Advertisement

Middle Childhood: An Evolutionary-Developmental Synthesis

  • Marco DelGiudice
Open Access
Chapter

Abstract

Middle childhood—conventionally going from about 6–11 years of age—is a crucial yet underappreciated phase of human development. On the surface, middle childhood may appear like a slow-motion interlude between the spectacular transformations of infancy and early childhood and those of adolescence. In reality, this life stage is anything but static: the transition from early to middle childhood heralds a global shift in cognition, motivation, and social behavior, with profound and wide-ranging implications for the development of personality, sex differences, and even psychopathology.

In the last two decades, converging theories and findings from anthropology, primatology, evolutionary psychology, endocrinology, and behavior genetics have revolutionized our understanding of middle childhood. In this chapter, I show how these diverse contributions can be synthesized into an integrated evolutionary-developmental model of middle childhood. I begin by reviewing the main evolved functions of middle childhood and the cognitive, behavioral, and hormonal processes that characterize this life stage. Then, I introduce the idea that the transition to middle childhood works as a switch point in the development of life history strategies and discuss three insights in the nature of middle childhood that arise from an integrated approach.

Middle childhood—conventionally going from about 6–11 years of age—is a crucial yet underappreciated phase of human development. On the surface, middle childhood may appear like a slow-motion interlude between the spectacular transformations of infancy and early childhood and those of adolescence. In reality, this life stage is anything but static: the transition from early to middle childhood heralds a global shift in cognition, motivation, and social behavior, with profound and wide-ranging implications for the development of personality, sex differences, and even psychopathology (Table 1).
Table 1

Development in middle childhood

Body growth

Eruption of permanent molars

Mid-growth spurt, followed by decelerating skeletal growth

Increased muscle mass

Increased adiposity and BMI (adiposity rebound)

Initial development of axillary hair and body odor

Increased sex differences in adiposity (F > M), bone strength, and muscularity (M > F)

Emergence of sex differences in vocal characteristics

Brain growth

Approaching peak of overall brain volume

Peak of gray matter volume

Continuing increase in white matter volume/integrity

Motor and perceptual skills

Increased gross motor skills (e.g., walking)

Increased fine motor skills

Local-global shift in visual processing preferences

Cognitive skills

Increased reasoning and problem-solving skills (e.g., concrete operations)

Increased self-regulation and executive functions (inhibition, attention, planning, etc.)

Increased mentalizing skills (multiple perspectives, conflicting goals)

Increased navigational skills (working memory, ability to understand maps)

Motivation and social behavior

Acquisition of cultural norms (e.g., prosociality)

Complex moral reasoning (conflicting points of view)

Increased pragmatic abilities (gossiping, storytelling, verbal competition, etc.)

Consolidation of status/dominance hierarchies

Changes in aggression levels (individual trajectories)

Development of disgust

Changes in food preferences (e.g., spicy foods)

Onset of sexual/romantic attraction

Increased frequency of sexual play

Increased sense of gender identity

Peak of sex segregation

Peak of sex differences in social play (including play fighting vs. play parenting)

Increased sex differences in physical aggression (M > F)

Emergence of sex differences in attachment styles

Psychopathology

Early peak of psychopathology onset (externalizing, anxiety, phobias, ADHD)

Peak onset of fetishistic attractions

Emergence of sex differences in conduct disorders (M > F)

Social context

Active involvement in caretaking, foraging, domestic tasks, helping

Expectations of responsible behavior

Attribution of individuality and personhood (“getting noticed”)

Behavior genetics

Increased heritability of general intelligence and language skills

New genetic influences on general intelligence, language, aggression, and prosociality

See the main text for supporting references

BMI body mass index, M male, F female, ADHD attention deficit hyperactivity disorder

In the last two decades, converging theories and findings from anthropology, primatology, evolutionary psychology, endocrinology, and behavior genetics have revolutionized our understanding of middle childhood. In this chapter, I show how these diverse contributions can be synthesized into an integrated evolutionary-developmental model of middle childhood. I begin by reviewing the main evolved functions of middle childhood and the cognitive, behavioral, and hormonal processes that characterize this life stage. Then, I introduce the idea that the transition to middle childhood works as a switch point in the development of life history strategies (Del Giudice et al. 2009, 2012; Del Giudice and Belsky 2011) and discuss three insights in the nature of middle childhood that arise from an integrated approach. This chapter was originally published as a short paper in the journal Child Development Perspectives (Del Giudice 2014a). It is reprinted here with updated references and a new section on the model’s implications for health development in a life course perspective (LCHD).

1 What Is Middle Childhood?

Middle childhood is one of the main stages of human development, marked by the eruption of the first permanent molars around age 6 and the onset of androgen secretion by the adrenal glands at about 6–8 years (Bogin 1997). In middle childhood, body growth slows considerably, usually following a small mid-growth spurt. At the same time, muscularity increases and the body starts accumulating fat (the adiposity rebound; Hochberg 2008), while sex differences in body composition become more pronounced (Del Giudice et al. 2009; Wells 2007). Figure 1 places middle childhood in the broader context of human growth from conception to adolescence.
Fig. 1

Developmental trajectories of human growth and sex hormones production, from conception to adolescence. Arrows show the landmark events that characterize middle childhood (Reproduced from Del Giudice 2014a)

In biological terms, middle childhood corresponds to human juvenility —a stage in which the individual is still sexually immature, but no longer dependent on parents for survival. In social mammals and primates, juvenility is a phase of intense learning—often accomplished through play—in which youngsters practice adult behavioral patterns and acquire essential social and foraging skills. Indeed, the duration of juvenility in primates correlates strongly with the size and complexity of social groups, as well as with cortical brain volume (Joffe 1997). Social learningin juvenility can be understood as investment in embodied capital—skills and knowledge that cost time and effort to acquire but increase an individual’s performance and reproductive success (Kaplan et al. 2000).

