No full-text available
To read the full-text of this research,
you can request a copy directly from the author.
Gene-environment interaction
... Developmental psychopathologists acknowledge that both biological vulnerabilities and environmental risk factors contribute to adjustment and maladjustment, and that apparent maladaptation can often be understood as adaptation to noxious environmental contexts (e.g., Cicchetti, 2006). This framework emphasizes interactions between individuals and their environments (Rutter & Sroufe, 2000;Sroufe & Rutter, 1984), which occur at multiple levels of analysis, including genetic, epigenetic, neurobiological, familial, and social (Cicchetti, 2007;Cicchetti & Dawson, 2002;Moffitt, Caspi, & Rutter, 2006). This is a transactional approach, as influence flows across all levels of analysis. ...
... Yet, biological vulnerabilities may be equally important. Recent research indicates quite clearly that an individual's genetic constitution may confer risk directly or through interactions with adverse environments (e.g., Caspi et al., 2002;Cicchetti, 2007;Jaffee et al., 2005). ...
... Finally, prevention researchers should evaluate the effects of biological risk and Biology  Environment interactions in predicting longterm treatment outcomes. Such efforts will lead to advances in our understanding of complex disorders, and to refined treatments for subgroups of patients with different etiologies (Cicchetti, 2007; see the following). ...
Most contemporary accounts of psychopathology acknowledge the importance of both biological and environmental influences on behavior. In developmental psychopathology, multiple etiological mechanisms for psychiatric disturbance are well recognized, including those operating at genetic, neurobiological, and environmental levels of analysis. However, neuroscientific principles are rarely considered in current approaches to prevention or intervention. In this article, we explain why a deeper understanding of the genetic and neural substrates of behavior is essential for the next generation of preventive interventions, and we outline 10 specific reasons why considering biological processes can improve treatment efficacy. Among these, we discuss (a) the role of biomarkers and endophenotypes in identifying those most in need of prevention; (b) implications for treatment of genetic and neural mechanisms of homotypic comorbidity, heterotypic comorbidity, and heterotypic continuity; (c) ways in which biological vulnerabilities moderate the effects of environmental experience; (d) situations in which Biology x Environment interactions account for more variance in key outcomes than main effects; and (e) sensitivity of neural systems, via epigenesis, programming, and neural plasticity, to environmental moderation across the life span. For each of the 10 reasons outlined we present an example from current literature and discuss critical implications for prevention.
... Moreover, recent research suggests that genes and environments are interrelated in complex relations that may have special meaning for understanding cross-generation durabilities in parenting behavior. Further, Conger, Belsky and Capaldi (2009) [54] mentioned recent studies by Cicchetti (2007) [57], Reiss and Leve (2007) [58] which investigated the interactions between social processes and specific sequences of DNA related to a wide scope of behavioral and emotional results. Furthermore, Conger, Belsky Alzheimer's Disease & Treatment [54], discussed the work of Sheese, Voelker, Rothbart and Posner (2007) [59] illustrating that specific parenting practices interact with molecular genetic modifications to influence emotions and behaviors of developing children. ...
... Moreover, recent research suggests that genes and environments are interrelated in complex relations that may have special meaning for understanding cross-generation durabilities in parenting behavior. Further, Conger, Belsky and Capaldi (2009) [54] mentioned recent studies by Cicchetti (2007) [57], Reiss and Leve (2007) [58] which investigated the interactions between social processes and specific sequences of DNA related to a wide scope of behavioral and emotional results. Furthermore, Conger, Belsky Alzheimer's Disease & Treatment [54], discussed the work of Sheese, Voelker, Rothbart and Posner (2007) [59] illustrating that specific parenting practices interact with molecular genetic modifications to influence emotions and behaviors of developing children. ...
Karraker and Coleman (2006) [1], extensively discussed that in recent years, research has been invested in expand- ing an understanding of the many individual and environ- mental factors impacting parenting and the influences of the differences in parenting styles on child developmental consequences (Karraker and Coleman, 2006) [1].
When I (Anat) began my psychotherapeutic practice, I worked with children in their natural environment, utilizing the ReachingOut approach, including work with parents as part of the therapeutic process. Early in my practice, I identi- fied that when parents undergo a transformation as part of the process, their children quickly respond to the transfor- mation.
As a result, the change in children’s behavior and well- being was quicker and more efficient than when I worked only with children. Following this as discussed in our previ- ous publications, I concluded that the parent’s involvement in the process was the most significant factor influencing change in children [2].
It is our basic assumption that if we wish to supply the compatible conditions to the specific needs of the child, we should shift the focus from our parenting aspirations which construct our attitudes and behaviors toward the child’s specific individual needs. This shift will force the par- ent to engage in constant internal awareness with regard to the notion that he is always driven by his psychic needs and fantasies which although unconscious may neverthe- less be crucial in guiding his decision-making process. We are therefore suggested to shift towards “conscious parent- ing” in terms of actions and reactions towards the children, based on a decision-making process of choosing the action and reaction which promotes in the best possible way the development of the child with his specific characteristics.
... Moreover, recent research suggests that genes and environments are interrelated in complex relations that may have special meaning for understanding cross-generation durabilities in parenting behavior. Further, Conger, Belsky and Capaldi (2009) [54] mentioned recent studies by Cicchetti (2007) [57], Reiss and Leve (2007) [58] which investigated the interactions between social processes and specific sequences of DNA related to a wide scope of behavioral and emotional results. Furthermore, Conger, Belsky Alzheimer's Disease & Treatment [54], discussed the work of Sheese, Voelker, Rothbart and Posner (2007) [59] illustrating that specific parenting practices interact with molecular genetic modifications to influence emotions and behaviors of developing children. ...
... Moreover, recent research suggests that genes and environments are interrelated in complex relations that may have special meaning for understanding cross-generation durabilities in parenting behavior. Further, Conger, Belsky and Capaldi (2009) [54] mentioned recent studies by Cicchetti (2007) [57], Reiss and Leve (2007) [58] which investigated the interactions between social processes and specific sequences of DNA related to a wide scope of behavioral and emotional results. Furthermore, Conger, Belsky Alzheimer's Disease & Treatment [54], discussed the work of Sheese, Voelker, Rothbart and Posner (2007) [59] illustrating that specific parenting practices interact with molecular genetic modifications to influence emotions and behaviors of developing children. ...
