Prepubertal Body Mass Index Research Articles

The pubertal growth spurt is diminished in children with severe obesity.

At the population level, there is a negative linear correlation between childhood body mass index (BMI) and pubertal height gain. However, in children with obesity, there are no studies showing whether the severity of obesity affects pubertal height gain. Moreover, how obesity in childhood affects pubertal timing is controversial, especially in boys. We aimed to investigate the impact of severe obesity in childhood on the pubertal growth spurt in both sexes. The study group consisted of 68 patients (32 boys) with childhood onset obesity followed in a Spanish university hospital. The QEPS growth model was used to calculate pubertal growth function estimates for each individual. The highest individual prepubertal BMI SDS value was related to the age at onset of pubertal growth and pubertal height gain. Results were compared to analyses from individuals in a community-based setting (n = 1901) with different weight status. A higher peak BMI in childhood was associated with less specific pubertal height gain in children with moderate-to-extreme obesity. For boys, the higher the BMI, the earlier the onset of pubertal growth. For girls with obesity, this correlation was not linear. Obesity in childhood impairs the pubertal growth spurt in a severity-related fashion. The higher the BMI in childhood, the lower the pubertal height gain in children with moderate-to-extreme obesity. For boys with obesity, the higher the BMI, the earlier the onset of pubertal growth. The results contribute to the research field of how weight status in childhood is related to pubertal timing and pubertal growth. The results have implications for understanding how childhood obesity is related to further growth.

Early Life Adversity and Pubertal Timing: Implications for Cardiometabolic Health.

To identify early life adversity (ELA) risk factors for earlier pubertal timing, itself a risk factor for poor cardiometabolic health, and to determine whether such ELA-related risk may be mediated by pre-pubertal body mass index (BMI). Subjects included 426 female participants in a prospective birth cohort study, the NICHD Study of Early Child Care and Youth Development. Survival analysis models were fit to examine ELA exposures, representing childhood socioeconomic status (SES), maternal sensitivity, mother-child attachment, and negative life events, along with child health indicators and covariates, in relation to pubertal timing outcomes, including age at menarche and ages at Tanner stage II for breast and pubic hair development. Higher childhood SES emerged as an independent predictor of older age at menarche, showing each one standard deviation increase in childhood SES corresponded to a 1.3% increase in age at menarche (factor change = 1.013; 1.003-1.022; p < .01), but did not predict breast or pubic hair development (ps > .05). In mediation analyses, indirect (mediated) effects of mother-child attachment on the pubertal timing outcomes, via pre-pubertal BMI, were all statistically significant (ps < .05). Higher childhood SES predicted directly, and secure (vs. insecure) mother-child attachment predicted indirectly (via pre-pubertal BMI), later pubertal timing, suggesting these factors may protect girls from earlier pubertal development. By extension, clinical implications are that intervention strategies designed to lessen ELA- and pre-pubertal obesity-related risk may be effective in remediating life course pathways linking ELA, accelerated pubertal development, and cardiometabolic risk.

Breastfeeding and timing of pubertal onset in girls: a multiethnic population-based prospective cohort study

