Timing Of Pubertal Development Research Articles

Pubertal timing: A life course pathway linking early life risk to adulthood cardiometabolic health.

To evaluate a series of prospective life course models testing whether the timing of pubertal development is a pathway through which prepubertal risk factors may influence adulthood cardiometabolic health. Subjects were 655 female participants in the NICHD Study of Early Child Care and Youth Development (SECCYD) and recent SECCYD 30-year follow-up, the Study of Health in Early and Adult Life (SHINE). Prepubertal risk factors included maternal menarcheal age, child race/ethnicity, child health status indicators, and child adversity indicators. Pubertal timing was indexed by breast development onset (Tanner stage [TS] II), pubic hair onset (TS II) and menarcheal age. Adulthood cardiometabolic risk (CMR) was indexed by a composite of waist circumference, systolic blood pressure, diastolic blood pressure, hemoglobin A1c, C-reactive protein, and high-density lipoprotein. Inspection of paths between the prepubertal risk factors, pubertal timing indicators, and adulthood CMR composite showed later breast development onset (-0.173, p < .01), later pubic hair onset (-0.182, p < .01), and later menarche (-0.145, p < .01) each predicted lower adulthood CMR, and each pubertal timing indicator mediated effects of prepubertal risk factors on adulthood CMR. Specifically, the timing of breast development onset and menarche mediated effects of maternal menarcheal age, Black (vs. White), Asian/PI (vs. White), child BMI percentile, and child SES on adulthood CMR (all ps < .05), and the timing of pubic hair onset mediated effects of maternal menarcheal age, Black (vs. White), and child BMI percentile on adulthood CMR (all ps < .10). Findings in the current study contribute to the broader literature by identifying pubertal development and its timing as a potentially important pathway through which early life exposures may shape adulthood cardiometabolic health and disease. These findings have important implications for novel opportunities for increased surveillance and potential intervention focusing on pubertal development as a target to improve health more broadly.

Pubertal development at age 14 is associated with male adolescents’ combustible cigarette smoking and dual use, but not with e-cigarette use – Findings from the UK Millennium Cohort Study

BackgroundAdolescent nicotine exposure via electronic cigarettes (e-cigarettes) is a global health concern. Pubertal development earlier than peers increases the risk of tobacco smoking compared to peers experiencing on-time or late maturation, yet relationships of pubertal timing with e-cigarettes are unknown. We examine whether early pubertal timing is associated with risk for e-cigarette use, tobacco cigarettes, or both by age 14. MethodsThe Millennium Cohort Study follows a representative cohort of 18,552 9-month-old children born 2000–2002 in the United Kingdom. Our sample includes 11,445 adolescents (5697 boys, 5748 girls) classified at age 14 as early, on-time, or late in pubertal development timing (PDT) relative to same-age, same-sex peers using the Pubertal Development Scale. Outcomes were use of e-cigarettes, tobacco cigarettes, or both by age 14. We included childhood liability confounders and demographics measured from age 7–11. ResultsFor girls, no PDT differences in age 14 e-cigarette or tobacco cigarette use were observed. All relative to on-time PDT boys, early maturing boys’ odds of tobacco cigarette use were 59% higher (OR=1.59, 95% confidence interval (CI)=1.08,2.35), and odds of dual-use were 49% higher (OR=1.49, CI=1.11,1.99), both compared to odds of never use. Among late PDT boys, dual-use odds were lower than never use by 35% (OR=0.65, CI=0.47,0.91) and lower than e-cigarette use only by 36% (OR=0.64, CI=0.42,0.97). ConclusionsAt age 14, PDT was not associated with e-cigarette use for either sex, yet it was linked with tobacco use and dual use among boys.

