Ciências Do Desenvolvimento 2.5

Developmental Psychopathology, Personality, and Temperament: Reflections on Recent
Behavioral Genetics Research

Author(s): JOEL T. NIGG and H. HILL GOLDSMITH
Source: Human Biology, Vol. 70, No. 2, Special Issue on Human Behavioral Genetics: Synthesis
of Quantitative and Molecular Approaches (April 1998), pp. 387-412
Published by: Wayne State University Press
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Developmental Psychopathology, Personality, and
Temperament: Reflections on Recent Behavioral
Genetics Research
JOELT. NIGG1ANDH. HILLGOLDSMITH2
Abstract Personality, temperament,andpsychopathology wereuntil

recently largelydistinct
areasof study,eachof whichemphasized par-
titioningofheritableandenvironmental variance.Theemergence ofthe
paradigm of developmental psychopathology alongwithapplication of
multivariate biometriemodelsto behavioral genetic data has defined a
secondphaseofresearch inthesedomains. Integrated researchhasbegun
to mapdimensional modelsof psychopathology
liability-threshold and
to evaluateempirically thecategorical versusdimensional etiologyof
traitsanddisorders. An interesting
pattern in thedatais thatpsychopa-
thology is probablynotmerely anextreme oftemperament orpersonality
inmanycases.Variations intemperament andpersonality arenowknown
tobe heavily influencedbyadditivegenetic andnonshared environmental
factorsandtoexhibit stableorincreasing across
heritability development.
Thispattern holdsforsomemeasuresof psychopathology butnotfor
others.Forexample,sharedenvironment effectsanddecreasing herita-
bilityinfluence muchadolescent psychopathology, andcomorbid prob-
lemsin youngchildren appearto be due in partto sharedenvironment
effects.Otherrecentbiometrie workon thecentral problem of comor-
bidityin psychopathology suggeststhatsharedgeneticcovariation ac-
countsforsomespecific butnotothers.
comorbidities A third phaseof
researchis nowunderway, studyof specificmolecular
featuring gene
mechanisms by meansof linkageandassociation studiesin relation to
behavioral phenotypes.Complementary integration of discoveriesfrom
biometrie behavioralstudiesandmolecular studiesis expected tobe the
normforthenearfuture.
presentsomewhatcontrasting
Personalityand psychopathology challenges
foraccommodationto evolutionarytheoryof humanbehavior.On the one
1 ofPsychology, State
Michigan University, 117.
MI48824-1
EastLansing,
2Department 1202
ofPsychology,
Department W.Johnson
Street, ofWisconsin,
University WI53706-
Madison
1611.
Human
Biology, v.70,no.2,pp.387^412.
1998,
April
© 1998
Copyright WayneState Detroit,
Press,
University 48201-1309
Michigan
KEYWORDS: COMORBIDITY,
PSYCHOPATHOLOGY,
TEMPERAMENT,
PERSONALITY,
ATTENTION HYPERACTIVITY
DEFICIT DISORDER

388 /NIGGANDGOLDSMITH
hand,wide variationin personalityand temperament is readilyexplainedby

thesocial contextof humanevolution(Bouchard1994). Indeed,evolutionary
theoryhas been suggestedas a means of integrating diversedevelopmental
and behavioralgeneticfindings(Scarr 1992). More difficult to accommodate
are major psychiatricconditions,which disable individualsand conferno
apparentsurvivaladvantageto theindividualor thegroup.One clue maybe
thatgeneticvariation,althoughimportant, does notfullyaccountfornormal
variationin personalityand temperament norforthepresenceor absence of
psychopathology. In short,gene effectsin thesedomainsare mediatedand
moderatedby experienceduringdevelopment.Thus genotype-environment
correlations and genotype-environment interactions(Plominet al. 1977), al-
though difficultto captureempirically,are likelynecessaryto explanatory
developmentalmodels.
Yet it is fittingthatthe guest editorsof this special issue of Human
Biology asked us to considerpersonality,temperament, and psychopathology
together.Increasingly,the developmentof personalityand temperament is
seen to be intertwined withdevelopmentof mentaland behavioraldisorders.
Such interrelation may be a fruitfulfocus foretiologicalresearchgenerally
and behavioralgeneticsinvestigation specifically[Careyand DiLalla 1994;
Nigg and Goldsmith1994; Gottesmanand Goldsmith1994; butfora critical
view see Maherand Maher(1994)]. At thesame timethebehavioralgenetics
literature
has consistedlargelyof separate,substantialbodies of researchon
(1) personality, (2) temperament, and (3) psychiatricdisorders,the last di-
vided intoliterature on childhoodand adultdisorders.
Ourgoal is therefore notto be exhaustive.Rather,we briefly summarize
establishedfindingsand highlightrecentdevelopments,notingintegrative
opportunities andexamples.We emphasizechildhoodanddevelopmental per-
spectivesand close withour view of thekey directionsforthefield.
Key Background: Some Definitions
Personality and Temperament. Several theoreticaltraditionsenergize

personality research.Of these,traitmodelshave been themainfocusof be-
havioralgeneticsresearchon personality.Althoughthe lens of behavioral
geneticsthusyieldsan incompleteview of thefieldof personality, we focus
on traitresearchhere.Personalitytraitsaregenerallyunderstood as governing
behaviorundera limitedset of incentivecontexts.Most of thetimebehavior
is activatedundertheinfluenceof severaltraits.Traittheorists[e.g.,Eysenck
and Eysenck(1985), John(1990), Tellegen(1985), Zuckerman(1991)] agree
thatneuroticism and extroversionare two of themajortraits.
Neuroticism, sometimes labeled negativeaffect,connotesvulnerability
to anxietyand depression,worry,and poor copingwithstress.Extroversion,
sometimeslabeled positive affect,implicatesactivitylevel, interestin so-

Psychopathology, and Personality/389
Temperamenty
cializingwithothers,and interpersonal warmth.Althoughthesemajortraits

were theorizedto have biogeneticunderpinnings (Eysenck and Eysenck
1985), the extent to which this is true has received ongoingempiricalinves-
tigation. A substantial literature describes neural,endocrine,and otherbio-
logical substrates of personality and temperament in animals and humans
(Bates and Wachs 1994; Zuckerman 1991). Indeed,biological models such
as that of Gray (1982) may lead to modification of traitconstructsand are
alreadyinfluencingpsychopathology research (Heath et al. 1994), but we
emphasizeneuroticism and extroversion for their illustrative utilityand ex-
tensivebehavioralgenetics research base. Trait researchers also agree that
personalityis hierarchically organized. That is, broadband higher-order fac-
torssuch as neuroticismand extroversion each comprise several narrower,
morehomogenoustraits.Lower-ordertraitsare underresearched, and it re-
mainsan empiricalquestionto what extent consideration of higher-order ver-
sus lower-order traitswill illuminategenetic influences or clarifyliabilityto
psychopathology.
The relationbetweentemperament and personality traitmodelscontin-
ues to evolve (Endler 1989; Goldsmith1983). Classically,temperament has
been viewed as a set of narrowerbiologically based characteristics. Person-
ality,in contrast, represents laterelaborationof experienceand development
and moresociallydetermined characteristics (Strelau 1987; Goldsmithet al.
1987). Yet themaindimensionsof temperament identified in current research
may map at least partiallyonto domainsof adultpersonality. example, For
Rothbartet al. (1995) suggestedthatthe temperamental constructof "ap-
proach"may map ontothepersonalitytraitof extroversion, "negativeaffec-
tivity"onto neuroticism, and "inhibitory control"onto constraint or consci-
entiousness. One exciting trend comprises empirical attemptsto link
temperament and personalityfroma developmentalperspective(Halverson
et al. 1994). In particular, theheterotypic continuity of earlytemperament in
itsdevelopmentto maturepersonality is underincreasinginvestigation [fora
reviewsee Rothbartand Ahadi (1994)]. Such effortsto unifytemperament
and personalityshouldenhancetheirusefulnessto understanding thedevel-
opmentof psychopathology.
Psychopathology. The prevailingoperationaldefinitionsof psychopa-

