Premature sexual development of children. Puberty is early and late in boys

Puberty is a genetically determined process of transforming a child’s body into an adult capable of reproduction. In a broad sense, the achievement of puberty includes not only a physiological process, but also social adaptation.

Currently, the average age of puberty in girls ranges from 8 to 13 years, and in boys from 9 to 14 years.

The timing of the onset of puberty is significantly influenced by the child’s gender, race, hereditary predisposition, environmental factors, nutritional status, and socioeconomic status. For example, obesity and exogenous supply of hormones can play an unfavorable role.

Physiology of sexual development

Male and female gonads are formed from one undifferentiated rudiment. The development of the gonads in both sexes in the early stages proceeds in the same way (indifferent stage). The gene that determines the differentiation of the gonad according to the male type is localized on the Y chromosome.

The basis for the development of the internal genital organs are the Wolffian (in boys) and Müllerian (in girls) ducts.

The formation of the external genitalia of the male fetus begins from the 8th week of the intrauterine period and occurs under the influence of dihydrotestosterone, formed from testosterone in the fetal testicles. Androgens are necessary for the differentiation of embryonic anlages according to the male type. Leydig cells, which produce androgens, function under the influence of placental chorionic gonadotropin. The genital tubercle forms the penis, and the external genital folds form the scrotum. At 18-20 weeks of intrauterine development, the formation of male-type external genitalia ends, although the process of lowering the testicles into the scrotum occurs much later, by 8-9 months of gestation. After birth, testosterone production is stimulated by pituitary gonadotropins.

When a female organism is formed, the fallopian tubes develop from the upper third of the Müllerian ducts; the middle part of the ducts merges to form the body and cervix. Wolffian ducts regress.

From the 12th to the 20th week of the intrauterine period, the vagina, clitoris, labia majora and minora, the vestibule of the vagina with separate external opening of the urethra and the entrance to the vagina are formed. In the female fetus, differentiation of the external genitalia occurs regardless of the state of the gonads.

The triggering mechanism of puberty associated with the activation of the neuroendocrine system is currently not clear enough. However, it is known that this process is initiated by the pulsed secretion of gonadotropin-releasing hormone (LH-RH) by neurons located in the nuclei of the hypothalamus. The development of the hypothalamic-pituitary-gonadal axis (gonadostat) occurs throughout the entire period of a child’s life, starting from intrauterine.

In a newborn child, the hypothalamic-pituitary-gonadal regulation is fully formed. In boys, this system functions up to 6-12 months, in girls up to 2-3 years of life. Then follows a long period (until puberty) of its oppression - the “juvenile pause”. Pulse secretion of LH-RH sharply decreases. Despite the low content of sex steroids in the blood, this period is critical for precocious sexual development (PPD) of central origin.

By the end of the “juvenile pause” - by 6-7 years in girls and by 8-9 in boys - adrenal androgens begin to be intensively synthesized, causing the development of secondary hair growth (pubic and axillary) in girls. In boys, this role is played mainly by androgens of testicular origin. This period preceding puberty is called the adrenarche phase.

The final formation of the gonadostat occurs during puberty. Activation of the LH-RH pulse secretion generator stimulates the production of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) of the pituitary gland, which are necessary for the formation of gonadal steroids - androgens and estrogens. The regulation of this system during reproductive age is based on the principle of feedback between these hormones.

In boys, the main hormone of puberty is testosterone, which is secreted by Leydig cells in the testes and partly in the adrenal cortex. Testosterone itself is inactive. In target organs, with the help of the enzyme 5α-reductase, it is converted into the active form - dihydrotestosterone. The increasing production of androgens by enlarged testicles causes the development of secondary sexual characteristics (lowering and deepening of the voice, male-type hair growth on the face and body, the transformation of vellus hair into terminal hair, increased secretion of sweat and a change in its smell, an increase in the size of the penis, pigmentation and the development of skin folding scrotum, nipple pigmentation, formation of a male type of face and skeleton, increase in prostate size), regulates spermatogenesis and sexual behavior.

The ovaries produce two main hormones that have the greatest impact on the condition and functioning of the female reproductive system - estradiol and progesterone.

