Why are early maturing girls less active? Links between pubertal development, psychological well-being, and physical activity among girls at ages 11 and 13

Previous research has shown that early maturing girls at age I I have lower subsequent physical activity at age 13 in comparison to later maturing girls. Possible reasons for this association have not been assessed. This study examines girls' psychological response to puberty and their enjoyment of physical activity as intermediary factors linking pubertal maturation and physical activity. Participants included 178 girls who were assessed at age 11, of whom 168 were reassessed at age 13. All participants were non-Hispanic white and resided in the US. Three measures of pubertal development were obtained at age I I including Tanner breast stage, estradiol levels, and mothers' reports of girls' development on the Pubertal Development Scale (PDS). Measures of psychological well-being at ages I I and 13 included depression, global self-worth, perceived athletic competence, maturation fears, and body esteem. At age 13, girls' enjoyment of physical activity was assessed using the Physical Activity Enjoyment Scale and their daily minutes of moderate-to-vigorous physical activity (MVPA) were assessed using objective monitoring. Structural Equation Modeling was used to assess direct and indirect pathways between pubertal development at age I I and MVPA at age 13. In addition to a direct effect of pubertal development on MVPA, indirect effects were found for depression, global self-worth and maturity fears controlling for covariates. In each instance, more advanced pubertal development at age I I was associated with lower psychological wellbeing at age 13, which predicted lower enjoyment of physical activity at age 13 and in turn lower MVPA. Results from this study suggest that programs designed to increase physical activity among adolescent girls should address the self-consciousness and discontent that girls' experience with their bodies during puberty, particularly if they mature earlier than their peers, and identify activities or settings that make differences in body shape less conspicuous.

The influence of chronic conditions and the environment on pubertal development. An example from medieval England

Adolescence is a unique period in human development encompassing sexual maturation (puberty) and the physical and psychological transition into adulthood. It is a crucial time for healthy development and any adverse environmental conditions, poor nutrition, or chronic infection can alter the timing of these physical changes; delaying menarche in girls or the age of peak height velocity in boys. This study explores the impact of chronic illness on the tempo of puberty in 607 adolescent skeletons from medieval England (AD 900-1550). A total of 135 (22.2%) adolescents showed some delay in their pubertal development, and this lag increased with age. Of those with a chronic condition, 40.0% (n=24/60) showed delay compared to only 20.3% (n=111/547) of the non-pathology group. This difference was statistically significant. A binary logistic regression model demonstrated a significant association between increasing delay in pubertal stage attainment with age in the pathology group. This is the first time that chronic conditions have been directly associated with a delay in maturation in the osteological record, using a new method to assess stages of puberty in skeletal remains.

Leptin signaling in Kiss1 neurons arises after pubertal development

The adipocyte-derived hormone leptin is required for normal pubertal maturation in mice and humans and, therefore, leptin has been recognized as a crucial metabolic cue linking energy stores and the onset of puberty. Several lines of evidence have suggested that leptin acts via kisspeptin expressing neurons of the arcuate nucleus to exert its effects. Using conditional knockout mice, we have previously demonstrated that deletion of leptin receptors (LepR) from kisspeptin cells cause no puberty or fertility deficits. However, developmental adaptations and system redundancies may have obscured the physiologic relevance of direct leptin signaling in kisspeptin neurons. To overcome these putative effects, we re-expressed endogenous LepR selectively in kisspeptin cells of mice otherwise null for LepR, using the Cre-loxP system. Kiss1-Cre LepR null mice showed no pubertal development and no improvement of the metabolic phenotype, remaining obese, diabetic and infertile. These mice displayed decreased numbers of neurons expressing Kiss1 gene, similar to prepubertal control mice, and an unexpected lack of re-expression of functional LepR. To further assess the temporal coexpression of Kiss1 and Lepr genes, we generated mice with the human renilla green fluorescent protein (hrGFP) driven by Kiss1 regulatory elements and crossed them with mice that express Cre recombinase from the Lepr locus and the R26-tdTomato reporter gene. No coexpression of Kiss1 and LepR was observed in prepubertal mice. Our findings unequivocally demonstrate that kisspeptin neurons are not the direct target of leptin in the onset of puberty. Leptin signaling in kisspeptin neurons arises only after completion of sexual maturation.

