The hypothalamus, the anterior pituitary gland and the gonads of the fetus, infant and pre-pubertal children are capable of processing hormones equivalent to adult levels.
Even while still a fetus in the uterus in the middle of pregnancy, serum levels of FSH and LH hormones have reached adult levels but then decreased as pregnancy steroid hormones are reversed. inhibition. After birth, when newborns escape the mother's estrogen and progesterone negative responses, the infant's FSH and LH are temporarily higher than those of adults during normal menstrual cycles. Estradiol is also temporarily secreted at par with the adult menstrual cycle and leads to follicular proliferation and follicular atrophy.
The negative response quickly returns, the ovarian steroids and gonadotropins decrease and remain very low until 6-8 years of age. During this time, the hypothalamus-pituitary system controls the gonadotropic hormones, and the gonadostat is highly sensitive to the negative effects of estrogen. The concentration of estradiol in these years was low about ìopg / ml.
In studies of gonadal dysplasia cases and children with hypogonadism, gonadostat was found to be 6-15 times more sensitive in terms of negative feedback than adults. Thus, gonadotropin secretion is partly inhibited by exceptionally low levels of estrogen.
The decrease in gonadotropin in children is not entirely due to the sensitivity to negative feedback. Even in children with hypogonadism (with genital dystrophy), FSH and LH at the age of 5-11 are similar to the low level of normal children of the same age. Because the Gn-RH-releasing hormone has a slight stimulation of the secretion of FSH and LH in subjects without this gonad. A nonsteroidal inhibition center for Gn-RH and gonadotropins has been shown to be effective.
Although peptide hormone levels are low during childhood and pre-puberty, the secretion of FSH and LH remains paced. It has been reported that the gonadotropin hormones of the pituitary gland, while acting at very low levels, also have responses to the exogenous Gn-RH, albeit at lower concentrations than during puberty, but also has the ability to stimulate the unripe gonads to secrete tiny amounts of steroids.
As puberty approaches, there are three critical changes in homeostatic endocrine function. That is:
Increases adrenocortical activity.
Reduced inhibition of gonadostat.
Increasing the interaction between peptides with each other and between peptides and ste-roid leads to increased pituitary activity.
Increases adrenocortical activity
Pubic and underarm hair growth is caused by increased secretion of the adrenal cortex male hormones (androgens) during puberty. This stage of puberty is called adrenocortical hyperactivity or pubic hair growth. There are also times when pubic hairs grow early, meaning that there is no other sign of sexual development. Early breast development is rare, but can still occur before other genital manifestations.
Increased adrenal hyperactivity is indicated by an increase in circulating DHA (dehydroepiandrosteron), DHAS (dehydroepiandrosteron sulíat) and androstenedion accompanied by an increased 17a-hydroxylase and 17-20-lyase activity (450cl7 enzyme) in the infant. Children 6-7 years old to adulthood (13-15 years old). This steroid secretion is accompanied by an increase in stimulation and increased internal differentiation (reticulum) of the adrenal cortex.
Usually an increase in adrenal cortex activity begins 2 years before there is a spike in body contour, before the increase in estrogen and gonadotropin hormones of puberty and the first mid-puberty period. Because of such a time relation, the secretory activity of adrenal androgens has been regarded as an initiating event of the ontogeny during the course of puberty.
