Prepubertal BMI Research Articles

Association between childhood obesity and infertility in later life: a systematic review of cohort studies

BackgroundThe global prevalence of childhood obesity has exhibited a troubling surge in recent years. Due to the raised questions regarding its potential correlation with infertility in adulthood, this systematic review has been undertaken to explore the relationships between childhood obesity, and infertility later in life.MethodsA comprehensive search was performed in three international databases (PubMed, Web of Science, and Scopus). All cohort (retrospective or prospective), case-cohort, and nested case-control studies until April 2022 which assessed the association of obesity in children and adolescents with male and female infertility indicators in later life were included. The quality of the included studies was assessed by Newcastle-Ottawa quality assessment checklists.ResultOut of the initial 32,501 documents, eleven eligible studies with a total sample size of 498,980 participants were included. Five studies focused on the number of offspring and indicated that obesity, especially in adolescence had an association with later life lower number of children, nulliparity, and childlessness in both men and women. Concerning conceiving problems, two studies showed that obesity before age 12 increased the risk of female fertility problems in the future. Two studies reported that obesity in early life raised the risk of impaired female reproductive system such as menstrual or ovulatory problems. As well as females, a study discovered that obesity in men during their 20s was linked to an elevated risk of low sperm motility and poor sperm morphology. Another study has reported men with higher pre-pubertal BMI had lower sex hormone-binding globulin; however, the same association was not seen between childhood BMI and semen quality.ConclusionThe evidence suggests a positive association between childhood obesity with infertility indicators in later life. Childhood weight reduction strategies are suggested to be implemented in societies in order to reduce infertility rates in later life.

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.

Association of mode of delivery with offspring pubertal development in Project Viva: a prospective pre-birth cohort study in the USA.

Is cesarean delivery associated with earlier offspring pubertal development? We identified that boys born by cesarean delivery developed puberty earlier, evidenced by an earlier age at peak height velocity and earlier attainment of puberty score > 1, than boys born by vaginal delivery. Cesarean delivery is posited to have long-term effects on health outcomes. However, few studies have examined whether mode of delivery is related to pubertal development. Prospective pre-birth cohort study consisting of 1485 mother-child pairs enrolled during pregnancy from obstetric practices and followed up until early adolescence (median age 12.9 years). Participant inclusion required data on mode of delivery and at least one measure of pubertal development. Participants are children from the Project Viva study. We abstracted information on delivery mode from electronic medical records from children followed since birth (1999-2002) and examined the following markers of pubertal development: age at peak height velocity (APHV); age at menarche (girls only); parent-reported pubertal development score; and child-reported pictograph Tanner pubic hair staging. We used multivariable regression models to examine associations of delivery mode with these four pubertal indices, adjusting for the following confounders: demographic and socioeconomic factors; maternal height, pre-pregnancy BMI, total gestational weight gain, pregnancy conditions, parity, and maternal age at menarche; paternal height and BMI; gestational age at delivery and birthweight-for-gestational-age z-score. In this study, 23.2% of children were born by cesarean delivery. Girls had an earlier APHV, had a higher pubertal score throughout childhood and in early adolescence, and were more likely to attain puberty score >1 and Tanner pubic hair Stage >1 earlier compared to boys. Mean (SD) age at menarche in girls was 12.4 (1.0) years. Boys born by cesarean delivery had significantly earlier APHV (β -0.23 years; 95% CI -0.40, -0.05) and higher risk of earlier attainment of puberty score > 1 (hazard ratio 1.09; 95% CI 1.01, 1.19) than boys born by vaginal delivery, after adjusting for confounders. These associations were not mediated by pre-pubertal BMI and were similar for planned (no labor) and unplanned (labor) cesarean delivery. No associations were observed between delivery mode and time to attain Tanner pubic hair Stage > 1 in boys. In girls, mode of delivery was not associated with any of the measured pubertal development markers. This study used, as secondary outcomes, parent- and child-reported measures of pubertal development, which may be more prone to error and misclassification than information collected by trained observers or physicians during clinical examinations. The findings may also not be generalizable to populations from different settings, because all participants lived in one geographic area, were well educated, and had health care. Our findings provide support for cesarean delivery as a potential indicator of identifying children who are likely to experience earlier pubertal development; however, more studies are needed to confirm or refute these observations. The project was funded by grants from the National Institutes of Health. The authors have no financial relationships or competing interests to disclose. N/A.

