scholarly journals Characterization of pubertal development of girls in rural Bangladesh

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0247762
Author(s):  
Jinhee Hur ◽  
Kerry J. Schulze ◽  
Andrew L. Thorne-Lyman ◽  
Lee S.-F. Wu ◽  
Saijuddin Shaikh ◽  
...  

This study aimed to describe the timing and patterns of pubertal maturation of girls living in rural Bangladesh. Starting in September 2015, a total of 15,320 girls from a birth cohort, aged 9 to 15 years at initial encounter, were visited twice at about a one year interval, typically in their birth month. Participants were asked to self-report extent of pubertal maturation, including breast development, pubic hair growth and age at menarche, if applicable. Pubertal stage (abbreviated as B2 and B3-4 for breast development and PH2 and PH3-4 for pubic hair growth) was assigned. Data from both visits were pooled, yielding a total of 29,377 age-related observations per pubertal characteristic. Probit regression models were used to estimate distributions of age at which each stage of pubertal development was attained. Before age 8, <3% of the study population initiated pubertal maturation as indicated by onset of breast development (B2). The median (95% confidence interval) age of B2 and B3-4 was 11.02 (11.00–11.04) and 12.82 (12.80–12.83) years, respectively; and 12.93 (12.91–12.94) and 14.29 (14.27–14.31) years for the onset (PH2) and advanced stage (PH3-4) of pubic hair growth, respectively. Median age at menarche was 13.17 (13.15–13.19) years, with 2.15 years of timespan from B2 to menarche. Girls in rural Bangladesh progressed through puberty following a well-documented sequence of sexual maturation stages. The age at which each pubertal milestone took place was somewhat later, but the tempo from breast development to menarche was comparable to that observed elsewhere. Our findings present a current norm of pubertal maturation in a typical, rural adolescent population in South Asia, which could help inform future studies and interventions to preserve or improve early adolescent health and development.

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):  
Io Ieong Chan ◽  
Man Ki Kwok ◽  
C Mary Schooling

Abstract Introduction Observational studies suggest earlier puberty is associated with higher adulthood blood pressure (BP), but these findings have not been replicated using Mendelian randomization (MR). We examined this question sex-specifically using larger genome-wide association studies (GWAS) with more extensive measures of pubertal timing. Methods We obtained genetic instruments proxying pubertal maturation (age at menarche (AAM) or voice breaking (AVB)) from the largest published GWAS. We applied them to summary sex-specific genetic associations with systolic and diastolic BP z-scores, and self-reported hypertension in women (n=194174) and men (n=167020) from the UK Biobank, using inverse-variance weighting meta-analysis. We conducted sensitivity analyses using other MR methods, including multivariable MR adjusted for childhood obesity proxied by body mass index (BMI). We used late pubertal growth as a validation outcome. Results AAM (beta per one-year later = -0.030 [95% confidence interval (CI) -0.055, -0.005] and AVB (beta -0.058 [95% CI -0.100, -0.015]) were inversely associated with systolic BP independent of childhood BMI, as were diastolic BP (-0.035 [95% CI -0.060, -0.009] for AAM and -0.046 [95% CI -0.089, -0.004] for AVB) and self-reported hypertension (odds ratios 0.89 [95% CI 0.84, 0.95] for AAM and 0.87 [95% CI 0.79, 0.96] for AVB). AAM and AVB were positively associated with late pubertal growth, as expected. The results were robust to sensitivity analysis using other MR methods. Conclusion Timing of pubertal maturation was associated with adulthood BP independent of childhood BMI, highlighting the role of pubertal maturation timing in midlife BP.


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.


2020 ◽  
Vol 105 (5) ◽  
pp. 1599-1607 ◽  
Author(s):  
Ingvild Særvold Bruserud ◽  
Mathieu Roelants ◽  
Ninnie Helén Bakken Oehme ◽  
Andre Madsen ◽  
Geir Egil Eide ◽  
...  

