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PubMed1992

Neuroendocrine mechanism of onset of puberty. Sequential reduction in activity of inhibitory and facilitatory N-methyl-D-aspartate receptors.

In humans and in several animal species, puberty results from changes in pulsatile gonadotropin-releasing hormone (GnRH) secretion in the hypothalamus. In particular, the frequency of pulsatile GnRH secretion increases at the onset of puberty, as can be shown by using hypothalamic explants of male rats of 15 and 25 d. Previous observations from us and others suggested that the initiation of puberty could involve a facilitatory effect of excitatory amino acids mediated through N-methyl-D-aspartate (NMDA) receptors. We found that GnRH secretion could be activated through NMDA receptors only around the time of onset of puberty (25 d). The aim of this study was to clarify why this activation did not occur earlier (at 15 d) and could no longer be observed by the end of puberty (at 50 d). We studied GnRH secretion in the presence of MK-801, a noncompetitive antagonist of NMDA receptors or AP-5, a competitive antagonist. We showed that, in the hypothalamus of immature male rats (15 d), a highly potent inhibitory control of pulsatile GnRH secretion in vitro was mediated through NMDA receptors. These data were confirmed in vivo because administration of the antagonist MK-801 (0.001 mg/kg) to immature male rats resulted in early pubertal development. Onset of puberty (25 d) was characterized by the disappearance of that NMDA receptor-mediated inhibition, thus unmasking a facilitatory effect also mediated through NMDA receptors. During puberty, there was a reduction in activity of this facilitatory control which was no longer opposed by its inhibitory counterpart. We conclude that a sequential reduction in activity of inhibitory and facilitatory NMDA receptors provides a developmental basis for the neuroendocrine mechanism of onset of puberty.

Animals↗
PubMed1991

Changes in metabolites, metabolic hormones, and luteinizing hormone before puberty in Angus, Braford, Charolais, and Simmental heifers.

We determined changes in insulin, glucose, free fatty acids (FFA), growth hormone (GH), insulin-like growth factor I (IGF-I) and LH before puberty in Angus, Braford, Charolais, and Simmental heifers. Our primary objective was to identify metabolites and metabolic hormones that serve as metabolic cues for onset of puberty. Angus (n = 12). Braford (n = 7), Charolais (n = 9), and Simmental (n = 7) heifers were assigned at weaning (289 +/- 25 d of age; 264 +/- 23 kg) to open-sided pens with slotted floors, and they were fed a corn silage-concentrate diet formulated to provide gains of .91 kg/d. Puberty was defined as the 1st d (d 0) that serum progesterone (determined in blood samples collected at weekly intervals) exceeded 1 ng/ml. Blood samples were collected before and after feeding at 15-min intervals for 8 h at 21-d intervals before puberty in a subsample of heifers (at least five per breed). Angus and Simmental heifers weighed less and were younger (P less than .05) at puberty than Charolais and Braford heifers. Serum FFA before feeding and frequency of LH release increased (P less than .05) from d-40 +/- 3 to d-17 +/- 3 in all breeds. Conversely, concentrations of insulin were greater (P less than .05) at -40 than at -17 d from puberty in Angus, but not in Braford, Charolais, or Simmental heifers. Frequency of GH release was greater at d -40 than at d -17 in Angus heifers; however, in Braford and Charolais heifers frequency of GH release was greater at d -17 than at d -40. Concentrations of IGF-I (measured every 2 wk) increased linearly (P less than .07) from d -56 to 0 from puberty in Angus but not in other breeds. In conclusion, frequency of LH release and concentrations of FFA increased before puberty in all breeds; however, consistent changes in other metabolites and hormones were observed only in Angus heifers.

Age Factors↗
PubMed1991

Breed effects and heterosis in advanced generations of composite populations for puberty and scrotal traits of beef cattle.