Karraker and Coleman (2006) [1], extensively discussed that in recent years, research has been invested in expanding an understanding of the many individual and environmental factors impacting parenting and the influences of the differences in parenting styles on child developmental consequences (Karraker and Coleman, 2006) [1]. When I (Anat) began my psychotherapeutic practice, I worked with children in their natural environment, utilizing the ReachingOut approach, including working with parents as part of the therapeutic process. Early in my practice, I identified that when parents undergo a transformation as part of the process, their children quickly respond to the transformation. As a result, the change in children’s behavior and well-being was quicker and more efficient than when I worked only with children. Following this as discussed in our previous publications, I concluded that the parent’s involvement in the process was the most significant factor influencing change in children [2]. It is our basic assumption that if we wish to supply the compatible conditions to the specific needs of the child, we should shift the focus from our parenting aspirations which construct our attitudes and behaviors toward the child’s specific individual needs. This shift will force the parent to engage in constant internal awareness with regard to the notion that he is always driven by his psychic needs and fantasies which although unconscious may nevertheless be crucial in guiding his decision-making process. We are therefore suggested to shift towards “conscious parenting” in terms of actions and reactions towards the children, based on a decision-making process of choosing the action and reaction which promotes in the best possible way the development of the child with his specific characteristics.
... Bio-psycho-social approaches that highlight the interplay of the child, parent, family, and other environmental factors are commonly used to depict the complexity of psychopathology during child development (1,2). The Developmental Psychopathology clinical and theoretical framework has widely demonstrated that parents and children often share psychopathological risk (3). ...
... On the other hand, the same studies posited that the mothers of children with DMDD can show poor caregiving capacities. Therefore, we can hypothesize that, consistently with a transactional standpoint, children with DMDD's and their mothers' symptoms could reinforce each other (1). ...
Epigenetic mechanisms, in particular DNA methylation, have been implicated in the etiopathogenesis of psychopathologies in adulthood. The significance of this mechanism in child psychopathologies, however, is much less recognized. Here, we examined whether global DNA methylation alteration was associated with the presence of disruptive mood dysregulation disorder (DMDD) in children. Moreover, in light of the relevance of the interplay between children and parents for the onset and maintaining of psychopathology during development, we measured the association between psychological symptoms, attachment styles, and global DNA methylation levels in healthy and DMDD mother-child dyads (mothers: N = 126, age = 38.3 ± 2.5 years; children: N = 150, age = 8.2 ± 0.9 years, gender ratio [f/m] = 72/78). We did not observe any significant differences in global DNA methylation levels in DMDD children when compared with healthy peers, and children's symptoms did not correlate with variations in this parameter. The mothers showed different levels of psychological symptomatology. Notably, mothers with high psychological symptomatology showed the lowest levels of global DNA methylation. Maternal global DNA methylation levels were associated with maternal hostility, interpersonal sensitivity, psychoticism, and general severity index. Moreover, we found an effect of maternal mental health on the severity of children's symptoms, independently from both maternal and child DNA methylation levels. Despite here DNA methylation does not appear to be involved in the maternal inheritance of vulnerability to depression, this biological link could still arise in later stages of the child's development.
... Second, this design is not able to identify any of the specific genetic variants that contribute to heritability estimates, nor does it identify the environmental experiences that comprise shared and nonshared environmental effects. Finally, these models do not directly index epigenetic processes (Wolffe & Matzke, 1999) or gene-environment interactions (Cicchetti, 2007). ...
... For example, although our results highlight the role of both shared and nonshared environmental factors, we are only able to speculate about the specific environmental variables comprising these effects. In addition, our analyses do not directly index epigenetic processes (Wolffe & Matzke, 1999) or gene-environment interactions (Cicchetti, 2007). Because of the exclusion of epigenetics and gene-environment in-teractions, estimates from traditional biometric models are considered approximations of genetic and environmental effects (McGue, 2010). ...
Decades of research have indicated the foundational importance of parenting to offspring outcomes during childhood and beyond. Unearthing the specific origins of parenting is therefore a critically important research objective. Extant research on this topic has suggested that parenting behaviors are multidetermined (Belsky, 1984) and are associated with a wide range of contextual and familial characteristics (e.g., ethnicity, community, family financial stress), as well as characteristics of the parents (e.g., personality) and their children (e.g., temperament). Behavioral genetic studies have further indicated that parenting behaviors are in fact heritable-that is, individual differences in parenting are at least partially a function of genetic differences between persons. Critically, however, the estimates of these genetic influences have varied dramatically across studies. It is also unclear how factors such as parent gender, child age, and methodological considerations may impact genetic influences on parenting behavior. In the current set of meta-analyses, we sought to quantitatively synthesize twin and adoption studies (n = 56) examining the etiology of parenting behavior, with the goal of more definitively cataloguing genetic and environmental effects on parenting. Results reveal significant effects of parental genetic makeup on parental behavior, but also highlight the genetic makeup of the child as a particularly prominent source of genetic transmission (via evocative gene-environment correlation). Environmental contributions to parenting also emerged as important, including both shared and nonshared environmental effects. Theoretical implications of these findings are discussed. (PsycINFO Database Record (c) 2013 APA, all rights reserved).
... Especially important, recent work suggests that genes and environments are interrelated in complex ways that may have special significance for understanding cross-generation continuities in parenting behavior. One of the most exciting lines of research in recent years has involved the investigation of interactions between social processes and specific patterns of DNA that lead to a wide range of behavioral and emotional outcomes (e.g., see Cicchetti, 2007; Reiss & Leve, 2007). Particularly important are studies demonstrating that specific parenting practices interact with molecular genetic variations to affect the emotions and behaviors of developing children (e.g., Sheese, Voelker, Rothbart, & Posner, 2007). ...
... A second major question involves the identification of Gene Environment interactions that will amplify intergenerational continuity in parenting behaviors that are involved, effective, and supportive of the developing child. Because almost all the Gene Environment interaction research reported to date with humans has focused on the prediction of psychopathology or illness (e.g., Cicchetti, 2007), we have no early evidence to cite in this promising area. However, research on this issue also has great importance for furthering understanding of the intergenerational transmission of parenting and applying this understanding to the development of more effective prevention and intervention programs. ...
The 5 studies in this special section both confirm prior findings regarding the intergenerational transmission of parenting and provide important new evidence regarding the intergenerational transmission of positive parenting and the developmental mediators that seem involved in that transmission. Consistent with earlier research, the findings suggest that harsh parenting in the 1st generation (G1) predicts similar behavior in the 2nd generation (G2) primarily through the exacerbation of G2 conduct problems. In contrast, replicated findings in this set of articles indicate that intergenerational continuities in positive parenting likely stem from the social and academic competencies such parenting engenders in the next generation. In addition, these 5 studies demonstrate that the evidence for intergenerational continuity in parenting is robust across diverse study samples, different types of measurement, different lengths of time, and after the introduction of a variety of control variables. Important next steps in this area of inquiry should include the study of moderator variables that will explain discontinuities as well as continuities in G1 and G2 parenting. Also important will be research on genetic and epigenetic processes that contribute to similarities and dissimilarities in parenting across generations.
