The Blackwell Handbook of Early Childhood Developmentpresents a comprehensive summary of research into child developmentfrom age two to seven. * * Comprises 30 contributions from both established scholars andemerging leaders in the field * The editors have a distinguished reputation in early childhooddevelopment * Covers biological development, cognitive development, languagedevelopment, and social, emotional and regulatory development * Considers the applications of psychology to the care andeducation of young children, treating issues such as poverty,media, and the transition to school * A valuable resource for students, scholars and practitionersdealing with young children
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List of Tables and Figures
Notes on Contributors
PART I Conceptual Frameworks
1 Nature and Nurture in Early Childhood
Methods in Research on Gene–Environment Processes
Stature and Physical Development
Genetically Informative Studies Clarify Environmental Mechanisms
Change and Development
Where the Environment Lives: Subjective Experience
2 Vulnerability and Resilience in Early Child Development
The Challenge of Defining Vulnerability and Resilience
Models of Vulnerability and Resilience
A Resilience Framework for Promoting Positive Development in Early Childhood
3 Family Influences on Early Development: Integrating the Science of Normative Development, Risk and Disability, and Intervention
Developmental Science of Normative Development
Developmental Science of Biological Risk and Disability
Summary and Future Directions
4 Developmental Pathways and Intersections among Domains of Development
Conceptual Framework for the Intersections of Domains
Interface of Developmental Domains: Examples Based on Differences in Temperament, Disability, and Negative Life Experience
PART II Early Biological and Physiological Development
5 Early Brain Development and Plasticity
The Basic Building Blocks
Mechanisms of Brain Development
Connections and Prenatal Plasticity
Plasticity and the Environment
Conclusions and Future Directions
6 Social Regulation of Stress in Early Child Development
The Neurobiology of Stress
Frontal Regulation of Stress
Animal Models of the Social Regulation of Stress
Psychobiological Studies of Stress and Emotion in Children
Summary and Future Directions
Historical Origins of Temperament
Approach and Withdrawal Systems
The Neural Substrates of Temperament
Behavioral Inhibition and a Synthesis of Temperament and Neuroscience
Continuity of Temperament across Childhood
Consequences of Individual Differences in Temperament
PART III Cognitive Development
8 Early Conceptual Development
Role of Experience
9 Executive Functions in Developing Children: Current Conceptualizations and Questions for the Future
Current Conceptualizations of Executive Function
Future Questions for Executive Function Research
Summary and Concluding Thoughts
10 Developing Social Understanding in a Social Context
How Is TOM Measured?
How is TOM Related to Other Abilities?
The Role of Social Context
Why is Theory of Mind Development Important?
11 Mathematical Thinking and Learning
How Does Mathematical Knowledge Develop?
What Do Young Children Know about Mathematics?
Early Childhood Mathematics Education
PART IV Language and Communicative Development
12 Language Experience and Language Milestones During Early Childhood
13 How Children Learn Language: A Focus on Resilience
Out of the Mouths of Babes
Language-Learning by Hand
Language-Learning Around the Globe
Does More or Less Input Matter?
Is Language Innate?
14 What Counts as Literacy in Early Childhood?
The Literate Child
So How Do We Define Literacy?
Two Straw Persons
The Key Early Literacy and Precursor Skills
Factors Related to Literacy Outcomes
Promoting Literacy Development at Home and in the Classroom
Assessing Individuals’ Literacy Skills and Evaluating Literacy in Society
Coming to a View of Literacy That Can Inform Early Childhood Practitioners
PART V Social, Emotional, and Regulatory Development
15 Getting Along with Others: Social Competence in Early Childhood
Definition and Conceptualization of Social Competence
Predictors of Social Competence in Young Children
Socialization Within the Family
Socialization by Peers
Interventions for Young Children’s Social Competence
Summary and Conclusion
16 Feeling and Understanding: Early Emotional Development
Emotional Development and Close Relationships
Early Emotional Vulnerability
Emotional Development and the Self
Development of Emotion Regulation
17 Temperament, Attention, and the Development of Self-Regulation
Development of Self- and Other-Regulation
Self-Regulation in the Toddler and Preschool Years
Years 1 to 3
Years 3 to 6
Environmental and Genetic Influences on Effortful Control
Future Prospects in Self-Regulation Research
18 Maladjustment in Preschool Children: A Developmental Psychopathology Perspective
Developmental Tasks and Problem Behaviors
Dimensions and Categories of Childhood Disorders
Internalizing (Emotional) Disorders
A Developmental Psychopathology Perspective on Young Children’s Problem Behavior
Individual Differences in Child Behavior
PART VI The Social Ecology of Early Development
19 Family Systems
What Is a Family System?
Family Systems Research
Looking Toward the Future: Closing the Gap Between Family Systems Theory and Research
20 Poverty During Early Childhood
Incidence of Poverty During Early Childhood
The Developmental Context of Poverty
Developmental Sequelae of Poverty During Early Childhood
Causal Inference and Practical Significance Dilemmas: Endogeneity, Effect Size, and Measurement Concerns
Measuring Family Economic Resources
Contextualizing Poverty During Early Childhood
21 Orphanages as a Developmental Context for Early Childhood
Ecology of Institutional Life
Developmental Problems Associated with Institutionalization
Disturbances of Attachment and Institutional Care
Other Problems in Young Children Associated with Institutional Rearing
Conclusions and Future Directions
22 Peer Relationships in Early Childhood
A Conceptual Framework
Descriptions of Early Peer Relations
Peer Relations as a Developmental Outcome
Peer Relations as Predictors of Child Developmental Outcomes
A Transactional Perspective
23 Child Care and Early Development
The Demographics of Child Care
The Child Care Microsystem
The Child Care Mesosystem
The Child Care Exosystem
The Child Care Macrosystem
24 The Social Ecology of the Transition to School: Classrooms, Families, and Children
A Conceptual Model of Early Schooling and Individual Differences
Conclusions and Trends Shaping the Transition Ecology in the Future
25 Media and Early Development
Early Media Use: Access, Experiences, and Parental Attitudes
How Do Children Learn from Media Presentations?
