No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
An Evolutionary Perspective on Family Studies: Differential Susceptibility to Environmental Influences
Abstract
An evolutionary perspective of human development provides the basis for the differential-susceptibility hypothesis which stipulates that individuals should differ in their susceptibility to environmental influences, with some being more affected than others by both positive and negative developmental experiences and environmental exposures. This paper reviews evidence consistent with this claim while revealing that temperamental and genetic characteristics play a role in distinguishing more and less susceptible individuals. The differential-susceptibility framework under consideration is contrasted to the traditional diathesis-stress view that "vulnerability" traits predispose some to being disproportionately affected by (only) adverse experiences. We raise several issues stimulated by the literature that need to be clarified in further research. Lastly, we suggest that therapy may differ in its effects depending on an individual's susceptibility.
© 2015 Family Process Institute.
... Since the genetic variant is not a risk or protective factor alone, research shows there is little or no effect on psychopathology in the absence of the environmental risk factors (Rutter, 2006). The diathesis-stress perspective stipulates that underlying predisposition/vulnerability (i.e., due to genetics or biological factors) place some individuals at higher risk than others (Hartman & Belsky, 2016;Zuckerman, 1999). The environment interacts with the diathesis to trigger negative responses to toxic stress. ...
... The environment interacts with the diathesis to trigger negative responses to toxic stress. In contrast, differential susceptibility perspective asserts that individuals more susceptible to adverse life experiences are, simultaneously, most likely to benefit from a supportive environment because they are more developmentally plastic (Hartman & Belsky, 2016;Zuckerman, 1999). This could be a case with more severe stressors such as GBV. ...
... Research on abused children (Cicchetti & Rogosch, 2012) showed that children with the greatest genetic susceptibility had the poorest level of functioning when abused but had the highest level of functioning when not abused. Conversely, less genetically susceptible children showed no effect of abuse on their functioning (Cicchetti & Rogosch, 2012;Hartman & Belsky, 2016). Thus, women victimized by GBV may be most vulnerable to its negative health effects. ...
Gender-based violence (GBV) and trauma can dysregulate and recalibrate environmentally sensitive physiological (i.e. central nervous, endocrine, and immune) systems placing survivors at risk for multiple health problems. The researchers build the case that the effects of GBV are likely to be particularly high impact and contribute to health disparities for marginalized survivors of GBV. Further, the researchers underscore a need for a multi-level bio-socio-ecological model that deciphers, characterizes, and explains individual differences in these effects and the need to establish an evidence base from which to derive interventions that address biological effects of toxic stress among marginalized survivors of GBV.
... Hartman & Belsky, 2015). The current study investigated whether the relation between perceived risk in the childhood family environment and daily suppressive and avoidant coping in adulthood varies as a function of individual differences in two putative indicators of neurobiological sensitivity. ...
... However, relations between early experiences and psychological responses to stress in adulthood have not always been replicated (e.g., Helitzer, Graeber, LaNoue, & Newbill, 2015). Individual differences in neurobiological sensitivity may provide insight into the variability seen in adult responses to stress subsequent to childhood family-related adversity (Hartman & Belsky, 2015). ...
... For example, it has been found that an indicator of genetic sensitivity (indexed by variation in cholinergic genes, which are involved in neural plasticity and learning) predicted the greatest negative affectivity in children exposed to maltreatment and the lowest negative affectivity in non-exposed children (Grazioplene, DeYoung, Rogosch, & Cicchetti, 2013). Although attention to this phenomenon in adulthood has been limited (Hartman & Belsky, 2015), it has been shown that maltreatment in childhood leads to greater negative affectivity among young adults who exhibit either physiological sensitivity to stress (Hagan, Roubinov, Mistler, & Luecken, 2015) or high sensory-processing sensitivity (Aron, Aron, & Davies, 2005). ...
Background and objectives:
Although it has been postulated that psychological responses to stress in adulthood are grounded in childhood experiences in the family environment, evidence has been inconsistent. This study tested whether two putative measures of neurobiological sensitivity (vagal flexibility and attentional capacity) moderated the relation between women's reported exposure to a risky childhood environment and current engagement in suppressive or avoidant coping in response to daily stress.
Design and methods:
Adult women (N = 158) recruited for a study of stress, coping, and aging reported on early adversity (EA) in their childhood family environment and completed a week-long daily diary in which they described their most stressful event of the day and indicated the degree to which they used suppression or avoidance in response to that event. In addition, women completed a visual tracking task during which heart rate variability and attentional capacity were assessed.
Results:
Multilevel mixed modeling analyses revealed that greater EA predicted greater suppression and avoidance only among women with higher attentional capacity. Similarly, greater EA predicted greater use of suppression, but only among women with greater vagal flexibility.
Conclusion:
Childhood adversity may predispose individuals with high neurobiological sensitivity to a lifetime of maladaptive coping.
... Given that many SPS individuals experience sensory bombardment (Aron & Aron, 1997), they are more susceptible to environmental influences, such as different cultural and social contexts. Hence, SPS individuals are more affected than others by negative environmental exposures (Hartman & Belsky, 2016), experiencing higher levels of stress (Aron et al., 2005;Liss et al., 2005). This can strongly affect the sensitivity genotype by increasing its phenotype expression (Pluess, 2015), activating the sympathetic nervous system (Shoenfeld et al., 2008), and eventually magnifying their sensitivity expression. ...
... Nevertheless, exposure to specific environmental stimuli can lead individuals to experience higher levels of sensory bombardment, increasing their level of sensitivity (Aron & Aron, 1997). Hence, negative experiences and environmental exposures to high levels of stress (Aron et al., 2005;Hartman & Belsky, 2016;Liss et al., 2005) might increase the phenotype expression of the sensitivity genotype (Pluess, 2015), and activate the sympathetic nervous system (Shoenfeld et al., 2008). Therefore, although about 1.4 billion people worldwide are highly sensitive, some countries or cultures are better suited for highly sensitive persons than others (Aron, 2013). ...
The medical clown is a healthcare practitioner whose character is strictly associated with the performer's own personality. In this study, the relationships between the level of sensory processing sensitivity (SPS), caregiving strategies and humour in Italian and Israeli clowns were examined. Participants were 159 medical clowns (97 Italian and 62 Israeli), ranging from 22 to 74 years of age, who completed a demographic questionnaire, the self-reported Highly Sensitive Person Scale, the Caregiving System Scale and the BenCor. Results showed that a higher SPS was related to higher hyperactivation and deactivation, and that hyperactivation was related to lower benevolent humour and greater corrective humour. Hyperactivation negatively predicts benevolent humour but positively predicts corrective humour, beyond the effect of SPS. Deactivation had no relationship to either benevolent or corrective humour. The results are also discussed in reference to the two culture groups and to previous studies conducted with general populations.
... Furthermore, a good parent-child relationship is protective against self-motivated alcohol use and attenuates peer-induced drinking behaviour in adolescents (23). Based on the evolutionary perspective of human development, Belsky proposed an operational perspective to study G×E called differential susceptibility to environmental influences, which hypothesizes that individuals differ in their susceptibility to environmental influences, with some being more susceptible to both negative and positive developmental experiences (especially those of rearing environments) and environmental exposures than others (24)(25)(26). Recently, a study based on the differential susceptibility framework assessed the interplay between the negative and positive environmental exposures and their effect on alcohol-related problems among youths, where they observed that adolescents and young adults carrying a susceptible allele of the SNP rs2290045 in the VGLUT2 gene exposed to stressful life events reported more alcohol-related problems if they were also exposed to poor parenting, whereas, in contrast, those exposed to good parenting reported lower alcohol-related problems (27). ...
Introduction
Risk-allele carriers of a Monoamine oxidase A (MAOA) gene, short-allele (MAOA-S) in males and long-allele (MAOA-L) in females, in the presence of a negative environment, are associated with alcohol misuse. Whether MAOA-S/L alleles also present susceptibility to a positive environment to mitigate the risk of alcohol misuse is unknown. Thus, we assessed the association of the three-way interaction of MAOA, maltreatment, and positive parent-child relationship with alcohol consumption among adolescents.
Methods
This prospective study included 1416 adolescents (females: 59.88%) aged 16 ̵ 19 years from Sweden, enrolled in the “Survey of Adolescent Life in Västmanland” in 2012. Adolescents self-reported alcohol consumption, maltreatment by a family (FM) or non-family member (NFM), parent-child relationship, and left saliva for MAOA genotyping.
Results and discussion
We observed sex-dependent results. Females carrying MAOA-L with FM or NFM and a good parent-child relationship reported lower alcohol consumption than those with an average or poor parent-child relationship. In males, the interactions were not significant. Results suggest MAOA-L in females, conventionally regarded as a “risk”, is a “plasticity” allele as it is differentially susceptible to negative and positive environments. Results highlight the importance of a good parent-child relationship in mitigating the risk of alcohol misuse in maltreated individuals carrying genetic risk. However, the interactions were not significant after adjusting to several environmental and behavioural covariates, especially parent’s alcohol use, negative parent-child relationship, and nicotine use (smoking and/or snus), suggesting predictor and outcome intersection. Future studies and frameworks for preventive strategies should consider these covariates together with alcohol consumption. More studies with larger sample sizes are needed to replicate the findings.
... Are gehiago, norbanako batzuk inguruneko alderdi espezifiko batzuen eraginpean ote dauden galdetzeaz gain, funtzionamenduaren eremuen arabera (gaitasun sozial edo akademikoa, funtzio exekutiboa, depresioa, jokabide oldarkorra, etab.) aldagarritasunik ba ote dagoen ere galdetu da [29]. Sentiberatasun diferentzialari buruzko deskribapen askok, inplizituki behintzat, sentikortasun-ezaugarri orokor bat dagoela argudiatzen dute. ...
Giza garapenean eragina dute norberaren testuinguru fisiko eta sozialen alderdiek. Hala ere, gizabanakoak desberdinak dira ingurunearekiko sentsibilitatean eta hari erantzuteko gaitasunean, sentiberagoak direlarik banako batzuk ingurune-baldintza berberen aurrean. Tradizioz, desberdintasun indibidual hauek diatesi-estresaren eredutik aztertu izan dira. Eredu horren arabera, pertsona batzuk, beren zaurgarritasun-ezaugarri endogenoengatik, neurri gabe zaurgarriak dira esperientzia negatiboen edo ondorio kaltegarrien aurrean, zaurgarritasun txikiagoko banakoekin alderatuta. Ikuspegi ebolutiboari jarraituta, badaude beste bi eredu teoriko, sentikortasun diferentzialaren eredua eta testuinguruarekiko sentsibilitate biologikoaren eredua, zeinek dioten gizabanako batzuek, sentikortasunaren ezaugarri indibidualengatik, neurrigabeago jasaten dituztela ingurumen-eragin negatibo zein positiboak. Hortaz, ingurune positiboetatik onura gehiago jasotzen dute, eta, aldi berean, zaurgarriagoak dira ingurune negatiboen aurrean. Azkenik, badago beste teoria berriago bat, sentsibilitate abantailatsuaren eredua, zeinak proposatzen duen gizabanako batzuek, beren sentikortasun-faktoreengatik, sentikorragoak direla ingurumen-abantailekin edo testuinguru positiboekin, eta onura ateratzen dutela horretatik, eta, hortaz, banako hauek abantailadunak direla ahalmen hori ez dutenen aldean.
... Family systems theories offer something that individual-focused illness theories do not: a strength-based framework for family care (McCubbin & McCubbin, 1993;Rolland, 2006Rolland, , 2018Walsh, 2016). A family-systems framework can expand our understanding of health conditions across healthcare settings, and family-focused interventions can improve health-related outcomes (Hartman & Belsky, 2016;Heru, 2000;Martire et al., 2010;Shields et al., 2012). Further, family systems models that apply an ecological and developmental lens expand our understanding of family resilience during the HCT process. ...
