Jump to content

Puberty

From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by 76.85.144.126 (talk) at 00:13, 30 August 2008 (→‎Male musculature and body shape: Removed vandalism.). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

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

1 Follicle-stimulating hormone - FSH
2 Luteinizing hormone - LH
3 Progesterone
4 Estrogen
5 Hypothalamus
6 Pituitary gland
7 Ovary
8 Pregnancy - hCG (Human chorionic gonadotropin)
9 Testosterone
10 Testicle
11 Incentives
12 Prolactin - PRL

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.[1] 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.[2] Estradiol levels rise earlier and reach higher levels in women than in men.

In males, 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 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,[3] a direct result of the later rise and lower adult male levels of estradiol.

Puberty onset

Onset is associated with high GnRH pulsing, which precedes the rise in sex hormones, LH and FSH[4]. Exogenous GnRH pulses cause the onset of puberty.[5] Brain tumors which increase GnRH output may also lead to premature puberty.[6]

The cause of this GnRH rise is contentious. Puberty begins consistently at around 47 kg for girls and 55 kg for boys. This dependence on bodyweight makes leptin a good candidate for causing GnRH rise. It is known that leptin has receptors in the hypothalamus[7] which synthesises GnRH. Furthermore, individuals who are deficient in the leptin pathway fail to initiate puberty[8]. The levels of leptin change in line with the onset of puberty, and then decline to adult levels.

Physical changes in males

Testicular size, function, and fertility

In boys, testicular enlargement is the first physical manifestation of puberty (and is termed gonadarche).[9] 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.[10] While 18-20 cc is reportedly an average adult size, there is wide variation in the normal population.[11]

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

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

Facial hair of a male that has been shaved

In the months and years following the appearance of pubic hair, other areas of skin which respond to androgens develop heavier hair (androgenic hair) in roughly the following sequence: underarm (axillary) hair, perianal hair, upper lip hair, sideburn (preauricular) hair, periareolar hair, and the rest of the beard area. Arm, leg, chest, abdominal, and back hair become heavier more gradually. There is a large range in amount of body hair among adult men, and significant differences in timing and quantity of hair growth among different ethnic groups.

Voice change

Under the influence of androgens, the voice box, or larynx, grows in both genders. This growth is far more prominent in boys, causing the male voice to drop 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 [citation needed]. 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.


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.

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 or diminished by antibacterial face washes and other compounds and typically fully 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 some 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 it is causing a lot of stress or anxiety in the boy.

Physical changes in females

Breast development

The first physical sign of puberty in females 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.[12] 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.[13]

Pubic hair

Pubic hair is often the second unequivocal change of puberty noticed, usually within a few months of thelarche.[14] 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.[13] 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.[14]

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).[15] Whitish secretions (physiologic leukorrhea) are a normal effect of estrogen as well.[12] In the next 2 years following thelarche, the uterus and ovaries increase in size, and follicles in the ovaries reach larger sizes.[16] The ovaries usually contain small follicular cysts visible by ultrasound.[17][18]

Menstruation and fertility

The first menstrual bleeding is referred to as menarche, and typically occurs about 2 years after thelarche.[14] The average age of menarche in American girls is about 11.75 years.[14] Menses (menstrual periods) are not always regular and monthly in the first 2 years after menarche.[19] Ovulation is necessary for fertility, but may or may not accompany the earliest menses.[20] In postmenarchal girls, about 80% of the cycles were anovulatory in the first year after menarche (about 13 years), 50% in the third (about 15 years) and 10% in the sixth year (about 18 years).[19] 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.[21] The word nubility is used commonly in the social sciences to designate achievement of fertility.

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).[13][22] 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%.[23]

Body odour, 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.[24]

Variations

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.[25].

Ethnic/racial differences have been recognized for centuries. For example, the average age of menarche in various populations surveyed in the last several decades has ranged from 12.0 to 18.5 years. The earliest mean is reported for African-American girls and the oldest for high altitude subsistence populations in Asia. However, it is clear that much of the higher age averages reflect nutritional limitations more than genetic differences and can change within a few generations with a substantial change in diet. The median age of menarche for a population may be an index of the proportion of undernourished girls in the population, and the width of the spread may reflect unevenness of wealth and food distribution in a population.

Genetic influence

Various studies have found direct genetic effects to account for at least 46% of the variation of timing of puberty in well-nourished populations.[26][27][28][29] The genetic association of timing is strongest between mothers and daughters. The specific genes affecting timing are not defined yet.[26] Among the candidates is an androgen receptor gene.[30]

Environmental factors

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

Nutritional factors are the strongest and most obvious environmental factors affecting timing of puberty.[26] 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 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.

Obesity influence

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. [31] Early puberty in girls can be a harbinger of later health problems. [32]

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.

Physical illness

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.