The Educational Lessons of Media
Engagement and Learning: Interactive Stories
Media, Gender, and Ethnicity
Social Policy and Media Exposure
PART VII Policy Issues
26 Evaluating Early Childhood Assessments: A Differential Analysis
27 Head Start: What Do We Know About Its Effectiveness? What Do We Need to Know?
The Head Start Program and the Families It Serves
The Federal Head Start Research Agenda
What Previous Research Summaries Have Concluded About Head Start Effectiveness
Recent Studies of Head Start Effects
Lessons from Head Start Research about Children’s Development
Lessons from Head Start Research for Programs
Summary and Conclusions
28 Early Childhood Policy: A Comparative Perspective
Three Types of Early Childhood Policies
Parental Leave Policies
Early Childhood Education and Care Policies
29 Promoting Social Competence in Early Childhood: Classroom Curricula and Social Skills Coaching Programs
Goals of Social Competence Interventions
Promoting Social-Emotional Learning and Social Competence
Preschool Curricula Designed to Promote Social-Emotional Learning in the Classroom
Social Competence Coaching Programs for Children with Skill Delays and Deficits
Promoting Generalized and Sustained Competencies
Summary and Future Directions
30 Treatment and Prevention of Conduct Problems: Parent Training Interventions for Young Children (2–7 Years Old)
The Importance of Early Intervention
Characteristics of Empirically Validated Interventions
Cognitive Behavioral Parent Training Programs for Children with Conduct Problems (Ages 2–7 Years)
Summary of Parent-Focused Interventions
Multi-focused Interventions: Combining Parent Training with Classroom Intervention
Key Features of Effective Programs
Summary of Effective Parent Interventions for Children Ages 2–7 Years
Policy Implications: Principles for Implementing Empirically Supported Prevention Programs
Blackwell Handbooks of Developmental Psychology
This outstanding series of handbooks provides a cutting-edge overview of classic research, current research and future trends in developmental psychology.Each handbook draws together 25–30 newly commissioned chapters to provide a comprehensive overview of a sub-discipline of developmental psychology.The international team of contributors to each handbook has been specially chosen for its expertise and knowledge of each field.Each handbook is introduced and contextualized by leading figures in the field, lending coherence and authority to each volume.
The Blackwell Handbooks of Developmental Psychology will provide an invaluable overview for advanced students of developmental psychology and for researchers as an authoritative definition of their chosen field.
Blackwell Handbook of Infant Development
Edited by Gavin Bremner and Alan Fogel
Blackwell Handbook of Childhood Social Development
Edited by Peter K. Smith and Craig H. Hart
Blackwell Handbook of Childhood Cognitive Development
Edited by Usha Goswami
Blackwell Handbook of Adolescence
Edited by Gerald R. Adams and Michael D. Berzonsky
The Science of Reading: A Handbook
Edited by Margaret J. Snowling and Charles Hulme
Blackwell Handbook of Early Childhood Development
Edited by Kathleen McCartney and Deborah A. Phillips
Blackwell Handbook of Language Development
Edited by Erika Hoff and Marilyn Shatz
© 2006, 2008 by Blackwell Publishing Ltd
except for editorial material and organization © 2006, 2008 Kathleen McCartney and Deborah Phillips
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The right of Kathleen McCartney and Deborah Phillips to be identified as the authors of the editorial material in this work has been asserted in accordance with the UK Copyright, Designs, and Patents Act 1988.
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs, and Patents Act 1988, without the prior permission of the publisher.
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This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought.
First published 2006
First published in paperback 2008 by Blackwell Publishing Ltd
Library of Congress Cataloging-in-Publication Data
Blackwell handbook of early childhood development/edited by Kathleen McCartney and Deborah Phillips.
p. cm. — (Blackwell handbooks of developmental psychology) Includes bibliographical references and index.
ISBN: 978-1-4051-2073-9 (hardcover: alk. paper) — ISBN: 978-1-4051-7661-3 (pbk.: alk. paper) 1. Child psychology. 2. Child development. I. Title: Handbook of early childhood development. II. McCartney, Kathleen. III. Phillips, Deborah. IV. Series.
BF721. B44 2006
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List of Tables and Figures
2.1 Concise glossary of concepts related to vulnerability and resilience in development
12.1 Milestones of phonological development in production
12.2 Milestones of lexical development in production
12.3 Milestones of morphosyntactic development in production
12.4 Milestones of communicative development
13.1 The resilient properties of language
14.1 Examples of early literacy accomplishments in five domains
21.1 Studies with multiple reports on the same sample followed by single-sample studies
28.1 Childbirth-related leave policies in the United States and other OECD nations
30.1 Summary of empirically validated prevention programs for young children (0–8 years) that are designed to prevent later development of substance abuse, violence, and delinquency: parent- and family-focused interventions
30.2 Summary of empirically validated prevention programs for young children (0–8 years) that are designed to prevent later development of substance abuse, violence, and delinquency: multi-focused interventions
4.1 Developmental web for two relationships
4.2 Developmental web for normative mean and nice social interactions
4.3 Developmental web biased toward nice interactions due to inhibited temperament
5.1 Neuron including cell body, axon, dendrites, and synapse
5.2 Developmental trajectories of mechanisms of brain development
6.1 Schematic of the hypothalamic-pituitary-adrenocortical (HPA) system
17.1 The development of executive functioning
24.1 The ecological and dynamic model of transition
25.1 Percent of parents who say each medium mostly helps/hurts children’s learning
30.1 Model of linking risk factors: unfolding chain of events in development of conduct disorder
Notes on Contributors
Sally Atkins-Burnett is Assistant Professor of Early Childhood Special Education at the University of Toledo.
Catherine C. Ayoub is Associate Professor of Education at the Harvard Graduate School of Education and Associate Professor of Psychology at the Harvard Medical School.
Rachel Barr is Assistant Professor of Psychology at Georgetown University.
Daniel Berry is a doctoral student in Human Development and Psychology at the Harvard Graduate School of Education.
Karen L. Bierman is Distinguished Professor of Psychology at Pennsylvania State University.
Marc H. Bornstein is Senior Investigator and Head of Child and Family Research at the National Institute of Child Health and Human Development.
Katherine Cahill is a doctoral student in Psychology at the University of Oregon.
Sandra L. Calvert is Professor of Psychology at Georgetown University and Director of the Children’s Digital Media Center.
Susan B. Campbell is Professor of Psychology at the University of Pittsburgh.
Joanna Cannon is a postdoctoral fellow in Developmental Psychology at the University of Chicago.
Rachel Chazan-Cohen is Senior Research Analyst at the Office of Planning, Research and Evaluation, Administration for Children and Families, US Department of Health and Human Services.
Jane W. Couperus is the Foundation for Psychocultural Research – Hampshire College Program in Culture, Brain, and Development Assistant Professor of Developmental Cognitive Neuroscience.
Eric Dearing is Assistant Professor of Psychology at the University of Wyoming.
Kirby Deater-Deckard is Professor of Psychology at Virginia Polytechnic Institute and State University.
Janet Eisenband is a doctoral student in Cognitive Studies in Education at Teachers College, Columbia University.
Stephen A. Erath is a student in Child Clinical Psychology at the Pennsylvania State University.
Richard A. Fabes is a Professor in the Department of Family and Human Development at Arizona State University.
Kurt W. Fischer is Charles Bigelow Professor of Education at the Harvard Graduate School of Education.
Nathan A. Fox is Professor of Human Development at the University of Maryland.