Introduction: Hematopoietic stem cell transplantation (HCT) greatly impacts the social, emotional, and physical well-being of the patient and their family. The transplant process imposes significant lifestyle restrictions that result in patient and family isolation, which has been further amplified during the COVID-19 pandemic era. While hospital systems recognize the importance of family engagement, the pandemic underscored the need to translate this philosophy more fully into practice. Method: We discuss the importance of engaging the family throughout the transplant experience to improve patient outcomes and overall family health and well-being. Results: We present the HCT family resilience model, a synthesis of multiple family and nursing theories and HCT concepts to better guide HCT family care. The theories and frameworks that inform our model address family functioning and growth in times of stress, coping strategies that promote positive family outcomes and resilience, and multicultural factors that may affect family experiences. A key contribution of our model is highlighting the role of family engagement in improving HCT family outcomes. Discussion: Application of a family systems lens highlights the essential role families play in the care of HCT patients and can foster family well-being. We offer the HCT family resilience conceptual model as a guide for practice and policy improvements to optimize care delivery for this patient and family population, as well as direction for future research.
... Therefore, genes involved in the dopaminergic system, which are relevant to the neural reward system, seem to play a role in the etiology of proactive aggression, as hypothesized by Chen et al. [30]. Furthermore, these results contribute to the debate on whether there is domain-specific or domaingeneral sensitivity [86]. In line with other research that advocates for domain-specific sensitivity [87,88], the findings of this study suggest that it is domain-specific as the COMT gene only interacts with the environment to predict the proactive form of aggression. ...
The aim of the study was to explore the possible vulnerability (diathesis-stress), susceptibility (differential susceptibility), or vantage (vantage sensitivity) properties of COMT gen Val158Met polymorphism to adverse and favorable parenting styles from both parents in relation to children’s reactive and proactive aggressive behavior. Within 279 eight-year-old children (125 girls and 154 boys) from Spain, reactive and proactive aggressive behavior was measured through the “Reactive and Proactive Questionnaire” (RPQ). Saliva samples were collected to genotype for the COMT Val158Met polymorphism via real-time PCR. Finally, parenting styles were assessed using the “Parenting Styles and Dimensions Questionnaire” (PSDQ). The results revealed that for boys, the Met allele was a vulnerability factor for proactive aggression in response to low-authoritative parenting from the father. For girls, it was the Val allele, the vulnerability variable to the high authoritarian style of the father, and the susceptibility factor to the authoritative style of the mother over proactive aggression. The results are discussed, considering possible sex differences. Our results indicate that the COMT Val158Met polymorphism is a biological variable that confers greater sensitivity to the environment.
... Drawing on the differential susceptibility hypothesis (Belsky, 2005;, we conceptualized emotion dysregulation as a susceptibility marker that may position emotionally dysregulated adolescents to be more sensitive to both positive and negative environmental influences, compared to less dysregulated adolescents. The differential susceptibility hypothesis suggests that individuals characterized by heightened susceptibility benefit more from supportive environments, but are also more negatively influenced by adverse environments, indicating a for-better-or-for-worse pattern (Belsky et al., 2007;Hartman & Belsky, 2016). Past research has shown that children higher in negative emotionality or difficult temperament exhibited more behavioral problems when faced with lower-quality rearing environments (e.g., poor parenting) and fewer behavioral problems when they were in higher-quality contexts (Belsky, 2005;Pluess & Belsky, 2009). ...
Introduction
In adolescence, life satisfaction is an early indicator of later psychological well‐being. However, researchers know little about how daily family relationships shape adolescent life satisfaction. The current study examined the day‐to‐day associations between parent–adolescent relationships and life satisfaction, and whether adolescent emotion dysregulation moderated these associations.
Methods
A total of 191 adolescents (Mage = 12.93, SDage = 0.75, 53% female) recruited from junior high schools in Taiwan participated in a 10‐day daily diary protocol. We conducted multilevel analyses to examine within‐family and between‐family processes.
Results
At the within‐family level, adolescents reported higher life satisfaction on days when parent–adolescent closeness was higher, but lower life satisfaction on days when parent–adolescent conflict was higher. At the between‐family level, higher parent–adolescent closeness was associated with greater life satisfaction on average, while parent–adolescent conflict was not related to adolescent life satisfaction. Cross‐level interactions indicated that within‐family changes in parent–adolescent closeness and conflict were only associated with life satisfaction for adolescents with higher levels of emotion dysregulation, indicating emotion dysregulation may intensify the role of daily parent–adolescent relationships in shaping adolescent life satisfaction.
Conclusions
This study expands current literature and provides novel evidence that changes in day‐to‐day parent–adolescent relationships have important implications for adolescent life satisfaction, especially for youth higher in emotion dysregulation. The findings underscore the importance of evaluating family and individual characteristics to better support adolescent well‐being.
... Several others 11,12 focus on other aspects of genetic support for differential susceptibility. Hartman and Belsky 13 reviewed literature with a focus on temperament and genetic characteristics that contribute to susceptibility. Rabinowitz and Drabick 14 reviewed the relationship between child genetic, endophenotypic, and phenotypic attributes related to parenting and social-emotional behaviors. ...
Differential susceptibility theory posits that some individuals, with specific characteristics, are more, or less susceptible than others, to both adverse and beneficial environmental influences. It offers a perspective for understanding the directional trajectories across the life course affected by daily context and individual characteristics, in order to identify influential components. The aim of this article is to describe differential susceptibility theory, critically evaluate research findings in which the theory is tested, and consider implications of differential susceptibility theory as a theoretical framework for nursing science. Preterm birth trajectories and outcomes research are used as a lens for this examination.
... Although most research focused on children, studies also found support for differential susceptibility in adults (Slagt et al., 2015). In adults, mostly candidate genes (such as Dopamine Receptor D4; DRD4, Monoamine oxidase A; MAOA, or Serotonin transporter polymorphism; 5-HTTLPR) have been used as markers for a susceptibility, but some support has been found for high sensitivity to the environment or openness to the environment as susceptibility markers (Hartman & Belsky, 2016;Slagt et al., 2015). Thus, it is important to take into account the differential susceptibility of the parents to not underestimate intervention effects . ...
In this randomized controlled trial, we investigated the effectiveness of the brief, home-based Video-feedback Intervention to promote Positive Parenting and Sensitive Discipline (VIPP-SD) in parents of 257 school-aged twin pairs (N = 514 children, Mage = 7.92, SD = 0.66), replicating a previous study testing the effectiveness of the intervention in parents with preschool-aged twins (Euser et al., 2021). We conducted two pretests (1 year apart) and one posttest 1 month after the intervention. An age-adequate twin-adapted version of the VIPP-SD was used in primary caregivers (91% female). We examined the main effect of the intervention on observed parental sensitivity and sensitive discipline and on attitudes toward sensitivity and sensitive discipline. We also investigated whether parents who are more susceptible to the environment, as measured by their self- and partner-reported current temperamental reactivity, benefitted more from the intervention. In our sample with older children, the VIPP-SD did not significantly change observed parental sensitivity or sensitive discipline in the intervention group compared to the control group. The VIPP-SD did improve parents' attitude toward sensitivity, but not toward discipline. Intervention effects were not moderated by temperamental reactivity of the parents, providing no support for the differential susceptibility hypothesis. Future research might examine the differential susceptibility hypothesis in parents using stress-reactivity or genetic susceptibility markers instead of self-reported reactive temperament. (PsycInfo Database Record (c) 2022 APA, all rights reserved).
... In a study, where Chinese centenarians were participating, it was found that the polymorphism SNP rs2069837 in IL6 was significantly associated with extreme longevity [5]. Another plausible reason why centenarians overcome COVID-19 better could be due to their characteristic genetic background, namely, how longevity and vulnerability genes are expressed [6][7][8]. Unique expression patterns of these genes could provide explanation for a superior ability of the centenarians' immune system to defend against SARS-CoV-2. Epigenetic changes might also contribute, since centenarians had to go through 2 world wars, hunger, and flu pandemics. ...
... However, the diathesis stress model focus on risk factors and excludes the possible influence of positive environments. An alternative approach to the diathesis stress model is the differential susceptibility theory, which suggests that susceptible individuals, rather than being solely responsive to negative environments, are also responsive to positive environments, in a "for better and for worse" manner Belsky and Pluess 2009;Hartman and Belsky 2016). ...
FKBP5 gene–environment interaction (cG × E) studies have shown diverse results, some indicating significant interaction effects between the gene and environmental stressors on depression, while others lack such results. Moreover, FKBP5 has a potential role in the diathesis stress and differential susceptibility theorem. The aim of the present study was to evaluate whether a cG × E interaction effect of FKBP5 single-nucleotide polymorphisms (SNPs) or haplotype and early life stress (ELS) on depressive symptoms among young adults was moderated by a positive parenting style (PASCQ pos ), through the frameworks of the diathesis stress and differential susceptibility theorem. Data were obtained from the Survey of Adolescent Life in Västmanland Cohort Study, including 1006 participants and their guardians. Data were collected during 2012, when the participants were 13 and 15 years old (Wave I: DNA), 2015, when participants were 16 and 18 years old (Wave II: PASCQ pos , depressive symptomology and ELS) and 2018, when participants were 19 and 21 years old (Wave III: depressive symptomology). Significant three-way interactions were found for the FKBP5 SNPs rs1360780 , rs4713916 , rs7748266 and rs9394309 , moderated by ELS and PASCQ pos , on depressive symptoms among young adults. Diathesis stress patterns of interaction were observed for the FKBP5 SNPs rs1360780 , rs4713916 and rs9394309 , and differential susceptibility patterns of interaction were observed for the FKBP5 SNP rs7748266 . Findings emphasize the possible role of FKBP5 in the development of depressive symptoms among young adults and contribute to the understanding of possible differential susceptibility effects of FKBP5 .
... While various studies have demonstrated individual differences in sensitivity to environmental influences on EXT (Lengua 2008;Pitzer et al. 2011;DiLalla et al. 2015;Rioux et al. 2015;De Laet et al. 2016;Janssens et al. 2017a;Tung et al. 2018), these studies focused on a narrow measurement of the environment, not addressing the issue of whether sensitive individuals are generally more sensitive to any environment, or rather are more sensitive to the effects of that particular environmental aspect or domain and might not be sensitive to others. This question was raised more generally in theoretical work regarding individual differences in environmental sensitivity and is questioning whether such differences are domain-general (individuals are either sensitive to many environmental influences or not/much less sensitive), or domain-specific (different individuals are sensitive to different environmental effects) (Belsky 2005;Belsky andPluess 2009, 2013;Ellis et al. 2011;Mitchell et al. 2013;Belsky and Hartman 2014;Hartman and Belsky 2015). While theoretical and evolutionary thinking favors the domain-specific perspective, suggesting that the effects of different environmental inputs could have either costs or benefits depending on the context, thus creating individual differences in sensitivity to each of these different inputs (Belsky 2005;Markovitch and Knafo-Noam 2021), there is almost no empirical work testing this question. ...
Externalizing behavior is substantially affected by genetic effects, which are moderated by environmental exposures. However, little is known about whether these moderation effects differ depending on individual characteristics, and whether moderation of environmental effects generalizes across different environmental domains. With a large sample (N = 1,441 individuals) of early adolescent twins (ages 11 and 13), using a longitudinal multi-informant design, we tested interaction effects between negative emotionality and both positive and negative aspects of three key social domains: parents, peers, and schools, on the phenotypic variance as well as the etiology of externalizing. Negative emotionality moderated some of the environmental effects on the phenotypic, genetic, and environmental variance in externalizing, with adolescents at both ends of the negative emotionality distribution showing different patterns of sensitivity to the tested environmental influences. This is the first use of gene-environment interaction twin models to test individual differences in environmental sensitivity, offering a new approach to study such effects.
