The onset of puberty is pivotal for human growth and development [1
]. However, among developed nations, there has been a secular trend of early pubertal timing over the past century, and in recent years, also in developing countries [2
]. Early pubertal timing has been recognized as a risk factor for adverse health outcomes in adulthood including obesity, hyperinsulinemia, type-2 diabetes, hypertension, coronary heart disease, depression and early mortality [4
]. Multiple inter-related social and environmental factors have been found to significantly influence pubertal timing, including nutrition and obesity, genetic factors, and general health status, race, and familial socioeconomic status (SES) [9
Adverse childhood experiences (ACEs), defined as experiences that threaten the child’s bodily, familial, or social safety or security, classically include maltreatment and household dysfunction to more targeted experiences of bullying, exposure to crime, victimization, and economic disadvantage [10
]. For the purposes of this meta-analysis, ACEs were defined as exposure to at least one significant form of the following childhood adversities: before the age of 18 years: physical abuse, sexual abuse, neglect (failure to provide and failure to supervise physically or emotionally), family dysfunction (parental death or serious illness, parental separation or divorce, parental incarceration, parental substance abuse, domestic violence, mental illness), low SES, and father absence (separation or divorce of the birth parents followed by absence of the birth father from the home).
ACEs are a major public health problem, with some estimates suggesting that about a third of the general population may be affected [11
]. A growing number of studies have examined ACEs as risk factors for early pubertal timing, however, the association has been a topic of enduring controversy [3
]. For example, Romans et al. [16
] have found associations between father absence and early puberty whereas similar results were not observed by Henrichs et al. [9
The life history theory provides a theoretical framework for explaining the individual differences in reproductive strategies from adolescence to adulthood, especially the role of family and ecological environment in regulating individual differences in puberty development and reproductive strategies. It attempts to explain the timing of reproductive development and events across the life span in terms of evolved strategies for distributing metabolic resources between the competing demands of growth, maintenance, and reproduction [17
]. Specifically, there are environmental conditions in which accelerated maturational development is an adaptive response serving to maximize reproduction opportunities. Based on the life history theory, three middle-level life history models have been advanced to explain why ACEs may increase risk of early pubertal timing. First, the psychosocial acceleration theory, first advanced by Belsky, Steinberg, and Draper, 1991 postulates that ecological stressors in and around the family create conditions that undermine parental functioning and lower the quality of parental investment [18
]. Under these conditions, parental investment is unreliable and/or not closely related to the reproductive success of offspring, girls are predicted to develop in a manner that accelerates pubertal maturation and sexual activity, and orients the individual towards unstable pair-bonds. Second, as a variant of the psychosocial acceleration theory, paternal investment theory parallels this logic but posits a more unique and central role for father and other men in the regulation of female pubertal timing, separate from the effects of other dimensions of psychosocial stress and support in the child’s environment [17
]. The third theory is an extension on the psychosocial acceleration theory and paternal investment theory and is referred to as the child development theory. The child development theory describes how the composition and quality of family environments might influence the length of childhood as a developmental strategy. According to child development theory, the benefits of a longer childhood (delay puberty) are increased in high-quality family contexts that foster the development of sociocompetitive competencies, while the costs of cutting short childhood (accelerate puberty) are reduced in adverse family contexts that do not significantly facilitate these competencies. Children should be selected to take advantage of the benefits of high-quality parental investment and reduce the costs of low-quality parental investment by contingently altering the length of growth and development prior to reproductive maturity [17
Activation of the hypothalamic-pituitary-adrenal (HPA) axis may be an underlying neuroendocrine mechanism linking ACEs and early pubertal timing, which governs both stress response and adrenarche, the first phase of pubertal maturation [20
]. ACEs can alter the response of the HPA axis, with chronic stressful experiences resulting in hyperactivation followed by downregulation of the stress system. The attenuated cortisol profile may actually hasten the pubertal timing because the stress function of the HPA axis is dampened, allowing the cascade of pubertal hormones via the HPG axis to commence [21
]. However, given the different forms of ACEs and the multiple indicators of HPA axis, more longitudinal studies are needed to understand the underlying mechanism better.
Variability in study design, methodology, subject characteristics, type of ACEs, and developmental timing limit the ability to draw definitive conclusions. The objective of this meta-analysis was to clarify the relationship between ACEs and early pubertal timing by means of a systematic examination of the literature, which may be beneficial for guiding future empirical and theoretical work in this area.
To our knowledge, this is the first meta-analysis to examine the association between ACEs and early pubertal timing and has extended previous studies by quantifying the effect size for early pubertal timing. Our finding suggests that sexual abuse, father absence, and growing up with challenging family circumstances were significantly associated with early pubertal timing among girls. Using Cohen’s categorization, the effect for sexual abuse and family dysfunction is small, while father absence is between small to medium. However, similar associations were not observed in other types of ACEs, or across total ACEs.
