Early Pubertal Timing Research Articles

Multimethod assessment of pubertal timing and associations with internalizing psychopathology in early adolescent girls.

Early pubertal timing has consistently been associated with internalizing psychopathology in adolescent girls. Here, we aimed to examine whether the association between timing and mental health outcomes varies by measurement of pubertal timing and internalizing psychopathology, differs between adrenarcheal and gonadarcheal processes, and is stronger concurrently or prospectively. We assessed 174 female adolescents (age 10.0-13.0 at Time 1) twice, with an 18-month interval. Participants provided self-reported assessments of depression/anxiety symptoms and pubertal development, subjective pubertal timing, and date of menarche. Their parents/guardians also reported on the adolescent's pubertal development and subjective pubertal timing. We assessed salivary dehydroepiandrosterone (DHEA), testosterone, and estradiol levels and conducted clinical interviews to determine the presence of case level internalizing disorders. From these data, we computed 11 measures of pubertal timing at both time points, as well as seven measures of internalizing psychopathology, and entered these in a Specification Curve Analysis. Overall, earlier pubertal timing was associated with increased internalizing psychopathology. Associations were stronger prospectively than concurrently, suggesting that timing of early pubertal processes might be especially important for later risk of mental illness. Associations were strongest when pubertal timing was based on the Tanner Stage Line Drawings and when the outcome was case-level Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) depression or Hierarchical Taxonomy of Psychopathology (HiTOP) distress disorders. Timing based on hormone levels was not associated with internalizing psychopathology, suggesting that psychosocial mechanisms, captured by timing measures of visible physical characteristics might be more meaningful determinants of internalizing psychopathology than biological ones in adolescent girls. Future research should precisely examine these psychosocial mechanisms. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

Psychosocial and energetic factors on human female pubertal timing: a systematized review.

Childhood psychosocial stressors have been proposed to favour fast life history strategies promoting earlier puberty in females. However, studies demonstrating this association often do not elucidate causal mechanisms, nor account for greater childhood energetic availability - also known to promote rapid growth and earlier puberty. To assess the extent to which such confounding has been considered, we conducted a systematized review to identify studies examining measures of both prepubertal growth (e.g. weight, height) and psychosocial stressors (e.g. adversity, father absence) in relation to female pubertal timing. A total of 1069 non-duplicated studies were identified across five databases. Twenty studies met selection criteria for critical review following independent screening of titles, abstracts and manuscripts. Within these studies, measures indicative of rapid childhood growth were more consistently associated with earlier pubertal timing than were measures of psychosocial stress. We discuss future research directions to investigate the impact of psychosocial stress on pubertal timing more robustly, including methodological and mechanistic considerations, and contextualization of findings by socioecological environments.

Association Between Paternal Separation During Early Childhood and Pubertal Timing Among Girls Using Longitudinal Birth Cohort in Japan.

IntroductionPrevious studies have shown that paternal absence leads to earlier pubertal timing among girls in high-income countries. Despite the low divorce rate in Japan, paternal separation is commonly seen due to a unique corporation system, tanshin funin, where employees relocate with their spouses and children. We examined paternal separation, including paternal absence (due to divorce or paternal death) and paternal tanshin funin, during early childhood as a predictor of earlier girl’s pubertal development, assessed as age at peak height velocity (PHV).MethodsThis study examined 15 214 girls from a longitudinal survey conducted in Japan from 2001 to 2016 by the Ministry of Health, Labor and Welfare. Paternal separation was determined by the occurrence through annual surveys conducted at ages 0.5 to 4.5 years. Outcome was defined as age at PHV between ages 6 to 15 years. We conducted linear regression, adjusted for potential confounders and other covariates.ResultsContinuous father cohabitation was seen in 88.7% of households, while paternal separation was experienced 1-2, 3-4 and 5 times (always) among 7.4%, 2.8% and 1.1% of households, respectively. Girls who confronted continuous paternal separation (5 times) experienced 0.42 years earlier [95% confidence interval (CI): -0.75, -0.10] age at PHV compared to their peers who always lived with their fathers.ConclusionGirls who experienced paternal separation throughout ages 0.5 to 4.5 years experienced PHV earlier.