Estrogens are the general collective name for a subclass of steroid hormones produced mainly by the follicular apparatus of the ovaries in women. Estrogens are also produced in small quantities by the testicles in men and the adrenal cortex in both sexes. More than 30 types of estrogens have been isolated from various human biological fluids, three of which are considered the main ones: estrone (E 1), 17-β-estradiol (E 2) and estriol (E 3). Estradiol and some estrone are synthesized in the ovaries. Estrone and estriol are formed mainly in the liver from estradiol, as well as in other tissues from androgens, mainly from androstenedione. The synthesis of estrogen in follicles is regulated by FSH.

Signs of the onset of puberty

As mentioned above, puberty is initiated by the pulsed nature of LH-RH secretion. In boys, the first sign of the onset of puberty is enlargement of the testicles. The testicles in the period from 1 year to the onset of puberty almost do not change in size, length is 2-2.5 cm, volume< 4 мл. Через 6 лет после начала пубертата яички достигают объема 18-20 см 3 , однако нужно учитывать индивидуальные различия среди мужчин.

Testicles have two main functions: hormone production and sperm production, with the former starting earlier and stimulating the latter. Already a year after the onset of puberty, sperm can be detected in the morning urine of boys (spermaturia). The penis (penis) begins to grow shortly after the testicles begin to grow. As the penis grows, erections occur, followed by wet dreams. On average, boys reach potential fertility by the age of 13, and full fertility by 14-16 years.

Under the influence of androgens, the larynx grows, the vocal cords lengthen and thicken, which makes the voice deeper. A change in voice usually accompanies a growth spurt in the body.

Hair growth (adrenarche) begins from the pubis, shortly after the start of testicular growth. Appearing in small quantities at the base of the penis, the hair gradually becomes thicker and occupies the entire pubic triangle, after which it spreads to the thighs and along the linea alba to the navel. Then, after several months and even years, hair begins to grow in the armpits, near the anus, on the upper lip, near the ears, around the nipples and on the chin. The sequence and rate of hair growth is subject to individual differences. Throughout life, hair continues to grow and become thicker on the arms, legs, chest, stomach and back.

By the end of puberty, young men develop a male type of skeleton: a narrow pelvis and a relatively wide shoulder girdle.

The growth of mammary glands (thelarche) is the first sign of puberty in girls and is observed on average at the age of 10.5 years. First, a small, painful lump appears under the areola on one or both sides. After 6-12 months, compaction begins to be noted on both sides, it increases in size, becomes softer and extends beyond the areola. Within 2 years, the mammary glands reach a mature size and shape, and the nipples become clearly defined. The size and shape of the mammary glands in girls have pronounced individual differences.

Pubic hair appears a few months after the mammary glands begin to grow. In 15% of girls, this symptom appears first. At first these are single hairs on the labia, spreading to the pubis within 6-12 months. Subsequently, the hair grows and covers the entire pubic triangle. Under the influence of estrogens, the vaginal epithelium thickens and cells begin to actively exfoliate from its surface, and the vascularization of the vagina increases. Follicles begin to grow in the ovaries.

When performing an ultrasound examination during this period, you can see many small cysts - follicles. The first menstruation (menarche) usually occurs 2 years after the start of breast growth.

During puberty, under the influence of high levels of estrogen, the pelvic bones grow in width, as a result of which the hips become wider. Adipose tissue increases, and by the end of puberty the volume of adipose tissue in girls is twice that of boys. Fat is deposited mainly in the area of the mammary glands, thighs, buttocks, shoulder girdle, and pubis.

Premature sexual development

PPD refers to the onset of pubertal symptoms before the age of 8 years in girls and 9 years in boys. This pathology may be caused by a disorder in the gonadostatic system at various levels. Most authors adhere to the pathogenetic classification of PPR.

There are true, or cerebral, forms of the disease, the pathogenesis of which is associated with premature pulsed secretion of LH-RH by the hypothalamus. Increased synthesis of sex steroids in these cases is due to excess production of pituitary gonadotropic hormones. A feature of true PPD is that it occurs as isosexual, and the biological changes in the body correspond to the stages of normal sexual development, but at an accelerated pace. Excessive secretion of sex steroids increases the growth rate and promotes rapid closure of growth plates.

False (peripheral) forms of PPR, independent of the secretion of gonadotropins, are associated with premature excessive production of steroid hormones by tumors of the gonads and adrenal glands, with McCuen-Albright-Braitsev syndrome, testotoxicosis. In these cases, the sequence of stages of puberty is distorted. False forms of the disease can spontaneously transform into true ones, which is associated with secondary activation of the hypothalamic-pituitary axis.