Sarah L. Friedman is a staff member of the National Institute of Child Health and Human Development. She is Scientific Coordinator of the NICHD Study of Early Child Care and Youth Development.
Bridget M. Gaertner is a doctoral student in Family Science at the Arizona State University.
Susan A. Gelman is Associate Dean for Social Sciences and Frederich G. L. Huetwell Professor of Psychology at the University of Michigan.
Abigail H. Gewirtz is Assistant Professor of Psychology at the University of Minnesota.
Herbert P. Ginsburg is Jacob H. Schiff Foundations Professor of Psychology and Education at Teachers College, Columbia University.
Susan Goldin-Meadow is Irving B. Harris Professor of Psychology at the University of Chicago.
Megan R. Gunnar is Professor of Child Development at the University of Minnesota.
Michael J. Guralnick is Director of the Center on Human Development and Disability and Professor of Psychology and Pediatrics at the University of Washington.
Erika Hoff is Professor of Psychology at Florida Atlantic University.
Jessica Kieras is a doctoral student in Psychology at the University of Oregon.
Kristin H. Lagattuta is Assistant Professor of Psychology at the University of California, Davis.
John M. Love is a senior fellow at Mathematica Policy Research Inc., Princeton, NJ.
Kathleen McCartney is Gerald S. Lesser Professor of Early Childhood Development at the Harvard Graduate School of Education.
Jennifer N. Martin is a doctoral student in Human Development at the University of Maryland.
Ann S. Masten is Distinguished McKnight University Professor and Distinguished University Professor of Child Psychology at the University of Minnesota.
Samuel J. Meisels is President of the Erikson Institute.
Charles A. Nelson is Richard David Scott Chair of Pediatrics at the Harvard Medical School and Research Director of the Developmental Medicine Center at Boston Children’s Hospital.
Lana Nenide is a doctoral student at the University of Wisconsin.
Sandra Pappas is a doctoral student in Developmental Psychology at Teachers College, Columbia University.
Deborah Phillips is Professor of Psychology at Georgetown University.
Robert C. Pianta is Professor and William Clay Parrish Jr. Chair in Education at the University of Virginia.
Tierney K. Popp is a doctoral student in Child Development and Family Studies at Arizona State University.
Michael I. Posner is Professor Emeritus at the University of Oregon and Adjunct Professor at the Weill Medical College in New York (Sackler Institute).
Helen Raikes is Professor, Department of Family and Consumer Sciences, University of Nebraska, Lincoln.
M. Jamila Reid is Co-Director of the Parenting Center and a research psychologist at the Department of Family and Child Nursing, at the University of Washington.
Sara Rimm-Kaufman is Assistant Professor of Educational Psychology at the University of Virginia.
Mary K. Rothbart is Professor Emeritus at the University of Oregon.
Jeanette Sawyer is a doctoral student in Clinical Psychology at Columbia University.
Lisa D. Settles is a member of the clinical faculty in the Department of Psychiatry and Neurology at Tulane University Health Sciences Center.
Anna T. Smyke is Research Instructor of Child and Adolescent Psychiatry at Tulane University.
Catherine E. Snow is Henry Lee Shattuck Professor of Education at the Harvard Graduate School of Education.
Susan J. Spieker is Professor of Family and Child Nursing at the University of Washington.
Amy Sussman is a researcher and adjunct faculty member in the Psychology Department at Georgetown University.
Louisa Banks Tarullo is a senior researcher at Mathematica Policy Research, Inc. in Washington, DC.
Ross A. Thompson is Professor of Psychology at the University of California, Davis.
Sara J. Van Winkle is a graduate student at the University of Wisconsin.
Deborah Lowe Vandell is a Professor in the Department of Educational Psychology at the University of Wisconsin-Madison.
Jane Waldfogel is Professor of Social Work and Public Affairs at Columbia University.
Carolyn Webster-Stratton is Professor and Director of the Parenting Clinic at the Department of Family and Child Nursing, University of Washington.
Marilyn C. Welsh is Professor of Psychology at the University of Northern Colorado.
Martha Zaslow is the Vice President for Research and Area Director for the Early Child Development content area at Child Trends.
Charles H. Zeanah is Professor of Psychiatry and Pediatrics and Director of Child and Adolescent Psychiatry at Tulane University.
In the first two years of life, infants develop amazing competencies across development, from controlled movements to representational thought to goal-directed attachment relationships. Our story picks up from this point through about age 7, the early childhood years. Early childhood, like infancy, represents a time of emerging skills – skills that make the 7-year-old seem more like an adult than an infant. In early childhood, children exchange magical and egocentric thinking for a theory of mind, the ability to execute a plan of action, and a rudimentary logic. Over time, “terrible” 2-year-olds become young children who can exhibit self-control by delaying gratification and inhibiting inappropriate responses. In a stunning feat, by the end of early childhood, children master most of the grammatical rules that adults use. Parents and teachers respond to these kinds of noticeable changes by using reasoning, encouraging independence, arranging play dates, and providing explicit opportunities for learning in their dealings with young children. Soon, children are reading, counting, developing friendships, choosing to engage in favorite activities, and more.
There are two main ways to study development at any age. The first is to chart the milestones that reflect changes observed in the average child, while the second is to assess individual differences among children. Both perspectives inform the knowledge base on early childhood development. Individual differences are of particular interest to those concerned with applied problems. For this reason, an understanding of early childhood necessitates an investigation of the contexts of development, what we refer to here as the social ecology of early development, including the family, peers, poverty, child care, and the media. To some extent, research on early childhood has informed policy issues, as reflected in work on assessment as well as evaluations of early interventions for children and parents. Comparative studies reveal vast differences across cultures in policies for children and families, which are more likely to reflect public will than research per se.
We began our editing task by reflecting on the emerging competencies in early childhood, the approaches social scientists use to study it, and methodological issues in the field. Then we constructed topics that represent our view of the landscape in early childhood development. We recruited leading scholars in developmental science to write relatively short, albeit comprehensive, reviews of the literature from both a theoretical and a conceptual perspective. To give the volume a unified voice, we asked authors to consider four organizing themes in their reviews: the role of early experiences as they shape the course of development; contributions of the cultural contexts within which children grow up; individual differences in developmental trajectories; and applications of development science to issues of practice and policy.
The result is a Handbook that we have organized into seven parts: Part I, Conceptual Frameworks; Part II, Early Biological and Physiological Development; Part III, Cognitive Development; Part IV, Language and Communicative Development; Part V, Social, Emotional, and Regulatory Development; Part VI, The Social Ecology of Early Development; and Part VII, Policy Issues. The four conceptual frameworks that open the Handbook provide a foundation for the field through their discussions of how to describe the interplay of genes and environments, how research on children’s vulnerability and resilience informs our understanding of individual differences, how the study of normal and atypical development can enhance our understanding of developmental processes, and how domains of development intersect.