BackgroundEarly puberty is associated with higher risk of adverse health and behavioral outcomes throughout adolescence and adulthood. US girls are experiencing earlier puberty with substantial racial/ethnic differences. We examined the association between breastfeeding and pubertal timing to identify modifiable risk factors of early puberty and potential sources of racial/ethnic differences in the timing of pubertal development.MethodsA prospective cohort study of 3331 racially/ethnically diverse girls born at Kaiser Permanente Northern California (KPNC) between 2004 and 06. All data were obtained from KPNC electronic clinical and administrative datasets. Mother-reported duration of breastfeeding was obtained from questionnaires administered at each ‘well-baby’ check-up exam throughout the baby’s first year and categorized as ‘Not breastfed’, ‘Breastfed < 6 months’, and ‘Breastfed ≥6 months’. Pubertal development data used Tanner stages assessed by pediatricians during routine pediatric checkups starting at age 6. Pubertal onset was defined as transition from Tanner Stage 1 to Tanner Stage 2+ for breast (thelarche) and pubic hair (pubarche). Weibull regression models accommodating for left, right, and interval censoring were used in all analyses. Models were adjusted for maternal age, education, race/ethnicity, parity and prepubertal body mass index (BMI). We also examined race/ethnicity as a potential effect modifier of these associations.ResultsNot breastfeeding was associated with earlier onset of breast and pubic hair development compared to breastfeeding ≥6 months (adjusted hazard ratio [HR]: 1.25; 95% confidence interval [CI]: 1.07–1.46; HR: 1.24; 95% CI: 1.05–1.46, respectively). Breastfeeding for < 6 months was also associated with the risk of earlier pubic hair development (HR: 1.14; 95% CI: 1.00–1.30, compared to breastfeeding ≥6 months). Inclusion of girls’ prepubertal BMI slightly attenuated the association between breastfeeding and timing of breast onset but remained significant. The association between not breastfeeding and early breast development may be stronger among African American girls (HR: 1.92; 95% CI: 1.01–3.66, compared to breastfeeding ≥6 months) than other racial/ethnic groups.ConclusionsBreastfeeding is an independent predictor of pubertal onset in girls, and the strength of the association may vary by race/ethnicity. Providing breastfeeding support and lactation education for high risk mothers may help prevent earlier pubertal onset and promote positive health outcomes later in life.

Pubertal development after unintended intrauterine exposure to oral contraceptives: a nationwide cohort study

To study the associations between exposure to oral contraceptives before conception and early in pregnancy and pubertal timing in boys and girls. Population-based cohort study. Not applicable. Overall, 15,800 children (70%) born during 2000-2003 into the Danish National Birth Cohort were categorized according to maternal use of combined oral contraceptive pills or progestin-only pills reported around gestational week 17: no exposure (reference), exposure 4months before conception, and exposure in early pregnancy. Children self-assessed pubertal status using Web-based questionnaires from 11years and biannually throughout puberty. None. Adjusted mean age differences (months) for attaining individual pubertal milestones and overall pubertal timing. Proportion mediated by prepubertal body mass index. In boys, intrauterine exposure to oral contraceptives showed a tendency toward slightly earlier mean age for voice break (months, -3.8; 95% confidence interval [CI] -6.5, -1.0) and first ejaculation (months, -2.9; 95% CI -5.9, 0.1) and a mean difference of -1.4months (95% CI -3.3, 0.4) for overall pubertal timing. Girls with intrauterine exposure tended to have slightly earlier age at menarche (months, -1.9; 95% CI -4.0, 0.3) and Tanner breast stages and had a mean difference of -0.9months (95% CI -2.7, 1.0) for overall pubertal timing. Exposure before conception was not associated with pubertal timing. Prepubertal body mass index did not play a mediating role. This study shows some evidence that intrauterine exposure to oral contraceptives might slightly affect pubertal timing.

Childhood Body Mass Index Is Associated with Risk of Adult Colon Cancer in Men: An Association Modulated by Pubertal Change in Body Mass Index.

The relative contribution of childhood and pubertal body mass index (BMI) for the risk of adult colorectal cancer is not known. The aim of this study was to evaluate the independent associations for childhood BMI and pubertal BMI change with risk of colorectal cancer in men. We included 37,663 men born in 1946 to 1961 who had weight and height measured at 8 (childhood) and 20 (young adult age) years of age available from the BMI Epidemiology Study. Information on colorectal cancer was retrieved from the Swedish National Patient Register (257 cases of colon cancer and 159 cases of rectal cancer). Childhood BMI at 8 years of age [HR, 1.19 per SD increase; 95% confidence interval (CI), 1.06-1.33], but not pubertal BMI change (HR, 1.02; 95% CI, 0.90-1.15), was associated with increased risk of colon cancer. Due to a significant interaction between childhood BMI and pubertal BMI change (P < 0.001), we stratified the analyses according to the median of pubertal BMI change. Childhood BMI was associated with risk of colon cancer in individuals with a pubertal BMI change above, but not below, the median (above: HR = 1.48, 95% CI, 1.26-1.74; below: HR = 0.95, 95% CI, 0.80-1.12). Neither childhood BMI nor pubertal BMI change was associated with rectal cancer. High childhood BMI was associated with increased risk of colon cancer only if it was followed by a pubertal BMI increase above the median. Further studies should evaluate prepubertal childhood BMI in relation to pubertal BMI change and BMI in middle age for the risk of colon cancer.