Anti-Müllerian hormone levels in girls and adolescents with Turner syndrome are related to karyotype, pubertal development and growth hormone treatment

In girls and adolescents with Turner syndrome (TS), is there a correlation between serum AMH levels and karyotype, spontaneous puberty and other biochemical markers of ovarian function, or growth hormone (GH) therapy? SUMMARY ANSWER: Serum anti-Müllerian hormone (AMH) correlates with karyotype, pubertal development, LH, FSH and are measurable in a higher percentage of TS patients under GH therapy. WHAT IS KNOWN ALREADY: Most girls with TS suffer from incomplete sexual development, premature ovarian failure and infertility due to abnormal ovarian folliculogenesis. Serum AMH levels reflect the ovarian reserve in females, even in childhood. STUDY DESIGN, SIZE, DURATION: Cross-sectional study investigating 270 karyotype proven TS patients aged 0-20 years between 2009 and 2010. PARTICIPANTS/MATERIALS, SETTINGS, METHODS: Studies were conducted at three University Children's hospitals in Europe. Main outcome measures were clinical data concerning pubertal development as well as laboratory data including karyotype, serum AMH, LH, FSH, estradiol (E2), inhibin B and IGF. RESULTS AND THE ROLE OF CHANCE: Serum AMH was detectable in 21.9% of all TS girls and correlated strongly with karyotypes. A measurable serum AMH was found in 77% of TS girls with karyotype 45,X/46,XX, in 25% with 'other' karyotypes and in only 10% of 45,X TS girls. A strong relationship was also observed for measurable serum AMH and signs of spontaneous puberty such as breast development [adjusted odds ratio (OR) 19.3; 95% CI 2.1-175.6; P = 0.009] and menarche (crude OR 47.6; 95% CI 4.8-472.9; P = 0.001). Serum AMH correlated negatively with FSH and LH, but did not correlate with E2 and inhibin B. GH therapy increased the odds of having measurable AMH in TS (adjusted OR 4.1; 95% CI 1.9-8.8; P < 0.001). LIMITATIONS, REASONS FOR CAUTION: The cross-sectional design of the study does not allow longitudinal interpretation of the data; for that further studies are needed. High percentage of non-measurable AMH levels in the cohort of TS require categorized analysis. WIDER IMPLICATIONS OF THE FINDINGS: Serum AMH levels are a useful marker of the follicle pool and thus ovarian function in pediatric patients with TS. These findings are in line with the published literature. The finding that GH therapy may affect AMH levels is novel, but must be confirmed by future longitudinal studies.

GH mutant (R77C) in a pedigree presenting with the delay of growth and pubertal development: structural analysis of the mutant and evaluation of the biological activity

A heterozygous missense mutation in the GH-1 gene converting codon 77 from arginine (R) to cysteine (C), which was previously reported to have some GH antagonistic effect, was identified in a Syrian family. The index patient, a boy, was referred for assessment of his short stature (-2.5 SDS) at the age of 6 years. His mother and grandfather were also carrying the same mutation, but did not differ in adult height from the other unaffected family members. Hormonal examination in all affected subjects revealed increased basal GH, low IGF-I concentrations, and subnormal IGF-I response in generation test leading to the diagnosis of partial GH insensitivity. However, GH receptor gene (GHR) sequencing demonstrated no abnormalities. As other family members carrying the GH-R77C form showed similar alterations at the hormonal level, but presented with normal final height, no GH therapy was given to the boy, but he was followed through his pubertal development which was delayed. At the age of 20 years he reached his final height, which was normal within his parental target height. Functional characterization of the GH-R77C, assessed through activation of Jak2/Stat5 pathway, revealed no differences in the bioactivity between wild-type-GH (wt-GH) and GH-R77C. Detailed structural analysis indicated that the structure of GH-R77C, in terms of disulfide bond formation, is almost identical to that of the wt-GH despite the introduced mutation (Cys77). Previous studies from our group demonstrated a reduced capability of GH-R77C to induce GHR/GH-binding protein (GHBP) gene transcription rate when compared with wt-GH. Therefore, reduced GHR/GHBP expression might well be the possible cause for the partial GH insensitivity found in our patients. In addition, this group of patients deserve further attention because they could represent a distinct clinical entity underlining that an altered GH peptide may also have a direct impact on GHR/GHBP gene expression causing partial GH insensitivity. This might be responsible for the delay of growth and pubertal development. Finally, we clearly demonstrate that GH-R77C is not invariably associated with short stature, but that great care needs to be taken in ascribing growth failure to various heterozygous mutations affecting the GH-IGF axis and that careful functional studies are mandatory.