Our aim, like that of other editors in this Blackwell series, is to provide a Handbook that is accessible to a broad audience, from students to researchers to practitioners. Each chapter offers an independent overview of a topic, which can be read as a stand-alone piece. Note, however, that the authors liberally reference other chapters in the volume to help readers make important connections across the field. Indeed, several authors read one another’s first drafts to discover not only common ground, but also points of diversion. One can easily imagine organizing an early childhood seminar around cross-chapter discussions of key developmental issues. In the final analysis, our aim has been to assemble a Handbook that will be useful to all within our field who seek to understand the developing child, to move the knowledge base forward, and apply this knowledge toward constructive policies and programs for all children.
Nature and Nurture in Early Childhood
Kirby Deater-Deckard and Katherine Cahill
Human development is shaped by dynamic transactions between genes and environments – genetic and environmental influences that can be independent or correlated, and additive or interactive in their effects. These effects cannot be elucidated without understanding how these transactions may be operating throughout the lifespan. The focus in developmental science has shifted toward testing models of how genes and environments work together to create human variability, as part of a much broader trend toward investigating biological and environmental factors in brain growth, functioning, and plasticity.
In the current chapter, we present research investigating the interplay between nature and nurture in early childhood development. We begin with an overview of the techniques used to ascertain genetic and environmental influences, and then turn to a description of what we know about the etiology of individual differences. We concentrate on the domains of physical development, cognitive and language skills, temperament, and the early signs of developing psychopathology. In addition, we consider recent developments in the study of gene–environment processes and molecular genetics, as they apply to early childhood.
Methods in Research on Gene–Environment Processes
Human genes and environments share remarkable similarities across populations. Indeed, humans share much of their genotype with many other species. However, there also is awesome variability in the form and function of genes and environments that give rise to equally remarkable variability across individuals, and it is the examination of the etiology of these individual differences that is at the root of contemporary quantitative and molecular genetics research (Plomin, DeFries, McClearn, & McGuffin, 2001). With few exceptions, behavioral and molecular genetic data are correlational. However, even correlational genetic designs yield data that are useful in pointing toward likely causal mechanisms, because they control for potential confounds between genetic and environmental influences – confounds that go undetected in most developmental studies of genetically related family members. Behavioral and molecular genetics research, in addition to experimental and quasi-experimental studies of the effects of familial and extra-familial experiences in development, are important contemporary approaches to understanding the contributions of both genes and environments to human development (Collins, Maccoby, Steinberg, Hetherington, & Bornstein, 2000).
Molecular genetic techniques
The Human Genome Project revealed that there are around 30,000 functional human genes – far fewer than the 100,000 that researchers expected to find. Genes are the functional parts of chromosomes that synthesize proteins. These proteins act as enzymes that are the building blocks for neurotransmitters, hormones, and other bio-chemicals. Human chromosomes come in pairs, and people have one allele (i.e., form) of a gene on one chromosome and one allele on the second. There are variations in alleles; some are longer or shorter or more complex than others, and these differences correspond to differences in protein synthesis and the production of chemicals involved in guiding human behavior. Base pairs are the unit of analysis in genome scans, and variability in base pairs at specific gene loci is related to variability in the production, destruction, and expression of enzymes. For instance, single base pair substitutions/single nucleotide polymorphisms (SNPs) and simple sequence repeats (SSRs) are structural variations that are associated with complex trait expression (Craig & McClay, 2003).
Consider as an example the dopamine receptor D4 gene (DRD4), which plays a role in determining the number of dopamine receptors in the brain. Having more dopamine receptors typically translates into greater dopamine activity in the brain, which is related to novelty seeking, attention problems – and, in more extreme cases, schizophrenia and disorganized attachment (Ebstein, Benjamin, & Belmaker, 2003). DRD4 alleles come in at least ten forms (Kluger, Siegfried, & Ebstein, 2002), but the most common are the 4- and 7-repeat alleles, often referred to as the short and long forms of DRD4, respectively. The long form is associated with higher levels of novelty seeking (Ebstein et al., 2003). DRD4 and the serotonin transporter 5-HTTLPR gene have received substantial attention in molecular genetics research, because they are thought to have widespread effects on complex human behaviors.
Molecular genetic techniques allow scientists to identify specific genes involved in the expression of complex human traits and behaviors, based on the analysis of structural differences in DNA like the differences just described in the DRD4 gene. Linkage and association approaches to studying genetic similarity (e.g., allele sharing and allelic frequency at specific locations on chromosomes) among family members have vastly increased our knowledge about individual genes implicated in some of the most widely studied human attributes, including how those genes are differentially expressed in individuals. More recent advances in molecular genetics have focused on understanding the complex processes involved in gene structure and functional expression.
A small number of genes involved in individual differences in early childhood have been identified, and little is understood about the intricacies of the expression of these genes in terms of their products (i.e., proteins, enzymes) and the effects of those gene products. Nevertheless, this research is progressing rapidly, and the work that has been done already greatly enriches our appreciation for the importance of examining gene–environment processes. The decades ahead will be filled with major discoveries regarding variation in structure and function of genes and networks of genes, their products, and the transactions between these and non-genetic factors. These will include discoveries arising from the search for relevant genes (based on genome scans) as well as from investigations of candidate genes in particular neurotransmitter systems implicated for specific attributes (based on existing knowledge from the human and animal biopsychology literatures).
Quantitative genetic techniques
Unlike molecular genetic approaches, quantitative genetic techniques are based on mathematical models that employ principles of population genetics to estimate the proportions of variance that are accounted for by genetic and environmental factors. Studies of sibling and parent–offspring pairs that vary in their genetic similarity (e.g., biological and non-biological relatives in intact, step, and adoptive families; twins; families that have used egg or sperm donation) allow for estimation of genetic, shared environmental, and non-shared environmental effects on outcomes of interest. If family members who are more genetically similar (e.g., identical versus fraternal twins) are more similar on a trait, then genetic variance or heritability is said to account for the greater similarity. If genetic similarity is controlled and family members continue to show similarity, shared environmental variance is said to be present. Non-shared environmental variance includes effects of all the non-genetic influences that lead to dissimilarity among family members, and includes measurement error (Reiss, Neiderhiser, Hetherington, & Plomin, 2000).
The overwhelming majority of research on the effects of nature and nurture in early childhood has employed quantitative techniques, but that trend is changing as molecular genetic techniques become more accessible (Plomin & Rutter, 1998). With this in mind, we turn to review the research on the contributions of genes and environments to children’s early physical, cognitive, and psychosocial development.
