As an overarching goal of my career, I seek to integrate evolutionary biology and developmental psychology—to create a new field of study, which David Bjorklund and I have called evolutionary developmental psychology (Ellis & Bjorklund, 2005; Bjorklund, Ellis, & Rosenberg, 2007). Along these lines, my research focuses on generating and testing evolutionary models of developmental experience. At one level, this focus involves theory development: advancing new models of how evolution has shaped the child’s brain to respond to specific features of family environments and the larger ecological context. This theoretical work has twice been recognized by the George A. Miller Award from the American Psychological Association. At another level, my work focuses on theory testing: examining the impact of fathers, family relationships, and socioecological conditions on children’s biological stress responses, timing of pubertal development, and first sexual experience and pregnancy. Although my research has shown replicable effects of families and ecological stress on these developmental outcomes, the size of these effects differ across individuals. That is, some children are more impacted by their rearing experiences than are others. Another focus of my research, therefore, is investigating differences between children in their neurobiological susceptibility to environmental influence.
Life History Theory and Sexual Development
Much of my theoretical and empirical work examines links between childhood experience and pubertal development. This work stands on the shoulders of a landmark theory, first presented in 1991 by Jay Belsky and colleagues (Belsky, Steinberg, & Draper, 1991), linking childhood experience, interpersonal orientation, and reproductive strategy. This theory posited that levels of stress and support in extra-familial environments influence family dynamics (marital relationships, parent-child relationships), thereby shaping children’s early emotional and behavioral development and, through it, subsequent sexual development and behavior in adolescence and beyond. Moreover, the theory asserted that this environmentally sensitive developmental system evolved as a means of matching individuals to their environments, and that this matching process functions to promote survival and reproductive success across varying ecological contexts. I have taken the lead role in a series of prospective, longitudinal investigations that have tested core propositions derived from this theory, particularly regarding relations between family environments and pubertal timing (Ellis et al., 1999, 2003; Ellis & Garber, 2000; Ellis & Essex, 2007; Tither & Ellis, 2008; Ellis, Shirtcliff et al., 2011).
Based on my theoretical and empirical work, my colleagues and I have advanced a series of revisions and extensions of Belsky’s original theory, including:
- A reanalysis of family environments to distinguish between harsh-conflictual and warm-supportive family dynamics and their relative effects on pubertal maturation (Ellis et al., 1999; here we found that girls who experienced more warm and supportive parenting in the pre-school years had later pubertal development).
- Development of a complementary theory of paternal investment that emphasizes the unique effects of fathers and other adult males in regulation of daughters’ sexual development (Ellis et al., 1999, 2003; Ellis & Garber, 2000; Ellis, 2004; Tither & Ellis, 2008; Deardorff, Ellis et al., 2010; Ellis, Schlomer et al., in press; this research has shown that girls who experience more biological father presence and involvement experience later puberty and engage in less risky sexual behavior, but that exposure to stepfathers has the opposite effect).
- Integration of the original model with sexual selection theory, leading to new hypotheses about sexually differentiated pathways and the role of self-perceived mate value in regulating sexual development and behavior (Jackson & Ellis, 2009; Jackson, Ellis, Schlomer, & Garber, submitted; here we found the female pubertal development was especially attuned to the quality of family relationships, and that male pubertal maturation exerted an indirect effect on sexual behavior through self-perceived mate value).
- Development of an alternative theory of the function of pubertal timing as a mechanism for calibrating the length of childhood to match the quality of family environments (Ellis, 2004; Ellis & Essex, 2007).
- Reconceptualization of childhood stress as constituting two fundamental dimensions of variation—harshness and unpredictability—that ultimately guide reproductive development (Ellis, Figueredo, et al., 2009; Brumbach, Figueredo, & Ellis, 2009; Belsky, Schlomer, & Ellis, in press; this work has shown that exposure to unpredictable family ecologies is linked to precocious sexual behavior).
- Incorporation of the importance of changes in childhood conditions during sensitive age periods as a critical factor in early pubertal development (Tither & Ellis, 2008; this work indicates that early changes in exposure to socially deviant fathers may provoke early puberty).
- Development of a mediational model linking socioeconomic status, psychosocial stress in families, fat deposition in middle childhood, and onset of puberty (Deardorff et al., 2010; Ellis & Essex, 2007; this work suggests that the accelerating effects of maternal depression and marital conflict on pubertal development may operate through changes in body mass index in middle childhood).