Although it seems obvious, there are also mismatches between the mechanisms of increased adrenal cortical activity and Gn-RH-pituitary-ovarian (gonadarche) ripening. Increased early adrenal cortex (early appearance of pubic hair and axillary hair before age 8) is not associated with early development of genital abnormalities. In the case of an increase in gonadotropin due to hypogonadism (gonadal dysplasia) or in the case of a hypogonadism of Kalmann's syndrome, there is an increase in adrenal cortical activity without an increase. sexual activity. When there was no increase in adrenocortical activity as in the case of cortisol-treated children with Addison's disease (adrenocortical insufficiency), there was an increase in sexual activity. Finally, in early puberty before age 6,
Androgen levels of the adrenal cortex were also not associated with changes in cortisol and ACTH levels in the fetus, puberty, and in old age. In addition, in cases such as chronic illness, surgical stress, recovery from adrenal insufficiency and anorexia nervosa, ACTH-stimulated cortisol secretion changes do not follow changes in andro- levels. genes in plasma. Thereby, the increased adrenocortical activity does not appear to be directly controlled by gonadotropic hormones or ACTH. An element of the pituitary that stimulates adrenocortical androgen secretion produced by a high molecular mass precursor. It is proopiomelanocortin (POMC), which also contains ACTH and beta-lipotropin, acting on ACTH that is formed and maintaining adrenal cortical activity. This substance has been considered to increase the activity of the adrenal cortex. However, in one study, the androgen-cortisol mismatch was found in the plasma of children and adults with Cushing's disease and ACTH birthplace tumors. It was seen that the proopiomelanocortin-related peptides including ACTH, beta-liptropin did not play a decisive role in initiating adrenocortical action. Studies have not demonstrated an association between melatonin secretion and increased adrenarche (adrenarche) activity. It can be said that the factors that inhibit the adrenocortical hyperactivity are still unknown. However, in one study, the androgen-cortisol mismatch was found in the plasma of children and adults with Cushing's disease and ACTH birthplace tumors. It was seen that the proopiomelanocortin-related peptides including ACTH, beta-liptropin did not play a decisive role in initiating adrenocortical action. Studies have not demonstrated an association between melatonin secretion and increased adrenarche (adrenarche) activity. It can be said that the factors that inhibit the adrenocortical hyperactivity are still unknown. However, in one study, the androgen-cortisol mismatch was found in the plasma of children and adults with Cushing's disease and ACTH birthplace tumors. It was seen that the proopiomelanocortin-related peptides including ACTH, beta-liptropin did not play a decisive role in initiating adrenocortical action. Studies have not demonstrated an association between melatonin secretion and increased adrenarche (adrenarche) activity. It can be said that the factors that inhibit the adrenocortical hyperactivity are still unknown. Studies have not demonstrated an association between melatonin secretion and increased adrenarche (adrenarche) activity. It can be said that the factors that inhibit the adrenocortical hyperactivity are still unknown. Studies have not demonstrated an association between melatonin secretion and increased adrenarche (adrenarche) activity. It can be said that the factors that inhibit the adrenocortical hyperactivity are still unknown.
The braking of "gonadostat"
Not associated with increased adrenal cortex activity. Is one of the factors that cause increased gonadal activity (gonadarche).
At the end of pre-puberty, there is a decrease in the inhibition of the pituitary-nervous system to the gonads, which increases the anterior pituitary response to Gn-RH. The pituitary gland becomes active again, the follicles respond to FSH and LH.
At the age of 8, that means between children and pre-puberty, FSH and LH are inhibited so it is very low. These mechanisms of inhibition on gonadotropin secretion are due to a highly negative-sensitive feedback mechanism in the hypothalamus and pituitary gland. It is also considered that the endogenous effect on Gn-RH causes gonadotropin levels to be reduced, even in children without gonads. Patients with gonadal dystrophy showed a significant increase in the first 2-3 years of life, then gradually decreased and decreased at the lowest at 6-8 years of age. At the age of 10-11 years old again increases again into puberty. However, the gonadotropin increases one more disruption in postmenopausal age. The secretion of baseline gonadotropins in children without gonads is of the same quality as in normal women.
While negative feedback inhibition may play a more important role in the early childhood years, central endogenous inhibition has become predominant in mid-age function and maintenance. until pre-puberty.
Neurosuppression or nerve damage that deprives the source of neurosuppression has been considered to be the pathogenesis of early puberty. Due to damage to the nerve body, the lower twin region becomes pinched or the anterior lower quadrant is destroyed. So the normal onset of puberty on the gonads is due to the phenomenon of re-pointing of the gonadotropic hormones. This hormone is synthesized and secreted by a combination of two processes: decreased endogenous suppression of Gn-RH and decreased sensitivity to estrogen negative feedback.
