Adrenarche

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Adrenarche is an early stage in sexual maturation that happens in some higher primates (including humans), typically peaks at around 20 years of age, [1] [2] and is involved in the development of pubic hair, body odor, skin oiliness, axillary hair, sexual attraction/sexual desire/increased libido and mild acne. During adrenarche the adrenal glands secrete increased levels of weak adrenal androgens, including dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and androstenedione (A4), but without increased cortisol levels. Adrenarche is the result of the development of a new zone of the adrenal cortex, the zona reticularis. [3] Adrenarche is a process related to puberty, but distinct from hypothalamic–pituitary–gonadal axis (HPG axis) maturation and function.

Contents

Occurrence

Levels of DHEA-S, a major adrenal androgen, throughout life in humans Dehydroepiandrosterone sulfate levels throughout life in human males and females.png
Levels of DHEA-S, a major adrenal androgen, throughout life in humans

Adrenarche occurs starting at the age of 6 years. [4] [5] After the first year of life, the adrenal glands secrete very low levels of adrenal androgens. [1] Adrenarche begins on average between age 5 to 8 in girls and between 7 and 11 in boys, and precedes puberty by about 2 years. [1] [4] [5] Unlike the physical changes that occur during puberty, adrenarche is primarily an emotional and psychological stage of development. [6] It continues throughout puberty, with adrenal androgen levels progressively increasing until reaching maximal levels in young adulthood, around the age of 20 years. [1] [5] Circulating DHEA-S levels specifically peak in humans at about age 19 or 20 years in females and around age 20 to 24 years in males. [2] Levels of corticosteroids like cortisol do not change with adrenarche. [1] Biological messengers[ which? ] during the onset of adrenarche are thought to signal in preparation for puberty.

Role in puberty

An initiator of adrenarche has not yet been identified. Researchers have unsuccessfully tried to identify a new pituitary peptide, to be called "adrenal androgen stimulating hormone". Others have proposed that adrenarchal maturation is a gradual process intrinsic to the adrenal glands that has no distinct trigger. A third avenue of research is pursuing a possible relationship with either fetal or childhood body mass and related signals such as insulin and leptin. Many children born small for gestational age (SGA) because of intrauterine growth restriction (IUGR) have an earlier onset of adrenarche, which raises the possibility that timing of adrenarche may be affected by physiological programming in infancy. Adrenarche also occurs prematurely in many children who are overweight, suggesting a possible relationship with body mass or adiposity signals.

The principal physical consequences of adrenarche are androgen effects, especially pubic hair (in which Tanner stage 2 becomes Tanner stage 3) and the change of sweat composition that produces adult body odor. Increased oiliness of the skin and hair and mild acne may occur. Pubic hair caused by adrenarche is usually transient and will disappear right before the onset of puberty. In most boys, these changes are indistinguishable from early testicular testosterone effects occurring at the beginning of gonadal puberty. In girls, the adrenal androgens of adrenarche produce most of the early androgenic changes of puberty: pubic hair, body odor, skin oiliness, and acne. In most girls the early androgen effects coincide with, or are a few months following, the earliest estrogenic effects of gonadal puberty (breast development and growth acceleration). As female puberty progresses, the ovaries and peripheral tissues become more important sources of androgens.

Parents and many physicians often infer (incorrectly) the onset of puberty from the first appearance of pubic hair (termed pubarche).[ citation needed ] However, the independence of adrenarche and gonadal puberty is apparent in children with atypical or abnormal development, when one process may occur without the other. For instance, adrenarche does not occur in many girls with Addison's disease, who will continue to have minimal pubic hair as puberty progresses. Conversely, girls with Turner syndrome will have normal adrenarche and normal pubic hair development, but true gonadal puberty never occurs because their ovaries are abnormal.

Premature adrenarche

Premature adrenarche is the most common cause of the early appearance of pubic hair ("premature pubarche") in childhood. In a large proportion of children it seems to be a variation of normal development requiring no treatment. However, there are three clinical issues related to premature adrenarche.

