scholarly journals SUN-594 Pubertal Timing and Hormonal Correlates in Male Obesity

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jean De Schepper ◽  
Evy Berlanger ◽  
Monique Van Helvoirt ◽  
Ann De Guchtenaere ◽  
Eddy Basslé ◽  
...  
Keyword(s):  
Pubertal Timing ◽  
Pubertal Development ◽  
Age Distribution ◽  
Delayed Puberty ◽  
Low Grade ◽  
Z Score ◽  
Early Puberty ◽  
Pubertal Onset ◽  
Genital Development ◽  
Low Grade Inflammation

Abstract An early, normal or delayed pubertal onset have been described in overweight/ obese males(1). A greater prepubertal adiposity has been associated with a greater risk for delayed puberty in males, but an underlying mechanism was not explored(2). We investigated whether an increased testosterone aromatization or an higher degree of low-grade inflammation might be more prevalent in obese males with a delay in genital development. Pubertal status assessment by Tanner staging and measurement of morning serum testosterone, estradiol, leptin, and hSCRP by standard laboratory methods were performed in 191 male adolescents, aged between 10 and 18.6 yr (median 12.8 yr) with overweight (BMI z-score > 1.3), starting an ambulatory (n = 138) or a residential weight loss program (n = 55). Their median (range) BMI z-score was 2.32 (1.34 – 3.38). Delayed / slow and early / rapid genital development was defined by a Tanner genital stage respectively above the 90th or below 10th percentile age distribution (national Flemish standards of 2004). In 3 males pubertal development was advanced, while in 34 it was delayed. In the remaining 154 adolescents genital stage was normally timed. Males with a delayed timing or progression of genital development were older (median(range) age:14.8 (11.6-18.6) yr vs 12.3 (10-18.6) yr; p< 0.005) and shorter (height sds: -0.55 (-1.90- 1.48) vs 0.49 (-3 – 3.19); p < 0.005), and had a higher birthweight (birthweight z-score: 0.15(-3.51-2.75) vs -0.34(-4.7-3.30); p = 0.058), but a similar BMI and waist z-score in comparison with males with a normally timed puberty. Median serum estradiol, leptin, and hSCRP concentrations did not differ significantly between those with a normal or a delayed pubertal onset or progression. In conclusion, pubertal delay is more frequently observed than early puberty in males referred to obesity clinics. Neither low grade inflammation nor increased estradiol production appear to be associated with a later onset of slower progression of genital development in male obesity. References (1) Li W et al. Int J Environ Res Public Health. 2017 Oct 24;14(10) (2) Lee JM et al. Arch Pediatr Adolesc Med. 2010 Feb;164(2):139-44.

scholarly journals Heritability of Testosterone Levels in 12-Year-Old Twins and Its Relation to Pubertal Development

2006 ◽  
Vol 9 (4) ◽  
pp. 558-565 ◽  
Author(s):  
Rosa A. Hoekstra ◽  
Meike Bartels ◽  
Dorret I. Boomsma
Keyword(s):  
Pubertal Development ◽  
Environmental Influences ◽  
Pubic Hair ◽  
Self Report ◽  
Early Puberty ◽  
Salivary Testosterone ◽  
Testosterone Levels ◽  
Genital Development ◽  
Opposite Sex ◽  
Hair Development

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.

Evaluation of delayed puberty: what diagnostic tests should be performed in the seemingly otherwise well adolescent?

2016 ◽  
Vol 101 (8) ◽  
pp. 767-771 ◽  
Author(s):  
Leah Abitbol ◽  
Stephen Zborovski ◽  
Mark R Palmert
Keyword(s):  
Diagnostic Tests ◽  
Pubertal Timing ◽  
Pubertal Development ◽  
Laboratory Data ◽  
Bone Age ◽  
Delayed Puberty ◽  
Future Research ◽  
Wide Variability ◽  
Height Prediction ◽  
Underlying Disorder