It is also thought that the central endogenous suppressive switch is due to decreased melatonin secretion by the pineal gland. In antiperspirants affected by the optical cycle, melatonin of the pineal gland has been shown to inhibit the secretion of the hypothalamus - pituitary. While melatonin may play a role in puberty in cases of pineal adenoma and in the pathophysiology of central-cause premature puberty, there is no evidence to support an important role in the initiation of puberty. in humans. In two large studies of the nocturnal rhythms of serum melatonin in children and adolescents (1-18), nocturnal decrease in me-latonin secretion led to the sole thought of initiating puberty. from a child's age declining throughout puberty.
Intriguing research on pubertal "gonadostat" decisive factors is continuing. Peptides associated with POMC appear to be unchanged during the transition period. The individual differentiation of the Gn-RH gene as well as its expression, which has been eloquently demonstrated in rodents, needs further research on primates.
The change and expansion of reciprocal relationships between Gn-RH - gonadotropin hormone - ovarian steroid
FSH levels increase through the stages of puberty. Paced immature Rhesus monkeys Gn-RH initiate the pituitary-gonadal machinery, which supports the endogenous Gn-RH that plays a key role in puberty formation and maintenance. puberty. Similar effects have been demonstrated in pre-pubertal girls. The normal maturation of puberty in women is also accompanied by changes in the face of the gonadotropin hormone in response to the hormone releasing hormone of the hypothalamus. FSH initially responded clearly to Gn-RH but then decreased and remained constant during puberty. In contrast, LH response is low in pre-puberty and increases sharply during puberty. It is based on the common knowledge that FSH increases initially and then stays flat in the middle of puberty, while LH tends to gradually increase and reach at the end of puberty to the same extent as that of adults. The increase in the amplitude and frequency of the Gn-RH rhythms is considered to be the factor that gradually increases the regulatory response of FSI and LH. Gn-RH acts on the gonadotropin-producing cells of the anterior pituitary gland, through surface receptors specific to Gn-RH. Thus, gonadal hormone cells increase the ability to respond to Gn-RH, initially synthesizing and then excretion of gonadotropic hormones. When gonadotropin is secreted, ovarian follicles are stimulated to synthesize steroids and secreted estrogen increases. Gn-RH acts on the gonadotropin-producing cells of the anterior pituitary gland, through surface receptors specific to Gn-RH. Thus, gonadal hormone cells increase the ability to respond to Gn-RH, initially synthesizing and then excretion of gonadotropic hormones. When gonadotropin is secreted, ovarian follicles are stimulated to synthesize steroids and secreted estrogen increases. Gn-RH acts on the gonadotropin-producing cells of the anterior pituitary gland, through surface receptors specific to Gn-RH. Thus, gonadal hormone cells increase the ability to respond to Gn-RH, initially synthesizing and then excretion of gonadotropins. When gonadotropin is secreted, ovarian follicles are stimulated to synthesize steroids and secreted estrogen increases.
The double-sided mechanism of estrogen reversal on the anterior pituitary gland has been observed. It is sufficiently rationale to say that in mid-puberty, estrogen increases LH secretion, in response to Gn-RH (positive feedback), while in combination with a inhibin it maintains a relatively inhibitory effect on FSH response (negative response).
Before puberty, gonadotropic hormone levels are low but still paced. Gn-RH initially increases the pace during sleep. LH is released in both sexes because the LH is met with endogenous Gn-RH. During the early stages of puberty, FSH and LH rate increase at night, both in amplitude and frequency, but mainly in frequency.
At the end of puberty, the rates increase during the day and decrease at night. The closer to actual puberty, the clearer this day and night difference. With very sensitive test methods, one can detect increases in FSH and LH both day and night in the months before breast development begins.
