Socioemotional Mechanisms of Children’s Differential Response to the Effects of Maternal Sensitivity on Child Adjustment

SYNOPSIS

Objective.

Children differ in the extent to which they reap the benefits of maternal sensitive care or suffer the adverse consequences of insensitive care, and these differences can be accounted for by biological characteristics. However, how susceptible children adapt to maternal sensitivity in ways that either maximize positive development or lead to maladjustment has yet to be determined. Here, we propose a novel model of socioemotional mechanisms by which the joint influences of maternal sensitivity and child biological characteristics influence child adjustment.

Design.

We propose a theoretical model, in which children’s vagal functioning and polymorphisms in serotonin transporter (5-HTTLPR) and dopamine receptor D4 (DRD4) genes confer susceptibility to the effects of maternal sensitivity on internalizing, externalizing, prosocial and moral behavior via changes in interpersonal strategies for emotion regulation, the threat response system, and empathy.

Results.

Theoretical and empirical support for the proposed mechanisms are provided.

Conclusions.

The proposed mechanistic model of susceptibility to maternal sensitivity offers a novel framework of for whom and how children are affected by early maternal care, highlighting multiple reciprocal, interacting influences across genes, physiology, behavior, and the environment.

INTRODUCTION

Maternal sensitivity in a child’s early years promotes the child’s acquisition of positive competencies, including prosocial behavior (e.g., Brophy-Herb et al., 2011; Kiang et al., 2004) and moral reasoning (Hinnant et al., 2013), whereas insensitive maternal care can lead to a range of adverse developmental outcomes, including poor relationships, internalizing and externalizing behavior problems, and psychopathology (Crockenberg & Leerkes, 2011; Kok et al., 2013; Leerkes et al., 2012; van der Voort et al., 2014). Despite robust evidence that maternal sensitivity is a salient influence on children’s development, associations between sensitive parenting and children’s socioemotional competence and behavior problems are small to modest in size (McLeod, Weisz, & Wood, 2007; McLeod, Wood, & Weisz, 2007; Verhage et al., 2016; Zeegers et al., 2017). Furthermore, meta-analytic work documents significant variation between and within studies in the effects of maternal sensitivity on subsequent child outcomes, warranting better understanding of child factors that can account for differences in magnitudes of effects of maternal sensitivity on child development (Zeegers et al., 2017).

Differential susceptibility models argue that some children are especially likely to flourish when reared by sensitive caregivers but flounder when reared by insensitive caregivers (Ellis et al., 2011). Differential susceptibility to the effects of a wide range of environments on outcomes across the lifespan can be indexed at phenotypic (e.g., temperament), endophenotypic (e.g., resting autonomic nervous system [ANS] functioning and ANS reactivity), and genetic levels (for reviews, see Belsky & Pluess, 2009; Rabinowitz & Drabick, 2017). Consistent with the differential susceptibility framework, various forms of maternal sensitivity (e.g., warmth, autonomy support, responsive care, physical comforting) have differential effects on prosocial behaviors and moral internalization, depending on children’s genotype (Knafo et al., 2011; Kochanska et al., 2011) or ANS reactivity (Scrimgeour et al., 2016). Relative to studies of positive adaptation, more investigations have demonstrated that the effects of maternal sensitivity on behavior problems, from infancy through adolescence, vary based on children’s genotype or ANS functioning (Bakermans-Kranenburg & van IJzendoorn, 2006; Berry et al., 2013; Davies & Cicchetti, 2014; Hastings & De, 2008; Nikitopoulos et al., 2014; Sulik et al., 2012; Windhorst et al., 2015). Despite ample evidence that children’s biological characteristics account for differences in their responsiveness to maternal sensitivity, little attention has been paid to how child biological characteristics may modify the impact of maternal sensitivity on children’s socioemotional and behavioral development.

Our primary aim is to propose three potential socioemotional mechanisms of biological susceptibility to the effects of early maternal sensitivity on subsequent adjustment. Mechanisms refer to the intervening processes that account (at least in part) for the effects of biological susceptibility to early maternal sensitivity on later child outcomes. In statistical terms, these mechanistic processes can be represented as mediating variables in a mediated moderation model. In a mediated moderation model, the effect of maternal sensitivity (i.e., exposure variable) on the mediator depends on the susceptibility factor (i.e., moderator), and the effect of the mediator on the outcome is constant (Morgan-Lopez & MacKinnon, 2006). In other words, mediators of susceptibility are produced by the joint contributions of maternal sensitivity and child biological susceptibility and directly influence child outcomes. Knowledge of mechanisms of susceptibility can therefore address how children are influenced by maternal sensitivity and for whom maternal sensitivity is most influential.

Notably, our proposed mechanistic model of biologically based differential susceptibility to maternal sensitivity is consistent with a biopsychosocial perspective on developmental psychopathology, which emphasizes multiple interacting factors, from genes to environment, that contribute to normative and nonnormative development (Calkins et al., 2013). Under the principle of multifinality, one of the central tenets of developmental psychopathology, the same risk or protective factors (e.g., insensitive or sensitive maternal care) can lead to different developmental outcomes (Cicchetti & Rogosch, 1996). Identifying why some children suffer maladaptive consequences of insensitive maternal care whereas others are less affected, and why some children show exceptional adjustment with sensitive maternal care, can shed light on the multiple pathways to both adaptive and maladaptive functioning (Rutter & Sroufe, 2000). Although the mechanisms we propose shed light on the different ways in which early maternal care may exert enduring effects on child development, these pathways are malleable and open to influence from later environmental exposures and life experiences.

First, we briefly set the scope of the proposed model, which is limited to maternal sensitivity in the first 5 years of life and to two types of biological susceptibility factors that play a prominent role in susceptibility theory and have received considerable attention in the empirical literature: genetic variability (specifically, sources of variability in the serotonin transporter and dopamine receptor genes) and variability in parasympathetic nervous system functioning (specifically, variability in vagal tone and reactivity). The remainder of the paper offers theoretical rationale and empirical support for three proposed mechanisms of biological susceptibility to maternal sensitivity: interpersonal strategies for emotion regulation, the threat response system, and empathy. Although other mechanisms are theoretically viable, these three are highlighted due to the strength of their theoretical support as well as the availability of empirical support. In areas with limited relevant literature, the review occasionally draws on studies of biological susceptibility to maternal sensitivity after 5 years of age or to a broader range of related caregiving environments. We conclude by discussing the limitations of the proposed theoretical model and directions for future research to advance theory and practice.