A special group includes the so-called gonadotropin-independent forms of PPR, in which the autonomous activation of the gonads is caused by genetic disorders. These variants of PPR have all the signs of advanced puberty - enlargement of the gonads, accelerated growth and bone maturation, and the formation of secondary sexual characteristics.

There are patients with the only sign of premature puberty: isolated development of secondary hair growth (premature pubarche) and isolated development of the mammary glands (premature thelarche). These are incomplete forms of PPR.

True precocious puberty

The cause of true PPR can be various lesions of the central nervous system (CNS) of a non-tumor nature (organic, inflammatory, etc.), as well as exposure to adverse factors in the prenatal period (trauma, hypoxia, infections). These children are often diagnosed with hydrocephalic syndrome. The cause of PPR may be arachnoid cysts of the bottom of the 3rd ventricle and the chiasmal-sellar region of the brain. Cysts form during embryogenesis, less often as a result of meningitis, encephalitis, or brain injury.

In some patients with true PPR, the cause of the disease cannot be identified. In such cases, when organic diseases of the central nervous system are excluded, a diagnosis of the idiopathic form of PPR is made. However, the improvement of research methods (the use of computer and magnetic resonance imaging) of the brain makes it possible to more often identify the cause of the cerebral form of PPR.

The constitutional nature of PPD can be assumed if, when collecting an anamnesis, it turns out that in relatives puberty began 2-3 years earlier.

Modern examination methods allow early visualization of CNS tumors.

Hamartoma is one of the most frequently detected tumor formations of the central nervous system in children with true PPR under the age of 3 years. Hypothalamic hamartoma is a benign tumor consisting of a cluster of differentiated nerve cells formed during embryogenesis. Essentially, it is a consequence of a malformation of nervous tissue. Intravital diagnostics became possible only with the introduction of magnetic resonance imaging into practice.

The leading syndrome of hypothalamic hamartomas is PPR, this is due to the fact that the neurosecretory cells of hamartomas secrete LH-RH, which stimulates the formation of LH in the pituitary gland with subsequent excessive production of steroid hormones in the gonads. It should be noted that disruption of the migration of embryonic cells secreting LH-RH can lead to ectopia of these cells, i.e. they can be located outside the hypothalamus. It is believed that PPR in this case develops through the endogenous pulsatile release of LH-RH alone or together with LH-RH secreting neurons of the hypothalamus. It has been suggested that PPR may be caused by the indirect action of glial factors, including the transformation of growth factor alpha, which stimulates the secretion of GnRH in the hypothalamus. Removal of a hamartoma does not inhibit sexual development in all cases. In these patients, secondary activation of astroglial cells in the tissues surrounding the hypothalamus can cause increased secretion of LH-RH, thereby maintaining the clinical picture of PPR.

In children with hamartoma, the disease manifests itself as true PPR at an early age. The incidence of the disease is the same in boys and girls. Neurological symptoms may include minor epileptic seizures in the form of violent laughter, memory loss, and aggressiveness.

Most tumors of the chiasm and hypothalamus in children are poorly differentiated gliomas. In the suprasellar region, astrocytomas are more often detected.

Brainstem gliomas causing PPR are common in neurofibromatosis type 1 (Recklinghausen disease). This disease has an autosomal dominant mode of inheritance and occurs with a frequency of 1:3500 newborns.

Failure of the gene responsible for the synthesis of the neurofibromin protein causes rapid, uncontrolled cell growth. The clinical picture is characterized by pigment spots on the skin ranging from light to dark brown. Neurofibromas are benign small neoplasms that are located on the skin, iris, and central nervous system. Multiple bone defects are characteristic. The pathognomonic symptom of this disease is the presence of pigment spots on the skin of a café-au-lait color larger than 0.5 cm. The pathogenesis of PPR in benign tumors and cysts of the central nervous system is not clear, but pubertal gonadostat indicators were detected in patients. The peculiarity of this process is that neurological symptoms (headaches, seizures, visual disturbances, and others) precede the symptoms of PPR.

