developmental psychopathology: concepts and...

Development and Psychopathology, 12 (2000), 265–296Copyright 2000 Cambridge University PressPrinted in the United States of America

Developmental psychopathology:Concepts and challenges

MICHAEL RUTTERaAND L. ALAN SROUFEb

aUniversity of London; and bUniversity of Minnesota

AbstractThe defining features of developmental psychopathology concepts include attention to the understanding of causalprocesses, appreciation of the role of developmental mechanisms, and consideration of continuities anddiscontinuities between normality and psychopathology. Accomplishments with respect to these issues are reviewedin relation to attachment disorders, antisocial behavior, autism, depressive disorder, schizophrenia, and intellectualdevelopment. Major research challenges remain in relation to measurement issues, comorbidity, gender differences,cognitive processing, nature–nurture interplay, heterotypic continuity, continuities between normal variations anddisorders, developmental programming, and therapeutic mechanisms in effective treatments.

Origins of a Developmental of the processes underlying both continuityPsychopathology Perspective and change in patterns. The focus was on the

how of developmental processes, rather thanKarl Popper (1972), the distinguished philos- on the charting of age-related progressions.opher of science, made the astute point that Many, perhaps most, causal processes weredefinitions need to be read from right to left,

viewed in terms of chain reactions operatingand not left to right. In other words, it makes

over time. Development was seen as an ac-no sense to ask what a word means. Rather,

tive, dynamic process that involved individu-we have to ask what is the concept or idea to

als processing (cognitively and affectively)which we wish to attach the descriptive term.

and adding meaning to their experiences, theSixteen years ago we succinctly referred to

biology of the individual influencing how in-developmental psychopathology as the study

dividuals respond to their experiences but, inof the origins and course of individual pat-

turn, the biology being shaped by those expe-terns of behavioral maladaption (Sroufe &

riences. Because development was likely toRutter, 1984). We went on to emphasize that

be affected by experiences that often occurredthe main aim was to provide an understanding

for the first time only in adult life (such asmarriage, rearing children, and establishing awork career), development was viewed as ex-We are greatly indebted to Dante Cicchetti for his invalu-

able suggestions on an earlier draft of this paper, as well tending into adult life—a life-span approach.as for his leadership of the field over many years. In addi- The end product of development was, there-tion, however, this account of developmental psychopath- fore, conceptualized, not as the attainment ofology has been possible only as the result of the creative

biological maturity or the highest level ofresearch of many pioneers from both developmental andcompetence or the stabilization of personalityclinical fields; we wish to express our deep appreciation

for their contributions, which have done so much to set traits but rather as the establishment of a co-an exciting and fruitful research agenda. herence of functioning as a thinking, feeling

Address correspondence and reprint requests to: Prof.human being. In this essay, we look back onSir Michael Rutter, Social, Genetic & Developmentalthe origins of the domain of developmentalPsychiatry Research Centre, Institute of Psychiatry, De

Crespigny Park, Denmark Hill, London SE5 8AF, UK. psychopathology, consider its current stand-

265

M. Rutter and L. A. Sroufe266

ing, review some of its accomplishments, and developmental operation of the complex mixof influences that give rise to resilience in thelook forward to the very considerable chal-

lenges that remain. face of adversity (Masten & Curtis, 2000;Rutter, in press-a; Sroufe, 1997), and to real-ize that individuals cannot be subdivided cate-

Positive influences on originsgorically into the vulnerable and invulnerable.There were many individuals who suffer inMany ideas, and many people, played critical

roles in the emergence of developmental psy- some ways but not in others (Luthar, Cic-chetti, & Becker, in press). Furthermore,chopathology as a key perspective on both de-

velopmental processes and the causes and some of the adverse outcomes take the formof serious patterns of social malfunction thatcourse of psychopathology. We make no at-

tempt to cover these in exhaustive fashion but, do not fit readily into any of the existingpsychiatric diagnostic categories (Richters &rather, provide a few disparate examples to

indicate the diversity of the roots of the per- Cicchetti, 1993; Rutter, in press-c). If riskprocesses are to be understood adequately, in-spective. In so doing, we have sought to pro-

vide a balanced overview of perspectives, vestigations need to include detailed longitu-dinal studies of risk populations, as well asrather than expound our own positions, al-

though doubtless our own views will have large-scale epidemiological studies. Hether-ington’s (1989; Hetherington & Clingempeel,colored our scientific vision to some extent.

We begin with risk research because it is 1992; Hetherington & Stanley–Hagan, 1997)studies of divorce and stepparenthood well il-paradigmatic of developmental psychopathol-

ogy (Sroufe & Rutter, 1984). At first, particu- lustrate this trend.Of all the specific features of development,larly in the United States, both the origins and

the outcomes of risk were viewed in diagno- the study of emergence of selective attach-ments, our second example, was possibly thesis-specific terms (Garmezy, 1974). Thus,

longitudinal studies were set up to examine most crucial in moving thinking in a develop-mental psychopathology direction. Early stud-the emergence of schizophrenia in the off-

spring of mothers with a schizophrenic disor- ies had made clear both the importance of se-lective attachments and the phases of earlyder. It soon became clear, however, that many

of the children who did not develop schizo- development that were involved in their estab-lishment (Bowlby, 1969). Ainsworth, Blehar,phrenia did show other forms of psychopath-

ology, and that the risks for such psychopath- Waters, and Wall’s (1978) recognition thatnot only were universals of development in-ology also derived from other forms of mental

illness in parents (Rutter, 1989a). Epidemio- volved but also patterns of attachment rela-tionships differed in the degree of securitylogical studies provided a further extension in

their demonstration that many of the risks provided and that these individual differencesmattered for later development moved devel-were found in families exhibiting discord, dis-

ruption and disharmony but where the parents opmental thinking into an individual differ-ences perspective. It was, however, an indi-had no diagnosable mental illness (Rutter &

Quinton, 1984). Studies of all manner of vidual differences perspective that involved akey shift from trait views. The individual dif-risks, both mild and severe, were consistent in

their demonstration of the extreme heteroge- ference initially lay in a dyadic relationship,and only later did this become transformedneity of outcome and in their indication that

it was the number of serious risks, rather than into something more akin to an individualcharacteristic (Sroufe, 1989). Also, the indi-the nature of any one, that was critical (Sam-

eroff, 2000). Given the same risk experience, viduality, as carried forward in time, wasthought to derive from a particular way ofsome children succumb with disorder whereas

others seem to escape largely undamaged. At- thinking about relationships, or cognitive set,termed an internal working model (Brether-tention, increasingly, came to be drawn to the

need to consider both risk and protective ton, 1995; Bretherton & Waters, 1985). Thefunctions of behavior were crucial. Thus, themechanisms (Rutter, 1990), to understand the

Developmental psychopathology: Concepts and challenges 267

approach behavior of attachment in the tod- no sense to assume one or the other. Instead,the research advantage lay in examining whatdler age period was viewed as (and empiri-

cally found to be) a precursor of later inde- was involved in the continuities and disconti-nuities between normal and abnormal behav-pendence (rather than dependence), if the

attachment relationships were secure (Sroufe, ior (Rutter, 1986a).A further stimulus came from the growth1983; Sroufe, Fox, & Pancake, 1983). A prob-

abilistic “pathways” model of development of findings and theories in the domain of life-span development (Baltes, Staudinger, & Lin-was a key feature (Rutter, 1989b; Sroufe,

Egeland, & Carlson, 1999). denberger, 1999; Hetherington, Lerner, &Perlmutter, 1988; Rutter & Rutter, 1993). TheA third area of research that was influential

concerned the study of cognitive processing importance of this field of inquiry derivedfrom the important changes in functioningof experiences. Findings in the fields of both

antisocial behavior (Dodge, Bates, & Pettit, that take place in adult life; the powerful im-pact of key experiences in adult life; the find-1990; Dodge, Pettit, Bates, & Valente, 1995)

and depression (Garber, Quiggle, Panak, & ing that people varied in the life trajectoriesthey took, and that it was misleading to seeDodge, 1991; Teasdale & Barnard, 1993)

showed the importance of individual differ- development as a single universal progressionthat varied only in its timing (see Emde &ences in the attributions that people make to

the experiences and personal interactions that Spicer, 2000); the importance of social con-text; and the extent to which what had seemedthey encounter. The importance of this body

of research lay in its emphasis on the active to be universals were much influenced by lifeexperiences. For example, it had been thoughtthinking and feeling processes that were in-

volved in the interplay between persons and that a thinning of the bone structure was aninevitable part of aging but it became appar-their environments. The findings pointed to

the need to move away from a sharp dichot- ent that this was very considerably attenuatedif the individuals continued to engage inomy between risk factors based on environ-

mental hazards and risk factors involved with strenuous physical exercise as they grew older(Lane, Bloch, Jones, Marshall, Wood, &personal attributes. A more dynamic apprecia-

tion of how the two worked together was re- Fries, 1986; Lane, Bloch, Wood, & Fries,1987).quired.