Heterosis effects were evaluated in F1, F2, and F3 generations of females and in the F1, F2, and combined F3 and F4 generations of males in three composite populations of beef cattle. Traits included weight, height, and condition scores at different ages, percentage of females reaching puberty at 368, 410, and 452 d, adjusted age, and adjusted weight of females at puberty and scrotal circumference and paired testicular volume of males. Breed effects were evaluated for the nine parental breeds (Red Poll [R], Hereford [H], Angus [A], Limousin [L], Braunvieh [B], Pinzgauer [P], Gelbvieh [G], Simmental [S], and Charolais [C]) that contributed to the three composite populations (MARC I = 1/4 C, 1/4 B, 1/4 L, 1/8 H, 1/8 A; MARC II = 1/4 G, 1/4 S, 1/4 H, 1/4 A; and MARC III = 1/4 R, 1/4 P, 1/4 H, 1/4 A). Breed effects were significant for all traits evaluated. Heterosis was significant for weight, height, and condition score at all ages and for most measures of puberty in each generation of each composite and for the mean of the three composite populations. Heterosis for age at puberty was largely independent of heterosis effects on 368-d weight. Heterosis was significant for scrotal circumference and paired testicular volume in each generation of each composite and for the mean of the three composite populations. Heterosis effects on scrotal measurements are mediated both through heterosis effects on growth rate and through factors that are independent of growth rate. Correlation coefficients among breed group means and correlations of breed rank for scrotal measurements with puberty traits of females were greater than or equal to .88 (P less than .01) for all puberty traits except weight at puberty, which was not associated with scrotal measurements. There was close agreement in heterosis observed for most traits and expectation based on retained heterozygosity. These results support the hypothesis that heterosis in cattle for size, puberty, and scrotal measurement traits is due to dominance effects of genes.

Analysis of Variance↗
PubMed1995

Body composition of gilts at puberty.

The relationship between body composition and the occurrence of puberty was evaluated using 93 Yorkshire x Landrace gilts. At approximately 60 d of age gilts were purchased and placed in a heated confinement unit where they were housed for the duration of the study. Ad libitum access to feed was provided throughout the study. Gilts were moved, mixed, and initially exposed to mature boars at approximately 120 d of age to encourage the earliest possible occurrence of puberty. Empty body weights of water, fat, protein, and ash at puberty were estimated using a deuterium dilution technique and prediction equations developed for this gilt population. There was considerable variation in age, weight, and all measures of body composition at puberty. Gilts were 138 to 240 d old and weighted 64.9 to 150.8 kg. Backfat thickness ranged from 17.5 to 44.0 mm. Gilts were composed of 32.4 to 64.3 kg of water, 15.6 to 53.9 kg of fat, 9.03 to 20.56 kg of protein, and 1.24 to 3.10 kg of ash. The coefficient of variation for fat to lean ratio at puberty was 15.39%. Linear and quadratic regressions showed that lifetime (birth to puberty) growth rate was not related to age at puberty (P > .10). Based on the variation in body composition observed it was concluded that the occurrence of puberty in gilts given ad libitum access to feed during rearing and initially exposed to mature boars at approximately 120 d of age was not related to certain minimum threshold amounts of body tissues or to a specific rate at which body tissue reserves were accumulated.

Animals↗
PubMed1996

Incidence of precocious puberty in developing beef heifers.

The objectives of this study were to determine the incidence of precocious puberty and effect of exposure to a bull on the incidence of precocious puberty in beef heifers. The experiment was conducted using 120 heifers during 1990 and 1991. Heifer calves were randomly assigned to be pastured in the presence (n = 30 heifers/yr) or absence (n = 30 heifers/yr) of a bull starting at 140 +/- 14 d of age for the duration of the study. Heifers were 402 +/- 14 d of age at the time the study was completed. Blood samples were collected weekly to determine the age of onset, duration and cessation of luteal function. Heifers were considered to have exhibited a precocious puberty when the onset of luteal function was before 300 d of age. There was no effect of exposure to a bull on the incidence of precocious puberty, and therefore the data were pooled. The incidence of precocious puberty was greater (P < .02; X2 = 5.5) in 1990 (25.0%; 15 of 60) compared with 1991 (8.3%; 5 of 60). There was no effect of year on age of precocious puberty (194 +/- 12.4 d of age), duration of cyclic luteal function (65 +/- 10.5 d), or the age at resumption of anestrus (260 +/- 15.3 d of age). Precocious puberty does occur in developing beef heifers; as many as 25% of heifers have transient luteal function before 300 d of age. However, exposure to a bull has no effect on the incidence of precocious puberty.