... Yet research examining the links between childhood maltreatment and developmental outcomes as moderated by DRD4 remains scant. As Hartman and Belsky (2016) reviewed, although testing the applicability of differential susceptibility to trauma survivors is practically meaningful, research has primarily centered on environmental stressors that are more moderate (e.g., insensitive parenting). Further, as they also noted, the findings from a handful of studies are mixed with regard to the differential susceptibility conferred by DRD4. ...
There is a call for integrative studies examining the roles of biological and psychosocial factors and their interrelations in shaping maternal postpartum psychopathology. Using longitudinal data from 198 primiparous mothers, we tested a biopsychosocial model for the etiology of maternal postpartum depressive symptoms that integrated childhood emotional maltreatment, couple relationship satisfaction, and oxytocin and dopamine D4 receptor genes (i.e., OXTR rs53576 and DRD4). Results indicate (a) two indirect effects from childhood emotional maltreatment and DRD4 to depressive symptoms at 1 year postpartum through couple relationship satisfaction at 6 months postpartum; (b) an interactive effect between DRD4 and couple relationship satisfaction at 6 months postpartum in predicting depressive symptoms at 1 year postpartum, which is in concert with the differential susceptibility hypotheses; and (c) no mediating effects or moderating effects (after adjusting for multiple testing with Bonferroni correction) involving OXTR rs53576. Notably, all associations were identified after controlling for several key covariates (e.g., maternal prenatal depressive symptoms). Last, robustness of the currently identified interactive effect involving DRD4 was demonstrated by an extensive set of additional analyses considering the effects of rGE, G by Covariates, and/or E by Covariates. Taken altogether, this study represents one of the initial efforts for a more sophisticated portrayal of how nature and nurture forces may work in conjunction with each other to shape new mothers’ psychopathology. Yet given the current modest sample size and candidate gene approach, our findings are preliminary, should be cautiously interpreted, and need to be replicated with more rigorous designs.
... Furthermore, since parenting is a dyadic activity, and possible effects of parenting quality might be moderated by child temperament (see e.g. Hartman & Belsky, 2016;Kiff, Lengua, & Zalewski, 2011), future studies should include parenting-temperament interactions in their investigations of the development of emotional eating. ...
This study assessed the association between parenting quality at age 15 and 28 months and emotional eating (EE) at age 12 and 16 years through serial mediation by suppression of emotions and alexithymia at 12 years. The sample included 129 children and their parents. Lower parental quality in infancy was related to more suppression of emotions, which in turn was related to more difficulty identifying emotions, and in turn to higher EE in adolescence. This serial mediation model was significant for EE at 12 years, and for EE at 16 years. If future studies reveal converging findings, this knowledge points to the need for programs preventing the development of EE in adolescence through increasing the quality of parenting in infancy.
... This score was built by combining the risk alleles of the above-mentioned genes associated with non-optimal parenting or social impairments based on previous literature (Feldman et al., 2014). Drawing on the differentialsusceptibility hypothesis (Hartman and Belsky, 2016;Pluess and Belsky, 2010), parenting quality might differentially affect offspring future own parenting quality depending on the genotype of the offspring (Brüne, 2012). Individuals with so-called "plasticity alleles" may benefit the most from the warm and accepting parent-child relationship qualities but may similarly be more prone to cold and rejecting parenting, that is they may be sensitive to the environment "for better and for worse". ...
Parenting qualities are known to transmit across generations, but less is known about genetic processes that may modify how strongly parenting quality carries across generations. We examined in prospective data whether oxytocinergic genes of offspring moderate the intergenerational transmission of warm and accepting parent-child relationship qualities. The sample comprised 1167 Finnish parents (G2, 62% female) and their mothers (G1). At the study baseline, G1 mothers (Mage = 38) reported parent-child relationship qualities towards G2 children (age range 3-18). After 28-34 years, G2 offspring reported parent-child relationship qualities towards their own children using the same questionnaire. A cumulative genetic score was computed for G2 by summing up previously identified four alleles associated with non-optimal parenting or social impairments across OXTR (rs1042778, rs2254298, rs53576) and CD38 (rs3796863) genes. Results indicated no interaction effects of G2 cumulative genetic score on the transmission of parent-child relationship qualities. Among single polymorphisms in OXTR, the interaction effects of rs53576 and rs1042778 were found. G1 maternal emotional warmth was associated with higher G2 emotional warmth among G2 participants with the OXTR rs53576 AA/AG genotype, but not among those with the GG genotype. G1 maternal acceptance was associated with higher G2 acceptance among those G2 participants with the OXTR rs1042778 GG/GT genotype, but not among those with the TT genotype. Oxytocinergic genes may influence sensitivity to quality of parent-child relationship, although this needs replication in future studies.
... This proven shift in the subcortical mode is a result of individually different susceptibility to qualities of environments through genetic factors as Bakermans-Kranenburg and van Ijzendoorn (2006) showed for the DRD4 dopaminergic system, behavior problems and parenting. Environments (e.g., parenting) are steering epigenetic processes and children's behavior is forming parenting (Hartman and Belsky, 2016). Taken together, there is empirical evidence that CAs and also protective factors are integrated into the interacting levels of behavior, environment, and gene-expression, as it is conceptualized in the model of genetic differential sensitivity to social environment (GDSE, Hengartner et al., 2013;Mitchell et al., 2013;McDonald et al., 2016;Moore and Depue, 2016). ...
Context: Families with high rates of childhood adversities (CAs) (multi problem families, MPF) have an increasing importance in public health-policy.
Objective: The present study addresses the relationship between risk- and protective factors and the severity and treatment-outcome of mental disorders.
Setting: Family-therapeutic home-based treatment for MPF. We examined a clinical sample (N = 1031) of children between the age of 4 to 17, and a non-clinical sample of 148 children. We hypothesized that of all children of the clinical group have a predominance of risk factors and a higher number of psychopathological symptoms. Furthermore, we hypothesized that children with a predominance of protective factors benefit stronger from psychotherapy.
Main Results: In the clinical sample, most children met the criteria of a psychopathological diagnosis (95.7%, as compared to 21.6% in the non-clinical sample) and showed significant higher rates of CAs and significant less protective factors as compared to the non-clinical sample. The clinical group showed a significant reduction of psychopathological symptoms and benefited equally well from treatment. The number of risk factors was a significant predictor for a child from the non-clinical sample to meet the criteria of a psychopathological diagnosis, while the number of protective factors significantly predicted the absence thereof.
Conclusion: Children and adolescents with high scores of CAs show significant associations with child psychiatric symptoms (d = 0.35; including all ICD-diagnosis such as, e.g., Asperger Syndrome, ADHD etc. with a higher rate of genetic etiology). Early life stressors, however, do not trigger an irreversible fate, as psychotherapy with young people with high numbers of risk factors does help to reduce psychopathological symptoms significantly (range of five outcome parameters: d = 0.31–0.72).
... Moreover, the effects of the genotype on changes in lipid metabolism traits showed opposite trends in participants with low-fat versus high-fat intake. The results are in line with the "differential susceptibility hypothesis," which proposes that vulnerability genes or risk alleles may function like plasticity genes because genetic risk can be modified by environmental exposures, including dietary factors (23)(24)(25)(26). In other words, some individuals might be more responsive to environmental influences in a "for-better-and-for-worse" manner because of the genetic background (24). ...
Compelling evidence indicates that lipid metabolism is into partly control of the circadian system. In this context, it has been reported that the Melatonin receptor 1B (MTNR1B) genetic variant influences the dynamics of melatonin secretion, which is involved in the circadian system as a chronobiotic. The objective was to analyze whether the MTNR1B rs10830963 genetic variant was related to changes in lipid levels in response to dietary interventions with different macronutrient distribution in 722 overweight/obese subjects from the POUNDS Lost. We did not find a significant association between the MTNR1B genotype and changes in lipid metabolism. However, dietary fat intake significantly modified genetic effects on 2-year changes in total and LDL cholesterol (p interaction=0.006 and 0.001, respectively). In the low-fat diet group, carriers of the sleep disruption G allele (minor allele), showed a greater reduction of total (β±SE=-5.782.88 mg/dL, p=0.04) and LDL cholesterol (β±SE=-7.192.37 mg/dL, p=0.003). Conversely, in the high-fat diet group, subjects carrying the G allele evidenced a smaller decrease in total (β±SE=5.812.65 mg/dL, p=0.03) and LDL cholesterol (β±SE=5.232.21 mg/dL, p=0.002). Subjects carrying the G allele of the circadian-rhythm related MTNR1B variant may present a bigger impact on total and LDL cholesterol when undertaking an energy restricted low-fat diet.
... Hartman and Belsky (2015) found that temperamental and genetic characteristics played a role in distinguishing children that were either more or less susceptible to parental influences. In particular, two temperamental patterns have emerged as being indicators of heightened susceptibility to rearing: negative emotionality, and a highly sensitive personality (Hartman & Belsky, 2015). By contrast, less susceptible individuals are less affected by rearing conditions, whether they are positive or negative. ...
This paper synthesises what is known about that factors that affect development during the first 1000 days (the period from conception to the end of the second year), how these factors have their impact, and what are the long-term effects of early exposures and experiences. Further details can be found on the Centre for Community Child Health website: http://www.rch.org.au/ccch/first-thousand-days/
... In the present study, we showed that the genetic effects on changes in glucose-metabolism traits depend on dietary fat and carbohydrate intakes. This opposite nutrigenetic effect could be partly explained by the "differential susceptibility hypothesis," which proposes that genes could be considered as plasticity factors because genetic risk can be modified by environmental exposures such as dietary habits (34)(35)(36)(37). Thus, although some individuals proved highly susceptible to environmental conditions, for better or worse, depending on the genotype, other individuals appeared to be hardly affected (35). ...
Background: Circulating branched-chain amino acids (BCAAs) and aromatic amino acids (AAAs) have been shown to be associated with insulin resistance and diabetes risk. The common rs1440581 T allele in the protein phosphatase Mg2+/Mn2+ dependent 1K (PPM1K) gene has been related to elevated BCAA concentrations and risk of type 2 diabetes.Objective: In the present study, we tested whether dietary fat and carbohydrate intakes influenced the association between the rs1440581 PPM1K genetic variant and glucose-metabolism traits during weight loss.Design: The rs1440581 PPM1K genetic variant was genotyped in a total of 757 nondiabetic individuals who were randomly assigned to 1 of 2 energy-restricted diets that differed in macronutrient composition (low-fat diet: 20-25% fat, 15% protein, and 60-65% carbohydrate; high-fat diet: 40-45% fat, 15% protein, and 40-45% carbohydrate). The changes in fasting glucose, fasting insulin, insulin resistance (homeostasis model assessment of insulin resistance) and homeostasis model assessment of β cell function (HOMA-B) were measured after a mean ± SD weight loss of 6.8 ± 3.4 kg over 10 wk and analyzed according to the presence of the T allele of rs1440581.Results: The rs1440581 T allele was associated with a smaller improvement in glucose concentrations after the 10-wk dietary intervention (β ± SE: 0.05 ± 0.02 mg/dL; P = 0.03). In addition, significant gene-diet interactions were shown for the rs1440581 PPM1K genetic variant in relation to changes in insulin and HOMA-B (P-interaction = 0.006 and 0.002, respectively). In response to the high-fat diet, the T allele was associated with a higher reduction of insulin (β ± SE: -0.77 ± 0.40 μU/mL; P = 0.04) and HOMA-B (β ± SE: -13.2 ± 3.81; P = 0.003). An opposite effect was observed in the low-fat diet group, although in this group the T allele was marginally (P = 0.10) and not significantly (P = 0.24) associated with insulin and HOMA-B, respectively.Conclusion:PPM1K rs1440581 may affect changes in glucose metabolism during weight loss, and this effect is dependent on dietary fat and carbohydrate intakes. This trial was registered at controlled-trials.com as ISRCTN25867281.