The fourth positive stimulus derived from The principles that unite these disparateexamples include the concept of developmentstudies of children with handicapping disor-

ders. The findings showed both the common- as an active dynamic process in which themeanings attributed to experiences alter theiralities in the course of development shown by

normal and handicapped children (Cicchetti & consequences, and the notion of individualpathways that diverge in both their originsSroufe, 1978) and also the marked differences

associated with certain disorders, such as au- and endings (Cicchetti & Rogosch, 1996).tism (Hermelin & O’Connor, 1970). Studiesof individuals with gross sensory handicaps

Limitations in traditional theoriesprovided an interesting mixture of the two

and concepts(O’Connor & Hermelin, 1978). What the re-search demonstrated was the very consider- In part, too, developmental psychopathology

perspectives arose because of limitations inable extent to which comparisons acrossgroups could be informative about the mecha- the traditional developmental and psychiatric

concepts as they applied during the 1970s.nisms involved in both normal and abnormaldevelopment. There was a need to avoid false Progress in psychiatry had been greatly

helped by the appreciation of the importancedecisions about whether there were continui-ties between normal and abnormal or whether of diagnosis and classification and by the de-

velopment of standardized approaches tothe presence of disorder marked a qualitativediscontinuity. The research was clear in its in- both. On the other hand, there was concern

about the unhelpful reification of diagnosticdication that both could be found, and it made


categories (Rutter & Shaffer, 1980). Instead of experiences as well as the years of biologi-cal growth.of being treated as useful working hypotheses,

Second, very little attention was being paiddiagnostic systems were becoming increas-to the transition into adult life. This is a curi-ingly constraining, with their implication thatous lack because, if development is seen ascategories represented some form of realthat which leads up to adulthood, its under-truth. It was not so much that the categoriesstanding necessarily required a study of adultlacked diagnostic validity (there was good ev-outcomes (see Cicchetti & Toth, 1995). Oneidence for at least partial validity of some ofmight suppose that what would characterizethe main diagnoses; Cantwell & Rutter, 1994)developmental psychology most of all wouldbut rather that there was too little appreciationbe a focus on longitudinal studies thatof the limitations in what was known. Allspanned the period from infancy to adult life.sorts of rules had been devised to differentiateIn fact, the opposite was more the case (Debetween disorder and normality without anRibaupierre, 1989). Most developmentalistsadequate understanding of the extent to whichspecialized in a very narrow age period, andso many psychopathological concepts weremost research was cross-sectional rather thandimensional (Achenbach, in press), with thelongitudinal.need to account for variations along the di-

Third, little attention was paid to the causalmensions and not just for the causes of ex-processes involved in individual differencestreme disorders. This was evident, for exam-in development. There were many exceptionsple, in the fields of disruptive behavior,to these limitations, and there was much thatanxiety, and depression. Much causal researchwas good in developmental research. Never-seemed to be based on the expectation thattheless, the perspectives needed to be broad-one single main cause for any disorder wouldened. Achenbach’s (1974) textbook, the firstbe found and that the cause would be diagno-labeled “developmental psychopathology,”sis specific. Too little attention was paid towas pioneering in that concern.the possibility that the mechanisms involved

Fourth, it had become increasingly obviousin causation might entail dynamic processesthat the prevailing developmental theoriesoperating over time, that indirect chain effectswere inadequate in a whole variety of ways.

might often be present, and that there mightTo begin with, most focused on the universals

be several different routes to the same out-of a progression through predetermined

come. Of course, there was a great deal ofstages, whether defined in terms of psycho-

value in the psychiatric research perspectives sexual stages (Freud, 1953), cognitive phasesthat were being taken, and, in addition, there (Gelman & Baillargeon, 1983; Piaget, 1970),were many exceptions to these apparent rigid- or social tasks and crises (Erikson, 1950),ities. Nevertheless, a broadening of perspec- with individual differences seen in terms of atives was needed. stage fixation or regression or a phase adapta-

Parallel, but different, concerns applied to tion.developmental psychology. To a considerable There were three main types of problem.extent, research seemed to be preoccupied First, most of the theories seemed to portraywith an undue concern to chart the universals an all-encompassing view of life, rather thanof developmental progression. Three main an attempt to provide an explanation for par-limitations stood out. First, there was a ten- ticular empirical phenomena. On the face ofdency to regard age as a sufficient explanation it, there seemed to be an untenable assump-for this progression (Wohlwill, 1970, 1973). tion that a single theory could account for allIt came to be appreciated that age constituted the complexities that were involved in devel-an ambiguous measure (Rutter, 1989c). Bio- opment. Second, theories failed to address alogical maturity was not a single thing; hor- host of crucial developmental issues. Little at-monal maturity and brain maturity, for exam- tention was paid to biological processes or ge-ple, did not proceed directly in parallel. Also, netic influences, and gender differences were

inadequately conceptualized. Third, all thenecessarily, age indexed the nature and extent


theories had a poor empirical basis, and re- levels, operate on a dimensional basis withvariations within the normal range being asso-search findings showed the many ways in

which the theories were seriously wrong on ciated with differences in risk. The causal pro-cesses operate over a long period of time, be-numerous essentials (Bowlby, 1988; Bryant,

1974; Piaget, 1970; Rutter, 1971a). ginning early in life. Thus, for example, it hasbeen found that infants of low birth weightOf course, these big theories had been im-

portant historically in ways that have stood have a substantially increased risk of cardio-vascular disease in later life (Barker, 1998;the test of time. Thus, psychoanalytic theory

was very important in drawing attention to the Nathanielsz, 1999). The finding is of interestbecause that is the opposite of the way inrole of mental mechanisms and of emotional

influences, Piagetian theory to the role of ac- which weight operates in middle age (whenthe risks are associated with being overweighttive cognitive processes, and Eriksonian the-

ory to the importance of social context and and not underweight). The notion of develop-mental programming (Bock & Whelan, 1991)social challenges. Nevertheless, they were

ceasing to serve a useful role, and it was nec- has come to the fore, whereby it is thoughtthat the body-regulating systems are adaptedessary to move on. Although it was clear that

good developmental research required a hy- in early life to low levels of nutrition and thatthe risk comes from being, therefore, mal-pothesis-testing approach, it was equally ap-

parent that it was completely implausible that adapted to high levels of nutrition in later life.The importance of social factors in the gene-any one theory could account for all develop-

mental phenomena. Bowlby’s (1969) judi- sis of somatic disease (including cardiovascu-lar conditions) has been well established for acious integration of perspectives in his formu-

lation of attachment theory provided a useful long time. McKeown (1976), in the 1950s and1960s, pointed out that the huge improve-alternative model.ments in infantile mortality and the increasein life expectancy in the first half of this cen-

The Current Standing of Developmentaltury were largely attributable to improved liv-

Psychopathologying conditions and improved nutrition, withmedical advances being of limited impor-Developmental psychopathology perspectives

have become mainstream now, in both devel- tance. The huge social disparities in levels ofillness are well documented (Acheson, 1998;opmental psychology and psychiatry, al-

though, quite properly, they do not constitute Townsend & Davidson, 1992; Wilkinson,1996), and psychological factors too have athe whole of either. Thus, with respect to psy-

chiatry, a major body of research is concerned well-demonstrated role (Marmot & Wilkin-son, 1999). Medicine has also long appreci-with the evaluation of methods of treatment

and of the delivery of services. Similarly, and ated that a single-risk factor can lead to quitediverse disorders (smoking is an obvious ex-equally appropriately, developmental psychol-

ogy is concerned with studying what is in- ample of this kind) and that the same diseaseend point may come from rather varied causalvolved in developmental processes as they

apply universally. Both of these are of interest pathways, as the study of comorbidity well il-lustrates (Rutter, 1997a). All of this closelyto developmental psychopathology, but they

do not constitute a key feature. parallels the perspective of developmentalpsychopathology. The perspective is a biolog-It is also relevant that the perspective rep-

resents an equally mainstream, modern, medi- ical one that encompasses medicine and be-havior equally. The importance of emphasiz-cal model. Thus, for example, with respect to

cardiovascular disease, it has long been recog- ing this is that, in the past, there has been atendency for behavioral scientists to wish tonized that there is multifactorial causation, in-

volving influences as diverse as cholesterol develop a special set of mechanisms and ofconcepts that apply specifically to psychologi-levels, clotting factors in the blood, smoking,

lack of exercise, obesity, and sex hormones. cal development, as if this were somehowseparate or different from the rest of bodilyMany of the risk factors, such as cholesterol


functioning. It is not. It is true, of course, that mental psychopathology perspective. First, anunderstanding of causal processes requiresthe study of cognitive and affective processes

is distinctive of psychology and psychiatry knowledge about how risk and protectivemechanisms operate. With rare exceptions, all(and vital in developmental psychopathology

perspectives), but this is part of biology and behavior is influenced by both genetic and en-vironmental factors, and knowing the propor-medicine and not separate from it.tion of the population variance accounted forby each is, on its own, uninformative about

Central Concepts of Developmentalhow the causal process operates. The need to

Psychopathologyfind out how causal processes operate has im-portant design implications for research. Re-Although there are many features of develop-

mental psychopathology that could be consid- views have considered those relevant to thestudy of environmental risks (Rutter, Pickles,ered important, we suggest that the defining

features can be reduced to the approach taken Murray, & Eaves, 2000), and those that applyto genetic research (Rutter et al., 1999a,to three key issues: (a) the understanding of

causal processes, (b) the concept of develop- 1999b; Rutter, in press-a). As already noted,it will usually be necessary to study the opera-ment, and (c) continuities and discontinuities

between normality and pathology. tion of causal processes as they operate overtime through direct and indirect chain effects,and a developmental perspective also requires

Causal processesquestioning how effects are carried forwardand how they influence the way the individualThe rising influence of behavior genetics in

recent years, supported by empirical research deals with later situations and circumstances.Second, behavior–genetic partitioning offindings (Rutter, Silberg, O’Connor, & Simo-

noff, 1999a, 1999b), has led many psycholo- population variance is entirely concerned withthe study of individual differences. That isgists and psychiatrists to think increasingly

that the study of causal processes can be re- only one of several types of causal questions.For example, both theoretical and publicduced to the partitioning of population vari-

ance into additive and nonadditive genetic, health considerations require attention to thecauses of differences in level of a trait or aand shared and nonshared environmental, ef-

fects. The findings have, undoubtedly, been disorder. Thus, for example, why has therebeen such a massive rise in the rate of soimportant in showing that genetic factors play

a major role in individual differences in all many psychosocial disorders in young peopleover the last 50 years (Rutter & Smith, 1995)?kinds of behavior. Among other things, the

genetic findings have been crucially important Or, why has there been a rise in the overallIQ level over this century (Anderson, 1982;in showing that genetic influences operate

with respect to normal variations in behavior Flynn, 1987)? Or, why are most forms of anti-social behavior so much more prevalent inas well as to diseases and disorders.