Human children are no exception to this pattern. Social learning is universally recognized as a key evolved function of middle childhood and is enabled by a global reorganization of cognitive functioning known as the five-to-seven shift (Weisner 1996). By age 6, the brain has almost reached its maximum size and receives a decreasing share of the body’s glucose after the consumption peak of early childhood (Fig. 1; Giedd and Rapoport 2010; Kuzawa et al. 2014). However, brain development proceeds at a sustained pace, with intensive synaptogenesis in cortical areas (gray matter) and rapid maturation of axonal connections (white matter; Lebel et al. 2008). The transition to middle childhood is marked by a simultaneous increase in perceptual abilities (including a transition from local to global visual processing), motor control (including the emergence of adult-like walking), and complex reasoning skills (Bjorklund 2011; Poirel et al. 2011; Weisner 1996). The most dramatic changes probably occur in the domain of self-regulation and executive functions: children become much more capable of inhibiting unwanted behavior, maintaining sustained attention, making and following plans, and so forth (Best et al. 2009; Weisner 1996; see also McClelland et al. 2017). Parallel improvements take place in mentalizing (the ability to understand and represent mental states) and moral reasoning, as children become able to consider multiple perspectives and conflicting goals (Jambon and Smetana 2014; Lagattuta et al. 2009).

In traditional societies, older relatives—especially parents and grandparents—are the main sources of knowledge for juveniles, supplemented by peers and—where available—professional teachers. Storytellin g—both fictional and based in real events—is a powerful technology for transmitting knowledge about foraging and social skills, avoidance of dangers, topography, wayfinding, and social roles and norms (Scalise Sugiyama 2011). Storytelling mimics the format of episodic memories, providing the child with a rich source of indirect experience (Scalise Sugiyama 2011). Intriguingly, episodic memory shows dramatic and sustained improvements across middle childhood (Ghetti and Bunge 2012).

However, children at this age are not just learning and playing. Cross-culturally, middle childhood is the time when children are expected to start helping with domestic tasks—such as caring for younger siblings, collecting food and water, tending animals, and helping adults prepare food (Bogin 1997; Lancy and Grove 2011; Scalise Sugiyama 2011; Weisner 1996). In favorable ecologies, juveniles can contribute substantially to family subsistence (Kramer 2011). Thanks to marked increases in spatial cognition—reflected in the emerging ability to understand maps—and navigational skills, children become able to memorize complex routes and find their way without adult supervision (Bjorklund 2011; Piccardi et al. 2014). The important role of juveniles in collecting and preparing food may explain why the emotion of disgust does not fully develop until middle childhood (Rozin 1990a).

The transition to middle childhood is typically associated with a strong separation in gender roles, even in societies where tasks are not rigidly assigned by sex. Spontaneous sex segregation of boys and girls peaks during these years, as does the frequency of sexually differentiated play (Del Giudice et al. 2009). On a broader social level, cross-cultural evidence shows that juveniles start “getting noticed” by adults—that is, they begin to be viewed fully as people with their own individuality, personality, and social responsibility (Lancy and Grove 2011).

In summary, the life stage of juvenility/middle childhood has two major interlocking functions: social learning and social integration in a system of roles, norms, activities, and shared knowledge. While children are still receiving sustained investment from parents and other relatives—in the form of food, protection, knowledge, and so forth—they also start to actively contribute to their family economy. By providing resources and sharing the burden of child care, juveniles can boost their parents’ reproductive potential. The dual nature of juveniles as both receivers and providers explains many psychological features of middle childhood and has likely played a major role in the evolution of human life history (Kramer 2011).

1.1 Adrenarche

The transition to middle childhood is coordinated by a remarkable endocrinological event: the awakening of the adrenal glands, or adrenarche (Auchus and Rainey 2004; Hochberg 2008). Starting at about 6–8 years—with much individual variation and only minor differences between males and females—adrenal glands begin to secrete increasing amounts of androgens (see Fig. 1), mainly dehydroepiandrosterone (DHEA) and its sulfate (DHEAS). Adrenal androgens have only minor effects on physical development, but they have powerful effects on brain functioning. DHEA and DHEAS promote neurogenesis and modulate gamma-aminobutyric acid (GABA) and glutamate receptors; moreover, DHEA can act directly on androgen and estrogen receptors. Even more important, adrenal androgens can be converted to estrogen or testosterone in the brain (Campbell 2006; Del Giudice et al. 2009). As sex hormones , adrenal androgens play a twofold role: They activate sexually differentiated brain pathways that had been previously organized by the hormonal surges of prenatal development and infancy (Fig. 1), and they further organize brain development along sexually differentiated trajectories (Del Giudice et al. 2009).

Adrenal androgens likely provide a major impulse for many of the psychological changes of middle childhood (Campbell 2006, 2011; Del Giudice et al. 2009), including the emergence and intensification of sex differences across domains (see Table 1). Since the age of adrenarche correlates strongly with that of gonadarche (the awakening of the testes/ovaries that marks the beginning of puberty; Hochberg 2008), human development shows a peculiar pattern in which sexually differentiated brain pathways are activated several years before the development of secondary sexual characteristics. This developmental pattern (shared by chimpanzees and, to a lesser extent, gorillas; Bernstein et al. 2012) results in a temporary decoupling between physical and behavioral development, consistent with the idea of middle childhood as a sexually differentiated phase of social learning and experimentation (Geary 2010). Moreover, adrenal androgens promote extended brain plasticity through synaptogenesis and may play an important role in shifting the allocation of the body’s energetic resources away from brain development and toward the accumulation of muscle and fat in preparation for puberty (Campbell 2006, 2011; see also Kuzawa et al. 2014).