Precocious puberty in relation to the COVID-19 pandemic. A survey among Argentine pediatric endocrinologists

Introduction. Puberty is manifested initially by the onset of secondary sexual characteristics as a result of hormonal changes that progressively lead to complete sexual maturity. In Argentina and worldwide, the lockdown resulting from the SARS-CoV-2 pandemic may have interfered in the onset and timing of pubertal development. Objective. To describe the perception of pediatric endocrinologists in Argentina regarding consultations for suspected precocious and/or rapidly progressive puberty during the pandemic. Materials and methods. Descriptive, observational, cross-sectional study. Anonymous survey among pediatric endocrinologists members of the Sociedad Argentina de Pediatría and/or the Asociación de Endocrinología Pediátrica Argentina administered in December 2021. Results. Out of 144 pediatric endocrinologists, 83 completed the survey (rate of response: 58%). All of them considered that consultation for precocious or early puberty increased, either in terms of early thelarche (84%), early pubarche (26%), and/or precocious puberty (95%). Ninety-nine percent agreed that this has occurred to a greater extent in girls. All survey respondents also consider that the diagnosis of central precocious puberty has increased. In total, 96.4% of respondents consider that the number of patients treated with GnRH analogs has increased. Conclusion. Our results about the perception of pediatric endocrinologists are consistent with data published in other regions on the increase in the diagnosis of precocious puberty during the COVID-19 pandemic. We underscore the need to develop national registries of central precocious puberty, and to disseminate the evidence for a timely detection and management.

Maternal thyroid disease in pregnancy and timing of pubertal development in sons and daughters

To study whether maternal thyroid disease in pregnancy is associated with pubertal timing in sons and daughters. Cohort study. National birth cohort and health registers. A total of 15,763 mothers and children from the Danish National Birth Cohort and its Puberty Cohort. Register-based and self-reported information on maternal thyroid diseases during pregnancy (hyperthyroidism, hypothyroidism, benign goiter, or no thyroid disease [reference group]). The adjusted mean age difference (months) at attaining several self-reported pubertal milestones collected every 6 months using an interval-censored regression and the average difference in age at attaining all pubertal milestones using the Huber-White robust variance estimation (primary outcome). Sons of mothers with hyperthyroidism had earlier pubertal development (average difference, -2.9 [95% confidence interval (CI), -5.0 to -0.7] months) than unexposed sons. Maternal hypothyroidism was not associated with pubertal development in sons (average difference, -1.2 [95% CI, -5.1 to 2.7] months). We observed nonstatistically significant indications of earlier pubertal development in sons of mothers with benign goiter (average difference, -1.9 [95% CI, -4.6 to 0.9] months). Maternal thyroid disease was not associated with pubertal development in daughters (average difference (months), hyperthyroidism, -0.8 [95% CI, -2.8 to 1.2]; hypothyroidism, 0.3 [95% CI, -3.1 to 3.8]; and benign goiter, 0.7 [95% CI, -2.0 to 3.4]). We found indications of earlier pubertal development in sons of mothers with hyperthyroidism. More research is needed to further investigate the observed sex-specific association.

Prepubertal BMI, pubertal growth patterns, and long-term BMI: Results from a longitudinal analysis in Chinese children and adolescents from 2005 to 2016.

To assess the effects of prepubertal BMI on pubertal growth patterns, and the influence of prepubertal BMI and pubertal growth patterns on long-term BMI among Chinese children and adolescents. A total of 9606 individuals aged between 7 and 18 years from longitudinal surveys in Zhongshan city of China from 2005 to 2016 were enrolled. Age at peak height velocity (APHV) and peak height velocity (PHV) were estimated using Super-Imposition by Translation and Rotation (SITAR) model. Associations between prepubertal BMI, APHV, PHV, and long-term overweight and obesity were assessed by linear regression and multinominal logistic regression. Scatter plots were elaborated to show the associations between prepubertal BMI and pubertal growth patterns according to prepubertal BMI categories. Prepubertal BMI Z-Score was positively correlated with long-term BMI Z-Score, and negatively correlated with APHV in both sexes. In addition, there was a negative association between prepubertal BMI Z-Score and PHV in boys. With 1-year decrease in APHV, risk of long-term underweight decreased by 92%, while overweight increased by 33% in boys. Corresponding risk of long-term underweight and overweight for girls decreased by 42% and increased by 20%, respectively. High prepubertal BMI levels were associated with earlier APHV and lower PHV, and the early onset of pubertal development could increase the risks of long-term overweight and obesity at 17-18 years of age both in boys and girls. Such evidence emphasized the importance of reducing prepubertal obesity risks combined with appropriate pubertal development timing, including later APHV and higher PHV, so as to prevent the obesity and related cardiovascular diseases in adulthood.