Abstract Context Discriminating adipose and glandular tissue is challenging when clinically assessing breast development. Ultrasound facilitates staging of pubertal breast maturation (US B), but has not been systematically compared to Tanner breast (Tanner B) staging, and no normative data have been reported. Objective To present normative references for US B along with references for Tanner B, pubic hair (PH), and menarche. Design, Setting, and Participants A cross-sectional sample of 703 healthy girls aged 6 to 16 years were examined. Main Outcome Measures Breast development was determined with US B and Tanner B staging. Tanner PH and menarcheal status were recorded. The age distributions of entry in US B, Tanner B, and PH stages and menarche were estimated with generalized linear and generalized additive models with a probit link. Method agreement was tested with weighted Cohen’s kappa. Results The median (±2SD) ages for thelarche, US B2 and Tanner B2, were 10.2 (7.7, 12.8) and 10.4 (8.0, 12.7) years. The median (±2SD) ages at Tanner PH2 and menarche were 10.9 (8.5, 13.3) and 12.7 (11.0, 16.2) years. Cohen’s kappa of agreement (95% confidence interval) between US B and Tanner B was 0.87 (0.85–0.88). When the methods disagreed, US B was usually more advanced. Conclusion Thelarche occurred at a slightly younger age when assessed with ultrasound compared to clinical Tanner staging, although the 2 methods had a very good agreement when determining pubertal breast maturation. A significant decrease of 2.8 months in age at menarche was observed during the past decade in Norwegian girls.


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).


2016 ◽  
Vol 30 (2) ◽  
pp. 109-112
Author(s):  
Poly Begum ◽  
Dipti Rani Saha ◽  
Md Kamrul Hassan

The parents of a 04-year-old girl bring her to a Gynaecologist because of breast development, appearance of pubic hair and periodic per vaginal bleeding. Her medical history is unremarkable. The parents are of average height, and the mother reports first menstruating when she was 11 years old. At physical examination, the girl is 100 cm tall , weighs 17 kg, and has a bodymass index of 17. Her pubertal development is classified as Tanner stage 3 breast development and Tanner stage 2 pubic hair development. She was diagnosed as a case of precocious puberity. Appearance of secondary sexual development before the age of 9 in a male child and before the age of 8 in a female child is called precocious puberty. When the cause of precocious puberty is premature activation of the hypothalamic-pituitary axis, it is called central or complete precocious puberty and she was a case of central precocious puberty. After proper consult she was treated by GnRHa suppressor of pituitary till 11 years of age.Bangladesh J Obstet Gynaecol, 2015; Vol. 30(2) : 109-112


Author(s):  
Jasmine A McDonald ◽  
Sinaida Cherubin ◽  
Mandy Goldberg ◽  
Ying Wei ◽  
Wendy K Chung ◽  
...  

Abstract Earlier pubertal development is only partially explained by childhood body mass index (BMI); the role of other factors like childhood infections is less understood. Using data from the LEGACY Girls Study (2011 – 2016), we prospectively examined the associations between childhood viral infections (Cytomegalovirus (CMV), Epstein Barr Virus (EBV), Herpes Simplex Virus 1 (HSV1), HSV2 and pubertal timing. We measured exposures based on seropositivity in pre-menarcheal girls (n=490). Breast and pubic hair development were classified based on mother-reported Tanner Stage (TS: TS2+ compared with TS1), adjusting for age, BMI, and sociodemographic factors. The average age at first blood draw was 9.8 years (Stdev=1.9 years). The prevalences were 31% CMV+, 37% EBV+, 14% HSV1+, 0.4% HSV2+, and 16% for both CMV+/EBV+. CMV+ infection without co-infection was associated with developing breasts an average of 7 months earlier (Hazard Ratio (HR)=2.12, 95% CI 1.32, 3.40). CMV+ infection without co-infection and HSV1+ and/or HSV2+ infection were associated with developing pubic hair 9 months later (HR 0.41, 95% CI 0.24, 0.71, HR 0.42, 95% CI 0.22, 0.81, respectively). Infection was not associated with menarche. If replicated in larger cohorts with blood collection prior to any breast development, this study supports that childhood infections may play a role in altering pubertal timing.


2020 ◽  
Author(s):  
Donghao Lu ◽  
Jurate Aleknaviciute ◽  
Ragnar Bjarnason ◽  
Rulla M Tamimi ◽  
Unnur A Valdimarsdóttir ◽  
...  

