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Puberty is the process of physical changes through which a child's Human body matures into an adult body capable of sexual reproduction. It is initiated by hormone signals from the Human brain to the : the ovary in a female, the in a male. In response to the signals, the gonads produce hormones that stimulate libido and the growth, function, and transformation of the brain, , muscle, blood, Human skin, hair, , and . Physical growth—height and weight—accelerates in the first half of puberty and is completed when an adult body has been developed. Before puberty, the external sex organs, known as primary sexual characteristics, are sex characteristics that distinguish males and females. Puberty leads to sexual dimorphism through the development of the secondary sex characteristics, which further distinguish the sexes.
On average, females begin puberty at age 10½ and complete puberty at ages 15-17; males begin at ages 11½-12 and complete puberty at ages 16-17. The major landmark of puberty for females is menarche, the onset of menstruation, which occurs on average around age 12½. For males, first ejaculation, spermarche, occurs on average at age 13. In the 21st century, the average age at which children, especially females, reach specific markers of puberty is lower compared to the 19th century, when it was 15 for females and 17 for males (with age at first periods for females and voice-breaks for males being used as examples). This can be due to any number of factors, including improved nutrition resulting in rapid body growth, increased weight and fat deposition, or exposure to endocrine disruptors such as , which can at times be due to food consumption or other environmental factors. However, more modern archeological research suggests that the rate of puberty as it occurs now is the intended way. Growth spurts began at around 10-12, but markers of later stages of puberty such as menarche had delays that correlated with severe environmental conditions such as poverty, poor nutrition, and air pollution. Puberty that starts earlier than usual is known as precocious puberty, and puberty which starts later than usual is known as delayed puberty.
Notable among the morphologic changes in size, shape, composition, and functioning of the pubertal body, is the development of secondary sex characteristics, the "filling in" of the child's body; from girl to woman, from boy to man. Derived from the Latin puberatum (age of maturity), the word puberty describes the physical changes to sexual maturation, not the psychosocial and cultural maturation denoted by the term adolescent development in Western culture, wherein adolescence is the period of mental transition from childhood to , which overlaps much of the body's period of puberty. The Oxford Dictionary of English Etymology, C. T. Onions ed. Oxford University Press, 1996, p. 720.
Two of the most significant differences between puberty in females and puberty in males are the age at which it begins, and the major involved, the and the .
Although there is a wide range of normal ages, females typically begin the process of puberty around age 10½; males at ages 11½—12. Puberty generally ends between 15—17 for females and 16–17 for males. Females attain reproductive maturity about four years after the first physical changes of puberty appear. In contrast, males accelerate more slowly but continue to grow for about six years after the first visible pubertal changes.Garn, SM. Physical growth and development. In: Friedman SB, Fisher M, Schonberg SK., editors. Comprehensive Adolescent Health Care. St Louis: Quality Medical Publishing; 1992. Retrieved on 2009-02-20
For males, the androgen testosterone is the principal sex hormone; while testosterone is produced, all males' changes are characterized as virilization. A substantial product of testosterone metabolism in males is the estrogen estradiol. The conversion of testosterone to estradiol depends on the amount of body fat and estradiol levels in males are typically much lower than in females. The male "growth spurt" also begins later, accelerates more slowly, and lasts longer before the epiphyses fuse. Although males are on average shorter than females before puberty begins, adult men are on average about 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 hormonal maturation of females is considerably more complicated than in males. The main , testosterone, estradiol, and progesterone as well as prolactin play important physiological functions in puberty. The production of Sex hormone in females starts with production of testosterone, which is typically quickly converted to estradiol inside the ovaries. However the rate of conversion from testosterone to estradiol (driven by FSH/LH balance) during early puberty is highly individual, resulting in very diverse development patterns of secondary sexual characteristics. Production of progesterone in the ovaries begins with the development of ovulatory cycles in females (during the lutheal phase of the cycle), before puberty low levels of progesterone are produced in the adrenal glands of both males and females. Estradiol levels rise earlier and reach higher levels in women than in men. While estradiol promotes growth of the breasts and uterus, it is also the principal hormone driving the pubertal growth spurt and epiphyseal maturation and closure.
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.