Some developmentalists (Baumrind, 1993) males than females (Moffitt, Caspi, Rutter, &Sylva, 2000), and why are depressive disor-and some neuroscientists (Rose, 1995) have

worried that this implies a genetic determin- ders (Bebbington, 1996) and eating disorders(Lucas, Beard, O’Fallon, & Kurland, 1991;ism. We do not share that concern. One of the

most important messages of genetic research Nielsen, 1990) more characteristic of womenthan men?has been that genetic influences are probabi-

listic and not deterministic, and that environ- It is important to appreciate that the causalprocesses involved in differences in level maymental factors and genetic factors are broadly

speaking of roughly equal importance not be the same as those involved in relationto individual differences (see Tizard, 1975,(Plomin & Rutter, 1998; Rutter & Plomin,

1997). with respect to the same point in relation tothe huge secular increase in average heightWe do, however, have three rather differ-

ent concerns that are central to a develop- during the first half of this century). A differ-


ent type of causal question concerns course. ate the importance of personal effects on theenvironment that are not genetically medi-Many disorders involve several distinct

phases. Thus, for example, in order for per- ated. Bell (1968) first pointed out, in a semi-nal paper, the importance of recognizing thesons to develop drug dependency, they must

first take the drug, they must progress to tak- need to determine the direction of socializa-tion effects. That there are important effectsing it regularly, and they must then develop a

psychological or pharmacological dependency of children on their environments has beenshown through a variety of research designson the substance. Factors that influence each

of these phases may be rather different (Rob- (Bell & Chapman, 1986); O’Connor, Deater–Deckard, Fulker, Rutter, and Plomin (1998)ins, Davis, & Wish, 1977), as well illustrated

by Robins’s (1993) study of heroin depen- showed that, with respect to antisocial behav-ior, most of the children’s effect on theirdency in Vietnam veterans. Also, the factors

associated with the onset of the first episode parents was not a function of genetic risk.Longitudinal research designs are ordinarilyof a depressive disorder may not be the same

as those associated with its repeated recur- necessary for differentiating between personaleffects on the environment and environmentalrence (Post, 1992).

A further type of causal question concerns effects on the person; as already noted, theyconstitute a key feature of a developmentalthe factors involved in the translation of an

individual liability into the commission of a psychopathology research perspective (Sroufe,in press).particular behavioral act such as attempting

suicide or undertaking a burglary. The predis- Person–environment interplay is character-ized by complex chains, sometimes involvingposing influences are often rather different

from those concerned with individual differ- heterotypic continuity. For example, avoidantattachment in infancy is associated with laterences in liability, and they involve factors

within the individual, such as alcohol intoxi- conduct problems, but avoidant attachment isalso associated with low self-esteem (Sroufe,cation, or situational factors, such as the avail-

ability of the means of the suicide or opportu- 1983), negative attributional biases (Suess,Grossman, & Sroufe, 1992), and rejection bynities for crime (see Rutter, Maughan, Meyer,

Pickles, Silberg, Simonoff, & Taylor, 1997, peers and teachers (Sroufe & Fleeson, 1988),all of which may predispose to conduct prob-for a discussion of these issues with respect

to antisocial behavior). lems. We are only beginning to understandhow these chain effects operate in predisposi-The third concern about the need to move

beyond partitioning the population variance in tion to psychopathology. Their understandingprovides an unavoidable tension between thethe study of causal processes is that nature

and nurture are not neatly separable in the need to seek simplification (the hallmark ofall good science) and the need to note com-way that was once envisaged (Bronfenbren-

ner & Ceci, 1994; Rutter, Dunn, Plomin, Si- plexity. Research has often suffered from un-warranted simplifying assumptions, but a truemonoff, Pickles, Maughan, Ormel, Meyer, &

Eaves, 1997; Rutter 1997b). Behavior geneti- understanding of biological processes usuallyshows that the complexity is explicable incists have produced an increasing body of evi-

dence on the importance of different types of terms of a limited set of unifying mechanismsand principles.gene–environment correlations and also

gene–environment interactions. In the tradi-tional way of tackling partitioning the vari-

The role of developmentance, these will all be included under genet-ics, although, by definition, they have their In 1984 (Sroufe & Rutter, 1984), we argued

that it was possible to understand the complexeffects through interplay with the environ-ment. links between early adaptation and later disor-

der only through detailed appreciation of theIn recent years, most of the discussion inthe literature has concerned gene–environ- nature of the developmental process itself.

This entails a progressive transformation andment correlations, but it is crucial to appreci-


reorganization of behavior as the developing the influences as restricted to the genetic andthe environmental. The genetic programmingorganism continually transacts with the envi-

ronment. We stressed that development neces- of development is probabilistic rather than de-terminative (Michel & Moore, 1995). Thus,sarily involved a change (because that is what

development is all about) but, also, that it in- neuronal migration is a key feature of earlybrain development, but the genetic program-volved a degree of continuity and the estab-

lishment of some coherence. It could be ar- ming provides a general instruction as towhere neurons are meant to go, rather than agued that the introduction of the notion of

development does not add anything to the control of what happens with each and everynerve cell (Goodman, 1994). It is because ofstudy of behavior because development, like

behavior, is subject to the same mix of genetic this probabilistic feature that one important el-ement in brain development concerns the se-and environmental influences that have to be

investigated and delineated. However, al- lective pruning of neurons that have not endedup in the right place. That means that there isthough that is the case, and although it is diffi-

cult to define the differences between devel- stochastic, or random, variation in develop-ment—what Molenaar, Boomsma, and Dolanopment and other forms of behavioral change

(Harris, 1957; Rutter, 1984), it misses the (1993) have called “the third force,” meaningbeyond genetic and environmental influences.point for three main reasons (Gottlieb, Wahl-

sten, & Lickliter, 1998; Wahlsten & Gottlieb, For example, each girl inherits two X chromo-somes, one from each parent, but only one of1997).

First, the overall, universally applicable these remains functionally active. One is inac-tivated, or “switched off,” and it seems thatpattern of biological development is deter-

mined by nonsegregating genes possessed by which one it is is randomly determined, as isthe case with various other biological pro-all humans. For example, over the course of

evolution, all humans have come to have cesses (see Goodman, 1991).The third consideration is that the study ofgenes that provide the possibility of language

(these genes not being possessed, e.g., by causal processes has to be concerned with thecarryforward of effects, whether they be ge-mice). Many of the universals of development

are of this kind (see, e.g., Kagan, 1981). netic or environmental. In each case, it is im-portant to ask about the nature of internalThese universals (the occurrence of which is

not influenced by either genes or experiences changes within the individual that are takingplace (Rutter, 2000). Thus, with respect tothat differ among children) are important be-

cause they may have important implications psychosocial experiences, these may involvevariations in brain structure (Cicchetti &for adaptation and maladaptation. Thus, there

are well-documented age-dependent differ- Tucker, 1994; Liu, Diorio, Tannenbaum,Caldji, Francis, Freedman, Sharma, Pearson,ences in vulnerability to particular kinds of

experiences, and there are age-dependent vari- Plotsky, & Meaney, 1997; O’Brien, 1997), oralterations in neuroendocrine functioningations in the incidence of disorders (Petersen,

1993; Rutter, 1986a; Sroufe, in press). Of (Hennessey & Levine, 1979), or modifica-tions of affect regulation (Sroufe, 1996), orcourse, it cannot be assumed that these varia-

tions are a consequence of biological matura- changes in cognitive set or cognitive process-ing (Dodge et al., 1990, 1995), or altered pat-tion, but that does constitute one possibility

requiring investigation. Moreover, with re- terns of interpersonal interaction (Pawlby,Mills, & Quinton, 1997; Pawlby, Mills, Tay-spect to certain well-established variations—

for example, the response to brain injury (see lor, & Quinton, 1997; Quinton & Rutter,1988).Vharga–Khadem, Isaacs, van der Werf,

Robb, & Wilson, 1992)—biological matura-The continuities and discontinuities betweention almost certainly is responsible.normality and psychopathologyThe second consideration with respect to

development is that, even when considering The central concern for developmental psy-chopathology is delineation of what is in-individual differences, it is misleading to see


volved in the continuities and discontinuities from research by scientists who would notidentify themselves as using developmentalbetween normality and pathology. Two points

are crucial in this connection. First, the key psychopathology (that would perhaps particu-larly apply to research in the field of adultissue concerns continuities and discontinuities

in mechanisms, and not just in measures. Sec- psychiatry). As noted in the introduction tothis paper, one of the marks of the achieve-ond, even with the same feature, it is often the

case that both continuities and discontinuities ment of a developmental psychopathologyperspective is that it has become mainstreamare present. For example, IQ functions dimen-

sionally as a predictor of educational attain- and is no longer easily separated off as a dif-ferent approach. Our aim, however, is to showment or social competence right across the

range, extending from profound retardation to something of the value of a developmentalpsychopathology perspective, rather than theabove-normal levels of functioning. On the

other hand, for the most part the causes of achievements of individuals who would iden-tify with this approach. We have chosen tosevere and profound retardation are quite dif-

ferent from the causes of the variations in IQ structure this section of the paper accordingto different types of psychopathology and, inwithin the normal range or, even, of mild

mental retardation (Cantwell & Rutter, 1994; looking forward into the next millennium, westructure the challenges in terms of issues andRutter, Simonoff, & Plomin, 1996). Similar

issues apply to many other forms of behavior. mechanisms, rather than disorders. Neverthe-less, in looking back into the past, we do drawFor example, the phenomenon of depression

clearly spans normality and disorder in a di- attention to some of the outstanding researchneeds with respect to the disorders that wemensional way, but it may also be the case

that bipolar affective psychoses are discontin- consider.uous with normal variations in mood (Perris,1992).

Attachment disordersA further point is that, regardless of

whether or not the underlying liability to psy- Attachment concepts have come to have anincreasing prominence in developmental re-chopathology is dimensional, with a contin-

uum spanning normality and disorder, cate- search in recent years. Six main trends maybe identified. First, many studies have showngorical decisions will often be required for

practical purposes. Thus, clinicians need to that early insecure attachment relationshipsare associated with a higher risk of later psy-decide whether or not to use antidepressant

medication or to admit somebody to hospital. chopathology (Belsky & Nezworski, 1988;Cassidy & Shaver, 1999; Sroufe, Egeland, &It is important to distinguish between these

practical requirements for having diagnostic, Carlson, 1999). Increasingly, clinical re-searchers have sought to apply attachmentor severity, categories and an understanding

of the underlying patterning of behavior. concepts to an understanding of the genesis ofdifferent forms of psychopathology in child-hood and adolescence and to the development

Past Value of Developmentalof methods of treating them. The findings em-

Psychopathologyphasize the importance of social relationshipsin human functioning and the extent to whichBecause developmental psychopathology, as

conceptualized by us, has been such a bur- they are affected in a wide range of disorders(Hinde, 1997). Nevertheless, there is a dangergeoning field in the last 2 decades, it would

require a textbook to discuss the many ad- that attachment concepts become too all ex-planatory. Attachment features do not consti-vances that have derived from adopting a de-

velopmental psychopathology perspective. In tute the whole of relationships (indeed, oneof Bowlby’s, 1969, key contributions, was thethis section of the paper, we therefore provide

only a limited set of examples to illustrate differentiation of attachment features fromother aspects of relationships), and insecuresomething of the range of accomplishments.