Abstract STUDY QUESTION Is pubertal timing associated with risk of premenstrual disorders (PMDs) in young adulthood? SUMMARY ANSWER Late pubertal development is associated with decreased premenstrual symptom burden and risk of PMDs in young adulthood. WHAT IS KNOWN ALREADY PMDs, including premenstrual syndrome and premenstrual dysphoric disorder, may begin during the teenage years. Few risk factors in early life have been identified for PMD development. STUDY DESIGN, SIZE, DURATION A prospective cohort study of 6495 female participants during 1996–2013. PARTICIPANTS/MATERIALS, SETTING, METHODS We included participants from the Growing Up Today Study (GUTS). Pubertal development was indicated by the timing of menarche, breast and pubic hair growth. Self-reported age at menarche was longitudinally assessed at enrollment (in 1996/2004 for GUTS I/II) and onwards, and classified as early (age ≤ mean − SD, 11.64 years), normative and late menarche (age ≥ mean + SD, 13.95 years). Timing of pubic hair and breast growth were assessed multiple times during follow-up via Tanner scales, and classified into early, normative and late development according to mean ± SD. Using a validated questionnaire based on the Calendar of Premenstrual Experiences, we assessed premenstrual symptoms and identified probable cases of PMDs in 2013. We examined the associations of timing of pubertal development with premenstrual symptom score and disorders using multivariable linear and logistic regressions, respectively. MAIN RESULTS AND THE ROLE OF CHANCE In 2013 (mean age = 26), 1001 (15.4%) individuals met criteria for a PMD. An inverse association was found between age at menarche and premenstrual symptom z-score (β −0.05 per year, 95% CI −0.07 to −0.03) and risk of PMDs (odds ratio (OR) 0.93 per year, 95% CI 0.88 to 0.99). Compared to individuals with normative menarche, individuals with late menarche had a lower risk of PMDs (OR 0.73, 95% CI 0.59 to 0.91), while individuals with early menarche had comparable odds (OR 0.98, 95% CI 0.81 to 1.18). Moreover, early growth of pubic hair was associated with increased premenstrual symptoms (z-score β 0.09 per year, 95% CI 0.02 to 0.17) and PMD risk (OR 1.28, 95% CI 1.04 to 1.56), independent of age at menarche. No associations were noted for breast development. LIMITATIONS, REASONS FOR CAUTION One major limitation is some misclassification of menarche due to recall. We, however, showed robust association among participants who were premenarcheal at baseline. WIDER IMPLICATIONS OF THE FINDINGS Our findings suggest that pubertal timing, particularly timing of menarche, is inversely associated with the risk of developing premenstrual symptoms in young adulthood, and that women with later menarche have significantly lower risk of PMDs. Information on PMDs should be provided to teenage girls and their parents. If these findings are confirmed in independent populations, prevention strategies and early detection programs may be considered for women with early pubertal development. STUDY FUNDING/COMPETING INTEREST(S) The work is supported by the National Institutes of Health and Swedish Research Council. TRIAL REGISTRATION NUMBER N/A


2021 ◽  
Vol 11 ◽  
Author(s):  
Megan M. Herting ◽  
Kristina A. Uban ◽  
Marybel Robledo Gonzalez ◽  
Fiona C. Baker ◽  
Eric C. Kan ◽  
...  

AimTo examine individual variability between perceived physical features and hormones of pubertal maturation in 9–10-year-old children as a function of sociodemographic characteristics.MethodsCross-sectional metrics of puberty were utilized from the baseline assessment of the Adolescent Brain Cognitive Development (ABCD) Study—a multi-site sample of 9–10 year-olds (n = 11,875)—and included perceived physical features via the pubertal development scale (PDS) and child salivary hormone levels (dehydroepiandrosterone and testosterone in all, and estradiol in females). Multi-level models examined the relationships among sociodemographic measures, physical features, and hormone levels. A group factor analysis (GFA) was implemented to extract latent variables of pubertal maturation that integrated both measures of perceived physical features and hormone levels.ResultsPDS summary scores indicated more males (70%) than females (31%) were prepubertal. Perceived physical features and hormone levels were significantly associated with child’s weight status and income, such that more mature scores were observed among children that were overweight/obese or from households with low-income. Results from the GFA identified two latent factors that described individual differences in pubertal maturation among both females and males, with factor 1 driven by higher hormone levels, and factor 2 driven by perceived physical maturation. The correspondence between latent factor 1 scores (hormones) and latent factor 2 scores (perceived physical maturation) revealed synchronous and asynchronous relationships between hormones and concomitant physical features in this large young adolescent sample.ConclusionsSociodemographic measures were associated with both objective hormone and self-report physical measures of pubertal maturation in a large, diverse sample of 9–10 year-olds. The latent variables of pubertal maturation described a complex interplay between perceived physical changes and hormone levels that hallmark sexual maturation, which future studies can examine in relation to trajectories of brain maturation, risk/resilience to substance use, and other mental health outcomes.


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.


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