thologytodayare descriptivesymptomlists containedin the fourthedition
ofDiagnosticand StatisticalManual ofMentalDisorders(DSM-IV) (Ameri-
can PsychiatricAssociation1994) or therelatedInternationalClassification
ofMentaland BehavioralDisorders(WorldHealthOrganization1993). Def-
initionsofpsychopathology outsidethecurrentprevailingnosology,however,
may withtimeprove more apt. The currentoperationaldefinitions of psy-
chopathologicalsyndromes remain unsatisfyingbecause of the lack of suffi-
cientempiricalsupport in some cases and the lack of a developmentalper-
spectivein general(Carson 1991). For themostpartpsychiatricsyndromes

are behaviorallydiagnosed and lack biological gold standardsto establish

diagnosis,althoughbiologicalcorrelatesmaysoon be acceptedforsome syn-
dromes.Indeed,theboundarybetween"normal"and "disordered"is recog-
nized as beingfuzzyformostdisorders,and itsdefinition in partrequiresthe
application of values particular to a given social and cultural context[for
sophisticated discussions see Wakefield (1992) and Lilienfeld and Marino
(1995)]. Furthermore, genetic contributions to behavioral dysfunction areun-
to
likely map optimally onto existingphenotypiccategories; excessive reli-
ance on thesedefinitions as phenotypes forgeneticresearchmayevenimpede
geneticunderstanding. Nevertheless, muchof theextantpsychopathology re-
searchhas focusedon psychiatricsyndromesfoundin the DSM-IV and its
predecessors.The DSM-IV lists some 400 mentaldisordersforadultsand
children,of whichwe mentiononlya handful.
Childhooddisordershave a shorterresearchhistorythando mostadult
disorders.In theDSM-IV disordersofchildhoodare in somecases conceived
simplyas child versionsof adult disorders(e.g., childhooddepression).In
othercases child-specific disordershave recentlybeen introduced to theadult
literature(e.g., attention
deficit hyperactivity disorder).Critically,theseop-
erationaldefinitions do notincorporate processesor mechanismsthatmight
cause or maintainthedisorderedfunctioning. This is in contrastto theinte-
grated perspectiveof developmentalpsychopathology(Cichetti 1993),
whereinchildhoodand laterdevelopingdisordersare thoughtto represent
departures fromless problematicdevelopmentalpathwaysinfluencedby in-
teracting biologicaland experientialriskand protectivefactors(Rutter1996;
Sroufeand Rutter1984). A longitudinal, developmental perspectiveis essen-
tial to understanding distal,proximal,and maintaining causes of psychopa-
thology,whetherthese causes are geneticor environmental. Furthermore,
developmentalpsychopathology assumes a transactionalsystemsmodel in
whichgenetic,biological,psychological,and psychosocialmechanismsare
dynamicallyrelatedby means of multidirectional causality.As a result,the
specificcontextsof behavioralexpressionare crucial to fullyappreciating
even geneticand biologicalcontributions. Finally,a developmentalpsycho-
pathologyperspective underscores the reciprocalimportance to scientificad-
vance of normaland disordereddevelopment,bolsteringan emphasison
studyingsuch normalrangefactorsas temperament and personalityin con-
junction with psychopathology.
Categories and Dimensions. As readersmightguess fromthediscussion

so far,a well-recognizedissue in psychopathology researchconcernswhether
disordersareproperly conceivedofas categoriesoras extremeson continuous
dimensions(Jensenet al. 1993). It can be arguedthatpsychiatric categories
representarbitrary cut pointsnear the extremesof dimensionallyoccurring
temperament and personality
traits(Eysenckand Eysenck1985). Indeed,the
notionof a continuousunderlying dimensionof liabilityto disorder,withthe

and PersonalityI 391
, Temperament,
Psychopathology
disorderoccurringbeyonda particularthreshold(Gottesman1991), has been

fundamental to contemporary biometriegeneticmethods.On theotherhand,
disordersreallymayreflectunderlingtaxa withuniquedeterminants (genetic
or otherwise),implyingdiscontinuities betweennormaland abnormaldevel-
opment.Meehl (1973, 1995) showedthattherelationbetweenthedistribution
of phenotypicscoresin a populationis complexlyrelatedto genotypicstruc-
tureand proposedsophisticatedstatisticalmethodologiesto investigatethis
question.Recentdevelopmentsin behavioralgeneticsmethodologyalso at-
temptto addresstheissue of dimensionalliabilityempiricallyratherthanas
an assumption[e.g., DeFries and Fulker(1988) and Eaves et al. (1993a)].
The developmentalrelationof temperament or personalityto psycho-
pathologymay be still more complex. For example,temperament or person-
alitymaypredispose an individualto a particulardisorder.Thus, neuroticism
maypredisposesomeoneto anxietydisorders(Carey and DiLalla 1994), and
inhibitedtemperament maypredisposea childto childhoodanxietydisorder
(Rosenbaum et al. 1993). More complex, parentpersonalitymay interact
withchild traitsto dampenor amplifychild behavioralproblems(Nigg and
Hinshaw1998). Anotherconsideration is genotype-environment correlations,
in which a child elicits differentialresponsesfromothersbecause of their
own geneticallyinfluencedtemperament and othercharacteristics(Scarrand
McCartney 1983). These are only some of the possibilities;one review
(Rothbartet al. 1995) tabulated 14 possible ways in which temperament or
personalitymay relate to the of
development psychopathology. The main
pointforourpurposesis thatbiometriemodelsthatevaluatethegeneticcor-
relationunderlying phenotypictraits(Carey 1988) can clarifytheseissues.
Genetic Methods. Althoughearlytwin,adoption,and familystudiesem-

phasizedmagnitudesof geneticcontribution to variabilityin a traitor disor-
der,thefieldhas steadily moved beyond question.Recentresearch,which
that
we termthe"secondphase" in this often
field, emphasizesfitting multivariate
twin,liability,longitudinal,and other biometrie models to test competing
etiologicaltheories.Othermodels testthe plausibilityof specificmodes of
gene action (e.g., single major gene effects,sex-linkedeffects)and devel-
opmentalprocesses.In general,thesebiometriemodels recognizetheprob-
able polygenicnatureof geneticinfluenceon behavioraltraits.Such models
enable investigationof additiveand nonadditivegeneticcontributions and
sharedand nonsharedenvironment contributions to covariationamong dis-
ordersand traitsas well as to liabilityfordisorder,ratherthanto thedisorder
itself(Falconer1965; Neale and Cardon 1992). Temperament and personality
traitsrepresent one possiblesourceofthehypothesized dimensionalvariation
in underlying liabilityto disorder.Integrated modelsthatrecognizethispoint
are one markerof thefield'srecententryintothissecondphase of biometrie
geneticresearchin psychiatric disorders,bothin theestablishedfieldof adult
psychiatric genetics and in the newerfieldof childor developmentalpsychi-