My current work on childhood experience and sexual development focuses on testing for causation using genetically informative designs. Although evolutionary theories of developmental experience posit that family environments have a causal influence on pubertal timing, alternative behavior genetic models suggest that this “influence” is spurious—a non-causal artifact of high genetic loading for traits associated with early pubertal development in dysfunctional families. To distinguish between these competing explanations, I have developed a genetically- and environmentally-controlled sibling-comparison methodology. Central to this design are comparisons between full biological sisters, discrepant in age, who experienced the dissolution of their biological parents’ union while growing up, and then lived primarily with their mother following the dissolution. If such siblings are 7 years apart in age, for example, then the childhood environment of the older sibling is characterized by 7 more years of residence in a biologically intact, father-present family, whereas the childhood environment of the younger sibling is characterized by 7 more years of residence in a biologically disrupted family without the birth father in the home.
My ongoing research, begun in New Zealand and continuing in the US, is examining the effects of these differences between sisters in exposure to family disruption/father absence (a non-shared environmental factor) on sexual development. In the New Zealand study (Tither & Ellis, 2008), this differential exposure had substantial effects on age at menarche, and in the US this differential exposure influenced risky sexual behavior in daughters (Ellis, Schlomer et al., in press). For example, we found that in divorced families in which the father had a history of socially deviant behavior, the younger sisters went through puberty almost a year earlier than their older sisters. They also went through puberty about a year earlier than other younger sisters who were not exposed to problematic fathers. Thus, girls with high levels of exposure to stress early in life (socially deviant fathers), who then had that stressor removed (divorce and exit of the father from the home), tended to go through quite early puberty.
Biological Sensitivity to Context
In recent years, researchers have made significant progress in understanding how environmental exposures interact with genotypes and phenotypes to differentially shape human development. It has become increasingly clear that individuals with different characteristics vary not only in whether and how much they are negatively affected (in terms of conventionally defined mental health outcomes) by environmental stressors and adversity, but also in the extent to which they are positively influenced by environmental resources and supports (Belsky, 2005; Boyce & Ellis, 2005; Ellis, Boyce et al., 2011). Most notable, however, is the recurrent finding that the very characteristics of individuals that make them disproportionately vulnerable to adversity sometimes also make them disproportionately likely to benefit from contextual support. That is, certain characteristics underlie sensitivity to environmental influence, for better and for worse. My collaborative work with W. Thomas Boyce suggests that one such characteristic is biological reactivity of the stress response systems to environmental and psychological challenge, which we have called biological sensitivity to context (Boyce & Ellis, 2005; Ellis & Boyce, 2008).
Biologically sensitive children are more affected by variations in parental investment, by good or bad school environments and teachers, and by various social programs and interventions. Our recent work indicates that the effects of parental supportiveness on pubertal development in early adolescence depends on biological sensitivity to context, with the combination of high parental supportiveness and high stress reactivity predicting the slowest pubertal maturation in early adolescence (Ellis, Shirtcliff et al., 2011). We expect, and are seeking to test the hypothesis, that many effects of childhood experiences on life history strategies (e.g., timing of puberty, age at first birth, number of offspring, quality of parental investment) will depend on biological sensitivity to context.
We have also proposed a conditional adaptation model of individual differences in development of biological sensitivity to context. Specifically, we hypothesized a curvilinear, U-shaped relation between early exposures to adversity and the development of biological sensitivity to context in children, with high context-sensitivity emerging in both highly stressful and highly protected early family environments (Boyce & Ellis, 2005; see also Ellis, Jackson, & Boyce, 2006). The curvilinearity hypothesis received provisional support in two studies of early development and psychopathology (Ellis, Essex, & Boyce, 2005).
We have recently revised the developmental theory of biological sensitivity to context and renamed this part of the theory the Adaptive Calibration Model (ACM; Del Giudice, Ellis, & Shirtcliff, 2010). The ACM is an evolutionary-developmental theory of individual differences in the functioning of the stress response system and associated behavioral strategies. According to the ACM, The stress response system has three main biological functions: (1) to coordinate the organism’s allostatic response to physical and psychosocial challenges; (2) to encode and filter information about the organism’s social and physical environment, mediating the organism’s openness to environmental inputs; and (3) to regulate the organism’s physiology and behavior in a broad range of fitness-relevant areas including defensive behaviors, competitive risk-taking, learning, attachment, affiliation and reproductive functioning. The information encoded by the system during development feeds back on the long-term calibration of the system itself, resulting in adaptive patterns of responsivity and individual differences in behavior. Several ongoing investigations should enable me and my collaborators to thoroughly examine relations between rearing experiences and calibration of the stress response systems.
In sum, my theoretical and empirical work attempts to connect three broad constructs: family environments, stress physiology, and sexual development. Guided by evolutionary theory, the fundamental goal of this work is to characterize major dimensions of stress experienced by children, and how different levels and types of family stress (e.g., absence of warmth vs. presence of conflict, chronically harsh vs. unpredictable home environments, early vs. middle childhood exposures) affect stress response systems and pubertal and sexual development.