Delayed puberty (DP) is defined as the lack of pubertal development by an age that is 2–2.5 SDs beyond the population mean. Although it generally represents a normal variant in pubertal timing, concern that DP could be the initial presentation of a serious underlying disorder has led to a diagnostic approach that is variable and may include tests that are unnecessary and costly. In this review, we examine available literature regarding the recommended diagnostic tests and aetiologies identified during the evaluation of youth with DP. We view this literature through the prism of the seemingly otherwise well adolescent. To provide further clinical context, we also evaluate the clinical and laboratory data from patients seen with DP in our centre over a 2-year period. The literature and our data reveal wide variability in the number of tests performed and raise the question of whether tests, other than gonadotropins, obtained in the absence of signs or symptoms of an underlying disorder are routinely warranted. Together this information provides a pragmatic rationale for revisiting recommendations calling for broad testing during the initial diagnostic evaluation of an otherwise healthy adolescent with DP. We highlight the need for further research comparing the utility of broader screening with a more streamlined approach, such as limiting initial testing to gonadotropins and a bone age, which, while not diagnostic, is often useful for height prediction, followed by close clinical monitoring. If future research supports a more streamlined approach to DP, then much unnecessary testing could be eliminated.

scholarly journals Delayed Puberty but Normal Fertility in Mice With Selective Deletion of Insulin Receptors From Kiss1 Cells

Endocrinology ◽  
2013 ◽  
Vol 154 (3) ◽  
pp. 1337-1348 ◽  
Author(s):  
Xiaoliang Qiu ◽  
Abigail R. Dowling ◽  
Joseph S. Marino ◽  
Latrice D. Faulkner ◽  
Benjamin Bryant ◽  
...  
Keyword(s):  
Pubertal Timing ◽  
Insulin Receptors ◽  
Reproductive Capacity ◽  
Delayed Puberty ◽  
Vaginal Opening ◽  
Early Puberty ◽  
Impaired Insulin ◽  
Fat Composition ◽  
Neuron Function ◽  
Insight Into

Abstract Pubertal onset only occurs in a favorable, anabolic hormonal environment. The neuropeptide kisspeptin, encoded by the Kiss1 gene, modifies GnRH neuronal activity to initiate puberty and maintain fertility, but the factors that regulate Kiss1 neurons and permit pubertal maturation remain to be clarified. The anabolic factor insulin may signal nutritional status to these neurons. To determine whether insulin sensing plays an important role in Kiss1 neuron function, we generated mice lacking insulin receptors in Kiss1 neurons (IRΔKiss mice). IRΔKiss females showed a delay in vaginal opening and in first estrus, whereas IRΔKiss males also exhibited late sexual maturation. Correspondingly, LH levels in IRΔKiss mice were reduced in early puberty in both sexes. Adult reproductive capacity, body weight, fat composition, food intake, and glucose regulation were comparable between the 2 groups. These data suggest that impaired insulin sensing by Kiss1 neurons delays the initiation of puberty but does not affect adult fertility. These studies provide insight into the mechanisms regulating pubertal timing in anabolic states.

scholarly journals Early life household intactness and timing of pubertal onset in girls: a prospective cohort study

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Sara Aghaee ◽  
Julianna Deardorff ◽  
Louise C. Greenspan ◽  
Charles P. Quesenberry ◽  
Lawrence H. Kushi ◽  
...  
Keyword(s):  
Cohort Study ◽  
Prospective Cohort Study ◽  
Prospective Cohort ◽  
Early Life ◽  
Pubertal Development ◽  
Pubic Hair ◽  
Interval Censoring ◽  
Early Puberty ◽  
Pubertal Onset ◽  
Increased Risk