Revisiting the critical weight hypothesis for regulation of pubertal timing in boys

ABSTRACTBackgroundRecent findings indicate that there is a body weight–sensing homeostatic regulation of body weight in postpubertal rodents and humans. It is possible that body weight sensing also might be involved in the regulation of pubertal timing. Although an early small study suggested that there is a critical body weight for pubertal timing in girls, most studies have focused on BMI and reported an inverse association between BMI and pubertal timing.ObjectivesIn the present longitudinal well-powered cohort study, we revisited the critical weight hypothesis and tested if prepubertal body weight is a more robust inverse predictor of pubertal timing than prepubertal BMI in boys.MethodWe included men born during 1945–1961 (old cohort; n = 31,971) and men born during 1981–1996 (recent cohort; n = 1465) in the large BMI Epidemiology Study (BEST) Gothenburg (combined BEST cohort n = 33,436). Men with information on prepubertal body weight and BMI at 8 y of age and age at peak height velocity (PHV; an objective measure of pubertal timing) were included.ResultsBody weight explained more of the variance in age at PHV than BMI in both the old cohort and the recent cohort (combined cohort, body weight 6.3%, BMI 3.6%). Both body weight (β: −0.24 SD/SD increase in weight; 95% CI: −0.25, −0.23) and BMI (β: −0.18 SD/SD increase in BMI, 95% CI: −0.19, −0.17) were inversely associated with age at PHV but the association for body weight was significantly more pronounced than the association for BMI (P < 0.001).ConclusionsIn conclusion, prepubertal body weight is a more robust inverse predictor of pubertal timing than prepubertal BMI in boys. We propose that body weight sensing constitutes a feedback mechanism to regulate pubertal timing.

Early puberty and risk for type 2 diabetes in men

Aims/hypothesisThe association between pubertal timing and type 2 diabetes, independent of prepubertal BMI, is not fully understood. The aim of the present study was to evaluate the association between pubertal timing and risk of adult type 2 diabetes, independent of prepubertal BMI, in Swedish men.MethodsWe included 30,697 men who had data for BMI at age 8 and 20 years and age at Peak Height Velocity (PHV), an objective assessment of pubertal timing, available from the BMI Epidemiology Study Gothenburg (BEST Gothenburg), Sweden. Information on type 2 diabetes (n = 1851) was retrieved from the Swedish National Patient Register. HRs and 95% CIs were estimated by Cox regression analysis. We observed violations of the assumption of proportional hazards for the association between age at PHV and the risk of type 2 diabetes and therefore split the follow-up period at the median age of type 2 diabetes diagnosis (57.2 years of age) to define early (≤57.2 years) and late (>57.2 years) type 2 diabetes diagnosis.ResultsAge at PHV was inversely associated with both early (HR 1.28 per year decrease in age at PHV, 95% CI 1.21, 1.36) and late (HR 1.13, 95% CI 1.06, 1.19) type 2 diabetes. After adjustment for childhood BMI, the associations between age at PHV and both early (HR 1.24, 95% CI 1.17, 1.31) and late (HR 1.11, 95% CI 1.05, 1.17) type 2 diabetes were similar. Moreover, early age at PHV predicted insulin treatment of type 2 diabetes (OR 1.25 per year decrease in age at PHV, 95% CI 1.17, 1.33). Assuming a higher risk among those with an age at PHV below the median, the population attributable factor indicates that 15% fewer of the diagnosed individuals would have developed type 2 diabetes had they not reached puberty early.Conclusions/interpretationThese findings indicate that early puberty may be a novel independent risk factor for type 2 diabetes.