2 The Transition to Middle Childhood as a Developmental Switch Point

The evolutionary model of middle childhood sketched in the previous section can be enriched and extended by considering the role of adrenarche as a developmental switch (Del Giudice et al. 2009). The concept of a developmental switch was introduced by West-Eberhard (2003); a switch is a regulatory mechanism that activates at a specific point in development, collects input from the external environment or the state of the organism, and shifts the individual along alternative pathways—ultimately resulting in the development of alternative phenotypes (morphological, physiological, or behavioral traits of an organism). For example, a switch may regulate the development of aggressive behavior so that safe conditions entrain the development of low levels of aggression, whereas threatening environments trigger high levels of aggression. Developmental switches enable adaptive plasticity —the ability of an organism to adjust its phenotype to match the local environment in a way that promotes biological fitness (West-Eberhard 2003). In other words, plastic organisms track the state of the environment—usually through indirect cues—and use this information to develop alternative phenotypes that tend to promote survival or reproduction under different conditions.

Developmental switches work in a modular fashion (see Fig. 2). Activation of a switch leads to the coordinated expression of different genes—both those involved in the regulatory mechanism itself and those involved in the production of the new phenotype. Moreover, alternative phenotypes (A and B in Fig. 2) involve the expression of modular packages of genes specific to each phenotype. Another key aspect of developmental switches is that they integrate variation in the environment with individual differences in the genes that regulate the switch. For example, different individuals may have genetically different thresholds for switching between aggressive and nonaggressive phenotypes. Finally, the embodied effects of past experiences and conditions (e.g., an individual’s previous exposure to stress or nutritional conditions early in life) may also modulate how the switch functions, allowing the organism to integrate information over time and across different life stages (Del Giudice 2014b; Ellis 2013). In many instances, the effects of past experience on developmental switches may be mediated by epigenetic mechanisms (see Meaney 2010).
Fig. 2

The concept of a developmental switch. A regulatory mechanism, which may operate through hormonal signals, integrates current and past information from the environment with the individual’s genotype. As a result, the individual’s developmental trajectory is shifted along alternative pathways—here, A and B—depending on whether a threshold is reached within the mechanism. The location of the threshold, the intensity of the signal, and the timing of the switch point all depend on the joint action of the current state of the environment, the embodied effect of past environmental conditions, and individual variation in the genes involved in the regulatory mechanism. Each alternative pathway involves the modular expression of a set of specific genes, in addition to the shared genes expressed in the new developmental stage. A developmental switch may integrate many sources of input from the environment or produce graded phenotypes rather than discrete alternatives such as A and B

The concept of a developmental switch point resembles that of a sensitive period , in that the organism is maximally responsive to some environmental input. The crucial difference is that, because genetic and environmental inputs converge in the regulatory mechanism, a developmental switch amplifies both environmental and genetic effects on the phenotype (West-Eberhard 2003). Indeed, the activation of a developmental switch exposes many new potential sources of genetic variation, including the genes involved in the regulatory mechanism and in the expression of the new phenotypes (Fig. 2).

2.1 A Switch Point in Life History Development

The role of adrenarche as a developmental switch is not limited to a single trait; in fact, the transition to middle childhood (or juvenile transition; Del Giudice et al. 2009) encompasses all the major domains of behavior—from learning and self-regulation to attachment and sexuality (see Table 1). My colleagues and I (Del Giudice and Belsky 2011; Del Giudice et al. 2009, 2012) have argued that the transition to middle childhood is a switch point in the development of life history strategies , which are coordinate suites of morphological, physiological, and behavioral traits that determine how organisms allocate their resources to key biological activities such as growth, reproduction, mating, and parenting (for a non-technical overview of life history theory, see Del Giudice et al. 2015). At the level of behavior, individual differences in life history strategy are reflected in patterns of self-regulation, aggression, cooperation and prosociality, attachment, sexuality, and so forth (Del Giudice and Belsky 2011; Del Giudice et al. 2009, 2011; Ellis et al. 2009). Although life history strategies are partly heritable, they also show a degree of plasticity in response to the quality of the environment, including the level of danger and unpredictability –embodied in the experience of early stress—and the availability of adequate nutritional resources. In a nutshell, dangerous and unpredictable environments tend to favor fast strategies characterized by early reproduction, sexual promiscuity, unstable relationships, impulsivity, risk taking, aggression, and exploitative tendencies, whereas safe and predictable environments tend to entrain slow strategies characterized by late reproduction, stable relationships, high self-control, aversion to risk, and prosociality. Slow strategies are also favored by nutritional scarcity when danger is low (see Del Giudice et al. 2016; Ellis et al. 2009).

Our argument is that adrenarche coordinates the expression of individual differences in life history strategy by integrating individual genetic variation with information about the child’s social and physical environment collected throughout infancy and early childhood (Belsky et al. 1991). The stress response system plays a major role in gathering and storing information about environmental safety, predictability, and availability of resources; adrenarche contributes by translating that information into adaptive, sexually differentiated patterns of behavior (Del Giudice et al. 2011; Ellis and Del Giudice 2014). Consistent with this view, both early relational stress and early nutrition have been found to modulate the timing of adrenarche (Ellis and Essex 2007; Hochberg 2008). It is no coincidence that the first sexual and romantic attractions typically develop in middle childhood, in tandem with the intensification of sexual play (Bancroft 2003; Herdt and McClintock 2000). By interacting with peers and adults, juveniles receive feedback about the effectiveness of their nascent behavioral strategies. The information collected during middle childhood feeds into the next developmental switch point, that of gonadarche (Ellis 2013); the transition to adolescence offers an opportunity for youth to adjust or revise their initial strategy before attaining sexual and reproductive maturity (Del Giudice and Belsky 2011).