Associations of Maternal Gestational Weight Gain and Obesity With the Timing of Pubertal Onset in Daughters.

Early puberty is associated with adverse health outcomes, but little is known regarding early-life determinants influencing pubertal timing. We examined the associations between maternal gestational weight gain (GWG) and the timing of the onset of breast development (thelarche) and pubic hair development (pubarche) in a cohort of 2,070 girls born in a Kaiser Permanente Northern California facility between 2005 and 2006. Using Weibull regression models accommodating interval censoring and adjusting for important confounders, we found that excess GWG was associated with increased risk of early thelarche (hazard ratio (HR) = 1.50, 95% confidence interval (CI): 1.26, 1.78) and early pubarche (HR = 1.35, 95% CI: 1.10, 1.66). Inadequate GWG was associated with early thelarche (HR = 1.36, 95% CI: 1.08, 1.71). The associations between excess or inadequate GWG and risk of earlier thelarche were stronger if mothers were obese before or at the beginning of pregnancy (body mass index ≥30 kg body weight per m height squared) (HR = 2.01, 95% CI: 1.53, 2.63; HR = 2.08, 95% CI: 1.45, 2.98, respectively). Similar associations were found for pubarche outcome. Inclusion of girls' prepubertal body mass index slightly attenuated these associations, but they remained significant. Monitoring of maternal weight before and throughout pregnancy might help prevent early pubertal onset and subsequent negative health outcomes.

Association of prepubertal obesity with pubertal development in Chinese girls and boys: A longitudinal study.

ObjectivesThe purpose of this study was to examine the association of prepubertal body mass index (BMI) and weight status with pubertal development in boys and girls in Chongqing, China.MethodsIn a longitudinal study, 1237 students (695 boys and 542 girls) were recruited from Chongqing, China, and examined at baseline, then followed every 6 months for three and a half years. Height, weight, testicular volume, and breast development were measured at every examination. Age of first spermatorrhea and menarche were obtained from self‐report. Subjects were divided into normal weight, overweight, and obese groups according to baseline BMI. Multivariable Cox regression analysis was used to examine the association of BMI and weight status with pubertal development.ResultsIn girls, higher prepubertal BMI increased the chance of earlier menarche (hazards ratio (HR): 1.205, 95% confidence interval (95% CI): 1.151‐2.261) and breast development (HR: 1.092, 95% CI: 1.045‐1.142). Girls in the overweight (HR: 2.605, 95% CI: 1.716‐3.956) and obese (HR: 2.565, 95% CI: 1.603‐4.103) groups had an increased risk of early menarche compared with those in the normal weight group, while only overweight was associated with an increased risk for earlier breast development (HR: 1.469, 95% CI: 1.024‐2.108). In boys, higher prepubertal BMI was significantly associated with the timing of first spermatorrhea (HR: 1.054, 95% CI: 1.004‐1.106) and testicular development (HR: 1.098, 95% CI: 1.063‐1.135). Overweight (HR: 1.672, 95% CI: 1.204‐2.322) and obesity (HR: 1.598, 95% CI: 1.135‐2.249) increased the hazard of earlier testicular development compared with the normal weight group, while no significant differences were detected among the three weight groups in terms of time to first spermatorrhea.ConclusionsHigher prepubertal BMI was associated with earlier puberty in both Chinese boys and girls.

Influence of puberty timing on adiposity and cardiometabolic traits: A Mendelian randomisation study.