... In our study, mothers of children with DMDD, carrying the G allele, showed higher symptoms, so that in those families, we observed youths and mothers (all G carriers) with psychopathological symptoms higher than A/A homozygotes. The biopsychosocial standpoint (Cicchetti, 2007) has documented the fact that the same genetic variation in the OPRM1 could explain some of the phenotypic variance observed in children and in mothers, suggesting that children's and mothers' emotional/behavioral functioning could have coadapted, giving rise to a familiar problematic configuration with a significant psychopathological risk. ...
The A118G single nucleotide polymorphism (SNP) of the μ-opioid receptor gene, with high expression of the A allele and low expression of the G allele, has been associated with emotional/behavioral dysregulation and depressive disorders and is recognized as a mediator of affiliative behavior. This study compared a sample of healthy children and their mothers with a sample of children with disruptive mood regulation disorder and their mothers, evaluating whether insecure attachment and psychopathological symptoms are associated with A allele- or G allele-carrying mothers and children and whether caregiving capacities are associated with A allele- or G allele-carrying mothers.
An insecure attachment style was more frequent in mothers and children carrying the G allele (G/G + A/G genotypes). In the clinical sample, G allele-carrying children scored higher than homozygous A/A ones on the subscales of Withdrawal and Conduct Problems. G-carrying mothers showed higher interpersonal sensitivity, depression, hostility, and paranoid ideation and provided less care than A/A mothers.
This study offers new insights into the associations between the A118G SNP of the μ-opioid receptor gene and emotional/behavioral functioning, attachment style in children, and psychopathology and caregiving ability in mothers.
... Even though the link between trauma, human development, and subsequent lifespan adaptation has long been established, a focus on child health policy formation [8][9][10][11][12][13][14][15][16][17][18] to guide the development of trauma-informed and trauma-focused intervention is only beginning to take shape as a standard of care in mental health systems. 19 Although many regional institutions in Canada are moving toward developing policies, guidelines, and education, implementation at the level of patient care lags. ...
Context:
There is a movement toward trauma-informed, trauma-focused psychiatric treatment.
Objective:
To examine Adverse Childhood Experiences (ACE) survey items by sex and by total scores by sex vs clinical measures of impairment to examine the clinical utility of the ACE survey as an index of trauma in a child and adolescent mental health care setting.
Design:
Descriptive, polychoric factor analysis and regression analyses were employed to analyze cross-sectional ACE surveys (N = 2833) and registration-linked data using past admissions (N = 10,400) collected from November 2016 to March 2017 related to clinical data (28 independent variables), taking into account multicollinearity.
Results:
Distinct ACE items emerged for males, females, and those with self-identified sex and for ACE total scores in regression analysis. In hierarchical regression analysis, the final models consisting of standard clinical measures and demographic and system variables (eg, repeated admissions) were associated with substantial ACE total score variance for females (44%) and males (38%). Inadequate sample size foreclosed on developing a reduced multivariable model for the self-identified sex group.
Conclusion:
The ACE scores relate to independent clinical measures and system and demographic variables. There are implications for clinical practice. For example, a child presenting with anxiety and a high ACE score likely requires treatment that is different from a child presenting with anxiety and an ACE score of zero. The ACE survey score is an important index of presenting clinical status that guides patient care planning and intervention in the progress toward a trauma-focused system of care.
... However, current progress in molecular genetics, while emphasising the pervasive influence of 'gene x environment' interactions, points to a kind of genetic probability rather than genetic determinism. Genes, in fact, do not work in isolation but influence the extent to which organisms are responsive to particular environments (Cicchetti, 2007). Thus, one may presume that genes account for a certain predisposition towards conservative or liberal ideologies, but environmental considerations are crucial in turning this into stable preferences and behavioural tendencies. ...
... By suggesting that both genetic and environmental factors combine to explain variability in brain function for selective attention in children from lower SES backgrounds, these lines of research led to a broader question: To what extent might environmental experiences interact with or serve to alter genetic associations with brain function? Advances in molecular genetics now permit the investigation of interactions between gene polymorphisms and specific environmental factors, i.e., gene × environment interactions (44)(45)(46)(47). Although the majority of the studies assessing gene × environment interactions are correlational in design (i.e., they rely on naturally occurring variation in environments), a growing body of work uses randomized, controlled trial studies to experimentally manipulate environmental factors (48)(49)(50)(51). ...
Significance
Selective attention is the ability to select and preferentially process specific information while simultaneously suppressing the processing of irrelevant, competing distractors. It is a fundamental ability linked to various cognitive skills and academic achievement. We describe the foundations and history of our research program, which spans from basic research on neural mechanisms and neuroplasticity of selective attention to translational research aimed at designing interventions to improve selective attention. We also present preliminary evidence for gene × intervention interactions in neural mechanisms of selective attention in children from lower socioeconomic status backgrounds. This program of research demonstrates the marked malleability of neural systems for selective attention and highlights the potential for changes in selective attention as a function of intervention.
... Contemporary developmental theories acknowledge and incorporate the contributions of biologically informed research. A framework that emphasizes the interactions between individuals and their environments (Rutter & Sroufe, 2000), which occur at multiple levels of analysis, including genetic, epigenetic, neurobiological, familial, and social (Cicchetti, 2007;Moffitt, Caspi, & Rutter, 2006) permits a conceptualization of maladaptation as an adaptation to noxious environmental contexts. In this transactional approach, family environments, social conditions, and psychological processes all affect biological processes, and biological functioning and predispositions influence the ways in which an individual selects and shapes the environment (Rutter, 2007). ...
... Moreover, this integration must include multiple levels of analysis (e.g., genetics, molecular neurobiology, brain function, cognitive-affective performance, symptoms, and disorders) in order to tease apart the many pathways to disorder versus health (Cicchetti & Blender, 2004;Cicchetti & Dawson, 2002;Masten, 2007). This dissertation builds on the perspectives set forth in prior work, which emphasized a developmental, multi-level approach to the study of psychopathology (e.g., Cicchetti, 2007;Cicchetti & Blender, 2004;Monk, 2008). Additionally, our framework incorporates the concept of transactional models and acknowledges the bidirectional effects between levels of analysis (Sameroff, 2010). ...
