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Role of Environmental Factors in the Timing of Puberty

Role of Environmental Factors in the Timing of Puberty

Puberty-timing measures have historically been used as indicators of adequate nu- trition and growth. More recently, these measures have been examined in relation to exposure to estrogenic or antiandrogenic agents, as well as other environmental factors. The scientific community has debated whether puberty timing is occurring earlier today than in the mid-1900s in the United States and, if so, whether envi- ronmental factors play a role; however, no one has asked a multidisciplinary panel to resolve this question. Thus, a multidisciplinary expert panel jointly sponsored by the US Environmental Protection Agency, the National Institute of Environmental Health Sciences, and Serono Symposia International was convened to examine the evidence of a secular trend, identify potential environmental factors of concern, and identify research needs regarding environmental factors and puberty timing at “The Role of Environmental Factors on the Timing and Progression of Puberty” workshop. The majority of the panelists concluded that the girls’ data are suffi- cient to suggest a secular trend toward earlier breast development onset and menarche from 1940 to 1994 but that the boys’ data are insufficient to suggest a trend during this same period. The weight-of-the-evidence evaluation of human and animal studies suggest that endocrine-disrupting chemicals, particularly the estrogen mimics and antiandrogens, and body fat are important factors associated in altered puberty timing. A change in the timing of puberty markers was considered adverse from a public health perspective. The panel recommended research areas to further our understanding of the relationships among environ- mental factors, puberty-timing outcomes, and other reproductive and adult dis- ease at the individual and population levels.
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Link Between Body Fat and the Timing of Puberty

Link Between Body Fat and the Timing of Puberty

thickness of premenarcheal and postmenarcheal girls of the same age and found extensive overlap; he concluded that there was no clear evidence of a threshold level of weight or fatness that is critical for the onset of men- arche. Nonetheless, evidence has accumulated in the past 30 years that points to a major influence of body fat as the timing of puberty, at least in girls. Although the role of environmental chemicals has not been ade- quately studied, the well-documented epidemic of obe- sity in American children provides a plausible explana- tion for the decreasing age in both the age of onset of breast development and the age of menarche. In this review, the studies presented support a link between these 2 phenomena. Although there are much fewer data concerning the possible link of obesity with early puberty in boys, this is reviewed and contrasted with the findings in girls.
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<p>Could long-term administration of melatonin to prepubertal children affect timing of puberty? A clinician&rsquo;s perspective</p>

<p>Could long-term administration of melatonin to prepubertal children affect timing of puberty? A clinician&rsquo;s perspective</p>

Abstract: Exogenous melatonin can be used to treat sleep disturbance in adults, children, and adolescents. While its short-term use is considered safe, there are some concerns that long-term use might delay children’s sexual maturation, possibly by disrupting the decline in nocturnal melatonin levels that occur at the onset of puberty. This narrative review aimed to summarize some of the current knowledge about the potential effects of exogenous melatonin on puberty. We found no clinical studies that experimentally tested the effects of melatonin on pubertal timing in children, but we reviewed the small number of observational studies. We also drew on animal data to try to answer our question. The photoperiod and melatonin-mediated seasonal transitions in sexual activity and breeding in some mammals across the seasons have been used as a model of sexual development in mammals, including humans. The switch from non-sexual activity (in the non-breeding period) to sexual activity (in the breeding period) has been likened to the onset of puberty as there are similarities between the two. We conclude that to investigate an association between melatonin and pubertal timing, it will be important to conduct long-term randomized controlled trials of latency age children and also examine the cellular and systems- level interactions between melatonin and kisspeptin, a recently identified neuropeptide with a locus of action at the gonadotropin releasing hormone neurons that is important in contributing to the timing of puberty onset.
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Preterm birth and the timing of puberty: a systematic review

Preterm birth and the timing of puberty: a systematic review

[18]. This hypothesis is supported by early data which showed that preterm birth was associated with earlier (6 months) onset of menarche, as compared to term controls [19]. To examine the hypothesis that preterm birth is associated with a stereotyped phenotypic devel- opmental trajectory, we carried out a systematic review looking at the association between preterm birth and the timing of puberty. Given the morbidity associated with both entities, if there proved to be relationship between the two this would have significant public health conse- quences. In addition, this information would be import- ant for clinicians counseling parents and eventually patients on the longer term consequences of preterm birth. We therefore asked the research question: in ado- lescents (Population), what are the effects of being born prematurely at <37 weeks (Exposure) versus being born at term (Comparison) on the timing of onset of puberty (Outcome), as reported in cohort, cross sectional or case control studies (Study design).
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Timing of Puberty in Overweight Versus Obese Boys

