Normal Sexual Development and Puberty

2021 ◽  
Author(s):  
Amanda French
Keyword(s):  
Sexual Development ◽  
Sex Steroids ◽  
Pubertal Development ◽  
Follicle Stimulating Hormone ◽  
Growth Spurt ◽  
Delayed Puberty ◽  
Health Issues ◽  
Reproductive Axis ◽  
Physical Changes ◽  
End Of Puberty

Puberty is the hormonally mediated process of physical changes that occur during the transition of childhood to adulthood.   Activation of the hypothalamic-pituitary-gonadal axis triggers the onset of puberty. Gonadotropin hormone-releasing hormone (GnRH) is the major regulator of the reproductive axis.  GnRH stimulates the anterior pituitary gland to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which in turn activate the gonads to produce sex steroids. Thelarche is stimulated by estrogen and is usually the first sign of puberty in girls. Adrenarche, although associated temporally with puberty, is mediated by the adrenal cortex and is unrelated to pubertal maturation. A growth spurt occurs mid-puberty.  Menarche, usually occurring 2-3 years after thelarche, is considered the end of puberty. After menarche, only about 1-2 additional inches of height are accrued.  Understanding what is considered the normal timeline of sexual development allows better recognition of precocious or delayed puberty, both of which may be associated with serious underlying health issues This review contains 4 tables, 5 figures, and 29 references. Keywords: puberty, pubertal development, hypothalamic-pituitary-gonadal axis, thelarche, menarche, normal sexual development

scholarly journals Should 45,X/46,XY boys with no or mild anomaly of external genitalia be investigated and followed up?

2018 ◽  
Vol 179 (3) ◽  
pp. 181-190 ◽  
Author(s):  
Laurence Dumeige ◽  
Livie Chatelais ◽  
Claire Bouvattier ◽  
Marc De Kerdanet ◽  
Capucine Hyon ◽  
...  
Keyword(s):  
Cell Function ◽  
Pubertal Development ◽  
External Genitalia ◽  
Growth Spurt ◽  
Normal Male ◽  
Early Management ◽  
Abnormal Growth ◽  
Renal Malformations ◽  
Male Phenotype ◽  
End Of Puberty

Objective Few studies of patients with a 45,X/46,XY mosaicism have considered those with normal male phenotype. The purpose of this study was to evaluate the clinical outcome of 45,X/46,XY boys born with normal or minor abnormalities of external genitalia, notably in terms of growth and pubertal development. Methods Retrospective longitudinal study of 40 patients followed between 1982 and 2017 in France. Results Twenty patients had a prenatal diagnosis, whereas 20 patients had a postnatal diagnosis, mainly for short stature. Most patients had stunted growth, with abnormal growth spurt during puberty and a mean adult height of 158 ± 7.6 cm, i.e. −2.3 DS with correction for target height. Seventy percent of patients presented Turner-like syndrome features including cardiac (6/23 patients investigated) and renal malformations (3/19 patients investigated). Twenty-two patients had minor abnormalities of external genitalia. One patient developed a testicular embryonic carcinoma, suggesting evidence of partial gonadal dysgenesis. Moreover, puberty occurred spontaneously in 93% of patients but 71% (n = 5) of those evaluated at the end of puberty presented signs of declined Sertoli cell function (low inhibin B levels and increased FSH levels). Conclusion This study emphasizes the need to identify and follow-up 45,X/46,XY patients born with normal male phenotype until adulthood, as they present similar prognosis than those born with severe genital anomalies. Currently, most patients are diagnosed in adulthood with azoospermia, consistent with our observations of decreased testicular function at the end of puberty. Early management of these patients may lead to fertility preservation strategies.