Timing of Pubertal Development in Boys and Girls With Congenital Heart Defects: A Nationwide Cohort Study.

BackgroundChildren with congenital heart defects (CHD) have an increased risk of developmental delay. It remains sparsely investigated if these patients also have a delayed pubertal development. In this nationwide cohort study, we evaluated if CHD was associated with timing of puberty using longitudinally collected data on pubertal milestones.Methods and ResultsWe used data from the Danish nationwide Puberty Cohort. Information on CHD was obtained from the Danish National Patient Register. Information on pubertal development was obtained from 15 780 children through questionnaires answered half‐yearly from 11 years until 18 years or full maturity. Using a multivariable regression model for censored time‐to‐event data, mean difference in age at attaining each pubertal milestone was estimated, including a combined pubertal marker. Compared with children without CHD, analyses were performed for both CHD overall and subdivided into simple and complex CHD. In a subanalysis, analyses were repeated in children born at term. In total, 137 children (62 boys and 75 girls) had a CHD diagnosis. Overall, no difference in age at pubertal timing was observed for children with CHD compared with unaffected children. The average differences were small for both boys (1.6 [95% CI, −2.6 to 5.7] months) and girls (1.0 [95% CI, −2.5 to 4.4] months). The same differences were observed when subdividing into simple or complex CHD and when restricting to children born at term.ConclusionsWe found no association between CHD and pubertal timing. For the group of children with complex CHD, we were unable to exclude a later pubertal timing.

Timing of pubertal development in boys and girls with congenital heart defects: a nationwide cohort study

Timing of pubertal development in boys and girls with congenital heart defects: a nationwide cohort study

Genetics of pubertal delay.

The timing of pubertal development is strongly influenced by the genetic background, and clinical presentations of delayed puberty are often found within families with clear patterns of inheritance. The discovery of the underlying genetic regulators of such conditions, in recent years through next generation sequencing, has advanced the understanding of the pathogenesis of disorders of pubertal timing and the potential for genetic testing to assist diagnosis for patients with these conditions. This review covers the significant advances in the understanding of the biological mechanisms of delayed puberty that have occurred in the last two decades.

Nausea During Pregnancy and Timing of Pubertal Development in Sons and Daughters: A Population-Based Cohort Study.

PurposeThe objective of this study was to explore whether maternal nausea in pregnancy, a potential surrogate marker of endogenous estrogen levels, was associated with age at attaining pubertal milestones in sons and daughters.Materials and MethodsThe study included a total of 14,612 boys and girls born in 2000–2003, from the Danish National Birth Cohort. Information on nausea was reported by mothers during pregnancy in telephone interviews scheduled around gestational week 12 and 30. Their children were invited every six months from 11 years of age until 18 years of full maturation to provide information on current pubertal status. Pubertal milestones included pubic hair, axillary hair and acne for both sexes, besides genital development, voice break and first ejaculation for boys, and breast development and menarche for girls. Mean monthly differences in age at attaining several pubertal milestones for boys and girls were estimated according to duration of nausea in the first trimester (0, 1–6, 7–11, 12 weeks). Further, we explored whether duration of nausea in the first two trimesters (0, 1–8, 9–15 or 16–28 weeks) and severity (measured by co-existence of vomiting and weight loss) were associated with pubertal timing.ResultsNeither maternal nausea in the first trimester nor duration or severity of nausea in the first two trimesters were associated with pubertal timing.ConclusionOur study does not support the hypothesis that nausea in pregnancy – as a surrogate marker of endogenous estrogen levels – is associated with age at attaining pubertal milestones in children.