Timing of Puberty in Overweight Versus Obese Boys

Briefly, 212 trained clinicians from the PROS and Academic Pediatric Association’s Continuity Research Network (CORNET) recruited patients between July 2005 and February 2010. Boys ages 6 to 16 years being seen for well-child visits were eligible for enrollment. Clinicians recorded weight to the nearest 0.5 kg and height to the nearest cm using their own office measuring devices and techniques, Tanner stages, testicular volume measurement (coded as ≤ 1, 2, 3, or ≥ 4 mL), and results of breast palpation for gynecomastia. If Tanner stage or testis volume appeared to fall between categories, clinicians assumed the lower stage or volume, as this would provide a conservative estimate of timing of puberty and would ensure consistency across multiple clinicians. Race/ethnicity was classified by clinicians as African American (regardless of any other race/ethnicity indication), Hispanic if this ethnicity was indicated (regardless of any other indication other than African American), and white if only this category was indicated. Practice locations were 17% in the Midwest, 24% in the
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Examination of US Puberty-Timing Data from 1940 to 1994 for Secular Trends: Panel Findings

Examination of US Puberty-Timing Data from 1940 to 1994 for Secular Trends: Panel Findings

Whether children, especially girls, are entering and progressing through puberty earlier today than in the mid-1900s has been debated. Secular trend analysis, based on available data, is limited by data comparability among studies in different popu- lations, in different periods of time, and using different methods. As a result, conclusions from data comparisons have not been consistent. An expert panel was asked to evaluate the weight of evidence for whether the data, collected from 1940 to 1994, are sufficient to suggest or establish a secular trend in the timing of puberty markers in US boys or girls. A majority of the panelists agreed that data are sufficient to suggest a trend toward an earlier breast development onset and menarche in girls but not for other female pubertal markers. A minority of panelists concluded that the current data on girls’ puberty timing for any marker are insufficient. Almost all panelists concluded, on the basis of few studies and reliability issues of some male puberty markers, that current data for boys are insufficient to evaluate secular trends in male pubertal development. The panel agreed that altered puberty timing should be considered an adverse effect, although the magnitude of change considered adverse was not assessed. The panel recommended (1) additional analyses of existing puberty-timing data to examine secular trends and trends in the temporal sequence of pubertal events; (2) the development of biomarkers for pubertal timing and methods to discriminate fat versus breast tissue, and (3) establishment of cohorts to examine pubertal markers longitudinally within the same individuals.
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Puberty in female wild boar (Sus scrofa) in Sweden

Puberty in female wild boar (Sus scrofa) in Sweden

In free-ranging wild boar it is difficult to monitor if a gilt shows oestrus and exhibits regular oestrus cycles. Therefore, the majority of studies of puberty in free-rang- ing female wild boar gilts are based on post-mortem mac- roscopic examinations of the reproductive organs. Yet, the definition of puberty in these studies varies, which make comparisons difficult. Most commonly signs of ovulation, which is presence of one or more corpora lutea (CL), is used to define if the female wild boar has reached puberty [4, 23]. However, others declare that ‘puberty is assumed in individuals with follicles more than 3 mm in diameter [24], i.e. without the necessity of the presence of one or more CL. In addition, wild boar females below 1 year of age have been categorized as being cyclic, i.e. having passed puberty, if found with follicles of 6  mm in diameter or larger [25]. The exact timing of when a female passes puberty cannot be detected by macro- scopic examination of reproductive organs. This method can only result in proportions of animals in a population that have passed puberty. If the exact timing of puberty needs to be studied, other methods such as repeated fecal [26] or blood [27, 28] sampling for progesterone analyses of fenced animals can be used. These methods are harder, or impossible to apply in free-ranging animals.
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RASopathies Are Associated With Delayed Puberty; Are They Associated With Precocious Puberty Too?

RASopathies Are Associated With Delayed Puberty; Are They Associated With Precocious Puberty Too?