Stature and Physical Development
A good place to start in considering research on gene–environment processes is with the literature on indices of stature – most scientists agree on what these observable attributes (i.e., phenotypes) are, and how they are best measured. There is also consensus on how these should be measured, and if used correctly, the measurement tools yield data that are highly reliable and valid. Quantitative genetics research has indicated substantial genetic variance in children’s height, weight, and body mass index (BMI). Several twin and adoption studies have revealed heritability estimates that increase from early to middle childhood (e.g., Cardon, 1994; Phillips & Matheny, 1990). A study of 14- to 36-monthold twins showed that, even at these young ages, an average of two-thirds of the variance was attributed to genetic factors. Shared environmental variance was highest at 20 and 24 months for all measures, but remained modest, with the exception of moderate shared environment for BMI at 20 and 24 months (Chambers, Hewitt, Schmitz, Corley, & Fulker, 2001).
Environmental effects on BMI are reflected in rapid generational changes, evidenced as increases in the rates of obesity in children in the US. From 1988 to 1994, the rate of obesity in 2- to 5-year-olds rose from 7.2% to 10.4% (Ogden, Flegal, Carroll, & Johnson, 2002). Environmental conditions are implicated because genetic influences do not change this rapidly. Correlational research revealing that breastfeeding in infancy reduces children’s risk for childhood obesity also points to the importance of early environmental experiences in physical development (Dietz, 2001). Yet the changing social conditions that promote overeating and sedentary lifestyle probably interact with genetic risk for obesity in some children (see below for more discussion of gene–environment interaction). It is to be hoped that researchers will continue to concentrate on identifying genetic variation as it interacts with environmental factors that put some children at increased risk for obesity and related health problems.
We now consider some of the psychological attributes in early childhood that have been investigated in genetically informative studies. Individual differences in children’s cognitive development include a number of interrelated domains of skill and performance, ranging from processing speed and capacity, to complex problem solving, to language understanding and use. We concentrate in the following section on the two areas of inquiry that have received the most attention among researchers studying early childhood development – general cognitive ability (e.g., intelligence or IQ) and verbal communication skills.
General cognitive ability
Typically, general cognitive ability is estimated to be moderately heritable, based on twin and adoption studies of preschoolers. Longitudinal studies also suggest that genetic influences on general cognitive ability increase over early and middle childhood, while shared environmental effects are modest and often disappear by middle childhood (Bishop, Price, Dale, & Plomin, 2003; Cherny, et al., 2001; McCartney, Harris, & Bernieri, 1990; Petrill et al., 1998; Plomin et al., 2001; Wilson, 1983). This may reflect developmental changes arising from shifts in the degree to which children have more control, and parents less control, over their environments and daily experiences (Scarr & McCartney, 1983). Nevertheless, interventions for improving cognitive performance have been shown to be effective (Ramey & Haskins, 1981), and it is important to emphasize that about half of the variance in cognitive abilities is accounted for by non-shared environmental influences.
Single-gene disorders and chromosomal abnormalities are the most common causes of major deficits in general cognitive ability. Down’s syndrome is a chromosomal abnormality characterized by the presence of a third twenty-first chromosome, and it is the most widespread cause of mental retardation in both males and females. The single-gene disorders of Fragile X syndrome and Rett syndrome are responsible for the second largest number of cases of mental retardation in males and females, respectively (Plomin et al., 2001). The single-gene disorder PKU is caused by a mutation of the PAH gene, and provides a clear example of how genes and environments work together. The mutation of the PAH gene prevents proper breakdown of phenylalanine, a substance commonly ingested through red meat and other foods. When phenylalanine levels build up, it damages the developing brain and leads to mental retardation and other symptoms. Maintaining a strict diet can prevent the great majority of the effects of PKU. Discovering the genes involved in disorders and how they function can open doors to developing environmental interventions that reduce or alleviate the effects of genetic problems (Plomin et al., 2001).
Language and communication
Many components of language and literacy development are moderately heritable. In this domain, the effects of the shared environment are often more evident, compared to the domain of general cognitive ability. Expressive language skills – compared to receptive skills – appear to be more genetically variable, and more of this genetic variance overlaps with genetic influences on general cognitive ability. In contrast, shared environmental influences appear to be more prominent for receptive language skills, compared with expressive skills (Young, Schmitz, Corley, & Fulker, 2001). Dale, Dionne, Eley, and Plomin (2000) reported heritability estimates of.25 and.39 for lexical and grammatical development, respectively, in 2-year-olds. Shared environmental effects were estimated at.69 for grammar and.48 for lexical development.
Common genetic and environmental processes are thought to underlie lexical and grammatical development, but it is less clear whether general verbal and non-verbal language development shares genetic and environmental influences (Dale et al., 2000). Verbal and non-verbal skills in 2-year-olds are moderately correlated, and less than half of this similarity is accounted for by common genetic influences (Price et al., 2000). Similarly, Dale et al. found low to moderate correlations between lexical and grammatical development and non-verbal skills. However, in contrast, Colledge et al. (2002) found extensive overlap in the genetic influence on verbal and non-verbal skills in 4-year-olds.
Genetic factors appear to be highly influential when it comes to more severe language and communication problems and disorders (Plomin et al., 2001). Dale et al. (1998) found that heritability in vocabulary development was greater, and shared environmental variance smaller, among those scoring in the lowest 5% of the performance range in their large and diverse sample of 2-year-old twins. Similarly, variance in vocabulary scores for children with persistent language problems in early childhood was largely accounted for by genetic factors, whereas variance in vocabulary scores for children with transient language problems was more likely to be accounted for by environmental factors (Bishop et al., 2003). The genetic basis of dyslexia and other reading and communication disorders is currently under intense study, and the results of this research will allow for a clearer understanding of how genes and environments work together in shaping children’s language development (Plomin et al., 2001).
To summarize, genetic variance is moderate to substantial in studies of cognitive and language functioning and performance in early childhood. There also is evidence for shared environmental influences; these are largest in early childhood, and dissipate with development. In contrast, non-shared environmental influences are present from early in life, and persist into middle childhood and beyond.
Next, we consider temperament and its component parts, as the domain of socialemotional development that has received the most attention in behavioral genetic research. The estimates of heritable and genetic variance in these studies vary to some degree, due to differences across study designs (e.g., measurement, twin or adoption study).
Temperament is the framework for personality. It is rooted in biologically based individual differences, is moderately stable over time and across settings, and is modified by gene-environment processes. Individual differences in temperament are observable from infancy and are implicated in many crucial aspects of children’s development and adaptation (Emde & Hewitt, 2001; Prior, 1999). Rothbart’s theory of temperament posits that there are multiple dimensions of behavior that represent reactivity to stimuli and regulation of those reactions (Rothbart & Bates, 1998). Relevant domains in this literature that we highlight here include negative affectivity, effortful control, extraversion/surgency, sociability, and adaptability (see Rothbart, Posner, & Kieras, this volume).