The development of socio-emotional functioning is a complex process that occurs over a protracted time period and requires coordinating affective, cognitive, and social faculties. At many points in development, the trajectory of socio-emotional development can be deleteriously altered due to a combination of environmental insults and individual vulnerabilities. The result can be psychopathology. However, researchers are just beginning to understand the neural and genetic mechanisms involved in the development of healthy and disordered socio-emotional functioning. In this dissertation, I propose a translational developmental neuroscience framework to understand socio-emotional functioning in both healthy and disordered populations. I then apply this framework to healthy socio-emotional development and autism spectrum disorders, selectively reviewing current literature in light of the framework. Next, three pieces of original research serve as examples of research on socio-emotional functioning in autism spectrum disorders guided by the framework: The first study examines the influence of a genetic variant (5-HTTLPR) on habituation of a socio-emotionally relevant brain structure, the amygdala, in autism spectrum disorders. The second study compares interactions of the amygdala with other areas in the brain in the context of a socio-emotional task and in the absence of a task in autism spectrum disorders. The third study examines the influence of the same genetic variant on another socially-relevant brain network, the default network. Lastly, I examine ways that the framework can help to identify future directions of research on socio-emotional development.
... Des avancées conceptuelles notables ont également été opérées : les chercheurs ont pleinement pris en compte la nature probabiliste, systémique et contextuelle des phénomènes psychopathologiques (Cicchetti, 2007b ;Masten, 2007 Rothbart & Bates, 2006). Un numéro entier de la revue Development and Psychopathology était récemment dédié à cette thématique (Cicchetti, 2007a). Notre connaissance croissante du fonctionnement cérébral et les régulières démonstrations du fait que le développement du cerveau est guidé par l'expérience militent pour de tels efforts intégratifs. ...
Anorexia nervosa is part of a continuum of eating disorders and body image disorders now very common in adolescence. Thin ideal and body dissatisfaction which affects most of adolescent females are precursors to the onset of a morbid process which may lead to the most serious forms of anorexia which are generally the ones that clinicians see. Community-based epidemiological studies of eating disorders in adolescents have shown that anorexia and subclinical anorexia might recover spontaneously but that they may be associated with an elevated risk for a broad range of physical and mental health problems during early adulthood. Severe forms of anorexia usually require hospitalization but individual and familial outpatient therapies have proved to be effective for less severe forms.
... Those concerned primarily with environmental features of development have become interested in gene-environment interaction (e.g., Belsky, Bakermans-Kranenburg, & van IJzendoorn, 2007), whereas those interested in biological bases of behavior or temperament have become concerned with the modifying role of environmental features (e.g., Rothbart & Bates, 2006). Recently, an entire issue of Development and Psychopathology was devoted to gene-environment interaction (Cicchetti, 2007a). Our expanding knowledge of brain functioning and the clear demonstrations of experiencedependent brain development support such integrative efforts. ...
So important is the perspective of development for understanding psychopathology that it spawned a new discipline-"developmental psychopathology"-which has seen remarkable advances since its introduction,, but has yet to completely fulfill its promise. To do this requires maintaining a thoroughgoing developmental perspective. When we take development seriously, there are implications for how we understand psychopathology, describe and conceptualize the origins and course of disorder, and interpret research findings. From this perspective, disorders are complex products of development; for example, we can view neurophysiological associates of disorder not as causes but as markers, the development of which we need to understand. Research on developmental psychopathology requires an examination of the history of problem behavior from early in life, and it unites multiple features of adaptation and maladaptation (contextual, experiential, physiological, and genetic).
... Research on the interplay between genes and environment is especially promising (Rutter, Moffitt, & Caspi, 2006). One approach would be to test potential moderating environmental effects on genetic expression (GeneÂEnvironment interaction; for a discussion of gene–environment interactions and developmental psychopathology, see Cicchetti, 2007 ). This would allow researchers to test whether a certain genotype makes children vulnerable to develop narcissistic personalities, but only so in the context of specific environmental stresses (e.g., dysfunctional parenting practices). ...
Narcissism is a dynamic form of personality characterized by a pervasive sense of grandiosity and self-importance, and by a need to obtain continuous self-validation from others. Very little is known about its etiology and development. What factors (e.g., temperament, parenting experiences) and processes (e.g., transactions between these factors over time) cause some children to become more narcissistic than others? When does narcissism first emerge, and how does narcissism develop over time? This article describes a framework for research on the etiology and development of narcissism, and recommends ten research priorities. This research should yield fundamental knowledge and should inform intervention efforts to minimize the negative impact narcissistic individuals have on themselves and on others.
Przedstawione zostały kluczowe dla opracowania konstrukcje teoretyczne: resiliencja indywidualna, resiliencja rodziny i przystosowanie szkolne. Indywidualna resiliencja została zoperacjonalizowana za pomocą trzech wskaźników: pozytywnej koncepcji własnej osoby, kompetencji emocjonalnej i społecznej oraz samokontroli/samoregulacji. Resiliencja rodzinna była mierzona jednowymiarową skalą, opisującą integrację i funkcjonalność wychowawczą rodziny. Przystosowanie szkolne było mierzone za pomocą trzech wskaźników: stres szkolny, sukces szkolny i asertywność w szkole. Próba liczyła 130 uczniów w wieku 17–18 lat. Analiza ścieżek (path analysis) wykazała, że resiliencja rodziny może wpływać na przystosowanie szkolne uczniów bezpośrednio oraz za pośrednictwem indywidualnej resiliencji.
Introduction - Developmental psychology and psychopathology : a mutual enrichment
On behalf of the research center Psycle (Psychology of Cognition, Language and Emotion Laboratory, Aix-Marseille University, France) in Aix-en-Provence, the tenth edition of the Ripsydeve colloquium was devoted to the transfer of knowledge “From research to practice”. The focus aimed at examining practice at the light of the most recent research results and at analyzing how research can be influenced by field questions. The rich reciprocal influence between research and practice that characterizes developmental psychology can be found also in developmental psychopathology: hence the second focus of the colloquium was “studies in developmental psychology and psychopathology”. To investigate autism, individual developmental trajectory is a central notion that allows to take into account the variety of clinical symptoms around a common hub, and the life-long variability of developmental profiles under the influence of interactions between endogeneous, exogeneous and experiential factors. Crosslinking studies on typical and atypical development allows us to keep in mind a dynamic representation of development and to measure the importance of reading the atypical trajectories in the framework of general developmental models.