Timing of Pubertal Development and Midlife Blood Pressure in Men and Women: A Mendelian Randomization Study.

Observational studies suggest earlier puberty is associated with higher adulthood blood pressure (BP), but these findings have not been replicated using Mendelian randomization (MR). We examined this question sex-specifically using larger genome-wide association studies (GWAS) with more extensive measures of pubertal timing. We obtained genetic instruments proxying pubertal maturation (age at menarche [AAM] or voice breaking [AVB]) from the largest published GWAS. We applied them to summary sex-specific genetic associations with systolic and diastolic BP z-scores, and self-reported hypertension in women (n = 194 174) and men (n = 167 020) from the UK Biobank, using inverse-variance weighted meta-analysis. We conducted sensitivity analyses using other MR methods, including multivariable MR adjusted for childhood obesity proxied by body mass index (BMI). We used late pubertal growth as a validation outcome. AAM (beta per 1-year later = -0.030 [95% confidence interval, -0.055 to -0.005] and AVB (beta -0.058 [95% CI, -0.100 to -0.015]) were inversely associated with systolic BP independent of childhood BMI, as were diastolic BP (-0.035 [95% CI, -0.060 to -0.009] for AAM and -0.046 [95% CI, -0.089 to -0.004] for AVB) and self-reported hypertension (odds ratio 0.89 [95% CI, 0.84-0.95] for AAM and 0.87 [95% CI, 0.79-0.96] for AVB). AAM and AVB were positively associated with late pubertal growth, as expected. The results were robust to sensitivity analysis using other MR methods. Timing of pubertal maturation was associated with adulthood BP independent of childhood BMI, highlighting the role of pubertal maturation timing in midlife BP.

Hypertensive disorders in pregnancy and timing of pubertal development in daughters and sons.

Do maternal hypertensive disorders affect pubertal development in daughters and sons? Pubertal development tended to occur earlier in daughters of mothers with 'preeclampsia, eclampsia or HELLP syndrome' (hemolysis, elevated liver enzymes and low blood platelets) or hypertension in pregnancy compared to daughters born of normotensive mothers. The existing literature suggests some or no association between preeclampsia and pubertal development in daughters, but not in sons. None of the previous studies has investigated the possible association between other types of hypertensive disorders (hypertension, eclampsia or HELLP syndrome) and pubertal timing in children. Longitudinal cohort study consisting of 15 819 mother-child pairs with information on maternal hypertensive disorders collected during pregnancy and information on pubertal development collected half-yearly from the age of 11 years and until fully developed or 18 years of age. Participants are children from the Puberty Cohort nested within the Danish National Birth Cohort. The exposure was register-based and self-reported information on maternal hypertensive disorders during pregnancy. The outcomes were children's self-reported information on pubertal development, including Tanner stage 1-5 (pubic hair (both daughters and sons) and breast development (daughters) or genital development (sons)), first menstrual bleeding (daughters) or first ejaculation (sons), voice break episode (sons), axillary hair development and acne occurrence (both daughters and sons). The main outcome was mean difference in age at attaining each pubertal milestone and a combined pubertal marker in children of mothers with hypertensive disorders in pregnancy (either hypertension (n = 490), 'preeclampsia, eclampsia or HELLP syndrome' (n = 419) or 'unspecific hypertensive disorders' (n = 334) with unexposed children as reference (n = 14 576)). In daughters of mothers with 'preeclampsia, eclampsia or HELLP syndrome', we observed tendencies of earlier pubertal timing (combined marker: -2.0 (95% CI: -3.9; 0.0) months). In daughters of mothers with hypertension, several pubertal milestones tended to occur earlier than in daughters of normotensive mothers; however, all 95% CIs overlapped the null resulting in a combined pubertal marker of -1.0 (95% CI: -3.2; 1.1) months. In sons of mothers with any of the hypertensive disorders, we observed no difference in pubertal timing (combined markers: 'preeclampsia, eclampsia or HELLP syndrome': 0.1 (95% CI: -2.0; 2.1) months; hypertension: -0.6 (95% CI: -2.3; 1.1) months; 'unspecific hypertensive disorders': 0.2 (95% CI: -1.9; 2.2) months). The study is subject to non-differential misclassification of self-reported information on maternal hypertensive disorders in pregnancy and current pubertal status; possibly causing bias toward the null. Hypertensive disorders in pregnancy might accelerate pubertal timing in daughters; however, more studies are needed for causal conclusions. The study was funded by the Faculty of Health at Aarhus University. The authors have no financial relationships or competing interests to disclose. N/A.