Abstract Background Girls who experience early-life familial stress may have heightened risk of early puberty, which has adverse implications for adolescent and adult health. We assessed the association between household intactness and pubertal onset using a racially/ethnically diverse cohort of girls from Northern California. Methods A prospective cohort study of 26,044 girls born in 2003-10. Girls living with both parents from birth up to 6 years were considered to come from “intact” households while others constituted “non-intact” households. Pubertal development was measured using pediatrician-assessed Tanner staging for breast and pubic hair. Pubertal onset was defined as the transition from Tanner Stage 1 to 2+ for breast (thelarche) and pubic hair (pubarche). Menarche data was collected from routine well-child questionnaires. Weibull regression models accommodating left, right, and interval censoring were used to determine risk of earlier thelarche and pubarche, and logistic regressions were used to assess the risk of early menarche (age < 12). Results Girls exposed to non-intact households before age 2 years were at increased risk for earlier thelarche and pubarche with significant effect modification by race/ethnicity, compared with girls from intact households. The associations were strongest among Black girls (adjusted hazard ratio [HR]: 1.60, 95% confidence interval [CI]: 1.29,1.98; HR: 1.42, 95%CI: 1.15,1.77 for thelarche and pubarche, respectively). There were no significant associations among Asian/Pacific Islanders. Girls who lived in non-intact households before age 2 years were also at increased risk for earlier menarche, but without race/ethnic interaction. Adjustment for prepubertal obesity did not change these associations. Associations between living in non-intact households after age 2 years and early puberty were weaker but still significant. Conclusions Exposure to a non-intact household early in life may increase the risk of early puberty in girls. Future psychosocial interventions focused on improving family cohesiveness and efforts to reduce childhood stress among families that are non-intact may mitigate these negative associations, thereby preventing future adverse health effects of early puberty and health disparities.

Psychological Effects of Precocious and Delayed Puberty

2010 ◽  
Author(s):  
Laura M. Derose ◽  
Julia A. Graber
Keyword(s):  
African American ◽  
Pubertal Development ◽  
Pubic Hair ◽  
Breast Development ◽  
Delayed Puberty ◽  
Sex Characteristics ◽  
African American Girls ◽  
Pubertal Onset ◽  
The Mean ◽  
Hair Development

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).

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 ◽  
...  
Keyword(s):  
Pubertal Timing ◽  
Pubertal Development ◽  
Age At Onset ◽  
Pubic Hair ◽  
Healthy Children ◽  
Pubertal Onset ◽  
Hair Development ◽  
The Impact ◽  
Age Of Menarche ◽  
Menarche Age

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 &gt;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.

Obesity Is Associated with Earlier Pubertal Onset in Boys

2019 ◽  
Vol 105 (4) ◽  
pp. e1667-e1672 ◽  
Author(s):  
Alexander S Busch ◽  
Brigitte Højgaard ◽  
Casper P Hagen ◽  
Grete Teilmann
Keyword(s):  
Intervention Program ◽  
Age Of Onset ◽  
Pubertal Timing ◽  
Pubertal Development ◽  
Inverse Correlation ◽  
Population Based ◽  
Normal Weight ◽  
Testicular Volume ◽  
Pubertal Onset ◽  
Tanner Staging

Abstract Context Pubertal timing in boys is associated with body mass index (BMI). Studies consistently report an inverse correlation of BMI and pubertal timing within the normal BMI range. However, observations in obese boys are conflicting with different studies reporting either early or delayed pubertal onset in obese boys. Objective We aimed to assess the association of male pubertal timing with age-specific BMI (zBMI) in obese boys. Design, Setting, and Participants A total of 218 obese boys (zBMI &gt; +2SD, with a median age at baseline of 10.8 years (range 4.2–17.0), were recruited as part of a prospective outpatient childhood obesity intervention program at Nordsjællands Hospital, Hillerød, Denmark, between 2009 and 2017. Serving as controls, we included 660 healthy boys participating in the population-based COPENHAGEN Puberty Study (-2SD &lt; zBMI ≤ +2SD, 2006–2014). Subanalyses were performed on overweight controls (+1SD &lt; zBMI ≤ +2SD). The clinical assessment of pubertal development by Tanner staging, including testis volume using a Prader’s orchidometer, was performed by trained physicians. The timing of pubertal milestones was estimated by probit analyses. Main Outcome Measures Timing of testicular volume ≥ 4 mL, genital stage ≥ 2, and pubarche. Results The mean (95% confidence interval [CI]) age of onset of pubertal event in obese boys was as follows: testicular volume ≥ 4 mL, 11.3 years (11.0–11.6); genital stage ≥ 2, 11.6 yrs (11.3–11.9); and pubarche, 11.9 years (11.5–12.3). Testicular volume ≥ 4 mL occurred significantly earlier in obese boys compared to controls (-2SD &lt; zBMI ≤ +2SD) (P = 0.01). We did not observe significant differences for either the timing of pubarche nor the genital stage ≥ 2 (P = 0.06 and P = 0.94, respectively) Conclusions We demonstrate that testicular enlargement in obese boys occurs significantly earlier compared to a population-based normal-weight reference cohort.