atricgenetics[e.g.,Belmakerand Biederman(1994)]. This newphaseofwork

represents an advance because thesemodels offera moresophisticated rep-
resentationof the multifactorial underpinnings of psychopathology, thus
buildingon thepreliminary workthatpartitioned geneticand environmental
sourcesof variance.
Finally,moleculargeneticapproachesthatuse linkageand association
studiesto examinespecificmolecularloci are now beingintegrated intobe-
havioralstudies.We viewthisas a coincidentthirdphaseofworkthatinforms
and is informedby thebiometriemodelsjust described.Because molecular
approachesper se are discussedby Alsobrookand Pauls (1998) (thisissue),
we confineour commentson molecularworkto a few illustrative findings
thatdemonstrate thepotentialin integratingthesedomains.
A rangeof othermethodologicaland conceptualissues in behavioral
geneticsresearchare beyondthe scope of thisbriefreview,includingsuch
importantissues as non-Mendelianeffects,theoreticalconsiderationsin
genotype-environment correlations,and empiricalexaminationsof the as-
sumptions ofbehavioralgeneticsresearch.Discussionof suchissuesinregard
to developmentalpsychopathology is providedby Goldsmith,Gottesmanet
al. (1997). A generalreviewof psychiatric geneticsis providedby McGuffin
et al. (1994).
A Word on Misconceptions. Beforeproceeding,we notethatpsychopa-
thologyand personality representdomainsforwhichgeneticmodelsrequire
carefulframingin lightof possible misconceptions about such models.One
misconception is thatemphasison geneticcontributionsto development, es-
peciallywhenlinkedto evolutionary theory,impliesbiologicaldeterminism
(and thusindirectly supportsconservativepoliticalideologies). In brief,we
do notbelievethisview is necessary,and we emphasizeagainthatbehavioral
geneticmodels describeindividualdifferenceswithina given population.
Thus theircontribution to predictionsregardingthelimitsof intervention on
a populationis minimalat best,and theyprovideno directinformation re-
gardingeithergroupdifferences or the developmentof one individual.Be-
cause of thisprincipleand because psychiatricdisordersare now knownto
reflectsome combinationof geneticand experientialdeterminants, uncover-
ingtheetiologyofpsychiatric ormentaldisorders(includingtheroleofgenes)
is expectedto shed lighton preventionby highlighting the developmental
conditionsunderwhichspecificconstitutional vulnerabilities
(or liability)de-
velop intopsychopathology. For example,preventiontrialsdemonstrate the
plasticityof humanantisocialbehaviorsdespitetheirpartiallyheritableun-
derpinnings [e.g.,Peplerand Rubin(1991)]. Nigg and Goldsmith(1994) pro-
vide furtherdiscussion.
Empirical Findings: Personality and Temperament

Established Findings. The geneticsofpersonality and temperament
entail
twoparallelresearchlines,recently intodialogue.Mostofthecurrent
entering

and Personality/393
Temperamenty
Psychopathology,
dataarisefromtwinstudies.Twinresearchhas shown(1) minimalheritability

fortraitsin the neonatalperiod (Riese 1990); (2) increasingheritability of
traitsthroughinfancyinto childhood(Matheny1989); (3) heritabilities of
major traits
approximating 0.50 forchildhood temperament (Goldsmith, Buss
et al. 1997; Schmitzet al. 1994) and foryoungto middleadultpersonality
traits(Eaves et al. 1989; Tellegenet al. 1988), withstableor slightlyincreas-
ing heritabilityin laterlife; (4) environmental variancegenerallyof thenon-
shared(within-family) type(Plomin and Daniels 1987); and (5) sharedex-
perience(betweenfamilyvariance) contributing littleto variationin these
traits.The temperament literature has reliedon parentratings, buttwinstudies
using laboratorymeasures appear supportive[e.g., Saudino and Eaton
(1991)].
A biggerissue is thatthe sparseadoptiondata available (usingparent
ratingsof temperament) oftenyieldsignificantly smallerestimatesof herita-
bility(Scarret al. 1981; Plominet al. 1991). This discrepancycould be due
to violationsof the equal environments assumptionof twinstudies,nonad-
ditivegene effectsinfluencing traitvariation,or undetectedbiases in rating
data,such as ratercontrasteffects.Ongoingstudiesusingtwinand adoption
data and laboratorymeasuresof temperament shouldclarifythepicture.
Of thenotedreplicatedfindings, perhapsthemostunexpectedwas the
importanceof nonsharedenvironment to individualdifferences in develop-
ment[see Plominand Daniels (1987) and accompanying commentaries]. Sys-
tematicempiricalinvestigation ofnonsharedenvironmental influencesis quite
recent(Heatherington et al. 1994; Pike and Plomin 1996; Rowe 1994). Per-
tinentcritiqueswere also slow to appear (Goodman 1991; Hoffman1991).
One issue is thatmanytwinsamples assess an incompleterangeof devel-
opmentallyrelevantenvironments (e.g., portionsof thesocioeconomicspec-
trumare oftenunderrepresented). As a result,bothheritability estimatesand
estimatesof the(un)importance of shared(between-family) environment ef-
fectsmay be biased. Furthermore, processor methodartifacts, such as rater
or siblingcontrasteffects,could lead to over-or underestimation of shared
environment influencesin twindata; whentheseeffectsarecontrolled, shared
environment effectsmay emergeforsome temperamental traits(Saudino et
al. 1995). Finally,quantitative modelshave lowerpowerto detectunspecified
shared environmenteffectsthan to detect heritableinfluences[see Rose
(1995) forfurther discussion].As we note in the next section,the picture
changessomewhatwhenmeasuresof psychopathology are considered.Fur-
theradvances are likely when specific measures of shared and nonshared
environment are incorporated intobiometrie models (as manystudiescur-
in
of
rentlyunderway)and a widerrange theoretically relevantenvironments
are sampled.These measures of environmental effects,however,are them-
selves likelyto reflect substantial genetic variation (Plomin and Bergeman
1991), probably because of the ubiquitous influence of personalityon the
perception and selection of environmental contexts. Such confoundscan be

addressedby incorporatingmultipleraters,multipletimepoints,and multiple

assessmentmethods.These confoundsalso can be a focus forfurther study
in theirown rightas genotype-environment correlations
(discussedlater).
RecentDevelopmentsin TemperamentResearch. Of current interest