The role of adrenarche as a switch point in life history development adds another level of complexity to the biological profile of juvenility. Figure 3 outlines an integrated evolutionary-developmental model that brings together the various strands of theory and evidence reviewed in this chapter.
Fig. 3

An integrated evolutionary -developmental model of middle childhood. Adrenarche is shown as a switch in the development of life history strategies, as well as a key mechanism underlying the normative changes of middle childhood and the emergence and intensification of sex differences. At a broader level, development in middle childhood serves two complementary functions, social integration and social competition

3 Three Insights in the Nature of Middle Childhood

3.1 Insight 1: Social Integration and Social Competition Are Complementary Functions of Middle Childhood

Evolutionary accounts of middle childhood typically focus on learning, helping, and other forms of social integration. A life history approach emphasizes the need to consider social competition as a crucial, complementary function of human juvenility. In the peer group, children compete for vital social resources—status, reputation, allies, and friends. While learning and play are relatively risk-free, they are not without consequences. The social position achieved in middle childhood is a springboard for adolescence and adulthood; popularity and centrality within the peer network put a child at a considerable advantage, with potentially long-term effects on mating and reproductive success (Del Giudice et al. 2009).

Physical and relational aggression are obvious tactics for gaining influence, but social competition also occurs through prosocial behaviors such as forming alliances, doing favors, and displaying valuable skills. Indeed, managing the balance between prosocial and coercive tactics is an important part of developing social skills (Hawley 2014). More broadly, competition shapes many aspects of cognitive and behavioral development in middle childhood; for example, increased pragmatic abilities allow children to gossip, joke, tease, and engage in verbal duels—all forms of social competition mediated by language (Locke and Bogin 2006). Intensifying social competition also contributes to explain the early peak of psychopathology onset observed in middle childhood, characterized by increasing rates of externalizing disorders (e.g., conduct disorder), anxiety disorders (including social phobia), and attention deficit hyperactivity disorder (ADHD; Del Giudice et al. 2009).

3.2 Insight 2: Sexual Selection Contributes to the Emergence and Intensification of Sex Differences in Middle Childhood

By determining children’s initial place in social networks and hierarchies, competition in middle childhood indirectly affects their ability to attract sexual and romantic partners later. In other words, middle childhood is a likely target for sexual selection —that is, natural selection arising from the processes of choosing mates (mate choice) and competing for mates (mating competition). My colleagues and I (Del Giudice et al. 2009) argued that sexual selection is one reason why sex differences emerge and intensify in middle childhood. In particular, sex differences in physical aggression increase markedly, in tandem with sex differences in muscularity and play fighting. At the same time, attachment styles begin to diverge between males and females, with insecurely attached boys becoming more avoidant and insecure girls becoming more preoccupied/ambivalent (Del Giudice 2009; Del Giudice and Belsky 2010). Different attachment styles are conducive to different social strategies and may be adaptive in regulating children’s nascent relationships with peers. There is initial evidence that attachment styles in middle childhood reflect the effects of prenatal sex hormones, which according to our model are activated by adrenal androgens (Del Giudice and Angeleri 2016). Sexual selection also has indirect implications for the development of psychopathology; for example, marked sex differences in the prevalence of conduct disorders become apparent at the beginning of middle childhood, likely reflecting the stronger role of aggression in boys’ social competition (see Del Giudice et al. 2009; Martel 2013).

3.3 Insight 3: In Middle Childhood, Heightened Sensitivity to the Environment Goes Hand in Hand with the Expression of New Genetic Factors

When an organism goes through a developmental switch point, inputs from the environment combine with the individual’s genotype to determine the resulting phenotype. For example, when adrenal androgens begin to increase during the transition to middle childhood, they activate many hormone-sensitive brain pathways that have been dormant since infancy. In doing so, they release previously hidden genetic variation (Del Giudice et al. 2009). Thus, middle childhood should be characterized by a mixture of heightened sensitivity to the environment—possibly mediated by newly activated epigenetic mechanisms (Meaney 2010) and expression of new genetic factors.

Evidence of increased sensitivity to the environment in middle childhood is not hard to find. Two intriguing and little-known examples concern the development of food preferences and erotic fetishes. In cultures where chili pepper is an essential part of the diet, children tend to dislike spicy food until middle childhood and then increase rapidly their preference for the flavor of chili as a result of social learning (Rozin 1990b). Fetishistic attractions also tend to form in middle childhood, with the onset of pleasurable sensations toward the object of the fetish (e.g., rubber, shoes) that later become fully eroticized (Lawrence 2009). The onset of fetishistic attractions is part of a generalized awakening of sexuality in middle childhood (Table 1) and illustrates the potential for rapid plasticity with long-lasting outcomes. Enhanced sensitivity to the environment extends beyond individual learning to acquiring social norms: for example, cross-cultural differences in prosocial behavior are absent in young children but emerge clearly during middle childhood (House et al. 2013).

On the genetic side of the equation, general intelligence and language skills increase markedly in heritability from early to middle childhood. In both cases, new genetic factors come into play around age 7 (Davis et al. 2009; Hayiou-Thomas et al. 2012). Studies of prosociality and aggression find the same pattern, with new genetic influences on behavior emerging during the transition to middle childhood (Knafo and Plomin 2006; van Beijsterveldt et al. 2003). These genetic findings dovetail with converging evidence that individual changes in levels of aggression are especially frequent during the transition to juvenility (Del Giudice et al. 2009).