Precocious and delayed puberty. Studies of FSH and LH production and metabolism

1980 ◽  
Vol 94 (4) ◽  
pp. 475-479 ◽  
Author(s):  
Salvatore Raiti ◽  
Noel K. Maclaren ◽  
F. A. Akesode
Keyword(s):  
Sexual Development ◽  
The Other ◽  
Delayed Puberty ◽  
Plasma Testosterone ◽  
Metabolic Clearance ◽  
Early Puberty ◽  
Hypogonadotrophic Hypogonadism ◽  
Constitutional Delay ◽  
Excretion Rates ◽  
End Of Puberty

Abstract. We measured the production rates and metabolic clearance, disappearance and excretion rates of FSH and LH as well as plasma testosterone and Δ4androstenedione in males with precocious and delayed puberty. In precocious puberty, we found modestly elevated FSH production early in puberty, reaching adult levels by midpuberty and remaining constant thereafter. LH production was low early in puberty, reached high levels at midpuberty and then fell. The plasma testosterone concentrations paralleled the changes in LH. This suggests that moderate FSH production is achieved by early puberty and adult levels are reached by midpuberty. On the other hand LH production is low early in puberty, reaches high levels by midpuberty and then falls again towards the end of puberty. Constitutional delay in sexual development probably consists of several syndromes due either to a delay in LH production or to FSH production or to both. One patient with hypogonadotrophic hypogonadism was also studied. He showed relatively normal LH production but very low FSH production.

The Interaction of Pubertal and Psychosocial Development During Adolescence

1991 ◽  
Vol 12 (8) ◽  
pp. 249-255
Author(s):  
Iris F. Litt
Keyword(s):  
Psychosocial Development ◽  
Developmental Process ◽  
Pubertal Development ◽  
Breast Development ◽  
Growth Spurt ◽  
Sex Characteristics ◽  
Hormonal Changes ◽  
Secondary Sex Characteristics ◽  
Is Development ◽  
Physical Changes

During the second decade of life, the physical changes of puberty interact with those of psychosocial and cognitive development to forge the young adult, who often bears little resemblance to the same individual as a child. This article reviews those elements of the developmental process that have an impact on the physician's ability to understand and care for the adolescent patient. PUBERTY Endocrine Changes Release of inhibition on the hypothalamus unleashes an outpouring of releasing hormones, which stimulate the secretion of gonadotropins and growth hormone by the pituitary. These are produced in a sleep-augmented, pulsatile fashion that characterizes the onset of pubertal development. As a result, within the few years between the onset and completion of puberty, levels of estradiol increase eightfold in females, and levels of testosterone increase 18-fold in males. These hormonal changes stimulate the growth spurt and development of secondary sex characteristics. Development of Secondary Sex Characteristics Breast Development. In females, one of the earliest signs of puberty is development of the breast bud. The subsequent progression of breast development is orderly and predictable, thus forming one of the bases for the categorization in females of the stages of puberty, often referred to as Tanner stages or SMRs (sex maturity ratings).

Evaluating the four most important salivary sex steroids during male puberty: testosterone best characterizes pubertal development

2019 ◽  
Vol 32 (3) ◽  
pp. 287-294
Author(s):  
Andreas Krebs ◽  
Karoline Dickhuth ◽  
Rebekka Mumm ◽  
Bernhard Stier ◽  
Jürgen Doerfer ◽  
...  
Keyword(s):  
Sex Steroids ◽  
Pubertal Development ◽  
Rank Correlation ◽  
Dehydroepiandrosterone Sulfate ◽  
Pubic Hair ◽  
Enzyme Linked Immunosorbent Assay ◽  
Pubertal Maturation ◽  
Maturation Stages ◽  
17 Hydroxyprogesterone ◽  
Physical Changes