Review of the Literature on Current Changes in the Timing of Pubertal Development and the Incomplete Forms of Early Puberty.

Puberty is a sensitive period of life characterized by the appearance of secondary sex characteristics which leads to a complete sexual maturation. It physiologically starts between the age of 8 and 13 years in girls and 9 and 14 years in boys. In the last two decades, several studies have showed that start of puberty has moved up to younger ages by 12–18 months, and some of the hypotheses trying to explain this change include the role of nutritional status and obesity and the influence of extrinsic factors such as exposure to endocrine-disrupting chemicals (EDCs), as well. The hypothalamic–hypophysis–gonadal axis develops during embryogenesis, and except for a period of activation immediately after birth, remains suppressed until the onset of pubertal development. At the beginning of puberty, the pulse generator is reactivated, probably due to progressive stimulatory influences on GnRH neurons from glial signals and neurotrasmitters. Kisspeptin and its receptor play a fundamental role in this phase. Premature Pubarche/Adrenarche, Premature Thelarche, and Premature Menarche are incomplete forms of precocious pubertal development that have their origin in endocrine mechanisms that only recently have started to be understood. It is important to distinguish these forms from the complete ones in order to reassure patients and parents about the non-evolution of pubertal progression and avoid non-useful treatments with analogous LHRH.

SUN-262 Total and Central Adiposity Is Associated with Earlier Puberty in Chilean Boys

Background. In recent years worldwide, there has been an increase in childhood obesity together with an advance in the age at which puberty begins in girls; however, in boys the evidence has been controversial (i.e. Crocker MK JCEM 2014, Lee JM pediatrics 2016). Objective. To determine whether total and central body obesity in pre-pubertal children evaluated since age 4 is associated with precocious puberty through the measurement of testicular volume. Methods. We included 527 boys for the Growth and Obesity Cohort Study longitudinal cohort. The anthropometric measures (weight, height, waist circumference) were registered and Body Mass index SDS calculated. Trained personnel valuated the onset of puberty through a Prader Orchidometer and precocious puberty was defined as reaching a testicular volume greater than 3 cc before 9 years of age in any of the testicles. The association between obesity (total body adiposity and central body adiposity) and precocious puberty, were analyzed through logistic regression models and the Odds Ratio (OR) and 95% confidence interval (CI) were estimated. Results. There was an increase in BMI SDS and prevalence of total obesity and central obesity through the years :at 6 - 7 yr, 0.99±1.32 SDS and 22.0% & 11.8 % respectively, and at Tanner 2 ,age 11.4±1.4 yr (n = 494) , 1.15±1.22 SDS and 28.6 % & 17.4% respectively. Forty ive boys initiated puberty before 9 yrs (9.1%). A positive and statistically significant association was found between total body obesity and precocious puberty from 4 to 7 years of age (i.e. between 5 and 6 years of age, OR: 2.68 95% CI: 1.09 - 6.57) and at the time of pubertal onset OR: 3.59 95% CI: 1.92 - 6.70. When analyzing BMI SDS as a continuous variable, the association remained positive and significant at birth and from 4 to 8 years of age and at the time of pubertal onset. Likewise, a positive and significant association was found between central obesity and precocious puberty from 4 to 7 years of age (example between 5 and 6 years, OR: 6.36 95% CI: 2.03-19.92). Conclusions. Total and central body obesity in boys aged 4 to 7 years is associated with earlier puberty. Our observation supports the association of adiposity and earlier pubertal events in Chilean boys. Early puberty might increase the risk of behavior problems. In addition, it has been postulated that precocious puberty in boys, could be related to higher incidence of testicular cancer in adulthood. Our results suggest that controlling the obesity epidemic could be useful in decreasing these risks. Additional studies are needed to understand the possible relationships among race/ethnicity, gender, BMI, and the timing of pubertal development