SCOPE OF THE REVIEW

Maternal Sensitivity

Specific dimensions of parenting behavior that often fall under the umbrella of maternal sensitivity include contingent responsiveness, the affective quality of mother-child interactions, and behavioral control/autonomy support (Kiff et al., 2011). Maternal sensitivity to children’s negative emotions or distress cues may include soothing, distracting, and modeling and encouraging adaptive problem-oriented responses (Leerkes et al., 2009). Maternal sensitivity to nondistress or positive cues, such as communication bids during play, may include encouraging attention to herself or joint attention to an object, infant-directed speech, expressions of shared delight, affective and behavioral synchrony, and autonomy support (Bornstein & Manian, 2013; Leerkes et al., 2009; Leerkes et al., 2012). In contrast, insensitive maternal behavior can take the form of undercontingent (e.g., unresponsive) or overcontingent (e.g., intrusive) behavior during mother-child interactions (Bornstein & Manian, 2013).

Although maternal sensitivity to her child’s cues is moderately stable across a child’s early years (e.g., Bornstein et al., 2020), the salience of specific caregiving behaviors and their relations to later outcomes may vary depending on the setting, the child’s needs and abilities, and the broader cultural context in which they were observed (Leerkes et al., 2012). For example, in infancy, prompt and appropriate responses to children’s social signals and distress cues may be particularly important indicators of sensitivity, whereas parental control behaviors, such as autonomy support, intrusiveness, and harshness or coerciveness, may be more germane in early childhood (Berry et al., 2013; Kiff et al., 2011; Windhorst et al., 2015). Furthermore, as children’s self-regulation and need for autonomy increases, parenting behaviors are increasingly governed by cultural expectations and social norms for how mothers and children should behave, and the measurement of maternal sensitivity may be more culturally bound (e.g., Leerkes et al., 2012).

Biological Susceptibility Factors

Biological susceptibility reflects children’s capacity to be responsive to their environment, and is related to processes that support engagement with the environment, such as emotional learning, cognition, active exploration, and social behavior. Several genetic polymorphisms have been identified as susceptibility factors, with particularly strong support for polymorphisms in the serotonin transporter promoter (5-HTTLPR) and dopamine receptor D4 (DRD4) genes (Papageorgiou & Ronald, 2013). Serotonin influences emotion regulation, emotional learning, decision making, and social behavior (Crişan et al., 2009). The short allele of the serotonin transporter (5-HTTLPR) gene is associated with less efficient serotonin transport and reduced levels of serotonin (Hariri et al., 2002), whereas the long form is associated with increased serotonin transcriptional efficiency and consequently higher rates of serotonin reuptake (Ficks & Waldman, 2014). Dopamine is involved in attention, motivation, reinforcement learning, social behavior, and approach orientation (Insel, 2003; Panskepp, 1986; Wise, 2004). The 7-repeat of the dopamine receptor D4 gene (DRD4) has been linked to low dopamine reception efficiency (Robbins & Everitt, 1999), although there are inconsistencies in this literature (Pappa et al., 2015).

Several indicators of ANS functioning have been considered within the susceptibility literature; in this review, we focus on vagal functioning, which reflects parasympathetically mediated influences of the vagus nerve on cardiac output (Porges, 2007). According to polyvagal theory and the neurovisceral integration model, higher vagal tone allows for rapid, incremental changes in cardiac output to meet environmental demands, while maintaining homeostasis, which facilitates adaptability to the environment and goal-directed behavior (Beauchaine, 2001; Bornstein & Suess, 2000; Porges, 1996, 2007; Thayer & Lane, 2000). During challenge, withdrawal of the vagal brake is thought to provide cardiac output required for engagement with or disengagement from the social environment, including focusing of attention and contingent changes in affect and behavior (e.g., Porges, 2007; Porges et al., 1996). Vagal tone is often indexed as resting high-frequency heart rate variability (HF-HRV) or resting respiratory sinus arrhythmia (RSA), which is the amount of variation in heart rate in a respiratory cycle during a resting period. Vagal reactivity is typically assessed by measuring changes in mean levels of vagal tone from a resting or baseline condition to a defined challenge. Measures of resting RSA indicate moderate heritability (Snieder et al., 1997) and are stable markers of individual differences in vagal functioning from infancy to childhood (Alkon et al., 2011; Bornstein & Suess, 2000; Weiner & McGrath, 2017), whereas measures of RSA reactivity stabilize by 5 years of age (Quigley & Moore, 2018). Low vagal tone and less vagal withdrawal in response to stressors in infancy and childhood have been associated with subsequent deficits in self-regulation and social, emotional, and behavioral problems in childhood, although null and contradictory associations have also been reported in the literature (Feldman, 2009; Field & Diego, 2008; Graziano & Derefinko, 2013; Porges, 2001; Porges et al., 1996).

PROPOSED MECHANISMS OF THE EFFECTS OF BIOLOGICAL SUSCEPTIBILITY TO MATERNAL SENSITIVITY

The current review offers a theoretical framework that proposes intermediary socioemotional mechanisms that are influenced by biological susceptibility to maternal sensitivity and directly influence child development. The proposed mechanisms speak to observable ways that biologically susceptible children tap into their “preparedness” to be conscious of themselves and their caregiving environment and to respond to maternal sensitivity, which contributes to their socioemotional and behavioral adjustment. We propose mechanistic roles for three broad constructs: interpersonal strategies for emotion regulation, the threat response system, and empathy (see Figure 1). Whereas these mechanisms are likely influential across development, they may be particularly salient during specific developmental stages, either due to the acquisition of capacities that support the underlying mechanism or the availability of measures to assess the construct.

Figure 1.

Proposed Mediated Moderation Model

Interpersonal Strategies For Emotion Regulation

Children who receive supportive and responsive maternal care early in life are thought to develop the expectation that others will be sensitive and responsive to their needs, and these mental schema of relationships (or internal working models; Main et al., 1985) serve as templates for effective interpersonal strategies for affect regulation across the lifespan (Mikulincer & Shaver, 2003). In contrast, children reared by inconsistent, unavailable, or frightening caregivers may adjust their interpersonal strategies in ways that are ultimately ineffective, either because their strategies are too exaggerated (e.g., children who amplify their bids for social support at the expense of close social ties), too dampened (e.g., children who withdraw from the environment rather than seek social support), or incoherent.

