scholarly journals Pubertal Onset in Boys and Girls Is Influenced by Pubertal Timing of Both Parents

2016 ◽  
Vol 101 (7) ◽  
pp. 2667-2674 ◽  
Author(s):  
Christine Wohlfahrt-Veje ◽  
Annette Mouritsen ◽  
Casper P. Hagen ◽  
Jeanette Tinggaard ◽  
Mikkel Grunnet Mieritz ◽  
...  

Context: Epidemiological evidence on maternal and paternal heritability of the wide normal variation within pubertal timing is sparse. Objective: We aimed to estimate the impact of parental pubertal timing on the onset of puberty in boys and girls. Design: Annual pubertal examinations of healthy children in a longitudinal cohort study. Information on parental timing of puberty (earlier, comparable to, or later compared to peers) and menarche age was retrieved from questionnaires. Participants: A total of 672 girls and 846 boys. Main Outcome Measures: Age at onset of pubic hair (PH2+), breasts (B2+), and menarche in girls; and PH2+, genital stage (G2+), and testis >3 mL with orchidometer (Tvol3+) in boys. Results: In boys, pubertal onset was significantly associated with pubertal timing of both parents. PH2+ and Tvol3+ were earlier: −11.8 months (95% confidence interval, −16.8, −6.8)/−8.9 (−12.8, −4.9), and −9.5 (−13.9, −5.1)/−7.1 (−10.4, −3.7) if the father/mother, respectively, had early pubertal development compared to late. In girls, menarche was significantly associated with both parents' pubertal timing: −10.5 months (−15.9, −5.1)/−10.1 (−14.3, −6.0) if father/mother had early pubertal development compared to late. For the onset of PH2+ and B2+ in girls, estimates were −7.0 months (−12.6, −1.4) and −4.1 (−10.6, +2.4)/−6.7 (−11.0, −2.5), and −6.7 (−11.0, −2.0) for fathers/mothers, respectively. Maternal age of menarche was significantly associated with the onset of all pubertal milestones except PH2+ in girls. Conclusions: Maternal as well as paternal pubertal timing was a strong determinant of age at pubertal onset in both girls and boys. Age at breast and pubic hair development in girls, which has declined most during recent years, seemed to be least dependent on heritability.

2016 ◽  
Vol 7 (6) ◽  
pp. 636-651 ◽  
Author(s):  
J. A. McDonald ◽  
S. M. Eng ◽  
O. O. Dina ◽  
C. M. Schooling ◽  
M. B. Terry

The decline in age of pubertal timing has serious public health implications ranging from psychosocial adjustment problems to a possible increase in reproductive cancers. One biologically plausible explanation for the decline is a decrease in exposures to infections. To systematically review studies that assess the role of infection in pubertal timing, Medline, Web of Science and EMBASE were systematically searched and retrieved studies were reviewed for eligibility. Eligible studies examined the association between infections, including microbial exposures, and physical pubertal characteristics (breast, genitalia and pubic hair development) or age at menarche. We excluded studies that were published in a language other than English, focused on precocious puberty, were case studies, and/or included youth with autoimmune diseases. We report on study design, population characteristics, measurement of infection and puberty and the main effects of infection on pubertal development. Based on our search terms we identified 1372 unique articles, of which only 15 human and five animal studies met our eligibility criteria. Not all studies examined all outcomes. Infection was associated with later breast development (4/4 human studies), with less consistent evidence for genitalia and pubic hair development. Seven studies assessed age at menarche with inconsistent findings (three supporting later, four no association). We conclude that a small but consistent literature supports that infection is associated with later breast development; the evidence for other pubertal events and age at menarche is less clear. Where fewer childhood infections coincide with the rise in incidence of hormone-related cancers.


