This cohort study, including 15,810 children born 2000–2003 in Denmark, aimed to investigate the association between father absence in pregnancy or during childhood and pubertal development in girls and boys. The children were followed from 11 years of age and throughout pubertal development. Mean age differences according to exposure groups were estimated for each pubertal marker separately and for a combined pubertal marker. The results suggested that father absence in pregnancy and during childhood was associated with earlier pubertal development in girls, and father absence from late childhood was associated with earlier pubertal development in boys. The paternal investment theory, the psychosocial acceleration theory and the energetics theory were explored, and did not seem to explain the observed associations.

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Purpose Cryptorchidism and hypospadias share several prenatal risk factors. However, in published studies, boys exposed to cigarette smoking during pregnancy have a higher risk of cryptorchidism and a lower risk of hypospadias. Using Danish register-based data, we revisited these findings with a cohort and sibling-matched design to investigate the potential effect of shared time-stable factors. Patients and Methods For the cohort study, we included 823,670 live-born, singleton boys born from 1991 to 2016. Crude and adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated using Cox regression models for each genital anomaly according to maternal cigarette smoking during pregnancy. For the sibling-matched design, we included 399,258 brothers and used a stratified Cox regression model creating family-adjusted results. Results In the cohort study, we found a higher risk of cryptorchidism (aHR = 1.18, 95% CI: 1.12, 1.24) and a lower risk of hypospadias (aHR = 0.84, 95% CI: 0.76, 0.93) when comparing boys exposed to cigarette smoking with non-exposed, and for increasing numbers of cigarettes smoked. In comparison, the sibling-matched analyses suggested a slightly weaker association for cryptorchidism and an association of similar magnitude for hypospadias, both in the same direction as in the cohort study. Conclusion Shared, familial confounding does not seem to explain earlier findings of higher risk of cryptorchidism and lower risk of hypospadias.

Background Breast feeding has been associated with improved infant health, but its impact on pubertal timing remains uncertain, particularly in boys. Objective The objective of this study was to investigate the association between duration of breast feeding and pubertal timing in boys and girls. Methods This population‐based cohort study included 13 511 boys and girls from the Puberty Cohort nested within the Danish National Birth Cohort. The children gave half‐yearly, self‐reported information on pubertal development through questionnaires (Tanner stages, age at menarche, first ejaculation, voice break, axillary hair growth, and acne). Information on breast feeding was provided by the mothers when the children were 6 months of age. We estimated mean differences (in months) in age at attaining each pubertal marker and for overall timing of puberty (combined estimate) for every additional month of exclusive breast feeding. Furthermore, we estimated differences in pubertal age when comparing children never exclusively breastfed and exclusively breastfed <4 months using children exclusively breastfed ≥4 months as reference. In sub‐analyses, we further adjusted for infant weight gain and childhood BMI at 7 years to investigate whether these variables mediated the association. Results Boys tended to reach pubertal markers later for every additional month of exclusive breast feeding (combined estimate: 0.2 (95% confidence interval [CI] 0.0, 0.4 months). Never exclusively breastfed boys reached pubertal markers earlier than the boys exclusively breastfed ≥4 months (combined estimate: −4.1 (95% CI −6.7, −1.6) months). Boys exclusively breastfed <4 months also reached pubertal markers earlier than those never exclusively breastfed but with smaller differences. In girls, duration of breast feeding was not associated with pubertal development. When including infant weight gain or childhood BMI, the results remained essentially unchanged. Conclusions Shorter duration of exclusive breast feeding was associated with earlier pubertal development in boys but not in girls.

STUDY QUESTION Do maternal hypertensive disorders affect pubertal development in daughters and sons? SUMMARY ANSWER Pubertal development tended to occur earlier in daughters of mothers with ‘preeclampsia, eclampsia or HELLP syndrome’ (hemolysis, elevated liver enzymes and low blood platelets) or hypertension in pregnancy compared to daughters born of normotensive mothers. WHAT IS KNOWN ALREADY The existing literature suggests some or no association between preeclampsia and pubertal development in daughters, but not in sons. None of the previous studies has investigated the possible association between other types of hypertensive disorders (hypertension, eclampsia or HELLP syndrome) and pubertal timing in children. STUDY DESIGN, SIZE, DURATION Longitudinal cohort study consisting of 15 819 mother–child pairs with information on maternal hypertensive disorders collected during pregnancy and information on pubertal development collected half-yearly from the age of 11 years and until fully developed or 18 years of age. PARTICIPANTS/MATERIALS, SETTING, METHODS Participants are children from the Puberty Cohort nested within the Danish National Birth Cohort. The exposure was register-based and self-reported information on maternal hypertensive disorders during pregnancy. The outcomes were children’s self-reported information on pubertal development, including Tanner stage 1–5 (pubic hair (both daughters and sons) and breast development (daughters) or genital development (sons)), first menstrual bleeding (daughters) or first ejaculation (sons), voice break episode (sons), axillary hair development and acne occurrence (both daughters and sons). The main outcome was mean difference in age at attaining each pubertal milestone and a combined pubertal marker in children of mothers with hypertensive disorders in pregnancy (either hypertension (n = 490), ‘preeclampsia, eclampsia or HELLP syndrome’ (n = 419) or ‘unspecific hypertensive disorders’ (n = 334) with unexposed children as reference (n = 14 576)). MAIN RESULTS AND THE ROLE OF CHANCE In daughters of mothers with ‘preeclampsia, eclampsia or HELLP syndrome’, we observed tendencies of earlier pubertal timing (combined marker: −2.0 (95% CI: −3.9; 0.0) months). In daughters of mothers with hypertension, several pubertal milestones tended to occur earlier than in daughters of normotensive mothers; however, all 95% CIs overlapped the null resulting in a combined pubertal marker of −1.0 (95% CI: −3.2; 1.1) months. In sons of mothers with any of the hypertensive disorders, we observed no difference in pubertal timing (combined markers: ‘preeclampsia, eclampsia or HELLP syndrome’: 0.1 (95% CI: −2.0; 2.1) months; hypertension: −0.6 (95% CI: −2.3; 1.1) months; ‘unspecific hypertensive disorders’: 0.2 (95% CI: −1.9; 2.2) months). LIMITATIONS, REASONS FOR CAUTION The study is subject to non-differential misclassification of self-reported information on maternal hypertensive disorders in pregnancy and current pubertal status; possibly causing bias toward the null. WIDER IMPLICATIONS OF THE FINDINGS Hypertensive disorders in pregnancy might accelerate pubertal timing in daughters; however, more studies are needed for causal conclusions. STUDY FUNDING/COMPETING INTEREST(S) The study was funded by the Faculty of Health at Aarhus University. The authors have no financial relationships or competing interests to disclose. TRIAL REGISTRATION NUMBER N/A.