In infancy, attachment behavioral strategies with mothers (e.g., appropriate proximity-seeking and contact maintenance following stressful situations and appropriate exploration of the environment during periods of relatively less stress; Sroufe & Waters, 1977) typically reflect the primary avenue for interpersonal emotion regulation. Patterns established in early childhood with primary caregivers are thought to generalize to other close relationships later in life (e.g., with peers or romantic partners; Bartholomew & Shaver, 1998), warranting examination of interpersonal strategies for emotion regulation across different close relationships, such as recruiting social support from peers (Cline et al., 2015). Children who are most equipped to reap the benefits of sensitive maternal care may develop efficient social engagement and support-seeking strategies with their mothers, and later with their peers and romantic partners, which contribute to positive socioemotional adjustment. In contrast, susceptible children exposed to insensitive maternal care may develop strategies that in the long-term impede emotion regulation and contribute to maladjustment.

Evidence of Susceptibility to Interpersonal Strategies for Emotion Regulation.

With respect to work on biological susceptibility to the effects of maternal sensitivity on interpersonal emotion regulation strategies, most research has focused on attachment security, perhaps given surprising findings from meta-analytic work that empirical relations between maternal sensitivity and attachment security/organization are only modest in size (e.g., Bakermans-Kranenburg et al., 2003; De Wolff & van IJzendoorn, 1997; van IJzendoorn et al., 1999; Verhage et al., 2016). Evidence of biological susceptibility to the effects of maternal sensitivity in the first year of life on infants’ attachment security has been found among children from diverse socioeconomic and ethnic backgrounds (for a review, see Golds et al., 2020). Consistent with prior work documenting risk associated with atypical RSA reactivity (e.g., Scrimgeour et al., 2016), infants who exhibited higher RSA during stressful parent-child interactions exhibited higher levels of attachment disorganization, but only if reared by mothers who were rated as negative-intrusive (Holochwost et al., 2014). Notably, these results were specific to attachment disorganization, a construct related to attachment insecurity but distinct in its focus on a lack of a coherent behavioral strategy for achieving attachment goals (Holochwost et al., 2014).

Most of the work on susceptibility to attachment has examined genetic variation as a susceptibility factor. Specifically, among carriers of the shorter alleles of the 5-HTTLPR and DRD4, maternal sensitivity in both stressful and nonstressful contexts has a pronounced impact on children’s attachment security, assessed categorically and continuously in terms of social-interactive behaviors within the attachment system, such as proximity-contact seeking, proximity maintenance, contact resistance, and avoidance (Barry et al., 2008; Leerkes et al., 2017). In a small study (N = 88), Barry et al. (2008) demonstrated that children who carried a short allele of the 5-HTTLPR gene exhibited less attachment security and were less likely to be securely attached at 15 months when exposed to more insensitive maternal care during typical, daily home activities at 7 months. Similarly, 5-HTTLPR short allele carriers were more likely to be classified as disorganized if their mothers showed low responsiveness during free play (Spangler et al., 2009), although these children may not have exhibited the “bright side” of susceptibility, or especially benefitted from high maternal responsiveness. Research with larger samples is needed to extend evidence to support our hypothesis that susceptible children with more sensitive caregivers demonstrate exceptionally robust and efficient maintenance of an attachment-exploration balance in early childhood. Furthermore, Kochanska et al. (2011) demonstrated that 5-HTTLPR short allele carriers are susceptible to the cumulative effects of maternal responsiveness from infancy to early childhood on positive child competencies. Although not directly tested, taken together, these findings suggest that 5-HTTLPR short allele carriers’ susceptibility to the effects of early maternal responsiveness on positive competencies may be accounted for by attachment security.

Whereas the DRD4 7-repeat allele has been identified as a susceptibility factor to the effects of maternal sensitivity on prosocial behavior and behavior problems, children without this allele may be susceptible to the effects of insensitive maternal care on attachment insecurity and disorganization. Leerkes and colleagues (2017) demonstrated that children without the 7-repeat allele who experienced more sensitive maternal care during distress-eliciting tasks had marginally higher attachment security in infancy. Similarly, children without the 7-repeat allele had the lowest rates of attachment disorganization (half the rate of their 7-present counterparts) if their mothers’ communication was non-aversive, but had the highest rates of disorganization (by twofold) if their mothers’ communication was aversive (Gervai et al., 2007). Research on behavior competence and problems has often focused on sensitivity during nondistressing, free play paradigms, whereas research on attachment has focused on sensitivity during distress-eliciting contexts (e.g., Gervai et al., 2007; Leerkes et al., 2017). Discrepancies in the identified susceptibility allele may be related to differences in the context in which sensitivity was observed.

However, null findings with respect to children’s susceptibility to the effects of maternal sensitivity on attachment security and disorganization have been reported, especially among samples from predominantly ethnic minority backgrounds (Golds et al., 2020). One explanation for the discrepancies is that it may be harder to detect susceptibility to the effects of maternal sensitivity without accounting for other environmental influences on attachment quality, such as economic hardship and maternal stress. Measurement invariance in the operationalization of maternal sensitivity across culturally diverse families may also contribute to the mixed pattern of findings. Null findings may also be attributed to assessment of maternal sensitivity over a broader age range (at 6 and 15 months child age), over a shorter duration (15 min), and through the use of global measures of maternal behavior. Furthermore, no studies have assessed children’s susceptibility to the effects of maternal sensitivity on mother-child attachment security and organization after infancy, or to patterns of attachment in other close relationships later in life (e.g., with peers, romantic partners), precluding examination of whether processes within the mother-child relationship have cascading effects across social domains.

Although less studied than attachment security and disorganization, social engagement and social support seeking may also represent interpersonal strategies for emotion regulation that account for children’s differential responsiveness to the effects of maternal sensitivity on subsequent adjustment. Infant girls who carry the 5-HTTLPR short allele display less orienting toward their mothers during a distressing situation, if their mothers also exhibit less sensitive behavior (Zhang et al., 2014). Less effective recruitment of maternal regulatory support may lead these infants to rely predominantly on their rudimentary self-regulatory abilities (e.g., thumb sucking), limiting opportunities to learn more sophisticated interpersonal regulatory strategies. In contrast, Zhang et al. (2014) found no evidence that the effects of maternal sensitivity on boys’ social orienting differed by 5-HTTLPR genotype; however, boys with both short alleles of 5-HTTLPR and 3 repeats of the MAOA-uVNTR polymorphism, which is involved in regulating serotonergic signals, exhibited more social orienting when exposed to higher levels of maternal sensitivity. Future research is needed to evaluate potential sex differences in how, and for whom, maternal sensitivity influences interpersonal emotion regulation strategies. Sex differences may be illuminated by consideration of multiple biological susceptibility factors, including other serotonin-related genes.