4 Implications for Health Development

The main focus of this chapter has been on psychological development, but the implications of the evolutionary-developmental synthesis extend to both mental and physical health. The transition to middle childhood seems to be a switch point for a number of growth and metabolic processes that have long-term impact on health, including the risk for obesity and type 2 diabetes (Hochberg 2008, 2010). These processes become apparent in middle childhood (e.g., anticipated onset of the adiposity rebound, rapid weight gain, onset of insulin resistance), but respond to the accumulated effects of early nutrition and other sources of stress, starting from prenatal life (e.g., intrauterine growth restriction; see Salsberry et al. 2017). From the standpoint of the model presented here, one can predict that metabolic changes in middle childhood will reflect both the “programming” effects of the early environment (Gluckman et al. 2005) and the activation of new genetic factors. Consistent with this view, a recent study has documented significant genetic correlations between puberty timing, insulin levels, type 2 diabetes, and cardiovascular disease (Day et al. 2015). Moreover, some of those factors are likely to be expressed in sexually differentiated ways, and the different patterns of health risk associated with early adrenarche and puberty in boys and girls may be usefully interpreted in light of different constraints on life history trade-offs in the two sexes (see Hochberg 2010). These predictions are consistent with the nonlinear and multilevel nature of developmental processes—one of the guiding principles of LCHD emphasized in this volume.

Another intriguing implication of this perspective is that the juvenile transition may be a promising—and still virtually unexplored—developmental window for intervention. While intervening to change early life conditions may be desirable in view of their long-term effects, this approach is not always possible or realistic. In addition, prenatal factors such as fetal nutrition and gestational stress may be especially difficult to target, as they do not simply mirror the mother’s conditions but reflect a complex—and partially conflictual—interplay between fetal and maternal factors (e.g., Del Giudice 2012; Gangestad et al. 2012; Haig 1993). However, the logic of developmental switches (Fig. 2) suggests that the activation of the mechanisms that initiate the switch (e.g., adrenarche) may correspond to a transient phase of instability and openness in the system. If so, it should be possible to exploit that phase to maximize the efficacy of focused interventions—including pharmacological ones. Of course, this would require a better understanding of how different hormonal and neurobiological systems interact during the transition to middle childhood; the existing evidence points to a central role of the hypothalamic-pituitary-adrenal (HPA) axis, the hypothalamic-pituitary-adrenal-thyroid (HPT) axis, and the insulin/insulin-like growth factor 1 (IGF-1) signaling systems as mediators of life history allocations, not just in humans but in other vertebrates as well (see Del Giudice et al. 2015; Ellis and Del Giudice 2014). Those systems might be used as direct targets for intervention, but also as “endophenotypes” or early indicators of the efficacy of interventions. Importantly, neurobiological systems such as the HPA axis regulate both metabolism and behavior—as components of coordinated life history allocations—so that many of the same processes may be relevant to both physical and mental health. The idea that intervening during a biological transition may afford more leverage to alter developmental trajectories resonates with two key principles of LCHD, that is, the nonlinearity of developmental processes and their time sensitivity.

Probably the most important take-home point of an evolutionary-developmental approach is that researchers should be more cautious in assuming that undesirable developmental outcomes reflect dysregulation of a biological system (e.g., see Kim et al. 2017) and more open to the possibility that those outcomes may be part of adaptive—or formerly adaptive—strategies for survival and reproduction. As I have argued in detail elsewhere (Del Giudice 2014b, c), a life history framework is especially useful in teasing out the logic of potentially adaptive combinations of traits, highlighting critical factors in the environment, and bridging behavioral development with physical growth trajectories. As an example, consider the association between intrauterine growth restriction and early maturation in children (Hochberg 2008, 2010). This can be interpreted as a manifestation of physiological dysregulation due to prenatal adversity or as an adaptive programming effect on children’s metabolic processes and life history trajectories. This alternative interpretation is supported by the association between low birth weight, anticipated puberty, and early childbearing in women (e.g., Nettle et al. 2013). A third possibility is that low birth weight partly reflects reduced energetic and metabolic investment by the mother during pregnancy, which may be adaptive as a component of a fast life history strategy. If so, the association between reduced fetal growth and earlier sexual maturation may not be fully causal, but rather result—at least in part—from shared genetic, or epigenetic, factors that influence life history strategy in both the mother and the offspring. Clearly, the implications for intervention are going to be quite different depending on which of these scenarios apply.

Another recent example is the finding that early adrenarche is associated with reduced white matter volume in the frontal lobe of children (Klauser et al. 2015). Again, the standard interpretation is that early DHEA exposure has a disruptive effect on neurodevelopmental processes; however, it is also possible that different trajectories of brain development—and even associated “symptoms” such as anxiety and aggressive behaviors—may instead reflect alternative strategies on a fast-slow continuum of life history variation. Ellis et al. (2012) present an extended analysis of adolescent risk-taking from this perspective and discuss several implications for the design of interventions. The LCHD principle that evolution both enables and constrains plasticity is especially relevant in this regard; evolutionary scenarios are not just interesting explanatory “stories,” but can illuminate limits as well as opportunities for intervention. For example, when considering mother-fetus interactions, the existence of partial conflicts of interest on nutrition, cortisol production, and so on suggests that interventions designed to favor the fetus may sometimes have detrimental side effects for the mother and vice versa (see Del Giudice 2014b; Haig 1993).

In considering potential adaptive explanations for apparently pathological outcomes, it is important to remember that biologically adaptive traits may carry substantial costs. Fitness is ultimately about reproductive success; natural selection does not necessarily promote psychological well-being or physical health and may sacrifice survival in exchange for enhanced reproduction. Moreover, even adaptive developmental processes may result in genuinely maladaptive outcomes for some individuals (Frankenhuis and Del Giudice 2012). It follows that the existence of substantial psychological, social, or health costs does not automatically qualify a trait or behavior as biologically maladaptive (see Del Giudice 2014b; Ellis et al. 2012; Ellis and Del Giudice 2014).