We propose a dimensional model of personality disturbance in which personality pathology develops as an emergent product defined by extreme values on interacting subsets of several major personality traits. Being at the extreme ends of the continua described in this model has marked effects on the threshold for eliciting those traits under stimulus conditions: marked effects on the extent to which the environment affects the neurobiological functioning underlying the traits. To explore the nature of development of extreme values on these traits, each trait is discussed in terms of three major issues: (1) the neurobiological variables associated with the trait; (2) individual variation in this neurobiology as a function of genetic polymorphisms; and (3) the effects of environmental adversity on these neurobiological variables through the action of epigenetic processes. It is noted that gene–environment interaction appears to be dependent on two main factors: (1) both genetic and environmental variables appear to have the most profound and enduring effects when they exert their effects during early postnatal periods, times when the forebrain is undergoing exuberant experience-expectant dendritic and axonal growth; and (2) environmental effects on neurobiology are strongly modified by individual differences in trait-like functioning of neurobiological variables. We present this model of the development of personality disturbance for its heuristic potential as an organizing framework for understanding personality disturbance, one that emphasizes the interaction between environmental and neurobiological variables in the development of this form of psychopathology.
This chapter reviews origins and progress in resilience science, with an emphasis on progress over the past decade in theory, findings, and translational applications for strategic intervention. In alignment with prevailing concepts in developmental systems theory, human resilience is defined as the potential or manifested capacity of an individual to adapt successfully through multiple processes to experiences that threaten his or her function, survival, or development. Resilience pathways, developmental cascades, gene-environment interactions, and other models salient in current resilience theory are delineated, including new approaches to testing resilience-related processes in such models. Findings on promotive and protective effects are discussed, focusing on widely replicated adaptive processes that develop in children, their families, other relationships, and key contexts as children develop. Resilience processes involving families, schools, peers, culture, and other socioecological systems are highlighted. Genetic and neurobiological processes are reviewed as a growingedge of resilience science. Intervention research based on resilience theory is discussed, together with translational implications for practice and policy based on the expanding body of knowledge about resilience processes. The chapter concludes with a review of enduring controversies, a summary of progress, and directions for the future.
Keywords:
resilience;
intervention;
risk;
adaptation;
adversity;
competence;
protective;
stress;
promotive;
stress inoculation
Background: It is uncertain how stressful life events, social support networks and psychological defense mechanisms interact with each other to ameliorate or exacerbate the impairment in social functioning experienced by patients with a diagnosis of social phobia. Objective: Compare the relationship of stress, social support and defense mechanisms between patients with social phobia and normal control subjects. Methods: 38 newly diagnosed patients with social phobia seen at the Zi Lang Hospital in Nantong between October 2009 and August 2010 were administered a Life Event Scale, the Social Support Rating Scale and the Defense Style Questionnaire. The results were compared with those for 38 normal controls. Results: There were no differences in the in the numbers of positive and negative life events between the two groups but the psychological impact of both positive and negative life events on the social phobia group were significantly greater than on the control group. Based on the results of the Social Support Rating Scale the mean (SD) scores of objective support, subjective support, total support and utilization of social support in the social phobia group were all significantly lower than those in the control group. Results of the Defense Style Questionnaire showed that compared to the control group the total score for immature defenses was significantly higher (i.e., respondents were more likely to report using these defenses) and the total score for the mature defenses was significantly lower in the social phobia group. The social phobia group was significantly more likely to report using the neurotic defenses of repression, avoidance, isolation, and increased social association but significantly less likely to report using the neurotic defenses of reaction formation, denial, and anticipation. Conclusion: Differential patterns of life events do not appear to be important in the etiology of social phobia. Compared to normal control subjects, patients with social phobia have a less developed social support network, are less likely to use available social support and are more likely to employ immature defense mechanisms. Copyright © 2011 by Editorial Department of Shanghai Archives of Psychiatry.
The Psychology of Politicians explores a topic which fuels public and media debate yet is under-researched and has potentially far-reaching consequences for the success of our political systems. Focusing on research with democratically elected representatives from the UK, Poland and Italy, and on the political behaviour of a former US President and voters' perceptions in the emerging democracy of Ukraine, this book is packed with psychological insights. Using quantitative and qualitative methodologies, the contributors chart the progress of the individual politician from selection as a candidate to becoming established in Parliament examining their qualities as communicators, thinkers and leaders. The impact of work and non-work pressures on their mental well-being and capacity to handle a crisis are probed and the roles of personality traits in politicians' values and in public perceptions of our elected representatives are highlighted.
So important is the perspective of development for understanding psychopathology that it spawned a new discipline — “developmental psychopathology” — which has seen remarkable advances since its introduction but has yet to completely fulfill its promise. To do this requires maintaining a thoroughgoing developmental perspective. When development is taken seriously, there are implications for how to understand psychopathology, describe and conceptualize the origins and course of disorder, and interpret research findings. From this perspective, disorders are complex products of development; for example, neurophysiological associates of disorder can be viewed not as causes but as markers, the development of which needs to be understood. Research on developmental psychopathology requires an examination of the history of problem behavior from early in life, and it unites multiple features of adaptation and maladaptation (contextual, experiential, physiological, and genetic).
The development of socioemotional functioning is a complex process that occurs over a protracted time period and requires coordinating affective, cognitive, and social faculties. At many points in development, the trajectory of socioemotional development can be deleteriously altered due to a combination of environmental insults and individual vulnerabilities. The result can be psychopathology. However, researchers are just beginning to understand the neural and genetic mechanisms involved in the development of healthy and disordered socioemotional functioning. We propose a translational developmental neuroscience framework to understand the transactional process that results in socioemotional functioning in both healthy and disordered populations. We then apply this framework to healthy socioemotional development, pediatric anxiety, pediatric depression, and autism spectrum disorder, selectively reviewing current literature in light of the framework. Finally, we examine ways that the framework can help to frame future directions of research on socioemotional development and translational implications for intervention.
A developmental psychopathology framework for conducting research on high-risk conditions and mental disorders across the life course is presented. After an account of its historical underpinnings, the interdisciplinary field of developmental psychopathology is described. Next, the definitional parameters and principles of developmental psychopathology are discussed and illustrations of these tenets are provided through examples from a number of high-risk conditions and mental disorders across the life span. Research on the genetic, neurobiological, and psychological correlates and sequelae of child maltreatment is used as an exemplar of a multiple-levels-of-analysis approach to investigating the development of psychopathology. Likewise, research demonstrates the psychological and biological determinants of resilience—the achievement of competent functioning despite the experience of significant adversity. This multilevel research is beginning to be translated into the development and implementation of prevention and intervention programs that hold promise for significantly strengthening our capacity to decrease the burden of mental illness for individuals, families, and society.