The temperament dimension of Negative affectivity includes anger, sadness, discomfort, and low soothability. Quantitative genetic research indicates that approximately one-third to two-thirds of the variance in negative affectivity is heritable (Goldsmith, Buss, & Lemery, 1997; Oniszczenko et al., 2003; Plomin, Pedersen, McClearn, Nesselroade, & Bergeman, 1988). Angry reactions to restraint and the initiating of fights are estimated to be heritable, and this genetic variance appears to contribute mainly to the observable stability of individual differences (Emde, Robinson, Corley, Nikkari, & Zahn-Waxler, 2001). Some evidence for shared environmental influence also has been found, and environmental sources of variance (shared and non-shared) contribute to both continuity and change in these behaviors across infancy and the preschool years (Emde et al., 2001).
Molecular genetic research has implicated dopamine and serotonin genes in negative emotionality. Infants who have at least one long DRD4 allele display less negative emotionality (Ebstein, Levine, Geller, Auerbach, Gritsenko, & Belmaker, 1998) and less anger in response to restraint (Auerbach, Faroy, Ebstein, Kahana, & Levine, 2001). Mothers’ reports of high levels of aggression in 4-year-olds were also found to be associated with the presence of the long form of DRD4 (Schmidt, Fox, Rubin, Hu, & Hammer, 2002). Twelve-month-olds who have two copies of the short form of the serotonin transporter 5-HTTLPR gene showed less pleasure than others during free play (Auerbach et al., 2001).
The dimension of Effortful control includes anticipation and enjoyment of low-intensity stimulation, perceptual sensitivity, and enhanced control of attention and impulses. High levels of effortful control are correlated with lower levels of negative emotionality (Rothbart, Ahadi, & Evans, 2000). Many studies have indicated moderate heritability in the components of effortful control, including task orientation, persistence, and related aspects of “difficult” temperament (Goldsmith et al., 1997; Lemery & Goldsmith, 2002; Manke, Suadino, & Grant, 2001). Molecular genetics research has linked the DRD4 gene to attentional control (Fan, Fossella, Sommer, Wu, & Posner, 2003), but this finding has not yet been replicated in young children. Shared environmental effects stemming from family socio-economic status and observed maternal warmth account for some of the variability in task persistence in early childhood (Petrill & Deater-Deckard, 2004).
Extraversion or surgency
The dimension of Extraversion or Surgency includes activity level, novelty seeking, positive affect, and low shyness. Activity level refers to the amount and intensity of physical movement and it is one of the most thoroughly researched dimensions of early childhood temperament. Overall, activity level has been found to be moderately heritable and to be relatively uninfluenced by shared environmental factors (Goldsmith et al., 1997). Among children at the extremes of activity level, the strength of genetic effects may increase (Manke et al., 2001), and the genetic effects on activity level appear to be moderately to highly stable across time points from infancy to 3 years of age (Saudino & Cherny, 2001). Variance in positive affect and general cheerfulness also appears to be mainly accounted for by heritability and non-shared environmental factors (Eid, Reimann, Angleitner, & Borkenau, 2003; Robinson, Emde, & Corley, 2001).
Research with newborns has identified genes in the serotonin and dopamine systems that are linked with temperament, especially components of temperament that relate to surgency. Among 2-week-olds, the presence of one or two alleles of the long form of the DRD4 gene was associated with higher scores on orientation, range of state, motor organization, and regulation of state (Ebstein et al., 1998). Additionally, an interaction between the DRD4 gene and the serotonin transporter 5-HTTLPR gene was found. Neonates without the long form of DRD4, and who also had only the short form of 5-HTTLPR, had significantly lower orientation scores than other infants (Ebstein et al., 1998). In a follow-up study of the infants in the Ebstein et al. study, Auerbach and colleagues (2001) found that the presence of the long form of DRD4 was associated with higher activity level at 12 months of age.
The temperament dimension of Sociability refers to the enjoyment of interpersonal interaction (contrasted with shyness and enjoyment of being alone). Sociability is moderately heritable, with one-quarter to three-quarters of the variance attributed to genetic influences. Some studies also show evidence of shared environmental effects (Eid et al., 2003; Plomin et al., 1988; Schmitz, 1994). Genetic effects on sociability and shyness are moderately to substantially stable across 14 to 36 months of age (Saudino & Cherny, 2001). As with surgency, the heritability of more extreme forms of sociability is greater than that found for moderate sociability (Manke et al., 2001). Molecular genetic research on shyness implicates the 5-HTTLPR gene in increased shyness in second graders (Arbelle et al., 2003), but related serotonin genes have not been found to predict shyness in 4-year-olds (Schmidt et al., 2002).
The dimension of Adaptability is often identified as an important component of temperament, and it includes flexibility, distress in response to novelty, emotional regulation, and high soothability. Adaptability is moderately heritable, and evidence for modest shared environmental effects is sometimes found (Oniszczenko et al., 2003; Rusalov & Biryukov, 1993). Goldsmith, Lemery, Buss, and Campos (1999) reported substantial shared environmental influence in 3- to 16-month-olds’ soothability scores. However, genetic effects accounted for all of the twin similarity in distress to novelty. The Ebstein et al. (1998) finding that the presence of the long form of DRD4 was associated with increased regulation of state in neonates suggests that genetic variation in the dopamine system also may play a role in adaptability.
To summarize, like the research on cognitive and language abilities, there is ample evidence of genetic influences in young children’s temperament attributes. These findings include moderate heritability estimates as well as associations with specific dopamine and serotonin genes. Also like the research on cognitive and language abilities, there is ample non-genetic variation – much of this is non-shared, but again there is evidence of some shared environmental variance depending on the particular attribute in question.
We turn briefly away from consideration of typical variation in cognitive and socio-emotional outcomes toward early indicators of psychopathology among young children. The environmental and genetic influences on psychopathology in early childhood vary depending on the type of symptom being examined, child age, and gender. The evidence for genetic variance is greatest and most consistent for externalizing problems. Internalizing problems (i.e., depression, anxiety, somatic problems) are moderately heritable throughout early and middle childhood, but the effects of the shared environment are less consistent (Murray & Sines, 1996; Schmitz, Fulker, & Mrazek, 1995). In one study, nearly one-quarter of the variance in girls’ internalizing problems from ages 4 through 12 years was attributed to the shared environment, but there were no shared environmental influences found for boys (Murray & Sines, 1996). With respect to age differences, Schmitz et al. showed that the effects of the shared environment decreased and the effects of genetics increased on both internalizing and externalizing problems (i.e., aggression, non-compliance, delinquency, attention problems) from early to middle childhood (but see Gjone, Stevenson, & Sundet, 1996, who did not find this pattern for externalizing problems). Other investigations of externalizing problems in early childhood converge to show similarly moderate to high heritability estimates (Arseneault et al., 2003; Dionne, Tremblay, Boivin, Laplante, & Perusse, 2003; van den Oord, Verhults, & Boomsma, 1996; van der Valk, van den Oord, Verhulst, & Boomsma, 2001; van der Valk, Verhulst, Stroet, & Boomsma, 1998; Zahn-Waxler, Schmitz, Fulker, Robinson, & Emde, 1996).