Herman-Giddens et al. [67
] first reported in 1997 that child sexual abuse increased the risk of girls’ pubic hair and breast development before age 8. Subsequent studies have consistently found that sexual abuse was associated with early pubertal timing [16
]. Recently, a cohort study of the Avon Longitudinal Study of Parents and Children (ALSPAC) mothers showing that total ACEs was not associated with age at menarche, while childhood sexual abuse was associated with lower age at menarche, which is consistent with our findings [54
]. Sexual abuse is often regarded as the most prevalent health problem children face with the most serious array of consequences, while in our study, early pubertal timing may be more affected by father absence instead of sexual abuse.
As early as the 1980s to the 1990s, Draper and Harpending [68
] and Belsky et al. [18
] began to focus on the association between father absence and reproductive behaviors in adulthood, which has received increased attention over recent years. Majority of these studies have indicated a significant association between father absence and early pubertal timing. A study from a large UK birth cohort (ALSPAC) demonstrated that girls from father-absent homes had earlier menarche than girls from father-present homes [46
]. The observed association between father absence and early pubertal timing has also been supported by other articles [20
]. Moreover, the earlier that father absence occurs, the earlier girls tend to experience puberty, there is evidence to suggest that exposure to father absence during the first five years of life is more strongly associated with early menarche than father absence later in childhood [24
It has been previously argued that the effects of age at menarche may be explained by low SES arising as a result of father absence, for example, decrease in family income, major financial problems [69
]. However, in this meta-analysis, we did not find a significant association between low SES and early pubertal timing. When we excluded studies in which pubertal timing measured by Tanner stage or PDS [12
], results suggested that girls living in low SES households may experience delayed onset of menarche (Cohen’s d
: 0.12, 95% CI: 0.003, 0.25). A longitudinal study on 1091 black and 986 white girls from the three sites in the United States found that high SES was a protective factor for the risk of early menarche among white girls but opposite among black girls [14
]. Given the challenges in methodology and definition of SES along with socially heterogeneous of study populations, it is difficult to draw firm conclusions concerning the relationship between low SES and early pubertal timing.
The association between family dysfunction and early pubertal timing was weak, we suspect that family dysfunction may be a proxy variable that represents a range of other family characteristics (including parental divorce, separation, mental illness, and family conflict) and have an effect similar to father absence. However, when we excluded three articles involving parental divorce or separation, the effect size was small but still significant. The effect of total ACEs on adolescent development was not significant. One explanation may be that there are great individual differences in the types, timing, duration, and severity of ACEs. Another explanation is that the association may differ depending on race/ethnicity. As demonstrated in prior research, high SES was a protective factor for the risk of early menarche among white girls but opposite among black girls [14
Overall, despite some inconsistencies across specific forms of ACEs with early pubertal timing, these results support that ACEs exposure may affect female reproductive function. Given the association between ACEs and early pubertal timing, clinicians should sensitively enquire about past childhood experiences, and tailor support accordingly, thus resetting their trajectory for lifelong health and reducing the risk of chronic diseases and conditions.
There are also several limitations. Firstly, most of the measurements relied on retrospective self-report which is subject to recall or reporting biases. Secondly, this sample was restricted to females, and these findings cannot be extrapolated to males. In addition, the analysis revealed substantial statistical heterogeneity, which allows for less confidence in the estimated effect sizes, but is not surprising given the methodological and analytic variances in the identified studies. We cannot rule out the effect of interactions of ACEs with other factors (parental early puberty history, physical activity, etc.) in the current meta-analysis because most studies did not adjust for these interactions, or partly adjusted for these factors as possible moderators. The current meta-analysis focused on specific types of ACEs (sexual abuse, physical abuse, neglect, father absence, low SES, and family dysfunction). Nevertheless, adversity is a heterogeneous concept (including types of ACEs not considered here, such as bullying, exposure to war, and natural disasters, etc.). Although most studies measured ACEs at any point in childhood or adolescence, we were unable to obtain sufficient information about the frequency, timing, and duration of ACEs. Additionally, studies without sufficient statistical information for the computation of effects were not included in our analysis. Nevertheless, the thorough search of literature ensures a full coverage of the existing evidence and makes the results more convincing. Moreover, the large sample of the study population derived from the included studies enhances the possibility of effect detection with reasonable statistical power.
These limitations also suggest some directions for future research. Identification of distinct dimensions, duration and sensitive periods of adverse childhood experience that differentially influence pubertal development are required to uncover mechanisms that explain how childhood adversity is associated with female reproductive strategies.