Caesarean delivery and pubertal timing in boys and girls: A Danish population-based cohort study.

There is considerable public and scientific interest in the declining age of pubertal timing. Prenatal and postnatal stress has been proposed to relate with earlier pubertal timing, but it remains unknown whether intrapartum stress may affect pubertal timing as well. This study aims to examine the potential effect of caesarean delivery on pubertal timing in boys and girls. This study was based upon the nationwide Puberty Cohort nested within the Danish National Birth Cohort (DNBC) from 2000 to 2003. A total of 15,731mother-child pairs with complete information on delivery mode and puberty were included in the main analysis. The delivery mode was categorised into non-instrumental vaginal delivery (reference), instrumental vaginal delivery, elective caesarean delivery before labour, emergency caesarean delivery during labour and un-specified caesarean delivery. Children's pubertal development were self-reported in web-based questionnaires from 11years of age and every 6months throughout puberty (2012-2019), including Tanner stages 2-5, menarche, voice break, first ejaculation, axillary hair growth and the onset of acne. Regression models for censored, normally distributed time-to-event data were used to estimate mean monthly differences in age at attaining the different pubertal milestones and the average of all these estimates for each sex (a combined indicator of pubertal timing). A total of 2810 participants were born by caesarean delivery (17.9%). Neither elective nor emergency caesarean delivery was associated with earlier age at achieving the pubertal milestones in boys or in girls. For the combined indicator, the mean age differences for elective caesarean delivery and emergency caesarean delivery were 0.1 (95% CI -1.1, 1.4) months and -0.7 (95% CI -2.0, 0.5) months in boys and 0.7 (95% CI -0.7, 2.0) and 0.2 (95% CI -1.3, 1.7) in girls. This study does not suggest a clinically important effect of caesarean delivery on children's pubertal timing.

Pubertal timing and functional neurodevelopmental alterations independently mediate the effect of family conflict on adolescent psychopathology

This study tested the hypothesis that early life adversity (ELA) heightens psychopathology risk by concurrently altering pubertal and neurodevelopmental timing, and associated gene transcription signatures. Analyses focused on threat- (family conflict/neighbourhood crime) and deprivation-related ELAs (parental inattentiveness/unmet material needs), using longitudinal data from 1514 biologically unrelated youths in the Adolescent Brain and Cognitive Development (ABCD) study. Typical developmental changes in white matter microstructure corresponded to widespread BOLD signal variability (BOLDsv) increases (linked to cell communication and biosynthesis genes) and region-specific task-related BOLDsv increases/decreases (linked to signal transduction, immune and external environmental response genes). Increasing resting-state (RS), but decreasing task-related BOLDsv predicted normative functional network segregation. Family conflict was the strongest concurrent and prospective contributor to psychopathology, while material deprivation constituted an additive risk factor. ELA-linked psychopathology was predicted by higher Time 1 threat-evoked BOLDSV (associated with axonal development, myelination, cell differentiation and signal transduction genes), reduced Time 2 RS BOLDsv (associated with cell metabolism and attention genes) and greater Time 1 to Time 2 control/attention network segregation. Earlier pubertal timing and neurodevelopmental alterations independently mediated ELA effects on psychopathology. Our results underscore the differential roles of the immediate and wider external environment(s) in concurrent and longer-term ELA consequences.

Parenting Styles as a Moderator of the Association between Pubertal Timing and Chinese Adolescents' Smoking Behavior.

Background: Pubertal timing refers to the timing of an individual regarding pubertal sexual maturation, both physiologically and psychologically. Existing research shows that pubertal timing is associated with behavioral problems. This study investigated the role of parenting style in the relationship between pubertal timing and Chinese adolescents’ smoking behavior. Methods: The study examined the association of pubertal timing, parenting style and adolescents’ smoking behavior, using the Pubertal Development Scale (Chinese version), Simplified Parenting Style Scale-Chinese version, and three items related to adolescents’ smoking situation. Participants were 1391 Chinese adolescents aged 11–16 years old (53.41% boys). Hierarchical linear regression analyses assessed the moderating role of parenting style on the association between pubertal timing and adolescent smoking behavior. Results: The results indicated that parenting style moderates the relationship between pubertal timing and adolescent smoking behavior. For male adolescents, father rejection moderated the relationship between early pubertal timing and smoking behavior. For female adolescents, father rejection, father emotional warmth, and mother emotional warmth moderated the relationship between pubertal timing and smoking behavior. Conclusions: Findings from the study highlight the importance of parenting style, which may influence the negative outcomes associated with early pubertal timing and can help improve interventions aimed at reducing these negative outcomes.