Parental Obesity and Offspring Pubertal Development: Project Viva

To investigate the association of preconception parental obesity (body mass index [BMI] ≥30kg/m2) with offspring pubertal development. Among 1377 children from a prospective prebirth cohort in Boston, we examined markers of puberty (age at peak height velocity [PHV], age at menarche, self-reported pubertal development score), and adrenarche (pictograph Tanner pubic hair staging). We used multivariable regression models to examine associations of maternal and paternal obesity with offspring pubertal indices, and applied marginal structural models to estimate the controlled direct effect not mediated by offspring prepubertal BMI. The prevalence of paternal obesity alone, maternal obesity alone, and biparental obesity were 10.5%, 10.1%, and 5%, respectively. After adjusting for demographic and socioeconomic factors, parental heights and maternal age at menarche, maternal obesity alone (vs neither parent with obesity) was associated with earlier age at PHV (β -0.30years; 95% CI -0.57, -0.03) and higher early adolescent pubertal score (0.29 units; 0.10, 0.48) in boys, but not with pubertal or adrenarchal outcomes in girls. Paternal obesity alone was not associated with any outcomes in either boys or girls. Biparental obesity was associated with earlier age at PHV in boys and earlier menarche in girls. Using marginal structural models with stabilized inverse probability weighting, maternal obesity alone had significant controlled direct effects on age at PHV (-0.31years; -0.62, 0.00) and on pubertal score (0.22 units; 0.00, 0.44) in boys, independent of prepubertal BMI. Maternal, but not paternal, obesity is associated with earlier pubertal development in boys, and such association is independent of prepubertal BMI.

The relationship between pubertal timing and markers of vascular and cardiac structure and function in men and women aged 60\u201364 years

Earlier age at menarche has been associated with higher risk of coronary heart disease, but the mechanisms underlying the association remain unclear. We assessed the relationship of pubertal timing, in both men (n = 672) and women (n = 713), with vascular (carotid intima-media thickness (cIMT), pulse wave velocity (PWV)) and cardiac (left ventricular (LV) structure and function) measures recorded at age 60–64 yrs in a British birth cohort study. Regression models found that earlier menarche was associated with higher (more adverse) LV mass, LV end diastolic volume and left atrial volume, but not with other cardiac measures, cIMT or PWV. Associations were attenuated after adjustment for either adult or childhood BMI (e.g. mean difference in LV mass per year later menarche: −4.2 g (95% CI:−7.0,−1.4) reducing to −2.2 g (95% CI:−4.7,0.4) after adjustment for adult BMI). There were no associations among men, despite those fully mature at 15 yrs having higher blood pressure than the least mature group by 10.21 mmHg (95% CI:19.45,0.98). Any effect of pubertal timing on vascular and cardiac structure and function is likely to be small and primarily confounded by pre-pubertal BMI and/or mediated through adult adiposity.

Voice break in boys-temporal relations with other pubertal milestones and likely causal effects of BMI.