BackgroundEarlier puberty is widely linked with future obesity and cardiometabolic disease. We examined whether age at puberty onset likely influences adiposity and cardiometabolic traits independent of childhood adiposity.Methods and findingsOne-sample Mendelian randomisation (MR) analyses were conducted on up to 3,611 white-European female and male offspring from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort recruited at birth via mothers between 1 April 1991 and 31 December 1992. Time-sensitive exposures were age at menarche and age at voice breaking. Outcomes measured at age 18 y were body mass index (BMI), dual-energy X-ray absorptiometry–based fat and lean mass indices, blood pressure, and 230 cardiometabolic traits derived from targeted metabolomics (150 concentrations plus 80 ratios from nuclear magnetic resonance [NMR] spectroscopy covering lipoprotein subclasses of cholesterol and triglycerides, amino acids, inflammatory glycoproteins, and others). Adjustment was made for pre-pubertal BMI measured at age 8 y. For negative control MR analyses, BMI and cardiometabolic trait measures taken at age 8 y (before puberty, and which therefore cannot be an outcome of puberty itself) were used. For replication analyses, 2-sample MR was conducted using summary genome-wide association study data on up to 322,154 adults for post-pubertal BMI, 24,925 adults for post-pubertal NMR cardiometabolic traits, and 13,848 children for pre-pubertal obesity (negative control). Like observational estimates, 1-sample MR estimates in ALSPAC using 351 polymorphisms for age at menarche (explaining 10.6% of variance) among 2,053 females suggested that later age at menarche (per year) was associated with −1.38 kg/m2 of BMI at age 18 y (or −0.34 SD units, 95% CI −0.46, −0.23; P = 9.77 × 10−09). This coefficient attenuated 10-fold upon adjustment for BMI at age 8 y, to −0.12 kg/m2 (or −0.03 SDs, 95% CI −0.13, 0.07; P = 0.55). Associations with blood pressure were similar, but associations across other traits were small and inconsistent. In negative control MR analyses, later age at menarche was associated with −0.77 kg/m2 of pre-pubertal BMI measured at age 8 y (or −0.39 SDs, 95% CI −0.50, −0.29; P = 6.28 × 10−13), indicating that variants influencing menarche also influence BMI before menarche. Cardiometabolic trait associations were weaker and less consistent among males and both sexes combined. Higher BMI at age 8 y (per 1 kg/m2 using 95 polymorphisms for BMI explaining 3.4% of variance) was associated with earlier menarche among 2,648 females (by −0.26 y, 95% CI −0.37, −0.16; P = 1.16 × 10−06), likewise among males and both sexes combined. In 2-sample MR analyses using 234 polymorphisms and inverse variance weighted (IVW) regression, each year later age at menarche was associated with −0.81 kg/m2 of adult BMI (or −0.17 SD units, 95% CI −0.21, −0.12; P = 4.00 × 10−15). Associations were weaker with cardiometabolic traits. Using 202 polymorphisms, later menarche was associated with lower odds of childhood obesity (IVW-based odds ratio = 0.52 per year later, 95% CI 0.48, 0.57; P = 6.64 × 10−15). Study limitations include modest sample sizes for 1-sample MR, lack of inference to non-white-European populations, potential selection bias through modest completion rates of puberty questionnaires, and likely disproportionate measurement error of exposures by sex. The cardiometabolic traits examined were heavily lipid-focused and did not include hormone-related traits such as insulin and insulin-like growth factors.ConclusionsOur results suggest that puberty timing has a small influence on adiposity and cardiometabolic traits and that preventive interventions should instead focus on reducing childhood adiposity.

Pubertal maturation and affective symptoms in adolescence and adulthood: Evidence from a prospective birth cohort.