5 Conclusions

We cannot make sense of human development without understanding middle childhood and its many apparent paradoxes. An evolutionary-developmental approach illuminates the complexity of this life stage and shows how different levels of analysis—from genes to society—can be tied together in a coherent synthesis. This emerging view of middle childhood can help developmental scientists appreciate its centrality in the human life history and stimulate ideas for research and intervention. The study of middle childhood may finally be ready to come of age, opening up promising avenues for a better understanding of health development across the life course.

References

  1. Auchus, R. J., & Rainey, W. E. (2004). Adrenarche–physiology, biochemistry and human disease. Clinical Endocrinology, 60, 288–296.CrossRefGoogle Scholar
  2. Bancroft, J. (Ed.). (2003). Sexual development in childhood. Bloomington: Indiana University Press.Google Scholar
  3. Belsky, J., Steinberg, L., & Draper, P. (1991). Childhood experience, interpersonal development, and reproductive strategy: An evolutionary theory of socialization. Child Development, 62, 647–670.CrossRefGoogle Scholar
  4. Bernstein, R. M., Sterner, K. N., & Wildman, D. E. (2012). Adrenal androgen production in catarrhine primates and the evolution of adrenarche. American Journal of Physical Anthropology, 147, 389–400.CrossRefGoogle Scholar
  5. Best, J. R., Miller, P. H., & Jones, L. L. (2009). Executive functions after age 5: Changes and correlates. Developmental Review, 29, 180–200.CrossRefGoogle Scholar
  6. Bjorklund, D. F. (2011). Children’s thinking: Cognitive development and individual differences (5th ed.). Belmont: Wadsworth.Google Scholar
  7. Bogin, B. (1997). Evolutionary hypotheses for human childhood. Yearbook of Physical Anthropology, 40, 63–89.CrossRefGoogle Scholar
  8. Campbell, B. C. (2006). Adrenarche and the evolution of human life history. American Journal of Human Biology, 18, 569–589.CrossRefGoogle Scholar
  9. Campbell, B. C. (2011). Adrenarche and middle childhood. Human Nature, 22, 327–349.CrossRefGoogle Scholar
  10. Davis, O. S. P., Haworth, C. M. A., & Plomin, R. (2009). Dramatic increase in heritability of cognitive development from early to middle childhood: An 8-year longitudinal study of 8,700 pairs of twins. Psychological Science, 20, 1301–1308.CrossRefGoogle Scholar
  11. Day, F. R., Bulik-Sullivan, B., Hinds, D. A., Finucane, H. K., Murabito, J. M., Tung, J. Y., et al. (2015). Genetic determinants of puberty timing in men and women: Shared genetic aetiology between sexes and with health-related outcomes. Nature Communications, 6, 8842.CrossRefGoogle Scholar
  12. Del Giudice, M. (2009). Sex, attachment, and the development of reproductive strategies. Behavioral and Brain Sciences, 32, 1–21.CrossRefGoogle Scholar
  13. Del Giudice, M. (2012). Fetal programming by maternal stress: Insights from a conflict perspective. Psychoneuroendocrinology, 37, 1614–1629.CrossRefGoogle Scholar
  14. Del Giudice, M. (2014a). Middle childhood: An evolutionary-developmental synthesis. Child Development Perspectives, 8, 193–200.CrossRefGoogle Scholar
  15. Del Giudice, M. (2014b). Early stress and human behavioral development: Emerging evolutionary perspectives. Journal of Developmental Origins of Health and Disease, 5, 270–280.CrossRefGoogle Scholar
  16. Del Giudice, M. (2014c). An evolutionary life history framework for psychopathology. Psychological Inquiry, 25, 261–300.CrossRefGoogle Scholar
  17. Del Giudice, M., & Angeleri, R. (2016). Digit ratio (2D:4D) and attachment styles in middle childhood: Indirect evidence for an organizational effect of sex hormones. Adaptive Human Behavior and Physiology, 2,1–10.Google Scholar
  18. Del Giudice, M., & Belsky, J. (2010). Sex differences in attachment emerge in middle childhood: An evolutionary hypothesis. Child Development Perspectives, 4, 97–105.CrossRefGoogle Scholar
  19. Del Giudice, M., & Belsky, J. (2011). The development of life history strategies: Toward a multi-stage theory. In D. M. Buss & P. H. Hawley (Eds.), The evolution of personality and individual differences, (pp. 154–176). New York: Oxford University Press.Google Scholar
  20. Del Giudice, M., Angeleri, R., & Manera, V. (2009). The juvenile transition: A developmental switch point in human life history. Developmental Review, 29, 1–31.CrossRefGoogle Scholar
  21. Del Giudice, M., Ellis, B. J., & Shirtcliff, E. A. (2011). The adaptive calibration model of stress responsivity. Neuroscience & Biobehavioral Reviews, 35, 1562–1592.CrossRefGoogle Scholar
  22. Del Giudice, M., Angeleri, R., & Manera, V. (2012). Juvenility and the juvenile transition. In R. J. R. Levesque (Ed.), Encyclopedia of adolescence, (pp. 1534–1537). New York: Springer.CrossRefGoogle Scholar
  23. Del Giudice, M., Gangestad, S. W., & Kaplan, H. S. (2015). Life history theory and evolutionary psychology. In D. M. Buss (Ed.), The handbook of evolutionary psychology – Vol 1: Foundations (2nd ed., pp. 88–114). New York: Wiley.Google Scholar