STUDY QUESTIONHow is timing of voice break related to other male pubertal milestones as well as to BMI?SUMMARY ANSWERWe provide a comprehensive temporal analysis of male pubertal milestones, including reproductive hormone dynamics, confirm voice break as a late milestone of male puberty and report a likely causal relationship between higher BMI and earlier age at voice break in men.WHAT IS KNOWN ALREADYVoice break represents a late pubertal milestone and recalled age at voice break is frequently used in epidemiological studies as a measure of puberty. In contrast, clinical studies use mainly testicular enlargement and/or genital tanner stage as the marker of pubertal onset. However, neither correlation of pubertal milestones nor reproductive hormone dynamics have been assessed in detail previously. Further, although BMI and puberty timing are known to be closely linked, cause and effect between these traits are not known.STUDY DESIGN, SIZE, DURATIONThe study included a population-based mixed cross-sectional and longitudinal cohort (2006–2014, COPENHAGEN Puberty Study) of 730 healthy Danish boys. Data for 55 871 male research participants from the 23andMe study were obtained, including genome-wide single nucleotide polymorphism data and age at voice break.PARTICIPANTS/MATERIALS, SETTING, METHODSWe performed a detailed evaluation of pubertal milestones and reproductive hormone levels (study population 1). A Mendelian randomization (MR) approach was used to determine the likely causal link between BMI and timing of voice break (study population 2).MAIN RESULTS AND THE ROLE OF CHANCEVoice break occurred at mean age 13.6 (95% CI: 13.5–13.8) years. At voice break, mean (95% CI) testosterone levels, LH levels and bi-testicular volume were 10.9 (10.0–11.7) nmol/L, 2.4 (2.2–2.5) IU/L and 24 (23–25) mL, respectively. Voice break correlated moderately strongly with timing of male pubertal milestones, including testicular enlargement, gonadarche, pubarche, sweat odor, axillary hair growth and testosterone above limit of detection (r2 range: 0.43–0.61). Timing of all milestones was negatively associated with age-specific BMI (all P ≤ 0.001). MR analyses inferred likely causal effects of higher BMI on earlier voice break in males (−0.35 years/approximate SD, P < 0.001).LIMITATIONS, REASONS FOR CAUTIONParticipation rate of the population-based cohort was 25%. Further, boys that were followed longitudinally were examined approximately every 6 months limiting the time resolution of pubertal milestones. Using adult BMI as exposure instead of prepubertal BMI in the MR analysis and the known inaccuracies of the testosterone immunoassay at low testosterone levels may be further limitations.WIDER IMPLICATIONS OF THE FINDINGSWe provide valuable normative data on the temporal relation of male pubertal milestones. Further, the likely causal relationship between BMI and puberty timing highlights the importance of preventing obesity in childhood.STUDY FUNDING/COMPETING INTEREST(S)This work was supported by Danish Agency for Science, Technology and Innovation (09-067 180); Danish Ministry of the Environment, CeHoS (MST-621-00 065); Capital Region of Denmark (R129-A3966); Ministry of Higher Education and Science (DFF-1331-00 113); Innovation Fund Denmark (InnovationsFonden, 14-2013-4); The International Center for Research and Research Training in Endocrine Disrupting Effects of Male Reproduction and Child Health. B.H., F.R.D., J.R.B.P. and K.K.O. are supported by the Medical Research Council (MC_UU_12015/2). The 23andMe study is supported by the National Human Genome Research Institute of the National Institutes of Health (R44HG006981). Members of the 23andMe Research Team are employees of 23andMe, Inc. and hold stock or stock options in 23andMe.TRIAL REGISTRATION NUMBERNCT01411527

Associations Between Maternal Obesity and Pregnancy Hyperglycemia and Timing of Puberty Onset in Adolescent Girls: A Population-Based Study.

Early puberty is associated with adverse health outcomes. We investigated whether in utero exposure to maternal obesity is associated with daughters' pubertal timing using 15,267 racially/ethnically diverse Kaiser Permanente Northern California members aged 6-11 years with pediatrician-assessed Tanner staging (2003-2017). We calculated maternal body mass index (BMI; weight (kg)/height (m)2) during pregnancy from the electronic health record data. Using a proportional hazards model with interval censoring, we examined the associations between maternal obesity and girls' pubertal timing, as well as effect modification by race/ethnicity and mediation by prepubertal BMI. Maternal obesity (BMI ≥30) and overweight (BMI 25-29.9) were associated with earlier onset of breast development in girls (hazard ratio (HR) = 1.39 (95% confidence interval (CI): 1.30, 1.49) and HR = 1.21 (95% CI: 1.13, 1.29), respectively), after adjustment for girl's race/ethnicity, maternal age, education, parity, and smoking during pregnancy. There was interaction by race/ethnicity for associations between maternal obesity and girls' pubic hair onset: Associations were strongest among Asian and non-Hispanic white girls (HR = 1.53 (95% CI: 1.24, 1.90) and HR = 1.34 (95% CI: 1.18, 1.52), respectively) and absent for African-American girls. Adjustment for girl's prepubertal BMI only slightly attenuated associations. Our results suggest the importance of maternal metabolic factors during pregnancy in the timing of girls' puberty and potential differences in the associations by race/ethnicity.

Associations Between Maternal Prepregnancy Body Mass Index and Gestational Weight Gain and Daughter's Age at Menarche: The Avon Longitudinal Study of Parents and Children.