... Second, we examined multiple domains of children's adjustment to school, including child pathology in terms of externalizing behavior problems (e.g., aggressive behavior), and child competence in terms of peer acceptance and ego-resilience (i.e., the capacity to negotiate uncertainty and stress in a way that is flexible, resourceful, and adaptive; Sroufe, 1991). In doing so, this investigation answered recent calls to examine a range of negative and positive adjustment outcomes to evaluate differential susceptibility patterns (Belsky & Pluess, 2009), and to document whether or not differences in environmental sensitivity affect various developmental domains equally (Hartman & Belsky, 2015;Pluess, 2015). ...
Consistent with models of environmental sensitivity (Pluess, 2015), research suggests that the effects of parents' behaviors on child adjustment are stronger among children who struggle to regulate their thoughts, feelings, and behaviors compared with children with better self-regulation. This study extended prior research by assessing maternal representations of the child, which presumably underlie mothers' parenting behaviors, to evaluate the moderating influence of preschoolers' self-regulation on relations between mothers' representations and changes in children's negative and positive developmental adjustment outcomes from preschool to first grade. Participants were 187 mothers and their preschoolers. Mothers' representations were assessed via the coherence of their verbal narratives regarding their preschooler and teachers reported on preschoolers' self-regulation. In preschool and first grade, examiners rated children's externalizing behavior problems and ego-resilience, and teachers rated children's externalizing behavior problems and peer acceptance. Consistent with the environmental sensitivity framework, the coherence of mothers' narratives predicted changes in adjustment among children with self-regulation difficulties, but not among children with better self-regulation. Preschoolers with self-regulation difficulties whose mothers produced incoherent narratives showed increased externalizing behavior problems, decreased ego-resilience, and lower peer acceptance across the transition to school. In contrast, preschoolers with better self-regulation did not evidence such effects when their mothers produced incoherent narratives. The implications of these findings for understanding and supporting children's adjustment during the early school years are discussed. (PsycINFO Database Record
... Finally, and perhaps most relevant, a number of studies have demonstrated that the DRD4 III polymorphism moderates the relation between environmental factors (including maternal stress) and children's behavior postnatally, such that those who inherit at least one 7-repeat allele are particularly sensitive to context, and this includes contexts that are good or bad (e.g., Zohsel, Buchmann, Blomeyer, Hohm, Schmidt, Esser, Brandeis, Banaschewski, & Laucht, 2014). Based on these findings, the 7-repeat (7R) allele on the third exon of the DRD4 gene, is considered among several candidates that promote individuals' s (bivalent) "Differential Susceptibility"(recent review in Hartman & Belsky, 2015; F o r P e e r R e v i e w DRD4 GENOTYPE, MATERNAL ANXIETY, AND FETAL MOVEMENTS 6 meta-analysis in Bakersmans- . The plasticity associated with the DRD4-III 7R variant stands in contrast to the shorter allele variants (2-6 repeats) that do not seem to impact individuals' response to context, whether good or bad. ...
We determined whether the combination of fetal genotype (dopamine D4 receptor; DRD4) and mothers' anxiety during pregnancy is associated with fetal behavior. Two hundred and six pregnant women underwent an ultrasound exam. Fetal movement measures (Movement Frequency, Total Activity, Movement Duration, and Longest Quiet Time) were derived from off-line coding. A moderating role of the DRD4-III polymorphism was found: Results indicate that higher levels of antenatal maternal anxiety symptoms were associated with more frequent fetal movements among fetuses carrying a 7R allele, but not among fetuses carrying shorter alleles. Total Activity did not show full moderation by DRD4, though the measure was correlated with maternal anxiety among fetuses in the Anxious Group with a 7R allele; not among fetuses without both factors. The findings provide the first evidence of a GXE interaction in association with fetal behavior. Results also demonstrate that some individuals are inherently more susceptible to uterine environmental influences than are others.
... Although environmental factors are not considered as causative in ASD and/or ADHD by themselves, they may act as risk or protective factors during sensitive developmental periods beginning in prenatal life through interactions with child characteristics, particularly in (genetically) susceptible individuals (Gardener et al., 2009;Hartman and Belsky, 2015;Pluess and Belsky, 2011;Sonuga-Barke and Halperin, 2010). During the embryonic stage intrauterine environmental influences are likely to modulate risk for developmental disorders (Gardener et al., 2011;Hallmayer et al., 2011). ...
Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) have overlapping characteristics and etiological factors, but to which extent this applies to infant- and preschool age is less well understood. Comparing the pathways to ASD and ADHD from the earliest possible stages is crucial for understanding how phenotypic overlap emerges and develops. Ultimately, these insights may guide preventative and therapeutic interventions. Here, we review the literature on the core symptoms, temperament and executive function in ASD and ADHD from infancy through preschool age, and draw several conclusions: (1) the co-occurrence of ASD and ADHD increases with age, severity of symptoms and lower IQ, (2) attention problems form a linking pin between early ASD and ADHD, but the behavioral, cognitive and sensory correlates of these attention problems partly diverge between the two conditions, (3) ASD and ADHD share high levels of negative affect, although the underlying motivational and behavioral tendencies seem to differ, and (4) ASD and ADHD share difficulties with control and shifting, but partly opposite behaviors seem to be involved.
From cradle to grave, human behaviour is greatly influenced by our emotional attachments to other people, animals, objects, places, and ideologies. In this volume, “Archaeologies of Attachment”, we seek to explore new approaches in archaeological thought to study these bonds from the Palaeolithic to the recent past. This introduction provides a basic overview of attachment, considers attachment as a more general explanatory concept for social bonds, and offers a short introduction into the rest of the chapters contained within.
Research on early biomarkers and behavioral precursors of autism has led to interventions initiated during the infant period that could potentially change the course of infant brain and behavioral development in autism. This article integrates neuroscience and clinical perspectives to explore how knowledge of infant brain and behavioral development can inform the design of infant autism interventions. Focusing on infants ≤12 months, we review studies on behavioral precursors of autism and their neural correlates and clinical trials evaluating the efficacy of infant autism interventions. We then consider how contemporary developmental social neuroscience theories of autism can shed light on the therapeutic strategies used in infant autism interventions and offer a new perspective that emphasizes improving child outcome and well-being by enhancing infant–environment fit. Finally, we offer recommendations for future research that incorporates brain-based measures to inform individualized approaches to intervention and discuss ethical issues raised by infant autism interventions. Readers are referred to Supplemental Table 1 for a glossary of terms used in this article.
This theoretical article revives a classical bridging construct, canalization, to describe a new model of a general factor of psychopathology. To achieve this, we have distinguished between two types of plasticity, an early one that we call 'TEMP' for 'Temperature or Entropy Mediated Plasticity', and another, we call 'canalization', which is close to Hebbian plasticity. These two forms of plasticity can be most easily distinguished by their relationship to 'precision' or inverse variance; TEMP relates to increased model variance or decreased precision, whereas the opposite is true for canalization. TEMP also subsumes increased learning rate, (Ising) temperature and entropy. Dictionary definitions of 'plasticity' describe it as the property of being easily shaped or molded; TEMP is the better match for this. Importantly, we propose that 'pathological' phenotypes develop via mechanisms of canalization or increased model precision, as a defensive response to adversity and associated distress or dysphoria. Our model states that canalization entrenches in psychopathology, narrowing the phenotypic state-space as the agent develops expertise in their pathology. We suggest that TEMP - combined with gently guiding psychological support - can counter canalization. We address questions of whether and when canalization is adaptive versus maladaptive, furnish our model with references to basic and human neuroscience, and offer concrete experiments and measures to test its main hypotheses and implications.
This chapter provides an overview of childhood physical abuse (CPA), abusive traumatic brain injury (TBI), childhood sexual abuse (CSA) and other sexual trauma, childhood emotional abuse (CEA), neglect, human trafficking, and secondary vicarious trauma. Acute and long-term consequences of TBI are described. Additionally, an overview is provided on the neurobiology of the stress response, potential lifelong hypothalamic-pituitary-adrenal (HPA) axis and stress system changes after adverse childhood experiences (ACEs), and the implications of stress systems changes on bio-behavioral health outcomes. Our data suggest that ACEs can result in long-term poor bio-behavioral health outcomes including homicide and other violent and non-violent criminal behavior perpetrated by survivors later in life. Our data also show that it is possible to change this trajectory in adult females. Part IV of this book provides evidence-based interventions for resilience and healing throughout the life course.KeywordsChildhood physical abuse (CPA)Abusive traumatic brain injury (TBI)Abusive head trauma (AHT)Childhood sexual abuse (CSA)Sexual traumaChildhood emotional abuse (CEA)NeglectHuman traffickingSecondary vicarious traumaAcute and long-term consequences of TBINeurobiology of the stress responseHypothalamic-pituitary-adrenal (HPA)Stress responseAdverse childhood experiences (ACEs)Bio-behavioral healthViolence - Violent behavior
Systemic family therapy (SFT) is the mental health profession and practice that focuses on family relationships. In this overview chapter, we describe the defining characteristics of the field that include (a) focus on family relational processes as the primary mechanism of treatment, (b) a broad definition of family, and (c) flexibility as to which family members are seen directly in treatment. After discussing the wide range of treatment goals addressed in SFT, we highlight recent research that demonstrates the importance of family relationships for mental and physical well‐being. Finally, we suggest some major themes and new developments that emerge from the chapters on the wide range of topics included in the four‐volume The Handbook of Systemic Family Therapy.
Classrooms are key social settings that impact children's mental health, though individual differences in physiological reactivity may render children more or less susceptible to classroom environments. In a diverse sample of children from 19 kindergarten classrooms (N = 338, 48% female, M age = 5.32 years), we examined whether children's parasympathetic reactivity moderated the association between classroom climate and externalizing symptoms. Independent observers coded teachers’ use of child-centered and teacher-directed instructional practices across classroom social and management domains. Children's respiratory sinus arrhythmia reactivity to challenge tasks was assessed in fall and a multi-informant measure of externalizing was collected in fall and spring. Both the social and the management domains of classroom climate significantly interacted with children's respiratory sinus arrhythmia reactivity to predict spring externalizing symptoms, controlling for fall symptoms. For more reactive children, as classrooms shifted toward greater proportional use of child-centered methods, externalizing symptoms declined, whereas greater use of teacher-dominated practices was associated with increased symptoms. Conversely, among less reactive children, exposure to more teacher-dominated classroom management practices was associated with lower externalizing. Consistent with the theory of biological sensitivity to context, considering variability in children's physiological reactivity aids understanding of the salience of the classroom environment for children's mental health.
This article outlines a conceptual framework for organising an intervention plan for family therapy before starting the sessions. This is based on an integrative coherent theory or frame of understanding called neuroaffective developmental psychology (NADP) (Hart 2008, 2011). NADP is an integration of attachment theory, neuropsychology, developmental psychology, and trauma theory. It has been developed as a tool to navigate in the complex world of emotional development, intersubjectivity, family therapy, and psychotherapy to create relevant intervention plans to meet the needs of an individual family or client. NADP is used as a theoretical frame of understanding, (a) to understand emotional development, personality vulnerabilities and disorders, and the maturation of emotional capacities within attachment‐based relationships, and (b) to translate this understanding into intervention plans discretely adjusted to the complexity of human development and the skills and agency of the professionals working with the families. The theory and clinical application of NADP as an organising frame within a family therapy setting is illustrated by a case example.