The patient population of borderline personality disorder (BPD) is heterogeneous; many different combinations of BPD symptoms can lead to a BPD diagnosis. We investigated to what extent the covariance among four main components of BPD is explained by shared genetic and environmental factors. Using an extended twin design, multivariate genetic models were applied to the scales of the PAI-BOR, a self-report questionnaire tapping four main features of BPD (affective instability, identity problems, negative relationships, and self-harm). Data on the four BPD scales were available for 5,533 twins and 1,202 siblings from the Netherlands, Belgium, and Australia. The correlations among the scales ranged from 0.23 to 0.50 and were best explained by a genetic common pathway model. This model specifies that genes and environment influence the covariance between four main features of BPD in qualitatively similar ways, through a single latent factor representing the BPD construct. The heritability of the latent BPD factor was 51% and the remainder of its variance was explained by unique environmental influences. For each BPD scale, except self-harm, around 50% of its variance was explained by the latent BPD factor. The remaining variance for each of the four scales was explained by genetic (4% for affective instability to 20% for self-harm) and environmental (38% for negative relationships to 67% for self-harm) factors that were specific to each scale.
A dimensional model of personality disturbance is presented that is defined by extreme values on interacting subsets of seven major personality traits. Being at the extreme has marked effects on the threshold for eliciting those traits under stimulus conditions: that is, the extent to which the environment affects the neurobiological functioning underlying the traits. To explore the nature of development of extreme values on these traits, each trait is discussed in terms of three major issues: (a) the neurobiological variables associated with the trait, (b) individual variation in this neurobiology as a function of genetic polymorphisms, and (c) the effects of environmental adversity on these neurobiological variables through the action of epigenetic processes. It is noted that gene-environment interaction appears to be dependent on two main factors: (a) both genetic and environmental variables appear to have the most profound and enduring effects when they exert their effects during early postnatal periods, times when the forebrain is undergoing exuberant experience-expectant dendritic and axonal growth; and (b) environmental effects on neurobiology are strongly modified by individual differences in "traitlike" functioning of neurobiological variables. A model of the nature of the interaction between environmental and neurobiological variables in the development of personality disturbance is presented.
Even though generalized anxiety disorder (GAD) is one of the most common of the anxiety disorders, relatively little is known about its precursors. Bowlby's attachment theory provides a framework within which these precursors can be considered. According to Bowlby, adult anxiety may be rooted in childhood experiences that leave a child uncertain of the availability of a protective figure in times of trouble.Furthermore, adult "current state of mind with respect to attachment" is thought to relate to adult anxiety. Both attachment-related components were assessed with 8 subscales of the Perceptions of Adult Attachment Questionnaire(PAAQ). Clinically severe GAD clients who were about to begin therapy reported experiencing less maternal love in childhood, greater maternal rejection/neglect, and more maternal role-reversal/enmeshment than did control participants.In keeping with a cumulative risk model, risk for GAD increased as indices of poor childhood attachment experience increased. GAD clients, in contrast to controls,also reported greater current vulnerability in relation to their mothers as well as more difficulty accessing childhood memories. Logistic regression analyses revealed that elevations on PAAQ subscales could significantly predict GAD vs.non-GAD status. Results and the implications for advancing the theory and treatment of GAD are discussed.
Associations between a functional polymorphism in the serotonin transporter gene and amygdala activation have been found in healthy, depressed, and anxious adults. This study explored these gene-brain associations in adolescents by examining predictive effects of serotonin transporter gene variants (S and L(G) allele carriers vs. L(A) allele homozygotes) and their interaction with diagnosis (healthy vs. patients) on amygdala responses to emotional faces.
Functional magnetic resonance data were collected from 33 healthy adolescents (mean age: 13.71, 55% female) and 31 medication-free adolescents with current anxiety or depressive disorders (or both; mean age: 13.58, 56% female) while viewing fearful, angry, happy, and neutral facial expressions under varying attention states.
A significant three-way genotype-by-diagnosis-by-face-emotion interaction characterized right amygdala activity while subjects monitored internal fear levels. This interaction was decomposed to map differential gene-brain associations in healthy and affected adolescents. First, consistent with healthy adult data, healthy adolescents with at least one copy of the S or L(G) allele showed stronger amygdala responses to fearful faces than healthy adolescents without these alleles. Second, patients with two copies of the L(A) allele exhibited greater amygdala responses to fearful faces relative to patients with S or L(G) alleles. Third, although weaker, genotype differences on amygdala responses in patients extended to happy faces. All effects were restricted to the fear-monitoring attention state.
S/L(G) alleles in healthy adolescents, as in healthy adults, predict enhanced amygdala activation to fearful faces. Contrary findings of increased activation in patients with L(A)L(A) relative to the S or L(G) alleles require further exploration.
There is much curiosity about interactions between genes and environmental risk factors for psychopathology, but this interest is accompanied by uncertainty. This article aims to address this uncertainty. First, we explain what is and is not meant by gene-environment interaction. Second, we discuss reasons why such interactions were thought to be rare in psychopathology, and argue instead that they ought to be common. Third, we summarize emerging evidence about gene-environment interactions in mental disorders. Fourth, we argue that research on gene-environment interactions should be hypothesis driven, and we put forward strategies to guide future studies. Fifth, we describe potential benefits of studying measured gene-environment interactions for basic neuroscience, gene hunting, intervention, and public understanding of genetics. We suggest that information about nurture might be harnessed to make new discoveries about the nature of psychopathology.
© 2006 Association for Psychological Science.
This paper presents a critical appraisal of resilience, a construct connoting the maintenance of positive adaptation by individuals despite experiences of significant adversity. As empirical research on resilience has burgeoned in recent years, criticisms have been levied at work in this area. These critiques have generally focused on ambiguities in definitions and central terminology; heterogeneity in risks experienced and competence achieved by individuals viewed as resilient; instability of the phenomenon of resilience; and concerns regarding the usefulness of resilience as a theoretical construct. We address each identified criticism in turn, proposing solutions for those we view as legitimate and clarifying misunderstandings surrounding those we believe to be less valid. We conclude that work on resilience possesses substantial potential for augmenting the understanding of processes affecting at-risk individuals. Realization of the potential embodied by this construct, however, will remain constrained without continued scientific attention to some of the serious conceptual and methodological pitfalls that have been noted by skeptics and proponents alike.
Social and biological explanations traditionally have been cast as incompatible, but advances in recent years have revealed a new view synthesized from these 2 very different levels of analysis. The authors review evidence underscoring the complementing nature of social and biological levels of analysis and how the 2 together can foster understanding of the mechanisms underlying complex behavior and the mind. Specifically, they review the utility of considering social influences on biological processes that are often viewed as outside the social domain including genetic constitution, gene expression, disease, and autonomic, neuroendocrine, and immune activity. This research underscores the unity of psychology and the importance of retaining multilevel integrative research that spans molar and molecular levels of analysis. Especially needed in the coming years is more research on the mechanisms linking social and biological events and processes.