Future comprehensive studies of pubertal development in patients with RASopathies are needed to investigate these important genotype–phenotype correlations. Such studies would provide insight into the pathways that regulate the timing of puberty and also ascertain the incidence of delayed and precocious puberty in these conditions. Because CPP may lead to adverse psychosocial functioning 29

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The effects of pubertal timing and dominance on the mating strategy, appearance and behaviour of men

The effects of pubertal timing and dominance on the mating strategy, appearance and behaviour of men

and is, in this respect, evidence against exposure to prenatal testosterone acting as a mechanism for the adjustment of developmental speed. However, structural differences in anatomy between the sexes leads to differences in the amounts of testosterone produced and in sensitivity to testosterone. Men have more than three times the amount of testosterone than women, 95% of which is produced by the testes (Rommerts 2004). Male foetuses will therefore be exposed to larger quantities of testosterone than female foetueses once the Leydig cells become active at around week 14, the time at which 2D4D is set. Furthermore, male foetuses may be more sensitive to testosterone than female (i.e. have more androgen receptors) since androgens are crucial to male neural and cardiovascular development (Brinkmann 2001). Testosterone, then, may simply not be available to a female foetus in sufficient quantity for use as a signal of maternal environment, while the female foetus itself may not be sufficiently sensitive to it. Human females loose little from this, since the penalties of too early maturity for a female are potentially catastrophic (e.g. gestating a child before the pelvic girdle has completed growth could lead to the death of both mother and infant) while males face no such cost. Early development becomes maladaptive for human females much earlier than it does for human males. Using early, postnatal experience to modulate developmental trajectory may be a better strategy for a human female. Jeha et al. (2006) report a case of extreme precocious puberty (with pubertal development occurring around 2-4 years) in the males of one family, linked to a specific genetic mutation in their luteinising hormone (LH) receptors, which presumably promotes Leydig cell activity in the absence of appropriate hormonal signals. Interestingly, although some females of the family shared the mutant allele, they did not demonstrate precocious puberty. This may imply that the timing of puberty in males is closely linked to Leydig cell activity. Since Leydig cells are active and responsive to maternal hormones in utero, foetal programming of
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been linked to elevated IGF-1 concentrations and insulin resistance, elevated adrenal andro- gen concentrations, exaggerated adrenarche, obesity, and consequently elevated concentra- tions of hormones such as leptin. It has been suggested that these factors could promote the activity of the gonadotropin-releasing hor- mone (GnRH) pulse generator, thereby influ- encing the timing of puberty. 34 In particular, Terry et al. have found that size at birth and infant weight gain from 4 months to 1 year of life are associated with earlier age at menar- che in girls. 35 Other studies in this field have
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Divergent roles of growth factors in the GnRH regulation of puberty in mice

Divergent roles of growth factors in the GnRH regulation of puberty in mice

IGF-1 treatment of male mice did not affect puberty in control or GnRH-IGFRKO animals (Figure 6B). These data suggest that, unlike in females, activation of IGF signaling alone in GnRH neu- rons cannot activate the GnRH pulse generator; activation of IGF signaling pathways must be combined with activation or inhibition of other pathways to activate the GnRH pulse generator in males. Alternatively, males may need higher IGF-1 doses to effect pubertal onset. The sexual dimorphism of the effects of IGF-1 treatment on puberty is striking, although not surprising. IGF-1 has been shown to interact with estradiol to affect puberty. Primate studies have shown that IGF-1 treatment decreases the negative feedback effects of estrogen on LH release to advance the onset of puberty (47). Fur- thermore, the effect of intracerebroventricular IGF-1 treatment on rodent LH release is enhanced if detectable levels of serum estra- diol are present (48). These effects are IGF-1R dependent (49). In addition, the timing of puberty in mammals is earlier in females than males, implying that activation of the GnRH pulse generator is under the control of additional and/or different signals, path- ways, and mechanisms. Indeed, the differential effects of IGF-1 on male and female pubertal timing may partly account for the sexual dimorphism of pubertal timing seen in mammals.
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Maternal pre-pregnancy body mass index, smoking in pregnancy, and alcohol intake in pregnancy in relation to pubertal timing in the children