Some of the examples that we give derive attachments are not themselves indicative of


psychopathology (Sroufe, 1988; Rutter, 1995). and other forms of observational methodswere needed.Research must meet the challenge of deter-

mining just how insecure attachment relation- Earlier research had shown that the old-style notion of fixed critical periods for devel-ships play a role in psychopathology, putting

competing explanations under research scru- opment were misleading, but new findings ofvarious kinds have highlighted the importancetiny and not just assuming the primacy of an

attachment paradigm (see Rutter, 2000b, and of age-defined periods of especial vulnerabil-ity (“sensitive periods”) to particular kinds ofRutter, Pickles, et al., 2000, for a discussion

of the broader issue of testing causal hypoth- stress or adversity. Thus, the follow-up studyof children placed in residential nurseries ineses).

Second, there has been a growing attention infancy, undertaken by Hodges and Tizard(1989a, 1989b), showed that antisocial behav-to the social development of children reared

in grossly abnormal environments. This ne- ior was more a function of current social cir-cumstances and adolescence than the situationcessitated several developments. To begin

with, it soon became apparent that the tradi- in very early childhood. By contrast, both thechildren who had been restored to the biologi-tional ways of classifying security and insecu-

rity were not always picking up the features cal parents (and often were living in discor-dant, disadvantageous circumstances) andthat seemed most distinctive of these children

reared in highly atypical circumstances (Von- those who had been adopted (and who weremainly in above-average quality homes) dif-dra & Barnett, 1999). Much earlier, Main and

Solomon (1986) had recognized the need for fered from controls in showing a pattern ofpeer relationships that lacked intensity and se-a category of “disorganized attachment” (see

review by van IJzendoorn, Schuengel, & lectivity. The features were not normal, butthey did not constitute a disorder in the usualBakermans–Kranenburg, 1999, on its quali-

ties), and this seemed to apply particularly to psychiatric sense. Like the findings of indis-criminate friendliness, the links with earlierchildren from grossly abnormal backgrounds.

In addition, because many of the children be- attachment relationships remain uncertain, butit seems very likely that, in some way, theing studied were substantially older than the

age period below 2 years for which the lack of opportunity to form selective attach-ments in early childhood predisposed to these“Strange Situation” had been developed, some

modifications of procedure were required later features in peer relationships and adultrelationships. Findings of this kind highlight(Waters, Vaughan, Posada, & Kondo–Ike-

mura, 1995). They were also necessary be- the need to understand how early selective at-tachments are related to other social relation-cause the scattered nature of unusual samples

often meant that the children needed to be as- ships in later life.A fourth important trend in the field of at-sessed in their own homes rather than in the

research laboratory. In addition, studies of tachment concerns the extrapolation of attach-ment concepts into adult life (Hazan &children reared in severely depriving Roma-

nian orphanages, and later adopted into North Shaver, 1994). Various measures of differentaspects of adult relationships have been devel-American (Chisholm, 1998) or UK families

(O’Connor, Bredenkamp, Rutter, & the En- oped. The adult attachment interview has fo-cused especially on the cognitive set of rela-glish and Romanian Adoptees [ERA] Study

Team, 1999; O’Connor, Rutter, & the ERA tionships that is thought to have been derivedfrom the individual’s relationships in earlyStudy Team, in press), showed a pattern of

somewhat indiscriminate friendliness to life (Main, Kaplan, & Cassidy, 1985; van IJ-zendoorn, 1995). From all points of view, itadults that was not well picked up by the

presses of the “Strange Situation” procedure makes sense to extend attachment conceptsinto adult life. After all, the loss of a love rela-when it was used with postinfancy age groups

(Goldberg, 1997; Marvin & O’Connor, 1999), tionship constitutes a major risk factor at allage periods after infancy, and there is a uni-although noted by Bowlby (1973) as indica-

tive of attachment problems. Both interview versal wish to seek security in close intimate


human relationships. On the other hand, much dertaken. Traditionally, the measurements ofsecurity of attachment have been categorical,work has still to be done sorting out the conti-

nuities and discontinuities across the life span. although it would seem conceptually thatthere are underlying dimensions. Well-vali-The early childhood measures are dyadic,

whereas the measures in adult life reflect indi- dated dimensional measures are needed, andare being developed, in order to examine con-vidual characteristics. Also, in order to extend

into older age, it will be necessary to alter tinuities and discontinuities across the span ofbehavioral variation (Waters et al., 1995).concepts in fairly substantial ways. In the

years ahead, it will be important to put to rig-orous test the various assumptions that under-

Antisocial behaviorlie the extrapolations across ages and acrossdifferent types of relationships. It has been appreciated for a long time that

antisocial behavior is heterogeneous, but untilA fifth trend has been the study of inter-generational continuities and discontinuities recently the ways of subdividing it had proved

rather unsatisfactory. A way forward was pro-(see Fonagy, Steele, Steele, Higgitt, and Tar-get, 1994). Strikingly, several studies have vided by the recognition by Patterson (1995;

Patterson & Yoerger, 1997), Moffitt (1993),found that the security of the mother’s adultattachments, as assessed by the Adult Attach- and others that the age of onset, together with

course, might prove to be a key differentiatingment Interview during her pregnancy, pre-dicted the security of the infant’s attachment feature. A distinction was drawn between life-

course-persistent antisocial behavior and ado-to its mother. Similar, the mothers’ prenatalrepresentation of their infant has also pre- lescence-limited antisocial behavior. Empiri-

cal research has broadly confirmed the valid-dicted the infants’ attachment security (Be-noit, Parker & Zeanah, 1997). Questions re- ity of this distinction (Lahey, Waldman, &

McBurnett, 1999; Rutter, Giller, & Hagell,main on the mediation mechanisms involvedand on the factors leading to differences in 1998). The life-course-persistent variety,

which is much more common in males (Mof-attachment security among children beingreared in the same family. fitt et al., 2000), is characterized by the first

manifestations of markedly disruptive behav-Over recent years, too, there has been theapplication of attachment concepts to all sorts ior in the preschool years, by an association

with hyperactivity–inattention, by poor peerof abnormal groups, but all too often the mea-sures used both depart considerably from relations, by difficult behavioral features (of-

ten involving aggressivity, impulsiveness, andstandard attachment measures and also lackproven validity (Rutter & O’Connor, 1999). sensation seeking), and by mild cognitive im-

pairment. Family discord and disruption standThe potential is rich, but there is a great needto bring together the kind of approaches used out as part of the mix of risk features, and

insecure attachment relationships are oftento study normal development and those de-vised to study disorder. In that connection, present (Aguilar, Sroufe, Egeland, & Carlson,

2000). By contrast, the adolescence-onset va-uncertainty continues over the precise mean-ing and boundaries of so-called attachment riety is much less characterized by these risk

features (although they may be present indisorders (Zeanah, 1996). The pattern of in-discriminate friendliness provides a close ap- mild degree), but poor parental supervision

and being part of an antisocial peer groupproximation to the prevailing concepts of onesort of reactive attachment disorder (disinhib- stand out as the main risk features. Although

males predominate to a slight extent, the sexited type), and it seems probable that that willstand the test of time, although questions are ratio is much near parity than is the case with

the life-course-persistent variety. Researchstill being posed as to how this relates to earlyselective attachments (Zeanah, in press). evidence, so far, is inconclusive on whether

or not the two groups differ qualitatively or,Much less work has been done with the otherform of attachment disorder (inhibited type), rather, quantitatively; and it is likely that there

are more than just two types (Nagin, Farring-and that remains an important task to be un-


ton, & Moffitt, 1995). Nevertheless, the dis- as there is good evidence of a much strongergenetic component in the liability for hyperac-tinction according to age of onset and devel-

opmental course has proved useful and is tive behavior than is the case for other formsof antisocial behavior (Rutter et al., 1998;likely to hold up as a key differentiator.

Because delinquency reaches its peak in Thapar, Harold, & McGuffin, 1998), and inshowing the importance of cognitive deficits,adolescence, there has often been an assump-

tion that aggression and disruptive behavior and of a pattern of correlates that differ fromthat evident for other forms of disruptive be-start at a low level and then increase over time

in vulnerable groups. The implication has havior (Taylor, Sandberg, Thorley, & Giles,1991; Taylor, 1994). Longitudinal studies,been that the search needs to be for factors

that foster antisocial behaviors. Longitudinal particularly those using latent variable analy-ses, have also shown that the developmentalstudies undertaken by Tremblay and his col-

leagues (Nagin & Tremblay, 1999; Tremblay, paths of hyperactivity and of antisocial behav-ior are somewhat different (Ferguson & Hor-Japel, Perusse, Boivin, Zoccolillo, Mont-

plaisir, & McDuff, in press; see also wood, 1993). It seems that hyperactivity is amarker for early disruptive behavior but thatLoeber & Hay, 1997) have called that as-

sumption into question. Their evidence sug- the continuation of antisocial behavior is de-pendent on these early associations, rathergests that the peak occurs during the pre-

school years and falls off thereafter. If than on any risk for later onset antisocial be-havior. Findings are much in line with thoseconfirmed by other studies, the implication is

that the search needs to be for factors that fail already considered with respect to life-course-persistent and adolescence-limited antisocialto inhibit aggressive–disruptive behavior, as

well as for factors that foster it. behavior. On the other hand, concerns havebeen expressed that the mere presence of hy-Traditionally, psychiatric classifications

have differentiated between oppositional–de- peractivity–inattention is too readily used asan indicator of constitutional origin, and thatfiant disorders and conduct disorders, the for-

mer being characterized by disruptive inter- the likelihood is that the phenomenon is moreheterogeneous than the diagnostic categorypersonal interactions and the latter by more

severe predatory or illegal acquisitive behav- suggests (Carlson, Jacobvitz, & Sroufe, 1995;Sroufe, 1997). Recent research on childrenior. A range of longitudinal studies have