Abstract Background During pubertal development in healthy boys, increased levels of different sex steroids occur which are responsible for sexual maturation and physical changes. However, relationships between various sex hormones and pubertal development stages have not been sufficiently studied. Methods The investigation included 165 normal boys (mean age 12.7±2.8 years, mean body mass index [BMI] 19.6±4.2 kg/m2). Pubic hair (PH) stages were stratified by Tanner and testicular volume (TV) by means of the Prader orchidometer and assigned to the prepubertal, pubertal and postpubertal development phase. Four different sex steroids (testosterone [TE], dehydroepiandrosterone [DHEA]/dehydroepiandrosterone-sulfate [DHEAS], androstenedione (AE), 17-hydroxyprogesterone [17-OHP]) were measured in saliva by enzyme-linked immunosorbent assay (ELISA) and as serum total steroids by different assays (radioimmunoassay [RIA], chemiluminescence immunoassay [CLIA], electrochemiluminescence immunoassay [ECLIA]). Validation of saliva-based ELISA tests included data related to inter- and intra-assay coefficients of variation (CVs), recovery and linearity. Results Using Spearman rank correlation, salivary steroids significantly correlated (p<0.001) with pubertal development: TE (TV r=0.74 and PH stages r=0.72), DHEA (r=0.58 and 0.62), AE (r=0.38 and 0.45) and 17-OHP (r=0.42 and 0.43). Correlations between salivary and serum concentrations of steroids were also statistically significant (p<0.001). Binomial logistic regression analysis revealed significant correlations between salivary TE and pubertal maturation during the development phases of prepuberty-puberty and puberty-postpuberty. Inclusion of further salivary steroids did not improve analysis results. Conclusions Salivary TE permits a good non-invasive characterization of pubertal maturation stages. The consideration of further salivary sex steroids did not improve diagnostic accuracy.

scholarly journals Update on the etiology, diagnosis and therapeutic management of sexual precocity

2008 ◽  
Vol 52 (1) ◽  
pp. 18-31 ◽  
Author(s):  
Vinicius Nahime Brito ◽  
Ana Claudia Latronico ◽  
Ivo J. P. Arnhold ◽  
Berenice Bilharinho Mendonça
Keyword(s):  
Precocious Puberty ◽  
Sex Steroids ◽  
Therapeutic Option ◽  
Receptor Gene ◽  
Pubertal Development ◽  
Protein A ◽  
Activating Mutations ◽  
Sexual Precocity ◽  
Gonadotropic Axis ◽  
Hormonal Evaluation

Precocious puberty is defined as the development of secondary sexual characteristics before the age of 8 years in girls and 9 years in boys. Gonadotropin-dependent precocious puberty (GDPP) results from the premature activation of the hypothalamic-pituitary-gonadal axis and mimics the physiological pubertal development, although at an inadequate chronological age. Hormonal evaluation, mainly through basal and GnRH-stimulated LH levels shows activation of the gonadotropic axis. Gonadotropin-independent precocious puberty (GIPP) is the result of the secretion of sex steroids, independently from the activation of the gonadotropic axis. Several genetic causes, including constitutive activating mutations in the human LH-receptor gene and activating mutations in the Gs protein a-subunit gene are described as the etiology of testotoxicosis and McCune-Albright syndrome, respectively. The differential diagnosis between GDPP and GIPP has direct implications on the therapeutic option. Long-acting gonadotropin-releasing hormone (GnRH) analogs are the treatment of choice in GDPP. The treatment monitoring is carried out by clinical examination, hormonal evaluation measurements and image studies. For treatment of GIPP, drugs that act by blocking the action of sex steroids on their specific receptors (cyproterone, tamoxifen) or through their synthesis (ketoconazole, medroxyprogesterone, aromatase inhibitors) are used. In addition, variants of the normal pubertal development include isolated forms of precocious thelarche, precocious pubarche and precocious menarche. Here, we provide an update on the etiology, diagnosis and management of sexual precocity.

scholarly journals Redundancy in the central tachykinin systems safeguards puberty onset and fertility

2018 ◽  
Author(s):  
Silvia León ◽  
Chrysanthi Fergani ◽  
Rajae Talbi ◽  
Serap Simavli ◽  
Caroline A. Maguire ◽  
...  
Keyword(s):  
Substance P ◽  
Reproductive Success ◽  
Sex Steroids ◽  
Delayed Puberty ◽  
Neurokinin A ◽  
Neurokinin B ◽  
Female Mice ◽  
Gnrh Release ◽  
Lh Release ◽  
Puberty Onset