Earlier puberty and menarche are associated with adverse health outcomes. Reported associations of maternal adiposity with daughter’s age at menarche are inconsistent. We examined associations between maternal prepregnancy body mass index (BMI; weight (kg)/height (m)2) and gestational weight gain (GWG) and daughter’s ages at menarche (n = 3,935 mother-offspring pairs), pubarche (Tanner stage 2 for pubic hair) (n = 2,942 pairs), and thelarche (Tanner stage 2 for breast development) (n = 2,942 pairs) in the Avon Longitudinal Study of Parents and Children, a prospective United Kingdom pregnancy cohort study (baseline 1991–1992). During a follow-up period of up to 17 years (1991–2008), mean menarcheal age was 12.6 (standard deviation, 1.2) years. Both maternal prepregnancy BMI and GWG were inversely associated with daughter’s age at menarche after adjustment for maternal age, parity, socioeconomic status, smoking, maternal menarcheal age, and ethnicity (mean differences were −0.34 months (95% confidence interval: −0.45, −0.22) per BMI unit and −0.17 months (95% confidence interval: −0.26, −0.07) per kg, respectively). Associations remained unchanged after adjustment for birth weight and gestational age but were attenuated to the null when results were adjusted for daughter’s prepubertal BMI. Similar results were found for ages at pubarche and thelarche. These findings indicate that greater prepregnancy BMI and GWG are associated with earlier puberty in daughters and that these associations are mediated by daughters’ prepubertal BMIs.

Association between excessive BMI increase during puberty and risk of cardiovascular mortality in adult men: a population-based cohort study

Being overweight during childhood and adolescence is associated with increased risk of cardiovascular disease in adulthood, but the relative contribution of prepubertal childhood BMI and BMI change during puberty to adult mortality due to cardiovascular disease is unknown. We assessed the contribution of these two distinct developmental BMI parameters for cardiovascular mortality in adult men. As a part of the ongoing population-based BMI Epidemiology Study (BEST) in Gothenburg, Sweden, men born between 1945 and 1961 with information on both their childhood BMI at age 8 years and BMI change during puberty were included in the study and followed up until December, 2013. Participants who died or emigrated before age 20 years were excluded from the analysis. BMI was collected from paediatric growth charts and mandatory military conscription tests. Childhood overweight (BMI of ≥17·9 kg/m2) was defined according to the Centers for Disease Control and Prevention's cutoff at 8 years of age, and BMI change during puberty was defined as the difference between young adult BMI and childhood BMI (BMI at age 20 years minus BMI at age 8 years). Information on mortality was retrieved from high quality national registers with the participants' ten-digit personal identity number. We used Cox proportional hazard regression to analyse the association between exposures and mortality. The ethics committee of the University of Gothenburg, Sweden, approved the study and waived the requirement for written informed consent. We followed 37 672 Swedish men from age 20 years for a mean of 37·8 years (1 422 185 person-years follow-up). 3188 all-cause deaths and 710 cardiovascular deaths occurred during follow-up. The correlation between childhood BMI and BMI change during puberty was marginal (r=0·06). BMI change during puberty, but not childhood BMI, was independently associated with adult all-cause and cardiovascular mortality in men. Boys that became overweight during puberty (HR 2·39; 95% CI 1·86-3·09) and boys who were overweight consistently throughout childhood and puberty (1·85; 1·28-2·67), but not boys overweight in childhood that normalised during puberty (0·99, 0·65-1·50), had increased risk of cardiovascular mortality compared with participants who were not overweight in childhood or as young adults. The association between BMI change during puberty and cardiovascular mortality was non-linear with a substantial association above a threshold of 6·7 units increase in BMI. Excessive BMI increase during puberty is a risk marker of adult cardiovascular mortality. These results indicate that BMI should be monitored during puberty to identify boys with increased risk of adult cardiovascular mortality. Swedish Research Council, the Swedish Government (under the Avtal om Läkarutbildning och Medicinsk Forskning [Agreement for Medical Education and Research]), the Lundberg Foundation, the Torsten Söderberg Foundation, the Novo Nordisk Foundation, the Knut and Alice Wallenberg Foundation, and the Anna Ahrenberg Foundation.

High normal post-load plasma glucose, cardiometabolic risk factors and signs of organ damage in obese children.