Age appropriate pubertal development in cystic fibrosis

No abstract

Effects of adolescent depressive symptoms, pubertal development, and interpersonal relationship satisfaction on sexual risk behaviors in adolescent romantic couples

This study examined links between adolescent depressive symptoms, actual pubertal development, perceived pubertal timing relative to one’s peers, adolescent-maternal relationship satisfaction, and couple sexual behavior. Assessments of these variables were made on each couple member separately and then these variables were used to predict the sexual activity of the couple. Participants were drawn from the National Longitudinal Study of Adolescent Health (Add Health; Bearman et al., 1997; Udry, 1997) data set (N = 20,088; aged 12–18 years). Dimensions of adolescent romantic experiences using the total sample were described and then a subsample of romantically paired adolescents ( n = 1,252) were used to test a risk and protective model for predicting couple sexual behavior using the factors noted above. Relevant measures from the Wave 1 Add Health measures were used. Most of the items used in Add Health to assess romantic relationship experiences, adolescent depressive symptoms, pubertal development (actual and perceived), adolescent-maternal relationship satisfaction, and couple sexual behavior were drawn from other national surveys or from scales with well documented psychometric properties. Results demonstrated that romantic relationships are part of most adolescents’ lives and that adolescents’ experiences with these relationships differ markedly by age, sex, and race/ethnicity. Further, each respective couple member’s pubertal development, perceived pubertal timing, and maternal relationship satisfaction were useful in predicting sexual risk-promoting and risk-reducing behaviors in adolescent romantic couples. Findings in this dissertation represent an initial step toward evaluating explanatory models of adolescent couple sexual behavior.

Effects of Adolescent Depressive Symptoms, Pubertal Development, and Interpersonal Relationship Satisfaction on Sexual Risk Behaviors in Adolescent Romantic Couples

This study examined links between adolescent depressive symptoms, actual pubertal development, perceived pubertal timing relative to one’s peers, adolescent-maternal relationship satisfaction, and couple sexual behavior. Assessments of these variables were made on each couple member separately and then these variables were used to predict the sexual activity of the couple. Participants were drawn from the National Longitudinal Study of Adolescent Health (Add Health; Bearman et al., 1997; Udry, 1997) data set (N = 20,088; aged 12-18 years). Dimensions of adolescent romantic experiences using the total sample were described and then a subsample of romantically paired adolescents (n = 1,252) were used to test a risk and protective model for predicting couple sexual behavior using the factors noted above. Relevant measures from the Wave 1 Add Health measures were used. Most of the items used in Add Health to assess romantic relationship experiences, adolescent depressive symptoms, pubertal development (actual and perceived), adolescent-maternal relationship satisfaction, and couple sexual behavior were drawn from other national surveys or from scales with well documented psychometric properties. Results demonstrated that romantic relationships are part of most adolescents’ lives and that adolescents’ experiences with these relationships differ markedly by age, sex, and race/ethnicity. Further, each respective couple member’s pubertal development, perceived pubertal timing, and maternal relationship satisfaction were useful in predicting sexual risk-promoting and risk-reducing behaviors in adolescent romantic couples. Findings in this dissertation represent an initial step toward evaluating explanatory models of adolescent couple sexual behavior.

Advanced pubertal status at age 11 and lower physical activity in adolescent girls

Objective To examine the relationship between pubertal timing and physical activity. Study design A longitudinal sample of 143 adolescent girls was assessed at ages 11 and 13 years. Girls' pubertal development was assessed at age 11 with blood estradiol levels, Tanner breast staging criteria, and parental report of pubertal development. Girls were classified as early maturers (n = 41) or later maturers (n = 102) on the basis of their scores on the 3 pubertal development measures. Dependent variables measured at age 13 were average minutes/day of moderate to vigorous and vigorous physical activity as measured by the ActiGraph accelerometer. Results Early-maturing girls had significantly lower self-reported physical activity and accumulated fewer minutes of moderate to vigorous and vigorous physical activity and accelerometer counts per day at age 13 than later maturing girls. These effects v.-ere independent of differences in percentage body fat and self-reported physical activity at age 11. Conclusion Girls experiencing early pubertal maturation at age 11 reported lower subsequent physical activity at age 13 than their later maturing peers. Pubertal maturation, in particular early maturation relative to peers, may lead to declines in physical activity among adolescent girls.

Temporal expression of G-protein-coupled receptor 54 (GPR54), gonadotropin-releasing hormones (GnRH), and dopamine receptor D2 (drd2) in pubertal female grey mullet, Mugil cephalus.