Aging↗
PubMed2006

Effect of timing of feeding a high-concentrate diet on growth and attainment of puberty in early-weaned heifers.

Precocious puberty (<300 d of age) can be successfully induced in a majority of heifers with early weaning and continuous feeding of a high-concentrate diet. The objective of this experiment was to determine the relative effects of timing of feeding a high-concentrate diet on age at puberty in early-weaned heifers. Sixty crossbred Angus and Simmental heifer calves were weaned at 112 +/- 2 d of age and 155 +/- 3 kg of BW and were fed a receiving diet for 2 wk. Heifers were blocked by age and BW, and assigned randomly to receive a high-concentrate (60% corn; H) or control (30% corn; C) diet during phase 1 (mean age 126 to 196 d) and H or C during phase 2 (mean age 196 to 402 d), resulting in 4 treatments (HH, n = 15; HC, n = 15; CH, n = 15; and CC, n = 15). Blood samples were collected weekly beginning at a mean age of 175 d and assayed for progesterone concentration to determine age at puberty. After 56 d on the experimental diets, BW of heifers fed the H diet during phase 1 were greater (P < 0.05) than those of heifers fed the C diet (mean age of 182 d; treatment x mean age, P < 0.01). After 70 d on the new diets (mean age of 266 d), heifers fed the H diet during phase 2 reached heavier BW (P < 0.05) than heifers fed the C diet, when compared within phase 1 diet groups (HH > HC; CH > CC). Body weights in HC and CH treatments differed from a mean age of 169 through 238 d, after which BW did not differ between these treatments. The ADG over the entire experimental period was greatest for the HH treatment (1.2 +/- 0.04 kg/d; P < 0.05), followed by the HC and CH treatments (1.0 +/- 0.03 and 1.0 +/- 0.02 kg/d, respectively), which were not different, and the CC treatment gained the least (0.7 +/- 0.04 kg/d; P < 0.05). Precocious puberty occurred in 67, 47, 47, and 20% of heifers in the HH, HC, CH, and CC treatments, respectively (HH > CC; P < 0.05). Mean age at puberty for the HH and HC treatments (271 +/- 17 and 283 +/- 17 d of age, respectively) was earlier (P < 0.05) than for the CC treatment (331 +/- 11 d of age). Age at puberty in the CH treatment (304 +/- 13 d of age) was intermediate to and not different from the other treatments. Heifers fed the H diet during phase 1 attained puberty earlier (P < 0.05) than heifers fed the C diet during phase 1. In conclusion, increasing dietary energy intake in early-weaned heifers, through feeding a high-concentrate diet from 126 to 196 d of age, decreased age at puberty regardless of the diet fed after 196 d of age.

Animal Feed↗
PubMed1982

Puberty in beef bulls: acrosome morphology and semen quality in bulls of different breeds.