Author(s):  
Laura M. Derose ◽  
Julia A. Graber

The timing of pubertal onset is marked by substantial variability within the range of normative development. Pubertal onset has mainly been measured by appearance of secondary sex characteristics—pubic hair development across sexes, and breast development in girls and testicular development in boys. This chapter provides statistics for the average age of pubertal onset, including findings for how average age differs by race. The two major types of pubertal disorders, precocious puberty and delayed puberty, are described, with a brief synopsis of the possible causes (for a comprehensive review of medical causes, see Grumbach and Styne 2003). The major focus of the chapter is on the psychological and behavioral consequences of precocious and delayed puberty. Although the majority of research on this topic has included nonclinical samples (onset or delay of puberty nearing 2 standard deviations [SD] from the mean), findings would be applicable to children who exhibit clinical precocious or delayed puberty (onset or delay of puberty >2 SDs from the mean). Finally, the chapter reviews the clinical practices for “treating” puberty that is normative by pediatric standards. Breast budding is generally the first sexual characteristic to appear in females, and is most commonly classified by Marshall and Tanner’s (1969) five stages of development. Breast development begins in the United States between ages 8 and 13, with a mean age of 9.96 for Caucasian girls and a mean age of 8.87 for African American girls (Herman-Giddens et al. 1997). Pubic hair development typically begins shortly after breast budding; however approximately 20 percent of girls experience pubic hair development prior to breast budding (Brooks-Gunn and Reiter 1990). Pubic hair development also begins between the ages of 8 and 13 years, with a mean age 10.5 years in Caucasian girls and 8.8 years for African American girls (Herman-Giddens et al. 1997). Menarche is a late sign of pubertal development in girls and occurs following the peak in height velocity and during the rapid increase in weight and body fat (Tanner 1978). The mean age of menarche in North America is 12.88 years for Caucasian girls and 12.16 years for African American girls (Herman-Giddens et al. 1997).


2018 ◽  
Vol 179 (5) ◽  
pp. 279-285 ◽  
Author(s):  
A German ◽  
M Shmoish ◽  
J Belsky ◽  
Z Hochberg

Background The relationship between pubertal onset and tempo and pubertal growth is controversial. We hypothesized that the age at onset of girls’ puberty predicts pubertal tempo and the rate of pubertal progression. Methods We analyzed the data of 380 girls from the prospective Study of Early Child Care and Youth Development (SECCYD) who were recruited in the USA from 1991 to 2006 and followed from birth to age 15.5 years. We used the following indicators: thelarche age (Tanner stage B2), pubarche age (P2), menarche age (M), the age when breast (B5) and pubic hair (P5) became fully mature, pubertal growth, pubertal duration (time from B2 to B5) and pubertal progression (time from B2 to M). We clustered the girls according to B2 age into early onset (EO; <9.4 years), intermediate (IO; 9.4–10.5 years), late onset (LO; >10.5 years). Results All indicators of pubertal onset and conclusion occurred earlier in the EOs than in the LOs; yet, the differences in the age at main pubertal milestones lessened as puberty progressed: 2 years for B2; −1.4 years for M; −1 year for B5. In EOs, puberty was 1 year (average) longer than in LOs. Although EOs grew 7 cm (average) more than LOs, their heights at B5 were comparable. There was a significant relationship between the thelarche age and puberty tempo (r = 0.23, P < 0.0001). Conclusions The study highlights the predictive nature of variation in the onset age of puberty on its progression and duration. These results are reassuring in this context and will add to clinicians’ and parental understanding of the expected milestones of puberty.


Author(s):  
Maria E Bleil ◽  
Susan J Spieker ◽  
Steven E Gregorich ◽  
Alexis S Thomas ◽  
Robert A Hiatt ◽  
...  

Abstract Objective  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). Methods  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. Results  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 &lt; .01), but did not predict breast or pubic hair development (ps &gt; .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 &lt; .05). Conclusions  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.


2021 ◽  
pp. 1-10
Author(s):  
Lea Oelkers ◽  
Mandy Vogel ◽  
Agnes Kalenda ◽  
Hans Christian Surup ◽  
Antje Körner ◽  
...  