LH sleep rate in children with unexplained premature puberty, in patients with anorexia nervosa in the intermediate stages between overgrowth and recovery and even patients without gonads, at age During puberty, their gonadotropins were as low as during childhood. The tempo of the Gn-RH was maintained independent of steroid feedback.
The cascade of events resulting from paced Gn-RH release, from the pre-puberty response and the negative central inhibition, the concentration of gonadotropins and steroids is increased. Since then appeared the secondary sexual properties and functions as those of the adult: menstruation for the first time and later ovulation. During the period 10-16 years old, endocrine events such as initial changes in LH rate, increase in sleep, later mainly increase in frequency, while amplitude increases less, during 24 hours of the day. High estradiol leads to first menstruation.
From mid-puberty to late puberty, a positive feedback between estradiol and LH leads to menstrual cycles with ovulation.
Although the main determinant of puberty is heredity, there are other factors that influence when puberty begins and puberty development such as location, exposure to light, and energy. general health, nutrition and psychological factor. For example, the child of early puberty families will also develop early puberty. Children near the equator, at low altitude, children in cities and those with average fat levels have puberty earlier than those in the northern latitudes, at a great height above sea level, in the countryside and at a normal weight. There is a clear relationship between the time of the first menstruation between mother and daughter, and between sisters. There is a relationship between puberty and the length of puberty, the earlier the puberty age, the longer the puberty period.
Puberty decreased in children in developed countries with good nutrition and healthy living conditions. Body weight did not appear to be as important as fat. Frisch claims the minimum weight to have a first menstrual period is 47.8kg.
It makes sense to hypothesize that the central mechanisms leading to maturity of the hypothalamus - pituitary - ovary axis and the action of this axis stimulate weight development and fat composition. of body. However, not all studies have reported a link between puberty initiation and body fat mass and the distribution of body fat. However, leptin identification revives the importance of the relationship between body fat and reproductive function.
Leptin is a peptide secreted in adipose tissue and circulating in the blood, a family of proteins, acting on central nervous neurons that regulate eating behavior and energy balance. The following comments support leptin's role in reproductive physiology:
Gives leptin, which accelerates the appearance of puberty in rodents.
Leptin levels increase in men during puberty.
Low leptin levels in athletes, patients with anorexia or delayed puberty.
Female mice lacking leptin are still genitalized but remain in pre-puberty and never ovulate. But when leptin is given, it is fertile.
In children, leptin increases until puberty begins. This leads to the thought of having leptin that leads to the onset of puberty. The higher the concentration of Leptin, the earlier menstruation begins to men. Teenage girls with unexplained early puberty also have high leptin levels. These associations suggest a relationship between the central nervous system and body fat during puberty and the messenger leptin.
After puberty, leptin levels return to pre-puberty levels. Probably because of testosterone suppression. Leptin levels are higher in women than in men. Leptin levels drop as puberty progresses. Thus, during puberty there is an increased sensitivity to leptin.
Stages of puberty development
Symptoms of puberty such as increased body size, development of the breast, increased adrenal cortex activity, and menstruation require an average period of 4-5 years (1.5-6 years). ).
In general, the first sign of puberty is a bulging, followed by enlarged breasts, enlarged nipples, raised with areola, breast bulging like a mound.
Two years after the onset of breast eruption, increased adrenal cortex activity and armpit hair appeared. About 20% of cases develop pubic hair early and consider it the first sign of puberty. The first menstruation is a sign of late appearances, occurring after the growth of the body.
An adult girl has a peak of body development 3 years earlier than a brother and after a year the high-speed doubled, reaching 6-1 lcm. On average, a girl reaches a peak of magnitude two years before breast tenderness and a year before her period. Reality has suggested that the magnitude increase is
due to estrogen and by association with an increase in growth hormone and insulin-like growth factor I (IGF-I, insulin-like grovvth factor-I). Androgens of the adrenal cortex do not play a role here because in patients with Addison's disease there is still a normal development of softness.