First, when pubic hair appears at an unusually early age in a child, premature adrenarche should be distinguished from true central precocious puberty, from congenital adrenal hyperplasia, and from androgen-producing tumors of the adrenals or gonads. Pediatric endocrinologists do this by demonstrating pubertal levels of DHEA-S and other adrenal androgens, with prepubertal levels of gonadotropins and gonadal sex steroids.

Second, there is some evidence that premature adrenarche may indicate that there was an abnormality of the intrauterine energy environment and of intrauterine growth. As mentioned above, premature adrenarche occurs more often in children with intrauterine growth retardation and in overweight children. Some of these same studies have demonstrated that some girls who display premature adrenarche may continue to have excessive androgen levels in adolescence. This can result in hirsutism or menstrual irregularities due to anovulation, referred to as polycystic ovary syndrome.

Third, at least one report [7] from 2008 found an increased incidence of behavior and school problems in a group of children with premature adrenarche compared with an otherwise similar control group. To date, such a relationship has neither been confirmed nor explained and there are no obvious management implications.

Other primates

Adrenarche occurs in only a small number of primates, and only chimpanzees and gorillas show a pattern of adrenarche development similar to humans. [8]

See also

Related Research Articles

<span class="mw-page-title-main">Dehydroepiandrosterone</span> Chemical compound

Dehydroepiandrosterone (DHEA), also known as androstenolone, is an endogenous steroid hormone precursor. It is one of the most abundant circulating steroids in humans. DHEA is produced in the adrenal glands, the gonads, and the brain. It functions as a metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids both in the gonads and in various other tissues. However, DHEA also has a variety of potential biological effects in its own right, binding to an array of nuclear and cell surface receptors, and acting as a neurosteroid and modulator of neurotrophic factor receptors.

<span class="mw-page-title-main">Androgen</span> Any steroid hormone that promotes male characteristics

An androgen is any natural or synthetic steroid hormone that regulates the development and maintenance of male characteristics in vertebrates by binding to androgen receptors. This includes the embryological development of the primary male sex organs, and the development of male secondary sex characteristics at puberty. Androgens are synthesized in the testes, the ovaries, and the adrenal glands.

In medicine, precocious puberty is puberty occurring at an unusually early age. In most cases, the process is normal in every aspect except the unusually early age and simply represents a variation of normal development. There is early development of secondary sex characters and gametogenesis also starts earlier. Precocious puberty is of two types: true precocious puberty and pseudoprecocious puberty. In a minority of children with precocious puberty, the early development is triggered by a disease such as a tumor or injury of the brain.

Delayed puberty is when a person lacks or has incomplete development of specific sexual characteristics past the usual age of onset of puberty. The person may have no physical or hormonal signs that puberty has begun. In the United States, girls are considered to have delayed puberty if they lack breast development by age 13 or have not started menstruating by age 15. Boys are considered to have delayed puberty if they lack enlargement of the testicles by age 14. Delayed puberty affects about 2% of adolescents.

<span class="mw-page-title-main">Virilization</span> Biological development of male sex characteristics

Virilization or masculinization is the biological development of adult male characteristics in young males or females. Most of the changes of virilization are produced by androgens.

<span class="mw-page-title-main">Lipoid congenital adrenal hyperplasia</span> Medical condition

Lipoid congenital adrenal hyperplasia is an endocrine disorder that is an uncommon and potentially lethal form of congenital adrenal hyperplasia (CAH). It arises from defects in the earliest stages of steroid hormone synthesis: the transport of cholesterol into the mitochondria and the conversion of cholesterol to pregnenolone—the first step in the synthesis of all steroid hormones. Lipoid CAH causes mineralocorticoid deficiency in affected infants and children. Male infants are severely undervirilized causing their external genitalia to look feminine. The adrenals are large and filled with lipid globules derived from cholesterol.

<span class="mw-page-title-main">Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency</span> Medical condition

Congenital adrenal hyperplasia due to 3β-hydroxysteroid dehydrogenase deficiency is an uncommon form of congenital adrenal hyperplasia (CAH) resulting from a mutation in the gene for one of the key enzymes in cortisol synthesis by the adrenal gland, 3β-hydroxysteroid dehydrogenase (3β-HSD) type II (HSD3B2). As a result, higher levels of 17α-hydroxypregnenolone appear in the blood with adrenocorticotropic hormone (ACTH) challenge, which stimulates adrenal corticosteroid synthesis.

Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency is an uncommon form of congenital adrenal hyperplasia (CAH) resulting from a mutation in the gene CYP17A1, which produces the enzyme 17α-hydroxylase. It causes decreased synthesis of cortisol and sex hormones, with resulting increase in mineralocorticoid production. Thus, common symptoms include mild cortisol deficiency, ambiguous genitalia in men or amenorrhea at puberty in women, and hypokalemic hypertension. However, partial (incomplete) deficiency often has inconsistent symptoms between patients, and affected women may be asymptomatic except for infertility.

Pubarche refers to the first appearance of pubic hair at puberty and it also marks the beginning of puberty. It is one of the physical changes of puberty and can occur independently of complete puberty. The early stage of sexual maturation, also known as adrenarche, is marked by characteristics including the development of pubic hair, axillary hair, adult apocrine body odor, acne, and increased oiliness of hair and skin. The Encyclopedia of Child and Adolescent Health corresponds SMR2 with pubarche, defining it as the development of pubic hair that occurs at a mean age of 11.6 years in females and 12.6 years in males. It further describes that pubarche's physical manifestation is vellus hair over the labia or the base of the penis. See Table 1 for the entirety of the sexual maturity rating description.

Gonadarche refers to the earliest gonadal changes of puberty. In response to pituitary gonadotropins, the ovaries in females and the testes in males begin to grow and increase the production of the sex steroids, especially estradiol and testosterone. The ovary and testis have receptors, follicle cells and leydig cells, respectively, where gonadotropins bind to stimulate the maturation of the gonads and secretion of estrogen and testosterone. Certain disorders can result in changes to timing or nature of these processes.

<span class="mw-page-title-main">Thelarche</span> Beginning of development of the breasts in the female

Thelarche, also known as breast budding, is the onset of secondary breast development, often representing the beginning of pubertal development. It is the stage at which male and female breasts differentiate due to variance in hormone levels; however, some males have a condition in which they develop breasts, termed gynecomastia. Thelarche typically occurs between the ages of 8 and 13 years with significant variation between individuals. However, the initial growth of breast tissue occurs during fetal development.

Underarm hair, also known as axillary hair or armpit hair, is the hair in the underarm area (axilla).

<span class="mw-page-title-main">Endocrine gland</span> Glands of the endocrine system that secrete hormones to blood

The Endocrine system is a network of glands and organs located throughout the body. It’s similar to the nervous system in that it plays a vital role in controlling and regulating many of the body’s functions. Endocrine glands are ductless glands of the endocrine system that secrete their products, hormones, directly into the blood. The major glands of the endocrine system include the pineal gland, pituitary gland, pancreas, ovaries, testicles, thyroid gland, parathyroid gland, hypothalamus and adrenal glands. The hypothalamus and pituitary glands are neuroendocrine organs.

<span class="mw-page-title-main">Hyperandrogenism</span> Excess androgens (male-related hormones) in the body

Hyperandrogenism is a medical condition characterized by high levels of androgens. It is more common in women than men. Symptoms of hyperandrogenism may include acne, seborrhea, hair loss on the scalp, increased body or facial hair, and infrequent or absent menstruation. Complications may include high blood cholesterol and diabetes. It occurs in approximately 5% of women of reproductive age.

<span class="mw-page-title-main">Dehydroepiandrosterone sulfate</span> Chemical compound

Dehydroepiandrosterone sulfate, abbreviated as DHEA sulfate or DHEA-S, also known as androstenolone sulfate, is an endogenous androstane steroid that is produced by the adrenal cortex. It is the 3β-sulfate ester and a metabolite of dehydroepiandrosterone (DHEA) and circulates in far greater relative concentrations than DHEA. The steroid is hormonally inert and is instead an important neurosteroid and neurotrophin.

<span class="mw-page-title-main">Estrogen insensitivity syndrome</span> Medical condition

Estrogen insensitivity syndrome (EIS), or estrogen resistance, is a form of congenital estrogen deficiency or hypoestrogenism which is caused by a defective estrogen receptor (ER) – specifically, the estrogen receptor alpha (ERα) – that results in an inability of estrogen to mediate its biological effects in the body. Congenital estrogen deficiency can alternatively be caused by a defect in aromatase, the enzyme responsible for the biosynthesis of estrogens, a condition which is referred to as aromatase deficiency and is similar in symptomatology to EIS.