Developmental Cascades from Polygenic and Prenatal Substance Use to Adolescent Substance Use: Leveraging Severity and Directionality of Externalizing and Internalizing Problems to Understand Pubertal and Harsh Discipline-Related Risk.

The current study leveraged the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort (n = 4504 White boys, n = 4287 White girls assessed from the prenatal period through 18.5years of age) to test a developmental cascade from genetic and prenatal substance use through pubertal timing and parenting to the severity of (regardless of type) and directionality (i.e., differentiation) of externalizing and internalizing problems to adolescent substance use. Limited associations of early pubertal timing with substance use outcomes were only observable via symptom directionality, differently for girls and boys. For boys, more severe exposure to prenatal substance use influenced adolescent substance use progression via differentiation towards relatively more pure externalizing problems, but in girls the associations were largely direct. Severity and especially directionality (i.e., differentiation towards relatively more pure externalizing problems) were key intermediaries in developmental cascades from parental harsh discipline with substance use progressions for girls and boys.

Erratum to: Childhood overweight and obesity and timing of puberty in boys and girls: cohort and sibling-matched analyses

Background Early puberty is a risk indicator for adult diseases. Identification of modifiable causes of earlier puberty is, therefore, warranted. We estimate the association between childhood body mass index (BMI) and pubertal timing in a cohort study and in a sibling-matched study to adjust for unobserved time-stable confounders shared within families. Methods For the cohort study, 11 046 of 22 439 (49%) invited children, born 2000-203, from the Danish National Birth Cohort (DNBC) had information on childhood BMI at 7 years and self-reported, half-yearly puberty information from 11 years on Tanner stages, menarche, voice break, first ejaculation, acne, and axillary hair. For the sibling-matched study, 1700 brothers and sisters were included among 86 820 live-born singletons from the DNBC. Results Childhood overweight (85th ≤ BMI Conclusions Childhood overweight and obesity were associated with earlier pubertal timing even after adjustment for unobserved time-stable confounders shared within families.

Association between pubertal development and elevated blood pressure in children.

Blood pressure (BP) increased with age and height development, but little was known about the effect of pubertal development on blood pressure in children. A cross‐sectional study was performed among 4146 children aged 7–12 years old in China. Pubertal development was assessed based on breast stages and testicular volume. The associations of pubertal development with BP levels and the rate of elevated blood pressure (EBP) were quantified using multiple linear and logistic regressions. We found that pubertal developmental level was positively correlated with BP, and children who experienced puberty onset and early pubertal timing had higher BP levels and prevalence of EBP. After adjusting for covariates, children experienced puberty onset had 3.84 and 2.24 mmHg increase in systolic blood pressure and diastolic blood pressure, and 70%, 53%, and 62% increased odds of EBP, ESBP, and EDBP, respectively, compared with those without puberty onset. Similar results were observed for children who had early pubertal timing. The change of BP in puberty is greater and the association between pubertal development and BP is stronger in girls than boys. These findings suggested that pubertal development could be an important independent factor and one critical period for the EBP progress. Monitoring and management of pubertal development are necessary particularly among girls.

The link between obesity and puberty: what is new?

The objective of this review is to assess the most recent literature on pubertal trends in boys and girls as well as evaluate genetic, epigenetic, and environmental factors implicated in the timing of pubertal progression. Recent studies confirm the previously described link between increased adiposity and earlier onset of puberty in girls, and more recent studies shed light onto the previously unclear situation in boys as a preponderance of recent longitudinal studies suggests that increased adiposity is linked with earlier pubertal timing also in boys. Discoveries of novel pathways highlights the complexity of pubertal development and suggest mechanistic links between nutrition, obesity, leptin, insulin resistance, and puberty. Furthermore, genetic and epigenetic variants can be linked to early puberty. Other factors, such as prenatal and postnatal environment, gut microbiota, and endocrine-disrupting chemicals have also been linked to both obesity and earlier puberty. Understanding how the interactions of these factors contribute the relationship between obesity and early pubertal onset is crucial as early puberty has been linked with long-term consequences, such as short stature, earlier type 2 diabetes, cardiovascular disease, and poor psychological and behavioral outcomes.