are
developmentalvariationin heritability and geneticand environmental con-
tributionsto developmentalchangein temperament expression.Resultsfrom
a majorlongitudinaltwininvestigation sponsoredby the MacArthurFoun-
dationareillustrative. Plominet al. (1993) reportedon temperament andother
data fortwinsassessed at 14 monthsand 20 monthsof age. Heritabilities of
the assessed majortemperament domains(inhibition, shyness,activity,task
orientation)were 0.30 forobservationaldata and 0.50 forparentratingsat
both14 monthsand 20 months,althoughsometraitsreflected a slightincrease
in heritability
(e.g., taskorientation) and othersrevealeda slightdecreasein
Notably,correlationsbetweenscores at thetwo timepointsav-
heritability.
eragedonly0.30, indicatingconsiderabledevelopmentalchangeduringthat
time.This changewas analyzedforseveraltemperament measures.We high-
lightfindingsforlaboratory-rated behavioralinhibition(Kagan et al. 1988)
because inhibitionhas interesting ramifications
forearlyriskof bothinter-
nalizingdisorders(e.g., anxietyin thecase of highinhibition)and external-
izingdisorders(low inhibition).Stabilityof inhibitionfrom14 monthsto 20
monthswas due entirelyto geneticstability(Plominet al. 1993). About25%
of thevariancein changescoresfrom14 monthsto 20 monthswas associated
withgeneticinfluences;the remainderof the change was due to nonshared
environment (and measurement error).Notably,a closely relatedconstruct,
shyness,revealedextensiveinfluenceof sharedenvironment on changefrom
14 monthsto 20 months,highlighting theimportanceof carefulphenotypic
definitionto geneticconclusions.Othertraitdomainsbesides inhibitionre-
vealed eithergeneticor nonsharedenvironment explanationsfordevelop-
mentalchange.Such findingsunderscorethe dynamicnatureof geneticin-
fluenceacross development,which has not always been appreciatedin
theoriesof psychopathology.
Withincreasedattention to thedevelopmental processesrelatedto tem-
perament(Halversonet al. 1994), assessmentin behavioralgeneticstudiesis
extendingbeyonddistressproneness,inhibition,and activitylevel. For in-
stance,Goldsmith,Buss et al. (1997) examinedtwinsimilarity forpositive
attentional
affectivity, focusing,and effortfulcontrol.Sharedenvironmental
factorsappearedto influencepositiveaffectivity, at least duringthetoddler
period.Geneticinfluenceswere strongforvariationin attentional capacities,
and effortfulcontrol,relatedto theabilityto inhibitactionand controlemo-
tion,was also geneticallyinfluenced.These findingsderivedfrommaternal
reportsoftemperament, butcurrent studiesfromvariouslaboratories areusing
laboratory-based observations. In additionto establishingquestionnaire-lab
correspondence bymeansofmultitrait, multimethod biometrieanalyses(Phil-

Psychopathology, , and Personality/395
Temperament
lips and Matheny1991), researchersneed to examinetemperamental simi-

betweenordinaryand adoptivesiblingsto establish
laritiesand differences
convergencewiththetwinresults(Saudino et al. 1995).
Recent Developments in PersonalityResearch. One ironyof the first

wave ofgeneticpersonality researchwas thattheuniformity offindings across
traitsbecame so predictableas to be viewed by some as uninteresting. An
important gap, however, was limited of
convergence genetic research with
thepopular"big five"conceptualization ofpersonality structure(extroversion,
neuroticism,agreeableness,conscientiousness, and openness). Loehlin's
(1992) reviewof thearea had to relyon studiesthatalmostwithoutexception
did not use instruments designedspecificallyto measurethe big fivetraits.
Recentresearchhas begunto fillthegap withstudiesdirectedat thebig five
(Reimannet al. 1997; Janget al. 1996). For example,Janget al. (1996)
reportedthefirsttwinstudyusingthelatestversionof theNeuroticism, Ex-
troversion, Openness (NEO) inventory (Costa and McCrae 1992), the most
popularassessmentinstrument forthebig five.Theymodeledunderpinnings
ofthebig fivepersonality traitsas well as 30 lower-order facetsofthesetraits.
Resultswere unsurprising forthebig five(moderateheritability and signifi-
cantnonsharedenvironment effects).However, their data reflectedan intrigu-
of in
ing degree variability genetic influence on variation in lower-order fac-
ets, even within one higher-order trait,suggesting that further analysis the
of
lower-order traitswill be useful.
One ofthemostinteresting personality traitsfroma psychopathologisťs
point of view is sensation seeking(Zuckerman1991), yetthistraithas his-
torically received limited behavioral geneticattention beyondone majortwin
sample. To address thisgap, Koopmans et al. (1995) evaluated Zuckerman's
originalscales, which included four sensation-seeking domains. Consistent
withearlierwork,thescales wereheritable.However,biometrieanalysissug-
gestedthatcorrelations amongthefoursensation-seeking subscaleswerenot
due to commonunderlyinggeneticinfluences.These findingssuggestthat
theoriesinvolvingsensationseekingin thedevelopmentof conductdisorder,
attentiondeficithyperactivity disorder,and substanceabuse disorderswill
need to attendto differential lower-order facetsof sensationseeking.
One questionthatrequiresempiricalclarification concernsthebiologi-
cal accuracyof competingtraitmodels currently in use. A firstattemptto
addressthisquestioncomparedthe degree of geneticoverlap in behaviors
assessed by theEysenckmodel and Cloninger's(1987) model (Heath et al.
1994). Heathet al.'s extensiveanalysescannotbe fullysummarizedhere,but
theynoted thatthe two personalitymeasuresappear to tap only partially
overlappingportionsof the geneticvariationin personality.Furtherstudies
using similarmethodsare needed to clarifythegeneticassociationbetween
competingtraitmodels.Overall,a keyfuturedirectionis to map empirically
thegeneticcommonality of temperament and traitconstructs.

Empirical Findings: Developmental Psychopathology

Severalfundamental issues meritconsideration:
(1) Do childbehavioral
disordersregardedas categoriesor dimensionsrevealpatternsof geneticand
environmental influencesimilarto thoseseen in temperament and personal-
ity?(2) What are the sources of comorbidity among disorders? This issue is
key because both phenotypic and genotypicoverlapsdoubtlesslyconfound
muchsingle-disorder research.(3) Are categoriesor dimensionsmostappro-
priateas modelsfortheetiologyof childdisorders?(4) Whatare thereasons
forheterogeneity withindisorders,and how are theseindividualdifferences
best parsedwithregardto genotypes?(5) Whatmechanisms(e.g., mainef-
fects,gene X environment cause disordersto develop?(6) What
interactions)
phenotypes arise from thesame genotype(instancesofpleiotropy)? We high-
lightattempts to address these problems,althoughproblems1, 2, and 3 have
receivedmoreattention thantheothers,and so thelast threequestionsstand
as keychallengesforthefuture.
Patternsof Effectin Child Problems