Russell-Silver syndrome is characterized by a complex of hereditary abnormalities (presumably an autosomal recessive type of inheritance): intrauterine and postnatal growth retardation and disorders of skeletal formation. Frequency of occurrence: 1:30,000 population. Children are born of short length (up to 45 cm) and low body weight (1.5-2.5 kg) during full-term pregnancy. Over the years, growth retardation persists, and therefore the final height in women is less than 150 cm, in men - slightly above 150 cm. Body weight in adults is normal or even overweight. Anomalies of the external genitalia are common: cryptorchidism, hypospadias, hypoplasia of the penis, scrotum. Asymmetry of the body (face, torso, leg length) is characteristic. The face is triangular in shape, pseudohydrocephalus, large forehead and hypoplasia of the lower jaw, high palate, often with a cleft, protruding ears. Clinodactyly of the fifth finger due to deviation of the distal phalanx, narrow chest, short arms, lumbar lordosis. Anomalies in the structure of the urinary system are often observed. Intelligence is usually normal. Sexual development begins to progress at 5-6 years of age and is gonadotropin-dependent. Elevated levels of LH and FSH in the setting of hypoglycemia are typical.

Tuberous sclerosis (Bourneville-Pringle syndrome) is one of the forms of phakomatosis and is characterized by congenital neuroectomesodermal dysplasia with the presence of benign tumors. Occurs with a frequency of 1:10,000 newborns, more often in boys. Presumably, the disease has an autosomal dominant mode of inheritance. Fibrous plaques are an obligate sign of this disease. In the brain, the size of these plaques varies from a few millimeters to several centimeters. They can be single or multiple. Depending on the location, plaques cause various clinical symptoms: headache, vomiting, decreased vision, epilepsy, convulsive paroxysms, hydrocephalus, signs of PPR.

True PPR may be caused by tumors that produce human choriogonic gonadotropin (hCG) (hCG-secreting tumors). These include germ cell tumors of the central nervous system, hepatoblastomas and other retroperitoneal tumors. Germ cell tumors develop from pluripotent germ cells. Many of these tumors can produce hCG during embryogenesis. In the process of disrupted migration, such cells can develop not only in the gonads, but also in other organs and tissues. Germ cell tumors account for 3-8% of all malignant neoplasms in childhood and adolescence. They are often combined with various genetic syndromes (Klinefelter syndrome, ataxia-telangiectasia, etc.).

Malignant germ cell tumors are 2-3 times more common in girls, and intracranial tumors are 2-3 times more common in boys. In the latter, PPR syndrome, associated with excessive secretion of hCG, is combined with symptoms of diabetes insipidus, increased intracranial pressure, narrowing of visual fields, hemiparesis, etc. Germ cell tumors localized in the brain are intensely vascularized and are therefore easily detected by contrast-enhanced computed tomography. Alpha-fetoprotein (AFP) and beta-hCG levels are elevated in serum and cerebrospinal fluid; testosterone levels correspond to puberty. An apparent increase in LH levels is detected (due to immunological cross-reactivity between hCG and LH). However, LH levels do not increase after GnRH stimulation. FSH levels are reduced.

Undescended testicles pose a risk of developing testicular tumors. In the clinical picture, attention should be paid to the volume of the testicles, which increase moderately and do not correspond to the signs of puberty. The reason for this phenomenon is that in children the gonadostat remains immature. From two gonadotropic hormones (FSH and LH), testicular tumor cells produce LH, which hyperplasias Leydig cells. At the same time, Sertoli cells, which require the action of FSH, remain intact. In boys, PPD develops in an isosexual pattern.

Germ tumors are divided into those that secrete beta-hCG and those that do not. In the diagnosis of germ cell tumors, the determination of AFP and beta-hCG plays an important role. One of the markers of a malignant tumor process is cancer embryonic antigen (CEA).

Chemotherapy plays a leading role in the treatment of germ cell tumors. Radiation therapy has very limited use and is effective in treating ovarian dysgerminomas. Surgical treatment is aimed at removing the primary tumor.

Hepatoblastoma is a malignant liver tumor that develops from an embryonic pluripotent anlage. The tumor is usually presented as a whitish-yellow nodule that grows into the liver tissue. Hepatoblastomas occur in children before the age of 3; after 5 years of age, this form of liver tumor is very rare. The exact causes of hepatoblastoma are not clear. Hepatoblastoma can be combined with other childhood tumors, for example, Wilms tumor (nephroblastoma). An increased risk of hepatoblastoma is observed in children who have had hepatitis B during the neonatal period, helminthic infestation, colon polyposis, metabolic disorders - hereditary tyrosinemia, glycogen storage disease type I, etc. In the initial period of development of hepatoblastoma there are no pronounced symptoms, progression is accompanied by symptoms of general intoxication and (rarely) symptoms of PPR due to hCG production by the tumor. Hepatoblastoma is a rapidly growing tumor with a high risk of hematogenous metastasis to the lungs, brain, bones and abdominal cavity. Treatment of hepatoblastoma is surgical, which consists of removing the tumor through partial hepatectomy. The survival prognosis for stage 1 of the disease for 2.5 years is 90% or more, for stage 4 - less than 30%.