Objective:
Sensory processing sensitivity (SPS) is a recently proposed construct that refers to a genetically influenced tendency to more strongly and deeply process a variety of information. The aim of the study was to examine whether SPS is associated with an autoimmune disease such as type 1 diabetes (T1D).
Research design and methods:
Participants were 128 adolescents (62 with T1D and 66 comparisons [without autoimmune disease]) and their parents who completed the Highly Sensitive Person Scale (HSPS) questionnaire, assessing SPS level.
Results:
Higher levels of SPS were found in the T1D group than in the comparison group. Furthermore, the frequency of SPS trait was significantly higher in the T1D group than in the comparison group.
Conclusions:
T1D is associated with higher levels of SPS. Hence, there is a need to develop interventions, treatments, and care focused on the needs of T1D patients with SPS temperament, aimed at better treatment adherence. Furthermore, longitudinal research is needed to evaluate whether SPS is a risk factor in the development of T1D.
Objective:
Previous studies have shown that individual differences in self-control emerge early in childhood and predict a range of important outcomes throughout childhood and adulthood. There is, however, less knowledge about the social origins of self-control, including the mechanisms by which early socioeconomic adversity may lead to lower levels of self-control. This study aimed to extend understanding of the link between socioeconomic adversity and self-control by (a) testing which individual aspects of socioeconomic risk uniquely predict lower self-control; (b) testing whether objective socioeconomic risk operates independently of, or via, subjective parental stress; and (c) examining the interplay of socioeconomic risk factors and individual differences in children's temperament as predictors of early self-control.
Method:
Data were from a UK population birth cohort of 18,552 children born in 2000 and 2001.
Results:
Multiple individual socioeconomic risk factors have independent associations with children's self-control, including low parental education, income, and occupational class; insecure housing tenure; and younger parenthood. Results point to independent additive effects of exposure to objective and subjective risk. There was evidence of mothers' subjective stress partially mediating objective socioeconomic risks but only weak evidence of hypothesized interaction effects between temperament and socioeconomic risk.
Conclusions:
Results were consistent with additive risk and bioecological perspectives.
The costs and limits of phenotypic plasticity are thought to have important ecological and evolutionary consequences, yet they are not as well understood as the benefits of plasticity. At least nine ideas exist regarding how plasticity may be costly or limited, but these have rarely been discussed together. The most commonly discussed cost is that of maintaining the sensory and regulatory machinery needed for plasticity, which may require energy and material expenses. A frequently considered limit to the benefit of plasticity is that the environmental cues guiding plastic development can be unreliable. Such costs and limits have recently been included in theoretical models and, perhaps more importantly, relevant empirical studies now have emerged. Despite the current interest in costs and limits of plasticity, several lines of reasoning suggest that they might be difficult to demonstrate.
Despite decades of research examining diathesis-stress models of emotional disorders, it remains unclear whether dysfunctional attitudes interact with stressful experiences to shape affect on a daily basis and, if so, how clinical and genetic factors influence these associations. To address these issues, we conducted a multi-level daily diary study that examined how dysfunctional attitudes and stressful events relate to daily fluctuations in negative and positive affect in 104 young adults. Given evidence that clinical and genetic factors underlie stress sensitivity, we also examined how daily affect is influenced by internalizing and externalizing symptoms and brain-derived neurotrophic factor (BDNF) genotype, which have been shown to influence neural, endocrine, and affective responses to stress. In multivariate models, internalizing symptoms and BDNF Val66Met genotype independently predicted heightened negative affect on stressful days, but dysfunctional attitudes did not. Specifically, the BDNF Met allele and elevated baseline internalizing symptomatology predicted greater increases in negative affect in stressful circumstances. These data are the first to demonstrate that BDNF genotype and stress are jointly associated with daily fluctuations in negative affect, and they challenge the assumption that maladaptive beliefs play a strong independent role in determining affective responses to everyday stressors. The results may thus inform the development of new multi-level theories of psychopathology and guide future research on predictors of affective lability.
We examined caregiver report of externalizing behavior from 12 to 54 months of age in 102 children randomized to care as usual in institutions or to newly created high-quality foster care. At baseline no differences by group or genotype in externalizing were found. However, changes in externalizing from baseline to 42 months of age were moderated by the serotonin transporter linked polymorphic region genotype and intervention group, where the slope for short-short (S/S) individuals differed as a function of intervention group. The slope for individuals carrying the long allele did not significantly differ between groups. At 54 months of age, S/S children in the foster care group had the lowest levels of externalizing behavior, while children with the S/S genotype in the care as usual group demonstrated the highest rates of externalizing behavior. No intervention group differences were found in externalizing behavior among children who carried the long allele. These findings, within a randomized controlled trial of foster care compared to continued care as usual, indicate that the serotonin transporter linked polymorphic region genotype moderates the relation between early caregiving environments to predict externalizing behavior in children exposed to early institutional care in a manner most consistent with differential susceptibility.
Background
Theory and research suggest that sensory processing sensitivity (SPS), found in roughly 20% of humans and over 100 other species, is a trait associated with greater sensitivity and responsiveness to the environment and to social stimuli. Self-report studies have shown that high-SPS individuals are strongly affected by others' moods, but no previous study has examined neural systems engaged in response to others' emotions.Methods
This study examined the neural correlates of SPS (measured by the standard short-form Highly Sensitive Person [HSP] scale) among 18 participants (10 females) while viewing photos of their romantic partners and of strangers displaying positive, negative, or neutral facial expressions. One year apart, 13 of the 18 participants were scanned twice.ResultsAcross all conditions, HSP scores were associated with increased brain activation of regions involved in attention and action planning (in the cingulate and premotor area [PMA]). For happy and sad photo conditions, SPS was associated with activation of brain regions involved in awareness, integration of sensory information, empathy, and action planning (e.g., cingulate, insula, inferior frontal gyrus [IFG], middle temporal gyrus [MTG], and PMA).Conclusions
As predicted, for partner images and for happy facial photos, HSP scores were associated with stronger activation of brain regions involved in awareness, empathy, and self-other processing. These results provide evidence that awareness and responsiveness are fundamental features of SPS, and show how the brain may mediate these traits.
In this study we examined whether parents are differentially susceptible to support from their spouse and adolescent child depending on their personality traits, and whether differences in susceptibility to support among parents, in turn are linked to the quality of support parents give to their children.
Participants in this three-wave longitudinal study were 288 two-parent Dutch families with an adolescent child. Fathers were on average 43.9 years old (SD = 3.7 years), mothers were 41.7 years old (SD = 3.3 years), and adolescents (50% girls) 14.5 years old (SD = 0.8 years).
We found that the association between support from children towards their parents and subsequent support from parents towards their children was more pronounced for parents high on openness, for better and for worse. Extraversion, agreeableness, conscientiousness, and emotional stability did not emerge as markers of differences in susceptibility. Also, parents did not differ in their susceptibility to support from their spouse, nor were differences in susceptibility found a year later when using data from a third wave.
We found very modest support for differential susceptibility, only for openness, and depending on the source of perceived support and on the timing of measurement.
We provide a theoretical and empirical basis for the claim that individual differences exist in developmental plasticity and that phenotypic plasticity should be a subject of study in its own right. To advance this argument, we begin by highlighting challenges that evolutionary thinking poses for a science of development and psychopathology, including for the diathesis-stress framework that has (fruitfully) guided so much empirical inquiry on developmental risk, resilience, and dysregulation. With this foundation laid, we raise a series of issues that the differential-susceptibility hypothesis calls attention to, while highlighting findings that have emerged over just the past several years and are pertinent to some of the questions posed. Even though it is clear that this new perspective on Person × Environment interaction is stimulating research and influencing how hypotheses are framed and data interpreted, a great many topics remain that need empirical attention. Our intention is to encourage students of development and psychopathology to treat phenotypic plasticity as an individual-difference construct while exploring unknowns in the differential-susceptibility equation.
Biased attention towards negative stimuli is a known vulnerability for affective psychopathology. However, factors that contribute to the development of this cognitive bias are largely unknown. Variation within the serotonin transporter gene (i.e., 5-HTTLPR) is associated with increased susceptibility to environmental influence and biased processing of negative stimuli. Using a passive viewing eye-tracking paradigm, this study examined gaze fixation for emotion stimuli in 91 US Army soldiers before and after deployment to Iraq. In addition, participants underwent genetic assay and provided in situ measures of war zone stress exposure. 5-HTTLPR short allele homozygotes were more likely than other genotype groups to develop a gaze bias towards negative stimuli as a function of increasing war zone stress, even when controlling for post-deployment PTSD and depression severity. Short allele homozygotes appear especially sensitive to environmental influence, which likely contributes to the development of cognitive vulnerability to anxiety and mood disorders.
We present results of a meta-analysis of gene-by-environment (G × E) studies involving the serotonin transporter genotype 5HTTLPR to evaluate empirical support for two competing conceptual frameworks in developmental psychopathology: diathesis-stress and differential susceptibility. From a diathesis-stress perspective, the cumulative negative effects of the short allele (ss and sl genotypes) and adverse environments on development have been stressed. From a differential-susceptibility perspective, carriers of the s allele are predicted to be more open to adverse as well as positive environments, for better and for worse. Studies with children and adolescents up to 18 years of age (N=9361) were included. We found 41 effect sizes (N=5863) for the association between negative environments and developmental outcomes with or without significant moderation by 5HTTLPR genotype and 36 effect sizes (N=3498) for the potentially 5HTTLPR-moderated association between positive environments and developmental outcomes. Five moderators were examined: age, ethnicity, genotyping (biallelic or triallelic) and methods used to assess environment and outcome. In the total set of studies, including studies with mixed ethnicities, we found that ss/sl carriers were significantly more vulnerable to negative environments than ll carriers, thus supporting the diathesis-stress model. In the Caucasian samples, however, ss/sl carriers also profited significantly more from positive environmental input than ll carriers. Associations between (positive or negative) environment and (positive or negative) developmental outcome were absent for ll carriers. The meta-analytic findings support the hypothesis that in Caucasian samples 5HTTLPR is a genetic marker of differential susceptibility. G × E interactions might be critically dependent on ethnicity.
Gene-environment interaction effects in predicting antisocial behavior in late childhood were investigated among maltreated and nonmaltreated low-income children (N = 627, M age = 11.27). Variants in three genes were examined: tryptophan hydroxylase 1 (TPH1), serotonin transporter linked polymorphic region (5-HTTLPR), and monoamine oxidase A (MAOA) upstream variable number tandem repeat. In addition to child maltreatment status, we considered the impact of maltreatment subtypes, developmental timing of maltreatment, and chronicity. Indicators of antisocial behavior were obtained from self-, peer, and adult counselor reports. In a series of analyses of covariance, child maltreatment and its parameters demonstrated strong main effects on early antisocial behavior as assessed by all report forms. Genetic effects operated primarily in the context of gene-environment interactions, moderating the impact of child maltreatment on outcomes. Across the three genes, among nonmaltreated children no differences in antisocial behavior were found based on genetic variation. In contrast, among maltreated children specific polymorphisms of TPH1, 5-HTTLPR, and MAOA were each related to heightened self-report of antisocial behavior; the interaction of 5-HTTLPR and developmental timing of maltreatment also indicated more severe antisocial outcomes for children with early onset and recurrent maltreatment based on genotype. TPH1 and 5-HTTLPR interacted with maltreatment subtype to predict peer reports of antisocial behavior; genetic variation contributed to larger differences in antisocial behavior among abused children. The TPH1 and 5-HTTLPR polymorphisms also moderated the effects of maltreatment subtype on adult reports of antisocial behavior; again, the genetic effects were strongest for children who were abused. In addition, TPH1 moderated the effect of developmental timing of maltreatment and chronicity on adult reports of antisocial behavior. The findings elucidate how genetic variation contributes to identifying which maltreated children are most vulnerable to antisocial development.