  24. Del Giudice, M., & Angeleri, R. (2016). Digit ratio (2D:4D) and attachment styles in middle childhood: Indirect evidence for an organizational effect of sex hormones. Adaptive Human Behavior and Physiology, 2, 1–10.CrossRefGoogle Scholar
  25. Ellis, B. J. (2013). The hypothalamic-pituitary-gonadal axis: A switch-controlled, condition-sensitive system in the regulation of life history strategies. Hormones and Behavior, 64, 215–225.CrossRefGoogle Scholar
  26. Ellis, B. J., & Del Giudice, M. (2014). Beyond allostatic load: Rethinking the role of stress in regulating human development. Development and Psychopathology, 26, 1–20.CrossRefGoogle Scholar
  27. Ellis, B. J., & Essex, M. J. (2007). Family environments, adrenarche and sexual maturation: A longitudinal test of a life history model. Child Development, 78, 1799–1817.CrossRefGoogle Scholar
  28. Ellis, B. J., Figueredo, A. J., Brumbach, B. H., & Schlomer, G. L. (2009). The impact of harsh versus unpredictable environments on the evolution and development of life history strategies. Human Nature, 20, 204–268.CrossRefGoogle Scholar
  29. Ellis, B. J., Del Giudice, M., Dishion, T. J., Figueredo, A. J., Gray, P., Griskevicius, V., et al. (2012). The evolutionary basis of risky adolescent behavior: Implications for science, policy, and practice. Developmental Psychology, 48, 598–623.CrossRefGoogle Scholar
  30. Frankenhuis, W. E., & Del Giudice, M. (2012). When do adaptive developmental mechanisms yield maladaptive outcomes? Developmental Psychology, 48, 628–642.CrossRefGoogle Scholar
  31. Gangestad, S. W., Caldwell Hooper, A. E., & Eaton, M. A. (2012). On the function of placental corticotropin-releasing hormone: A role in maternal-fetal conflicts over blood glucose concentrations. Biological Reviews, 87, 856–873.CrossRefGoogle Scholar
  32. Geary, D. C. (2010). Male, female: The evolution of human sex differences. Washington, DC: American Psychological Association.CrossRefGoogle Scholar
  33. Ghetti, S., & Bunge, S. A. (2012). Neural changes underlying the development of episodic memory during middle childhood. Developmental Cognitive Neuroscience, 2, 381–395.CrossRefGoogle Scholar
  34. Giedd, J. N., & Rapoport, J. L. (2010). Structural MRI of pediatric brain development: What have we learned and where are we going? Neuron, 67, 728–734.CrossRefGoogle Scholar
  35. Gluckman, P. D., Hanson, M. A., & Spencer, H. G. (2005). Predictive adaptive responses and human evolution. Trends in Ecology & Evolution, 20, 527–533.CrossRefGoogle Scholar
  36. Haig, D. (1993). Genetic conflicts in human pregnancy. QUARTERLY REVIEW OF BIOLOGY, 68, 495–532.CrossRefGoogle Scholar
  37. Hawley, P. H. (2014). Ontogeny and social dominance: A developmental view of human power patterns. Evolutionary Psychology, 12, 318–342.CrossRefGoogle Scholar
  38. Hayiou-Thomas, M. E., Dale, P. S., & Plomin, R. (2012). The etiology of variation in language skills changes with development: A longitudinal twin study of language from 2 to 12 years. Developmental Science, 15, 233–249.CrossRefGoogle Scholar
  39. Herdt, G., & McClintock, M. (2000). The magical age of 10. Archives of Sexual Behavior, 29, 587–606.CrossRefGoogle Scholar
  40. Hochberg, Z. (2008). Juvenility in the context of life history theory. Archives of Disease in Childhood, 93, 534–539.CrossRefGoogle Scholar
  41. Hochberg, Z. (2010). Evo-devo of child growth III: Premature juvenility as an evolutionary trade-off. Hormone Research in Pædiatrics, 73, 430–437.CrossRefGoogle Scholar
  42. House, B. R., Silk, J. B., Henrich, J., Barrett, H. C., Scelza, B. A., Boyette, A. H., et al. (2013). Ontogeny of prosocial behavior across diverse societies. Proceedings of the National Academy of Sciences USA, 110, 14586–14591.CrossRefGoogle Scholar
  43. Jambon, M., & Smetana, J. G. (2014). Moral complexity in middle childhood: Children’s evaluations of necessary harm. Developmental Psychology, 50, 22–33.CrossRefGoogle Scholar
  44. Joffe, T. H. (1997). Social pressures have selected for an extended juvenile period in primates. Journal of Human Evolution, 32, 593–605.CrossRefGoogle Scholar
  45. Kaplan, H., Hill, K., Lancaster, J., & Hurtado, A. M. (2000). A theory of human life history evolution: Diet, intelligence, and longevity. Evolutionary Anthropology, 9, 156–185.CrossRefGoogle Scholar
  46. Kim, P., Evans, G. W., Chen, E., Miller, G., & Seeman, T. (2017). How socioeconomic disadvantages get under the skin and into the brain to influence health development across the lifespan. In N. Halfon, C. B. Forrest, R. M. Lerner, & E. Faustman (Eds.), Handbook of life course health-development science. Cham: Springer.Google Scholar
  47. Klauser, P., Whittle, S., Simmons, J. G., Byrne, M. L., Mundy, L. K., Patton, G. C., et al. (2015). Reduced frontal white matter volume in children with early onset of adrenarche. Psychoneuroendocrinology, 52, 111–118.CrossRefGoogle Scholar
  48. Knafo, A., & Plomin, R. (2006). Prosocial behavior from early to middle childhood: Genetic and environmental influences on stability and change. Developmental Psychology, 42, 771–786.CrossRefGoogle Scholar