suggested that this categorical distinction is reared in institutions supports this concern.Studies of both children in well-run residen-probably misleading. Oppositional–defiant

behavior is more characteristic of the earlier tial nurseries in the United Kingdom (Roy,Rutter, & Pickles, 2000a, 2000b), and of chil-years of childhood, but if it continues it tends

to lead into conduct disorder (Lahey et al., dren from very poor quality Romanian or-phanages (Kreppner, O’Connor, Rutter, & the1999). In other words, the slightly different

manifestations probably reflect what is char- ERA Study Team, 2000), have both shownstrong associations with hyperactivity–inat-acteristic of different age periods rather than

of different disorders. tention. Of all the forms of unusual behavior,this stands out as the one that is the more dis-Longitudinal studies have shown that hy-

peractive–inattentive behavior is a risk factor tinctive. Whether or not the particular charac-teristics of the hyperactivity–inattention arefor later antisocial behavior, particularly for

that which persists into adult life (Farrington, the same as those found with the diagnosticcategory in children reared in more ordinaryLoeber, & van Kammen, 1990). On the other

hand, psychiatric diagnostic conventions have circumstances remains quite uncertain. Thegenetic evidence is also important in indicat-tended to place attention-deficit disorder with

hyperactivity as a strongly constitutional, and ing that the genetic liability applies to a muchbroader range of hyperactivity–inattentionin some respects “organic,” condition that is

rather different from the broad run of antiso- than that which is included in the extreme di-agnostic category (Rutter, Maughan, et al.,cial behavior. Findings have to some extent

confirmed this concept (Taylor, 1999), insofar 1997; Thapar et al., 1998).


Research in the field of antisocial behavior an increase in disruptive behavior and heavydrinking. The Dunedin longitudinal study inhas also been important in throwing new light

on the role of early experiences. When re- New Zealand showed much the same butadded to the finding in an important wayviewed some years ago (Rutter, 1981), it was

concluded that it was unusual for even mark- through its demonstration that, although thestimulus was clearly biological, the mediatingedly adverse early experiences to have endur-

ing effects that were independent of later cir- mechanism was almost certainly social. Theeffect of early puberty in girls was found tocumstances. That finding still holds true

(although there are some important excep- be dependent on the girls’ entering an olderpeer group (as also found by Stattin & Mag-tions, as research into the adoptees from Ro-

mania has shown, for at least some outcomes; nusson, 1990) and that the effect was confinedto coeducational schools, where, presumably,O’Connor et al., in press; Rutter, O’Connor,

Beckett, Castle, Croft, Groothues, Krepp- the presence of males increased the likelihoodof an antisocial ethos (Caspi, Lyman, Mof-ner, & the ERA Study Team, in press). How-

ever, the question had been posed the wrong fitt, & Silva, 1993; Caspi & Moffitt, 1991).The importance of interplay between na-way. What has been found to be important is

the considerable extent to which early experi- ture and nurture has also been brought out ingenetic studies of antisocial behavior (Rutter,ences shape and influence later experiences

(Rutter, Champion, Quinton, Maughan, & 1997b). Gene–environment correlations arefrequent and gene-environment interactionsPickles, 1995). Indeed, it is rather unusual for

later experiences to be independent of earlier are also evident (Bohman, 1996; Cadoret,Yates, Troughton, Woodworth, & Stewart,ones. Although the direct effects of early ex-

periences on functioning many years later are 1995; Cadoret, 1985; Rutter et al., 1998). In-dividuals showing antisocial behavior interactquite small, the indirect effects are very much

greater (Sroufe et al., 1999). These continui- with other people in ways that frequentlybring about further stressful or risky circum-ties and experiences play a substantial role in

enhancing behavioral characteristics, either in stances. This is strikingly evident, for exam-ple, in the strong tendency for antisocialan adaptive or maladaptive direction (Caspi &

Moffitt, 1991, 1993, 1995). individuals to marry or cohabit with other an-tisocial individuals (Krueger, Moffitt,On the other hand, research has also shown

the major importance of experiences in ado- Caspi, & Bleske, 1998). Indeed, this assorta-tive mating tendency is actually quite a lotlescence and adult life, provided that they

bring about either a radical alteration in life stronger than the tendency for antisocial par-ents to have antisocial children (Farrington,opportunities or a substantial alteration in a

person’s self-concept or cognitive set. This Barnes, & Lambert, 1996).has been shown, for example, with respect toarmy experiences when they bring about dis-

Autismcontinuities from the past for disadvantagedyouths (Elder, 1986; Sampson & Laub, 1996) At first sight, it might seem that autism is the

diagnostic category least likely to require aand for a cohesive, harmonious marriage(Zoccolillo, Pickles, Quinton, & Rutter, 1992; developmental psychopathology perspective.

As traditionally diagnosed, it stands out as aQuinton, Pickles, Maughan, & Rutter, 1993;Laub, Nagin, & Sampson, 1998). Depending severely handicapping disorder that appears

qualitatively quite distinct from normality.on whether or not the experiences in later lifeshow continuities or discontinuities with early Nevertheless, there are two ways in which this

view has proved, at least partially, mistaken.experiences, the consequence may be eitheran accentuation (Caspi & Moffitt, 1993) or a Psychiatric writings in the 1960s tended to

consider autism as a variety of infantile psy-turning-point effect (Rutter, 1996).Magnusson’s Swedish longitudinal study chosis, with parallels being drawn with schiz-

ophrenia. Much research indicated that the(Stattin & Magnusson, 1990) showed that anunusually early menarche was associated with differences between autism and schizophrenia


far outweighed the similarities and that also it noff, 1996) might also provide part of thecognitive basis for autism. Doubts have beenwas probably highly misleading to consider

autism as a psychosis that involved some raised about both (Griffith, Pennington,Wehner, & Rogers, 1999; Plaisted, Swetten-break with a previous normality (Rutter,

1972). Research by Hermelin and O’Connor ham, & Rees, 1999) but they warrant furtherstudy.(1970) and their colleagues was the first to

show the value of an experimental psycholog- A second area of autism research where a de-velopmental psychopathology perspective hasical approach that sought to examine the cog-

nitive features in greater detail and to link been useful concerns the delineation of the di-agnostic boundaries. Genetic research has beenthem with the social deficits. Nevertheless,

there were considerable difficulties in know- important in indicating that the phenotype, asdefined by genetic liability evident from twining just how the cognitive deficits might lead

to the particular social features that are diag- and family studies, extends far beyond the tra-ditional boundaries of the diagnosis of autismnostic of autism (Rutter, 1983).

A major step forward was provided by the as a major handicapping condition (Bailey,Palferman, Heavey, & Le Couteur, 1998; Rut-application of “theory of mind” concepts,

originally derived from studies of normal chil- ter, 2000a; Rutter, Maughan, et al., 1997).This broader phenotype, or lesser variant, ofdren (Baron–Cohen, Leslie, & Frith, 1985).

Subsequent research has confirmed that most autism may occur in as many as one in five ofthe first-degree relatives of individuals withautistic individuals lack the mentalizing skills

to know what another person is likely to be autism, and the possibility that autistic fea-tures might extend even further into the gen-thinking, given knowledge of the social con-

text or past happenings (Frith, 1989; Baron– eral population, although not considered plau-sible a few years ago, cannot now be ruledCohen, 1995; Happe, 1994). The detailed

findings provide good grounds for the infer- out entirely.One further feature to mention, with re-ence that this cognitive deficit plays a major

role in autistic individuals’ severe limitations spect to recent autism research, concerns thefinding that atypical varieties of autism mayin the development of reciprocal relation-

ships. One difficulty, however, has been the derive from congenital blindness (Brown,Hobson, & Lee, 1997) and profound early so-fact that autism is manifest before age 2 years

in most instances, well before normal children cial and nutritional deprivation (Rutter, An-dersen–Wood, Beckett, Bredenkamp, Castle,show theory of mind skills when tested in the

usual way. In part, this is probably a conse- Groothues, Kreppner, Keaveney, Lord,O’Connor, & the ERA Study Team, 1999).quence of the fact that the particular experi-

mental situation used does not pick up theory The clinical pictures associated with these un-usual risk factors seem somewhat differentof mind skills that are demonstrable in more

naturalistic circumstances (Dunn, 1988, 1996). from “ordinary” autism, and it is doubtfulwhether they have much direct relevance forIn addition, the focus shifted to earlier emerg-

ing cognitive skills, such as joint attention, the causation of autism arising in more ordi-nary circumstances. Nevertheless, the findingsthat might constitute precursors of theory of

mind or an alternative cognitive route to the do raise important questions about the hetero-geneity of autism and the possibly differentsocial dysfunction (Sigman & Ruskin, 1999).

Although theory of mind deficits constitute a routes by which it may arise.plausible explanation for social dysfunction, itis not so obvious that they could account for

Depressive disordersthe repetitive stereotyped behaviors that arealso characteristic of autism. For that and Up until about a generation ago, depressive

disorders were rarely diagnosed in childhoodother reasons, research has sought to deter-mine whether a lack of central coherence because psychoanalytic theory claimed that

they could not occur in the young (see Rutter,(Happe, 1996) or deficits in particular aspectsof executive planning (Pennington & Ozo- 1986b). The situation changed as people be-


came more sceptical about the unvalidated tween depressive disorders arising for the firsttime in childhood and those arising in adoles-claims of psychoanalytical theory, and as em-

pirical observations, and especially the use of cence or later (Duggal, Carlson, Sroufe, &Egeland, in press).standardized interview methods, made it clear

that depressive phenomena could and did oc- One of the striking features of depressivedisorders is that they become much more fre-cur in children. The pendulum has now rather

swung to the opposite extreme, depressive quent at some point during the adolescent ageperiod and that this increase in frequency isdisorders being diagnosed with a high fre-

quency (Lewinsohn, Rohde, & Seeley, 1998). much stronger in females than males (Silberg,Pickles, Rutter, Hewitt, Simonoff, Maes, Car-Indeed, there have even been claims that bipo-

lar disorders are extremely common in high- bonneau, Murrelle, Foley, & Eaves, 1999).Clearly, a developmental perspective is likelyrisk groups (see Biederman, Faraone, Mil-

berger, Guite, Meck, Chen, Mennin, Marrs, to be useful in investigating why depressionbecomes so much more common during theOuellette, Moore, Spencer, Norman, Wilens,

Kraus, & Perrin, 1996). A key problem is teenage years and why the sex ratio altersfrom, roughly, parity in childhood to athat, at one extreme, feelings of depression

are simply a normal part of the human condi- marked female preponderance in adulthood(Peterson, 1993). Again, the evidence is thintion but that, at the other extreme, they consti-

tute a serious psychosis. A key issue, from a on the ground, but findings from the Virginiatwin study suggest that genetic influences re-developmental perspective, is whether or not

the depressive disorders arising in early life lated to both life events and depression play asignificant role (Silberg et al., 1999).are the same as those occurring in adulthood.