The G-protein-coupled receptor 54 (muGPR54) cDNA was cloned from the brain of the grey mullet, and its expression level, as well as those of the gonadotropin-releasing hormones (GnRH1, GnRH2, GnRH3) and dopamine receptor D2 (drd2), in the brain, pituitary and ovary of pubertal fish (early, intermediate, advanced) were determined by real-time quantitative RT-PCR (QPCR). The muGPR54 cDNA has an open reading frame of 1140 bp with a predicted 380 amino acid peptide, containing seven putative transmembrane domains and putative N-glycosylation and protein kinase C phosphorylation sites. QPCR results showed that the early stage of puberty in grey mullet is characterized by significantly high levels of expression of GPR54, GnRH and drd2 in the brain relative to the intermediate and advanced stages, except for GnRH1 that increased at the advanced stage of puberty. In the pituitary, drd2 expression declined significantly at the advanced stage relative to levels at the intermediate stage. Ovarian expression of GPR54 significantly increased from the intermediate stage of puberty relative to the early stage while that of GnRH1 acutely increased at the advanced stage of puberty. The ovarian expression of drd2 decreased as puberty progressed, but the changes were not significant. The results suggest the possible role of GPR54 and GnRH in positively regulating pubertal development in grey mullet and the dopaminergic inhibition of reproductive function mediated by drd2.

Pubertal impairment in Nhlh2

Pubertal development is impaired in mice lacking the basic helix-loop-helix transcription factor Nhlh2. The mechanisms underlying changes in reproduction in Nhlh2-deficient mice (Nhlh2-/-) are unclear. Here we show that hypothalamic gonadotropin-releasing hormone-1 (GnRH-1) content is reduced in adult Nhlh2-/- mice as is the number of GnRH-1 neurons localized to mid- and caudal hypothalamic regions. This reduction was detected postnatally after normal migration of GnRH-1 neurons within nasal regions had occurred. Phenotype rescue experiments showed that female Nhlh2-/- mice were responsive to estrogen treatment. In contrast, puberty could not be primed in female Nhlh2-/- mice with a GnRH-1 regimen. The adenohypophysis of Nhlh2-/- mice was hypoplastic although it contained a full complement of the five anterior pituitary cell types. GnRH-1 receptors (GnRHRs) were reduced in Nhlh2-/- pituitary gonadotropes as compared to wild type. In vitro assays indicated that Nhlh2 expression is regulated in parallel with GnRHR expression. However, direct transcriptional activity of Nhlh2 on the GnRHR promoter was not found. These results indicate that Nhlh2 plays a role in the development and functional maintenance of the hypothalamic-pituitarygonadal axis at least at two levels: 1) in the hypothalamus by regulating the number and distribution of GnRH-1 neurons and, 2) in the developing and mature adenohypophysis.

Bone mineral density in healthy female adolescents according to age, bone age and pubertal breast stage

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Relationship between bone ageand pubertal breast stage to bone biomarkers and bone mineral density in healthy brazilian female adolescents

Background and Aims Bone metabolism involves understanding many factors, especially during puberty, when bone turnover is significant and the bone mass peak must be achieved as a protective factor of future bone health. The objective was to evaluate the behavior of formation and resorption bone biomarkers (BB) in function of biological maturation in female adolescents.Methods Evaluation of formation and resorption BB, osteocalcin (OC), bone alkaline phosphatase (BAP) and carboxyterminal telopeptide (S-CTx) by correlating them with bone mineralization, bone age and pubertal development in healthy female adolescents. Seventy-two volunteers were subdivided into groups according to chronological age/bone age (BA): 10 11 years (n=12), 12 13 years (n=16), 14 15 years (n=15) and 16 19 years (n=29). The following were evaluated: weight (kg), height (m), BMI (kg/m2), calcium intake (3-day 24h food recalls (mg/day), puberty events (Tanner stages), serum OC (ng/mL), BAP (U/L), S-CTx (ng/mL) and bone mineral density (BMD) as calculated by DXA (g/cm2) in the spine (L1-L4), proximal femur and whole body. The project was approved by the UNESP Ethics Committee.Results BB showed similar behaviors, with higher mean values for 10 12 years and when adolescents were in the B2-B3 Pubertal Maturation Stage (B2: BAP=110.16 U/L, OC=33.81ng/mL, S-CTx=1.66 ng/mL and B3: BAP=136.50 U/L, OC=39.15ng/mL and S-CTx=1.88 ng/mL; p<0.001). Mean BB values decreased with advancing BA and pubertal maturity.Conclusions BB values showed parallelism with peak height velocity and significant negative correlation with BMD in the different evaluated sites, with chronological and BA ; higher BMD values correlated with lower bone biomarker values.