Gonadotropin-independent PPR

The clinical picture of McCune-Albright-Braitsev syndrome consists of the following symptoms: asymmetrical light brown skin pigmentation, which resembles a geographical map; polyostotic fibrous osteodysplasia; PPR and other endocrinopathies. The disease is described only in girls.

The causes of endocrine disorders in McCune-Albright-Braitsev syndrome are caused by mutations of the Gs-alpha protein. The mutant protein activates adenylate cyclase in the LH and FSH receptors on ovarian cells, thereby stimulating the secretion of estrogen in the absence of gonadotropic hormones. It is assumed that Gs-alpha mutations occur in the early stages of embryogenesis. As a result, clones of cells carrying mutant proteins are formed.

The first signs of the disease are associated with characteristic light brown pigment spots on the skin that are present in a newborn or appear during the first year of life.

Fibrocystic dysplasia manifests itself in the form of lesions of long tubular bones. The changed bones become deformed and pathological fractures occur.

PPR in McCune-Albright-Braitsev syndrome is more often detected after the first year of life and occurs in waves. As a rule, the first manifestation is uterine bleeding. They are detected long before the onset of thelarche and adrenarche. Uterine bleeding is caused by a short-term increase in estrogen levels. The ovaries are of normal size, but large persistent follicular cysts can be found in them. Some patients have elevated levels of gonadotropic hormones. In such cases, we can talk about true PPR.

Other endocrine disorders include nodular euthyroid goiter, pituitary adenomas (Itsenko-Cushing syndrome, thyrotoxicosis and increased levels of other hormones).

Testosterone toxicosis is caused by excessive unregulated secretion of testosterone by hyperplastic Leydig cells. It is a familial, autosomal dominant disorder with incomplete penetrance that occurs in males. Excess testosterone production is caused by a point mutation in the LH receptor gene. Mutant genes cause intracellular activation of Leydig cell metabolism in the absence of LH.

Secondary sexual characteristics usually appear at 3-5 years of age, and the first symptoms of androgenization can be observed as early as 2 years of age. The timbre of the voice changes, a masculine physique, acne vulgaris, enlargement of the penis, erections are characteristic, the growth and maturation of the skeleton accelerates. The volume of the testicles is increased, but does not correspond to the degree of androgenization. The clinical picture of testotoxicosis is similar to true PPR.

When studying the gonadostat, high testosterone levels are detected with prepubertal LH and FSH levels. There is no reaction of LH and FSH to the test with luliberin (LH-RH), as well as pulsed spontaneous secretion of LH, characteristic of the puberty period.

A testicular biopsy reveals well-developed convoluted seminiferous tubules, an excess of mature Leydig cells, and germ cells at different stages of spermatogenesis. In some convoluted seminiferous tubules, degenerating germ cells are detected. In adults, the results of the GnRH test are normal; Some patients with damage to the spermatogenic epithelium have elevated FSH levels. In most men with familial testotoxicosis, fertility is not impaired.

Read the end of the article in the next issue.

V.V. Smirnov 1, Doctor of Medical Sciences, Professor
A. A. Nakula

GBOU VPO RNIMU im. N. I. Pirogova, Ministry of Health of the Russian Federation, Moscow

The diagnosis of precocious puberty can be made if the first signs of puberty appear before the age of seven in girls, and before the age of eight in boys. There are two types of disease: true and false. The first is characterized by the appearance of sexual characteristics along with the maturation of the gonads. The false form of the disease implies the presence of signs of puberty without the development of the gonads.

Signs of precocious puberty are much more common in girls. These include profuse acne in the face, early first menstruation, intense growth of hair on the pubis and armpits. There is also a strong body odor, which indicates a change in the balance of hormones, and there is a sharp growth and enlargement of the breasts.

In boys, this condition develops less frequently and is characterized by rapid body growth, enlarged testicles, profuse acne, hair growth in the armpits, face and pubic area, a deepening of the voice and a strong body odor.

