertal changes, and occasionally earlier. On average, potential fertility in boys is reached at 13 years old, but full fertility will not be gained until 14–16 years of age.
Pubic hair often appears on a boy shortly after the genitalia begin to grow. In girls, the first appearance of pubic hair is termed pubarche. 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 many 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.
In the months and years following the appearance of pubic hair, other areas of skin that respond to androgens may develop androgenic hair. The usual sequence is: underarm (axillary) hair, perianal hair, upper lip hair, sideburn (preauricular) hair, periareolar hair, and the beard area. As with most human biological processes, this specific order may vary among some individuals. 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. Facial hair is often present in late adolescence, but may not appear until significantly later. Facial hair will continue to get coarser, darker and thicker for another 2–4 years after puberty. Some men do not develop full facial hair for up to 10 years after the completion of puberty. Chest hair may appear during puberty or years after. Not all men have chest hair.
Under the influence of androgens, the voice box, or larynx, grows in both sexes. 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. Before puberty, the larynx of boys and girls is about equally small. 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 15 years. It usually precedes the development of significant facial hair by several months to years.
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.
Often, the fat pads of the male breast tissue and the male nipples will develop during puberty; sometimes, especially in one breast, this becomes more apparent and is termed gynecomastia. It is usually not a permanent phenomenon.
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 not be prevented or diminished easily, but it typically fully diminishes at the end of puberty. However, it is not unusual for a fully grown adult to suffer the occasional bout of acne, though it is normally less severe than in adolescents. Some may desire using prescription topical creams or ointments to keep acne from getting worse, or even oral medication, due to the fact that acne is emotionally difficult and can cause scarring.
The first physical sign of puberty in girls is usually a firm, tender lump under the center of the areola 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 noticeable change in puberty, usually within a few months of thelarche. It is referred to as pubarche. 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.
The mucosal surface of the vagina also changes in response to increasing levels of estrogen, becoming thicker and 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 two years following thelarche, the uterus, ovaries, and the follicles in the ovaries increase in size. The ovaries usually contain small follicular cysts visible by ultrasound.
The first menstrual bleeding is referred to as menarche, and typically occurs about two years after thelarche. The average age of menarche in girls is 11.75 years. The time between menstrual periods (menses) is not always regular in the first two 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 year and 10% in the sixth year. Initiation of ovulation after menarche is not inevitable. A high proportion of girls with continued irregularity in the menstrual cycle several years from menarche will continue to have prolonged irregularity and anovulation, and are at higher risk for reduced fertility. Nubility is used to designate achievement of fertility.
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. On average, at 10 years, girls have 6% more body fat than boys.
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 one or more years. Another androgen effect is increased secretion of oil (sebum) from the skin. This change increases the susceptibility to acne, a skin condition that is characteristic of puberty. Acne varies greatly in its severity.
The definition of the onset of puberty depends on perspective (e.g., hormonal versus physical) and purpose (establishing population normal standards, clinical care of early or late pubescent individuals, etc.) The most commonly used definition of the onset of puberty is physical changes to a person's body. These physical changes are the first visible signs of neural, hormonal, and gonadal function changes.
The age at which puberty begins varies between individuals and populations. The age at which puberty begins is affected by both genetic factors and by environmental factors such as nutritional state and social circumstances. An example of social circumstances is the Vandenbergh effect; a juvenile female who has significant interaction with adult males will enter puberty earlier than juvenile females who are not socially overexposed to adult males.
The average age at which puberty begins is affected by race. For example, the average age of menarche in various populations surveyed has ranged from 12 to 18 years. The earliest average onset of puberty is for African-American girls and the latest average onset for high altitude subsistence populations in Asia. However, 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.
Researchers have identified an earlier age of the onset of puberty. However, they have based their conclusions on a comparison of data from 1999 with data from 1969. In the earlier example, the sample population was based on a small sample of white girls (200, from Britain). The later study identified as puberty as occurring in 48% of African-American girls by age nine, and 12% of white girls by that age.
The average age at which the onset of puberty occurs has dropped significantly since the 1840s. Researchers refer to this drop as the 'secular trend'. In every decade from 1840 to 1950 there was a drop of four months in the average age of menarche among Western European females. In Norway, girls born in 1840 had their menarche at an average age of 17 years. In France the average in 1840 was 15.3 years. In England the average in 1840 was 16.5 years. 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.
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 yet known. Among the candidates is an androgen receptor gene.
Researchers have hypothesized that early puberty onset may be caused by certain hair care products containing estrogen or placenta, and by certain chemicals, namely phthalates, which are used in many cosmetics, toys, and plastic food containers.
If genetic factors account for half of the variation of pubertal timing, environment factors are clearly important as well. One of the first 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.
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.
Bisphenol A (BPA) is a chemical used to make plastics, and is frequently used to make baby bottles, water bottles, sports equipment, medical devices, and as a coating in food and beverage cans. Scientists are concerned about BPA's behavioral effects on fetuses, infants, and children at current exposure levels because it can effect the prostate gland, mammary gland, and lead to early puberty in girls. BPA mimics and interferes with the action of estrogen-an important reproduction and development regulator. It leaches out of plastic into liquids and foods, and the Centers for Disease Control and Prevention (CDC) found measurable amounts of BPA in the bodies of more than 90 percent of the U.S. population studied. The highest estimated daily intakes of BPA occur in infants and children. Many plastic baby bottles contain BPA, and BPA is more likely to leach out of plastic when its temperature is increased, as when one warms a baby bottle or warms up food in the microwave.
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 obesity 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 dietary fiber intakes, as occur with typical vegetarian diets, are associated with later onset and slower progression of female puberty.
Scientific researchers have linked early obesity with a drop of puberty onset in girls. They have cited obesity as a cause of breast development before nine years and menarche before twelve years. Early puberty in girls can be a harbinger of later health problems.
The average level of daily physical activity has also been shown to affect timing of puberty, especially in females. 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 and cholesterol.
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.
Mental illnesses occur in puberty. The brain undergoes significant development by hormones which can contribute to mood disorders such as Major depressive disorder, bipolar disorder, dysthymia and schizophrenia. Girls aged between 15 and 19 make up 40% of anorexia nervosa cases.
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.
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 15 years for an average girl and 18 years for an average boy. Potential fertility (sometimes termed nubility) usually precedes completion of growth by 1–2 years in girls and 3–4 years in boys. Stage 5 typically represents maximal gonadal growth and 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 onset of this neurohormonal process may precede the first visible body changes by 1–2 years.
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 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. The period of hormonal activity until several months after birth, followed by suppression of activity, may correspond to the period of infant sexuality, followed by a latency stage, which Sigmund Freud described.
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. An American physiologist, Ernst Knobil, found that the GnRH signals from the hypothalamus induce pulsed secretion of LH (and to a lesser degree, FSH) at roughly 1-2 hour intervals. The LH pulses are the consequence of pulsatile GnRH secretion by the arcuate nucleus that, in turn, is the result of an oscillator or signal generator in the central nervous system ("GnRH pulse generator"). In the years preceding physical puberty, Robert M. Boyar discovered that the gonadotropin pulses occur only during sleep, but as puberty progresses 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.
Some investigators have attributed the onset of puberty to a resonance of oscillators in the brain. By this mechanism, the gonadotropin pulses that occur primarily at night just before puberty represent beats.
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.
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 dihydrotestosterone in target organs (especially that of the bowels).
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.
Redirecting to Puberty