Studying on African dwarves, it was found that the main factor responsible for the development of normal puberty was IGF-I. The growth hormone acts through a locally produced mediator, the insulin-like growth factor I (IGF-I). In addition, growth hormone can directly stimulate cartilage development. The normal development of puberty requires a combination of growth hormone, insulin-like growth factor I and sex steroids.
The increase in IGF-I during puberty is associated with sexual development and is the result of the interaction between sex steroids and growth hormones. In particular, the increase in sex steroids increases growth hormones. This hormone in turn stimulates the production of IGF-I. However, studies have also shown that sex steroids can have a direct effect on bone growth, independent of growth hormone. So the Laron-type dwarves - who have a genetic defect in the growth hormone receptor and are unable to stimulate the production of growth factor I like insulin - still achieve their size at puberty due to their response. corresponding to sex steroids. However, normal growth rates during puberty require a combination of sex steroids and growth hormone effects. Sex steroids also limit the body's height by stimulating the closure of long bone oils. The main sex steroid that is involved in the body's growth during puberty is probably estrogen, for both men and women. For men, the estrogen comes from the aroma of androgen.
The hormone produced most by the pituitary is growth hormone. In addition to the stimulation of IGF-I on cartilage, the growth hormone also stimulates the production of IGF-I in a number of tissues throughout the body, especially in the liver, the main source of circulating IGF-I. The production of IGF-I-carrying protein (IGFP-I, insulin-like grovvth fac-tor binding protein-I) is regulated by insulin. IGFP-I levels decrease during puberty due to a relative increase in insulin in the blood that occurs during puberty in response to an increase in insulin resistance. This change increases the IGF-I activity. This is an important intermediate element of development.
As with gonadotropins, growth hormone is secreted in the rhythm of the dollar and during puberty the amplitude of the rhythms increases, especially during sleep. Therefore, sleep is an important condition to help the body grow. The tail with a large rhythm range means the age with rapid body development. The growth response, for growth hormones, is an increase in the amplitude of the rhythm, not an increase in baseline value. Children grow slowly, have a small rate of growth hormone. Growth hormone secretion rate is regulated by stimulation of growth-releasing hormone and inhibition of somatropin-inhibiting hormone-releasing hormone. Both substances are transferred from the nucleus of the hypothalamus through the vascular system to the pituitary gland. This mechanism is influenced by different levels of estrogen and androgen.
Before puberty, sex steroid hormones are not involved with growth hormones because of their low concentrations. However, during puberty, the secretory activity of the growth hormone is independent of the sex steroid hormone. Growth hormone secretion must be very sensitive to the stimulating effects of estrogen because the growth hormone pre-emits any signs of sexual development.
The level of estrogen required to stimulate the shell growth of long bones is small. A dose of 100 nanograms of estradiol/kg body weight increases the amplitude of secretory rhythms and maximizes enlargement in those without gonads. These doses are not enough to stimulate the breasts much, keratosis of vaginal tissue or increase sex hormone globulin. The effects of the aforementioned low doses of estrogens are certain, as girls achieve height growth early during puberty with a serum estradiol content of 20 pg/ml, ie only 1/6. of adults. Furthermore, at low doses, estrogen stimulates the secretion of IGF-I, while at high doses inhibits IGF-I secretion.
Estrogen is a core hormone for both men and women. For men, if there is a decrease in the function of aromatase, there will be a lack of estrogen, the body grows slowly and bone density decreases. Analysing the decrease of testosterone and testosterone in the circulation in the elderly, it was found that the amount of hormone with bioavailable value in the blood is oestrogen, a certain constant marker of bone density in men as well as in women. .
For men, androgens and estrogens are both needed to achieve the required bone mass.