In some cases, during early sexual development, not all of the listed signs appear and develop, but only some of them. This situation most often does not require special treatment, only some correction of the diet and control over the psycho-emotional state. However, the child should definitely be shown to a doctor.

Early sexual development can begin for various reasons. Most often, it is a definite signal about some kind of disorder in the child’s body. There are several pathological conditions that lead to premature sexual development:

Tumors in the brain or spinal cord;
- the period after suffering an acute form of certain infectious diseases (meningitis or meningoencephalitis);
- abnormalities in the development of the brain of a congenital nature, hydrocephalus;
- the period after radiation therapy or chemotherapy;
- suffered traumatic brain injuries;
- ischemia (acute vascular insufficiency);
- McCune-Albright genetic disease, characterized by bone damage leading to early osteoporosis and skin pigmentation disorders;
- hereditary diseases of the adrenal glands, in which hormones are produced in excess;
- diseases of the thyroid gland, both hereditary and acquired;
- disturbances in the functioning of the pituitary gland, which lead to a failure in the production of hormones;
- various tumors of the testicles, ovaries or mediastinum;
- chromosomal abnormalities.

The clinical picture depends entirely on the cause that led to premature puberty. If the pathology was caused by a tumor, congenital anomalies or chromosomal abnormalities, then the first signs appear very early. Girls experience bleeding from the vagina, which is small and irregular. The formation of secondary sexual characteristics occurs much later.

In boys, an early erection first occurs, and then secondary sexual characteristics develop: hair growth, penile development, some disturbance in body proportions, accompanied by increased ossification or the occurrence of early osteoporosis.

At the same time, disturbances in the functioning of the central nervous system occur. This is how children can lag behind in mental development and become more passive and uninitiative. But quite often, intellectual development is fully consistent with age and even ahead of it. A child may try to behave like an adult, parodying adult life. Sometimes sexual aggressiveness is also observed.
Children can withdraw into themselves, get tired quickly, they are not attentive and very aggressive. The teacher can also pay attention to this in class. Sometimes constant thirst occurs and appetite increases. Children have difficulty withstanding temperature changes and complain of headaches.
In some cases, cachexia develops. Mental disorders can lead to rude behavior, running away from home and engaging in prostitution or drug addiction. As a rule, children simply do not understand what is happening to them.

With false precocious puberty, the same clinical picture is observed, but the changes are transient in nature and regress over time, and the functional activity of the endocrine glands is completely restored.

For proper treatment, it is necessary to make a timely diagnosis and determine the type of disease. At the same time, weight and height indicators are taken into account and correlated with age. After this, the level of hormones in the blood is checked. If a tumor is suspected, computed tomography or magnetic resonance imaging is performed. If a child has genetic disorders, the altered gene is identified.

The preschool period is one of the main periods in sexual development. Check to see if there really is cause for concern.

Most new parents know how to read how their child is developing. Say when an ordinary child learns to sit down, walk, pronounce the first words or grab a toy. We are perfectly marked when it comes to cognitive development, motor, or physical. But sexual development is a dark forest for many parents. Many parents even believe that something begins to happen in this area only when the child enters the period of maturation. Nothing could be more wrong. The sexual development of a child begins at the moment of birth.

Early childhood is also the beginning of the acquisition of sexual identity, that is, the consciousness of being a boy or a girl and the ability to distinguish between genders based on various characteristics, including. genitals. We are dealing with this already in the second half of the 2nd year of life. During this period, the boy begins to identify with his father, and the girl with her mother. Children become interested in other people's genitals and want to compare them with their own.

Between the ages of 3 and 7 years, an unusually large number of questions arise in a child’s development.

1. Children touching their genitals serves to release and receive pleasure - it is natural that a child repeats activities that bring him pleasant sensations. When a child touches his genitals in the presence of others, for example in a preschool, he should be informed that public touching is not nice. Then you should not punish the child and react with fear, but just show him the boundaries of intimacy. Over time, children begin to control this area and do not do this in the presence of others.

2. Spying on others, such as parents in the toilet or other children, and asking questions related to gender, fertilization or childbirth. Their goal is to obtain information. Children at this age willingly show their bodies and compare them with the bodies of others. This is a way of helping yourself with very difficult emotions.