As children’s social spheres broaden, social engagement and social support seeking with peers may become an increasingly salient interpersonal emotion regulation strategy. Children may be susceptible to the effects of maternal caregiving on social wariness with peers, which may limit opportunities for social support. Among preschoolers, children who experienced more maternal protectiveness and exhibited lower baseline vagal tone or greater vagal reactivity to a challenge exhibited more social wariness with familiar and unfamiliar peers (Hastings et al., 2008). Other work has failed to demonstrate that support-seeking coping strategies mediate susceptibility to cumulative risk (e.g., harsh parenting, low warmth, traumatic events) on internalizing and externalizing behavior problems in middle childhood (Cline et al., 2015). Given that early close relationships are thought to set the stage for the development of lifelong strategies for interpersonal emotion regulation, examination of parental care after early childhood may account for null findings; alternatively, peer social engagement may be more salient during periods of social transition (e.g., transition to school, adolescence). Future research is needed to evaluate sensitive periods, or unique phases in the life cycle during which time brain and bodily structures and functions are especially susceptible to the presence or absence on specific experiences (Bornstein, 1989), for biological susceptibility to the effects of maternal sensitivity on the proposed mechanisms, which should take into consideration physiological and psychological mechanisms that regulate sensitivity to environmental influences during this period (cf. Bornstein, 1989).

Effects of Interpersonal Emotion Regulation on Adjustment.

Interpersonal emotion regulation is directly related to a wide range of outcomes across the lifespan. During infancy, orienting toward one’s mother is an effective way to self-regulate (Calkins & Dedmon, 2000). Narrative and meta-analytic reviews indicate that attachment security in infancy is modestly associated with internalizing and externalizing behavior problems (NICHD Early Child Care Research Network, 2006). Children with insecure attachment are at heightened risk for psychopathology (Fearon et al., 2010; Madigan et al., 2013), especially externalizing behavior problems (Groh et al., 2014; Groh et al., 2017). Attachment security has been linked to prosociality (e.g., Gross et al., 2015; Kim & Kochanska, 2017; Shaver et al., 2016). Disorganized attachment is a risk factor for behavior problems, especially aggressive and externalizing conditions (e.g., Fearon et al., 2010; Lyons-Ruth et al., 1997; van IJzendoorn et al., 1999) and psychopathology in adolescence (e.g., Carlson, 1998). Disorganized attachment in childhood may be a more powerful predictor of future problems than organized attachment (e.g., van IJzendoorn et al., 1999). As children enter preschool and kindergarten, high levels of wary and reticent behavior with peers predict subsequent social, emotional, and academic problems (Hastings et al., 2008). In general, children’s ability to enlist social support is related to fewer internalizing and externalizing behavior problems, and peer social support may be particularly important in adolescence (Cline et al., 2015).

Threat Response System

Children may adapt to early maternal care in ways that influence the threat response system, which is evident across attentional, cognitive, emotional, and behavioral domains of functioning and encompasses both automatic and effortful aspects of threat responses (e.g., Lazarus & Folkman, 1984; Luecken et al., 2006). The process of responding to threats first involves the detection of threat cues and may also involve effortful cognitive control of one’s attention toward threat cues in the environment. If a threat is detected, resources required to cope with the situation are appraised (primary threat appraisal); this appraisal then influences emotional reactivity to the situation as well as selection and implementation of emotional and cognitive self-regulatory strategies (secondary threat appraisal; Lazarus & Folkman, 1984). Children who received harsh and unpredictable maternal care may tailor their attentional, cognitive, emotional, and behavioral threat-related responses toward defensive responding necessary for survival in such environments (Ellis et al., 2017), but these adaptations may set children on trajectories toward internalizing and/or externalizing problems.

Biases in identifying and processing threat cues, such as angry and fearful faces (Bar-Haim et al., 2007), may initially allow children to selectively process salient signals in their environment and either mobilize behavior or withdraw from threats to preserve a sense of security and safety (Ellis et al., 2011). Earlier in life, attentional biases to threat are normative; meaningful differences in attentional biases to threat and interpretational biases emerge around 7 to 10 years of age, when children typically acquire the cognitive skills (e.g., effortful cognitive control) needed to inhibit these attentional biases and form mental representations of others’ intentions (Field & Lester, 2010). When threat-related attentional biases and cognitive threat appraisals become more stable and are applied to a broader range of interpersonal contexts, they may undermine effective emotion regulation and impede intrapersonal and interpersonal functioning (Field & Lester, 2010; Gibb et al., 2009; Grych & Fincham, 1990; Pollak, 2008; Schlomer et al., 2015).

Other cognitive and behavioral strategies for minimizing exposure to and coping with threatening situations may have specific consequences for the development of internalizing and externalizing behavior problems. Angry reactivity and hostile attribution biases, or the tendency to over-attribute threat, may be accompanied by beliefs that one must be prepared to fight and defend oneself; by middle childhood, these beliefs may lead to aggressive behavior with peers (Werner, 2012) and confer specific risk for externalizing behavior problems in adolescence (Dodge et al., 2015; Mueller et al., 2014; Schlomer et al., 2015). In contrast, acoccchildAAvoidant cognitive coping may facilitate attempts to avoid threatening situations but may impede the use of beneficial coping strategies and can increase risk for the onset or recurrence of anxiety or depressive disorders by adolescence (Aldao et al., 2010; Rood et al., 2009). Children who are most sensitive to cues of threat and safety, as well as to the availability and quality of maternal support to manage potential threats, may also be most likely to adapt their threat responses based on the quality of early maternal care, and these adaptations may confer risk for the development of future behavior problems.

Evidence of Susceptibility to the Threat Response System.

Growing evidence suggests that the effects of the caregiving environment on children’s threat-related cognitive processes differ depending on children’s genotypes. Among a small sample of European American adolescents, 5-HTTLPR short allele homozygotes were more likely to over-identify angry faces, if their mothers had ever experienced a major depressive episode (Jacobs et al., 2011). A cross-sectional study demonstrated that 5-HTTLPR short allele homozygotes who had more cumulative risk indicators (exposure to harsh parenting and parental warmth in middle childhood, and lifetime traumatic events, mainly in the home and neighborhood) reported less frequent use of behavioral avoidance strategies (e.g., distraction coping strategies) and more internalizing and externalizing behavior problems in middle childhood (Cline et al., 2015). Furthermore, results from mediated moderation analyses demonstrated children’s self-reported distraction coping strategies had a small, significant mediated effect of the interaction effect of genotype (s/s 5-HTTLPR) and cumulative stress on caregiver and teacher-reported internalizing problems (specifically, symptoms of generalized anxiety and dysthymia; Cline et al., 2015). However, distraction coping did not mediate children’s susceptibility to the effects of early environmental adversity on externalizing behavior problems. These results suggest differential pathways to internalizing versus externalizing behavior problems, and assessment of multiple outcomes in future studies would allow for examination of differential biological susceptibility to internalizing versus externalizing problems. In addition, given these studies examined correlates of maternal sensitivity, but not maternal sensitivity per se, it is not clear whether 5-HTTLPR short allele homozygotes are differentially responsive to maternal sensitivity.