The higher prevalence of affective symptoms among women compared to men emerges in adolescence, and it has been associated with pubertal maturation. However, it remains unclear whether pubertal timing has long-term influences on affective symptoms. Using data from the British 1946 birth cohort, we investigated whether pubertal timing was associated with affective symptoms over the life course, distinguishing those with symptoms in adolescence only, symptoms in adulthood only, and symptoms in both adolescence and adulthood. In females, there was no evidence that early pubertal maturation was a risk factor for affective symptoms. However, those with particularly late menarche (≥15 years) showed a lower risk of adult-onset affective symptoms (odds ratio = 0.54, 95% confidence interval = 0.31, 0.95). This effect of late pubertal timing was not explained by a range of sociobehavioral factors. In contrast, in males, late pubertal timing was associated with increased risk of adolescent-onset affective symptoms that tracked into adulthood (odds ratio = 2.10, 95% confidence interval = 1.44, 3.06). This effect was partly explained by low prepubertal body mass index. Sex-specific effects of pubertal timing on the long-term risk of affective symptoms might be due to different effects of gonadal hormonal on the central nervous system, as well as different social experiences during puberty.

Genome-wide association study of sexual maturation in males and females highlights a role for body mass and menarche loci in male puberty.

Little is known about genes regulating male puberty. Further, while many identified pubertal timing variants associate with age at menarche, a late manifestation of puberty, and body mass, little is known about these variants' relationship to pubertal initiation or tempo. To address these questions, we performed genome-wide association meta-analysis in over 11 000 European samples with data on early pubertal traits, male genital and female breast development, measured by the Tanner scale. We report the first genome-wide significant locus for male sexual development upstream of myocardin-like 2 (MKL2) (P = 8.9 × 10(-9)), a menarche locus tagging a developmental pathway linking earlier puberty with reduced pubertal growth (P = 4.6 × 10(-5)) and short adult stature (p = 7.5 × 10(-6)) in both males and females. Furthermore, our results indicate that a proportion of menarche loci are important for pubertal initiation in both sexes. Consistent with epidemiological correlations between increased prepubertal body mass and earlier pubertal timing in girls, body mass index (BMI)-increasing alleles correlated with earlier breast development. In boys, some BMI-increasing alleles associated with earlier, and others with delayed, sexual development; these genetic results mimic the controversy in epidemiological studies, some of which show opposing correlations between prepubertal BMI and male puberty. Our results contribute to our understanding of the pubertal initiation program in both sexes and indicate that although mechanisms regulating pubertal onset in males and females may largely be shared, the relationship between body mass and pubertal timing in boys may be complex and requires further genetic studies.

Timing of puberty and physical growth in obese children: a longitudinal study in boys and girls

To assess whether puberty and physical growth vary in obese when compared to normal-weight children. One hundred obese pre-pubertal children (44 boys; mean age (±SD): 9.01 ± 0.62 years; 56 girls; 8.70 ± 0.57 years) were compared to 55 normal-weight controls (27 boys; 9.17 ± 0.26 years; 28 girls; 8.71 ± 0.62 years). All study participants were followed prospectively with 6-monthly follow-up visits. At each study visit, height, weight, body mass index (BMI) and pubertal stage were assessed. Obese children entered puberty and achieved later stages of puberty earlier than controls (onset of puberty: boys: 11.66 ± 1.00 vs. 12.12 ± 0.91 years, P = 0.049; girls: 9.90 ± 0.78 vs. 10.32 ± 1.70, P = 0.016; late puberty: boys: 13.33 ± 0.71 vs. 14.47 ± 1.00 years, P < 0.001; girls: 11.54 ± 0.99 vs. 12.40 ± 1.02, P = 0.001). Pre-pubertal BMI standard deviation score (SDS) was inversely associated with both age at the onset of puberty (β = -0.506, P < 0.001) and age at late puberty (β = -0.514, P < 0.001). Obese children also showed an earlier age at peak height velocity (PHV) (boys: 12.62 ± 0.82 vs. 13.19 ± 0.96 years, P = 0.01; girls: 11.37 ± 0.89 vs. 12.77 ± 0.76, P < 0.001) and a lower PHV (boys: 7.74 ± 1.49 vs. 9.28 ± 1.64 cm year(-1) , P < 0.001; girls: 7.60 ± 1.64 vs. 8.29 ± 1.03, P = 0.03). Height SDS progressively declined over the study period in the obese group (P for trend <0.001), whereas there were no significant changes in the control group (P for trend = 0.5). Obese boys and girls presented an earlier onset of puberty and completion of puberty and an impaired height gain during puberty.