Obesity in both boys and girls associated with earlier pubertal timing

Chen LK, Wang G, Bennett WL, Ji Y, Pearson C, Radovick S, et al. Trajectory of Body Mass Index from Ages 2 to 7 Years and Age at Peak Height Velocity in Boys and Girls. J Pediatr 2021;230:221-9.e5. https://doi.org/10.1016/j.jpeds.2020.11.047

Family Experiences and Parent Personality as Antecedents of Pubertal Timing in Girls and Boys.

Pubertal timing may be influenced by typical variations in early family environmental events, but questions remain concerning the roles of specific parenting factors, developmental age of exposure to events, moderation by child temperament, and comparability of effects for girls and boys. This study focused on these questions utilizing longitudinal data from 733 same-sex twins (45% girls) in the U.S.; family context was measured at ages 1-3, 4-5, and 6-7 years and pubertal status was assessed annually via self-report at ages 9-15, enabling estimates of pubertal timing. Home environment at ages 4-5 years predicted pubertal timing better than home environment at other ages for both girls and boys, but parent personality was more predictive than home experiences (e.g., divorce, parental harshness, family conflict). Thus, effects of family environment must be considered within the context of parent characteristics, encouraging caution in implicating early environmental experiences as direct influences on early pubertal timing.

The Role of Pubertal Timing in the Development of Peer Victimization and Offending From Early- to Mid-Adolescence

We used latent growth curve analysis to extend research on associations between early puberty and adverse peer relations by examining the role of pubertal timing in the developmental trajectories of peer victimization and offending from early- to mid-adolescence. We made use of three-wave longitudinal data collected annually from a cohort of Swedish adolescents ( N = 1,515, 51% girls, [Formula: see text]age at T1 = 13.0 years). The results revealed negative developmental trends for peer victimization and offending. Early pubertal timing was linked to higher initial levels and a steeper decrease of peer victimization and offending. The only effect of pubertal timing that differed between the genders was that the initial level of offending was stronger for boys than girls. In conclusion, the negative impact of early pubertal timing on peer victimization and offending occurs in the early stages of adolescence and disappears thereafter.

Childhood obesity and multiple sclerosis: A Mendelian randomization study

Background: Higher childhood body mass index (BMI) has been associated with an increased risk of multiple sclerosis (MS). Objective: To evaluate whether childhood BMI has a causal influence on MS, and whether this putative effect is independent from early adult obesity and pubertal timing. Methods: We performed Mendelian randomization (MR) using summary genetic data on 14,802 MS cases and 26,703 controls. Large-scale genome-wide association studies provided estimates for BMI in childhood (n = 47,541) and adulthood (n = 322,154). In multivariable MR, we examined the direct effects of each timepoint and further adjusted for age at puberty. Findings were replicated using the UK Biobank (n = 453,169). Results: Higher genetically predicted childhood BMI was associated with increased odds of MS (odds ratio (OR) = 1.26/SD BMI increase, 95% confidence interval (CI): 1.07–1.50). However, there was little evidence of a direct effect after adjusting for adult BMI (OR = 1.03, 95% CI: 0.70–1.53). Conversely, the effect of adult BMI persisted independent of childhood BMI (OR = 1.43; 95% CI: 1.01–2.03). The addition of age at puberty did not alter the findings. UK Biobank analyses showed consistent results. Sensitivity analyses provided no evidence of pleiotropy. Conclusion: Genetic evidence supports an association between childhood obesity and MS susceptibility, mediated by persistence of obesity into early adulthood but independent of pubertal timing.

Childhood adversity, pubertal timing and self-harm: a longitudinal cohort study.