Evidence suggests 5-HTTLPR long allele homozygotes may be susceptible to the effects of maternal care on threat-related attentional biases. In a small, cross-sectional study of mostly middle-class, European American mother-child dyads, using a modified dot-probe task Gibb et al. (2011) demonstrated 5-HTTLPR accounted for differences in the effects of maternal criticism on school-aged children’s attentional biases (prolonged attention/disengagement) for facial displays of emotion. Adjusting for maternal depression history status, short allele carriers showed attentional biases away from angry faces when exposed to high levels of maternal criticism. Among long allele homozygotes, exposure to maternal criticism was associated with attentional allocation to angry faces (although the statistical significance of this relation was not reported).

Furthermore, evidence suggests that children with the high-expressing 5-HTTLPR genotype are more susceptible to environmental influences on externalizing behavior problems, via behavioral responses to threatening contexts. In a longitudinal study of ethnically diverse, socioeconomically disadvantaged families, Davies and Cicchetti (2014) reported that children who were homozygous for the L_a variant of 5-HTTLPR demonstrated susceptibility to the effects of maternal unresponsiveness at age 2 on angry behavioral reactivity (e.g., dominant posturing, expressions of anger or hostility) to conflict at age 3 and on changes in experimenter-rated externalizing symptoms from ages 3 to 4. Evidence of biological susceptibility to angry reactivity and externalizing symptoms met strict evidentiary criteria. Moreover, consistent with a mediated moderation model of susceptibility, children’s behavioral reactivity was a statistically significant mediator of the interaction effect of 5-HTTLPR genotype and maternal unresponsiveness on changes in externalizing symptoms.

DRD4 7-repeat allele carriers are also susceptible to environmental influences on threat appraisals (Schlomer et al., 2015). Among a mostly European American community sample of adolescents from two-parent families, Schlomer et al. (2015) demonstrated susceptibility to the effects of adolescents’ perceptions of positive interparental relationships on their appraisals of the consequences of interparental conflict, which included appraisals of both indirect (e.g., impending parental divorce) and direct threat (e.g., “afraid they will yell at me too”). Children with the DRD4 7-repeat allele were more affected by perceived interparental positivity than their counterparts without this allele; 7-repeat carriers demonstrated a significant, negative association between perceived interparental positivity and threat appraisals. Moreover, results from Schlomer et al.’s (2015) multiple-group path models suggested that threat appraisals account for children’s susceptibility to the effects of perceived interparental relationship conflict/positivity on internalizing psychopathology. However, Schlomer et al.’s (2015) study did not evaluate externalizing behavior problems, leaving unanswered questions about whether this path is specific to internalizing problems or whether, as suggested in the proposed model, it would predict a range of outcomes.

Threat–related cognitive biases may also mediate adolescents’ cumulative genetic susceptibility, based on being a carrier of both the DRD4 7-repeat and the 5-HTTLPR short alleles, to the effects of social environmental quality on aggression. In a large, five-wave longitudinal study of African American youth, Simons et al. (2011) demonstrated that children who carried at least one copy of the DRD4 7-repeat and of the 5-HTTLPR short alleles were more susceptible to the effects of supportive, non-adverse social conditions (including parenting, peer, school, and neighborhood quality) across childhood and adolescence on “hostile orientation” (characterized by less trait anger, a less hostile view of relationships, and weaker beliefs that one should have a reputation for toughness) in early adulthood. Results from regions of significance analyses were consistent with the “for better and for worse” pattern predicted by susceptibility theories. Moreover, consistent with the proposed mediated moderation model, changes in hostile orientation from early adolescence to early adulthood mediated children’s susceptibility to increases in aggression from 5^th grade (M_age = 10.5 years) to ages 20–21 years.

There is also promising empirical support that vagal functioning confers susceptibility to the effects of maternal sensitivity on attentional, emotional, and behavioral aspects of the threat response system. Recent evidence suggests young children with lower vagal tone are susceptible to the effects of sensitive parenting on executive functioning skills involved in the threat response system (e.g., response inhibition, cognitive flexibility; Gueron-Sela et al., 2017). Whereas inhibitory control may be adaptive in more stable, predictable environments, the ability to shift attention toward threats (which may have tradeoffs with ability to inhibit attention) may be more adaptive in hostile or unpredictable environments (Ellis et al., 2017). Furthermore, executive functioning deficits among children with lower vagal tone may place these children on a pathway toward behavior problems. Among an ethnically and socioeconomically diverse sample, Skibo, Sturge-Apple, and Suor (2020) demonstrated that children with lower vagal tone were more susceptible to the effects of maternal sensitivity on children’s effortful control at 3.5 years of age, which in turn predicted greater maternal report of child anger (but not sadness) regulation at 5 years of age. Effortful control may be particularly relevant to regulation of approach-oriented emotions, such as anger (Skibo et al., 2020). Finally, poor vagal functioning may also confer susceptibility to the effects of early caregiving environments on cognitive and behavioral flexibility later in life. Among a sample of adult women, Hagan and colleagues (2017) demonstrated that vagal reactivity accounted for variability in the effects of childhood emotional abuse (trauma and perceived maternal care during childhood) on avoidant cognitive coping (Hagan et al., 2017). Neither Skibo et al. (2020) or Hagan et al. (2017) evaluated a mediated moderation model, and future work is needed to evaluate whether children’s effortful control and cognitive and behavioral coping strategies account for biologically based differences in the effects of maternal sensitivity on subsequent internalizing and externalizing behavior problems.

Effects of the Threat Response System on Adjustment.

Within the threat response system, there may be general pathways toward maladjustment, as well as specific pathways toward internalizing or externalizing behavior problems. Children who are slower to disengage from threat and children who are more likely to appraise situations as threatening are more likely to exhibit a range of behavioral problems across the lifespan; therefore, threat appraisals and disengagement from threat may be common mechanism for biological susceptibility to either internalizing or externalizing behavior problems. Biases in identifying and processing threatening cues are associated with children’s clinically significant, as well as subclinical, internalizing problems (Jenness et al., 2015; Puliafico & Kendall, 2006), including among low-income ethnic minority groups (Raver et al., 2017). Prospective analyses suggest that threat appraisals are associated with both internalizing and externalizing problems (Mueller et al., 2015). Threat appraisals may precipitate feelings of anxiety, helplessness, or sadness, and over time these internalizing symptoms may develop into externalizing problems (Mueller et al., 2015). When accompanied by feelings of anger, threat appraisals lower inhibition and concern for negative consequences, engender a desire for retaliation and revenge, and facilitate angry behavioral reactivity (Schlomer et al., 2015).