In a randomized controlled trial we tested the role of genetic differences in explaining variability in intervention effects on child externalizing behavior. One hundred fifty-seven families with 1- to 3-year-old children screened for their relatively high levels of externalizing behavior participated in a study implementing Video-feedback Intervention to promote Positive Parenting and Sensitive Discipline (VIPP-SD), with six 1.5-hr intervention sessions focusing on maternal sensitivity and discipline. A moderating role of the dopamine D4 receptor (DRD4) variable-number tandem repeat (VNTR) exon III polymorphism was found: VIPP-SD proved to be effective in decreasing externalizing behavior in children with the DRD4 7-repeat allele, a polymorphism that is associated with motivational and reward mechanisms and Attention Deficit Hyperactivity Disorder (ADHD) in children. VIPP-SD effects were largest in children with the DRD4 7-repeat allele whose parents showed the largest increase in the use of positive discipline. The findings of this first experimental test of (measured) gene by (observed) environment interaction in human development indicate that children may be differentially susceptible to intervention effects depending on genetic differences.
Guided by the affective spillover hypothesis and the differential susceptibility to environmental influence frameworks, the present study examined how associations between interparental conflict and mothers' parenting practices were moderated by serotonin transporter (5-HTT) and oxytocin receptor (OXTR) genes. A sample of 201 mothers and their 2-year old child participated in a laboratory-based research assessment. Results supported differential susceptibility hypotheses within spillover frameworks. With respect to OXTR rs53576, mothers with the GG genotype showed greater differential maternal sensitivity across varying levels of interparental conflict. Mothers with one or two copies of the 5-HTTLPR S allele demonstrated differential susceptibility for both sensitive and harsh/punitive caregiving behaviors. Finally, analyses examined whether maternal depressive symptoms and emotional closeness to their child mediated the moderating effects. Findings suggest that maternal emotional closeness with their child indirectly linked OXTR with maternal sensitivity. The results highlight how molecular genetics may explain heterogeneity in spillover models with differential implications for specific parenting behaviors. Implications for clinicians and therapists working with maritally distressed parents are discussed.
This report describes the state of the art in distinguishing data generated by differential susceptibility from diathesis-stress models. We discuss several limitations of existing practices for probing interaction effects and offer solutions that are designed to better differentiate differential susceptibility from diathesis-stress models and quantify their corresponding implications. In addition, we demonstrate the utility of these methods by revisiting published evidence suggesting that temperamental difficulty serves as a marker of enhanced susceptibility to early maternal caregiving across a range of outcome domains in the NICHD Study of Early Child Care and Youth Development. We find that, with the exception of mother reports of psychopathology, there is consistent evidence in the Study of Early Child Care and Youth Development that the predictive significance of early sensitivity is moderated by difficult temperament over time. However, differential susceptibility effects emerged primarily for teacher reports of academic skills, social competence, and symptomatology. In contrast, effects more consistent with the diathesis-stress model were obtained for mother reports of social skills and objective tests of academic skills. We conclude by discussing the value of the application of this work to the next wave of Gene × Environment studies focused on early caregiving experiences.
Positive affect has been implicated in the phenomenological experience of various psychiatric disorders, vulnerability to develop psychopathology and overall socio-emotional functioning. However, developmental influences that may contribute to positive affect have been understudied. Here, we studied youths' 5-HTTLPR genotype and rearing environment (degree of positive and supportive parenting) to investigate the differential susceptibility hypothesis (DSH) that youth carrying short alleles of 5-HTTLPR would be more influenced and responsive to supportive and unsupportive parenting, and would exhibit higher and lower positive affect, respectively. Three independent studies tested this gene-environment interaction (GxE) in children and adolescents (age range 9-15 years; total N=1874). In study 1 (N=307; 54% girls), positive/supportive parenting was assessed via parent report, in study 2 (N=197; 58% girls) via coded observations of parent-child interactions in the laboratory and in study 3 (N=1370; 53% girls) via self report. Results from all the three studies showed that youth homozygous for the functional short allele of 5-HTTLPR were more responsive to parenting as environmental context in a 'for better and worse' manner. Specifically, the genetically susceptible youth (that is, S'S' group) who experienced unsupportive, non-positive parenting exhibited low levels of positive affect, whereas higher levels of positive affect were reported by genetically susceptible youth under supportive and positive parenting conditions. These GxE findings are consistent with the DSH and may inform etiological models and interventions in developmental psychopathology focused on positive emotion, parenting and genetic susceptibility.
Despite an extensive history underscoring the role of social processes and child contributions to the development of executive functions (C. Lewis & J. Carpendale, 2009; L. S. Vygotsky, 1987), research on these relations is sparse. To address this gap, 68 mother-child dyads were examined to determine whether maternal attention-directing behaviors (attention maintaining, attention redirection) and toddlers' temperament predicted executive processes during preschool (mean age = 4.5 years, SD = 0.46)-delay and conflict inhibition. Maternal attention maintaining was associated with high levels of conflict inhibition for inhibited and exuberant children, whereas attention redirection was associated with low levels of delay and conflict inhibition for inhibited children. Therefore, maternal attention-directing behaviors may enhance the development of executive functions but only for children with inhibited and exuberant temperaments.
The costs and limits of phenotypic plasticity are thought to have important ecological and evolutionary consequences, yet they are not as well understood as the benefits of plasticity. At least nine ideas exist regarding how plasticity may be costly or limited, but these have rarely been discussed together. The most commonly discussed cost is that of maintaining the sensory and regulatory machinery needed for plasticity, which may require energy and material expenses. A frequently considered limit to the benefit of plasticity is that the environmental cues guiding plastic development can be unreliable. Such costs and limits have recently been included in theoretical models and, perhaps more importantly, relevant empirical studies now have emerged. Despite the current interest in costs and limits of plasticity, several lines of reasoning suggest that they might be difficult to demonstrate.
Hypothesizing that genetic factors partially govern sensitivity to interpersonal cues, we examined whether a polymorphism (5-HTTLPR) in the serotonin transporter gene would moderate spouses' sensitivity to positive and negative partner affect. Before and after marital discussions, participants from 76 couples (total n = 150) reported their affective states. Spouses carrying the short allele of the 5-HTTLPR were more responsive to their partner's preinteraction positive affect and anxiety/nervousness, compared with spouses with two long alleles. These data support the contention that the serotonin system influences affective responses to social stimuli. In contrast to the view that the 5-HTTLPR primarily affects response to adverse experiences, these results suggest that this polymorphism moderates sensitivity to positive as well as negative affect.
Most individuals successfully maintain psychological well-being even when exposed to trauma or adversity. Emotional resilience or the ability to thrive in the face of adversity is determined by complex interactions between genetic makeup, previous exposure to stress, personality, coping style, availability of social support, etc. Recent studies have demonstrated that childhood trauma diminishes resilience in adults and affects mental health. The Dopamine receptor D4 (DRD4) exon III variable number tandem repeat (VNTR) polymorphism was reported to moderate the impact of adverse childhood environment on behaviour, mood and other health-related outcomes. In this study we investigated whether DRD4-exIII-VNTR genotype moderates the effect of childhood adversities (CA) on resilience. In a representative population sample (n = 1148) aged 30-34 years, we observed an interactive effect of DRD4 genotype and CA (β = 0.132; p = 0.003) on resilience despite no main effect of the genotype when effects of age, gender and education were controlled for. The 7-repeat allele appears to protect against the adverse effect of CA since the decline in resilience associated with increased adversity was evident only in individuals without the 7-repeat allele. Resilience was also significantly associated with approach-/avoidance-related personality measures (behavioural inhibition/activation system; BIS/BAS) measures and an interactive effect of DRD4-exIII-VNTR genotype and CA on BAS was observed. Hence it is possible that approach-related personality traits could be mediating the effect of the DRD4 gene and childhood environment interaction on resilience such that when stressors are present, the 7-repeat allele influences the development of personality in a way that provides protection against adverse outcomes.
The serotonin transporter polymorphism has been linked--often in interaction with environmental adversity--to a variety of outcomes, including affective disorders. This polymorphism is widely viewed as relating to anxiety traits. A different view is that it relates instead to impulsivity (vs. control) in reacting to emotions. In a test of the latter view, 303 students were genotyped on this polymorphism and completed self-reports bearing on impulsive reactions to emotions (including both negative and positive emotions in separate measures), impulsive tendencies that do not stem from emotions, and childhood adversity. The impulsivity measures reflected three latent variables: pervasive influence of feelings, feelings (including positive feelings) triggering action, and failure to carry through on intentions (with no mention of emotion). Interactions between genotype and adversity emerged for both emotion-related aspects of impulsivity. Theoretical implications of the findings are discussed.
The manifestation of alcohol dependence at different developmental stages may be associated with different genetic and environmental factors. Taking a developmental approach, we characterized interaction between the dopamine receptor 4 variable number tandem repeat (DRD4 VNTR) polymorphism and developmentally specific environmental factors (childhood adversity, college/Greek organization involvement, and delayed adult role transition) on alcohol dependence during emerging and young adulthood. Prospective data were obtained from a cohort of 234 White individuals (56% women, 44% men) who were followed up at ages 18 through 34. A longitudinal hierarchical factor model was estimated to model a traitlike persistent alcohol dependence factor throughout emerging and young adulthood and 2 residual statelike alcohol dependence factors limited to emerging adulthood and young adulthood, respectively. We accounted for those alcohol dependence factors by modeling 3 two-way interaction effects between the DRD4 VNTR polymorphism and the 3 developmentally specific environment factors. Carriers of the DRD4 long allele showed greater susceptibility to environmental effects; they showed more persistent symptoms of alcohol dependence as childhood adversity increased and more alcohol dependence symptoms limited to emerging adulthood as college/Greek organization involvement increased. Alcohol dependence among noncarriers of the long allele, however, did not differ as a function of those environments. Although replication is necessary, these findings highlight the importance of repeated phenotypic assessments across development and modeling both distal and proximal environments and their interaction with genetic susceptibility at specific developmental stages.
The moderating effects of biological sensitivity to context (physiological and behavioral stress reactivity) on the association between the early teacher-child relationship and the development of adolescent mental health problems were examined in a community sample of 96 children. Grade 1 measures of biological sensitivity to context included physiological (i.e., slope of mean arterial pressure across a 20- to 30-min stress protocol) and behavioral (i.e., temperamental inhibition/disinhibition) markers. Grade 1 measures of the teacher-child relationship included positive (i.e., closeness) and negative (i.e., conflict) qualities. Mental health symptoms were assessed at Grades 1 and 7. Results of a multiple regression analysis indicated substantial association of the teacher-child relationship with the development of adolescent mental health symptoms, especially for more reactive children. In addition to teacher-child relationship main effects, all four Reactivity x Teacher-Child Relationship interaction terms were statistically significant when controlling for Grade 1 symptom severity, suggesting that both physiological and behavioral reactivity moderate the association of both adverse and supportive aspects of the teacher-child relationship with Grade 7 symptom severity over and above Grade 1 severity. There were important differences, depending on which stress reactivity measure was considered. The importance of these findings for recent theoretical arguments regarding biological sensitivity to context and differential susceptibility is discussed.