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.[33]

Stress and social factors

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.

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

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 American girls and ~ 18 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[clarification needed] typically represents maximal gonadal growth and attainment of adult hormone levels.

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:

  1. The brain's hypothalamus begins to release pulses of GnRH.
  2. Cells in the anterior pituitary respond by secreting LH and FSH into the circulation.
  3. The ovaries or testes respond to the rising amounts of LH and FSH by growing and beginning to produce estradiol and testosterone.
  4. Rising levels of estradiol and testosterone produce the body changes of female and male puberty.

The onset of this neurohormonal process may precede the first visible body changes by 1-2 years.

Components of the endocrine reproductive system

The arcuate nucleus of the hypothalamus is the driver of the reproductive system. It has neurons which generate and release pulses of GnRH into the portal venous system of the pituitary gland. The arcuate nucleus is affected and controlled by neuronal input from other areas of the brain and hormonal input from the gonads, adipose tissue and a variety of other systems.

The pituitary gland responds to the pulsed GnRH signals by releasing LH and FSH into the blood of the general circulation, also in a pulsatile pattern.

The gonads (testes and ovaries) respond to rising levels of LH and FSH by producing the steroid sex hormones, testosterone and estradiol.

The adrenal glands are a second source for steroid hormones. Adrenal maturation, termed adrenarche, typically precedes gonadarche in mid-childhood.

Major hormones

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" 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 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).

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.

Historical shift

The age at which puberty occurs has dropped significantly since the 1840s.[34][35][36] 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 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.

