-
Human Reproduction (Oxford, England) Dec 2020Is earlier puberty more likely a result of adiposity gain in childhood than a cause of adiposity gain in adulthood?
STUDY QUESTION
Is earlier puberty more likely a result of adiposity gain in childhood than a cause of adiposity gain in adulthood?
SUMMARY ANSWER
Pre-pubertal fat mass is associated with earlier puberty timing but puberty timing is not associated with post-pubertal fat mass change.
WHAT IS KNOWN ALREADY
Age at puberty onset has decreased substantially in the last several decades. Whether reducing childhood adiposity prevents earlier puberty and if early puberty prevention itself also has additional independent benefits for prevention of adult adiposity is not well understood.
STUDY DESIGN, SIZE, DURATION
Prospective birth cohort study of 4176 participants born in 1991/1992 with 18 232 repeated measures of fat mass from age 9 to 18 years.
PARTICIPANTS/MATERIALS, SETTING, METHODS
We used repeated measures of height from 5 to 20 years to identify puberty timing (age at peak height velocity, aPHV) and repeated measures of directly measured fat mass from age 9 to 18 years, from a contemporary UK birth cohort study to model fat mass trajectories by chronological age and by time before and after puberty onset. We then examined associations of these trajectories with puberty timing separately in females and males.
MAIN RESULTS AND THE ROLE OF CHANCE
In models by chronological age, a 1-year later aPHV was associated with 20.5% (95% confidence interval (CI): 18.6-22.4%) and 23.4% (95% (CI): 21.3-25.5%) lower fat mass in females and males, respectively, at 9 years. These differences were smaller at age 18 years: 7.8% (95% (CI): 5.9-9.6%) and 12.4% (95% (CI): 9.6-15.2%) lower fat mass in females and males per year later aPHV. Trajectories of fat mass by time before and after puberty provided strong evidence for an association of pre-pubertal fat mass with puberty timing, and little evidence of an association of puberty timing with post-pubertal fat mass change. The role of chance is likely to be small in this study given the large sample sizes available.
LIMITATIONS, REASONS FOR CAUTION
Participants included in our analyses were more socially advantaged than those excluded. The findings of this work may not apply to non-White populations and further work examining associations of puberty timing and fat mass in other ethnicities is required.
WIDER IMPLICATIONS OF THE FINDINGS
Previous research has relied on self-reported measures of puberty timing such as age of voice breaking in males, has lacked data on pre-and post-pubertal adiposity together and relied predominantly on indirect measures of adiposity such as BMI. This has led to conflicting results on the nature and direction of the association between puberty timing and adiposity in females and males. Our work provides important clarity on this, suggesting that prevention of adiposity in childhood is key for prevention of early puberty, adult adiposity and associated cardiovascular risk. In contrast, our findings suggest that prevention of early puberty without prevention of childhood adiposity would have little impact on prevention of adult adiposity.
STUDY FUNDING/COMPETING INTEREST(S)
The UK Medical Research Council and Wellcome (Grant ref: 102215/2/13/2) and the University of Bristol provide core support for Avon Longitudinal Study of Parents and Children (ALSPAC). L.M.O.K. is supported by a UK Medical Research Council Population Health Scientist fellowship (MR/M014509/1) and a Health Research Board (HRB) of Ireland Emerging Investigator Award (EIA-FA-2019-007 SCaRLeT). J.A.B. is supported by the Elizabeth Blackwell Institute for Health Research, University of Bristol and the Wellcome Trust Institutional Strategic Support Fund (204813/Z/16/Z). L.D.H. and A.F. are supported by Career Development Awards from the UK Medical Research Council (grants MR/M020894/1 and MR/M009351/1, respectively). All authors work in a unit that receives funds from the UK Medical Research Council (grant MC_UU_00011/3, MC_UU_00011/6). No competing interests to declare.
TRIAL REGISTRATION NUMBER
N/A.