Several findings are crucial in drawing Research from many research groups butespecially that from Brown and Harris (1978)conclusions. First, longitudinal studies have

made it clear that children who suffer from a has shown the high frequency with which theonset of depressive disorder in adult life hasdepressive disorder have a greatly increased

risk of a recurrence of depressive disorders in been preceded by a stressful life event thatcarries long-term threat. On the other hand, itadult life (Harrington, Fudge, Rutter, Pick-

les, & Hill, 1990; Weissman, Wolk, Gold- is obvious that many people have life eventswithout developing depression, and it hasstein, Moreau, Adams, Greenwald, Klier,

Ryan, Dahl, & Wickramaratne, 1999). How- been necessary to consider why there are suchmarked individual differences in response toever, it is also relevant that very few of the

recurrences in adult life take the form of a apparently similar circumstances. Three fea-tures have seemed influential. First, manybipolar disorder. That has been true even

when samples have consisted of severe de- studies have shown that adverse experiencesin childhood are associated with an increasedpressive disorders in childhood that have led

to hospital admission (Weissman et al., 1999). liability to depressive disorder in adult life(Harris, Brown, & Bifulco, 1990). Second, theSecond, there is some evidence from ques-

tionnaire studies that depressive phenomena personal meaning of the event seems to influ-ence its impact (Brown & Harris, 1978,(not necessarily disorders) show a lower ge-

netic component in childhood than they do in 1989). Third, there is evidence that geneticfactors may play a role in susceptibility to lifeadolescence or adult life (Thapar & McGuf-

fin, 1994). Early-onset depressive disorders stressors (Kendler, Kessler, Walters, Mac-Lean, Neale, Heath, Corey, & Eaves, 1995;may also be more likely to be associated with

antisocial problems in the individual and in Silberg et al., 2000).For a long time, it has been implicitly as-the family (Harrington, Rutter, Weissman,

Fudge, Groothues, Bredenkamp, Pickles, sumed that all depressive disorders can betreated as equivalent (apart from, perhaps, bi-Rende, & Wickramaratne, 1997), although

this finding requires replication. The data are polar and severe melancholic varieties). How-ever, recent findings have raised queries as totoo sparse for firm conclusions, but it seems

that there may be important differences be- whether the factors involved in the onset of


the first episode of the disorder may not be investigated features of gender differencesand of age changes in frequency of depressivethe same as those involved in later recur-

rences (Brown, Harris, & Hepworth, 1994). disorder, including features that maintain onor deflect individuals from a depressionThe issue is an important one, if only because

most depressive disorders are recurrent (Judd, pathway.1997). The evidence suggests that genetic fac-tors may be more important in the lifetime lia-

Schizophreniability to depression than in the onset of thefirst episode (Kendler et al., 1995), and that Like autism, schizophrenia was long consid-

ered as a severe disorder that provided adepressive-style attributions may also play arole in the persistence or recurrence of depres- sharp, qualitative departure from normality. It

was not obvious that a developmental per-sion (Teasdale & Barnard, 1993). Psychiatricclassifications have tended to draw sharp dis- spective would be useful because it was so

uncommon for schizophrenic psychoses to be-tinctions between depressive disorders on theone hand and anxiety disorders on the other, gin in childhood.

Nevertheless, it has become increasinglydespite the fact that, at an individual level,there is very considerable overlap. Twin-study appreciated that a developmental perspective

is needed. (See Cicchetti & Cannon, 1999, forfindings indicate that both anxiety and depres-sive disorders probably reflect the same ge- an overview of the issues involved in relating

neurodevelopment to psychopathology.) Of-netic liability and that this may well reside,to a considerable extent, in the temperamental ford and Cross (1969) pointed to the evidence

that about half of schizophrenic psychosesfeature of neuroticism (Eley & Stevenson,1999; Kendler, 1996). with an onset in adult life had been preceded

by substantial nonpsychotic abnormalities inAlthough there is good reason for conclud-ing that adverse life experiences play a sub- childhood. In the 40-odd years since then, the

evidence that it is so has steadily mounted,stantial role in the genesis of depressive disor-ders (see Rutter, in press-c), a caveat is with the impact from prospective longitudinal

studies of the general population being crucialnecessary. Very little of the research is longi-tudinal, and because, in adults, the life experi- (Done, Johnstone, Frith, Golding, Shep-

herd, & Crow, 1991; Jones, Rodgers, Mur-ences and the depressive symptomatology arereported by the same informant, some of the ray, & Marmot, 1994). It is not just that social

and behavioral abnormalities may be evidentassociation may reflect reporting bias. Also,few of the studies have used genetically sensi- in childhood (although that is the case) but

also that there are developmental delays in ative designs, and it is relevant that genetic fac-tors play a role in the individual differences in substantial proportion of individuals who later

develop schizophrenia. A neurodevelopmentalthe likelihood of experiencing and of reactingadversely to stress events, and that the genetic concept of schizophrenia has come to the fore

(Cannon & Murray, 1998; Harrison, 1997;factors may also overlap with those that un-derlie depressive disorders (Kendler & Kar- Murray & Woodruff, 1995). At first, it was

thought that the neurodevelopmental riskskowski–Shuman, 1997; Thapar et al., 1998).An immense amount has been learned were specific to schizophrenia. Recent find-

ings have begun to cast doubt on whether thatfrom the study of depressive disorders inadults. There is a growing body of research is, strictly speaking, so. It seems that rather

similar risks may apply in the case of affec-findings on comparable disorders occurring inyoung people. Nevertheless, the adoption of a tive psychoses, although the findings are

stronger in the case of schizophrenia (Jones,developmental perspective has raised a num-ber of important queries that have yet to be 1997). Genetic findings, like those in autism,

have shown that the genetic liability extendsfully resolved. There is a need for more longi-tudinal research that is explicitly focused on beyond schizophrenic psychoses to include

schizotypal and paranoid disorders (Kendlerunderstanding the details of risk and protec-tive mechanisms and that focuses on the less et al., 1995). The evidence is still in favor of


a substantial degree of diagnostic specificity, ment at that early age. On the other hand,early brain injuries are perhaps more likelybut it is necessary to extend the concept of

schizophrenia beyond psychoses, to include than later ones to result in global intellectualimpairment (Vharga–Khadem et al., 1992).some forms of personality disorder. Precisely

how and where to draw the boundaries is, Also, adverse intellectual sequelae are morelikely if the injury is associated with epi-however, still unclear.

There is good evidence that genetic factors lepsy—suggesting that active brain dysfunc-tion, rather than loss of function, may be criti-play a substantial role in schizophrenia (Mol-

din & Gottesman, 1997), and the notion that cal. The results of research are clear cut inindicating marked age-dependent variations init is a psychogenic disorder has largely been

abandoned (with good reason). Nevertheless, response to brain injury, but the differenceslie more in the pattern of sequelae than inone of the most striking findings in recent

years has been the evidence that schizophre- whether or not cognitive impairment occurs.Until recently, the available evidence hasnia has a much increased rate among people

of West Indian origin living in the United given no clear indication of gene–environ-ment interactions in relation to intellectual de-Kingdom. The rate is higher than that in the

West Indies and is higher than in other ethnic velopment, but new findings have suggestedthat genetic influences are less when childrengroups within the United Kingdom (McKen-

zie & Murray, 1999). Careful analysis of pu- are reared in less advantageous environments(Rowe, Jacobson, & van den Oord, 1999).tative causal influences indicates that some

form of psychosocial stress or adversity that The possible importance of nature–nurture in-terplay needs to be reconsidered.impinges differentially on people of West In-

dian background in the United Kingdom is In most psychological theorizing about in-tellectual development, dietary factors havelikely to be responsible. Whether or not this

form of schizophreniform disorder, in which played a negligible role. It has, therefore, beenquite surprising that well-conducted research,psychosocial factors appear relatively strong,

is different from other forms of schizophrenia both naturalistic and experimental, comparingthe effects of natural breast milk and formularemains to be established.milk on the later intellectual development ofprematurely born children has shown substan-

Intellectual developmenttial benefits of breast milk (Lucas, Morley, &Cole, 1998). It has been argued that someIt used to be said that if you were going to

have a head injury it would be better to have form of developmental programming may un-derlie the finding. The research is sound andit early because the effects were so much

less—the so-called Kennard principle (1942). well designed, but, as with all forms of re-search, independent replication with other re-Research evidence has shown that this is a

somewhat misleading oversimplification search groups is required before too much isbuilt into this finding, however compelling(Rutter, 1982, 1993). The age of the individ-

ual at the time of brain injury clearly is a most the evidence from one set of investigations.Moreover, the effect may not apply to full-important factor, but its effects are somewhat

more complicated than the original principle term babies (Richards, Wadsworth, Rahimi–Foroushani, Hardy, Kuh, & Paul, 1998).suggested. Contrasted with the situation in

adults, lateralization effects following brain Numerous studies over the years haveshown that IQ scores in the first few yearsinjuries in infancy are negligible. That is to

say, unlike the situation in adults, left-brain of life are of negligible value for intellectualfunctioning in adolescence and adulthood.injuries do not result in specific verbal defi-

cits, and right-brain injuries do not lead to cir- The findings had seemed to suggest a sharpdiscontinuity between earlier and later intel-cumscribed visuospatial deficits. It seems that

either there is a transfer of functions across lectual functioning. There were many reasonswhy there should be a degree of discontinuity,the hemisphere when one side is damaged, or

there is greater plasticity in brain develop- particularly because language skills become


increasingly important in cognitive perfor- that are available for the assessment of psy-chopathology in childhood and adolescence,mance during childhood. Also, animal studies

had shown that with maturation, different as well as in adult life (Shaffer, Lucas, &Richters, 1999). A rich assortment of ques-parts of the brain may come to be responsible

for the same cognitive functions (Goldman– tionnaire, interview, observational, and psy-chometric measures have been developed andRakic, Issernoff, Schwartz, & Bugbee, 1983).