Threat-related information processing biases have been linked with children’s aggressive behavior and psychopathic traits (e.g., Kimonis et al., 2008; Shippell, Vasey et al., 2003). Children with a hostile attribution bias, or the tendency to over-attribute threat, may also believe that one must be prepared to fight and defend oneself; these beliefs may lead to aggressive behavior (Dodge et al., 2015; Mueller et al., 2015; Schlomer et al., 2015). For example, children who frequently make hostile attributions about others’ ambiguous behaviors may impulsively respond in a defensive manner or choose to engage in aggressive behaviors to meet their self-defensive goals (Dodge et al., 2015). A cross-sectional study among primarily middle- to upper-class, European American children found that children’s hostile attributions regarding physical and relational provocations were associated with higher aggression with peers (Werner, 2012). Children’s behavioral reactivity to threatening situations, such as dominant posturing and expressions of anger or hostility, may also be related to children’s externalizing behavior problems (Davies & Cicchetti, 2014).

Empathy

Empathy is the internal capacity to understand others’ intentions, resonate with others’ emotions, and care for others’ well-being (Decety, 2015; Stern & Cassidy, 2018). Empathy requires multiple domains of functioning, including cognitive (e.g., perspective-taking), emotional (e.g., emotion awareness), and behavioral responding. As children develop, they are increasingly able to recruit more sophisticated skills (e.g., cognitive perspective-taking) to express empathy. In infancy, pre-empathic responses include affect mirroring and emotional contagion; by the second year, children are capable of empathic responses, such as helping others in distress (Stern & Cassidy, 2018). As children’s cognitive abilities mature, they also are better equipped to understand others’ emotions and engage in perspective-taking. Finally, by middle childhood, empathic responses are more frequently directed outside of the family, as children’s social sphere expands and becomes increasingly focused on peers (Stern & Cassidy, 2018).

Sensitive mothers direct their children’s attention to the broader social world, promote awareness of opportunities in the environment, and organize children’s thoughts and behaviors in ways that support the development of empathy; susceptible children may be best equipped to reap the benefits of sensitive maternal care on the development of empathy (Ellis et al., 2017). By contrast, when reared by less sensitive mothers, susceptible children may be more likely to meet others’ emotions with unempathic, self-focused, or dysregulated reactions. In turn, children’s empathy shapes the development of moral competence, prosocial behavior, and externalizing behavior problems.

Evidence of Susceptibility to Empathy.

According to theory, both parental sensitive responsiveness and children’s biological predispositions influence empathy (Robinson, 2009). Although no known studies have directly evaluated susceptibility to the effects of maternal sensitivity on children’s empathy, preliminary research suggests children may be susceptible to family environmental influences on multiple components of empathy, across emotional, cognitive, and behavioral domains. As noted earlier, some evidence supports children’s susceptibility to the effects of positive parenting on prosocial behavior (Knafo et al., 2011). Knafo and colleagues (2011) demonstrated that positive maternal parenting practices (warmth, induction, reasoning, and autonomy support) predict mother-reported prosocial behavior, but only among children carrying the dopamine receptor D4 7-repeat allele. Given the close link between empathy and prosocial behavior, this study suggests that biological factors, including dopamine-system genes, may confer susceptibility to environmental influences on children’s empathy. However, prosocial behavior is not a pure measure of empathy and may be influenced by external factors not necessarily related to empathy (e.g., fear of punishment, compliance with authority, desire to be liked or praised, desire for social affiliation).

Children may be susceptible to the effects of maternal depression, which is associated with lower maternal sensitivity (Ashman & Dawson, 2002; Goodman & Gotlib, 1999), and to the effects of childhood maltreatment on cognitive components of empathy. Among an economically and ethnically diverse community sample overselected for risk of conduct problems, Blandon et al. (2008) demonstrated that children’s resting RSA conferred susceptibility to the effects of maternal depressive symptoms on children’s emotional awareness (i.e., understanding of one’s own emotions and empathy) at age 7: The negative relation between maternal depressive symptoms at age 4 and children’s emotional awareness at age 7 was only significant among children with higher RSA at age 4. In addition, there was a three-way interaction between children’s age, children’s resting RSA, and maternal depressive symptoms on change in children’s emotional awareness, such that children with higher RSA appear more strongly influenced by the effects of maternal depressive symptoms on the development of emotional awareness (Blandon et al., 2008). Similarly, Flasbeck et al. (2019) demonstrated that 5-HTTLPR short allele carriers were susceptible to the effects of childhood maltreatment on perspective-taking, a cognitive form of empathy, in adulthood, regardless of diagnostic status and depressive symptoms.

Effects of Empathy on Adjustment.

A large body of evidence demonstrates links between empathy, prosocial behavior, and moral reasoning. Empathy is associated with prosocial behavior, such as greater caring for others in distress, resource sharing, and greater likelihood of helping someone in need or distress (Eisenberg & Miller, 1987; Eisenberg et al., 2010; Eisenberg et al., 2013; Myers et al., 2013; although some studies have demonstrated null associations, e.g., Cowell et al., 2017). Experimental and intervention designs, although less often implemented, have also supported a causal link between empathic responding and children’s prosocial behavior (Eisenberg et al., 2010; Williams et al., 2014). Empathy, especially understanding others’ needs and intentions, is thought to be critical for moral reasoning, especially children’s developing understanding of why it is wrong to harm others (Decety, 2015; Eisenberg et al., 2010; Eisenberg et al., 2013; Eisenberg, 1986; Hinnant et al., 2013; Hoffman, 2000; Miller et al., 1996). Research among children from diverse cultures supports a positive association between children’s empathy-related responding and moral reasoning (for a review, see Malti & Ongley, 2013).

Empathy may also contribute to the development of children’s behavior problems. Empathy is widely theorized to inhibit aggression and antisocial behavior (Eisenberg et al., 2010; Miller & Eisenberg, 1988). Conversely, difficulty feeling empathy, which comprises a core component of callous-unemotional traits, is a substantial risk factor for antisocial and aggressive behavior and conduct disorders (Eisenberg et al., 2013; Malti & Ongley, 2013; Miller & Eisenberg, 1988; Robinson, 2009). Experimental evidence from intervention research supports a causal link between empathy-related responding and children’s aggressive and antisocial behavior (Eisenberg et al., 2010). However, the negative association between empathy and aggression may become stronger with age, and may not be apparent before early childhood (6 years of age), as young children’s assertiveness and lack of social inhibition may relate to both aggressive behavior and the tendency to approach others who express distress (Eisenberg et al., 2010; Eisenberg et al., 2013; Miller & Eisenberg, 1988; Robinson, 2009). In contrast to the robust effects of empathy on moral competence, prosocial behavior, and externalizing behavior problems, there is mixed evidence for a relation between empathy and youth internalizing behavior problems, especially among less well-regulated children who may become overwhelmed by their empathic response (e.g., Gambin & Sharp, 2016).