Semen characteristics were evaluated every 2 wk from 7 through 13 mo of age in 31 beef bulls representing six breed groups (Hereford, Angus, Hereford x Angus crossbreeds, Angus x Hereford crossbreds, Red Poll and Brown Swiss). Breeds differed in age at puberty, defined as the age at which an ejaculate was first obtained that contained a minimum of 50 x 10(6) total spermatozoa with at least 10% progressive motility (Hereford, 326 +/- 9 d; Angus, 295 +/- 4 d; Hereford x Angus, 300 +/- 8 d; Angus x Hereford, 296 +/- 9 d; Red Poll, 283 +/- 9 d and Brown Swiss, 264 +/- 9 d). Significant breed differences also were observed in concentration of spermatozoa, progressive motility, seminal protein concentration, abnormal spermatozoa and acrosomal morphology. Considerable variation was observed for the majority of pubertal traits among the 31 bulls, indicating that differences in stage of pubertal development existed among and within breeds of beef bulls between 7 and 13 mo of age. However, adjustment of data to age at puberty negated breed differences (P greater than .10), indicating that the pubertal patterns of change occurring in each semen characteristic were similar for the breeds evaluated. Concentration of spermatozoa, progressive motility, seminal protein concentration, percentage spermatozoa with normal head and tail morphology and percentage spermatozoa with normal acrosomal morphology increased (P less than .01) from puberty through 16 wk after puberty in all bulls and all breds. During the first 6 wk after puberty, rapid increases (P less than .01) were observed in percentage spermatozoa exhibiting normal head morphology (excluding acrosomes) and progressive motility, and a rapid decrease (P less than .01) was observed in percentage spermatozoa with proximal cytoplasmic droplets, with values at +6 wk approaching those reported for mature bulls. Percentage spermatozoa with normal acrosomal morphology and concentration of spermatozoa improved more slowly and had not reached mature levels by 16 wk after puberty. Because age at puberty varied by 62 d among breeds and 88 d among bulls and important characteristics of semen quality improved slowly after puberty, careful evaluation of the stage of pubertal development in individual bulls is recommended before selecting young bulls for natural breeding or artificial insemination. Additional investigations are needed to define the patterns of pubertal development through sexual maturity in beef bulls and to establish relationships to fertility.

Acrosome↗
PubMed1982

Onset of puberty in heifers of diverse beef breeds and crosses.

Puberty traits of straightbred and crossbred heifers (n = 301) were evaluated under pasture conditions. Breed groups represented were straightbred Hereford and Red Poll, reciprocal crosses of these two breeds, Angus X Hereford, Angus X Charolais-Cross, Brahman X Hereford and Brahman X Angus. Breed group was an important (P less than .01) source of variation in heifer weights and in age at puberty. Straight-bred Red Poll and Red Poll cross heifers were youngest at puberty, Angus X Hereford and Angus X Charolais-Cross were intermediate, and straightbred Hereford and Brahman crosses were oldest at the onset of puberty. At the beginning of their first mating season at 19.5 mo of age, 96% of the straightbred Red Polls, 95% of Red Poll crosses, 81% of Angus X Herefords, 89% of Angus X Charolais-Crosses, 68% of straightbred Herefords, 48% of Brahman X Herefords and 74% of the Brahman X Angus had attained puberty. Results of a diallel analysis of Hereford-Red Pool matings indicated that maternal influence of the Red Poll breed was superior (P less than .01) to Herefords for body weight up to 24 mo of age and incidence of puberty at 11.5 mo. Red Polls also exceeded Herefords in direct effects for puberty percentage at 11.5, 15 and 19.5 mo of age. Heterosis was significant for puberty percentage and weight. Breed group differences in pregnancy rate at 24 mo were not significantly.

Animals↗
PubMed1983

Estimating the impact of management decisions on the occurrence of puberty in beef heifers.

Age and weight at puberty in beef heifers were hypothesized to be jointly dependent random variables with the joint distribution conditional upon values of exogenous variables such as breed, date of birth and postweaning rate of gain. A statistical model was specified that tested the joint dependency hypothesis and measured the impact of variation in the explanatory variables on puberty. Model parameters were estimated by two-stage least-squares procedures from data on 556 beef heifers: 190 raised at the Northern Agricultural Research Center (NARC), Havre, Montana and 366 raised at the Livestock and Range Research Station (LARRS), Miles City, Montana. Results did not support the hypothesis that age and weight at puberty were jointly dependent; weight at puberty did depend upon age at puberty, but age at puberty did not depend upon weight at puberty when postweaning level of nutrition was known. Thus, the appropriate probability distribution was a conditional univariate probability distribution on age. Results were consistent with past research in that breed and breed-cross differences existed, and heifers heavier at weaning and fed higher levels of postweaning nutrition reached puberty at an earlier age and heavier weight.