The occurrence of early childhood adversity is strongly linked to later self-harm, but there is poor understanding of how this distal risk factor might influence later behaviours. One possible mechanism is through an earlier onset of puberty in children exposed to adversity, since early puberty is associated with an increased risk of adolescent self-harm. We investigated whether early pubertal timing mediates the association between childhood adversity and later self-harm. Participants were 6698 young people from a UK population-based birth cohort (ALSPAC). We measured exposure to nine types of adversity from 0 to 9 years old, and self-harm when participants were aged 16 and 21 years. Pubertal timing measures were age at peak height velocity (aPHV - males and females) and age at menarche (AAM). We used generalised structural equation modelling for analyses. For every additional type of adversity; participants had an average 12-14% increased risk of self-harm by 16. Relative risk (RR) estimates were stronger for direct effects when outcomes were self-harm with suicidal intent. There was no evidence that earlier pubertal timing mediated the association between adversity and self-harm [indirect effect RR 1.00, 95% confidence interval (CI) 1.00-1.00 for aPHV and RR 1.00, 95% CI 1.00-1.01 for AAM]. A cumulative measure of exposure to multiple types of adversity does not confer an increased risk of self-harm via early pubertal timing, however both childhood adversity and early puberty are risk factors for later self-harm. Research identifying mechanisms underlying the link between childhood adversity and later self-harm is needed to inform interventions.

Early life adversity, pubertal timing, and epigenetic age acceleration in adulthood.

Given associations linking early life adversity, pubertal timing, and biological aging, we examined the direct and indirect effects of early life trauma on adult biological aging (via age of menarche). Participants were premenopausal women (N=183). Path models evaluated whether early life trauma predicted early pubertal timing and thereby, adult epigenetic age acceleration (indexed via four epigenetic clocks: Horvath DNAm Age, Hannum DNAm Age, DNAm PhenoAge, and DNAm GrimAge). Secondary analyses explored the effects of type of trauma (abuse and neglect) and adult chronic stress status (caregiver of child with autism and non-caregiver). Early life trauma and earlier age at menarche independently predicted accelerated aging based on one of the four epigenetic clocks, DNAm GrimAge, though early life trauma was not associated with age of menarche. Childhood abuse, but not neglect, predicted faster epigenetic aging; results did not differ by chronic stress status. Early trauma and early menarche appear to exert independent effects on DNAm GrimAge, which has been shown to be the strongest epigenetic predictor of mortality risk. This study identifies a potential correlate or determinant of accelerated epigenetic aging-menarcheal age. Future research should address the limitations of this study by using racially diverse samples.

Association between Early Spermarche and Suicide Attempts in Boys: the Korea Youth Risk Behavior Web-based Survey.

BackgroundPuberty is a biologically and psychologically unstable period, and pubertal changes differ by sex. However, most previous studies on pubertal timing and suicide have focused on girls. This study investigated the association between early spermarche and suicide attempts in boys.MethodsWe analyzed a nationally representative sample of Korean adolescents (The Korea Youth Risk Behavior Web-Based Survey, KYRBS) that included approximately 35,000 boys annually from 2011 to 2015. Pubertal timing in boys was defined by spermarche. Complex sampling logistic regression analyses were performed to evaluate the odds ratios (ORs) for suicide attempts between the early and average spermarche groups.ResultsThe ORs for suicide attempts in boys with early spermarche were significantly higher than those in boys with average spermarche after adjustment for age, perceived stress, depressive symptoms, and suicidal ideation. The ORs from 2011 to 2015 were as follows: 1.782 (P < 0.001), 1.490 (P = 0.002), 1.693 (P < 0.001), 1.541 (P = 0.001), and 1.393 (1.024–1.895; P = 0.035), respectively.ConclusionThese findings suggest that early pubertal timing is a risk factor for suicide attempts in Korean boys after adjustment for depressive symptoms, perceived stress, and suicidal ideation, which have been previously reported as risk factors for suicide attempts. Therefore, careful attention should be paid to the prevention of suicide in boys who experience early spermarche in Korea.

Early Life Adversity and Pubertal Timing: Implications for Cardiometabolic Health.

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). 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. 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 < .01), but did not predict breast or pubic hair development (ps > .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 < .05). 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.

Placental weight Z-score and pubertal timing: A population-based cohort study.