Molecular genetics research has revealed potential gene–gene interactions that affect certain aspects of early childhood psychological health. Gene–gene interaction is said to occur when the effect of one gene’s expression on a trait is moderated by the effect of another gene. One example is found in a study of disorganized infant–caregiver attachment. Infants from a low-risk sample were found to have four times the risk for a disorganized attachment classification if they had a specific form of the DRD4 gene. In addition, the presence of a particular SNP on the DRD4 gene had no main effect on attachment classification but increased the risk of disorganized attachment for children who also had the risk allele to ten times that of children who had neither the risk allele nor the risk SNP (Lakatos et al., 2002).
Up to this point, we have summarized findings regarding additive genetic and non-genetic effects on individual differences measures. However, these effects are not independent, nor do they operate in isolation from each other. Contemporary genetic theories of development place an emphasis on transactions between the genotype and the environment – specifically, gene–environment correlations and interactions.
Gene–environment correlation (rg-e) refers to the non-independence of individuals’ genetic make-up and the environments in which they exist. The pairing of genetic and environmental factors that interact to influence individual development is not random. Passive and non-passive types of rg-e have been identified using quantitative genetic techniques (Plomin, 1994). Gene–environment correlation can be estimated through quantitative genetic models that include actual measures of the environmental variables of interest, and not just measures of the developmental outcome of interest (Plomin, 1994).
Passive rg-e occurs when biological parents provide environmental conditions for their children that are correlated with their genetic make-up. For example, children who are highly sociable are more likely to have biological parents who also are fairly sociable because sociability is moderately heritable. These parents may expose their children to more people and social interaction than do other parents, and so these children will have many opportunities to further enhance their social skills. These children may develop to experience high levels of social interaction and positive reinforcement from others, and this may appear to be a result of their early exposure to high levels of interpersonal interaction. However, because the experiences they had may have arisen in part from genetic influences, so too do their later outcomes. Often, results from studies of related family members lead to conclusions of environmental causation, but the same findings could also indicate the presence of passive genetic influence. For instance, maternal education has been found to predict aspects of preschoolers’ theory of mind development (Pears & Moses, 2003). One might conclude that well-educated mothers interact with their children in ways that promote their understanding of others’ minds. Alternatively, the same genetically influenced cognitive abilities that facilitated the mothers’ educational attainment might promote early theory of mind understanding in the children. Determining the appropriate interpretation of such findings can be resolved only by using genetically informative study designs that measure the outcomes and relevant environmental factors of interest (Petrill & Deater-Deckard, 2004).
Non-passive rg-e arises when individuals either seek out environments and experiences that are correlated with their genetically based propensities (active rg-e) or elicit responses based on their genetically based attributes that further reinforce those attributes (evocative or reactive rg-e). As an example of active rg-e, children who are low in activity level, a partially heritable trait, may select hobbies and peers that do not promote physical activity. These environmental factors are consistent with their genetically influenced tendencies and may make it less likely that their activity levels increase. Evocative rg-e may be experienced by children struggling with early reading skills, partly on the basis of their genetic make-up, who elicit negative attention from their teachers in a way that serves to further dampen their persistence with and interest in reading. Evocative rg-e also has been implicated in children’s externalizing problems. Children’s genetically influenced aggressive and inattentive behavior typically evokes harsh discipline or rejection from parents, teachers, and peers (Anderson, Lytton, & Romney, 1986; O’Connor, Deater-Deckard, Fulker, Rutter, & Plomin, 1998). These social responses may reinforce and promote continued growth in behavioral problems.
Maternal expression of warmth toward children is another process that appears to include evocative rg-e. Mothers’ reports of their positive feelings toward each of their children, as well as their observed warmth and responsiveness with each of their children, vary as a function of how genetically similar sibling children are to each other. Genetically unrelated adoptive siblings receive only modestly correlated levels of warmth from their adoptive mothers, whereas fraternal twins receive moderately similar levels of warmth from their mothers. Identical twins tend to receive warmth from their mothers that is very highly correlated. This pattern suggests that differences in children’s genetically influenced responsiveness and engagement with their mothers elicit different levels of maternal warmth and emotional reciprocity with their children (Deater-Deckard & O’Connor, 2000; Deater-Deckard & Petrill, 2004).
Gene–environment interaction (g × e) occurs when environmental conditions moderate the effects of genes or when genes moderate the effects of environmental conditions. There are many ways in which gene-environment interactions can affect how children’s temperament, cognitive skills, and psychological health develop. Children at genetic risk for a “poor” outcome on a particular variable may develop in a typical way if the environmental conditions they experience reduce the genetic effect. Alternatively, risk-inducing environmental conditions may compound the obstacles faced by children already at genetic risk for certain problems, more than for children without that genetic risk. Many children are likely to also experience resilience as an outcome of g × e. The effects of problematic environmental circumstances may be weakened or eradicated by protective genetic factors.
The best examples of g × e in human developmental science come from Caspi et al.’s (2002) work in the Dunedin Multidisciplinary Health and Development Study. Variation in the form and function of a gene involved in synthesizing monoamine oxidase A (MAOA), which metabolizes a neurotransmitter that is central to the control of emotion and behavior, appears to interact with children’s experiences of maltreatment. For males who had the form of the gene that is related to adequate levels of MAOA production, childhood maltreatment was only modestly predictive of adult antisocial behavior. For males who had the form of the gene that is related to inadequate levels of MAOA production, childhood maltreatment was a strong predictor of adult antisocial behavior (Caspi et al., 2002).
Caspi et al. (2003) also reported evidence for another g × e involving protection against stressful life events; it is an important representative study, although its relevance to g × e in early childhood is less clear than the other finding just described above. Among young adults who had experienced stressful life events, those who had two copies of a particular form of a gene involved in the production of serotonin were less likely than those with one or no copies of the form of the gene to have developed depression. These examples clearly demonstrate the important role genetic variation can play in providing protection against environmental risk. Continuing to identify g × e processes that occur in early childhood and carry protection or risk for individuals should be one of the central goals of genetics research in developmental science.
Genetically Informative Studies Clarify Environmental Mechanisms
The gene–environment transactions described above should not be interpreted to indicate that genes are more important than environments in determining how children develop. Indeed, genetically informative studies elucidate the ways in which non-genetic influences operate in development, by providing tools for identifying with much greater precision the transactions between specific environmental factors and general genetic influence effects. As molecular genetic techniques lead to replications of findings with respect to specific genes, those genetic variables can then be added to these gene–environment process models, leading to even further precision (Plomin & Rutter, 1998).