Theoretical considerations and new empirical evidence suggest that children's development cannot simply be explained by either genes or environment but that their interaction is important to understanding child behavior. In particular, a genetic polymorphism, the exon III repeat region of the dopamine receptor D4, has been the focus of interest regarding differential susceptibility to parental influence. To study environmental and genetic influences on children's prosocial behavior, 168 twin pairs (mean age = 44 months) participated in an experiment that assessed prosocial behavior via three measures: compliant prosocial behavior elicited in response to social requests, self-initiated prosocial behavior enacted voluntarily, and mothers' rating of children's behavior. Genetic effects accounted for 34% to 53% of the variance in prosocial behavior. The rest of the variance was accounted for by nonshared environment and error. Parenting measures of maternal positivity, negativity, and unexplained punishment did not correlate significantly with children's prosocial behavior. However, when parenting was stratified by presence or absence of the child's dopamine receptor D4 7-repeat allele in an overlapping sample of 167 children to model differential susceptibility to parental influence, a richer picture emerged. Positive parenting related meaningfully to mother-rated prosocial behavior, and unexplained punishment related positively to self-initiated prosocial behavior, but only among children carrying the 7-repeat allele. The findings demonstrate that a molecular genetic strategy, based on genotyping of common polymorphisms and combined with a classic twin approach, provides a richer description of how genes and environment interact to shape children's behavior, and allows for the identification of differential sensitivity to parental influence.
In the current paper we present new empirical data and meta-analytic evidence for the role of dopamine-related genes as a susceptibility factor interacting with the rearing environment for better and for worse, that is, increasing children's susceptibility to both the adverse effects of unsupportive environments and the beneficial effects of supportive rearing. In Study 1 we examined the readiness of 91 7-year-old children to donate their money to a charity (UNICEF). We tested whether the association between attachment and donating behavior was moderated by the presence of the dopamine receptor D4 (DRD4) 7-repeat allele. The attachment story completion task was used to assess attachment as an index of the quality of the rearing environment. Children with secure attachment representations donated more but only if they had the DRD4 7-repeat allele. In Study 2 we present the results of a meta-analysis of gene-environment studies on children up to 10 years of age involving dopamine-related genes (dopamine receptor D2, DRD4, dopamine transporter). The cumulative negative effects of these "risk genes" and adverse rearing environments have been stressed, but potentially cumulative positive effects of these same genes interacting with positive rearing environments remained largely unnoticed. We examined the associations between negative and positive rearing environments and developmental outcomes as moderated by dopamine-related gene polymorphisms. Children with the less efficient dopamine-related genes did worse in negative environments than the comparisons without the "genetic risk," but they also profited most from positive environments. Findings are discussed in light of evolutionary theory, and illustrated with some practical implications of differential susceptibility.
Existing studies of the effect on infant temperament of the 48 base pair variable number of tandem repeats polymorphism in exon 3 of the dopamine D4 receptor gene, DRD4 VNTR, and the serotonin transporter-linked polymorphic region, 5-HTTLPR, have provided contradictory results, and age seems to be an important factor. The present study investigated the effect of these two polymorphisms on the stability of infant temperament between 4 and 9 months of age. Furthermore, the effect of a recently discovered single nucleotide polymorphism which modulates the 5-HTTLPR (rs25531) was investigated in relation to infant temperament. The study sample consisted of 90 infants, who were assessed by parental report at the two ages under consideration using the Revised Infant Behavior Questionnaire. It was found that infants carrying the 7-repeat allele of the DRD4 VNTR had higher levels of Negative Affect. Furthermore, there was an interaction between DRD4 VNTR and 5-HTTLPR genotype such that infants with the DRD4 VNTR 7-repeat allele and the highest expressing 5-HTTLPR genotype (L(A) L(A) ) had the highest level of Negative Affect. These effects were largely driven by scores on the Falling Reactivity scale. Genetic effects were stable across age. The results emphasize the need for developmental studies of genetic effects on temperament.
Research on differential susceptibility to rearing suggests that infants with difficult temperaments are disproportionately affected by parenting and child care quality, but a major U.S. child care study raises questions as to whether quality of care influences social adjustment. One thousand three hundred sixty-four American children from reasonably diverse backgrounds were followed from 1 month to 11 years with repeated observational assessments of parenting and child care quality, as well as teacher report and standardized assessments of children's cognitive-academic and social functioning, to determine whether those with histories of difficult temperament proved more susceptible to early rearing effects at ages 10 and 11. Evidence for such differential susceptibility emerges in the case of both parenting and child care quality and with respect to both cognitive-academic and social functioning. Differential susceptibility to parenting and child care quality extends to late middle childhood. J. Belsky, D. L. Vandell, et al.'s (2007) failure to consider such temperament-moderated rearing effects in their evaluation of long-term child care effects misestimates effects of child care quality on social adjustment.
Evolutionary-biological reasoning suggests that individuals should be differentially susceptible to environmental influences, with some people being not just more vulnerable than others to the negative effects of adversity, as the prevailing diathesis-stress view of psychopathology (and of many environmental influences) maintains, but also disproportionately susceptible to the beneficial effects of supportive and enriching experiences (or just the absence of adversity). Evidence consistent with the proposition that individuals differ in plasticity is reviewed. The authors document multiple instances in which (a) phenotypic temperamental characteristics, (b) endophenotypic attributes, and (c) specific genes function less like "vulnerability factors" and more like "plasticity factors," thereby rendering some individuals more malleable or susceptible than others to both negative and positive environmental influences. Discussion focuses upon limits of the evidence, statistical criteria for distinguishing differential susceptibility from diathesis stress, potential mechanisms of influence, and unknowns in the differential-susceptibility equation.
Over a series of 7 studies that used diverse samples and measures, this research identified a unidimensional core variable of high sensory-processing sensitivity and demonstrated its partial independence from social introversion and emotionality, variables with which it had been confused or subsumed in most previous theorizing by personality researchers. Additional findings were that there appear to be 2 distinct clusters of highly sensitive individuals (a smaller group with an unhappy childhood and related variables, and a larger group similar to nonhighly sensitive individuals except for their sensitivity) and that sensitivity moderates, at least for men; the relation of parental environment to reporting having had an unhappy childhood. This research also demonstrated adequate reliability and content, convergent, and discriminant validity for a 27-item Highly Sensitive Person Scale.
This article reviews how a temperament approach emphasizing biological and developmental processes can integrate constructs from subdisciplines of psychology to further the study of personality. Basic measurement strategies and findings in the investigation of temperament in infancy and childhood are reviewed. These include linkage of temperament dimensions with basic affective-motivational and attentional systems, including positive affect/approach, fear, frustration/anger, and effortful control. Contributions of biological models that may support these processes are then reviewed. Research indicating how a temperament approach can lead researchers of social and personality development to investigate important person-environment interactions is also discussed. Lastly, adult research suggesting links between temperament dispositions and the Big Five personality factors is described.
Evidence that adverse rearing environments exert negative effects particularly on children presumed "vulnerable" for temperamental or genetic reasons may actually reflect something else: heightened susceptibility to the negative effects of risky environments and to the beneficial effects of supportive environments. Building on Belsky's (1997, 2005) evolutionary-inspired proposition that some children are more affected-both for better and for worse-by their rearing experiences than are others, we consider recent work on child vulnerability, including that involving measured genes, along with evidence showing that putatively vulnerable children are especially susceptible to both positive and negative rearing effects. We also consider methodological issues and unanswered questions in the differential-susceptibility equation.
The efficacy of interventions might be underestimated or even go undetected as a main effect when it is hidden in gene-by-environment (G×E) interactions. This review moves beyond the problems thwarting correlational G×E research to propose genetic differential susceptibility experiments. G×E experiments can test the bright side as well as the dark side of the moderating role of genotypes traditionally considered to represent vulnerability to negative conditions. The differential susceptibility model predicts that carriers of these risk genotypes profit most from interventions changing the environment for the better. The evolutionary background of G×E and differential susceptibility is discussed, and statistical methods for the analysis of differential susceptibility (versus diathesis stress) are reviewed. Then, based on results from 22 randomized G×E experiments, meta-analytic evidence for the differential susceptibility model is presented. Intervention effects are much stronger in the susceptible genotypes than in the nonsusceptible genotypes. The final sections suggest possibilities to broaden the G component in the G×E equation by including genetic pathways, and to broaden the E component by including methylation level and gene expression as promising ways to probe the concept of the environment more deeply and address the perennial issue of what works for whom. Expected final online publication date for the Annual Review of Psychology Volume 66 is November 30, 2014. Please see http://www.annualreviews.org/catalog/pubdates.aspx for revised estimates.
Background
Childhood dysregulation, which reflects deficits in the capacity to regulate or control one's thoughts, emotions and behaviours, is associated with psychopathology throughout childhood and into adulthood. Exposures to adversity during the prenatal period, including prenatal depression, can influence the development of dysregulation, and a number of candidate genes have been suggested as moderators of prenatal exposure, including polymorphisms in the promoter region of the serotonin transporter gene (5-HTTLPR). We examined whether prenatal depression and child 5-HTTLPR interact to predict childhood dysregulation.Method
Sample of N = 213 mother–child pairs from the Maternal Adversity, Vulnerability and Neurodevelopment (MAVAN) project. Mothers reported the IBQ-R at 3 and 6 months, and the ECBQ at 18 and 36 months, from which measures of dysregulation were extracted. Mothers' self-reported symptoms of depression on the CES-D at 24–36 weeks of gestation, and at 6, 12, 24 and 36 months postnatal. 5-HTTLPR genotype was extracted from buccal swabs. Mixed-model and confirmatory analyses were conducted.ResultsPrenatal depression and 5-HTTLPR interacted to predict dysregulation from 3 to 36 months, within a model of strong differential susceptibility.Conclusion
Children with S or LG alleles, when exposed to prenatal depression, have higher levels of dysregulation, and when exposed to lower or little prenatal depression, have higher capacity for regulation. Our findings support efforts to identify, support and treat prenatal depression.
Evidence that adverse rearing environments exert negative effects particularly on children presumed “vulnerable” for temperamental or genetic reasons may actually reflect something else: heightened susceptibility to the negative effects of risky environments and to the beneficial effects of supportive environments. Building on Belsky's (1997, 2005) evolutionary-inspired proposition that some children are more affected—both for better and for worse—by their rearing experiences than are others, we consider recent work on child vulnerability, including that involving measured genes, along with evidence showing that putatively vulnerable children are especially susceptible to both positive and negative rearing effects. We also consider methodological issues and unanswered questions in the differential-susceptibility equation.
We examined Genotype × Environment (G × E) interactions between children's genotypes (the serotonin transporter linked promoter region [5-HTTLPR] gene) and maternal responsive care observed at 15, 25, 38, and 52 months on three aspects of children's competence at 67 months: academic skills and school engagement, social functioning with peers, and moral internalization that encompassed prosocial moral cognition and the moral self. Academic and social competence outcomes were reported by both parents, and moral internalization was observed in children's narratives elicited by hypothetical stories and in a puppet interview. Analyses revealed robust G × E interactions, such that children's genotype moderated the effects of maternal responsive care on all aspects of children's competence. Among children with a short 5-HTTLPR allele (ss/sl), those whose mothers were more responsive were significantly more competent than those whose mothers were less responsive. Responsiveness had no effect for children with two long alleles (ll). For academic and social competence, the G × E interactions resembled the diathesis-stress model: ss/sl children of unresponsive mothers had particularly unfavorable outcomes, but ss/sl children of responsive mothers had no worse outcomes than ll children. For moral internalization, the G × E interaction reflected the differential susceptibility model: whereas ss/sl children of unresponsive mothers again had particularly unfavorable outcomes, ss/sl children of responsive mothers had significantly better outcomes than ll children.