How to react? Don't shout, don't punish or shame, just talk. You need to explain to your child in which places nudity is allowed - for example, on the beach, in the bathroom or sauna, and in which places the body should be covered. This is a good opportunity to talk about the right to intimacy and who and under what circumstances can examine and touch a child’s naked body, for example, a doctor during an examination. Preschool is a good time to clarify rules and social norms. Children at this age learn, among other things, that they cannot marry their parents or siblings.

The conversation itself, however, is not enough. What we say must be connected with what we show. Parents should not walk naked around the apartment. Such behavior can, at a later age, cause the child to refuse any thoughts about the opposite sex. Or vice versa - it can awaken a child’s unhealthy interest.

How to react if a child catches his parents during lovemaking? If this happens, you should talk to him about it and explain this situation to him in an appropriate way for his age. We can say that the parents love each other very much, the father and mother cuddle, it is pleasant for them, and thanks to this the child was born.

3. Any children's activity that is related to the topic of sexual development. Games at the doctor's, family, dad and mom. They serve to calm curiosity and gain knowledge, while also being stimulating, enjoyable, and provide valuable peer-to-peer experiences. More often they involve examining the genitals, touching them, acting out the role of spouses, rarely simulating sexual relations in clothes, especially naked. Fun “to be a doctor” arises from the desire to know the differences in the body structure of the other sex.

4. Children's creativity. Children can draw shapes with clearly marked genitals, sculpt them out of plasticine, or even make rhymes with words related to the theme of love relationships. They can also sketch their ideas about relationships. But no need to worry. Most of this fun is part of proper development. But parents should still be careful. If, in addition, during such fun, the child expresses a lot of negative emotions, one can suspect that someone has acted badly in relation to his sexual development.

The boundary in sexual development is the 5th year of a child’s life. Then the number of games based on display decreases, the need for privacy grows in return, and a natural feeling of shame begins to develop. Parents then play a very important role - they must respect the child’s shyness and take care of his intimacy. A girl at this age may ask to be covered when changing clothes on the beach. You can’t make fun of her and remind her that a year earlier she took off her clothes without any problems. You should also not forcefully assist the child during washing and satisfying physiological needs. Shared bathing between parents and child should end around 3 years of age. Bathing five-year-olds is more about instructing them on how to bathe properly than about helping them. It's good to be attentive and responsive to your child's needs. When we see his awkwardness, or we hear: “Mom, go, I’ll do it myself,” we should allow independence.

After 6-7 years of life, you can expect less interest in the sexual sphere.

Until 8-9 years of age (prepubertal period), the hypothalamic-pituitary-gonadal system is inactive: neither LH (luteinizing hormone) nor sex steroids (estradiol in girls and testosterone in boys) are detected in the blood serum. It is believed that the activity of the hypothalamus and pituitary gland at this time is under the influence of inhibitory neurons, which have so far been little studied.

Approximately 3 years before the appearance of the first clinical signs of sexual development in children during sleep, it is already possible to detect PH in the blood serum (prepubertal period). This sleep-induced LH secretion is pulsatile and is probably associated with episodic releases of hypothalamic GnRH. As puberty approaches, the amplitude and, to a lesser extent, the frequency of nocturnal LH pulses increase, which leads to enlargement and maturation of the gonads and the beginning of the secretion of sex hormones. As a result of the joint activity of the hypothalamus, pituitary gland and gonads in the early stages of sexual development, secondary sexual characteristics appear in children. In the middle of puberty, pulsed LH secretion is recorded not only at night, but also during the day. The interval between pulses is 90-120 minutes.

At the same or slightly later date, girls begin menstrual cycles and ovulation. A positive feedback loop is formed, due to which the level of estrogen increasing in the middle of the menstrual cycle causes a clear increase in the level of LH in the blood serum.

The factors that normally activate or inhibit GnRH-secreting hypothalamic neurons (the so-called GnRH pulse generator) are unknown. In experiments on monkeys, activation of this generator is caused by a decrease in the tone of hypothalamic GABAergic neurons, accompanied by increased activity of the glutamatergic system. In all likelihood, other CNS mediators also take part in this process in humans and monkeys.

It is GnRH that is the main, if not the only hormone that triggers the process of sexual development in children. Thus, by administering GnRH in a pulse mode, it is possible to induce sexual development in immature animals and humans, as well as in cases of gonadotropin deficiency.

Many circumstances make it difficult to understand hormonal changes during puberty:

pituitary gonadotropins are heterogeneous; their different isoforms are present in the blood. During puberty in children, biologically more active isoforms may predominate.