ABSTRACTThe tachykinin neurokinin B (NKB, Tac2) is critical for GnRH release. NKB signaling deficiency leads to infertility in humans. However, some patients reverse this hypogonadism resembling the fertile phenotype of Tac2KO and Tacr3KO (encoding NKB receptor, NK3R) mice despite the absence of NKB signaling. Here, we demonstrate that in the absence of NKB signaling, other tachykinins (substance P and neurokinin A [NKA], encoded by Tac1) may take over to preserve fertility. The complete absence of tachykinins in Tac1/Tac2KO mice leads to delayed puberty onset in both sexes and infertility in 80% of females (but not males), in contrast to the 100% fertile phenotype of Tac1KO and Tac2KO mice separately. Furthermore, we demonstrate that NKA controls puberty onset and LH release through NKB-independent mechanisms in the presence of sex steroids and NKB-dependent mechanisms in their absence. In summary, tachykinins interact in a coordinated manner to ensure reproductive success in female mice.

Precocious Puberty: Diagnosis, Evaluation, and Management

1993 ◽  
Vol 14 (9) ◽  
pp. 336-367
Keyword(s):  
The United States ◽  
Gonadotropin Releasing Hormone ◽  
Growth Spurt ◽  
Transitional Stage ◽  
Pubertal Growth Spurt ◽  
Adrenal Androgen ◽  
Secondary Sexual Characteristics ◽  
Pubertal Growth ◽  
Sexual Characteristics ◽  
Physical Changes

Puberty is a transitional stage associated with many changes, both physical and emotional. The endocrinologic changes, consisting of two processes, gonadarche and adrenarche, result in the development of secondary sexual characteristics and the pubertal growth spurt. Gonadarche, the maturation of the gonads, is initiated by the episodic pulsatile secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus. Adrenarche refers to the increase in adrenal androgen secretion (the mechanism responsible for this is unknown). Both of these processes cause an increase in sex steroid secretion, which results in the physical changes of puberty. In the United States, normal puberty occurs between 8 to 13 years in girls and 9 to 14 years in boys.

MiR-664-2 impacts pubertal development in a precocious-puberty rat model through targeting the NMDA receptor-1†

2019 ◽  
Vol 100 (6) ◽  
pp. 1536-1548 ◽  
Author(s):  
Minda Ju ◽  
Liu Yang ◽  
Jing Zhu ◽  
Zhejun Chen ◽  
Mizhen Zhang ◽  
...  
Keyword(s):  
Precocious Puberty ◽  
Bioinformatics Analysis ◽  
Pubertal Development ◽  
Follicle Stimulating Hormone ◽  
Gonadotropin Releasing Hormone ◽  
Untranslated Regions ◽  
Vaginal Opening ◽  
Protein Levels ◽  
Pulsatile Gnrh ◽  
Puberty Onset

Abstract Precocious puberty (PP) commonly results from premature activation of the hypothalamic–pituitary–gonadal axis (HPGA). Gonadotropin-releasing hormone (GnRH) is the initial trigger for HPGA activation and plays an important role in puberty onset. N-methyl-D-aspartate (NMDA) can promote pulsatile GnRH secretion and accelerates puberty onset. However, the mechanism of N-methyl-D-aspartate receptors (NMDARs) in PP pathogenesis remains obscure. We found that serum GnRH, luteinizing hormone (LH), follicle-stimulating hormone (FSH), estrogen (E2) levels, hypothalamic NMDAR1, and GnRH mRNA expression peaked at the vaginal opening (VO) day. Next, the hypothalamic NMDAR1 mRNA and protein levels in rats treated with danazol, a chemical commonly effecting on the reproductive system, were significantly increased at the VO day (postnatal day 24) compared to controls, accompanied by enhanced serum GnRH, LH, FSH, and E2 levels. Further, microRNA-664-2 (miR-664-2) was selected after bioinformatics analysis and approved in primary hypothalamic neurons, which binds to the 3′-untranslated regions of NMDAR1. Consistently, the miR-664-2 expression in hypothalamus of the Danazol group was decreased compared to Vehicle. Our results suggested that attenuated miR-664-2 might participate in PP pathogenesis through enhancing the NMDAR1 signaling.

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