See also

References

  • Gordon, Catharine M. (2005). "Chapter 4: Physiology of puberty". In Emans SJH, Goldstein DP, Laufer, MR, eds. (ed.). Pediatric and Adolescent Gynecology (5th ed. ed.). Philadelphia: Lippincott, Williams & Wilkins. pp. pp. 120–155. ISBN 0781744938. {{cite book}}: |edition= has extra text (help); |editor= has generic name (help); |pages= has extra text (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: multiple names: editors list (link)
  • Gungor, Neslihan (2002). "Chapter 21: Nutritional disorders: integration of energy metabolism and its disorders in childhood". In Sperling, MA ed. (ed.). Pediatric Endocrinology (2nd ed. ed.). Philadelphia: Saunders. pp. pp. 689–724. ISBN 0721695396. {{cite book}}: |edition= has extra text (help); |editor= has generic name (help); |pages= has extra text (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  • Marshall, William A. (1986). "Chapter 8: Puberty". In Falkner F, Tanner JM, eds. (ed.). Human Growth: A Comprehensive Treatise (2nd ed. ed.). New York: Plenum Press. pp. pp. 171–209. ISBN 0-306-41952-1. {{cite book}}: |edition= has extra text (help); |editor= has generic name (help); |pages= has extra text (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: multiple names: editors list (link)
  • Rosenfield, Robert L. (2002). "Chapter 16: Female puberty and its disorders". In Sperling, MA ed. (ed.). Pediatric Endocrinology (2nd ed. ed.). Philadelphia: Saunders. pp. pp. 455–518. ISBN 0721695396. {{cite book}}: |edition= has extra text (help); |editor= has generic name (help); |pages= has extra text (help)
  • Styne, Dennis M. (2002). "Chapter 18: The testes: disorders of sexual differentiation and puberty in the male". In Sperling, MA ed. (ed.). Pediatric Endocrinology (2nd ed. ed.). Philadelphia: Saunders. pp. pp. 565–628. ISBN 0721695396. {{cite book}}: |edition= has extra text (help); |editor= has generic name (help); |pages= has extra text (help)
  1. ^ Marshall (1986), p. 176–7
  2. ^ 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.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ Abbassi V (1998). "Growth and normal puberty". Pediatrics. 102 (2 Pt 3): 507–11. PMID 9685454.
  4. ^ Plant TM (2001). "Leptin, growth hormone, and the onset of primate puberty". J. Clin. Endocrinol. Metab. 86 (1): 458–60. PMID 11232044. {{cite journal}}: Unknown parameter |month= ignored (help)
  5. ^ Essential Reproduction, M Johnson, Blackwell Publishers, 6Rev Ed edition (29 Jun 2007)
  6. ^ Precocious Puberty, MERCK, http://www.merck.com/mmpe/sec19/ch282/ch282h.html, May 16th 08
  7. ^ Meister B, Håkansson ML (2001). "Leptin receptors in hypothalamus and circumventricular organs". Clin. Exp. Pharmacol. Physiol. 28 (7): 610–7. doi:10.1046/j.1440-1681.2001.03493.x. PMID 11458889. {{cite journal}}: Unknown parameter |month= ignored (help)
  8. ^ Clayton PE, Trueman JA (2000). "Leptin and puberty". Arch. Dis. Child. 83 (1): 1–4. PMC 1718397. PMID 10868988. {{cite journal}}: Unknown parameter |month= ignored (help)
  9. ^ Styne (2002), p. 598
  10. ^ Jones, Kenneth W. (2006). Smith's Recognizable Patterns of Human Malformation. St. Louis, Mo: Elsevier Saunders. ISBN 0-7216-0615-6.
  11. ^ Marshall (1986), p. 180
  12. ^ a b Marshall (1986), p. 187
  13. ^ a b c Marshall (1986), p. 188
  14. ^ a b c d 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.
  15. ^ Gordon (2005), p. 151
  16. ^ Marshall (1986), p. 186–7
  17. ^ Rosenfield (2002), p. 462
  18. ^ Siegel MJ, Surratt JT (1992). "Pediatric gynecologic imaging". Obstet. Gynecol. Clin. North Am. 19 (1): 103–27. PMID 1584537.
  19. ^ a b Apter D (1980). "Serum steroids and pituitary hormones in female puberty: a partly longitudinal study". Clin. Endocrinol. (Oxf). 12 (2): 107–20. doi:10.1111/j.1365-2265.1980.tb02125.x. PMID 6249519.
  20. ^ Marshall (1986), p. 196-7
  21. ^ Southam AL, Richart RM (1966). "The prognosis for adolescents with menstrual abnormalities". Am. J. Obstet. Gynecol. 94 (5): 637–45. PMID 5906589.
  22. ^ Hips widen during female puberty coulmbia.edu
  23. ^ Gungor (2002), p. 699-700
  24. ^ Rosenfield (2002), p. ?
  25. ^ AJ Giannini, AE Slaby A speculation on oranges,puberty, marriage contracts and frozen food. M.D. 25(5):51-52, 1981
  26. ^ a b c 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
  27. ^ Mustanski BS, Viken RJ, Kaprio J, Pulkkinen L, Rose RJ (2004). "Genetic and environmental influences on pubertal development: longitudinal data from Finnish twins at ages 11 and 14". Dev Psychol. 40 (6): 1188–98. doi:10.1037/0012-1649.40.6.1188. PMID 15535766. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  28. ^ Treloar SA, Martin NG (1990). "Age at menarche as a fitness trait: nonadditive genetic variance detected in a large twin sample". Am. J. Hum. Genet. 47 (1): 137–48. PMC 1683767. PMID 2349942. {{cite journal}}: Unknown parameter |month= ignored (help)
  29. ^ Kaprio J, Rimpelä A, Winter T, Viken RJ, Rimpelä M, Rose RJ (1995). "Common genetic influences on BMI and age at menarche". Hum. Biol. 67 (5): 739–53. PMID 8543288. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  30. ^ Comings DE, Muhleman D, Johnson JP, MacMurray JP (2002). "Parent-daughter transmission of the androgen receptor gene as an explanation of the effect of father absence on age of menarche". Child Dev. 73 (4): 1046–51. doi:10.1111/1467-8624.00456. PMID 12146732.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  31. ^ Phil McKenna, "Childhood obesity brings early puberty for girls" "New Scientist" March 5, 2007 http://www.newscientist.com/article/dn11307-childhood-obesity-brings-early-puberty-for-girls.html
  32. ^ Molly, M. Ginty, "US Girls' Early Puberty Attracts Research Flurry" "Women's eNews" http://www.womensenews.org/article.cfm/dyn/aid/3113
  33. ^ Are Bisphenol A (BPA) Plastic Products Safe for Infants and Children?
  34. ^ Finley, Harry. "Average age at menarche in various cultures". Museum of Menstruation and Women's Health. Retrieved 2007-08-02. {{cite news}}: Cite has empty unknown parameter: |coauthors= (help)
  35. ^ Whincup, P H (2001-05-05). "Age of menarche in contemporary British teenagers: survey of girls born between 1982 and 1986". BMJ. 322: 1095–1096. doi:10.1136/bmj.322.7294.1095. PMID 11337438. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  36. ^ "Girls maturing slightly earlier". BBC News. 2001-05-03. Retrieved 2007-08-02. {{cite news}}: Cite has empty unknown parameter: |coauthors= (help)

Further reading

  • 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. (1997). "Secondary sexual characteristics and menses in young girls seen in office practice: a study from the Pediatric Research in Office Settings network". Pediatrics. 99 (4): 505–12. doi:10.1542/peds.99.4.505. PMID 9093289. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) 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 (1985). "Clinical longitudinal standards for height and height velocity for North American children". J. Pediatr. 107 (3): 317–29. PMID 3875704. {{cite journal}}: Unknown parameter |month= ignored (help) Highly useful growth charts with integrated standards for stages of puberty.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Puberty&oldid=235092451"