Maternal pre-pregnancy body mass index, smoking in pregnancy, and alcohol intake in pregnancy in relation to pubertal timing in the children

During the last century, a trend toward earlier age at onset of puberty has been reported in girls, whereas the trend to- ward earlier age at menarche has leveled off in some coun- tries since the 1960s [1, 2]. A trend is less clear in boys [2]. A change in timing of puberty over time is of concern be- cause early pubertal timing has been associated with in- creased risk of adult diseases such as type 2 diabetes, cardiovascular diseases, testicular cancer, and breast cancer [3]. Identification of modifiable risk factors for earlier pu- bertal timing is, therefore, warranted. A potential modifi- able risk factor for earlier pubertal timing is childhood obesity, which has been suggested to be responsible for some of the trend [4, 5]. Prenatal exposures have also been suggested to interfere with pubertal timing through fetal growth restriction or overnutrition as well as endocrine dis- ruption of androgenic or estrogenic activity [5, 6]. Maternal obesity, smoking, and alcohol intake during pregnancy may lead to either fetal growth restriction [7, 8] or overnutrition [9] and may change the intrauterine hormonal milieu to- wards either increased androgenic activity [10] or increased estrogenic activity [11, 12]. Hence, these maternal expo- sures may potentially interfere with pubertal timing in the children. In girls, earlier puberty has been observed after prenatal exposure to maternal obesity [13–19] and smoking [20 – 23]. No association for prenatal exposure to alcohol has been reported in girls in all [22, 24–26] but one small study [27]. In boys, some evidence support an earlier puber- tal timing after prenatal exposure to smoking [23, 28 – 30], whereas results has been inconclusive for prenatal exposure to maternal obesity [31] and prenatal alcohol consumption [26, 32, 33]. If these associations reflect causal relations, they may open up for a potential for preventive actions as they are relatively frequent and modifiable [34–36].
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Public Health Implications of Altered Puberty Timing

Public Health Implications of Altered Puberty Timing

of precocious puberty in girls: the suggested age limits are 6 years in black American girls, 7 years in white American girls, and 8 years in European girls. In boys, a similar trend is not apparent, and definitions of precocity are the same around the world; however, it is pertinent to consider the consequences of early puberty in both boys and girls at the individual and population levels. Early puberty has clinical significance for individual children and their families that may necessitate counseling and intervention. On the population level, secular trends in the timing of puberty may influence behavioral disorders and adult health, which can be reflected in cancer morbidities (eg, breast, testis) and metabolic diseases (eg, polycystic ovary syndrome [PCOS], metabolic syndrome). This has implications in children’s health risk assessment that need to be considered in the continuous development of guidelines for reproductive and developmental toxicity testing and screening of endocrine disrupters. This review discusses the implications of secular
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Environmental Factors and Puberty Timing: Expert Panel Research Needs

Environmental Factors and Puberty Timing: Expert Panel Research Needs

A summary of selected examples of single environmen- tal chemicals whose exposure at specific dosages may lead to puberty-timing alterations is presented in Table 1. This table is organized by mode of action (MOA). Estrogen receptor (ER) agonists (also called estrogen agonists or estrogens) and ER antagonists compete with the endogenous estrogen hormones estradiol and es- trone for binding to the classical ER. Such agonists and antagonists bind to the ER and activate or repress, re- spectively, transcription of ER-dependent genes and thereby enhance or diminish estrogenic activity in vivo (eg, induce uterine weight increase/decrease, accelerate/ delay puberty). After in utero exposure to a potent es- trogen agonist, gross reproductive malformations may result in female rats, presumably by altering the devel- opment of reproductive organs that are responsive to estrogen action. Examples of estrogen agonists that are present as environmental contaminants include 2,2- bis(p-hydroxyphenyl)-1,1,1-trichloroethane (HPTE), a metabolite of the pesticide chemical methoxychlor, and
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Gender nonconforming youth: current perspectives