The Relationship of Pre-pubertal BMI Status to Post-pubertal BMI Status: An 8 Year Cohort Study

Objective: To investigate body mass index (BMI) percentile trends in a longitudinal cohort through puberty and to identify factors associated with post-pubertal overweight/obese BMI percentile status. Methods: A retrospective cohort study of 760 children over eight years in a large academic healthcare system. Each child had one pre-puberty visit during 1999-2000 while aged 6-11 and one post-puberty visit during 2006-2007. Demographic and BMI data was collected on all subjects. For pre-pubertal overweight/obese subjects (BMI ≥ 85th percentile), additional data was reviewed. Results: Overall, rates of overweight/obesity increased from 39% to 46% from pre to post puberty, respectively. Neither race/ethnicity nor gender was associated with increased post-pubertal BMI percentile. Twenty percent of children with normal pre-puberty BMI percentile progressed to being overweight/obese. A high normal pre-pubertal BMI (72nd-84th percentile) was predictive of post-pubertal overweight/obese status. Having a post-puberty overweight/ obese BMI percentile was 20.4 times more likely if the pre-puberty BMI was ≥ 85th percentile. Pre-puberty overweight/ obese subjects were less likely to be obese post-puberty if they met with a nutritionist/dietician. Few overweight/obese subjects had a provider-documented diagnosis of overweight/obese pre-puberty and weight related co-morbidities doubled through puberty, but neither influenced post-pubertal BMI percentile status. Conclusions: A pre-pubertal BMI at high normal (72nd-84th percentile), or a BMI ≥ 85th percentile, but not race/ ethnicity or gender, are risk factors for an overweight/obese BMI status post-puberty. Most children do not out grow their overweight/obese status through puberty, signifying the need for improved, earlier identification of and intervention for the pre-pubertal overweight/obese children and those near overweight (BMI ≥ 72nd percentile).

Distinct Variants at LIN28B Influence Growth in Height from Birth to Adulthood

We have studied the largely unknown genetic underpinnings of height growth by using a unique resource of longitudinal childhood height data available in Finnish population cohorts. After applying GWAS mapping of potential genes influencing pubertal height growth followed by further characterization of the genetic effects on complete postnatal growth trajectories, we have identified strong association between variants near LIN28B and pubertal growth (rs7759938; female p = 4.0 x 10(-9), male p = 1.5 x 10(-4), combined p = 5.0 x 10(-11), n = 5038). Analysis of growth during early puberty confirmed an effect on the timing of the growth spurt. Correlated SNPs have previously been implicated as influencing both adult stature and age at menarche, the same alleles associating with taller height and later age of menarche in other studies as with later pubertal growth here. Additionally, a partially correlated LIN28B SNP, rs314277, has been associated previously with final height. Testing both rs7759938 and rs314277 (pairwise r(2) = 0.29) for independent effects on postnatal growth in 8903 subjects indicated that the pubertal timing-associated marker rs7759938 affects prepubertal growth in females (p = 7 x 10(-5)) and final height in males (p = 5 x 10(-4)), whereas rs314277 has sex-specific effects on growth (p for interaction = 0.005) that were distinct from those observed at rs7759938. In conclusion, partially correlated variants at LIN28B tag distinctive, complex, and sex-specific height-growth-regulating effects, influencing the entire period of postnatal growth. These findings imply a critical role for LIN28B in the regulation of human growth.

Age at puberty and the emerging obesity epidemic.