The end of the last millennium witnessed an unprecedented degree of public awareness regarding mental disorder as well as motivation for policy change. Like Sartorius, we contend that the continued stigmatization of mental illness may well be the central issue facing the field, as nearly all attendant issues (e.g., standards of care, funding for basic and applied research efforts) emanate from professional, societal, and personal attitudes towards persons with aberrant behavior. We discuss empirical and narrative evidence for stigmatization as well as historical trends regarding conceptualizations of mental illness, including the field's increasing focus on genetic and neurobiological causes and determinants of mental disorder. We next define stigma explicitly, noting both the multiple levels (community, societal, familial, individual) through which stigma operates to dehumanize and delegitimize individuals with mental disorders and the impact of stigma across development. Key developmental psychopathology principles are salient in this regard. We express concern over the recent oversimplification of mental illness as "brain disorder," supporting instead transactional models which account for the dynamic interplay of genes, neurobiology, environment, and self across development and which are consistent with both compassion and societal responsibility. Finally, we consider educational and policy-related initiatives regarding the destigmatization of mental disorder. We conclude that attitudes and policy regarding mental disorder reflect, in microcosmic form, two crucial issues for the next century and millennium: (a) tolerance for diversity (vs. pressure for conformity) and (b) intentional direction of our species' evolution, given fast-breaking genetic advances.
Genomics and neuroscience, 2 areas of science fundamental to psychiatry, have undergone revolutionary changes in the past 20 years. Yet methods of diagnosis and treatment for patients with mental disorders have remained relatively unchanged. Indeed, during the same time, the public health burden of mental disorders has grown alarmingly. Mental disorders are now among the largest sources of medical disability worldwide1 and, like AIDS and cancer, they are urgent and deadly.2,3
The study of resilience has two core characteristics: it is fundamentally applied in nature, seeking to use scientific knowledge to maximize well-being among those at risk, and it draws on expertise from diverse scientific disciplines. Recent advances in biological processes have confirmed the profound deleterious effects of harsh caregiving environments, thereby underscoring the importance of early interventions. What remains to be established at this time is the degree to which insights on particular biological processes (e.g., involving specific brain regions, genes, or hormones) will be applied in the near future to achieve substantial reductions in mental health disparities. Aside from biology, resilience developmental researchers would do well to draw upon relevant evidence from other behavioral sciences as well, notably anthropology as well as family, counseling, and social psychology. Scientists working with adults and with children must remain vigilant to the advances and missteps in each others' work, always ensuring caution in conveying messages about the "innateness" of resilience or its prevalence across different subgroups. Our future research agenda must prioritize reducing abuse and neglect in close relationships; deriving the "critical ingredients" in effective interventions and going to scale with these; working collaboratively to refine theory on the construct; and responsibly, proactively disseminating what we have learned about the nature, limits, and antecedents of resilient adaptation across diverse at-risk groups.
The author begins by providing a brief historical perspective on the ways in which brain-behavior relations have been viewed in the field of developmental psychology. He then examines some of the changing theoretical perspectives, empirical discoveries, and technological advances that have played a major role in rejuvenating scientific interest in investigating the relations between neurobiological and behavioral development in normal persons and in individuals who are at high risk for, or who have, mental disorders. Next, the author provides a historical and present-day perspective on normal brain development on humans. In the penultimate section of the chapter, schizophrenia disorders are used to elucidate insights that can be gained on normal brain development from psychopathology, as well as to illustrate how knowledge of normal neural development can provide important insights into the genesis and epigenesis of this serious mental disorder. Finally, the author concludes by proferring future interdisciplinary research directions. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Genes associated with behavioral dimensions and disorders are beginning to be identified. Although it is difficult and expensive to find genes associated with behavior, it is relatively easy and inexpensive to use genes that have already been identified. We describe how genes are found, but the main goal of this article is to outline what developmentalists can do with genes once they are found and, hence, to encourage the use of DNA markers in developmental research. We suggest that genes can be used to answer questions about developmental continuities, about psychopathological patterns, and about environmental risk mechanisms. Developmental questions include the causal mechanisms involved in heterotypic continuity. Questions on psychopathological patterns address heterogeneity (Do gene-behavior associations apply to disorders or to separate components representing risk or protective factors?), comorbidity (Are gene-behavior associations diagnosis-specific?), and the links between normality and disorder (Does a gene-behavior association for a disorder extend to related dimensions of normal variation and vice versa?). Questions about environmental risk mechanisms are informed by study of gene-environment interaction (Are individuals who are at genetic risk more sensitive to specific psychosocial risks?) and gene-environment correlation (Are individuals who are at genetic risk more likely to be exposed to psychosocial risk?).
The authors predict that in a few years, many areas of psychology will be awash in specific genes responsible for the widespread influence of genetics on behavior. As the focus shifts from finding genes (genomics) to understanding how genes affect behavior (behavioral genomics), it is important for the future of psychology as a science that pathways between genes and behavior be examined not only at the molecular biological level of cells or the neuroscience level of the brain but also at the psychological level of analysis. After a brief overview of quantitative genetic research, the authors describe how genes that influence complex traits like behavioral dimensions and disorders in human and nonhuman animals are being found. Finally, the authors discuss behavioral genomics and predict that DNA will revolutionize psychological research and treatment early in the 21st century.
The focus of this article is on the interface between research on resilience-a construct representing positive adaptation despite adversity--and the applications of this work to the development of interventions and social policies. Salient defining features of research on resilience are delineated, as are various advantages, limitations, and precautions linked with the application of the resilience framework to developing interventions. For future applied efforts within this tradition, a series of guiding principles are presented along with exemplars of existing programs based on the resilience paradigm. The article concludes with discussions of directions for future work in this area, with emphases on an enhanced interface between science and practice, and a broadened scope of resilience-based interventions in terms of the types of populations, and the types of adjustment domains, that are encompassed.
The genetic influences on behavior are even more difficult to tease out than the genetic bases of complex diseases. But
McGuffin
et al.
discuss how the ultimate availability of the complete genome sequences of many individuals will offer a solution to this problem.
The sequencing of the human genome has opened the door to obtaining extensive maps of markers for single nucleotide variations
among people. This information will allow the use of allelic association, a method for identifying the genes that contribute
to variations in behavior among people and to complex behavioral disorders.
