Dataset Information

Association between the onset age of puberty and parental height.

ABSTRACT: BACKGROUND:The onset age of physiological puberty is greatly variable. This variability has been attributed to environmental factors and to genetic factors although a very little is explained by genome-wide associations studies. Previously, we reported the existence of an association between the onset age of puberty and final height. It is known that final height is associated with parental height (specifically, with the "target height"). We hypothesized that the variability of the onset age of puberty contributes to the attainment of a final height which is similar to the target height. We hypothesized that whenever a child's height-percentile differs from the target height percentile (we called this difference the "height gap"), the onset of puberty is advanced or delayed so that they are closer or even equal at the end of pubertal growth. The association between height gap and onset age of puberty was investigated in the reported study. METHODS:The study is an observational retrospective study on growth during puberty in 170 Israeli (60 girls) and 335 Polish children (162 girls). Anthropometric measurements were analyzed by multivariable linear regression with the onset age of the pubertal growth spurt (PGS) as the dependent variable, and two independent variables "height gap" and body mass index (BMI)-both standardized. RESULTS:The adjusted coefficient of determination (adj R2) between the onset age of the PGS and the two independent variables was 0.69 (Israeli girls), 0.50 (Israeli boys, BMI excluded), 0.25 (Polish girls) and 0.13 (Polish boys). A prediction model for the onset age of puberty is presented. CONCLUSIONS:The association between the "height gap" and the onset age of puberty suggests that the variability of this age is part of the targeted process of statural growth. The proposed model may explain idiopathic cases of precocious and delayed puberty.

SUBMITTER: Limony Y

PROVIDER: S-EPMC6347184 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Association between the onset age of puberty and parental height.

Limony Yehuda Y Koziel Slawomir S Friger Michael M

PloS one 20190125 1

<h4>Background</h4>The onset age of physiological puberty is greatly variable. This variability has been attributed to environmental factors and to genetic factors although a very little is explained by genome-wide associations studies. Previously, we reported the existence of an association between the onset age of puberty and final height. It is known that final height is associated with parental height (specifically, with the "target height"). We hypothesized that the variability of the onset ...[more]

PMID: 30682183

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Project description:ImportanceBone health in early life is thought to influence the risk of osteoporosis in later life.ObjectiveTo examine whether puberty timing is associated with bone mineral density accrual up to adulthood.Design, setting, and participantsThis cohort study used data from the Avon Longitudinal Study of Parents and Children, a prospective population-based birth cohort initiated in 1991 to 1992 in southwest England. The participants were 6389 healthy British people who underwent regular follow-up, including up to 6 repeated bone density scans from ages 10 to 25 years. Data analysis was performed from June 2018 to June 2019.ExposuresAge at puberty from estimated age at peak height velocity (years).Main outcomes and measuresGains per year in whole-body bone mineral density (grams per square centimeter), assessed by dual-energy x-ray absorptiometry at ages 10, 12, 14, 16, 18, and 25 years and modeled using linear splines.ResultsA total of 6389 participants (3196 [50.0%] female) were included. The mean (SD) age at peak height velocity was 13.5 (0.9) years for male participants and 11.6 (0.8) years for female participants. Male participants gained bone mineral density at faster rates than did female participants, with the greatest gains in both male participants (0.139 g/cm2/y; 95% CI, 0.127-0.151 g/cm2/y) and female participants (0.106 g/cm2/y; 95% CI, 0.098-0.114 g/cm2/y) observed between the year before and 2 years after peak height velocity. When aligned by chronological age, per 1-year older age at puberty was associated with faster subsequent gains in bone mineral density; the magnitudes of faster gains were greatest between ages 14 and 16 years in both male participants (0.013 g/cm2/y; 95% CI, 0.011-0.015 g/cm2/y) and female participants (0.014 g/cm2/y; 95% CI, 0.014-0.015 g/cm2/y), were greater in male participants (0.011 g/cm2/y; 95% CI, 0.010-0.013 g/cm2/y) than in female participants (0.003 g/cm2/y; 95% CI, 0.003-0.004 g/cm2/y) between ages 16 and 18 years, and were least in both male participants (0.002 g/cm2/y; 95% CI, 0.001-0.003 g/cm2/y) and female participants (0.000 g/cm2/y; 95% CI, -0.001 to 0.000 g/cm2/y) between ages 18 and 25 years. Despite faster gains, older age at puberty was associated with persistently lower bone mineral density, changing from 0.050 g/cm2 (95% CI, -0.056 to -0.045 g/cm2) lower at age 14 years to 0.047 g/cm2 (95% CI, -0.051 to -0.043 g/cm2) lower at age 25 years in male participants and from 0.044 g/cm2 (95% CI, -0.046 to -0.041 g/cm2) to 0.034 g/cm2 (95% CI, -0.036 to -0.032 g/cm2) lower at the same ages in female participants.Conclusions and relevancePeople with older pubertal age should be advised on how to maximize bone mineral density and minimize its decrease in later life to help prevent fracture and osteoporosis.