BackgroundRecent studies have shown that puberty starts at younger ages than previously. It has been hypothesized that the increasing prevalence of childhood obesity is contributing to this trend. The purpose of this study was to analyze the association between prepubertal body mass index (BMI) and pubertal timing, as assessed by age at onset of pubertal growth spurt (OGS) and at peak height velocity (PHV), and the secular trend of pubertal timing given the prepubertal BMI.Methodology/Principal FindingsAnnual measurements of height and weight were available in all children born from 1930 to 1969 who attended primary school in the Copenhagen municipality; 156,835 children fulfilled the criteria for determining age at OGS and PHV. The effect of prepubertal BMI at age seven on these markers of pubertal development within and between birth cohorts was analyzed. BMI at seven years was significantly inversely associated with age at OGS and PHV. Dividing the children into five levels of prepubertal BMI, we found a similar secular trend toward earlier maturation in all BMI groups.Conclusion/SignificanceThe heavier both boys and girls were at age seven, the earlier they entered puberty. Irrespective of level of BMI at age seven, there was a downward trend in the age at attaining puberty in both boys and girls, which suggests that the obesity epidemic is not solely responsible for the trend.

Association of prepubertal body composition in healthy girls and boys with the timing of early and late pubertal markers

BackgroundIt is controversial whether prepubertal body composition is implicated in the timing of puberty onset. ObjectiveThe objective was to investigate whether body composition in the 2 y preceding the start of the pubertal growth spurt—a marker of puberty onset—is associated with the attainment of early and late pubertal markers in healthy German boys and girls. DesignMultivariate-adjusted regression analyses were performed in 215 participants of the DOrtmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study for whom body mass index (BMI) and its components fat mass/height2 (FM/m2) and fat-free mass/height2 (FFM/m2) 1 and 2 y before the onset of the pubertal growth spurt (age at takeoff; ATO) and information on early life exposures were available. In addition, age at peak height velocity (APHV) and menarche were examined. ResultsHigher BMIs and FM/m2z scores 1 and 2 y before ATO showed modest associations with chronological age at ATO among girls only (girls: P for = trend 0.05–0.1, adjusted for early life factors; boys: P = 0.2–0.6). FFM/m2z scores were not related to age at ATO (P for trend = 0.5–0.8). Conversely, prepubertal BMI and FM/m2 more clearly predicted APHV and puberty duration (APHV minus ATO) in both sexes and age at menarche in girls (girls: adjusted P for trend <0.0001–0.03; boys: P = 0.01–0.046). ConclusionThis longitudinal study suggests that prepubertal body composition in healthy boys and girls may not be critical for the initiation of the pubertal growth spurt but instead affects the progression of pubertal development, which results in earlier attainment of later pubertal stages.

Age at voice break in Danish boys: effects of pre‐pubertal body mass index and secular trend

Voice break is a late, but characteristic event in male puberty. Assessment of age at voice break may be a relevant marker for epidemiological studies of male pubertal development. We investigated the timing of voice break and its association with explanatory variables [calendar year of admission in the boys choir and pre-pubertal body mass index (BMI)] by survival analysis techniques based on retrospective analyses of age at voice break in 463 Danish choir boys who were studied over a 10-year period. We found an overall median age at voice break of 14.0 [13.9-14.6] years, and a statistically significant downwards trend in age at voice break in the 10-year period (1994-2003) (log-rank test p = 0.0146). There was a statistically significant difference in age at voice break between boys in the different BMI quartiles in pre-puberty (p = 0.00822) with a tendency towards early voice break with increasing BMI standard deviation scores. Thus boys in the heaviest quartile at 8 years of age had an increased risk of early voice break (RR of 1.74 [1.14-2.65]) approximately 6 years later, compared with boys in the thinnest quartile. The earlier voice break seen during the 10-year observation period could however not exclusively be explained by a general increase in BMI in that period. Our findings indicate that puberty, as assessed by age at voice break in boys, may be starting earlier in Denmark as it has been observed in the USA, and suggest a relationship between pre-pubertal BMI and the timing of puberty.