To evaluate normoglycemic overweight/obese (Ow/Ob) children whose post-load plasma glucose (2hPG) cut-point may be significantly associated with cardiometabolic risk factors (CMRFs) and whether this cut-point predicts preclinical signs of organ damage. One thousand seven hundred and thrity four normoglycemic Ow/Ob children were stratified into quintiles of 2hPG, the sixth group was constituted by 101 children with impaired glucose tolerance (IGT). Moving from the lower quintiles of 2hPG to IGT, the groups differed for Prepubertal stage, BMI, fasting PG, insulin levels, blood pressure, and lipids. To evaluate the best cut-off of 2hPG related to CMRFs, the area under the receiver operating characteristic curve and the Youden's index was calculated. Insulin resistance, high blood pressure, and high triglyceride/HDL-C ratio were associated with a 2hPG cut-off of 110 mg/dl. Children with 2hPG ≥110 mg/dl showed 1.3-3.2 fold higher risk to have high levels of ALT (as surrogate of nonalcoholic fatty liver disease) or increased carotid intima-media thickness. This study, performed in a large cohort of Ow/Ob children, shows that an atherogenic risk profile and preclinical signs of organ damage are associated with post-challenge elevations in plasma glucose still considered in the high normal range.

Maternal pre-pregnancy BMI, gestational weight gain, and age at menarche in daughters.

Life course theory suggests that early life experiences can shape health over a lifetime and across generations. Associations between maternal pregnancy experience and daughters' age at menarche are not well understood. We examined whether maternal pre-pregnancy BMI and gestational weight gain (GWG) were independently related to daughters' age at menarche. Consistent with a life course perspective, we also examined whether maternal GWG, birth weight, and prepubertal BMI mediated the relationship between pre-pregnancy BMI and daughter's menarcheal age. We examined 2,497 mother-daughter pairs from the 1979 National Longitudinal Survey of Youth. Survival analysis with Cox proportional hazards was used to estimate whether maternal pre-pregnancy overweight/obesity (BMI≥25.0kg/m(2)) and GWG adequacy (inadequate, recommended, and excessive) were associated with risk for earlier menarche among girls, controlling for important covariates. Analyses were conducted to examine the mediating roles of GWG adequacy, child birth weight and prepubertal BMI. Adjusting for covariates, pre-pregnancy overweight/obesity (HR=1.20, 95% CI 1.06, 1.36) and excess GWG (HR=1.13, 95% CI 1.01, 1.27) were associated with daughters' earlier menarche, while inadequate GWG was not. The association between maternal pre-pregnancy weight and daughters' menarcheal timing was not mediated by daughter's birth weight, prepubertal BMI or maternal GWG. Maternal factors, before and during pregnancy, are potentially important determinants of daughters' menarcheal timing and are amenable to intervention. Further research is needed to better understand pathways through which these factors operate.

The physiology and timing of male puberty

To describe available markers of male puberty, discuss associations between adiposity and pubertal timing and to review recent evidence of a possible secular trend in male pubertal timing. An expert panel reviewing existing American pubertal data from boys in 2005 could not confirm a secular trend in male pubertal timing. National Health and Nutrition Examination Survey III findings have been confirmed by the National Institute of Child Health and Human Development study reporting a mean age of 10.4 years for Caucasian boys entering Tanner stage G2. Furthermore, the Copenhagen Puberty Study reported a 3 months decline in pubertal onset during a 15-year period (from 11.92 years in 1991 to 11.66 years in 2008).A negative association between obesity and early puberty was found in the National Institute of Child Health and Human Development study, in contrast to the positive association found in a Danish study. Other studies have not been able to document an association between prepubertal BMI and age at pubertal onset. Evaluation of Tanner stage and especially assessment of testicular volume should both be used in epidemiological studies. We speculate that the association between fat mass and pubertal timing may be nonlinear and recent studies may indicate a small decline in age at pubertal onset in boys.