Topics: Adiposity; Adolescent; Adult; Child; Cohort Studies; Female; Humans; Infant; Ireland; Longitudinal Studies; Male; Prospective Studies; Puberty
PubMed: 33242326
DOI: 10.1093/humrep/deaa213 -
The Journal of Pediatrics Jul 2020To test the association between early puberty and telomere length in preadolescent girls and mothers from a large representative sample of US females.
OBJECTIVE
To test the association between early puberty and telomere length in preadolescent girls and mothers from a large representative sample of US females.
STUDY DESIGN
We analyzed data from 1194 preadolescent girls and 2421 mothers from the Fragile Families and Child Wellbeing Study. Participants were from a population-based birth cohort (1998-2000) born in large US cities. Telomere length was assessed by quantitative polymerase chain reaction from saliva samples provided by preadolescent girls and mothers of preadolescent youth. Mothers completed a questionnaire about their child's pubertal development to determine concurrent Tanner stages and provided self-reports of her own age at menarche. Linear regression models were used to estimate the association between pubertal development (status and timing) and telomere length.
RESULTS
Early pubertal timing but not pubertal status was associated with shorter telomere length in preadolescent girls (P < .01). Early age at menarche was associated with shorter telomere length in a sample of mothers of preadolescent youth (P < .05).
CONCLUSIONS
Results provide evidence for the association between early puberty and shorter telomeres evidenced by associations in both preadolescent girls and mothers. Future research should address the limitations of this study by using longitudinal measurements of pubertal development assessed through medical examinations and repeated assessments of telomere length to capture telomere attrition.
Topics: Adolescent; Child; Child Development; Female; Humans; Menarche; Mothers; Puberty; Retrospective Studies; Telomere; Telomere Homeostasis; Young Adult
PubMed: 32586523
DOI: 10.1016/j.jpeds.2020.02.075 -
International Journal of Molecular... Mar 2021Chronic stress is encountered in our everyday life and is thought to contribute to a number of diseases. Many of these stress-related disorders display a sex bias.... (Review)
Review
Chronic stress is encountered in our everyday life and is thought to contribute to a number of diseases. Many of these stress-related disorders display a sex bias. Because glucocorticoid hormones are the main biological mediator of chronic stress, researchers have been interested in understanding the sexual dimorphism in glucocorticoid stress response to better explain the sex bias in stress-related diseases. Although not yet demonstrated for glucocorticoid regulation, sex chromosomes do influence sex-specific biology as soon as conception. Then a transient rise in testosterone start to shape the male brain during the prenatal period differently to the female brain. These organizational effects are completed just before puberty. The cerebral regions implicated in glucocorticoid regulation at rest and after stress are thereby impacted in a sex-specific manner. After puberty, the high levels of all gonadal hormones will interact with glucocorticoid hormones in specific crosstalk through their respective nuclear receptors. In addition, stress occurring early in life, in particular during the prenatal period and in adolescence will prime in the long-term glucocorticoid stress response through epigenetic mechanisms, again in a sex-specific manner. Altogether, various molecular mechanisms explain sex-specific glucocorticoid stress responses that do not exclude important gender effects in humans.
Topics: Adolescent; Animals; Child; Child Development; Embryonic Development; Genetic Association Studies; Glucocorticoids; Gonadal Hormones; Humans; Hydrocortisone; Puberty; Sex Characteristics; Sex Factors; Steroids; Stress, Physiological; Stress, Psychological
PubMed: 33808655
DOI: 10.3390/ijms22063139 -
Developmental Cognitive Neuroscience Apr 2021Total amygdala volumes develop in association with sex and puberty, and postmortem studies find neuronal numbers increase in a nuclei specific fashion across...