DEVELOPMENTAL CASCADES

Developmental science has long held an interest in developmental cascades, or the cumulative effects of functioning in one developing system across levels within and across systems, and across time, which shape the course of development (Masten & Cicchetti, 2010). Consistent with a developmental cascades model of change, we view the proposed mechanisms as reciprocally influencing each other across development. During infancy, when children are dependent on their caregivers for survival, interpersonal strategies for emotion regulation are critical to learning and skill development (Calkins, 2015). Through learning mechanisms (e.g., fear and reward learning), mother-child attachment may account for changes in empathy and in the threat response system, setting in motion developmental cascades that place children on trajectories toward adjustment or maladjustment. Children may internalize qualities of secure mother-child attachment, laying the foundation for acquiring competencies later in life, such as empathic responding in other interpersonal relationships and subsequent prosociality (Ainsworth et al., 1974; Masten & Cicchetti, 2010; Robinson, 2009; Shaver et al., 2016). In contrast, children’s dysregulated responses to maternal negative affect may crystallize into broader forms of externalizing problems through coercive parent-child processes that entrain aggressive behavior patterns (Davies & Cicchetti, 2014). In addition to disrupting parent-child dynamics, children’s insecure attachment to caregivers may result in impaired empathy (e.g., misunderstanding emotion cues and intentions of others), which may also precede the formation of hostile attribution biases that are consolidated in middle childhood (Field & Lester, 2010). Threat appraisals, in turn, may activate a social defense system that includes angry emotional responses and negative scripts for coping with interpersonal conflict (Schlomer et al., 2015; Simons et al., 2011).

CAVEATS AND LIMITATIONS

Limitations of the Existing Literature

We offer a novel theoretical model of socioemotional mechanisms that may account for variability in children’s susceptibility to the effects of sensitive maternal caregiving. The model and the literature on which it is based face several notable limitations. Many, although not all, of the studies reviewed relied on small samples (Ns ranging from 62 to 889). In addition, the few studies that reported effect sizes for interaction effects found small effects (except DiLalla et al., 2009; Kochanska et al., 2011). Small sample sizes and small effect sizes both may lower statistical power to detect interaction effects and contribute to inconsistent and null findings. Larger sample sizes may increase power to detect evidence of susceptibility. Including proposed mechanisms in mediated moderation models may also increase power to detect susceptibility to later adjustment via the indirect paths by reducing unexplained variability in the outcome (O’Rourke & MacKinnon, 2015).

Based on the extant literature, it is not clear how well the proposed mechanisms of susceptibility to maternal sensitivity will generalize across diverse samples or to different environmental contexts. Most studies have not addressed the possibility of differences by children’s ethnicity (although Propper et al., 2007, demonstrated a three-way interaction between ethnicity, DRD4, and parenting on externalizing behavior). Ethnic differences in biological susceptibility may occur due to ethnic differences in the meaning of specific parenting behaviors and/or ethnic-specific genetic effects (Bakermans-Kranenburg & van IJzendoorn, 2011; Williams et al., 2003). Although few studies have evaluated sex as a moderator of susceptibility, sex-specific susceptibility factors are possible, as are sex differences in the mechanisms by which susceptibility unfolds (Corwyn & Bradley, 2016; Eisenberg et al., 2012; Ramchandani et al., 2010; Rabinowitz & Drabick, 2017; Silveira et al., 2016; Somers, Jewell, et al., 2018). Susceptibility to maternal sensitivity may be harder to detect amidst contextual stressors such as poverty that exert strong influences on maternal sensitivity and on child development (Conradt et al., 2013). Alternatively, for children reared in resource-poor environments, maternal sensitivity may have a more pronounced impact on development, especially among biologically susceptible children. Inappropriate, or lack of, adjustment for potential confounds (e.g., ethnicity, socioeconomic status) may also influence patterns of findings (Keller, 2014; Tielbeek et al., 2015).

Model Caveats

Consistent with a spectrum of susceptibility across biological systems, as well as Belsky & Pluess’s (2009) conjecture that different susceptibility factors are manifestations of the same underlying predisposition, the proposed model makes an assumption that different susceptibility factors operate through similar mechanisms. However, it is possible that mechanisms of susceptibility to maternal sensitivity function differently depending on the biological indicator of susceptibility. Our ability to test the specificity of mechanisms is limited given that research typically only examines a single susceptibility factor. Alternatively, children’s susceptibility may exist on a spectrum that reflects the cumulative effects of multiple susceptibility factors (e.g., Belsky & Pluess, 2009; Brett et al., 2015; Cicchetti & Rogosch, 2012).

FUTURE DIRECTIONS

Empirically evaluating the proposed mechanisms in a longitudinal mediated moderation model is a logical next step for future research. Few studies have evaluated longitudinal mediated moderation models of children’s susceptibility (for exceptions, see Cline et al., 2015; Davies & Cicchetti, 2014; Simons et al., 2011; Somers, Luecken, et al., 2018). Multilevel mediated moderation models may also be employed to account for susceptibility to the effects of maternal sensitivity on developmental trajectories of behavioral problems or competencies (e.g., Brody et al., 2012). Although some researchers have evaluated mechanisms of susceptibility using multiple-group path models (e.g., Schlomer et al., 2015), these models may be better suited for understanding how susceptibility influences outcomes within a group of susceptible children, rather than understanding joint contributions of child biological and caregiving environmental factors on outcomes via proximal mechanisms, among the larger population.