Furthermore, as physical and emotional differences set them apart from people in their same age group, early-maturing females develop relationships with older people. For instance, some early-maturing females have older malefriends, "attracted to the females' womanly physique and femaleish innocence." While having an older malefriend might improve popularity among peers, it also increases the risk of alcohol and drug use, increased sexual relations (often unprotected), eating disorders and bullying.
Generally, later onset of puberty in females produces positive outcomes. They exhibit positive behaviors in adolescence that continue to adulthood.
Early-maturing males develop "more aggressive, law-breaking, and alcohol abusing" behaviors, which result in anger towards parents and trouble in school and with the police. Early puberty also correlates with increased sexual activity and a higher instance of teenage pregnancy, both of which can lead to depression and other psychosocial issues.
On the other hand, late-maturing males develop lower self-esteem and confidence and generally have lower popularity among peers, due to their less-developed physiques. Also, they experience problems with anxiety and depression and are more likely to be afraid of sex than other males.
Research by Øster (1968) found that with the onset and continuation of puberty, the proportion of males able to pull back their foreskins increased. At ages 12–13, Øster found that only 60% of males were able to retract their foreskins; this increased to 85% by ages 14–15, and 95% by 16–17. He also found that 1% of those unable to fully retract experienced phimosis at ages 14–17, the remainder were partially able to. The findings were supported by further research by Kayaba et al (1996) on a sample of over 600 males, and Ishikawa and Kawakita (2004) found that by age 15, 77% of their sample of males could retract their foreskins. Beaugé (1997) reports that males may assist the development of retractile foreskin by manual stretching.
Once a male is able to retract his foreskin, penile hygiene should become an important feature of his routine body care. Although the American Academy of Pediatrics states there is "little evidence to affirm the association between circumcision status and optimal penile hygiene", various studies suggest that males be educated about the role of hygiene, including retracting the foreskin while urinating and rinsing under it and around the glans at each bathing opportunity. Regular washing under the foreskin was found by Krueger and Osborn (1986) to reduce the risk of numerous penile disorders, however Birley et al. (1993) reports excessive washing with soap should be avoided because it dries the oils out of the tissues and can cause non-specific dermatitis.
Changes of the vulva initiated by estradiol as well as its direct effects also appear to influence the functioning of the lower urinary tract.
The age at which puberty begins varies between individuals; usually, puberty begins between 10 and 13 years of age. 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 mouse who has significant interaction with adult male mice will enter puberty earlier than juvenile females who are not socially overexposed to adult males.
The average age at which puberty begins may be affected by ethnicity as well. 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 females 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 females 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 females (200, from Britain). The later study identified as puberty as occurring in 48% of African-American females by age nine, and 12% of white females by that age. Based on a publication from The Ribbon, a newsletter of the Cornell University Program on Breast Cancer and Environmental Risk Factors in New York States ((BCERF), Vol 6, No. 1, Winter 2001.)
One possible cause of a delay in the onset of puberty past the age 14 in females and 15 in males is Kallmann syndrome, a form of hypogonadotropic hypogonadism (HH). Kallmann syndrome is also associated with a lack of sense of smell (anosmia). Kallmann syndrome and other forms of HH affect both men and women. It is caused by a failure in HPG axis at puberty which results in low or zero gonadotropin (LH and FSH) levels with the subsequent result of a failure to commence or complete puberty, secondary hypogonadism and infertility. (2025). 9780199545131, Oxford University Press. ISBN 9780199545131
A 2006 study in Denmark found that puberty, as evidenced by breast development, started at an average age of 9 years and 10 months, a year earlier than when a similar study was done in 1991. Scientists believe the phenomenon could be linked to obesity or exposure to chemicals in the food chain, and is putting females at greater long-term risk of breast cancer.
Researchers have hypothesized that early puberty onset may be caused by certain hair care products containing estrogen or placenta, and by certain chemicals, namely , which are used in many cosmetics, toys, and plastic food containers.
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 affect the prostate gland, mammary gland, and lead to early puberty in females. 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.
The onset of this neurohormonal process may precede the first visible body changes by 1–2 years.
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 ovary) respond to rising levels of LH and FSH by producing the steroid sex steroid, testosterone and estrogen.
The are a second source for steroid hormones. Adrenal maturation, termed adrenarche, typically precedes gonadarche in mid-childhood.
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.