Timing of pubertal development in boys born with cryptorchidism and hypospadias: a nationwide cohort study.

Pubertal development may be altered in boys with cryptorchidism and hypospadias, but existing knowledge is inconsistent. Therefore, we investigated the association between cryptorchidism and hypospadias and pubertal development in a large cohort study. Boys in the Puberty Cohort, a cohort nested within the Danish National Birth Cohort, were included in this study. Information on cryptorchidism and hypospadias was retrieved from the Danish National Patient Register. From 11 years until 18 years or full pubertal development, information on physical markers of pubertal development was provided biannually, including Tanner stages, axillary hair, acne, voice break, and first ejaculation. In multivariate regression models for interval censored data, the mean (95% confidence intervals [CIs]) differences in months in obtaining the pubertal markers between boys with and without the anomalies were estimated. Among 7698 boys, 196 (2.5%) had cryptorchidism and 60 (0.8%) had hypospadias. Boys with hypospadias experienced first ejaculation and voice break 7.7 (95% CI: 2.5–13.0) months and 4.5 (95% CI: 0.3–8.7) months later than boys without hypospadias. The age at attaining the Tanner stages for gonadal and pubic hair growth was also higher, though not statistically significant. Pubertal development seemed unaffected in boys with mild as well as severe cryptorchidism. In conclusion, hypospadias may be associated with delayed pubertal development, but pubertal development seems unaffected by cryptorchidism. The relation between hypospadias and later pubertal development may be due to the underlying shared in utero risk or genetic factors.

Association of pubertal development with adiposity and cardio-metabolic health in girls and boys–Findings from generation XXI birth cohort study

Introduction There is increasing evidence that the timing of pubertal development is associated with adult adiposity and cardio-metabolic health. In regard to the effect of early timing of pubertal development on worse cardio-metabolic health, some aspects remain largely unaddressed–if the effect is detectable already in childhood or, on the contrary, only occurs after adolescence; if this occurs also in males or only in females; and if this is or not independent of childhood adiposity. Accordingly, we aimed to evaluate the association of pubertal development with adiposity and cardio-metabolic health in girls and boys at 10 years of age and clarify if that association is independent of body mass index (BMI) previous to the onset of puberty Methods This study included 4550 children recruited from the birth cohort Generation XXI in 2005/2006, from Porto, Portugal. Pubertal development was evaluated at the 10 years old follow-up evaluation, by trained nurses through the Tanner scale and categorized into 1–pre-pubertal and ≥ 2–pubertal and post-pubertal. Girls were also categorized according to menarche stage and boys by testicular volume ( Results After taking previous BMI into account, Tanner stage ≥ 2 remained associated with weight [girls β = 3.03 kg (2.57;3.50); boys β = 1.29 kg (0.88;1.71)], height [girls β = 3.81 cm (2.21;4.42); boys β = 2.45 cm (1.93;2.97)], waist circumference [girls β = 2.64 cm (2.11;3.18); boys β = 0.81 cm (0.34;1.29)], fat-free mass index [girls β = 0.33 kg/m2 (0.18;0.47); boys β = 0.18 kg/m2 (0.04;0.31)], HDL-cholesterol [girls β = −1.64 mg/dL (−2.87; − 0.41); boys β = −1.51 mg/dL (−2.62; − 0.41)], and only in girls, BMI [β = 0.67 (0.51;0.83)], glucose [β = 1.59 mg/dL (0.85; 2.33)], insulin [β = 1.73 μU/mL (1.02; 2.44)] and HOMA-IR [β = 0.40 (0.24; 0.57)]. Considering only testicular volume to define pubertal development the results were similar to the previous ones for boys, while having had menarche was only significantly associated with higher weight [β = 0.60 kg (0.29;0.91)] and BMI [β = 0.17 kg/m2 (0.07; 0.28)]. Conclusions Independently of previous BMI, girls and boys with a more advanced pubertal development at 10 years of age had worse cardio-metabolic health. These pre-adolescents should be a target for prevention of impaired levels of cardio-metabolic indicators.