The placenta provides nutrients, oxygen, and hormonal support for adequate fetal growth and development of the hormonal axes, which are important for pubertal timing later in life. We investigated if an indicator of poor placental function, low gestational age-specific Z-score for placental weight at birth, was associated with earlier pubertal timing. The study is based on a population-based cohort of 15195 singleton boys and girls (68% of 22439 invited) born 20 to 43weeks of gestation (2000-2003) nested within the Danish National Birth Cohort. Placental Z-score was estimated from data collected at birth. Between 2012 and 2018, the children returned half-yearly web-based questionnaires from age of 11years on status of the pubertal milestones: Tanner stages, voice break, first ejaculation, menarche, acne, and axillary hair. We estimated adjusted monthly differences in mean age at attaining the pubertal milestones and pubertal timing overall with placental Z-score continuously and as restricted cubic splines. Further, we explored whether growth by birthweight Z-score and body mass index Z-score around 7years mediated the associations. Placental Z-score was positively associated with age at attaining most of the pubertal milestones in girls, particularly for age at menarche, but not in boys. Effect sizes were modest, and when combining all pubertal milestones, one standard deviation increase in placental Z-score was associated with 0.5months (95% confidence interval [CI] 0.2, 0.9) later pubertal timing overall in girls. The associations in girls were largely mediated through fetal growth. Assuming that placental Z-score correlates with placental function, these findings suggest that placental dysfunction (low placental Z-score) advances pubertal timing in girls slightly by reducing fetal growth. Future studies need to evaluate whether placental weight sufficiently captures intrauterine growth of importance for pubertal development and search for other potential candidates reflecting placental function.

Association of Early-Life Adversity With Measures of Accelerated Biological Aging Among Children in China

A growing body of literature suggests that exposure to early-life adversity (ELA) is associated with accelerated biological aging, offering 1 mechanism through which ELA may be associated with an increased risk for age-related disease. These investigations, however, have been predominantly cross-sectional and focused on adults and females. To evaluate associations of threat-related (ie, physical abuse) and deprivation-related (ie, emotional neglect) ELA exposure with cellular and reproductive strategy metrics of biological aging among boys and girls with specific genetic backgrounds around the period of pubertal onset. In this cohort study, 997 boys and girls in grade 1 to grade 3 from 3 large elementary schools were recruited from Bengbu, Anhui Province, China, and were followed up from March 21, 2016 (baseline; wave 1), for 4 consecutive years, through March 25, 2019. The outcome was accelerated biological aging in both cellular and reproductive strategy metrics: telomere attrition and age at thelarche (for girls) and testicular maturation (for boys). Multi-informant assessment of exposure to threat-related and deprivation-related ELA was done at baseline (wave 1) and 1-year follow-up (wave 2). The polygenic risk score (PRS) was computed based on 17 single-nucleotide variations for early pubertal timing. Of the 997 participants (579 girls [58.1%]; mean [SD] age at baseline, 8.0 [0.8] years), 550 (55.2%) reported exposure to threat-related ELA and 443 (44.4%) reported exposure to deprivation-related ELA. Threat-related ELA was associated with onset of thelarche 2.6 months earlier and deprivation-related ELA with onset of thelarche 3.3 months earlier in exposed girls than in unexposed peers; these associations were observed only among girls with a low PRS. Among boys, a similar pattern was found. Threat-related ELA was associated with testicular volume of 4 mL or more 1.4 months earlier and deprivation-related ELA was associated with testicular volume of 4 mL or more 2.3 months earlier than in unexposed peers but only among those with a low PRS. Boys and girls with greater exposure to threats showed a significantly higher percentage of telomere length change during 1-year follow-up, but only among those with low PRS (boys: β = 1.50; 95% CI, 0.80-2.21; P < .001; girls: β = 2.40; 95% CI, 1.78-3.05; P < .001) and moderate PRS (boys: β = 1.09; 95% CI, 0.43-1.75; P = .001; and girls: β = 1.27; 95% CI, 0.77-1.77; P < .001). No associations of deprivation-related ELA with percentage of telomere length change were found. This study suggests that the accelerating association of ELA with biological aging might occur at an earlier age and in a genetic background-dependent and dimension-specific manner.