Selected ChildhoodSyndromes. Family and behavioralgeneticdata on
variouschild disordersare oftensparse; recentreviewsincludethe articles
by Pauls (1990), Lombrosoet al. (1994), and Rutteret al. (1990). One focus
of researchhas been the disruptivebehaviordisorders,especiallyattention
deficithyperactivity disorder(ADHD), which oftenoverlaps withopposi-
tionaldefiantdisorder(ODD) and conductdisorder(CD). These disruptive
disordersare of particular interestbecause of theirheavydemandson clinical
servicesand likelihoodof latercostlyoutcomeswithregardto criminality,
substanceabuse, and achievementproblems.Consideredas phenotypic cate-
gories,ADHD overlapsapproximately 50% withODD and CD (Biederman
et al. 1991). All threedisordersand especiallyCD shareempiricallinkswith
laterdevelopingantisocialand delinquentbehaviorpatterns,the subjectof
manygeneticstudiesin theirown right(Gottesmanand Goldsmith1994).
Youngerchildren,however,have only recentlycome underthe purviewof
geneticresearchon clinicalproblems,revealingsome surprising findings.
Early familystudiesconfoundedADHD and ODD or CD; familyre-
searchin thisdomainchangedmarkedlyin themid-1980swiththeemerging
consensusthatADHD (or hyperactivity) and ODD/CD (or aggressionand
conduct problems) were partiallyseparable empirically(Hinshaw 1987).
Familydata subsequentto themid-1980sfoundseparablefamilypatternsof
psychopathology. ADHD was morecommonin familiesofboys,whereasCD
was not;antisocialpersonality disorder,alcoholism,and maternaldepression
accruedwithcomorbidCD ratherthanwithADHD per se (Biedermanet al.
1987; Faraoneet al. 1991; Lahey et al. 1988).
When ADHD behaviorsare considereddimensions,twindata reveal
highheritability (about 0.7) forparentalratingsof hyperactivity(Goodman

Temperament
and Stevenson1989; Stevenson1992) and attentionproblems(Gjone et al.

1996a) with nonsharedenvironment accountingfor the remainingeffects.
Thus forthesesymptoms thepattern is similarto whatis seen in temperament
research.In supportof an oligogeneticmodelforADHD, a recentsegregation
analysisoffamilydatafitted modelsconsistent witha majorgeneeffect(Fara-
one etal. 1992). However,segregation analysescan producespuriousfindings
of majorgene effects;thereal testwill come withmoleculargeneticassoci-
ationand linkagestudies(notedlater).Furthermore, the statisticalevidence
to date suggestsgeneticheterogeneity forADHD (Goldsmith,Gottesmanet
al. 1997), whichwill pose a challengeto molecularstudies.
Aggressionand CD reveal a less clear-cutetiologywithregardto her-
itablemechanisms.Studiesof CD per se are few,withmuchof theresearch
focusedon delinquency.However,severalreviewsofCD andaggressionhave
suggestedthatchildhoodCD revealsonlymodestheritability and significant
effectsof sharedenvironment (Lyonset al. 1995; Rutteret al. 1990), although
one recentretrospective twinstudyfailedto supportthispatternand found
higherlevels of heritabilityforchildconductproblems(Slutskeet al. 1997).
Nevertheless, on balance,thefindingsforantisocialbehaviorproblemsstand
in contrastto the patternseen with eitherhyperactivity or temperament
research.
For comparisonwe brieflynoteresearchon anxietyconditionsin child-
hood, whichhave receivedattentionin only a handfulof studies.The most
recentstudywe foundexaminedseveralanxietymeasuresin twinsat three
ages in childhood(Topolski et al. 1997). Topolski et al. foundthatshared
environment effectswere crucialwithregardto separationanxietydisorder
butthatmodestheritability (0.3-0.4) and nonsharedenvironment effectsbest
fittedoveranxiousdisorderin childhood;several interesting developmental
variationswere also noted.
In short,some measuresofpsychopathology (hyperactivity, generalized
anxiety) appear to echo patternsin temperament and personality research,but
othermeasures(e.g., conductproblems,separationanxiety)reveala different
patternof underpinnings thatincludesmodestsharedenvironment effects.
BroadbandChildProblemDimensions. Severalrecentstudieshave inves-

tigatedthe Child Behavior Checklist(CBCL) (Achenbach 1991), a broad-
band,empiricallyderivedratingscale of childbehaviorproblemsthatis the
workhorseof NorthAmericanchild clinical and researchassessment.Such
in contrastto clinicaldisordersbecause theempirically
researchis of interest
derivedscales of theCBCL differfromtheDSM-IV criteriaand thusrepre-
senta somewhatdifferent model of psychopathology. The two higher-order
factorsin thisschemeare internalizing (depressed,anxious,and withdrawn
behaviors)and externalizing (aggressive,defiant,and overactivebehaviors).
Edelbrocket al. (1995) foundsignificant forinternalizing
heritability
and externalizingbehaviorbutreportedsharedenvironment effectsand some-

whatlowerheritability fordelinquencyin adolescence.Gjone et al. (1996b)

examinedthreeage cohortsof twins.They foundconsistentand highheri-
tabilitiesin youngerchildrenforbothinternalizing and externalizing behav-
iors, but internalizingheritabilitydecreased with increased age, whereas
sharedenvironment as thechildrenapproached
effectsincreased, particularly
adolescence.
Van den Oord et al. (1996) extendedthetwinanalysisto preschoolers
and looked at broadband(externalizingand internalizing) and narrow-band
scale scores.Sharedenvironment effectsalongwithadditivegeneeffects were
notedforexternalizingbehaviors,but no sharedenvironment effectswere
observedforinternalizing behaviorsin thisyoungergroup.Strikingly, shared
environment effectswere substantialforthetotalproblemsscale, suggesting
thatcovariationamong problembehaviorsin early developmentmay be
shaped by sharedenvironment factors.Significantsiblingcontrasteffects
were found for the overactivityscale (a precursorof hyperactivity in
childhood).
In sum,thesestudiessuggestthatthedevelopmentalpatternof causal
effectson psychopathology in children(decreasingheritability forinternal-
izing,important shared environment effectsforcomorbid problemsand for
adolescentdifficulties)are sometimesdifferent fromthe generallyaccepted
patternof resultsin thetemperament and personality literature.
Comorbidityamong Child Problems. The just-notedfindingswithre-

gardto covariationamongproblembehaviorsare relevantto theproblemof
comorbidity, whichplaguesresearchon nearlyall disorders.We takethecase
of ADHD as illustrative. Several recentstudieshave attemptedto map the
genetic architecture of ADHD' s salientcomorbidities,whichincludeconduct
and oppositionaldisorders,depression,anxiety(Biedermanet al. 1991), and
achievementand learningproblems(Hinshaw 1992). For example,results
froman Australiancommunitytwinsample suggestedthatheritability was
moderateforCD withbothsharedand nonsharedenvironmental influences
playinga role, whereasheritability was high forsymptomsof ADHD and
ODD withonlynonsharedenvironmental influencescontributing
(Waldman
et al. 1996), echoingpatterns elsewherein theliterature.
Covariationof ODD
and CD symptoms withADHD symptoms, however,was almostentirely due
to commongeneticinfluences,whereascovariationbetweenODD and CD
symptoms was due to commongenetic,sharedenvironmental, and nonshared
environmental influences(Waldmanet al. 1996). Thus thedata suggestthat
sharedenvironment plays a role only sometimesin the developmentof co-
morbidity in child psychopathology. In contrast,
recenttwinand familydata
fromtheColoradoReadingProject,usinga clinicalsamplereferred forlearn-
ing problems,suggestthatthecomorbidity of ADHD and depressivesymp-
tomatology is notdue to geneticcovariation(Willcuttand Pennington1997).