Nevertheless, it had seemed surprising that al- for many of them there is good evidence oftheir reliability and validity. It might well bemost no continuity was evident. About 20

years ago, researchers began to adopt differ- thought that we have got as far as we can inthe field of measurement, but there are sub-ent strategies for studying cognitive function-

ing in infancy, recognizing that different skills stantial unresolved problems. In many re-spects, the most pervasive, and perhaps themight be needed at this early age. The result

was the development of methods for attention most surprising, finding has been the pooragreement between parents, teachers, andand habituation. These showed substantial in-

dividual differences that, contrary to findings children on almost all aspects of psychopath-ology, and also of family experiences (Achen-with developmental milestones of a traditional

kind, did show modest continuities with intel- bach, McConaughy, & Howell, 1987;Elander & Rutter, 1996; Simonoff, Pickles,lectual performance as assessed in the usual

ways in middle childhood (Bornstein & Sig- Meyer, Silberg, Maes, Loeber, Rutter, Hew-itt, & Eaves, 1997).man, 1986; Colombo, 1993; McCall & Car-

riger, 1993). Many questions remain, and it There are many reasons why this might beso. Thus, for example, children in rating theirhas not proved easy to define tests that are

applicable across more than quite narrow age own behavior may focus particularly on thecontrast between how they are feeling now (orperiods. Even so, the findings have been im-

portant in showing that there are continuities what they are doing now) as compared withhow things were some time ago. Parents, onas well as discontinuities in intellectual

achievement and that the continuities are het- the other hand, are more likely to comparechildren with their siblings or with other chil-erotypic. That is to say, although it seems

likely that the underlying function remains dren whom they know. Teachers, too, willmake comparisons with other children butbroadly the same over development, its sur-

face manifestations differ markedly. will have a much larger sample of comparisonavailable to them. Inevitably, too, parents willfocus more on what they have perceived in

Looking Forward Into the 21st Centurythe context of the home, whereas teachers willdo so in the context of the school, the situa-As illustrated by this selective review of some

key findings, considerable progress has been tional demands of the two settings beingrather different.made in understanding many of the features

presented by the domain of development psy- Evidence has accumulated that, with somebehaviors such as hyperactivity, parents maychopathology. Even so, it is equally apparent

that major research challenges remain. In this exaggerate the contrasts between siblings,leading to an artifactually low correlation be-final section of the paper, we outline a few of

these key challenges. We make no attempt at tween ratings of the behavior of the twins orsiblings (Simonoff, Pickles, Hervas, Silberg,being exhaustive in our coverage, but we do

seek to highlight issues that have broad impli- Rutter, & Eaves, 1998). But the problem goesmore broadly than that. It is not just that thecations beyond the specifics of a particular

trait or disorder. agreement between informants is modest butalso that the correlates tend to be rather differ-ent. Thus, for example, genetic influences on

Measurement issuesbehavior as rated by children tend to be lowerthan as rated by parents (Hewitt, Silberg, Rut-The last few decades have seen major im-

provements in the methods of measurement ter, Simonoff, Meyer, Maes, Pickles, Neale,


Loeber, Erickson, Kendler, Heath, Truett, are being found as risk correlates of one disor-der may, in fact, be the risk factors for someReynolds, & Eaves, 1997; Eaves, Silberg,

Meyer, Maes, Simonoff, Pickles, Rutter, other form of psychopathology with which ithappens to be associated), and because, ifNeale, Reynolds, Erickson, Heath, Loeber,

Truett, & Hewitt, 1997; Eley & Stephenson, properly handled, the investigation of themechanisms underlying comorbidity may be1999). Interest has also grown with respect to

the ways in which ratings may be biased by highly informative on risk and protective fac-tors more generally.the current mental state of the person making

the rating (such as the effects of parental de-pression on the parental ratings Boyle & Pick-

Gender differencesles, 1997; Brewin, Andrews, & Gotlib, 1993).The findings of such comparisons have been The existence of major gender differences in

rates of particular forms of psychopathologyinformative, but it has to be said that themechanisms involved in the similarities and has been well recognized for many years

(Earls, 1987; Eme, 1979, 1992), althoughdifferences among informants remain verypoorly understood. Their elucidation requires their meaning has been ill understood (Rutter,

1970; Gualteri & Hicks, 1985; Taylor & Rut-systematic epidemiological–longitudinal stud-ies focused on testing specific hypotheses ter, 1986). Thus, autism, attention-deficit hy-

perkinetic disorder, developmental languageabout possible explanations.disorders, and delinquency all show a markedmale preponderance, whereas adolescence-on-

Comorbidityset eating disorders (such as anorexia and bu-limia nervosa) and depressive disorders in theAfter years of neglect, the issue of comorbid-

ity has become the “flavor of the moment,” years after childhood are both substantiallymore frequent in females. In all cases, it iswith the literature full of papers on its occur-

rence and patterning. Unfortunately, many of necessary to check that the gender differencesare not artifactual. For example, Zoccolillothe studies are not as informative as they

might be because the research has not been (1993) has suggested that conduct disordersin girls are much more frequent than usuallyplanned in a way that provides an adequate

test of competing mechanisms. The fact that appreciated but that the diagnostic thresholdfor a number of symptoms needs to be differ-supposedly separate forms of psychopathol-

ogy frequently co-occur in the same individ- ent for girls than for boys. Likewise, Crick(1996) has argued that much aggression inual has been well demonstrated in numerous

epidemiological studies (Angold, Costello, & girls has been overlooked because it is of adifferent form from that in boys. As both No-Erkanli, 1999; Caron & Rutter, 1991). The

key question is what the co-occurrence len–Hoeksema (1987) and Moffitt et al.(2000) have sought to demonstrate, it is possi-means; it is likely that some, perhaps much,

is artifactual, deriving from mistaken assump- ble to postulate a range of different explana-tions and to undertake appropriate researchtions in diagnostic concepts and boundaries.

Alternatively, both may derive from the same tests to choose between competing hypothe-ses. Clearly, there is a need to understand theset of intercorrelated risk factors. Or, yet

again, the presence of one form of psycho- processes underlying these quite marked gen-der differences. We do not even knowpathology may, through its effects, constitute

a risk mechanism for another form of psycho- whether the causes of gender differences arethe same across different disorders or whetherpathology. There are numerous examples in

internal medicine of all of these (Rutter, quite different risk processes are operating.On the face of it, it is not obvious that the1997a), and they provide useful models for

research strategies. It is crucially important to explanation for the male excess in delin-quency and in autism would be the same.determine the meanings of comorbidity, both

because its presence is likely to confuse and However, it would be premature to entirelyreject the possibility of a unifying explana-distort the meaning of findings (because what


tion. The point is that this major phenomenon, to obtain a better understanding of how theyare involved in the risk processes. For exam-gender differences in rates of specific psycho-

pathology, requires systematic study, and this ple, the evidence suggests that a depresso-genic attributional style may be more impor-is likely to involve somewhat different re-

search strategies to those ordinarily employed. tant in the persistence or recurrence ofdepression than in its original onset (Teas-That is because the topic being investigated

concerns differences between groups in level, dale & Barnard, 1993). In addition, there is anequally pressing need to understand the con-rather than individual differences within a sin-

gle population. nections between brain and mind. The devel-opment of functional brain-imaging tech-niques, as represented at first by positron

Cognitive processingemission tomography (PET scans) (Bremner,Innis, Ng, Staib, Salomon, Bronen, Duncan,The study of cognitive processing has consti-

tuted one of the major growth areas in psy- Southwick, Krystal, Rich, Zubal, Dey,Soufer, & Charney, 1997), and more recentlychology over the last few decades. Two some-

what different phenomena seem to be by magnetic resonance imagery (MRI scans)provide one possible way forward (Rugg,important in relation to psychopathology

(Rutter, 1987). On the one hand, there are dis- 1997; Fletcher, Happe, Frith, Baker, Dolan,Frackowiak, & Frith, 1995; Schultz, Gauthier,orders, such as autism, where the underlying

problem seems to lie in the presence of cogni- Klin, Fulbright, Anderson, Volkmar, Skudlar-ski, Lacadie, Cohen, & Gore, 2000). In addi-tive deficits for particular kinds of mental pro-

cesses. Similar arguments have been put in re- tion, however, studies of experiential effectson cognitive styles, and on their changinglation to schizophrenia (Frith, 1992) and

antisocial behavior (Moffitt, 1993). On the manifestations with age, are needed.Sometimes functional imaging is “sold” asother hand, some disorders seem to be charac-

terized by unusual styles of cognitive process- a means of seeing the brain in action, and ofidentifying the parts of the brain that are mal-ing, rather than deficits as such. That seems

to apply, for example, to affective disorders functioning in the case of particular forms ofpsychopathology. That is, however, a some-and their associated depressogenic attributions

(Teasdale & Barnard, 1993) and antisocial be- what misleading way of putting things. Whatthe scans show is the part of the brain wherehavior with its associated tendency to make

hostile attributions with respect to other peo- the main metabolic activity, as reflected inblood flow, is taking part during particularple’s actions (Dodge & Schwartz, 1997;

Coie & Dodge, 1997). In some cases, too, it cognitive tasks. That provides a most valuablemeans of differentiating among supposedlyremains uncertain which type of cognitive

feature applies. For example, attention deficits separate cognitive functions, and it shouldalso be possible to determine whether thehave long been considered as fundamental in

hyperactivity disorders. However, despite ear- same brain areas are used to solve specificcognitive tasks by normal individuals and bylier views to the contrary, the evidence now

suggests that the basis does not lie in any de- individuals with psychopathological disor-ders. There is no doubt that this linking offect in selective attention (Schachar, 1991).

