Life history theory emerged in the biological sciences as an explanatory framework for understanding variation in fitness (i.e. survival and reproduction; Stearns, 1992). At a first level of analysis, life history theory is used to explain and predict species-typical adaptations to past evolutionary pressures (De Vries et al., 2023; Stearns & Rodrigues, 2020). Life history characteristics (e.g., pubertal development, reproductive outcomes), however, are not fixed within a species and a portion of this within-species variation reflects developmentally plastic adaptations (Del Giudice, 2020; Ellis et al., 2009; Frankenhuis et al., 2019; Nettle et al., 2013). As a result, at a second level of analysis, life history theory can be used to predict within-species variation that results from varying ecological conditions and developmental environments (Ellis et al., 2009; Rickard et al., 2014).

Owing to early work by Belsky and colleagues (J. Belsky et al., 1991; Draper & Harpending, 1982; Ellis et al., 1999; Ellis, 2004; Ellis & Del Giudice, 2019; Ellis & Garber, 2000), this latter application of life history theory has been the subject of research for over 30 years. Sometimes referred to as psychosocial acceleration theory (Ellis, 2004), life history informed research on human development has largely focused on associations between early environments (e.g., father absence, economic difficulties, maternal depression, and other early developmental and parenting factors) and reproductive development (J. Belsky et al., 2012; Dinh et al., 2022; Ellis & Garber, 2000; James et al., 2012; Webster et al., 2014). Although some debate remains about whether these associations reflect causal environmental influences or genetic confounding (Barbaro et al., 2017; Ellis et al., 2012; Gaydosh et al., 2018; Mendle et al., 2006; Schlomer & Cho, 2017; Schlomer & Marceau, 2022), research in Western populations suggests that associations between these early environments and life history related outcomes, such as pubertal development (James et al., 2012; Sung et al., 2016; Webster et al., 2014), timing of sexual debut (Hartman et al., 2018; James et al., 2012; Schlomer & Sun, 2022; Zito & De Coster, 2016), and number of sexual partners (J. Belsky et al., 2012; Schlomer & Sun, 2022; Simpson et al., 2012), is reliable, especially among women. There is some inconsistency, however, in whether these associations are more broadly generalizable since research on many non-Western populations and non-human animals have failed to reproduce these patterns (Royauté et al., 2018; Sear et al., 2019; Sohn, 2017).

Despite the relatively reliable associations, possible mechanisms (including genetic confounding) for how early environmental influences affect life history characteristics are unclear. A central tenet of life history theory applied to development is that organisms have evolved to detect and encode information from the early environment and entrain developmental pathways toward different suites of correlated life history characteristics (Del Giudice, 2020; Ellis, 2004; Ellis et al., 2009). Because such conditional adaptations are the hypothesized result of evolutionary selective processes, it follows that there must be one or more biological mechanisms that mediate early environment/life history outcome associations.

Recent research in human development has increasingly pointed to changes in DNA methylation (DNAm) as a possible mechanism that links early environmental experiences with later disease and mortality risk (Fransquet et al., 2019). DNA methylation is the addition of a methyl group to DNA at a cytosine-guanine dinucleotide (CpG) and variability in DNA methylation results in changes to gene expression. Moreover, variability in DNA methylation is also associated with chronological aging. For example, Horvath (2013) found that variation in a set of 353 methylated CpG's predicted chronological age with a relatively small degree of error. The Horvath clock computes “DNAm age” or “epigenetic age”, which reflects not only chronological age, but also the biological age of the sample. While the exact “ticking” mechanism of the Horvath clock is still largely unknown, the ticking rate is fastest within the first year of life and remains at an accelerated pace before leveling off to a linear increase past approximately age 20 (Horvath & Raj, 2018). This ticking pattern suggests epigenetic modifications are crucial for developmental processes, particularly during the first two decades of life.

The Horvath clock, as well as other “first-generation” clocks (e.g., Hannum et al., 2013), have been extensively studied in the literature, including research on physical development. As an index of biological aging, the Horvath clock is an accurate predictor of chronological age and though it performs well in samples of children and adolescence (Binder et al., 2018; Horvath, 2013; Simpkin et al., 2017), the association is not perfect. The difference between predicted epigenetic age and chronological age is known as age acceleration wherein some individuals are biologically older (or younger) than their chronological age. The finding that epigenetic age acceleration is only partially heritable (Horvath, 2013; Marioni et al., 2015) has led to increasing interest in examining possible environmental determinants. For example, human development studies in children that incorporate epigenetic clocks have largely focused on determining if severe forms of early adversity (e.g., abuse, neglect) are related to biological aging (Beijers et al., 2023; Colich et al., 2020). This research has also given rise to so called “second generation clocks” that tend to focus on indicators of health and disease in adulthood rather than aging per se (D. W. Belsky et al., 2020, Belsky et al., 2022; Lu et al., 2019).

