Pubertal development and risk of premenstrual disorders in young adulthood

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

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Infection and pubertal timing: a systematic review

Journal of Developmental Origins of Health and Disease ◽

10.1017/s2040174416000313 ◽

2016 ◽

Vol 7 (6) ◽

pp. 636-651 ◽

Cited By ~ 2

Author(s):

J. A. McDonald ◽

S. M. Eng ◽

O. O. Dina ◽

C. M. Schooling ◽

M. B. Terry

Keyword(s):

Psychosocial Adjustment ◽

Animal Studies ◽

Pubertal Timing ◽

Pubertal Development ◽

Pubic Hair ◽

Population Characteristics ◽

Breast Development ◽

Age At Menarche ◽

Eligibility Criteria ◽

Hair Development

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.

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Early Life Adversity and Pubertal Timing: Implications for Cardiometabolic Health

Journal of Pediatric Psychology ◽

10.1093/jpepsy/jsaa082 ◽

2020 ◽

Author(s):

Maria E Bleil ◽

Susan J Spieker ◽

Steven E Gregorich ◽

Alexis S Thomas ◽

Robert A Hiatt ◽

...

Keyword(s):

Early Life ◽

Pubertal Timing ◽

Pubertal Development ◽

Pubic Hair ◽

Cardiometabolic Health ◽

Age At Menarche ◽

Early Life Adversity ◽

Child Attachment ◽

Related Risk ◽

Hair Development

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 < .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). 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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Association between factors related to the pregnancy, neonatal period, and later complications (especially asthma) and menarcheal age in a sample of Lebanese girls

BMC Women s Health ◽

10.1186/s12905-020-01101-7 ◽

2020 ◽

Vol 20 (1) ◽

Author(s):

Josephine Sakkal ◽

Souheil Hallit ◽

Georges Nicolas

Keyword(s):

Neonatal Period ◽

Pubertal Timing ◽

Age At Menarche ◽

Cross Sectional ◽

Menarcheal Age ◽

Time In Literature ◽

Secondary Objective ◽

Mother’S Age ◽

Nicu Admission ◽

Timing Of Menarche

Abstract Background Studies about the majority of the factors that may potentially influence the pubertal timing and menarche were controversial. The objective was to evaluate the association between factors related to the pregnancy, neonatal period, and the complications that may happen later in life and the menarcheal age in a sample of Lebanese girls admitted or not to the NICU at birth. Our secondary objective was to try to find, for the first time in literature, a correlation between respiratory distress at birth and the need of oxygen therapy with the age of the first menses in these girls. Methods It is a cross-sectional retrospective study, conducted between January and March 2019. Our sample included all the 2474 girls born in Notre-Dame-de-Secours hospital, between 2000 and 2005; the sample consisted of 297 girls (97 girls admitted to the NICU and 200 randomly chosen to participate in our study with a ratio of 1:2 (1 girl admitted to the NICU vs 2 girls born in the nursery). Results Asthma later in life was significantly associated with lower age at menarche in girls, whereas a higher mother’s age at menarche and a higher gestational age were significantly associated with higher age at menarche in girls. When taking each cause of NICU admission as an independent variable, showed that a higher mother’s age at menarche was significantly associated with higher age at menarche in girls, whereas a higher number of days of phototherapy, a preeclampsia in the mother during pregnancy and asthma later in life in the girl were significantly associated with a lower age at menarche in girls. Conclusion The timing of menarche seems to be associated with many factors in Lebanese girls that should not be disregarded by physicians.

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Dietary Intake of Selenium in Relation to Pubertal Development in Mexican Children

Nutrients ◽

10.3390/nu11071595 ◽

2019 ◽

Vol 11 (7) ◽

pp. 1595 ◽

Cited By ~ 1

Author(s):

Yun Liu ◽

Karen E. Peterson ◽

Brisa N. Sánchez ◽

Andrew D. Jones ◽

Alejandra Cantoral ◽

...