  49. Kramer, K. L. (2011). The evolution of human parental care and recruitment of juvenile help. Trends in Ecology and Evolution, 26, 533–540.CrossRefGoogle Scholar
  50. Kuzawa, C. W., Chugani, H. T., Grossman, L. I., Lipovich, L., Muzik, O., Hof, P. R., et al. (2014). Metabolic costs and evolutionary implications of human brain development. Proceedings of the National Academy of Sciences of the United States of America, 111, 13010–13015.CrossRefGoogle Scholar
  51. Lagattuta, K. H., Sayfan, L., & Blattman, A. J. (2009). Forgetting common ground: Six- to seven-year-olds have an overinterpretive theory of mind. Developmental Psychology, 46, 1417–1432.CrossRefGoogle Scholar
  52. Lancy, D. F., & Grove, M. A. (2011). Getting noticed: Middle childhood in cross-cultural perspective. Human Nature, 22, 281–302.CrossRefGoogle Scholar
  53. Lawrence, A. A. (2009). Erotic target location errors: An underappreciated paraphilic dimension. Journal of Sex Research, 46, 194–215.CrossRefGoogle Scholar
  54. Lebel, C., Walker, L., Leemans, A., Phillips, L., & Beaulieu, C. (2008). Microstructural maturation of the human brain from childhood to adulthood. NeuroImage, 40, 1044–1055.CrossRefGoogle Scholar
  55. Locke, J. L., & Bogin, B. (2006). Language and life history: A new perspective on the development and evolution of human language. Behavioral and Brain Sciences, 29, 259–280.PubMedGoogle Scholar
  56. Martel, M. M. (2013). Sexual selection and sex differences in the prevalence of childhood externalizing and adolescent internalizing disorders. Psychological Bulletin, 139, 1221–1259.CrossRefGoogle Scholar
  57. McClelland, M., Morrison, F., Gestsdóttir, S., Cameron, C., Bowers, E. D., Duckworth, A., Little, T., & Grammer. J. (2017). Self-regulation. In N. Halfon, C. B. Forrest, R. M. Lerner, & E. Faustman (Eds.), Handbook of life course health-development science. Cham: Springer.Google Scholar
  58. Meaney, M. J. (2010). Epigenetics and the biological definition of gene x environment interactions. Child Development, 81, 41–79.CrossRefGoogle Scholar
  59. Nettle, D., Dickins, T. E., Coall, D. A., & de Mornay Davies, P. (2013). Patterns of physical and psychological development in future teenage mothers. Evolution, Medicine, and Public Health, 2013, 187–196.CrossRefGoogle Scholar
  60. Piccardi, L., Leonzi, M., D’Amico, S., Marano, A., & Guariglia, C. (2014). Development of navigational working memory: Evidence from 6- to 10-year-old children. British Journal of Developmental Psychology, 32, 205–217.CrossRefGoogle Scholar
  61. Poirel, N., Simon, G., Cassotti, M., Leroux, G., Perchey, G., Lanoë, C., Lubin, A., Turbelin, M. R., Rossi, S., Pineau, A., & Houdé, O. (2011). The shift from local to global visual processing in 6-year-old children is associated with grey matter loss. PloS One, 6, e20879.CrossRefGoogle Scholar
  62. Rozin, P. (1990a). Development in the food domain. Developmental Psychology, 26, 555–562.CrossRefGoogle Scholar
  63. Rozin, P. (1990b). Getting to like the burn of chili pepper: Biological, psychological, and cultural perspectives. In B. G. Green, J. R. Mason, & M. R. Kare (Eds.), Chemical senses – Volume 2: Irritation. New York: Dekker.Google Scholar
  64. Salsberry, P., Tanda, R., Anderson, S. E., & Kamboj, M. K. (2017). Pediatric type 2 diabetes: Prevention and treatment through a life course health development framework. In N. Halfon, C. B. Forrest, R. M. Lerner, & E. Faustman (Eds.), Handbook of life course health-development science. Cham: Springer.Google Scholar
  65. Scalise Sugiyama, M. (2011). The forager oral tradition and the evolution of prolonged juvenility. Frontiers in Psychology, 2, 133.CrossRefGoogle Scholar
  66. van Beijsterveldt, T. C. E. M., Bartels, M., Hudziak, J. J., & Boomsma, D. I. (2003). Causes of stability of aggression from early childhood to adolescence: A longitudinal genetic analysis in Dutch twins. Behavior Genetics, 33, 591–605.CrossRefGoogle Scholar
  67. Weisner, T. S. (1996). The 5–7 transition as an ecocultural project. In A. Sameroff & M. Haith (Eds.), The five to seven year shift: The age of reason and responsibility (pp. 295–326). Chicago: University of Chicago Press.Google Scholar
  68. Wells, J. C. K. (2007). Sexual dimorphism of body composition. Best Practice & Research Clinical Endocrinology & Metabolism, 21, 415–430.CrossRefGoogle Scholar
  69. West-Eberhard, M. J. (2003). Developmental plasticity and evolution. New York: Oxford University Press.Google Scholar

Copyright information

© The Author(s) 2018

This chapter is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license and indicate if changes were made. The images or other third party material in this chapter are included in the work's Creative Commons license, unless indicated otherwise in the credit line; if such material is not included in the work's Creative Commons license and the respective action is not permitted by statutory regulation, users will need to obtain permission from the license holder to duplicate, adapt or reproduce the material.

Authors and Affiliations

  1. 1.Department of PsychologyUniversity of New MexicoAlbuquerqueUSA

Personalised recommendations