Relatively few attempts have been made, however, to test whether epigenetic age acceleration is related to developmental outcomes in childhood or adolescence given much of the research in this field has focused on adult populations. For example, several studies of adults have examined the relation between AAM and epigenetic age (Hamlat et al., 2021; Lu et al., 2018; Maddock et al., 2021). In these studies, however, epigenetic age acceleration was collected after AAM and the hypotheses center on determining if and to what degree variation in AAM is related to later epigenetic aging. Notably, a handful of non-retrospective studies focused on child and adolescent development have been conducted. In a cross-sectional study of children (approximately age 12 years), Suarez et al. (2018) reported a relationship between an accelerated Horvath epigenetic age and higher height- and weight-for-age. This study also found that age acceleration was linked to advanced pubertal development measured by Tanner Stage (Tanner & Whitehouse, 1976) as well as the Pubertal Development Scale (Peterson et al., 1988). Subsequent research using children between the ages of 8 to 16 has similarly shown that Horvath epigenetic age acceleration is related to Tanner Stage development (Sumner et al., 2019) and also the rate at which children progress through the Tanner stages (Sumner et al., 2023). Because variation in AAM is known to be related to epigenetic age acceleration, the causal direction is unclear in these cross-sectional studies.

Improving on the limitations of cross-sectional studies, prospective studies on the relation between epigenetic age acceleration and pubertal development also suggest an association, though results are mixed. First, using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), Simpkin et al. (2017) found no relation between epigenetic age acceleration at age 7 and pubertal timing (measured via peak height velocity), though there was some evidence for an association with pubic hair development among boys. Age at menarche was not assessed in this study. Second, using a sample of N = 94 Chilean girls, Binder et al. (2018) used an averaged epigenetic age acceleration measure collected when children were approximately 10 and 11.5 years and found an approximately 5-month difference in AAM between girls with accelerated epigenetic age and girls with decelerated epigenetic age. More recently, Bolhuis et al. (2022) used life history theorizing to hypothesize that epigenetic age acceleration would mediate the association between parent-child attachment insecurity and AAM. No significant associations were detected, however. The null finding between epigenetic age acceleration and AAM might be attributed the small effect size detected (β = −0.10) in a low-risk sample, the small sample size (N = 85), and/or the dichotomous measure of menarche used (occurred/not occurred). In sum, these studies suggest there may be an association between epigenetic age acceleration and reproductive development, but additional research is needed.

The purpose of the current study was to examine if epigenetic age acceleration measured during middle childhood would prospectively predict life history-hypothesized accelerated reproductive development. Measuring age acceleration during middle childhood may be particularly important given arguments that middle childhood is a critical switch point in the development of life history strategies (see Del Giudice, 2014). More specifically, it was hypothesized that female children with accelerated epigenetic age at chronological age 7 years would exhibit faster life history strategies, characterized by earlier age at menarche, earlier age at first sexual intercourse, and higher sexual partner number. In doing so, a longitudinal path model of possible direct and indirect effects of epigenetic age acceleration on these outcomes was tested (Schlomer & Sun, 2022). Epigenetic age acceleration was indexed using the Horvath clock given that it is one of the most widely studied clocks, numerous loci within the 353 clock CpG's are found in genes related to cellular development, it is validated for use in child and adolescent samples, and reflects a measure of biological aging that, unlike second generation clocks, is not tied to adult health or disease (Horvath, 2013; Horvath & Raj, 2018). To our knowledge this is the only study to prospectively examine the associations between epigenetic age acceleration and down-stream life history outcomes other than AAM and is the only study to do so within a single model. Moreover, this is the only study to investigate the relationship between epigenetic age acceleration and behavioral aspects of reproductive development (i.e., age at first sex, number of sexual partners). The current study improves upon prior research by using a larger sample, prospective prediction, and continuous measures of AAM and other outcomes.