Infantile acne is a form of acne that begins in very young children. Typical symptoms include inflammatory and noninflammatory lesions, papules and pustules most commonly present on the face. No cause of infantile acne has been established but it may be caused by increased sebaceous gland secretions due to elevated androgens, genetics and the fetal adrenal gland causing increased sebum production. Infantile acne can resolve by itself by age 1 or 2. However, treatment options include topical benzyl peroxide, topical retinoids and topical antibiotics in most cases.

Puberty is the process of physical changes through which a child's body matures into an adult body capable of sexual reproduction. It is initiated by hormonal signals from the brain to the gonads: the ovaries in a female, the testicles in a male. In response to the signals, the gonads produce hormones that stimulate libido and the growth, function, and transformation of the brain, bones, muscle, blood, skin, hair, breasts, and sex organs. 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.

Adrenal steroids are steroids that are derived from the adrenal glands. They include corticosteroids, which consist of glucocorticoids like cortisol and mineralocorticoids like aldosterone, adrenal androgens like dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione (A4), and neurosteroids like DHEA and DHEA-S, as well as pregnenolone and pregnenolone sulfate (P5-S). Adrenal steroids are specifically produced in the adrenal cortex.

<span class="mw-page-title-main">Adrenopause</span> Decline in secretion and levels of adrenal androgens

Adrenopause is the decline in secretion and levels of adrenal androgens such as dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) from the zona reticularis of the adrenal glands with age. Levels of adrenal androgens start to increase around age 7 or 8 years (adrenarche), peak in early adulthood around age 20 to 25 years, and decrease at a rate of approximately 2% per year thereafter, eventually reaching levels of 10 to 20% of those of young adults by age 80 years. It is caused by the progressive apoptosis of adrenal androgen-secreting cells and hence involution of the zona reticularis. It is analogous to andropause in men and menopause in women, the abrupt or gradual decline in production of sex hormones from the gonads with age.

References

  1. 1 2 3 4 5 6 Mark A. Sperling (10 April 2014). Pediatric Endocrinology E-Book. Elsevier Health Sciences. pp. 485–. ISBN   978-1-4557-5973-6.
  2. 1 2 Mohammed Kalimi; William Regelson (13 July 2011). Dehydroepiandrosterone (DHEA): Biochemical, Physiological and Clinical Aspects. Walter de Gruyter. pp. 132–. ISBN   978-3-11-081116-2.
  3. ↑ Parker, LN (1991). "Adrenarche". Endocrinology and Metabolism Clinics of North America. 20 (1): 71–83. doi:10.1016/S0889-8529(18)30282-2. PMID   2029889.
  4. 1 2 Kenneth L. Becker (2001). Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. pp. 711–. ISBN   978-0-7817-1750-2.
  5. 1 2 3 A. Y. Elzouki; H. A. Harfi; H. Nazer; F. B. Stapleton; William Oh; R. J. Whitley (10 January 2012). Textbook of Clinical Pediatrics. Springer Science & Business Media. pp. 3681–. ISBN   978-3-642-02202-9.
  6. ↑ "Everything You Need to Know About Adrenarche: A Surge in Hormones That Happens Before Puberty". Parents. Retrieved 2019-12-31.
  7. ↑ Dom, Lorah D. (May 2008). "Differences in Endocrine Parameters and Psychopathology in Girls with Premature Adrenarche versus On-time Adrenarche". J Pediatr Endocrinol Metab. 21 (5): 439–448. doi:10.1515/jpem.2008.21.5.439. PMC   3677514 . PMID   18655525.
  8. ↑ Cutler Jr, GB; Glenn, M; Bush, M; Hodgen, GD; Graham, CE; Loriaux, DL (1978). "Adrenarche: a survey of rodents, domestic animals, and primates". Endocrinology. 103 (6): 2112–8. doi:10.1210/endo-103-6-2112. PMID   155005.
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