Data from 508 Caucasian children in the NICHD Study of Early Child Care and Youth Development shows that the DRD4 (but not 5-HTTLPR) polymorphism moderates the effect of child-care quality (but not quantity or type) on caregiver-reported externalizing problems at 54 months and in kindergarten and teacher-reported social skills at kindergarten and first grade-but not thereafter. Only children carrying the 7-repeat allele proved susceptible to quality-of-care effects. The behavior-problem interactions proved more consistent with diathesis-stress than differential-susceptibility thinking, whereas the reverse was true of the social-skills' results. Finally, the discerned Gene × Environment interactions did not account for previously reported parallel ones involving difficult temperament in infancy.
This book proposes that psychopathology is best understood as the interaction between 3 factors: biology–genetics, personality, and stressful events. These, in combination with social and familial factors, create vulnerability in the individual. Using this framework, the author synthesizes for his readers the most current research available on each of the major disorders including anxiety, mood, antisocial personality, substance abuse, pathological gambling, and schizophrenic disorders. The author's intent is to provide teachers, graduates students, clinicians, researchers, and theorists with an up-to-date coursebook, a single source of information on the major psychological disorders. The volume covers their history, diagnosis, prevalence, prognosis, course, outcome,comorbidity, demographic characteristics, genetics, biochemistry, and neurophysiology. An important finding is that while anxiety, depression, and antisocial personality represent extremes of normal personality dimensions, schizotypic personality and schizophrenic disorder are a taxon, not continuous with normal dimensions of personality. This comprehensive and authoritative book will be a valuable new resource. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
This study examined infants' negative emotionality as moderating the effect of parent-child mutually responsive orientation (MRO) on children's self-regulation (n=102). Negative emotionality was observed in anger-eliciting episodes and in interactions with parents at 7 months. MRO was coded in naturalistic interactions at 15 months. Self-regulation was measured at 25 months in effortful control battery and as self-regulated compliance to parental requests and prohibitions. Negative emotionality moderated the effects of mother-child, but not father-child, MRO. Highly negative infants were less self-regulated when they were in unresponsive relationships (low MRO), but more self-regulated when in responsive relationships (high MRO). For infants not prone to negative emotionality, there was no link between MRO and self-regulation. The "regions of significance" analysis supported the differential susceptibility model not the diathesis-stress model.
In this investigation, gene-environment interaction effects in predicting resilience in adaptive functioning among maltreated and nonmaltreated low-income children (N = 595) were examined. A multicomponent index of resilient functioning was derived and levels of resilient functioning were identified. Variants in four genes (serotonin transporter linked polymorphic region, corticotropin releasing hormone receptor 1, dopamine receptor D4-521C/T, and oxytocin receptor) were investigated. In a series of analyses of covariance, child maltreatment demonstrated a strong negative main effect on children's resilient functioning, whereas no main effects for any of the genotypes of the respective genes were found. However, gene-environment interactions involving genotypes of each of the respective genes and maltreatment status were obtained. For each respective gene, among children with a specific genotype, the relative advantage in resilient functioning of nonmaltreated compared to maltreated children was stronger than was the case for nonmaltreated and maltreated children with other genotypes of the respective gene. Across the four genes, a composite of the genotypes that more strongly differentiated resilient functioning between nonmaltreated and maltreated children provided further evidence of genetic variations influencing resilient functioning in nonmaltreated children, whereas genetic variation had a negligible effect on promoting resilience among maltreated children. Additional effects were observed for children based on the number of subtypes of maltreatment children experienced, as well as for abuse and neglect subgroups. Finally, maltreated and nonmaltreated children with high levels of resilience differed in their average number of differentiating genotypes. These results suggest that differential resilient outcomes are based on the interaction between genes and developmental experiences.
The S-allele of the 5-HTTLPR has been identified as a genetic vulnerability factor, being associated with an increased risk for affective disorders and/or maladaptive traits (e.g. neuroticism), especially after exposition to negative life-events (LEs). Alternatively, it has been hypothesized that this genetic risk factor might constitute a genetic plasticity factor. That is, S-allele carriers are not only vulnerable to the negative effects of a preponderance of stressful LEs but also disproportionally benefit from a preponderance of positive environmental influences. We tested this hypothesis in 357 subjects who were genotyped for the 5-HTTLPR and provided self-reports of neuroticism, life-satisfaction and LEs. Results showed a relatively increased number of positive LEss to be associated with reduced neuroticism (men: β = -0.501, P < 0.05, women: β = -0.369, P < 0.005) and increased life satisfaction (β = 0.494, P < 0.001) within SS-homozygotes. Within SL-heterozygotes, similar tendencies were found. No associations were detected in LL-homozygotes. Extreme Group comparisons revealed a genotype × LE interaction (F(2,198) = 5.593, P < 0.005), with SS-homozygotes having experienced predominantly positive LEs exhibiting reduced neuroticism (women: F(1,34) = 4.764, P < 0.05; men: F(1,17) = 2.092, P = 0.17), and increased life satisfaction (F(1,53) = 4.057, P < 0.05), as compared to LL-homozygotes having experienced predominantly positive LEs. Our data support the idea that the S-allele of the 5-HTTLPR is associated with an overall increased reactivity to environmental influences, be they positive or negative in nature. These findings constitute a promising add-on to earlier data and support the plasticity hypothesis.
A difficult or undercontrolled temperament, as well as harsh parental discipline or a lack of warmth, has long been regarded as risk factors for the development of externalizing problems. In addition, it has been suggested that children with difficult temperament are especially susceptible to rearing influences. We investigated the impact of early temperament and parenting and their interactions on externalizing behavior at school age.
Participants were 148 boys and 160 girls from a prospective longitudinal study on a high-risk sample. At ages 3 months and 2 years, temperament was assessed by a highly structured parent interview and standardized behavioral observations. Maternal parenting was assessed by videotaped behavioral observation and a parent questionnaire. Externalizing problems at age 8 years were measured by the Child Behavior Checklist.
Using hierarchical linear regression analyses, we found that externalizing problems were predicted by psychosocial adversity and poor self-control, whereas no main effect for restrictive parenting or maternal empathy was found. Fearful-inhibited boys were positively affected by empathic and sensitive parenting, whereas girls who were low in self-control and/or fearful developed less externalizing problems with restrictive parenting.
Our results partly support the differential susceptibility hypothesis. In addition, they point toward gender-specific pathways in the development of externalizing problems.
The aims of this study were to review studies on the molecular genetics of child temperament and prospectively analyze infant temperament as a function of the interaction between infant and mother: 5-HTT, DRD4, and MAO-A functional polymorphisms and the mother's emotional state.
A prospective study of 317 newborns and their mothers was performed. Infant temperament and the mother's anxiety and confidence in caregiving were evaluated at 8 and 32 weeks after childbirth using the Mother and Baby Scale. The mother's emotional state was evaluated using the Edinburgh Postpartum Depression Scale and the State-Trait Anxiety Inventory. These variables were correlated with 5-HTTLPR and Stin2 variants in the 5-HTT gene and the DRD4 variable number tandem repeats Exon 3 and MAO-A variable number tandem repeats genotypes of both the infants and their mothers.
The irritability scores of infants with the 5-HTTLPR s allele showed a linear relationship with their mothers' anxiety of caregiving at 8 (p = .011) and 32 weeks (p = .001), whereas the irritability of infants carrying the HTTLPR ll genotype was independent of their mothers' anxiety.
The review of the literature in this field and the results of this study support that the 5-HTTLPR polymorphism moderates the influence of the mother's anxiety on infant irritability.
Research chronicling links between a polymorphism in the serotonin-transporter gene (5-HTTLPR) and neuroticism has yielded inconsistent results. One possible explanation for this inconsistency is that any gene-phenotype association is obscured by a gene-X-environment (GXE) interaction. We studied a healthy non-clinical sample (N=118) to determine whether the 5-HTTLPR interacts with current life events in predicting neuroticism. The differential-susceptibility hypothesis led to the prediction of such an interaction, reflecting the fact that individuals with short alleles would be affected more by both negative and positive life events than those homozygous for long alleles. Participants completed questionnaires concerning recent life events and neuroticism. The 5-HTTLPR was genotyped using a standard protocol with DNA extracted from oral fluid. For those homozygous for the short allele, more negative life events proved related to greater neuroticism, whereas more positive life events proved related to less neuroticism. No such association emerged in the case of those homozygous for the long allele. Whereas neuroticism is likely to be an especially stable trait in individuals homozygous for the long allele, this may be less so the case for those carrying short alleles.
The current investigation examined the differential susceptibility of parents to the effects of marital quality on changes in parenting. We predicted that parents who were high on the personality constructs Negative Affect and Constraint would be more susceptible to the effects of marital quality on their level of sensitivity. Sensitivity was assessed at 3.5 and 13 months for both mothers and fathers during a triadic interaction. Consistent with the differential susceptibility theory, results suggested that when mothers were high on Negative Affect and when fathers were high on Constraint, their marital quality was associated with changes in sensitivity. This investigation suggests that personality factors may create "vulnerabilities" in parents that make them differentially susceptible to the effects of the family environment on parenting.
A randomized prevention design was used to investigate a moderation effect in the association between a polymorphism in the SCL6A4(5HTT) gene at 5-HTTLPR and increases in youths' risk behavior initiation. Participation in the Strong African American Families (SAAF) program was hypothesized to attenuate the link between 5-HTTLPR status and risk behavior initiation. Youths (N = 641, M age = 11.2 years) were assigned randomly to a SAAF or control condition. Risk behavior initiation across 29 months was linked positively with the 5-HTTLPR genotype and negatively with SAAF participation. Control youths at genetic risk initiated risk behavior at twice the rate of SAAF youths at genetic risk and youths not at genetic risk in either condition.
Inconsistencies regarding developmental effects of non-maternal childcare may be caused by neglecting the possibility that children are differentially susceptible towards such experiences.
Interactions between difficult/negative child temperament and childcare type, quantity, and quality on teacher-rated behavior problems and social competence at 54 months and in kindergarten were investigated via multiple regression using data from the NICHD Study of Early Child Care.
Childcare quality interacted with infant negativity in predicting behavior problems and social competence, whereas effects of quantity and type were independent of child temperament. Consistent with Belsky's (1997) differential susceptibility hypothesis, children with difficult temperaments as infants exhibited both more behavior problems when faced with low quality care and fewer when experiencing high quality care than children with easy temperaments.
Negatively-emotional infants appear to be more affected by the quality of care they experience - both negatively and positively - than other young children.
The research explores the antecedents and consequences of attachment disorganization from a prospective longitudinal perspective. The relations of attachment disorganization/disorientation to endogenous (e.g., maternal medical history, infant temperament) and environmental (e.g., maternal caregiving quality, infant history of abuse) antecedents and to behavioral consequences from 24 months to 19 years are examined. For the 157 participants in the longitudinal study, attachment disorganization was correlated significantly with environmental antecedents (e.g., maternal relationship and risk status, caregiving quality, and infant history of maltreatment), but not with available endogenous antecedents. Infant history of attachment disorganization was correlated with consequent variables related to mother-child relationship quality at 24 and 42 months, child behavior problems in preschool, elementary school and high school, and psychopathology and dissociation in adolescence. Structural models suggest that disorganization may mediate the relations between early experience and later psychopathology and dissociation. The findings are considered within a developmental view of psychopathology, that is, pathology defined in terms of process, as a pattern of adaptation constructed by individuals in their environments.