Temperament
The same Colorado Reading Projectdata were used to examine co-

morbidityof ADHD and reading disability. Initial studies of cross-
concordanceof readingdisabilityand ADHD (as categories)and of spelling
difficulties and hyperactivitysuggesteda geneticcontribution to comorbidity
in at least a subsetof thesubjects(Gilger et al. 1992; Stevenson et al. 1993).
More recently,Gillis-Lightet al. (1995) fitted a bivariate biometrie twin
model to the Colorado sample,relying on dimensional measures of hyper-
activityand readingdisability.They reportedthat70% of thecovariationin
readingdifficulties and hyperactivity scores was attributable to geneticco-
variation.Extensionof such methodsto samplesnot selected on thebasis of
learningdisorderis needed to assess generalizability. For example,Faraone
et al. (1993), reporting on a clinical sample selectedon thebasis of ADHD,
foundthatADHD and learningdisabilitiesdid notcosegregatein familydata.
They suggestedthatnonrandommatingbe consideredin evaluatingcomor-
bidity.Overall,data suggestthatforADHD comorbidconditionsoftenoccur
because of commongeneticinfluenceswithcomorbiddepressionbeing an
exception.
Mechanisms
ExtremesAnalysis. As notedearlier,the fundamental questionof dimen-

sionalliabilityor underlyinglatenttaxa has provokedfurther methodological
developmentsin behavioralgeneticsresearchthatcan be relatedto devel-
opmentalpsychopathology (Goldsmith,Buss et al. 1997; Rende and Plomin
1995). One methodis DeFries and Fulker's (1988) approach,which uses
regressionequationsto determinewhetherthe magnitudeof geneticand/or
environmental effectsat theextreme(disorder)scores on a traitdifferfrom
thosealong therestof thedistribution. If themagnitudesdiffer, thatsuggests
differentetiologies for the scores among disorderedand nondisordered
subjects.
Rende et al. (1993), studyingadolescentself-report depressivesymp-
tomsin a representative community sample,foundthatheritability was non-
significantfortheextremescores(in contrastto theremainderof scores)and
thatsharedenvironment effectswereimportant at theextremes.A follow-up
studyusingparentratingsof externalizing and internalizingsymptoms in the
same samplefounda weakerbutsimilarpattern. was
Heritability onlyslightly
(and statistically
nonsignificantly)lowerfortheextreme15% of theadoles-
cent sample (Deater-Deckardet al. 1997) forboth externalizingand inter-
nalizingsymptoms.
Gjone et al. (1996b), in theirNorwegiantwin sample, echoed these
resultsforinternalizingsymptomsin findingthatheritability decreasedat the
extremesand sharedenvironment effectsincreased (but the effectwas ob-
in
servedonly youngerchildren, not in In
adolescents). contrast, however,in
Gjone' s data of
heritability externalizing behavior remained stable or in-

creasedat theextremes,whereassharedenvironment effectsremainedstable

or decreased.Confirming the externalizingfindings,Rhee et al. (1995) and
Slutske et al. (1997) foundthatheritability of extremeand normalrange
symptoms ofhyperactivity and conductproblems,respectively, did notdiffer.
of
Overall,these studiesillustratethatthe assumption differential ge-
neticetiologiesforpsychopathology categoriesversusrelatednormalrange
variabilitymustbe examinedempirically.It is onlysometimestrueand may
varywithdevelopmentalstage.However,an important limitation of all these
studieswas theirrelianceon extremescores in communitysamples rather
thanexaminationof actualclinicalcases ofdisorder.Generalizability to clini-
cal cases remainsunknown,and it will be of interestto see thesame methods
appliedto symptomscoresacrossnormalcases and clinicalcases of disorder
together.
Furthermore, the precedingstudies all used variationsof the rather
straightforward DeFries and Fulker(1988) regressionmethod.In a second
approach,Eaves et al. (1993b) developed a sophisticatedmethodforlatent
class geneticanalysis,also usinga community twinsample.In contrastto the
previousfindings, theirapproachsupportedtheexistenceof a low-frequency
(about 3%) latentclass forADHD symptoms(Eaves et al. 1993b) and the
existenceof up to fourlatentclasses forchildhoodCD symptoms(Eaves et
al. 1993a).
Thus it appearson thebasis of initialstudiesthatwhentheunderlying
assumptionsof the statisticalmodel are dimensional(the liabilitymodel),
resultshave tendedto supporta dimensionallatentstructure, especiallyfor
externalizingbehavior.When assumptionsare categorical,however,as in
segregationanalysisor latentclass analyses,supportforlatenttaxa emerges.
Applicationof variousmethodologicalapproachesto thesame data sets and
inclusionof clinicalcases are needed.
Gene-Environment Interaction. We underscorethe shortageof develop-

mentalpsychopathology researchon genotype-environment interactions.
The
importance ofinteractionin thedomainofantisocialbehaviorsandaggression
maybe criticalto thefinalexplanationof thistroublingbehavioralarena.A
classic animalstudyby Hood and Cairns(1989) is instructive. These inves-
tigatorsbredmiceforaggression;afterseveralgenerations theyachievedtwo
populationswhosedistributions of aggressivebehaviorwerenonoverlapping,
thatis, geneticallydifferent
populationsforaggression.Pups fromeach popu-
lation were randomlyassigned to two different rearingenvironments: one
socially normative,the otherisolative.The pups fromthe two populations
could notbe distinguished in termsof aggressivebehaviorwhentheywere
raisedin thenormative social environment,whereasthedifferenceswerelarge
when theywere raised in the nonnormative environment.Thus genetically
mediateddifferences in aggressionbetweenthepopulationswerelargelyplas-
tic to rearingexperienceswithinone generation.Otherstudiesof aggression

Temperament
using inbredstrainsof mice also reveal gene-environment interaction,al-

thoughresultscan differdependingon the procedureused to measureag-
gression(Roubertoux1996).
Aggressionin these animals is at best only partiallysatisfyingas a
model forhumanconductproblems,althoughthe findingsare suggestive.
Human behavioralgeneticstudieshave also begun to examine interaction
phenomenamoreclosely.Severalstudiesnow convergein finding thatsevere
and chronicantisocialbehaviordevelopswithcontributions frombothgenetic
risk and environmental risk [e.g., Cadoret et al. (1995) and Eaves et al.
(1993a)]. Furtherexaminationof specificenvironmental riskfactorsin con-
junctionwithbehavioralgeneticmethodsis thenextstep.
Gene-Environment Correlation. Genotypesand environments are corre-

latedbecause parentstransmit bothgenesandfamilyenvironment tooffspring
andbecause people elicitresponsesfromand selecttheirenvironments in part
because of theirgenotype(Scarr and McCartney1983). Designs to evaluate
gene-environment correlationsare knownbut have been implementedsel-
dom. One simpletestforgene-environment is to use an adoption
correlations
designand evaluatewhetherchildrenat geneticriskfora disorderexperience
more of the environmental risks for thatdisorderthan do childrennot at
geneticrisk.For example,both Ge et al. (1996), using the Iowa adoption
sample,and O'Conner et al. (1996), usingtheColoradoadoptionprojectdata,
foundthatadoptedchildrenat geneticriskforantisocialbehavior(because
of theirbiologicalparents'antisocialhistory)weremorelikelyto experience
negativeor hostileparentingin theiradoptivehomesthanwerechildrennot
at geneticrisk.The presumedmechanismforthiseffectis the child's own
aversivebehaviorsthatare, in part,geneticallymediated.Hostile parenting
is thoughtto amplifyand maintainthe child's antisocialbehavior.Future
researchalong theselines will be of greatinterest.
TrinucleotideRepeatPolymorphisms. A keyfindingforgeneticmodelsof
behavioraldisordershas been the discoveryin recentyearsof a previously
unknownmechanismof mutationinvolvingtheexpansionof unstabletrinu-
cleotiderepeats(identicalnucleotidesequences) at some alleles, leadingto
failureof gene activity.At leasttwoof theapproximately elevenneurological
disorders known to exhibit this etiology have psychiatricsequellae:
Huntington'sdisease and fragileX syndrome.Several of thesediseases ex-
hibitanticipation;thatis, the illness occurs earlierin developmentin each
subsequentgeneration.The phenomenain neurologicaldisordersis typically
associatedwithmorethan35 repeatsin affectedindividuals[foran overview
see Gusella and McDonald (1996)]. The discoveryof these mutationshas
generatedconsiderableinterestin the psychopathologyliteraturebecause
some psychiatricconditionsexhibitincompletepenetrance,unclearpatterns
of inheritance, and possibly anticipation-like familypatterns,althoughthe