Keyword(s):

Dietary Intake ◽

Pubertal Timing ◽

Pubertal Development ◽

Pubic Hair ◽

Specific Pattern ◽

Lower Probability ◽

Cross Sectional ◽

Mexican Children ◽

Future Work

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

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Childhood growth and development and DNA methylation age in mid-life

Clinical Epigenetics ◽

10.1186/s13148-021-01138-x ◽

2021 ◽

Vol 13 (1) ◽

Author(s):

Jane Maddock ◽

Juan Castillo-Fernandez ◽

Andrew Wong ◽

George B. Ploubidis ◽

Diana Kuh ◽

...

Keyword(s):

Weight Gain ◽

Growth And Development ◽

Linear Growth ◽

Disease Risk ◽

Pubertal Timing ◽

Pubertal Development ◽

Cardiovascular Disease Risk ◽

Relative Weight ◽

Late Childhood ◽

Age At Menarche

Abstract Background In the first study of its kind, we examine the association between growth and development in early life and DNAm age biomarkers in mid-life. Methods Participants were from the Medical Research Council National Survey of Health and Development (n = 1376). Four DNAm age acceleration (AgeAccel) biomarkers were measured when participants were aged 53 years: AgeAccelHannum; AgeAccelHorvath; AgeAccelLevine; and AgeAccelGrim. Exposure variables included: relative weight gain (standardised residuals from models of current weight z-score on current height, and previous weight and height z-scores); and linear growth (standardised residuals from models of current height z-score on previous height and weight z-scores) during infancy (0–2 years, weight gain only), early childhood (2–4 years), middle childhood (4–7 years) and late childhood to adolescence (7–15 years); age at menarche; and pubertal stage for men at 14–15 years. The relationship between relative weight gain and linear growth and AgeAccel was investigated using conditional growth models. We replicated analyses from the late childhood to adolescence period and pubertal timing among 240 participants from The National Child and Development Study (NCDS). Results A 1SD increase in relative weight gain in late childhood to adolescence was associated with 0.50 years (95% CI 0.20, 0.79) higher AgeAccelGrim. Although the CI includes the null, the estimate was similar in NCDS [0.57 years (95% CI − 0.01, 1.16)] There was no strong evidence that relative weight gain and linear growth in childhood was associated with any other AgeAccel biomarker. There was no relationship between pubertal timing in men and AgeAccel biomarkers. Women who reached menarche ≥ 12 years had 1.20 years (95% CI 0.15, 2.24) higher AgeAccelGrim on average than women who reached menarche < 12 years; however, this was not replicated in NCDS and was not statistically significant after Bonferroni correction. Conclusions Our findings generally do not support an association between growth and AgeAccel biomarkers in mid-life. However, we found rapid weight gain during pubertal development, previously related to higher cardiovascular disease risk, to be associated with older AgeAccelGrim. Given this is an exploratory study, this finding requires replication.

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SUN-594 Pubertal Timing and Hormonal Correlates in Male Obesity

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.1081 ◽

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.

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Earlier age at menarche as a transdiagnostic mechanism linking childhood trauma with multiple forms of psychopathology in adolescent girls

Psychological Medicine ◽

10.1017/s0033291719000953 ◽

2019 ◽

Vol 50 (7) ◽

pp. 1090-1098 ◽

Cited By ~ 7

Author(s):

Natalie L. Colich ◽

Jonathan M. Platt ◽

Katherine M. Keyes ◽

Jennifer A. Sumner ◽

Nicholas B. Allen ◽

...

Keyword(s):