The impact of childhood body mass index on timing of puberty, adult stature and obesity: a follow-up study based on adolescent anthropometry recorded at Christ's Hospital (1936–1964)

To examine the impact of childhood body mass index (BMI) on timing of puberty, adult stature and obesity. A retrospective school-based cohort follow-up study. A total of 1520 men born between 1927 and 1956 with serial height and weight measurements from the age of 9 to 18, followed up in adulthood at a mean age of 63 years. Prepubertal (child) BMI; age at peak height velocity (APHV); adult leg length, waist and hip circumference (self-reported), and height and weight (measured). Boys with a higher childhood BMI tended to have an earlier puberty (per s.d. increase in child BMI: -0.31 years, 95% confidence interval (CI): -0.23 to -0.39, P < 0.001). Childhood BMI correlated strongly and positively with adult adiposity, as measured by BMI (1.24 kg/m(2), 95% CI: 1.04-1.45, P < 0.001), waist (1.94 cm, 95% CI: 1.50-2.37, P < 0.001) and hip (1.91 cm, 95% CI: 1.55-2.28, P < 0.001). It correlated inversely with leg length (-0.40 cm, 95% CI: -0.68 to -0.12, P = 0.005), but not significantly with height or trunk length. Boys with a later puberty tended to be taller (per s.d. increase in APHV: 0.57 cm, 95% CI: 0.17-0.97, P = 0.006) and less adipose as adults (-0.55 kg/m(2), 95% CI: -0.33 to -0.77, P < 0.001). The long-term consequences of childhood obesity into adulthood are well known, but the potential impact on early pubertal maturation is less well appreciated. The factors that contribute to the onset and persistence of childhood obesity require more public health focus.

Diabetes control deteriorates in girls at cessation of growth: relationship with body mass index.

Diabetic patients, particularly girls, often experience poor metabolic control during puberty and adolescence. The aim of this study was to investigate metabolic control during adolescence, especially in relation to pubertal stages, growth, insulin treatment and body mass index (BMI). We studied the records of 38 (consecutive) girls with prepubertal onset of Type 1 diabetes mellitus. Data from the age of 10 to 18-20 years were obtained with regard to glycaemic control, growth, age at menarche, final height and BMI, and analysed in relation to both chronological age and age at menarche. HbA1c was lowest 3 years before menarche; mean (+/- sd) 7.6 (+/- 1.2). After the pubertal growth spurt, there was a marked impairment of metabolic control, the highest level of HbA1c occurring 3 years after menarche. Mean age at menarche was 13.3 (+/- 1.1) years and mean linear growth after menarche only 4.7 cm, giving a final height of 164.9 (+/- 5.3) cm which is 2.7 cm below the Swedish mean. During adolescence the degree of correlation between BMI and HbA1c continuously increased, pointing out the effect of body fat on metabolic control in this age group. The level of HbA1c at 10 years of age could not predict the metabolic control after cessation of puberty, but prepubertal BMI appears to be a risk factor for both obesity and poor glycaemic control in late adolescence. The highest HbA1c was found after cessation of growth. Prepubertal BMI is a possible predictor of metabolic control in adolescent diabetic girls.

Pubertal Growth of the Short Normal Girl

Objectives: To determine the timing, magnitude and duration of the pubertal spurt for short normal and average height girls, to compare these with Tanner’s standard and to investigate predictors of pubertal growth. Methods: The growth of 46 short normal and 55 control girls, identified at school entry, was monitored throughout puberty. Height and weight were measured at 6-month intervals from which body mass index (BMI) was derived. Annual velocities were calculated and used to estimate the age and magnitude of peak height velocity (PHV). Age of menarche was recorded to the nearest month. Parents provided information on the child’s medical and social history. Results: The mean age at PHV, the magnitude of PHV and age at menarche were similar for both groups and close to Tanner’s 50th centile values. Pre-pubertal BMI predicted age at menarche for short and control girls, accounting for 17% of the variance. There was a tendency for early maturing girls of average stature to have greater PHV. However, this relationship was not observed in short girls, nor did any other variable, genetic or environmental, predict the timing or magnitude of their pubertal spurt. Conclusions: Delayed puberty in short normal girls is unlikely and their growth during puberty is comparable to girls of average height. The pubertal variables measured remain close to Tanner’s original standards for both groups, suggesting the lack of a secular trend towards earlier puberty in girls. The onset of menstruation is influenced by pre-pubertal BMI. However, the clinician should be aware that short normal girls have normal pubertal growth and that no genetic or environmental variable can predict the timing or magnitude of their growth spurt.