existenceof anticipationforpsychiatricsyndromesawaits rigorousdemon-

stration(Petroniset al. 1995). For example,considerablediscussionwas gen-
eratedby reportsthata mildervariantof thisphenomenon(a 7-repeatallele
on the dopamineD4 receptorgene) was relatedto the personalitytraitof
noveltyseeking(Ebsteinet al. 1996) andthento ADHD (LaHoste etal. 1996).
However,thepersonalityfindingcould notbe replicated(Pogue-Geileet al.
1996) and so is now open to question.The ADHD claim stillawaits repli-
cationattempts.
Yet thepatternof nonreplicated effectstypicalof psychiatricmolecular
researchis notentirelythecase. Notably,replicationnow has been achieved
withregardto linkageof ADHD and the dopaminetransporter gene (Cook
et al. 1995) by Waldmanet al. (1997), usinga moresophisticatedstatistical
strategy thanCook did. Likewise,morepromisingon thepersonality frontis
an associationstudyof a polymorphism on theregulatory regionof the se-
rotonintransporter gene,whichappearsto be relatedto thepersonality trait
of neuroticism, withimplicationsforanxietyand mood disorders(Lesch et
al. 1996). Finally,the usefulnessof using narrowlydefinedcognitivephe-
notypes(ratherthancomplexbehavioralsyndromesfromDSM-IV) in mo-
lecularstudieswas demonstrated by Grigorenkoet al. (1997) in an elegant
linkage studyof developmentaldyslexia. Grigorenkolinkedphonological
processing(thecognitivecoreofdyslexia)to markerson chromosome6. Such
studiesrepresent thethirdphase of researchin whichadvances in measure-
mentof thebehavioralphenotypeare integrated withlinkageand association
studiesof candidateloci.
It is important to notethattheseintriguing preliminaryfindingsare in
thecontextof smallsingle-geneeffectsand onlypartiallyheritabledisorders.
We now know thatgenes explainonly partof thepicturein even the most
severeformsof psychopathology and in all of personality.
Heritabilities
tend
to hoveraround0.50 formostdisordersand traits(and identicaltwincon-
cordancefordisordersis always less than 1.0). Presumably,the combined
actionof particulargeneticpotentialsand activatingenvironmental risks(by
meansof gene-environment interactions
or correlations)influencesindividual
differences in personalityand psychopathology.
Integrating Personality or Temperament and Psychopathology:

Examples. Initialeffortsto identify theoverlapof extremetemperament
per se and measuresof psychopathologydemonstrate thatclinicaldiagnoses
are notmerelyproxiesforextremetemperament (Maziade et al. 1990a). In-
stead,and notsurprisingly,
temperament and familyfactorsappearto interact
in predicting (Maziade et al. 1990b).
psychopathology
In an exemplarof methodologythatcapitalizeson personality research
to advancepsychopathology models,Kendler,Neale et al. (1993) investigated
thegeneticassociationof neuroticismand majordepressionin women.Bio-
metricmodelsindicatedthat70% of thecorrelation betweenneuroticism and

and Personality/403
, Temperament,
Psychopathology
liabilityto majordepressionwas due to sharedgeneticvarianceand 20% was

due to sharedenvironmental factors.Kendler,Kessler et al. (1993) fitteda
structural equation model to theirdata incorporating both specificenviron-
mental risk factorsand personality(neuroticism) to assess a completeetio-
logical model of depression. The model explained over 50% of thevariance
in liabilityto depression,withthestrongest predictorsbeing(in order)stress-
fullifeevents,genes,priordepression,and neuroticism. Resultssuggestthat
neuroticism cannotstandin forall othercontributors to liabilityfordepression
but is one significantindex of liability.Such models may become thenorm
in futurebehavioralgeneticmodelingof childdisordersalso.
Summary. We have attempted to illustratekey findingsin temperament,

personality, and psychopathology.One overarchingtheme is that simply
equating behavior problemsor psychopathology withextremesof tempera-
mentand personalityis problematicdevelopmentally. Not onlydoes herita-
to
bilityappear change at the extremes for some measures, such as internal-
izingsymptoms, butalso the of
developmentalpattern geneticfindings is not
parallel across domains. In particular, althoughheritability tends to increase
across developmentfortemperament and personality, it appearsto decrease
across development(at least throughadolescence) forseveral measuresof
psychopathology. Furthermore, thescarcityof sharedenvironment effectsin
and
temperament personality research stands in somewhat strikingcontrast
to thepresenceof notable,if modest,sharedenvironment effectsin psycho-
pathologystudiesin communitysamples.Finally,it is clear thatcloser ex-
aminationofnarrow-band measuresis neededto identify specificgeneeffects.
It is less clear whetherthatstrategywill help in determining specificshared
and nonsharedenvironment effects,but it may. Inclusionof clinic-referred
samples in analysisof extremeswill be of keen interest.Expansionof de-
velopmentalstudiesof psychopathology to includethe otherend of the life
span (aging) has begun and, although discussedhere,will be of interest
not
fora completeaccountof developmentalpsychopathology. Finally,therapid
explosion of molecular research on
capitalizing polymorphisms in brain-
relevantcandidategenes portendsfurther integrationof behavioral and mo-
lecularapproaches.
Conclusion: The Challenges Ahead

Ratherthanconcludingwithanswers,we concludewithselectedques-
tionsthatwe believe our reviewpointstoward.These questionsare, in our
view, centralto realizingthepotentialof behavioralgeneticsresearchto il-
luminateindividualdifferencesand developmentalpsychopathology.
models(second-phasebiomet-
1. How can sophisticatedmultifactorial
rie research)and linkage and association studiesof molecularcandidates