Age Factors↗
PubMed1987

Influence of biostimulation by mature bulls on occurrence of puberty in beef heifers.

The objective of this study was to determine if biostimulation of prepuberal beef heifers by mature bulls would alter proportions of heifers exhibiting puberty, or age or weight at puberty. Angus (A), A X Hereford (H) and Tarentaise X HA heifers (n = 103) were stratified by age and weight within breed-type and location of birth and allotted randomly to the following treatments: 1) heifers exposed to mature bulls (T1; n = 52) or 2) heifers isolated from bulls (T2; n = 51). At the start of the experiment, heifers in T1 and T2 were 287 +/- 2 and 286 +/- 2 d of age, respectively. Male-to-female ratio for T1 was 1:26. Heifers in T1 and T2 were maintained in drylots separated by .5 km. Heifers were observed for estrus twice daily for 152 d. Puberty was characterized by the following criteria: 1) behavioral estrus, 2) presence of a palpable corpus luteum (d 9; estrus = d 0) and 3) a rise in serum progesterone above 1 ng/ml (d 9). Proportions of heifers reaching puberty by 11, 12, 13, 14 and 15 mo of age did not differ (P greater than .10) between treatments. Percentages of heifers reaching puberty by the end of the experiment were 84 and 89% for T1 and T2, respectively. Age and weight at puberty did not differ (P greater than .10) between treatments and averaged 370 +/- 7 d and 293 +/- 4 kg, respectively. Results from this experiment indicated that presence of mature bulls did not alter proportions of beef heifers reaching puberty, or age and weight at puberty.

Animals↗
PubMed1995

Endocrine basis for puberty in heifers and ewes.

Maturation processes that culminate in puberty and sexual maturity are initiated before birth, continue through prepuberty (> 50 days before puberty) and peripuberty (50 days before puberty) and are completed early after puberty. The hypothalamus is the primary site of change during transition to sexual maturity. Maturation of the hypothalamus results from decreased negative feedback of oestradiol that leads to increased frequency of release of LH pulses. Increased tonic release of LH pulses during sexual maturation is the primary endocrine factor that regulates the onset of puberty in ewe lambs and heifers. Increased frequency of release of LH pulses enhances development of ovarian follicles which produce enough oestradiol to induce behavioural oestrus and a preovulatory surge of gonadotrophins. In later stages of peripuberty, ovulation or luteinization of follicles results in transient increases in progesterone for shorter periods than is typical for luteal phases of the oestrous cycle of mature ewes and cows. Transient increases in progesterone are not generally preceded by behavioural oestrus. After the demise of the transient luteal structures, puberty is attained with occurrence of the first behavioural oestrus that is accompanied by ovulation and development of a corpus luteum with a typical lifespan. At puberty, all components of the hypothalamic-pituitary-ovarian axis are in place for oestrous cycles to be expressed. Factors that can influence the pubertal rise in release of LH pulses are genotype, gender, season of year when pubertal age is attained, growth or nutritional intake, social cues or treatment with exogenous progestins. Sexual maturation continues after puberty with an enhanced probability of pregnancy occurring from actions of ovarian steroids at the uterus.

Animals↗
PubMed1989

Puberty in the syndrome of septo-optic dysplasia.

To determine the patterns of puberty associated with the syndrome of septo-optic dysplasia, 13 older children with optic nerve hypoplasia and hypopituitarism were studied. Three patterns of puberty were observed: early, rapidly progressive puberty (group 1); appropriately timed puberty (group 2); and delayed puberty associated with gonadotropin deficiency (group 3). In the six patients in group 1, puberty began at an early bone age. Pubertal changes progressed rapidly and the bone age advanced faster than chronologic time so that, despite a normal to increased growth rate, growth potential was lost. Group 2 comprised three patients with multiple pituitary hormone deficiencies but without gonadotropin deficiency who had the timing and progression of puberty expected in hypopituitarism. The four patients in group 3, all with multiple pituitary hormone deficiencies, had gonadotropin deficiency requiring sex steroid replacement.