Bone Age Advancement in Prepubertal Children With Obesity and Premature Adrenarche: Possible Potentiating Factors

Obesity and premature adrenarche (PA) are both associated with bone age (BA) advancement of unclear etiology, which may lead to earlier puberty, suboptimal final height and obesity in adulthood. Our objective was to understand the hormonal and anthropometric characteristics of BA advancement in a spectrum of prepubertal children with and without obesity and PA. In this cross-sectional study of 66 prepubertal children (35 PA, 31 control, 5-9 years), BMI z-score, hormonal values and response to an oral glucose tolerance test were the main outcome measures. Subjects were divided into tertiles by BA divided by chronological age (BA/CA), an index of BA advancement. Subjects in the top tertile for BA/CA had the highest dehydroepiandrosterone sulfate (DHEAS), free testosterone (%), hemoglobin A(1C), BMI z-score, and weight (P < 0.05). BMI z-score (r = 0.47), weight (r = 0.40), free testosterone (%) (r = 0.34), and DHEAS (r = 0.30) correlated with BA/CA (P < 0.02). Regression analysis showed greater BA/CA in PA compared to controls after controlling for weight (0.21 ± 0.56, P < 0.004). An exploratory stepwise regression model showed that weight, estradiol, and DHEAS were the strongest predictors of BA/CA accounting for 24% of its variance. Obesity was highly associated with BA advancement in this study of prepubertal children. In addition, children with PA had greater BA/CA at any given weight when compared to controls. These findings suggest a possible hormonal factor, which potentiates the effect of obesity on BA advancement in children with obesity and/or PA.

BMI Changes During Childhood and Adolescence as Predictors of Amount of Adult Subcutaneous and Visceral Adipose Tissue in Men

OBJECTIVEThe amount of visceral adipose tissue is a risk factor for the metabolic syndrome. It is unclear how BMI changes during childhood and adolescence predict adult fat distribution. We hypothesized that there are critical periods during development for the prediction of adult subcutaneous and visceral fat mass by BMI changes during childhood and adolescence.RESEARCH DESIGN AND METHODSDetailed growth charts were retrieved for the men participating in the population-based Gothenburg Osteoporosis and Obesity Determinants (GOOD) Study (n = 612). Body composition was analyzed using dual-energy X-ray absorptiometry and adipose tissue areas using abdominal computed tomography at 18 to 20 years of age.RESULTSThe main finding in the present study was that subjects with increases in BMI Z score of more than 1 SD during adolescence had, independent of prepubertal BMI, both larger subcutaneous (+138%; P < 0.001) and visceral adipose tissue areas (+91%; P < 0.001) than subjects with unchanged BMI Z-score. In contrast, subjects with increases in BMI Z score of more than 1 SD during late childhood had a larger amount of adult subcutaneous adipose tissue (+83%; P < 0.001) than subjects with unchanged BMI Z score but an unaffected amount of visceral adipose tissue. BMI changes during adolescence predict both visceral and subcutaneous adipose tissue of the abdomen, whereas BMI changes during late childhood predict only the subcutaneous adipose tissue.CONCLUSIONSThe amount of visceral adipose tissue in young adult men was associated with BMI changes specifically during adolescence, whereas the amount of subcutaneous adipose tissue was associated with BMI changes during both late childhood and adolescence.

Pubertal Timing Is an Independent Predictor of Central Adiposity in Young Adult Males

The role of puberty and normal variations in pubertal timing for the development of obesity in men is unclear. The aim of the current study was to investigate the impact of pubertal timing and prepubertal BMI (kg/m(2)) for young adult BMI and fat mass distribution. Detailed growth charts from birth to age 18-20 years were retrieved for the men participating in the population-based Gothenburg Osteoporosis and Obesity Determinants study. Age at peak height velocity (PHV) and BMI at age 10 years were estimated for 579 subjects, and PHV was used as an assessment of pubertal timing. The fat mass characterization and distribution were analyzed using dual X-ray absorptiometry and peripheral as well as abdominal computed tomography at age 18.9 +/- 0.5 years. We demonstrate that age at PHV is an independent negative predictor of young adult BMI and whole-body fat mass. Interestingly, age at PHV is an independent negative predictor of central, but not peripheral, fat mass. In contrast, BMI at 10 years of age predicts both central and peripheral subcutaneous fat mass. In conclusion, we demonstrate that early pubertal onset specifically predicts a central fat mass distribution, while a predominantly subcutaneous obese phenotype is strongly predicted by a high prepubertal BMI.