There are associated cognitive impairments, brain function with the workings of the mindis going to increase our understanding of cog-although it is uncertain how far they show

specificity, but also there seem to be more nitive and affective processing, but on its ownit will not identify brain pathology. It is im-stylistic problems in terms of impulsivity and

a difficulty in delaying gratification (Sonuga– portant to appreciate that changes in behaviorbrought about by psychological treatmentsBarke, Taylor, Sembi, & Smith, 1992; Scha-

char, Tannock, Marriott, & Logan, 1995). In may also alter brain functioning as shown onscans, as illustrated by the case of obsessive–each of these cases, there is still a need to

determine the degree of diagnostic specificity compulsive disorder (Baxter, Schwartz, Berg-man, Szuba, Guze, Mazziotla, Alazraki, Selin,of the cognitive features, and there is a need


Ferug, Munford, & Phelps, 1992). Neverthe- ations in affect regulation, and changes incognitive set or styles of cognitive processing.less, this is going to constitute one of the

highly important technologies that will help As discussed more fully elsewhere (Rutteret al., 2000), there is also a major need to pro-us understand brain–mind interrelationships.

At present, there are few such studies in de- vide a much better understanding of environ-mental risk mechanisms. We know a goodvelopmental journals, but we predict that the

situation is likely to change radically during deal about what are key risk indicators, butwe know much less about the environmentalthe next decade.risk processes that they reflect. Research inthe past has made clear that it is easy to mis-

Nature–nurture interplaytake risk indicators and risk mechanisms, andthat the theoretical policy implications areAs already noted, with respect to the past, the

study of the details of nature–nature interplay quite different according to which is which.For example, in relation to both childhoodare likely to constitute another major growth

area during the years ahead. The importance (Rutter, 1971b; Ferguson, Horwood, & Lyn-skey, 1992) and adult life (Harris, Brown, &of personal effects on the environment, and of

gene–environment correlations and interac- Bifulco, 1986), it has become evident that pa-rental loss is not usually a major risk mecha-tions, has been well demonstrated, but we still

lack adequate understanding of the role of nism. It is, however, a risk indicator becauseit tends to be associated with deficits in par-these mechanisms in the emergence of psy-

chopathology. Thus, almost all of the research enting that do constitute something closer toa risk mechanism. Research in the field of di-into person effects on the environment have

concerned very short-term effects (the study vorce and remarriage has also brought out theimportant point that it should not be consid-by Maccoby & Jacklin, 1983, constituting one

of the few exceptions). Findings in the field ered as a time-limited event but rather as aprocess in which the family interactions be-of antisocial behavior suggest that these may

be particularly important during the preschool fore and after the marriage breakup are as im-portant as the breakup itself (Block, Block, &years, and that the effects may be quite long

lasting (O’Connor et al., 1998), but very few Gjerde, 1986; Cherlin, Furstenberg, Chase–Lansdale, Kiernan, Robins, Morrison, &relevant data are available. The topic is a most

important one because it necessarily changes Teitler, 1991). Studies have begun to addressthe possible mediating factors that are in-the way in which both genetic and environ-

mental risk mechanisms have to be thought volved in these risk processes operating overtime (O’Connor, Thorpe, Dunn, Golding, &about. If genetically influenced susceptibili-

ties operate indirectly, rather than directly, it the ALSPAC Study Team, 1999b), and moreresearch of this kind is clearly indicatedmay be that the search needs to be not for the

susceptibility genes for depressive disorder (Gottlieb, 1997).but rather the susceptibility genes for reactiv-ity to environmental stressors. Similarly, if

Heterotypic continuityenvironmental effects are mainly evident ingenetically vulnerable individuals, we need to Several examples of heterotypic continuity

have already been given. The social deficitsunderstand how individual characteristicsplay a role in people’s responses to the envi- in adult life associated with severe develop-

mental disorders of receptive language consti-ronment.It is also important that we determine what tute another (Howlin, Mawhood, & Rutter, in

press). It is important to appreciate, however,it is that environmental effects do to the or-ganism that enables the sequelae to be carried that to establish heterotypic continuity, it is

not enough to show that one behavior followsforward to a later age. As already noted,mechanisms to be considered are heteroge- another during development. Such consecu-

tive occurrence could occur for a whole vari-neous, spanning changes in brain structure,changes in neuroendocrine function, alter- ety of reasons. Rather, it is crucial to show


that the different behaviors thought to repre- Bishop, Eley, Oliver, Price, Purcell, Steven-son, & Plomin, 1998). So far, the findings,sent heterotypic continuity have comparable

correlates. Very little research of that kind has from a twin study, apply only to 2 years ofage (which is rather too early to determinebeen undertaken. Genetic research strategies

would be informative. Thus, for example, is language disorders), and the sample was bi-ased in certain key respects. Nevertheless, thethere the same genetic liability for the mea-

sures of attention and habituation in infancy findings are provocative in showing that ge-netic influences for the extremes were muchand for the measures of general intelligence

in later childhood and adolescence? Similar stronger than for variations within the normalrange. The comparison of so-called individualquestions arise with respect to the neurodevel-

opmental precursors of schizophrenia. Do heritability and group heritability (the latterreferring to the difference between the ex-they constitute a diagnostically nonspecific

risk factor or are they indexing a specific ge- tremes and the normal variation) provides ameans of determining whether the differencesnetic liability to schizophrenia? Again, geneti-

cally sensitive designs would provide an an- are statistically significant (DeFries & Fulker,1985). So far, there has been very little sys-swer. Of course, the correlates to be examined

should include psychosocial risk factors as tematic research testing for continuities anddiscontinuities across the range of behavioralwell as genetic ones. Thus, with respect to the

links between a lack of early selective attach- variation, and there are substantial practicalproblems in view of the very large numbersments and a pattern of indiscriminate friendli-

ness later, as shown by adoptees from Roma- that are required to do this. Nevertheless, itdoes remain an important research priority fornia, it is necessary to ask whether the

correlates are similar. That is, is there evi- the future.dence not only of within-individual continuitybetween the two, but are the correlates simi-

Developmental programminglar? The fact that both show the same associa-tion with duration of privation begins to pro- Animal studies have provided strong evidence

for the existence of certain forms of develop-vide evidence of heterotypic continuity, butmuch more needs to be done. The negative mental programming by which environmental

input influences brain structure and develop-findings with respect to disruptive behaviorshow that disproof is possible. Thus, although ment. This is best established with respect to

the role of visual input in the development ofhyperactivity–inattention in Romanian adopt-ees was associated with the duration of priva- the occipital brain area underlying later visual

function (Blakemore, 1991). The practical im-tion, disruptive behavior was not (Kreppneret al., 2000) indicating that it probably had portance of the phenomenon is shown in hu-

man studies by the evidence that an uncor-somewhat different origins.rected squint in early childhood leads to alater loss of binocular vision. Hormonal influ-

Continuities and discontinuities betweenences in animals have also been shown to af-

normal variations and disorderfect the sexual differentiation of the brain(Gorski, 1996). In the fields of biology andSimilar issues apply to the study of continui-

ties and discontinuities between normal varia- internal medicine, there are also parallels withrespect to the development of immunity andtions in behavior and disorder that might re-

flect an extreme on the same dimension. The responses to diet (Bock & Whelan, 1991). Inthe field of psychopathology, there is a possi-need, again, is to determine whether the corre-

lates are the same or different. The example ble parallel in the case of the effects of pro-found early social privation on the later devel-of severe mental retardation has already been

given with respect to discontinuity. Recent opment of close confiding friendships andlove relationships. We have already noted thefindings suggest that the same might apply

with respect to normal variations in language extent to which such social deficits seem topersist in spite of a radical change for the bet-and severe language delay (Dale, Simonoff,


ter in the environment. The concept of devel- lessons for the understanding of both normaldevelopment and disorder. For example, theyopmental programming, at least as extended

more broadly, remains a controversial one, have shown the importance of a pathways ap-proach to causal processes that recognizesand much has still to be learned about the bio-

logical processes that it reflects. The issues, both direct and indirect effects, and which ac-cepts that a single risk factor may have di-however, are of obvious importance, and fur-

ther research into the phenomenon is much verse consequences and that a single disorderoutcome may arise by a variety of routes. Itneeded.is likely that, with full understanding of themechanisms involved, these complexities will

Therapeutic mechanisms in treatment reduce to a limited set of unifying processes,but the striving for parsimony needs to be

Studies of treatment, as such, are not a centraltempered by a frank appreciation of the com-

feature of developmental psychopathology,plexities that have to be explained. Similarly,

but an understanding of the mechanisms in-developmental psychopathology approaches

volved in psychotherapeutic efficacy are, be-have underlined the importance of consider-

cause of the light they may throw on develop-ing both continuities and discontinuities in de-

mental processing generally (Rutter et al.,velopment and of examining age-indexed

submitted). The work of Clark and his col-variations in vulnerability to specific influ-

leagues in the field of panic disorders pro-ences and of variations in onset and life

vides a good example of what can be done incourse as indices of psychopathological heter-

this connection (Clark, 1996; Clark & Fair-ogeneity. Concepts of risk and protective

burn, 1997), and the studies of Patterson andmechanisms, of resilience, of nature–nurture

his colleagues have begun to do the same inand person–environment interplay, of the

the field of antisocial disorders (Forgatch &cognitive and affective processing of experi-

DeGarmo, 1999). The effects of attachment-ences, of dimensional risk and protective pro-

based interventions are similarly informativecesses and psychopathological outcomes, and

(van IJzendoorn, 1995). The field is, however,of the interplay between different domains of

very underexplored up to now. The compari-development have all proved informative. But

son of experimental and control groups willmuch work lies ahead. Developmental psy-

not, on its own, give this information. Whatchopathology arose out of a recognition of the

is needed is the demonstration that, within thevalue of combining developmental and clini-

treated group, there is a systematic dose–res-cal perspectives but also out of an apprecia-

ponse relationship between changes in thetion of the limitations of the grand theories of

postulated mediated mechanism and changesthe day. There is a continuing need to remain

in the target feature of psychopathology.sceptical about the new evangelisms that have

Much greater use of this research stratagemcome to take their place, but equally the im-

should be made.perative must be to replace doubt with pro-grammatic research that truly tests competinghypotheses and which has the potential ofConclusionsproviding a real understanding of the range ofcausal processes as they apply across the spanDevelopmental psychopathology perspectives

have already provided many useful leads and of behavioral and developmental variation.

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