Timing of puberty and synchronization of seasonal rhythms by simulated natural photoperiods in female Siberian hamsters

2007 ◽  
Vol 293 (1) ◽  
pp. R413-R420 ◽  
Author(s):  
Matthew P. Butler ◽  
Justin J. Trumbull ◽  
Kevin W. Turner ◽  
Irving Zucker
Keyword(s):  
Pubertal Development ◽  
Somatic Growth ◽  
Life History Trait ◽  
Delayed Puberty ◽  
Summer Solstice ◽  
Early Puberty ◽  
Seasonal Rhythms ◽  
Siberian Hamsters ◽  
Natural Photoperiod ◽  
Timing Of Puberty

The timing of puberty is a critical life history trait of short-lived species; spring-born individuals mature rapidly and breed in the season of birth, whereas young born in mid- to late summer delay puberty until the next spring. The cues that govern the transition from rapid to delayed maturation in natural populations remain unknown. To identify ecologically relevant photoperiod cues that control timing of puberty, we monitored nine cohorts of female Siberian hamsters ( Phodopus sungorus) born every 2 wk from 4 wk before to 12 wk after the summer solstice in a simulated natural photoperiod (SNP). Hamsters born by the summer solstice underwent rapid somatic growth and achieved puberty that summer; among females born 2–4 wk after the solstice, some delayed puberty by many weeks, whereas others manifested early puberty. Hamsters born 6 or more weeks after the solstice generally delayed puberty until the following spring. The transition from accelerated to delayed pubertal development in the SNP occurred at day lengths that induce early puberty when presented as static photoperiods. Despite differences in timing of birth and timing of puberty, fall and subsequent spring seasonal events occurred at similar calendar dates in all cohorts. We found no evidence that prenatal photoperiod history influenced postnatal development of female hamsters. Considered together with a parallel study on males, the present findings point to sex differences in responsiveness to natural photoperiod variations. In both sexes, incrementally changing photoperiods exert a strong organizing effect on seasonal rhythms.

scholarly journals Pubertal development and risk of premenstrual disorders in young adulthood

2020 ◽  
Author(s):  
Donghao Lu ◽  
Jurate Aleknaviciute ◽  
Ragnar Bjarnason ◽  
Rulla M Tamimi ◽  
Unnur A Valdimarsdóttir ◽  
...  
Keyword(s):  
Young Adulthood ◽  
Lower Risk ◽  
Pubertal Timing ◽  
Pubertal Development ◽  
Pubic Hair ◽  
Premenstrual Symptom ◽  
Age At Menarche ◽  
Z Score ◽  
Premenstrual Symptoms ◽  
Timing Of Menarche

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

scholarly journals Endocrine-Disrupting Chemicals and Early Puberty in Girls

Children ◽  
2021 ◽  
Vol 8 (6) ◽  
pp. 492
Author(s):  
Anastasios Papadimitriou ◽  
Dimitrios T Papadimitriou
Keyword(s):  
Growth Pattern ◽  
Secular Trend ◽  
Pubertal Timing ◽  
Endocrine Disrupting Chemicals ◽  
The Other ◽  
Minor Effect ◽  
Early Puberty ◽  
Pubertal Onset ◽  
Endocrine Disrupting ◽  
A Minor

In recent decades, pubertal onset in girls has been considered to occur at an earlier age than previously. Exposure to endocrine-disrupting chemicals (EDCs) has been associated with alterations in pubertal timing, with several reports suggesting that EDCs may have a role in the secular trend in pubertal maturation, at least in girls. However, relevant studies give inconsistent results. On the other hand, the majority of girls with idiopathic precocious or early puberty present the growth pattern of constitutional advancement of growth (CAG), i.e., growth acceleration soon after birth. Herein, we show that the growth pattern of CAG is unrelated to exposure to endocrine-disrupting chemicals and is the major determinant of precocious or early puberty. Presented data suggest that EDCs, at most, have a minor effect on the timing of pubertal onset in girls.

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