One of the distinguishing principles that has guided research conducted within a developmental psychopathology perspective is that knowledge of normal development is necessary to comprehend psychopathology and that, conversely, the examination of maladaptive and psychopathological development can elucidate the normal functioning of individuals (Cicchetti, 1984, 1990a, 1990b, 1993; Rutter, 1986; Sroufe, 1990; Werner, 1948). Because all pathology can be conceived as a disturbance, distortion, or degeneration of normal functioning, in order to understand psychopathology it is essential that the normal functioning with which psychopathology is compared be fully grasped (Cicchetti, 1984, 1990a; Kaplan, 1967; Rutter & Garmezy, 1983). Likewise, understanding how mental disorders evolve and how aberrations in the organization of component developmental systems that exist among disturbed individuals eventuate may be informative for elucidating critical components of normal development.

Questions concerning the long-term effects of early experience on psychological development in humans continue to stir up controversy. There are, at present, great diversity and contradictions among extant conceptual models and inadequate data to resolve these differences. Limited opportunities to use experimental approaches and the inherent restrictions of observational approaches in research on humans implies that alternative research designs are needed. This article examines the use of “natural experiments” as a method for testing hypotheses concerning the effects of early experience on psychological development. The benefits and limitations of using natural experiments are reviewed and several case illustrations are considered.

During the past 10 years researchers studying children adopted from Romanian orphanages have had the opportunity to revisit developmental questions regarding the impact of early deprivation on child development. In the present paper the effects of deprivation are examined by reviewing both the early and more recent literature on studies of children who spent the first few years of life in institutions. Special attention is given to the Canadian study of Romanian adoptees in which the author has been involved. Findings across time and studies are consistent in showing the negative impact of institutionalization on all aspects of children's development (intellectual, physical, behavioral, and social–emotional). Results of studies show, however, that institutionalization, although a risk factor for less optimal development, does not doom a child to psychopathology. However, the impact of institutionalization is greater when coupled with risk factors in the postinstitutional environment. Methodological and conceptual difficulties in research with institutionalized samples of children are discussed and future directions for research are considered.

This paper provides an overview of the largest longitudinal investigation of institutionalized children less than 2 years old ever conducted. The Bucharest Early Intervention Project is an ongoing randomized controlled trial of foster placement as an alternative to institutionalization in abandoned infants and toddlers being conducted in Bucharest, Romania. In addition to describing the contexts in which this study is imbedded, we also provide an overview of the sample, the measures, and the intervention. We hope that the natural experiment of institutionalization will allow us to examine directly the effects of intervention on early deprivation. We hope it will provide answers to many of the critical questions that developmentalists have asked about the effects of early experience, the timing of deprivation, and the ameliorating effects of early intervention and provide clues to which underlying neurobiological processes are compromised by, and resilient to, dramatic changes in early experience.

Adoption provides a unique opportunity for the study of child development. Because adopted children are raised in families in which they have no genetic relationship with their parents, and possibly none with their siblings, they provide a rare opportunity to study the relative importance of genetic, shared environmental, and nonshared environmental influences on the development of child characteristics and behaviors. Because children are adopted from a variety of circumstances and at a wide range of ages, studies of adopted children and their families provide researchers the opportunity to examine the short- and long-term influences of a wide range of environments on children's development. Because children are adopted into homes with a range of characteristics (e.g., multiracial homes), adoption provides the opportunity to study the range of influences of these homes on child development. Adoption research that focuses on each of these areas is reviewed in this article. We present conclusions about the value of adoption in psychological research and some reasons why many psychologists ignore the opportunities presented by studying adoptive families, as well as potential useful directions for future research with adopted children and their families.

Analyzing gene–brain–behavior linkages in childhood neurodevelopmental disorders, a research approach called “behavioral neurogenetics,” has provided new insights into understanding how both genetic and environmental factors contribute to complex variations in typical and atypical human development. Research into etiologically more homogeneous disorders, such as fragile X syndrome, in particular, allows the use of more precise metrics of genetic risk so that we can more fully understand the complex pathophysiology of childhood onset neurodevelopmental disorders. In this paper, we review our laboratory's behavioral neurogenetics research by examining gene–brain–behavior relationships in fragile X syndrome, a single-gene disorder that has become a well-characterized model for studying neurodevelopmental dysfunction in childhood. Specifically, we examine genetic influences, trajectories of cognition and behavior, variation in brain structure and function, and biological and environmental factors that influence developmental and cognitive outcomes of children with fragile X. The converging approaches across these multilevel scientific domains indicate that fragile X, which arises from disruption of a single gene leading to the loss of a specific protein, is associated with a cascade of aberrations in neurodevelopment, resulting in a central nervous system that is suboptimal with respect to structure and function. In turn, structural and functional brain alterations lead to early disruption in emotion, cognition, and behavior in the child with fragile X. The combination of molecular genetics, neuroimaging, and behavioral research have advanced our understanding of the linkages between genetic variables, neurobiological measures, IQ, and behavior. Our research and that of others demonstrates that neurobehavior and neurocognition, genetics, and neuroanatomy are all different views of the same intriguing biological puzzle, a puzzle that today is rapidly emerging into a more complete picture of the intricate linkages among gene, brain, and behavior in developing children. Understanding the complex multilevel scientific perspective involved in fragile X will also contribute to our understanding of normal development by highlighting developmental events throughout the life span, thereby helping us to delineate the boundaries of pathology.