Introduction: Current health literature suggests that there has been a decline in the age of pubertal onset and that pubertal onset/duration of puberty may, besides weight status, be influenced by socioeconomic context. Objective: The goal of this study was to determine whether pubertal onset/duration and puberty-triggering hormones luteinizing hormone (LH) and follicle-stimulating hormone (FSH) vary according to socioeconomic status (SES). Moreover, we aimed to propose cutoff values of serum LH and FSH for predicting gonadarche in boys. Methods: 2,657 apparently healthy children and adolescents between 5.5 and 18 years from the area of Leipzig were recruited from the LIFE Child study. Age at pubertal onset/end of puberty was given in 738/573 children, respectively. Anthropometric parameters of puberty, blood measurements of LH and FSH, and questionnaires assessing SES were evaluated. Results: Lower SES was associated with earlier thelarche and longer duration of puberty in overweight/obese girls, whereas age of menarche was not affected. In boys with low SES, a trend versus earlier puberty onset can be seen. Lower SES was significantly associated with boys’ age at mutation. No significant differences in boys’ and girls’ serum levels of LH and FSH during puberty according to SES were observed. Serum LH levels of 0.56 IU/L and serum FSH levels of 1.74 IU/L showed the best prediction of gonadarche in boys. Conclusion: Puberty onset/duration and boys’ age at mutation is affected by SES. The proposed cutoff levels for serum LH and FSH could provide a serological tool to determine gonadarche in boys.


Author(s):  
Nana-Hawa Yayah Jones ◽  
Jane C. Khoury ◽  
Yingying Xu ◽  
Nicholas Newman ◽  
Heidi J. Kalkwarf ◽  
...  

Abstract Objectives Physical examinations to characterize pubertal maturation may be unacceptable for children enrolled in research studies. Studies confirm the utility of pubertal self staging for research, but there has been limited comparison of self examination with hormone biomarkers. Our objective was to assess concordance of pubertal self staging with hormone biomarkers of puberty. Methods Participants were enrolled in the Health Outcomes and Measures of the Environment Study, a longitudinal pregnancy and birth cohort study. At age 12 years, 139 females and 112 males completed pubertal self staging including breast and pubic hair development in females and pubic hair development in males. No clinical physical examination was performed. Hormone concentrations were measured in 102 females and 96 males including serum dehydroepiandrosterone sulfate, luteinizing hormone, and follicle-stimulating hormone in all; estradiol in females; and testosterone in males. Results Estradiol was significantly associated with female breast stage, even when adjusted for BMI, with geometric least squares means (95%CI) of 13.2 (8.7, 20.2), 38.3 (29.9, 49.1), 59.4 (39.8, 88.6), and 81.2 (45.6, 144) pg/mL for breast stage 1–2, 3, 4, and 5, respectively. Testosterone was significantly associated with male pubic hair stage, with adjusted geometric least squares means (95%CI) of 37.6 (19.9, 71.1), 43.4 (27.7, 68.3), 126 (78.4, 203), 275 (146, 521), and 559 (237, 1319) ng/dL for pubic hair stage 1, 2, 3, 4, and 5, respectively. Conclusions Self assessed pubertal development was positively associated with hormonal biomarkers of puberty.


2006 ◽  
Vol 9 (4) ◽  
pp. 558-565 ◽  
Author(s):  
Rosa A. Hoekstra ◽  
Meike Bartels ◽  
Dorret I. Boomsma

AbstractThe aim of this study was to estimate the heritability of variation in testosterone levels in 12-year-old children, and to explore the overlap in genetic and environmental influences on circulating testosterone levels and androgen-dependent pubertal development. Midday salivary testosterone samples were collected on 2 consecutive days in a sample of 183 unselected twin pairs. Androgen-induced pubertal development was assessed using self-report Tanner scales of pubic hair development (boys and girls) and genital development (boys). A significant contribution of genetic effects to the variance in testosterone levels was found. Heritability was approximately 50% in both boys and girls. The remaining proportion of the variance in testosterone levels could be explained by nonshared environmental influences. The relatively high correlation between testosterone levels of opposite-sex dizygotic twins suggests that sex differences in genes influencing variation in testosterone levels have not yet developed in preand early puberty. Variance in pubertal development was explained by a large genetic component, moderate shared environmental influences, and a small nonshared environmental effect. Testosterone levels correlated moderately (r = .31) with pubertal development; the covariance between testosterone levels and pubertal development was entirely accounted for by genetic influences.