Gender nonconforming youth: current perspectives

any social transitions until adolescence is not to ward off a transgender identity but rather that 1) it would be advanta- geous that a child experiences the first stages of physical puberty for that child to best make a determination of the gender that feels most authentic to him/her; 2) given devel- opmental stages of childhood, facilitating a social transition from one gender to another at a young age may create a form of cognitive constriction – the child may be prema- turely blocked from considering any other possibilities once moved into a cross-gender status and socially constricted from further childhood gender exploration because now they know the cross-gender identity is what everyone has come to expect from them; 3) socially transitioning a child at a very young age may preclude the child from maintaining a realistic understanding of their body and historical status – as a penis-bodied (once a boy) or a vagina-bodied (once a girl) person. In informing their practices, this model, like the live in your own skin model, relies on the data gathered about “persisters” and “desisters”, both at their own clinic in the Netherlands and in other international studies, par- ticularly those conducted at the Centre for Addiction and Mental Health (CAMH) gender program in Toronto. In the most recent review of these studies, it was found that 63% of the children seeking services at a gender clinic at a young age, and diagnosed with gender dysphoria, no longer had that diagnosis at puberty, while 37% did have the diagnosis consistently from early childhood to adolescence. 20 Since
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PRECOCIOUS PUBERTY

PRECOCIOUS PUBERTY

entiation.” Normal and abnormal sexual development has been reviewed by Wilkins.3 A fairly large number of patients with hypophyseal precocity resulting from hypo-.. thalamic lesions has[r]

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International Adoption, “Early” Puberty, and Underrecorded Age

International Adoption, “Early” Puberty, and Underrecorded Age

been signi fi cantly underrecorded, a lack of height gain is to be expected. On the assumption that the high rate of early puberty is genuine, researchers have hypothesized that it is caused by nutritional deprivation before adop- tion followed by catch-up after adop- tion. 4,6,7 This theory is said to gain support from a limited experiment on male rats, 4 although there is no evi- dence that it extends to nonadopted children who have recovered from postnatal undernutrition. 6 The theory has been made problematic by the fi nding, fi rst reported in a Belgian study, that children not underweight or only slightly underweight at the time of their adoption have gone on to develop PP. 2 The Belgian researchers proposed an alternative theory that early puberty is caused by endocrine disrupters and in particular by high levels of a pesticide found in both in- ternationally adopted and nonadopted migrant children with PP. 2 A high PP risk among children who migrate with their parents would invalidate the underrecorded age theory because there is little reason to doubt their age. However, a later Danish study revealed no increased risk of PP among migrant children, suggesting that environmental chemical exposure in the state of origin is not a factor. 5 A Spanish study cast additional doubt on both the pesticide and catch-up theories. It corroborated the Danish fi nding that migrant children are not at increased risk of PP, but it also corroborated the Belgian fi nding that children who have received suf fi cient nutrition before adoption can also be at risk of PP. Children adopted do- mestically in Spain, who were ade- quately nourished before adoption, had a PP risk 18 times higher than that in nonadopted children. 3 In light of their fi ndings, the Spanish re- searchers proposed that psychologi- cal factors in fl uence PP. 3 Childhood
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An empirical study on impact of puberty among children in young age with special reference to Tiruppur

An empirical study on impact of puberty among children in young age with special reference to Tiruppur

Dermatological problems of adolescence are mainly related to fluctuations in hormone levels mainly androgens. They include acne, hair problems and excessive sweating. The paper will teach about girl children’s proper eating habits and too prevent them from early puberty.

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Growth and Normal Puberty

Growth and Normal Puberty

measurements were obtained annually in children 6 to 17 years of age. A substantial number of children were enrolled in this study from six cities in the states of Kansas, Massachusetts, Minnesota, Missouri, Ohio, and Tennessee; these children were considered to be representative of the population of youth in the United States. The other longitudinal studies during puberty were those of Lee 4

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Anorexia nervosa in males: similarities and differences to anorexia nervosa in females

Anorexia nervosa in males: similarities and differences to anorexia nervosa in females

with a biological statement of ripeness to reproduce. If the personal perception of fatness as an aspect of body shape is the only factor determining anorexia nervosa coupled with the quest to rid the body of it, the male, who traditionally at the end of puberty has only about 12% of his body as fat, has less distance to travel in this respect than the female (whose body fat comprises about 25% of her body weight by this time). Of course other excesses of fat may be superim- posed, especially these days. Our clinical view is that elimination of such fatness in the female is simply a marker of the profound psychobiological changes that accompany it and which provide her with the haven she needs. However, these differences between the male and the female may be important in terms of incidence, prevalence and outcome.
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