Project description:BACKGROUND:Systemic inflammation may play a role in shaping breast composition, one of the strongest risk factors for breast cancer. Pubertal development presents a critical window of breast tissue susceptibility to exogenous and endogenous factors, including pro-inflammatory markers. However, little is known about the role of systemic inflammation on adolescent breast composition and pubertal development among girls. METHODS:We investigated associations between circulating levels of inflammatory markers (e.g., interleukin-6 (IL-6), tumor necrosis factor receptor 2 (TNFR2), and C-reactive protein (CRP)) at Tanner stages 2 and 4 and breast composition at Tanner stage 4 in a cohort of 397 adolescent girls in Santiago, Chile (Growth and Obesity Cohort Study, 2006-2018). Multivariable linear models were used to examine the association between breast composition and each inflammatory marker, stratifying by Tanner stage at inflammatory marker measurement. Accelerated failure time models were used to evaluate the association between inflammatory markers concentrations at each Tanner stage and time to menarche. RESULTS:In age-adjusted linear regression models, a doubling of TNFR2 at Tanner 2 was associated with a 26% (95% CI 7-48%) increase in total breast volume at Tanner 4 and a 22% (95% CI 10-32%) decrease of fibroglandular volume at Tanner 4. In multivariable models further adjusted for body fatness and other covariates, these associations were attenuated to the null. The time to menarche was 3% (95% CI 1-5%) shorter among those in the highest quartile of IL-6 at Tanner 2 relative to those in the lowest quartile in fully adjusted models. Compared to those in the lowest quartile of CRP at Tanner 4, those in the highest quartile experienced 2% (95% CI 0-3%) longer time to menarche in multivariable models. CONCLUSIONS:Systemic inflammation during puberty was not associated with breast volume or breast density at the conclusion of breast development among pubertal girls after adjusting for body fatness; however, these circulating inflammation biomarkers, specifically CRP and IL-6, may affect the timing of menarche onset.

Project description:Introduction The relationship between the characteristics of puberty growth and the stature (height and overweight and obesity) in late adolescence was not clear. We aimed to explore the effects of puberty growth patterns on the stature in late adolescence. Methods A total of 13,143 children from a longitudinal cohort from 2006 to 2016 in Zhongshan city of China were included. The Preece–Baines growth curve was fitted for each individual child, and the age at peak height velocity (APHV), peak height velocity (PHV), and age at take-off (TOA) were obtained from the Preece–Baines model. To compare the difference in height in late adolescence (at 18 years old) at different pubertal height growth patterns (height spurt timing, intensity, and duration), the height at baseline was matched by using the propensity score matching. The log-binomial model was applied to assess the association between the three pubertal height growth patterns (timing, intensity, and duration) and overweight and obesity status in late adolescence, controlling the urbanity and body mass index (BMI) at baseline. Results After matching the baseline height, boys and girls in three pubertal patterns with early timing (P < 0.01), small intensity (P < 0.01), and short duration (P < 0.01) of height spurt had the lowest final height in the late adolescence. A 16% increase and 45% increase of risk for overweight and obesity were significantly associated with the early APHV in boys and girls, respectively, relative risk (RR) in boys, 1.16(95% confidence interval, CI: 1.03–1.30), P = 0.011; RR in girls, 1.45(1.21–1.75), P < 0.001. A 21% increase and 59% increase of risk for overweight and obesity were significantly associated with small PHV in boys and girls, respectively, RR in boys, 1.21(1.07–1.36), P < 0.001; RR in girls, 1.59(1.30–1.95), P < 0.001; and an 80% increase of risk for overweight and obesity with small spurt duration in girls (RR = 1.80; 95% CI: 1.49, 2.18; P < 0.001). Conclusion Pubertal growth patterns, including earlier puberty onset timing, smaller puberty intensity, and shorter puberty spurt duration, had a positive association with lower height risks and higher overweight and obesity risks in late adolescence.

