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Puberty refers to the process of physical changes and accelerated sexual development by which a child's body becomes an adult body capable of reproduction. Pubescence is the process of first reaching puberty and a pubescent is one in the early stages of the process.
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.
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, 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) refer to the bodily changes of sexual maturation rather than the psychosocial and cultural aspects of adolescent development.
The physical changes of puberty 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. 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 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.
I LOVE VAGINAS!!!!!!
Menstruation and fertility
The first menstrual bleeding is referred to as menarche. The average age of menarche 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.
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 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.
The physical changes of puberty 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 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).
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 Tanner 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.
Pubic hair in boys
Pubic hair often appears in 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 Tanner 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.
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 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, 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.
- Main article: Puberum dysphonia
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, probably 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.
Variations of normal puberty
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 limitationns 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 popultion. 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.
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.
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).
Table 1: Ages of attainment of pubertal stages of American girls
3rd %ile 50th %ile 97th %ile B2 8y 10m 10y 11m 13y 0m B3 9y 10m 11y 11m 14y 0m B4 10y 6m 12y 11m 15y 5m PH2 9y 0m 11y 3m 13y 6m PH3 9y 8m 11y 11m 14y 3m PH4 10y 5m 12y 7m 14y 11m 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 white and African-American girls at some stages (Table 2).
Table 2: Recent survey on American girls by race
White girls 3rd %ile 50th %ile 97th %ile 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 12y 7m 14y 9m PH5 12y 5m 14y 7m 16y 8m Menarche 10y 6m 12y 10m 15y 3m Peak height velocity 10y 12y 2m 14y African-American 3rd %ile 50th %ile 97th %ile 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
Table 3: Ages of attaining stages of puberty for American boys
3rd % 50th % 97th% PH2 9y 11m 12y 0m 14y 1m PH3 11y3m 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 Testicular size 4 cc or 2.5 cm 9y 6m 11y 6m 13y 6m 6 cc or 3 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 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.
Puberty as a neurohormonal process
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.
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.
Historical shift in the onset of puberty
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 and 17.5 for boys. 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.
Puberty as a problem
- See Precocious puberty
- See Delayed puberty
- See Menarche, gonadarche, pubarche, thelarche, adrenarche.
- 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, 35–43.
- Brooks-Gunn, J. and Petersen, A. (eds) (1983) Girls at Puberty: Biological and Psycho-social Perspectives, New York: Plenum Press.
- Brooks-Gunn, J. and Warren, M. (1985) The effects of delayed menarche in different contexts: dance and nondance students, Journal of Youth and Adolescence 11: 121-33.
- 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.
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