To our knowledge, this is the largest prospective study of diverse adolescent girls to demonstrate that early-life exposure to family non-intactness is associated with earlier puberty. Girls who lived in a non-intact household before the age of 2 years were at greatest risk of experiencing earlier puberty compared with girls living in intact households. Later exposure (age 2–6 years) was also associated with early puberty, but not as strongly as exposure before age 2. Our study suggested that there may be racial/ethnic differences in these associations, where the associations were strongest among Black girls. Inclusion of prepubertal BMI did not substantially attenuate associations and, therefore, does not appear to be a likely mediator of these associations.
Our findings extend the previous knowledge regarding the associations between early-life family structures and pubertal timing in girls. Our results corroborate previous studies demonstrating that father absence is a risk factor of early puberty [9,10,11,12,13,14,15], as well as the studies that hypothesized that children may be particularly sensitive to stressful environments during the first few years of life [6]. There are several potential mechanisms explaining our observation.
First, infant attachment insecurity may be one mechanism through which girls living in non-intact households before age 2 years are experiencing earlier pubertal onset. Attachment security is the positive bond that develops between infant and caregiver that allows the infant to feel comfort while in the caregiver’s company [8]. Research shows that infants living in single-parent households are more likely to display attachment insecurity compared with infants living in dual-parent (e.g., intact) households [22]. Belsky and colleagues tested the hypothesis that girls with insecure attachment at 15 months would undergo earlier pubertal maturation in a cohort of 373 female infants who were followed over a period of 15 years [8]. The study found that girls with insecure infant attachment were more likely to experience earlier pubertal onset, earlier pubertal completion, and earlier menarche, compared with girls with secure infant attachment, lending evidence to the theory that family and rearing experiences are instrumental in determining pubertal and sexual developmental trajectories [8]. Our findings corroborate these observations.
Second, animal studies suggest there may be underlying biological mechanisms explaining the observed associations. For instance, a 2008 study found that maternal pup licking and grooming in rats correlates with estrogen receptor bioactivity, affecting female offspring pubertal timing [8, 23]. Female pups experiencing greater maternal care were less likely to engage in sexual activities and less likely to achieve pregnancy [8, 23]. It is possible that greater parental care in humans may also differentially affect the hypothalamic pituitary gonadal axis and other biological pathways involved in human sexual development. However, this theory is only plausible if the quality and amount of parental care varies substantially between single- and dual-parent households and is beyond the scope of the current study. In addition, there is a theory that pheromonal signaling may be one of the underlying mechanisms describing family intactness and pubertal timing. It has been postulated that proximity to the biological father may delay sexual development in girls as an evolutionary anti-inbreeding tactic to optimize quality of offspring [24]. Future studies further examining these mechanisms will provide greater insight.
The presence of race/ethnic differences in the association between household intactness and timing of pubertal onset may provide some explanation for why minority girls are experiencing an even greater decline in age of pubertal onset compared to other race/ethnic girls. In our race/ethnicity-stratified models, we found that White, Black, and Latinx girls, but not Asian/Pacific Islander or Other ethnicity girls, were at substantially greater risk of experiencing earlier breast onset, with Black and Latinx girls having the strongest associations. Although Black and Latinx have reportedly higher rates of childhood obesity and obesity-related conditions [25], our data did not demonstrate that the observed associations between family intactness and pubertal onset were explained by prepubertal BMI. Rate of single motherhood is disproportionately high in Black communities [16], which our data also demonstrated (i.e., nearly half of the girls living in a non-intact household by age 6). This, compounded by exposures to other stressors these communities often face (e.g., systemic racism), may partially explain the racial/ethnic differences in timing of puberty. Further, a previous study reported that socioeconomic status indicators such as mother’s marital status and lower family income accounted for up to 50% of the increased risk of earlier menarche found in Black and Latinx girls [26]. Other individual-level factors such as socioeconomic status, perceived stress, or adverse childhood events may further explain the differences [27].
Lastly, emerging research demonstrates that social and built environments are strong predictors of health outcomes independent of individual-level factors [27,28,29,30,31,32]. Living on a single income in the San Francisco Bay Area, a region with notoriously high cost of living, may pressure single parents to live in less optimal neighborhoods than intact families that are likely to have higher household incomes. Further, neighborhood characteristics may partially explain race/ethnic differences in pubertal timing [33]. We controlled for neighborhood-level household income at birth but did not consider changes in address, and therefore changes in neighborhood quality that could have occurred during the girl’s childhood, especially following family dissolution. Additionally, our measure of neighborhood-level household income was based on 2010 Census data and thus represents a single point in time. It may not accurately reflect changes in neighborhoods resulting from housing development, gentrification, and other factors that may be independent sources of stress. Future studies that include these multi-level factors and their changes over time will shed light on the contexts in which household intactness is associated with pubertal timing, and how these factors may influence associations by race/ethnicity. Such knowledge will help elucidate the complex interplay of race/ethnicity, socioeconomic status, neighborhood, stress and child development. This will in turn help the design of upstream interventions to slow the hastening of onset of pubertal development and race/ethnic health disparities due to earlier pubertal timing in minority populations.
This study has several limitations. Lack of detailed information on family structure prevented us from distinguishing single mother vs. single father households, presence of same-sex parenting, presence of other adult caregivers in the home, number and ages of siblings or other household members, and other circumstances pertaining to child guardianship including foster care status. Having a more robust understanding of a child’s living arrangements would permit us to explore in more detail the nuances of family structure and parent involvement on pubertal maturation. Second, because this study was based on EHR data, we did not have information on other potential confounders such as mother’s age at menarche, individual-level household income, perceived stress, food and nutrition intake, and physical activity. Last, we used EHR-based Tanner Stages assessed primarily by pediatricians. Although these data are far better than parent- or child-reported Tanner Stages, they may not be as precise as assessments by trained endocrinologists. However, these limitations of the study are outweighed by numerous strengths. Because of the availability of the EHR data, we were able to conduct one of the largest prospective cohort studies with availability of objective measures of clinical outcomes (e.g., Tanner Stages, BMI), and other relevant confounder variables, providing an unparalleled opportunity to rigorously and efficiently examine the association of intact household status on onset of puberty. Other notable strengths of the study include a diverse cohort with substantial representation of race/ethnic groups, lack of which has been a major limitation in previous studies.