2011 ◽  
Vol 23 (1) ◽  
pp. 85-99 ◽  
Author(s):  
Bruce J. Ellis ◽  
Elizabeth A. Shirtcliff ◽  
W. Thomas Boyce ◽  
Julianna Deardorff ◽  
Marilyn J. Essex

AbstractGuided by evolutionary–developmental theories of biological sensitivity to context and reproductive development, the current research examined the interactive effects of early family environments and psychobiologic reactivity to stress on the subsequent timing and tempo of puberty. As predicted by the theory, among children displaying heightened biological sensitivity to context (i.e., higher stress reactivity), higher quality parent–child relationships forecast slower initial pubertal tempo and later pubertal timing, whereas lower quality parent–child relationships forecast the opposite pattern. No such effects emerged among less context-sensitive children. Whereas sympathetic nervous system reactivity moderated the effects of parent–child relationships on both breast/genital and pubic hair development, adrenocortical activation only moderated the effect on pubic hair development. The current results build on previous research documenting what family contexts predict variation in pubertal timing by demonstrating for whom those contexts matter. In addition, the authors advance a new methodological approach for assessing pubertal tempo using piecewise growth curve analysis.


2020 ◽  
Vol 105 (10) ◽  
pp. e3650-e3659
Author(s):  
Jia Zhu ◽  
Henry A Feldman ◽  
Christine Chordas ◽  
Ari J Wassner ◽  
Peter E Manley ◽  
...  

Abstract Context Children with brain tumors may have pubertal onset at an inappropriately young chronologic age. Hypothalamic-pituitary irradiation ≥18Gy has been found to be a risk factor; age at irradiation is associated with pubertal timing. However, the underlying mechanisms are unknown. Objective To determine the impact of body mass index (BMI) and catch-up growth on pubertal timing in females treated for medulloblastoma and other embryonal tumors. Design, Setting, and Patients Retrospective cohort analysis of 90 female patients treated for medulloblastoma and other embryonal tumors at Dana-Farber Cancer Institute/Boston Children’s Hospital from 1996 to 2016. Eighteen individuals met inclusion criteria, with a mean ± SD follow-up period of 11.9 ± 3.4 years. Main Outcome Measures Multiple linear regression models for age at pubertal onset and bone age discrepancy from chronologic age at pubertal onset assessed the joint influences of age at irradiation, hypothalamic irradiation dose, undernutrition duration, BMI standard deviation score (SDS) at pubertal onset, and catch-up BMI SDS. Results The mean ± SD age of pubertal onset was 9.2 ± 1.3 years and hypothalamic radiation dose was 31.9 ± 9.9 Gy. There was a direct relationship between age at irradiation and age at pubertal onset (β = 0.323 ± 0.144 [standard error] year per year; P = 0.04) that was significantly attenuated after adjusting for BMI SDS at pubertal onset (P = 0.5) and catch-up BMI SDS (P = 0.08), suggesting that BMI is a mediator. Conclusions Both absolute and catch-up BMI SDS at pubertal onset are significant mediators of pubertal timing and bone age discrepancy in pediatric medulloblastoma and other embryonal tumors, and thus, are targetable risk factors to optimize pubertal timing.


Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1595 ◽  
Author(s):  
Yun Liu ◽  
Karen E. Peterson ◽  
Brisa N. Sánchez ◽  
Andrew D. Jones ◽  
Alejandra Cantoral ◽  
...  

Alterations in pubertal timing have been associated with long-term health outcomes. While a few reports have shown that dietary intake of selenium is associated with fertility and testosterone levels in men, no human studies have considered the association between selenium and pubertal development in children. We examined the cross-sectional association of childhood dietary intake of selenium with pubertal development among 274 girls and 245 boys aged 10–18 years in Mexico City. Multiple logistic and ordinal regression models were used to capture the association between energy-adjusted selenium intake (below Recommended Dietary Allowance (RDA) vs. above RDA) and stages of sexual maturity in children, adjusted for covariates. We found that boys with consumption of selenium below the RDA had lower odds of a higher stage for pubic hair growth (odds ratio (OR) = 0.51, 95% confidence interval (95% CI): 0.27–0.97) and genital development (OR = 0.53, 95% CI: 0.28–0.99) as well as a lower probability of having matured testicular volume (OR = 0.37, 95% CI: 0.15–0.88) compared with boys who had adequate daily dietary intake of selenium (above RDA). No associations were found in girls. According to our results, it is possible that inadequate consumption of selenium may be associated with later pubertal development in boys, suggesting a sex-specific pattern. Future work with a larger sample size and measures of selenium biomarkers is needed to confirm our findings and improve understanding of the role of this mineral in children’s sexual development.


Sign in / Sign up

Export Citation Format

Share Document