Total amygdala volumes develop in association with sex and puberty, and postmortem studies find neuronal numbers increase in a nuclei specific fashion across development. Thus, amygdala subregions and composition may evolve with age. Our goal was to examine if amygdala subregion absolute volumes and/or relative proportion varies as a function of age, sex, or puberty in a large sample of typically developing adolescents (N = 408, 43 % female, 10-17 years). Utilizing the in vivo CIT168 atlas, we quantified 9 subregions and implemented Generalized Additive Mixed Models to capture potential non-linear associations with age and pubertal status between sexes. Only males showed significant age associations with the basolateral ventral and paralaminar subdivision (BLVPL), central nucleus (CEN), and amygdala transition area (ATA). Again, only males showed relative differences in the proportion of the BLVPL, CEN, ATA, along with lateral (LA) and amygdalostriatal transition area (ASTA), with age. Using a best-fit modeling approach, age, and not puberty, was found to drive these associations. The results suggest that amygdala subregions show unique variations with age in males across adolescence. Future research is warranted to determine if our findings may contribute to sex differences in mental health that emerge across adolescence.
Topics: Adolescent; Amygdala; Child; Female; Humans; Male; Neural Pathways; Puberty; Sex Characteristics
PubMed: 33476872
DOI: 10.1016/j.dcn.2020.100883 -
Journal of Sleep Research Jun 2023Sleep health tends to worsen during adolescence, partially due to pubertal-related changes that, in combination with social and psychological factors, can lead to...
Sleep health tends to worsen during adolescence, partially due to pubertal-related changes that, in combination with social and psychological factors, can lead to long-lasting impairments in sleep health and affective functioning. Discrepant findings between subjective and objective measures of sleep in relation to affect have been reported in studies of adults; however, few investigations have assessed both subjective and objective sleep quality in a single sample, and fewer have examined this in the context of pubertal development. We aimed to (1) characterise pubertal associations with subjective sleep satisfaction, objective sleep efficiency, and objective and subjective sleep duration in adolescents; (2) examine the longitudinal association between daily affect and sleep metrics; and (3) test whether pubertal stage moderated this association. Eighty-nine participants (64% female, ages 13-20) completed an ecological momentary assessment (EMA) and actigraphy protocol. Independent of age, advanced pubertal stage was associated with lower subjective sleep satisfaction but not with objective sleep indices. Subjective sleep satisfaction was associated with within-person trajectories of negative affect, but not with positive affect. Pubertal stage and sleep satisfaction did not interact to predict within-day negative or positive affect. These findings are consistent with previous reports showing that objective and subjective sleep health are associated differently with puberty, and that subjective sleep health is associated with daily affect. Pubertal stage may be a more important indicator of subjective sleep quality in adolescence than is chronological age, most likely due to hormonal changes and psychological adjustment to the physical changes associated with the pubertal transition.
Topics: Adult; Humans; Adolescent; Female; Male; Sleep; Puberty; Sleep Initiation and Maintenance Disorders; Sleep Quality; Sleep Duration; Actigraphy
PubMed: 36514260
DOI: 10.1111/jsr.13805 -
Clinical Endocrinology Nov 2021Puberty is a process of transition from childhood to adult reproductive capacity, governed by the reactivation of the hypothalamic-pituitary-gonadal axis after a long... (Review)
Review
Puberty is a process of transition from childhood to adult reproductive capacity, governed by the reactivation of the hypothalamic-pituitary-gonadal axis after a long period of dormancy in mid-childhood. As such, the reproductive hormones are in a state of flux during the adolescent years, and interpretation of both the onset of healthy, concordant puberty and the differentiation of precocious, delayed or disordered puberty, can be challenging. This review is focused on the description of the endocrine axes in healthy puberty and the markers of disorders of puberty that can aid diagnosis and management for patients with these conditions. It will cover the hypothalamic, pituitary and gonadal hormone systems, the dynamic changes that occur during puberty, conditions leading to precocious, delayed or absent puberty and other syndromes with disordered puberty, and the biochemical diagnosis of these different disorders of puberty.