There has been substantial evidence for more than three decades that the major psychiatric illnesses such as schizophrenia, bipolar disorder, autism, and alcoholism have a strong genetic basis. During the past 15 years considerable effort has been expended in trying to establish the genetic loci associated with susceptibility to these and other mental disorders using principally linkage analysis. Despite this, only a handful of specific genes have been identified, and it is now generally recognized that further advances along these lines will require the analysis of literally hundreds of affected individuals and their families. Fortunately, the emergence in the past three years of a number of new approaches and more effective tools has given new hope to those engaged in the search for the underlying genetic and environmental factors involved in causing these illnesses, which collectively are among the most serious in all societies. Chief among these new tools is the availability of the entire human genome sequence and the prospect that within the next several years the entire complement of human genes will be known and the functions of most of their protein products elucidated. In the meantime the search for susceptibility loci is being facilitated by the availability of single nucleotide polymorphisms (SNPs) and by the beginning of haplotype mapping, which tracks the distribution of clusters of SNPs that segregate as a group. Together with high throughput DNA sequencing, microarrays for whole genome scanning, advances in proteomics, and the development of more sophisticated computer programs for analyzing sequence and association data, these advances hold promise of greatly accelerating the search for the genetic basis of most mental illnesses while, at the same time, providing molecular targets for the development of new and more effective therapies.
Endophenotypes, measurable components unseen by the unaided eye along the pathway between disease and distal genotype, have emerged as an important concept in the study of complex neuropsychiatric diseases. An endophenotype may be neurophysiological, biochemical, endocrinological, neuroanatomical, cognitive, or neuropsychological (including configured self-report data) in nature. Endophenotypes represent simpler clues to genetic underpinnings than the disease syndrome itself, promoting the view that psychiatric diagnoses can be decomposed or deconstructed, which can result in more straightforward-and successful-genetic analysis. However, to be most useful, endophenotypes for psychiatric disorders must meet certain criteria, including association with a candidate gene or gene region, heritability that is inferred from relative risk for the disorder in relatives, and disease association parameters. In addition to furthering genetic analysis, endophenotypes can clarify classification and diagnosis and foster the development of animal models. The authors discuss the etymology and strategy behind the use of endophenotypes in neuropsychiatric research and, more generally, in research on other diseases with complex genetics.
The Human Genome Project has been the first major foray of the biological and medical research communities into “big science.” In this Viewpoint, we present some of our experiences in organizing and managing such a complicated, publicly funded, international effort. We believe that many of the lessons we learned will be applicable to future large-scale projects in biology.
Empirical investigations of resilience over the past 30 years have examined a wide range of psychosocial correlates of, and contributors to, this phenomenon. Thus far, theoretical treatments of resilience have focused almost exclusively on psychosocial levels of analysis to derive explanatory models. However, there have been no formal discussions of either theory or research that have examined the biological contributors to, or correlates of, competent functioning despite the experience of adversity. This paper seeks to fill this gap and sets forth a preliminary theoretical framework and outline of empirical strategies for studying the biological underpinnings of resilience. The initial sections of the paper discuss the particular suitability of a transactional organizational theoretical perspective as a conceptual foundation for including a biological level of analysis within the extant theoretical framework of resilience. Subsequently, other important theoretical considerations for the inclusion of a biological perspective on resilience are discussed, including the avoidance of an approach that would reduce resilience to merely a biological process, the application of the constructs of multifinality and equifinality to a biological perspective on resilience, as well as a general discussion of the potential for utilization of brain imaging and other technologies in the study of resilience. The possible relation between the mechanisms of neural plasticity and resilience are examined in some detail, with specific suggestions concerning research questions needed to examine this association. Sections of the paper discuss the likely relation of several areas of brain and biological functioning with resilience, including emotion, cognition, neuroendocrine and immune functioning, and genetics. The paper concludes with a discussion of the implications of a biological perspective on resilience for preventive interventions.
Advances in genotyping and sequencing technologies, coupled with the development of sophisticated statistical methods, have afforded investigators novel opportunities to define the role of sequence variation in the development of common human diseases. At the forefront of these investigations is the use of dense maps of single-nucleotide polymorphisms (SNPs) and the haplotypes derived from these polymorphisms. Here we review basic concepts of high-density genetic maps of SNPs and haplotypes and how they are typically generated and used in human genetic research. We also provide useful examples and tools available for researchers interested in incorporating haplotypes into their studies. Finally, we discuss the latest concepts for the analysis of haplotypes related to human disease, including haplotype blocks, the International HapMap Project, and the future directions of these resources.
Adaptation is a central organizing principle throughout biology, whether we are studying species, populations, or individuals. Adaptation in biological systems occurs in response to molar and molecular environments. Thus, we would predict that genetic systems and nervous systems would be dynamic (cybernetic) in contrast to previous conceptualizations with genes and brains fixed in form and function. Questions of nature versus nurture are meaningless, and we must turn to epigenetics--the way in which biology and experience work together to enhance adaptation throughout thick and thin. Defining endophenotypes--road markers that bring us closer to the biological origins of the developmental journey--facilitates our understanding of adaptive or maladaptive processes. For human behavioral disorders such as schizophrenia and autism, the inherent plasticity of the nervous system requires a systems approach to incorporate all of the myriad epigenetic factors that can influence such outcomes.
Gene-environment interplay is a general term that covers several divergent concepts with different meanings and different implications. In this review, we evaluate research evidence on four varieties of gene-environment interplay. First, we consider epigenetic mechanisms by which environmental influences alter the effects of genes. Second, we focus on variations in heritability according to environmental circumstances. Third, we discuss what is known about gene-environment correlations. Finally, we assess concepts and findings on the interaction between specific identified genes and specific measured environmental risks. In order to provide an understanding of what may be involved in gene-environment interplay, we begin our presentation with a brief historical review of prevailing views about the role of genetic and environmental factors in the causation of mental disorders, and we provide a simplified account of some of the key features of how genes 'work'.
Resilient functioning, the attainment of unexpected competence despite significant adversity, is among the most intriguing and adaptive phenomena of human development. Although growing attention has been paid to discovering the processes through which individuals at high risk do not develop maladaptively, the empirical study of resilience has focused predominantly on detecting the psychosocial determinants of the phenomenon. For the field of resilience to grow in ways that are commensurate with the complexity inherent to the construct, efforts to understand underlying processes will be facilitated by the increased implementation of interdisciplinary research designed within a developmental psychopathology framework. Research of this nature would entail a consideration of psychological, biological, and environmental-contextual processes from which pathways to resilience might eventuate (known as equifinality), as well as those that result in diverse outcomes among individuals who have achieved resilient functioning (know as multifinality). The possible relation between the mechanisms of neural plasticity and resilience and specific suggestions concerning research questions needed to examine this association are discussed. Examples from developmental neuroscience and molecular genetics are provided to illustrate the potential of incorporating biology into the study of resilience. The importance of adopting a multiple-levels-of-analysis perspective for designing and evaluating interventions aimed at fostering resilient outcomes in persons facing significant adversity is emphasized.