Adolescent↗
PubMed1996

Serum concentrations of free and total insulin-like growth factor-I, IGF binding proteins -1 and -3 and IGFBP-3 protease activity in boys with normal or precocious puberty.

OBJECTIVE: Circulating IGF-I and IGF binding protein-3 (IGFBP-3) levels both increase in puberty where growth velocity is high. The amount of free IGF-I is dependent on the IGF-I level and on the concentrations of the specific IGFBPs. Furthermore, IGFBP-3 proteolysis regulates the bioavailability of IGF-I. However, the concentration of free IGF-I and possible IGFBP-3 proteolytic activity in puberty has not previously been studied. SUBJECTS AND MEASUREMENTS: We investigated serum levels of easily dissociable IGF-I concentrations and ultrafiltrated free IGF-I levels by specific assays in 60 healthy boys and in 5 boys with precocious puberty before and during GnRH agonist treatment. In addition, total serum IGF-I, IGFBP-1 and IGFBP-3 levels as well as IGFBP-3 protease activity were determined. RESULTS: Free (dissociable and ultrafiltrated) IGF-I concentrations were significantly higher in pubertal boys than in prepubertal children and correlated significantly with the molar ratio between IGF-I and IGFBP-3 (r = 0.69, P < 0.0001 and r = 0.54, P = 0.0008, respectively) and inversely with IGFBP-1 (r = -0.47, P < 0.0001 and r = -0.43, P = 0.0003, respectively). Multiple regression analysis suggested that IGFBP-3 level, and not IGFBP-1, was the major determinant of the free IGF-I serum level in normal boys. Free IGF-I levels were elevated in boys with precocious puberty and decreased during GnRH treatment. IGFBP-3 proteolysis was constant throughout puberty (mean 20%). CONCLUSIONS: We conclude that easily dissociable and ultrafiltrated free IGF-I serum levels are increased in boys with normal and precocious puberty and suggest that the increased free IGF-I serum concentration in puberty primarily reflects changes in total concentrations of IGF-I and IGFBPs secondary to increased GH secretion, but that it is not influenced by changes in IGFBP-3 proteolysis.

Adolescent↗
PubMed2005

Secular trend of timing of puberty.

During the last decades, a secular trend of growth and timing of puberty occurred consisting of increased adult height and earlier onset of puberty. In The Netherlands although the most recent survey showed an increase of final height again, the timing of puberty onset appears to level off, and in boys pubertal onset was even slightly retarded. Different findings were reported from the United States, where a strong advancement of the onset of puberty was observed in both white and black girls, although the effect was more evident in black girls. Timing of puberty follows a familial pattern and therefore seems to be controlled by genetic factors, whereas environmental factors may influence and mediate the genetic regulation. Environmental factors such as nutritional status, chronic diseases, migration to a healthy environment, frequent infectious diseases, pollution and exposure to insecticides are all thought to influence the endocrine regulation status and therefore differentiation and development of endocrine organs. In this chapter, the physiologic mechanisms of puberty onset with the different regulatory aspects, as well as pathologic processes interfering with the onset of puberty will be discussed.

Adolescent↗
PubMed2005

Constitutional delay of growth and puberty: from presentation to final height.

This retrospective study evaluated clinical characteristics of patients with constitutional delay of growth and puberty (CDGP) at presentation, during puberty and at final height. The records of 151 children (105 boys, 46 girls) with CDGP were reviewed and the results were evaluated with respect to findings in healthy Turkish schoolchildren. CDGP was twice as frequent in boys as in girls. Height and weight deficit and short sitting height of the children were evident at presentation and continued up to final height. Mean age of onset of puberty was retarded by 2.5 years in girls and by 3 years in boys. The time between onset of puberty and pubertal growth spurt was shorter in both girls and boys than in the controls. Peak growth velocity was compromised in both girls and boys. Forty-one patients (30 boys, 11 girls) reached final height (FH). Mean FH was shorter than both target height and predicted adult height. The Bayley-Pinneau method was found to be a better predictor of FH than either the Tanner-Whitehouse method or target height. FH also showed correlation with the father's height. There was no effect of testosterone treatment on final height. Height deficit at onset of puberty, shorter duration between onset of puberty and pubertal growth spurt, compromised peak growth velocity and short upper segment due to delayed puberty, are findings which may explain the decreased final height of children with CDGP.