Project description:Background: Maternal height has been confirmed to be associated with offspring stunting in low- and middle-income countries (LMICs), but only limited studies have examined the paternal-offspring association, and few studies have examined the joint effect of maternal and paternal height on stunting. Objective: To investigate the association between parental height and stunting of children aged under five in LMICs. Methods: We obtained data from the Demographic and Health Surveys (DHS) conducted in 14 LMICs from 2006 to 2016. The association between maternal and paternal height and height-for-age z score (HAZ) of children aged under five was analyzed using a linear regression model in consideration of complex survey design, and regression coefficients (β) with 95% confidence intervals (CIs) were reported. Then, the association between maternal and paternal height quintile and child stunting was analyzed using a modified Poisson regression approach with robust error variance in consideration of complex survey design with adjustment for covariates. The effect estimates were expressed as relative risks (RRs) with 95% CIs. Results: A total of 50,372 singleton children were included and the weighted prevalence of stunting was 34.5%. Both maternal height and paternal height were associated with child HAZ (β = 0.047; 95% CI, 0.043, 0.050; and β = 0.022; 95% CI, 0.018, 0.025, respectively). Compared with those born to the tallest mothers and fathers, children from the shortest mothers and the shortest fathers had higher risks of stunting (adjusted RR = 1.89; 95% CI, 1.78, 2.01; adjusted RR = 1.56; 95% CI, 1.47, 1.65, respectively). The mother-offspring associations are substantively larger than the father-offspring associations for each corresponding height quintile. Children from the shortest parents had the highest risk of stunting compared with children from the tallest parents (adjusted RR = 3.23; 95% CI, 2.83, 3.68). Conclusions: Offspring born to short parents are at increased risk of stunting in LMICs, and this intergenerational effect is partly driven by maternal intrauterine influence. This suggests the importance of improving the nutritional status of children and adults in LMICs, especially female caregivers.

Project description:Advanced parental age is a well-replicated risk factor for autism spectrum disorder (ASD), a neurodevelopmental condition with a complex and not well-defined etiology. We sought to determine parental age associations with ASD-related outcomes in subjects at high familial risk for ASD. A total of 397 younger siblings of a child with ASD, drawn from existing prospective high familial risk cohorts, were included in these analyses. Overall, we did not observe significant associations of advanced parental age with clinical ASD diagnosis, Social Responsiveness Scale, or Vineland Adaptive Behavior Scales scores. Instead, increased odds of ASD were found with paternal age < 30 years (adjusted odds ratio [AOR] = 2.83 and 95% confidence intervals [CI] = 1.14-7.02). Likewise, younger age (<30 years) for both parents was associated with decreases in Mullen Scales of Early Learning early learning composite (MSEL-ELC) scores (adjusted β = -9.62, 95% CI = -17.1 to -2.15). We also found significant increases in cognitive functioning based on MSEL-ELC scores with increasing paternal age (adjusted β associated with a 10-year increase in paternal age = 5.51, 95% CI = 0.70-10.3). Results suggest the potential for a different relationship between parental age and ASD-related outcomes in families with elevated ASD risk than has been observed in general population samples. Autism Res 2020, 13: 998-1010. © 2020 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Previous work suggests that older parents have a greater likelihood of having a child with autism. We investigated this relationship in the younger siblings of families who already had a child with autism. In this setting, we found a higher likelihood of autism, as well as poorer cognitive scores, in the siblings with younger fathers, and higher cognitive scores in the siblings with older parents. These results suggest that parental age associations may differ based on children's familial risk for autism.

Dataset Information

Association between the onset age of puberty and parental height.

Publications

Association between the onset age of puberty and parental height.

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