The results of determining the content of immunoreactive LH depend on the method used, so the data obtained in different laboratories differ.

gonadotropins are released into the blood in pulses, with LH and FSH acting synergistically on gonadal maturation. Therefore, single determinations of gonadotropin concentrations are not informative. Serial determinations of their level in the blood (every 10-20 minutes for 12-24 hours) are more significant.

There are sex differences in the maturation of the hypothalamus and pituitary gland, and the concentration of LH in the blood serum during puberty increases earlier in boys than in girls.

Studies of the effects of estrogen deficiency in boys have brought greater understanding to the effects of sex steroids (testosterone in boys and estradiol in girls) on bone growth and maturation. Both with aromatase deficiency and with defects in estrogen receptors in boys, the closure of the epiphyseal growth plates is delayed and tall stature develops. These data indicate a role for estrogens, rather than androgens, in skeletal maturation and growth arrest. Estrogens also stimulate the secretion of growth hormone, which, together with sex steroids, causes rapid acceleration of growth during puberty.

The age of onset of puberty varies and corresponds more to the degree of bone maturation than to chronological age. The first sign of sexual development in girls is a slight swelling of the mammary glands (at 10-11 years), after 6-12 months. pubic hair begins to grow. It usually takes another 2-2.5 years before the first menstruation (menarche); this interval can reach 6 years. In the United States, 95% of girls aged 12 and 99% of girls aged 13 have at least one sign of puberty. Growth peaks in girls early (usually between 11 and 12 years of age) and always precedes menarche. The average age of menarche is 12.75 years. However, the intervals between accelerated growth, development of mammary glands, pubic hair growth, and maturation of the internal and external genitalia vary widely.

In boys, the first sign of the onset of puberty is enlargement of the testicles (volume - more than 3 ml, longitudinal diameter - 2.5 cm) and thinning of the skin of the scrotum. Then pigmentation of the scrotum, enlargement of the penis and pubic hair growth occur. In the middle of puberty, children develop armpit hair. Acceleration of growth is recorded already during sexual development (at the IV-V stages of maturation of the genital organs, usually at the age of 13-14 years), i.e. approximately 2 years later than in girls. Growth can continue after 18 years.

The age at which puberty begins depends on genetic and environmental factors. In the 20th century The age at menarche has progressively decreased, which is probably due to improvements in nutrition and general health of the population. However, in the last 30-40 years this age has stabilized. African-American girls develop secondary sexual characteristics earlier than white girls. In ballerinas, gymnasts and other athletes who remain thin from early childhood and experience enormous physical exertion, sexual development and menarche occur much later, and oligomenorrhea or amenorrhea is often observed in adulthood. Such observations confirm the idea of a close connection between energy metabolism and the activity of the GnRH pulse generator and the mechanisms of initiation and maintenance of sexual development in children. This connection is probably mediated by hormonal signals emanating from fat cells (leptin and other peptides).

Androgens from the adrenal cortex also play an important role in sexual development in children. The level of dehydroepiandrosterone (DHEA) and its sulfate in the blood serum begins to increase at approximately 6-8 years of age, i.e., long before the increase in LH or sex hormones and, especially, before the appearance of the earliest physical signs of sexual development in children. This process is called adrenarche. Of all the adrenal C19-steroids present in the blood, the level of DHEA sulfate is the highest and practically does not fluctuate throughout the day. The result of a one-time determination of its concentration in the blood can serve as an indicator of the secretion of adrenal androgens. Although adrenarche precedes gonadal activation (gonadarche) by several years, there is apparently no cause-and-effect relationship between these processes, since one can occur without the other (for example, in precocious puberty or adrenal insufficiency).

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Children can withdraw into themselves, get tired quickly, they are not attentive and very aggressive. The teacher can also pay attention to this in class. Sometimes constant thirst occurs and appetite increases. Children have difficulty withstanding temperature changes and complain of headaches.

In some cases, obesity or cachexia develops. Mental disorders can lead to rude behavior, running away from home and engaging in prostitution or drug addiction. As a rule, children simply do not understand what is happening to them.

Treatment depends entirely on the causes of the disease. For tumors, radical therapy is performed. Infections are actively treated depending on the type of pathogen.

Hormonal correction is carried out using drugs such as gonadotropin-releasing, naferelin. In this case, special attention should be paid to the psycho-emotional state of the child in order to ensure that he is comfortable among his peers.

Ekaterina, www.site