Adolescent Girls ◽

Pubertal Timing ◽

Adolescent Psychopathology ◽

Pubertal Development ◽

Externalizing Disorders ◽

Age At Menarche ◽

Multiple Forms ◽

Early Life Adversity ◽

Early Maturation ◽

Nationally Representative

AbstractBackgroundAlthough early life adversity (ELA) increases risk for psychopathology, mechanisms linking ELA with the onset of psychopathology remain poorly understood. Conceptual models have argued that ELA accelerates development. It is unknown whether all forms of ELA are associated with accelerated development or whether early maturation is a potential mechanism linking ELA with psychopathology. We examine whether two distinct dimensions of ELA – threat and deprivation – have differential associations with pubertal timing in girls, and evaluate whether accelerated pubertal timing is a mechanism linking ELA with the onset of adolescent psychopathology.MethodsData were drawn from a large, nationally representative sample of 4937 adolescent girls. Multiple forms of ELA characterized by threat and deprivation were assessed along with age at menarche (AAM) and the onset of DSM-IV fear, distress, externalizing, and eating disorders.ResultsGreater exposure to threat was associated with earlier AAM (B = −0.1, p = 0.001). Each 1-year increase in AAM was associated with reduced odds of fear, distress, and externalizing disorders post-menarche (ORs = 0.74–0.85). Earlier AAM significantly mediated the association between exposure to threat and post-menarche onset of distress (proportion mediated = 6.2%), fear (proportion mediated = 16.3%), and externalizing disorders (proportion mediated = 2.9%).ConclusionsAccelerated pubertal development in girls may be one transdiagnostic pathway through which threat-related experiences confer risk for the adolescent onset of mental disorders. Early pubertal maturation is a marker that could be used in both medical and mental health settings to identify trauma-exposed youth that are at risk for developing a mental disorder during adolescence in order to better target early interventions.

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Childhood growth and development and DNA methylation age in mid-life

10.1101/2020.12.02.20242529 ◽

2020 ◽

Author(s):

Jane Maddock ◽

Juan Castillo-Fernandez ◽

Andrew Wong ◽

George B Ploubidis ◽

Diana Kuh ◽

...

Keyword(s):

Early Childhood ◽

Weight Gain ◽

Growth And Development ◽

Linear Growth ◽

Pubertal Timing ◽

Relative Weight ◽

Late Childhood ◽

Age At Menarche ◽

Z Score ◽

Z Scores

ABSTRACTBackgroundIn the first study of its kind, we examine the association between growth and development in early life and DNAm age biomarkers in mid-life.MethodsParticipants were from the Medical Research Council National Survey of Health and Development(n=1,376). Four DNAm age acceleration(AgeAccel) biomarkers were measured when participants were aged 53y:AgeAccelHannum, AgeAccelHorvath, AgeAccelLevine and AgeAccelGrim. Exposure variables included relative weight gain (standardised residuals from models of current weight z-score on current height, and previous weight and height z-scores) and linear growth (standardised residuals from models of current height z-score on previous height and weight z-scores) during infancy (0-2y, weight gain only), early childhood(2-4y), middle childhood(4-7y) and late childhood to adolescence(7- 15y), age at menarche and pubertal stage for men at 14-15y. The relationship between relative weight gain and linear growth and AgeAccel was investigated using conditional growth models. We replicated analyses from the late childhood to adolescence period and pubertal timing among 240 participants from The National Child and Development Study(NCDS).ResultsA 1 SD increase in relative weight gain in late childhood to adolescence was associated with 0.50y(95% CI:0.20,0.79) higher AgeAccelGrim. This was replicated in NCDS (0.57y(95%CI:-0.01, 1.16). A I SD increase in linear growth during early childhood was associated with lower AgeAccelLevine(−0.39y [95% CI:-0.74,-0.04) however we did not have the data to replicate this finding in NCDS. There was no strong evidence that relative weight gain and linear growth in childhood was associated with any other AgeAccel biomarker. There was no relationship between pubertal timing in men and AgeAccel biomarkers. Women who reached menarche ≥12y had 1.20y(95% CI:0.15,2.24) higher AgeAccelGrim on average than women who reached menarche <12y; however this was not replicated in NCDS.ConclusionsOur findings generally do not support an association between growth and AgeAccel biomarkers in mid-life. However, rapid weight gain during pubertal development, which we found to be related to older AgeAccelGrim and had previously been related to higher cardiovascular disease risk, warrants further investigation.

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

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2016-1073 ◽

2016 ◽

Vol 101 (7) ◽

pp. 2667-2674 ◽

Cited By ~ 27

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 >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.

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Common Childhood Viruses and Pubertal Timing: The LEGACY Girls Study

American Journal of Epidemiology ◽

10.1093/aje/kwaa240 ◽

2020 ◽

Author(s):

Jasmine A McDonald ◽

Sinaida Cherubin ◽

Mandy Goldberg ◽

Ying Wei ◽

Wendy K Chung ◽

...

Keyword(s):

Viral Infections ◽

Pubertal Timing ◽

Pubertal Development ◽

Tanner Stage ◽

Pubic Hair ◽

Breast Development ◽

Blood Collection ◽

Cmv Infection ◽

Blood Draw ◽

Childhood Infections

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.

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