Background
Among industrialized nations, and the United States in particular, the average age of menarche has decreased over the past century [
1‐
3]. This trend is of public health concern as early menarche, commonly defined as onset of menses before age 12, is associated with multiple poor health outcomes in adults from increased cardiovascular and metabolic diseases to breast cancer and all-cause mortality [
4‐
6]. Early menarche has also been linked to increased health risk behaviors, earlier sexual debut, and depression [
7‐
9].
Early menarche is likely the result of multiple influences on early endocrine development. Epidemiological studies have found that early menarche is associated with multiple inter-related social and environmental factors, including nutrition and obesity [
10‐
12], genetic factors [
13,
14], and general health status [
15], with differences noted by race/ethnicity and familial socioeconomic status [
16‐
18]. Among social factors with potential influence on early menarche, a growing body of literature points to exposure to childhood adversities as a risk factor for early menarche, including childhood sexual abuse [
9,
19‐
34]. The adverse impacts of biological father absence and the presence of non-related males in the home have also been suggested, though the evidence remains mixed [
26,
35‐
41]. To the best of our knowledge, studies to date have not considered the effects of a broader range of related childhood adversities on menarche. As adversities tend to cluster together, identifying specific adversities associated with early menarche could help identify particular environmental influences on endocrine pathways, should they exist. Elucidating the types of adversities associated with early onset of menarche is critical not only for guiding research on the impact of stressors on neuroendocrine development but also informing the design of targeted interventions for children exposed to specific adversities and potentially mitigating the impact of early pubertal development. This study assesses the joint predictive effects on age of menarche of a broad range of childhood adversities, including absence of biological father in the home and childhood sexual abuse, utilizing a large nationally representative sample from the United States, the National Comorbidity Survey Replication (NCS-R).
Discussion
Childhood adversities predict earlier onset of menarche in this large national sample of women, after statistical adjustment for BMI and race/ethnicity. The prevalence of early menarche is elevated at high levels of co-occurring adversities, specifically in the 5% of the population with more than five adversities. Among respondents reporting between one and four adversities (51% of the sample), the prevalence of early menarche was not significantly higher than those reporting no adversities (44% of the sample).
While risk for early menarche appears to increase with a greater number of childhood adversities, the variable for the count of adversities (Model 1 in Table
3) imposes an assumption that each adversity is associated with an identical increase in the risk for early menarche. The 26% increase found with Model 1 is an average across all the adversities. Figure
1, in contrast, does not make this assumption. This apparent contradiction demonstrates the difficulty in selecting between different models of the association between adversities and early menarche. The findings appear to go against a simple, linear relationship and suggest that a threshold model is a better fit to the overall pattern in the data. That is, risk for early menarche appears to increase above a certain number of adversities.
These analyses were also designed to identify contributions of specific childhood adversities on early menarche (Model 2 in Table
3); findings are consistent with the suggestion in the literature that childhood sexual abuse is associated with earlier onset of menarche. As observational studies have limited ability to distinguish between effects of specific adversities and more generalized effects of childhood environment in the context of highly clustered adversities, this study included a much broader range of childhood adversities than prior studies. Specifically, of the 11 adversities, childhood sexual abuse had the strongest association with early menarche when each adversity was examined in a separate model. In models adjusting for co-occurrence among the five adversities most strongly associated with early menarche, only childhood sexual abuse remained associated with early menarche at a statistically significant level. Absence of biological father during childhood, theorized to affect early menarche due to early triggering of sexual development, was not associated with early menarche in this study.
These results are consistent with prior studies in finding that stressors in childhood may have biological influences on endocrine development resulting in early menarche, a key developmental milestone with important social and biological consequences that extend across adulthood. However, the evidence regarding specific mechanisms is mixed. Theories related to paternal investment, suggested by Draper and Harpending [
55] as well as Belsky [
56], hypothesizing that the absence of the biological father during childhood would trigger early sexual development have received some support. However, in this study, absence of the biological father was not associated with early menarche. The current findings are congruent with those of Ellis [
36,
37], in that the impact of early father absence on early menarche does not exist independent of other moderating factors in the environment. At the same time, the finding that sexual abuse prior to menarche is the strongest predictor of early menarche may implicate a related pathway. Several previous studies have also found that childhood sexual abuse is associated with early menarche [
19,
28,
30,
31,
57,
58], including a recent study showing links between childhood sexual abuse and early menarche in a large sample of African-American women [
29] as well as a study suggesting a dose-response relationship between severity of sexual abuse and early menarche [
34]. None of these studies including the current study, however, has included information on timing of pre-menarchal development of secondary sexual characteristics, which may contribute to increased risk for sexual abuse. Similarly, while beyond the scope of this study, examination of the differential impact of childhood adversities such as absence of biological father at different developmental stages (i.e., early childhood versus early adolescence) would help elucidate the specific pathways for the influence of childhood adversities on pubertal development.
This study has several limitations. Most importantly, we rely on retrospective reporting of both childhood adversities and age of menarche. A large literature examining associations of recalled childhood adversities with health outcomes has proven valuable despite the known limitation of retrospective assessment [
59]. However, it is possible that certain adversities such as sexual abuse will be recalled more readily than others. Previous studies on recalled age of menarche found participant recall to be accurate within one year in 90% of cases between the teenage years and 30 years after the event [
60,
61]. As some of the study participants were in their 50s and 60s, it is possible that there is more recall bias with underreporting of childhood adversities and inaccurate timing of menarche among the older birth cohorts. In addition, data on BMI were available only from the time of interview as an adult, not from the period preceding menarche. This limitation is partially addressed by including participants’ BMI at the time of the interview in final analyses, as adult obesity and childhood obesity are highly correlated [
62,
63]. However, the self-reported adult height and weight to calculate BMI add an additional potential inaccuracy to these data (i.e., BMI is likely to be underestimated). Finally, information on the exact timing was not available for all adversities considered in the analysis, in particular for absence of biological father. It is possible in these cases that the adversity occurred after menarche and was misclassified in this study. Definitions have been constructed in these cases to minimize the possible impact of misclassification. It is unlikely that the remaining misclassification would result in bias in any particular direction.
Interpretation of the findings should also consider the absence of information on maternal age at menarche in this study and in most other studies of this topic. As noted by Moffitt and colleagues [
24], early menarche may lead to early sexual debut and early marriage. Given that early age at marriage is a strong predictor of divorce, children of mothers with early age at marriage may be more likely to grow up in disadvantaged settings, in which they are at risk for a wide variety of childhood adversities. In this scenario, genetic transmission of age at menarche may underlie the observed associations between childhood adversities and early menarche. A study by Wise and colleagues included statistical control for maternal age at marriage, which would adjust in part for this pathway [
29]. In that study, sexual abuse and physical abuse remained significantly associated with early menarche, although with associations of lesser magnitude than identified in this study.
Competing interests
The authors declared that they have no competing interests.
Authors’ contributions
KH conceptualized the study, conducted the literature review, participated in the design and analyses, drafted the initial manuscript, and approved the final manuscript as submitted. HLM participated in review of the analyses, critically reviewed and revised the manuscript, and approved the final manuscript as submitted. EM conceptualized and designed the study, reviewed and revised the manuscript, and approved the final manuscript as submitted. DS assisted in conceptualizing and designing the study, reviewed and revised the manuscript, and approved the final manuscript as submitted. NS participated in the design of the study, carried out the analyses, reviewed and revised the manuscript, and approved the final manuscript as submitted. JAB designed the study, directed the analyses, reviewed and revised the manuscript, and approved the final manuscript as submitted. All authors read and approved the final manuscript.