Maternal diabetes mellitus and timing of pubertal development in daughters and sons: a nationwide cohort study

To study the association between maternal diabetes and timing of pubertal development in daughters and sons. Prospective cohort study. Not applicable. A total of 15,822 mother-child pairs included in the Danish National Birth Cohort and the Puberty Cohort with prospectively collected, register-based and self-reported information on maternal diabetes and self-reported information on pubertal development. None. Adjusted mean monthly difference in age at attaining pubertal milestones in children born of mothers with diabetes compared with children born of mothers without diabetes. A total of 502 children were born of mothers with diabetes during pregnancy. In daughters exposed to gestational diabetes mellitus, we observed advanced onset in all pubertal milestones. The associations were statistically significant with regard to pubic hair Tanner stage 2 (-4.8months) (95% confidence interval [CI] -7.7, -2.0), pubic hair Tanner stage 3 (-2.2months) (95 % CI -4.4, 0.0), pubic hair Tanner stage 5 (-6.0months) (95% CI -10.8, -1.2), and menarche (-2.5months) (95 % CI -4.9, 0.0). We observed no tendencies between maternal type 1 or type 2 diabetes mellitus and pubertal development in daughters. We observed no associations between maternal diabetes and pubertal development in sons. Our findings suggest that gestational diabetes mellitus may accelerate the pubertal development in daughters. Our results did not support an association between type 1 or type 2 diabetes mellitus and daughters' pubertal development, as well as between any type of maternal diabetes and sons' pubertal development.

Race disparities in pubertal timing: Implications for cardiovascular disease risk among African American women.

Compared to white girls, sexual maturation is accelerated in African American girls as measured by indicators of pubertal development, including age at first menses. Increasing epidemiological evidence suggests that the timing of pubertal development may have strong implications for cardio-metabolic health in adolescence and adulthood. In fact, younger menarcheal age has been related prospectively to poorer cardiovascular risk factor profiles, a worsening of these profiles over time, and an increase in risk for cardiovascular events, including non-fatal incident cardiovascular disease and cardiovascular-specific and all-cause mortality. Yet, because this literature has been limited almost exclusively to white girls/women, whether this same association is present among African American girls/women has not been clarified. In the current narrative review, the well-established vulnerability of African American girls to experience earlier pubertal onset is discussed as are findings from literatures examining the health outcomes of earlier pubertal timing and its antecedents, including early life adversity exposures often experienced disproportionately in African American girls. Gaps in these literatures are highlighted especially with respect to the paucity of research among minority girls/women, and a conceptual framework is posited suggesting disparities in pubertal timing between African American and white girls may partially contribute to well-established disparities in adulthood risk for cardio-metabolic disease between African American and white women. Future research in these areas may point to novel areas for intervention in preventing or lessening the heightened cardio-metabolic risk among African American women, an important public health objective.