Topics: Adolescent; Adult; Child; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Humans; Luteinizing Hormone; Puberty; Puberty, Precocious
PubMed: 34368982
DOI: 10.1111/cen.14578 -
Problemy Endokrinologii Sep 2021The precocious puberty is an urgent problem of pediatric endocrinology characterized by clinical and pathogenetic heterogeneity. The appearance of secondary sex...
The precocious puberty is an urgent problem of pediatric endocrinology characterized by clinical and pathogenetic heterogeneity. The appearance of secondary sex characteristics before the age of 8 years in girls and 9 years in boys requires timely diagnosis and the appointment of pathogenetically justified treatment in order to achieve the target indicators of final growth and prevent social deprivation. The developed clinical guidelines are the main working tool of the practitioner. They briefly and structurally present the main information about the epidemiology and modern classification of рrecocious puberty, methods of its diagnosis and treatment based on the principles of evidence-based medicine.
Topics: Child; Female; Humans; Male; Puberty; Puberty, Precocious
PubMed: 34766494
DOI: 10.14341/probl12821 -
International Journal of Environmental... Jun 2022Manganese (Mn) and lead (Pb) have been associated with the deregulation of the neuroendocrine system, which could potentially favor the appearance of precocious puberty...
Manganese (Mn) and lead (Pb) have been associated with the deregulation of the neuroendocrine system, which could potentially favor the appearance of precocious puberty (PP) in environmentally exposed children. This study aims to evaluate the exposure to Mn and Pb and their potential effects in anticipating puberty in school-aged children living near a ferromanganese alloy plant in Bahia, Brazil. Toenail, occipital hair and blood samples were collected from 225 school-aged children. Tanner’s scale was used for pubertal staging. Mn in blood (MnB), toenail (MnTn) and hair (MnH) and blood lead (PbB) levels were measured by graphite furnace atomic absorption spectrometry. Puberty-related hormone concentrations were determined by chemiluminescence. The age at which girls’ breasts began to develop was inversely correlated with weight-for-age, height-for-age and BMI-for-age Z-scores (p < 0.05); pubarche also had similar results. Mn biomarker levels did not present differences among pubertal classification nor among children with potential PP or not. Furthermore, Mn exposure was not associated with the age of onset of sexual characteristics for either girls or boys. However, PbB levels were positively correlated with boys’ pubic hair stages (rho = 0.258; p = 0.009) and associated with the age of onset of girls’ pubarche (β = 0.299, 95%CI = 0.055−0.542; p = 0.017). Testosterone and LH concentrations were statistically higher in boys with an increased PbB (p = 0.09 and p = 0.02, respectively). Prospective studies are needed to better assess the association between exposure to Mn and Pb and the early onset of puberty.
Topics: Alloys; Child; Environmental Exposure; Female; Humans; Ions; Iron; Lead; Male; Manganese; Puberty; Puberty, Precocious
PubMed: 35742410
DOI: 10.3390/ijerph19127158 -
The Journal of Adolescent Health :... Mar 2021Risk markers for breast cancer include earlier onset of menarche (age at menarche [AAM]) and peak height velocity (PHV). Insulin-like growth factor-1 (IGF-1) is...
PURPOSE
Risk markers for breast cancer include earlier onset of menarche (age at menarche [AAM]) and peak height velocity (PHV). Insulin-like growth factor-1 (IGF-1) is associated with pubertal milestones, as well as cancer risk. This study examined the relationships between pubertal milestones associated with breast cancer risk and hormone changes in puberty.
METHODS
This is a longitudinal study of pubertal maturation in 183 girls, recruited at ages 6-7, followed up between 2004 and 2018. Measures included age at onset of puberty, and adult height attained; PHV; AAM; adult height, and serum IGF-1, and estrone-to-androstenedione (E:A) ratio.