Hormones and steroids
There is theoretical concern, and animal evidence, that environmental hormones and may affect aspects of prenatal or postnatal sexual development in humans. (1996). 9780316875462, Little, Brown. ISBN 9780316875462
Nutritional influence
factors are the strongest and most obvious environmental factors affecting timing of puberty.
Obesity influence and exercise
Scientific researchers have linked early obesity with an earlier onset of puberty in females. They have cited obesity as a cause of breast development before nine years and menarche before twelve years. Early puberty in females can be a harbinger of later health problems.Molly, M. Ginty, "US Girls' Early Puberty Attracts Research Flurry", Women's eNews
Physical and mental illness
Mental illnesses occur in puberty. The brain undergoes significant development by which can contribute to mood disorders such as major depressive disorder, bipolar disorder, dysthymia and schizophrenia. Females aged between 15 and 19 make up 40% of anorexia nervosa cases.
Neurohormonal process
The endocrine reproductive system consists of the hypothalamus, the pituitary gland, the , and the , 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:
Components of the endocrine reproductive system
The arcuate nucleus of the hypothalamus is the driver of the reproductive system. It has 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 , adipose tissue and a variety of other systems.
Major hormones
Lay summary:
Endocrine perspective
The endocrine system becomes functional by the end of the first Pregnancy 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 . 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.
! rowspan="2" Hormone
! rowspan="2" Units
! rowspan="2" Prepubertal
Stage 1
! rowspan="2"Stage 2
! rowspan="2" Stage 3
! rowspan="2" Stage 4
! colspan="2" Stage 5 mIU/mL 2.7 (<1.0–5.5) 4.2 (<1.0–9.0) 6.7 (<1.0–14.6) 7.7 (2.8–15.0) Follicular
Luteal7.6 (3–18)
6.6 (3–18)U/L <0.1 (<0.1–0.2) 0.7 (<0.1–2.8) 2.1 (<0.1–6.8) 3.6 (0.9–8.1) Follicular
Luteal3.8 (1.6–8.1)
3.5 (1.5–8.0) mIU/mL 4.0 (<1–5) 4.6 (<1.0–7.2) 6.8 (3.3–10.5) 7.4 (3.3–10.5) Follicular
Luteal10.3 (6–15)
6.0 (3.4–8.6)U/L 2.1 (<0.5–5.4) 3.5 (<0.5–6.6) 4.9 (0.7–9.0) 6.2 (1.1–11.3) Follicular
Luteal6.6 (1.9–10.8)
5.4 (1.8–10.5)Estradiol pg/mL 9 (<9–20) 15 (<9–30) 27 (<9–60) 55 (16–85) Follicular
Luteal50 (30–100)
130 (70–300)Estrone pg/mL 13 (<9–23) 18 (10–37) 26 (17–58) 36 (23–69) Follicular
Luteal44 (30–89)
75 (39–160)Progesterone ng/dL 22 (<10–32) 30 (10–51) 36 (10–75) 175 (<10–2500) Follicular
Luteal35 (13–75)
(200–2500)Hydroxyprogesterone ng/dL 33 (<10–84) 52 (10–98) 75 (10–185) 97 (17–235) Follicular
Luteal48 (12–90)
178 (35–290) μg/dL 49a (20–95)
106b (40–200)129 (60–240) 155 (85–290) 195 (106–320) – 220 (118–320) ng/dL 35a (<10–70)
127b (72–180)297 (150–540) 328 (190–620) 394 (240–768) – 538 (215–855) Androstenedione ng/dL 26 (<10–50) 77 (40–112) 126 (55–190) 147 (70–245) – 172 (74–284) Testosterone ng/dL 10 (<10–22) 18 (<10–29) 26 (<10–40) 38 (24–62) – 40 (27–70) Notes: Values are mean plasma levels, with ranges in parentheses. a = Pre-adrenarche. b = Post-adrenarche. (Adrenarche, or increased adrenal androgen section, occurs as a separate event and can precede puberty onset by 1 to 2 years.) Sources:
Stages
See also
Sources
(2025). 9780781744935, Lippincott Williams & Wilkins. ISBN 9780781744935
(2025). 9780721695396, Saunders. ISBN 9780721695396
(1986). 9780306419522, Plenum Press. ISBN 9780306419522
Further reading
(1996). 9780316875462, Little, Brown. ISBN 9780316875462
External links
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