Adolescent↗
PubMed1980

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

We measured the production rates and metabolic clearance, disappearance and excretion rates of FSH and LH as well as plasma testosterone and delta 4-androstenedione 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.

Adolescent↗
PubMed1991

Drug treatment in precocious puberty.

Precocious puberty, as defined by the onset of pubertal development before the age of 8 years in girls or 9 years in boys, can be classified into central and peripheral aetiologies. Central precocious puberty (CPP) results from early activation of the hypothalamic-pituitary-gonadal axis and has similar physical and hormonal characteristics to normal puberty. Extrapituitary gonadotrophin secretion or independent sex steroid secretion results in peripheral precocious puberty (PPP). Precocious puberty is characterised by rapid growth and advancement of skeletal age. The skeletal advancement is greater than the growth increase, so that final adult height is compromised. Long-acting gonadotrophin releasing hormone (GnRH) agonists are the current therapy of choice for central precocious puberty, having demonstrated effectiveness in halting the precocious development associated with this condition with minimal side effects. GnRH agonists are not effective as therapy for peripheral precocious puberty, but a number of other agents have been used with some success. These include androgen antagonists, testolactone, ketoconazole, and medroxyprogesterone acetate. The use of GnRH agonists has been associated with an increase in predictions of final height; however, continuing studies in treated cohorts are necessary to determine the true benefit of any of these agents on increasing ultimate height.

Adolescent↗
PubMed2004

Pineal attrition, loss of cognitive plasticity, and onset of puberty during the teen years: is it a modern maladaptation exposed by evolutionary displacement?

Cognitive plasticity, a developmental trait that promotes acquisition of complex skills such as language or playing musical instruments, diminishes substantially during puberty. The loss of plasticity has been attributed to surge of sex steroids during adolescence, but the phenomenon remains poorly understood. We hypothesize that pineal involution during puberty may contribute to plasticity decay. The pineal gland produces melatonin, the level of which declines dramatically during onset of puberty. Emerging evidence suggest that melatonin may modulate cognitive plasticity, independent of the effects of sex steroids, and low sex steroids and high melatonin may be simultaneously required to maintain cognitive plasticity. Potential mechanisms by which melatonin may modulate plasticity are examined within the sleep and hippocampal long-term potentiation frameworks. Implications for psychiatric conditions that involve sleep disorders and learning dysfunctions such as schizophrenia and autism are discussed, and the potential adaptive roles of postprandial and postcoital sleep are explored. From the Darwinian perspective, development and reproductive maturity may represent distinct phases that require tailored cognitive strategies to maximize fitness. While cognitive flexibility and susceptibility to new skills may be paramount during development, reduced cognitive flexibility and increased cognitive determinism may enable more efficient responses to stimuli during adulthood. Thus, cognitive plasticity and cognitive determinism may represent trade-off adaptations and different dimensions of intelligence. The decline of plasticity and emergence of puberty during the second decade may be relics of prehistoric times when the human lifespan was short and the environment was relatively simple and static. Today, when the environment is more complex and dynamic, and humans are living far longer, the early obsolescence of plasticity during puberty may represent a Darwinian inefficiency exposed by evolutionary displacement. Regulation of plasticity may be a systemic phenomenon, as exemplified by the association of learning disability with allergic conditions, a form of immune plasticity dysfunction. Ramifications for other plastic functions that decline during puberty such as wound healing and hyaline cartilage regeneration are explored. Like the plasticity of immunity and cognition, the plasticity of hyaline cartilage during youth may enable hosts to respond to ecologic opportunities and generate the optimally adapted adult phenotype. Pineal involution may represent a potential target for therapeutic extension or restoration of plasticity after puberty. Extending plasticity may have far-reaching consequences for human evolution.

Adolescent↗