The uneven cognitive phenotype in the adult outcome of Williams syndrome has led some researchers to make strong claims about the modularity of the brain and the purported genetically determined, innate specification of cognitive modules. Such arguments have particularly been marshaled with respect to language. We challenge this direct generalization from adult phenotypic outcomes to genetic specification and consider instead how genetic disorders provide clues to the constraints on plasticity that shape the outcome of development. We specifically examine behavioral studies, brain imaging, and computational modeling of language in Williams syndrome but contend that our theoretical arguments apply equally to other cognitive domains and other developmental disorders. While acknowledging that selective deficits in normal adult patients might justify claims about cognitive modularity, we question whether similar, seemingly selective deficits found in genetic disorders can be used to argue that such cognitive modules are prespecified in infant brains. Cognitive modules are, in our view, the outcome of development, not its starting point. We note that most work on genetic disorders ignores one vital factor, the actual process of ontogenetic development, and argue that it is vital to view genetic disorders as proceeding under different neurocomputational constraints, not as demonstrations of static modularity.

The prenatal and early postnatal periods constitute a time of rapid development when the brain is in a state of both heightened plasticity and vulnerability. Premature infants and infants of diabetic mothers represent two experiments of nature that allow researchers to observe how the developing brain responds to early biological challenge of either a global or regionally specific nature. We outline a set of organizing principles for conceptualizing the mechanisms by which early adverse experience may be encoded in the brain and subsequently expressed in behavior. We then review the available literature on developmental outcomes for infants born premature and infants of diabetic mothers. Research examining the relative influence of experience and maturation in the development of preterm infants indicates that advance experience does not accelerate the advent of specific cognitive capacities, but may enhance performance once the particular ability has emerged. Long-term follow-up of preterm infants also reveals evidence for plasticity and cognitive improvement into early adolescence for later maturing executive functions. Finally we offer an integrated model for investigating cognitive outcomes in infants of diabetic mothers that incorporates data from animal, electrophysiological, and behavioral measures.

The human brain is functionally altered through experience, a phenomenon known as plasticity. Relevant experiences may be negative, as in brain injury. Adult brain injury results in permanent impairment. However, it has been assumed that early injury leads to substantial functional recovery. Animal studies suggest several predictions regarding whether this principle generally holds true. These studies indicate that the timing of brain injury, relative to the expected course of neurodevelopment, impacts the extent of recovery. Injuries occurring during the period of cell migration are particularly detrimental. However, outcome must be assessed longitudinally because apparent recovery in childhood may reverse as the brain matures. Moreover, recovery of one function may come at the expense of others. Whether these findings characterize outcome following preterm birth is the focus of this review. Preterm birth is associated with high rates of neurodevelopmental disability, primarily due to hypoxic–ischemic events. Periventricular brain structures and white matter tracts are particularly vulnerable to damage. Through school age, preterm children exhibit diminished levels of global intellectual function, attention, memory, and reasoning skills relative to full-term peers. It is questionable whether these deficits persist. Because few studies have followed recent cohorts into young adulthood, it is argued that outcome cannot be reliably described based on the available literature. Moreover, important contributors to later development have been neglected, including both genetic and experiential factors. With improved assessment, it may be possible to develop interventions based on the individual child's constellation of genetic, biological, and sociodemographic risks.

This paper examines the advantages that arise from an individual differences approach to children's coping and vulnerabilities. It suggests that the basic motivational and attentional systems involved in temperament constitute relatively primitive coping mechanisms. With development, these primitive coping skills are aided by representational and other cortical functions, allowing the coping process to begin before a stressful event and thereby increasing the child's capacity to plan an effective coping option and to enhance self-control. Such an emphasis on motivational and attentional differences allows us to take advantage of children's diverse personalities as “experiments of nature” and to better understand the temperamental patterns that contribute to adaptive and maladaptive outcomes.

False belief understanding was investigated in maltreated (N = 203), low socioeconomic status (SES) nonmaltreated (N = 143), and middle SES nonmaltreated (N = 172) 3- to 8-year-old children. Contrasts among the three groups provided an opportunity to examine the impact of family contextual influences on theory of mind development. Specifically, child maltreatment served as an “experiment of nature” in order to elucidate theory of mind abilities. Two false belief tasks and language assessments were administered. Among children with a verbal mental age of 49 months or greater, maltreatment was related to delays in the development of theory of mind, beyond the influence of chronological age and SES. The occurrence of maltreatment during the toddler period, onset during the toddler years, and physical abuse were features of maltreatment associated with delay in the development of theory of mind. Findings are discussed in terms of the influence of harsh caregiving on the development of theory of mind. Implications for the understanding of normal developmental processes are highlighted.

Human variability in temperament allows a unique natural experiment where reactivity, self-regulation, and experience combine in complex ways to produce an individual personality. Personality disorders may result from changes in the way past memories filter new information in situations of emotional involvement with others. According to this view, disorders are specific to their initiating circumstances rather than a general difficulty that might extend to classes of information processing remote from triggers for the disorder. A different view suggests a more general deficit in attentional control mechanisms that might extend to a wide range of situations far from those related to the core abnormality. This paper outlines methods for examining these views and presents data from the study of borderline personality disorder, arguing in favor of high negative emotionality being combined with a deficit in an executive attentional control network. Because this attentional network has already been well described in terms of anatomy, the cognitive operations involved, development, chemical modulators, and effects of lesions and candidate genes, these findings may have implications for understanding the disorder and its treatment. We consider these implications in terms of a general approach to the study of personality development and its disorders.