Estimates of heritability obviously implicate genetic influences, but potential causal roles of environmental factors that are correlated and interacting with the involved genes cannot be dismissed. In addition, environmental changes likely produce changes in the gene–environment transactions that shape children’s attributes and experiences. Furthermore, the gene–environment transactions underlying individual differences on any particular trait may not be uniform across populations and historical eras. For instance, shared environmental variance is typically negligible in quantitative genetic studies of cognitive performance by the time participants are school-age, but shared environmental effects may be far more pronounced in populations living in more extremely deprived environmental conditions arising from poverty or social exclusion (Turkheimer, Haley, Waldron, D’Onofrio, & Gottesman, 2003). Developmental science will only benefit from a broadening of the research base in a way that includes participants from more socio-economic and ethnic groups, although doing so raises challenges, both ethical and methodological.
Quantitative genetic research reveals that a considerable amount of the variance in young children’s developmental outcomes arises from non-shared environmental influences. The environment has profound influence on children’s development, and this can be seen particularly well in behavioral genetic studies in which genetic similarity among family members is employed statistically in the computations of effects (Plomin, 1994). These powerful non-shared environmental effects can be accounted for by using genetically informative designs (Reiss et al., 2000).
One aspect of young children’s environments that has received a great deal of attention as a potential source of non-shared environmental influence is sibling differences in their experiences of interaction with the same shared parents. Our own study of 3-year-old identical twins indicated that the differences in mothers’ warmth with each of their children predicted up to one-quarter of the difference in behavior problems within twin pairs (Deater-Deckard et al., 2001). The twin in each pair who received more maternal warmth tended to be happier, less aggressive, and more compliant than his or her sibling. This difference does not arise from genetic differences between the twins, because they are genetically identical.
Cataloging the mechanisms involved in non-shared environmental variation in outcomes of interest will help to explain why family members are often so dissimilar. Nevertheless, doing so will be difficult. Non-shared environment estimates also include error variance and non-genetic influences that operate in a non-systematic (and therefore unpredictable) way (Reiss et al., 2000; Turkheimer & Waldron, 2000). Also, the most direct test for these influences involves examining identical-twin differences, and because these sibling pairs are unique compared to all others (e.g., always same sex, same age, physically very similar), the findings may not generalize to non-identical-twin populations.
Shared environmental influences – those aspects of the environment that make family members similar – also can be identified using quantitative genetic methods. During early childhood, general cognitive ability includes moderate shared environmental variance. The same twin study of 3-year-olds just described revealed that much of the shared environmental variance in the preschool-aged twins’ cognitive ability was due to overlapping variance between task orientation (an aspect of temperament), family socio-economic status, and maternal warmth (Petrill & Deater-Deckard, 2004). In general, developmental research investigating family processes will be improved to the extent that the measurement captures both global and child-specific environments within families. Such measures, when incorporated into quantitative genetic designs, will allow for more precise specification of shared and non-shared environmental mechanisms.
Change and Development
Gene–environment processes are not static over time. Environments evolve, and the expressions of genes change as well. For example, in spite of very clear evidence of genetic variance in measures of temperament in early childhood, these genetic signals are not apparent in neonates (Reise, 1990) – a developmental period when infant temperament can play a powerful role in the quality of the parent–child relationship when it is first being established. Nevertheless, this genetic signal grows in strength over the first two years of life (Matheny, 1983).
The correlations and interactions between genes and environments also can change. Gene–environment processes also vary between population groups and across eras within populations. This dynamism requires that if the interplay between genes and environments is to be fully understood, investigations of gene–environment processes must be conducted within a developmental context and with serious consideration to the environmental, historical, and systemic conditions of the population under study.
Therefore, research examining gene–environment transactions must be guided by developmental theories. Scarr and McCartney (1983) proposed one such framework, in which predictions were made regarding developmental shifts in the relative contribution of various forms of gene–environment correlation mechanisms. According to their theory, as children become more self-controlled and competent, they exercise a greater deal of control over their own environments. As a result, the theory states that passive forms of gene–environment correlation will wane as non-passive forms (implicated in the elicitation of and selection into certain types of experiences) become more influential. There have been very few explicit tests of this hypothesis (for a rare example, see McCartney et al., 1990), yet if it is true, it has major implications for the way in which we interpret findings based on family studies in early versus late childhood. For example, research has shown fairly consistent evidence of a modest-to-moderate positive correlation between parental use of physical punishment and child aggressive behavioral problems (Gershoff, 2002). Most researchers believe that this correlation reflects a bi-directional process between parent and child – the parent who is harsh elicits escalating problem behaviors in the child, and the child who is more difficult to manage elicits harsher treatment by the parent. However, it also is possible that this bi-directional process may be primarily parent-driven when children are very young, but primarily child-driven when those children get older. Furthermore, these interpersonal processes may reflect complex gene–environment correlation and interaction mechanisms. Only genetically sensitive designs incorporating longitudinal data can be used for drawing such conclusive inferences about the nature of bi-directional gene–environment transactions in development.
Where the Environment Lives: Subjective Experience
Children’s subjective experiences are another environmental arena that is correlated with and interacts with genetic influences. Siblings who are more genetically similar report more similar retrospective accounts of their rearing environments and relationships with their parents, compared to less genetically similar siblings (Plomin, 1994). This may be due to evocative and passive gene–environment correlation effects. However, it is plausible that there are genetic influences on social information-processing mechanisms involved in selective attention and memory – mechanisms that influence how it is that children perceive and construe their experiences. Quantitative and molecular genetics research that focuses on children’s perceptions of their family environments will be able to test whether this is the case.
Measuring young children’s subjective experiences is a topic that has received renewed attention in recent years. Children’s styles of social information processing, especially with respect to understanding other people’s intentions, have been implicated in the explanation as to why some at-risk children show increasing tendencies toward aggression over time while others do not (Crick & Dodge, 1994). The internal environments children construct also likely contribute to the non-shared environmental variance often revealed in quantitative genetic studies. Recent research demonstrates that children’s self-reported social cognitions offer similar and improved predictive validity compared to parent and teacher reports (Measelle, Ablow, Cowan, & Cowan, 1998). Developmental researchers should take seriously the assessment of both the external/objective and internal/subjective components of children’s experiences if at all possible when investigating gene-environment transactions that shape early childhood development.
The evidence from quantitative genetic and, more recently, molecular genetic studies is clear in showing that genetic and environmental influences are operating together to produce the wide variations that we see between children in their physical and psychological functioning. However, much more work needs to be done. Researchers of early childhood must prepare themselves for integrating findings and research methods from molecular biology with the very best procedures currently used in mainstream developmental psychology. We should continue to refine even more precisely our operationalizations of the developmental outcomes that are of the utmost importance, as well as the environmental factors that are of greatest influence and that are most amenable to intervention.
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