Osteoporosis and spinal fractures are less common in blacks than in whites. It is determined by race. Spine density increases rapidly and significantly increase during puberty. The increase in bone density at puberty reaches 10-20%, ensuring a bone accumulation for 10-20 years of osteoporosis prevention. Calcium supplementation in adulthood also helps to significantly increase bone density and bone mass in osteoporosis prevention. Menstrual irregularities often weigh themselves to be determined due to lack of estrogen. If due to lack of estrogen, it must be treated. The effect of sex steroids on bone mass increases bone mass, accumulating primarily in the hip bones and vertebrae of women in the years following the first menstrual period (age 11-14) and later in life. Maturity (age 18) is very important.
The lifestyle and nutritional status of the mother before birth and after birth play a significant role in helping the baby grow taller, heavier and more mature. Studies on twins show that if the surrounding environment is appropriate, sooner or later, the period of menstruation is determined by genetics.
Age at first menstruation in the US is 9.1-17.7, with the average age being 12.8 years. According to classical documents, the first menstruation age is 13-16 years old. The ultimate sign of pubertal endocrine is the positive growth of estrogen feedback on the hypothalamus and pituitary gland. This feedback stimulates the formation of a peak of LH in the middle of the menstrual cycle leading to ovulation. The first periods are usually ovarian, irregular, and bleeding frequently. Ovulation failure lasts up to 12-18 months from the first menstrual period. But it has also been found that pregnancy has occurred before the first menstrual period. The frequency of oocyte increases as puberty progresses. However, up to 25-50% of young women do not ovulate in the first 4 years from their first menstrual period.
Summarize the facts of puberty
Puberty is the next result of mature steps. The hypothalamus-pituitary-gonad system is differentiated and active throughout the life of the fetus and infant. It is then inhibited to reduce activity throughout the child's age due to a combination of two events: an increase in the sensitivity of gonadostat to estrogen negative responses and inhibition of endogenous central nervous system. All parts below the Gn-RH, that is, below the central nervous system, are capable of responding at all ages.
After a decade of Gn-RH dysfunction from adolescence to puberty, the secretion of Gn-RH is resumed (reactivation of the hypothalamus-pituitary - ovary axis. ) and leads to the onset of gonads.
If suppression of endogenous activity of the central nervous system persists or there is an inability to respond to any of the underlying components, it will lead to delayed or non-pubertal treatment.
FSH and LH rise slightly before age 10, followed by an increase in estradiol. Increasing the rate of 'LH' is initially seen only when sleeping, then gradually spread to the whole day. In adults, the beats are approximately 1.5-2 hours apart.
The estrogen of the gonads increases due to gonadarche (increased gonadal activity), breast development, distribution of fat according to femininity, development of the vagina and uterus. Spinal growth is the result of low secretion of first gonadal hormones, increasing growth hormone secretion. When the growth hormone secretes, it stimulates the secretion of IGF-I.
3 / Androgens of the adrenal cortex due to increased activity of the adrenal glands and androgens of the gonads to a lower level, causing pubic and axillary hair growth. The increased activity of the adrenal cortex (adrenarche), albeit at a low level, always plays a role in the development of the spine. While temporarily associated with gonadarche, adrenarche remained independent, not functionally related.
In mid-puberty, the estrogen of the gonads is fully secreted, which develops the endometrium and induces the first menstrual period.
After the first period, many subsequent cycles do not ovulate. By the time the full estrogen response is present, the hypercoagulation peak reaches a peak and leads to oocyte release. This event occurs towards the end of puberty.
Staging puberty according to Tanner
Stage 1 (pre-puberty)
No pubic hair
Slightly raised breasts and spines, enlarged areola. Average of 9.8 years old
Thin and thin, pale colour mainly along the large lips
The breasts are raised, can not distinguish the areola breast. Average age 11.2 years
Dark, coarse, possibly curly, strabismus on the pubic Average: 11.4 years old
Are areola, prominent spines above breast Average 12.1 years old
Adult hair type, much but limited above pubic Average: 12.0 years old
The areola is reduced, the same plane as the breast. Average age: 14.6 years
Adult hair type increased in volume Average: 13.7 years old