Accounting for nuances in the caregiving environment would also enhance our understanding of the mechanisms that underlie children’s susceptibility to maternal sensitivity. Some researchers have differentiated between sensitivity to distress or nondistress cues (Leerkes et al., 2009; Leerkes et al., 2012). Sensitivity to children’s nondistress or social cues are central to “serve and return” interactions that facilitate children’s regulatory development (Bernard, Meade, & Dozier, 2013); however, the beneficial effects of these interactions may only be evident if mothers are also contingently responsive to their children’s negative emotions or distress cues (Leerkes et al., 2009). Therefore, a model that only examines maternal sensitivity in one context or averages maternal sensitivity across stressful and play contexts may not capture the unique effects of maternal sensitivity to distress versus nondistress cues on child outcomes. Maternal sensitivity to distress can be further discriminated by the specific negative emotion expressed by the child or elicited by the context (e.g., fear, anger, sadness), which may be differentially related to child outcomes (Hastings & De, 2008; Leerkes, Weaver, & O’Brien, 2009). In addition, maternal caregiving can be influenced by intrapersonal characteristics (e.g., depressive symptoms) as well as characteristics of the family and household environment, such as interparental conflict, availability of maternal social support, and availability of alternative caregivers, to whom children may also be susceptible (e.g., Beach et al., 2014; El-Sheikh, Harger, & Whitson, 2001; El-Sheikh & Whitson, 2006; Somers, Jewell, et al., 2018; Somers, Luecken, et al., 2018; Sturge-Apple et al., 2016). Future research may elucidate whether specific mechanisms of susceptibility depend on the aspects of maternal sensitivity expressed in a specific emotional context, and whether the mechanisms proposed in this model account for susceptibility to broader contexts.

Maternal sensitivity may also influence the development or expression of children’s biological susceptibility. Theoretical accounts suggest that susceptibility is shaped by innate biological characteristics as well as by experience (Del Giudice et al., 2011). Some studies provide evidence that susceptibility changes over time (e.g., Berry et al., 2013; Gueron-Sela et al., 2017), either as part of normative developmental changes or in response to substantial environmental change (Ellis et al., 2011). Maternal sensitivity may influence children’s vagal tone and reactivity (Beauchaine, 2001; Johnson et al., 2017) and gene expression (Hostinar & Gunnar, 2013), and over time biological embedding of caregiving experiences may condition some children to become more or less susceptible to their environment (Del Giudice et al., 2011; Pluess, 2015; Quigley & Moore, 2018). Epigenetic changes (e.g., DNA methylation) may not only be a biological mechanism of gene-environment interplay (Bush & Boyce, 2016; van IJzendoorn et al., 2011), but changes in methylation levels may also represent a marker of plasticity or context-sensitivity across development (Bush & Boyce, 2016; van IJzendoorn et al., 2010; van IJzendoorn et al., 2011). Future work is needed to develop an integrated model of socioemotional and biological mechanisms of differential susceptibility to maternal sensitivity, including changes in biologically based susceptibility.

Although maternal sensitivity is relatively stable in infancy (Spanglar et al., 1994; Leerkes et al., 2009), toddlerhood (Bornstein et al., 2020), early childhood (Johnson et al., 2017), and middle childhood (Buck, 2014), it is not immutable and, over time, may be shaped by child characteristics. Bioecological models of development posit that children are influenced by parenting, and influence parenting behaviors (Kiff et al., 2011; Padilla-Walker et al., 2012). Children’s biologically-based characteristics may influence their capacity or willingness to communicate their needs, as well as the clarity of their distress or social cues, which in turn may influence their parents’ ability to be sensitive. Evocative effects have been documented, such that parents modify their caregiving based on child biological factors including dopamine- and serotonin-related genes and vagal tone (Berry et al., 2013; Elam et al., 2017; Hastings & De, 2008; Kennedy et al., 2004; Plomin et al., 2013).

Longitudinal research is needed that incorporates both transactional and interactive processes between child characteristics and parenting (Kiff, Lengua, & Zalewski, 2011). The joint contributions of early maternal care and children’s biological susceptibility may influence children’s socioemotional adjustment, which in turn may influence later maternal care. Children’s coercive style of interacting with caregivers may lead to greater reactivity to negative events and escalating aggressive behavior over time, both within parent-child interactions and across broader social contexts (Davies & Cicchetti, 2014; Simons et al., 2011), whereas children’s prosocial behavior may lead to improvements in parenting over time (Padilla-Walker et al., 2012). Furthermore, child biological and biologically based temperamental characteristics (e.g., behavioral inhibition, negative emotionality) may not only influence the extent to which parenting influences children, but may also influence the extent to which children influence parents’ behavior and well-being (Boyce & Ellis, 2005; Kiff et al., 2011; Slagt et al., 2016; Somers et al., 2019). For example, DRD4 confers susceptibility to transactional relations between children’s self-regulation and maternal sensitive parenting (Cho et al., 2016). Susceptibility may amplify the strength of transactional processes between child and environmental characteristics, and these transactional processes in turn may represent powerful mechanisms by which susceptibility influences child adjustment.

Research has traditionally adopted a developmental time scale to evaluate transactions between child characteristics and maternal parenting over a span of years, and research that adopts a more micro-time-scale could offer a window into individual differences in potentially causal mechanisms of how maternal sensitivity during parent-child interactions influences children’s socioemotional adjustment. Children’s emotion reactivity to their parents’ positive and negative emotions is distinct from other temperamental markers of susceptibility, such as negative emotionality (Slagt et al., 2018). Work is needed to evaluate whether children’s differential emotion reactivity within the context mother-child interactions acts as a mechanism by which children’s susceptibility to the effects of maternal sensitivity influences development. Over time, the effects of micro-level adjustments during mother-child interactions may accumulate to influence environmentally susceptible children’s developmental trajectories.

IMPLICATIONS FOR THEORY, PRACTICE, AND POLICY

A burgeoning body of evidence offers empirical support that variations in serotonergic, dopaminergic, and autonomic nervous systems confer susceptibility to the effects of early maternal sensitivity on children’s competencies and behavior problems from infancy through mid-adolescence. Our proposed theoretical model suggests that children’s vagal functioning and polymorphisms in serotonin transporter (5-HTTLPR) and dopamine receptor D4 (DRD4) genes confer susceptibility to the effects of maternal sensitivity on interpersonal strategies for emotion regulation, the threat response system, and empathy; in turn, these adjustments place children on trajectories toward adjustment or maladjustment. Knowledge of the mechanisms by which children differentially respond to maternal sensitivity offers promising new directions for the development of biopsychosocial theories of the lasting influence of early maternal caregiving. Integrating a developmental psychopathology perspective with theories of differential susceptibility can offer insight into the multiple reciprocal, interacting influences across genes, physiology, behavior, and the environment that shape whether and how children adapt to reap the benefits of maternal sensitivity or become disproportionately adversely affected by maternal insensitivity. Though trajectories established early in life are pivotal in shaping subsequent adjustment, development is probabilistic, and children continue to be shaped by, as well as elicit, changes in the environment. Furthermore, given this plasticity in children’s development, information on mediation and moderation of the effects of maternal sensitivity may be used to tailor prevention and intervention programs to account for whom specific programs are most likely to be effective and for the processes by which programs influence child adjustment.