RESULTS
PHV was greatest in early, and least in late maturing girls; length of the pubertal growth spurt was longest in early, and shortest in late maturing girls. Earlier AAM was related to greater PHV. IGF-1 concentrations tracked significantly during puberty; higher IGF-1 was related to earlier age of PHV, earlier AAM, greater PHV, and taller adult height. Greater E:A ratio was associated with earlier AAM.
CONCLUSIONS
Factors driving the association of earlier menarche and pubertal growth with breast cancer risk may be explained through a unifying concept relating higher IGF-1 concentrations, greater lifelong estrogen exposure, and longer pubertal growth period, with an expanded pubertal window of susceptibility.
Topics: Adult; Body Height; Breast Neoplasms; Child; Female; Humans; Insulin-Like Growth Factor I; Longitudinal Studies; Menarche; Puberty
PubMed: 32888770
DOI: 10.1016/j.jadohealth.2020.07.016 -
Human Reproduction Update Aug 2022Globally, the ages at pubertal onset for girls and boys have been decreasing during recent decades, partly attributed to excess body fat accumulation. However, a growing... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Globally, the ages at pubertal onset for girls and boys have been decreasing during recent decades, partly attributed to excess body fat accumulation. However, a growing body of literature has recognized that endocrine disrupting chemicals (EDCs) may play an important role in this global trend, but the association has not yet been fully established.
OBJECTIVE AND RATIONALE
EDCs can interfere with normal hormone function and metabolism and play a role in pubertal onset. We aimed to systematically identify and evaluate the current evidence on the timing of pubertal onset in girls and boys following prenatal or postnatal exposures to xenobiotic EDCs.
SEARCH METHODS
Following PRISMA guidelines, we performed a systematic literature search of original peer-reviewed publications in the PubMed database through a block search approach using a combination of index MeSH and free text search terms. Publications were considered if they covered biomarkers of prenatal or postnatal exposures to xenobiotic EDCs (European Commission's list of category 1 EDCs) measured in maternal or child biospecimen and pubertal onset defined by the progression of the following milestones (and assessed in terms of the following measures): menarche (age), thelarche (Tanner staging) and pubarche (Tanner staging), in girls, and genital stage (Tanner staging), testicular volume (ml) and pubarche (Tanner staging), in boys.
OUTCOMES
The literature search resulted in 703 references, of which we identified 52 publications fulfilling the eligibility criteria for the qualitative trend synthesis and 23 publications for the meta-analysis. The qualitative trend synthesis provided data on 103 combinations of associations between prenatal or postnatal exposure to EDC compounds groups and puberty outcomes and the meta-analysis enabled 18 summary risk estimates of meta-associations.
WIDER IMPLICATIONS
Statistically significant associations in the qualitative trend synthesis suggested that postnatal exposure to phthalates may be associated with earlier thelarche and later pubarche. However, we did not find consistent evidence in the meta-analysis for associations between timing of pubertal onset in girls and boys and exposures to any of the studied xenobiotic EDCs. We were not able to identify specific pre- or postnatal windows of exposure as particularly critical and susceptible for effects of EDCs. Current evidence is subject to several methodological challenges and inconsistencies and evidence on specific exposure-outcome associations remains too scarce to firmly confirm EDC exposure as a risk factor for changes in age of pubertal onset in the general child population. To create a more uniform foundation for future comparison of evidence and to strengthen pooled studies, we recommend the use of more standardized approaches in the choice of statistical analyses, with exposure transformations, and in the definitions and assessments of puberty outcomes. The impact of mixtures of EDC exposures on the association also remains unestablished and would be valuable to elucidate for prenatal and postnatal windows of exposure. Future large, longitudinal epidemiological studies are needed to clarify the overall association.
Topics: Child; Endocrine Disruptors; Female; Humans; Longitudinal Studies; Male; Menarche; Pregnancy; Puberty; Xenobiotics
PubMed: 35466359
DOI: 10.1093/humupd/dmac013