Urinary bisphenol A and pubertal development in Chinese school-aged girls: a cross-sectional study

BackgroundAnimal studies suggest that bisphenol A (BPA) may perturb pubertal development in females. However, evidence from human studies is limited.MethodsThis was a cross-sectional study to investigate the association between BPA exposure and pubertal development in school-aged girls. A total of 655 girls aged 9–18 years were selected from three schools in Shanghai, from May to June 2011. We collected one single spot urine sample from each girl. Urine BPA concentrations were measured by modified high-performance liquid chromatography and categorized according to LOD and the median of those above LOD. Pubertal development status was assessed by using Tanner staging, and age at menarche was collected as a milestone for mid-puberty. Modified Poisson regression was used to estimate adjusted prevalence ratios (PRs) and 95% confidence intervals (CIs).ResultsAfter adjustment for potential confounders, girls with detected BPA were more likely to have delayed menarche, a mid-puberty event, compared with girls with undetectable BPA; the prevalence ratios (PR) were 0.73 (0.56, 0.95) for those with moderate BPA(LOD-median) and 0.72 (0.52, 0.99) for those with high BPA(>median), respectively. Girls aged 9–12 years with detected BPA were more likely to have reached pubic hair stage 2, the indicator of pubarche; while among girls aged >15 years, those with detected BPA were less likely to have reached pubic hair stage 5, the late stage of pubic hair development.ConclusionsBPA exposure was associated with alterations in the timing of pubertal development. Results in the present study should be interpreted with caution because of its cross-sectional nature and the limited sample size in each age group.

The age of onset of pubertal development in healthy Thai boys in Khon Kaen, Thailand

Abstract Background There is variation of the age of onset of puberty in a population. The secular trends in the timing of pubertal development have decreased in some parts of the world. Objective To determine the age of pubertal development in healthy Thai boys in Khon Kaen, Thailand and compare it with that in previous studies of Thai boys. Methods A descriptive, cross-sectional study was performed in 316 school boys aged 5–16 years between May and July 2011. Development of the genitals and pubic hair was determined by Tanner staging, and testicular volume was assessed using a Prader orchidometer. All boys were examined by a male pediatrician. Results Genital stage of puberty in boys occurred at a median age of 11.3 years and a mean ± SD age of 11.3 ± 1.3 (mean ± SD, range 8.0–14.9) years, and pubarche occurred at a median age of 12.8 years and a mean ± SD of 12.5 ± 1.2 years (range 9.1–14.9) years. Conclusions No secular trend towards earlier age at pubertal onset for gonadarche in Khon Kaen boys, but pubarche seems to be later than found in previous studies in Thai boys.

Maternal Preeclampsia and Androgens in the Offspring around Puberty: A Follow-Up Study.

BackgroundChildren born after preeclampsia may have a dominant androgen profile in puberty compared with other children. Circulating androgen concentrations at 11–12 years of age were compared between offspring born after preeclampsia, and children whose mothers did not have preeclampsia.MethodsA total of 611 mother-offspring pairs were followed up 11 (daughters) or 12 (sons) years after birth: 218 pairs in the preeclampsia group, and 383 pairs without preeclampsia. Circulating total testosterone, androstenedione, dehydroepiandrosterone sulfate (DHEAS), and insulin-like growth factor I (IGF-I) were measured in the children. In boys, testicular volume was also measured.ResultsAmong girls born after preeclampsia, DHEAS concentrations were higher than in unexposed girls (p<0.001), however, girls born after preeclampsia with severe features had the lowest DHEAS levels. In contrast, testosterone concentrations were highest in girls born after preeclampsia with severe features, both compared to other girls in the preeclampsia group, and compared to unexposed girls (p<0.001). For boys, testosterone concentrations were higher in the preeclampsia group compared with unexposed boys (p<0.001), and boys born after preeclampsia with severe features had the lowest concentrations of DHEAS. Compared with unexposed boys, testicular volume (p = 0.015) and IGF-I (p = 0.004) were higher for boys in the preeclampsia group, except for boys in the clinically severe preeclampsia group.ConclusionsIn utero exposure to preeclampsia is associated with androgen hormonal patterns in early puberty that depend on clinical severity of preeclampsia and sex of the offspring. The hormonal differences may reflect different timing of pubertal development, and may have consequences for future health of the offspring.