(third-phasemolecularresearch)best be integrated?Are both typesof re-

searchstillnecessary?Our impressionis thatthesetwo approachescomple-
mentone anotherand will continueto do so at least in thenearfuturein the
domainof developmentalpsychopathology. For one thing,themode and ex-
tentof geneticinfluenceon developmentalbehavioralsyndromesare notyet
fullycharacterized.For example, if ADHD is really a productof genetic
heterogeneity (e.g., similaroutcomesfrommultipleloci), this information
frommodelingstudieswill be crucial to accuratelinkagestudies.Another
issue is thatcomorbidity is the rule in psychopathology, yet the extentof
overlappinggeneticinfluenceon comorbidsyndromesis not well mapped.
Behavioralstudiesare neededto completesuch mappingto determine which
phenotypesare mostpromisingformolecularstudy(i.e., narrowermarkers
or specificsyndromesubtypes).Likewise,the apparentpolygenicnatureof
mostdevelopmentalpsychopathology suggeststhatparticularmolecularap-
proaches,such as the searchforquantitative traitloci, may be moreadvan-
tageous thanothers.Finally,moleculardesignscannotreadilyidentifykey
environmental effectsforwhichmodifiedbehavioralgeneticdesignsmaybe
uniquelyuseful.However,integration of molecularstudieswithstudyof en-
vironmentalcontextswill be an importantstep in the next generationof
research.
2. What are the unsharedenvironmental effects?The importanceof
nonsharedenvironment in personalitydevelopment is onlypartiallyreplicated
in psychopathology research,butit remainsan important finding.Yet itbegs
thequestionof specifyingtheeffects.Possibly,thesereflectinteractions be-
tweenfamilyeventspreviouslythoughtto includesharedenvironment (e.g.,
parentaldivorce)and theuniquetemperaments of thesiblingsinvolved.But
demonstration of specificnonsharedeffectsin a geneticdesignwill be a real
step forward.As such,behavioralgeneticdesignsthatfeaturemeasuresof
theoretically importantnonshared(and shared) environmental causal vari-
ables will be key. Such effectsmightinclude indexes of prenatalinsults,
differentialparent-child interactions, parent X child personalitycontrasts,
childpeer groups,and school experiences,to namejust a few.
3. Are sharedenvironmental effectsbeingwritten offprematurely? Ex-
aminationof changesin proportionof gene and sharedand unsharedenvi-
ronment effectsacrosscriticalenvironments remainssparse[Rose (1995) also
makes thispoint],even thoughseveralcriticalenvironmental riskcontexts
are now knownin developmentalpsychopathology. Particularlyfordevel-
opmentalpsychopathology, in contrastto temperament and personality,evi-
dence is accruingthatsharedenvironment effectsmaybe crucialin theonset
of disorder,especiallyforadolescentpsychopathology and forcomorbidcon-
ditions.Studyof thesedisordersshouldincludemeasuresof specifichypoth-
esized sharedenvironment effectsin an effortto accountforthosefindings.
of
Examples likely candidates are parentalpsychopathology, maritaldiscord,
and social support.

, and Personality/405
, Temperament
Psychopathology
4. What is transmitted in heritabletraitsand disorders,and in which

etiologicalsubtypes is the heritable geneticprocessoperative?For example,
forADHD heritability is consistently foundto be highin twinstudies.As-
suming thatthese effects are replicatedwithclinicalcases, adoptionsamples,
and observationaldata (ratherthanonlyparentratings),a questionfollows:
Giventhatthedisorderis complexand heterogeneous, whatprocessis closer
to the genes thanthe observablesyndromeof behaviors?Althoughreliance
on rare categoricalmarkersis problematic(Deutsch and Kinsborne1990),
dimensionalmarkersmay be useful.For example,Nigg et al. (1997) found
thatabnormalitiesof attentionalorientingwere exhibitedby childrenwith
ADHD and theirbiologicalbutnotadoptiveparents.Familyandtwinresearch
as well as moleculardesigns should more routinelyexamine such narrow
neurocognitive or biological markersin conjunctionwithbehavioralpheno-
types. The recent studyby Grigorenkoet al. (1997) is an example of the
designs needed. For behavioraldisordersexamplesof potentialreductionist
candidateswould be brainneurotransmitter action,executive,attentional, or
otherprefrontal cognitivefunctions, and narrower behavior dimensions (e.g.,
activitylevel).
5. Temperamentand personalitytheorynow predictparticularneuro-
psychologicaland neurophysiological correlates.These neuropsychological
correlatesare possiblecandidatesforlaboratory measuresof psychiatric syn-
for
dromes, example, the deficits in leftcortical EEG activationrelatedto
depressionin adultsand children(Davidson 1992). An intriguing exampleof
a genetictwinstudyof EEG event-related potentials providedby Katsanis
is
et al. (1997). Thus integration of these perspectivesin behavioralgenetic
designsintendedto addresstheunderpinnings of existingsyndromaldefini-
tions,althoughambitious, is a promisingway forward.Heritability of the
and
putativeneuropsychological neurophysiological is
correlates virtually un-
known, butinitialdata indicate that
it be
may quitehigh(Katsanis et al. 1997).
Phase 1 behavioralgeneticsresearchis stillneededin thisdomain,as well as
phase2 modelingofgeneticand environmental mechanismsinfluencing these
behavioraland cognitivemarkers,in preparation forfruitful 3
phase linkage
and associationstudies.In short,a simultaneousconsideration of severallev-
els of analysis(i.e., behavioral,cognitive,neuropsychological, or biological)
withbehavioralgeneticdesignsis muchneeded to studylinksbetweenper-
sonalityand psychopathology.
Conclusion. Behavioralgeneticsresearchin relationto temperament, per-

sonality,and psychopathology has entereda new phase as a resultof several
developmentsin recentyears.First,theimportance of liabilityto disorderhas
focusedincreasingscientificattention
on personalityandtemperament as pos-
sible diatheses.Second, continuitiesbetweentemperament and personality
are now beginningto be mapped.Third,multivariate biometriemodels and
molecularstudieshave replacedsingleheritability estimatesas themethods

of choice to answeretiologicaland geneticquestionswithregardto devel-

opmentalpsychopathology. On theone hand,advancesin moleculargenetics
will help to specifysome of thegeneticvariationthathas been identified by
quantitative designs.However,specification of environmental activatingand
maintaining causes in relationto geneticetiologyis no less important and
maybe bestaccomplishedthroughmoresophisticated quantitativedesigns.
Theoretically,themostimportant paradigmshiftunderwaymaybe to-
wardbothempiricalstudyofwhether particular
syndromes, ordisorders
traits,
reallyare dimensionsor categoriesetiologicallyand the initialmappingof
thegeneticarchitecture underlying thephenotypicstructure of mentaldisor-
ders as currently classified,which could lead to an etiologicallyinformed
nosology.Integrated geneticdesignsare drawingincreasingattention in sci-
entificdiscussion[e.g., Scarr(1997) and Waldman(1997)]. It is hoped that
growingcross-fertilization amongdisciplines,includingbehavioralgenetics
researchers, and ecologicallymindedscientists,will help to
neuroscientists,
resolvetheetiologyof society'smostvexingbehavioraland mentaldisorders.
AcknowledgmentsThisresearch wassupportedbytheNational
Institute
ofMental
Healththrough
grantsMH51560(awardedtoH. HillGoldsmith)
andR03-MH57422
(awardedtoJ.Nigg).
Received21 January
1997; revision 23 June1997.
received
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Developmental Psychopathology, Personality, and Temperament: Reflections on Recent

Behavioral Genetics Research

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JOELT. NIGG1ANDH. HILLGOLDSMITH2

Abstract Personality, temperament,andpsychopathology wereuntil

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hand,wide variationin personalityand temperament is readilyexplainedby

Key Background: Some Definitions

Personality and Temperament. Several theoreticaltraditionsenergize

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cializingwithothers,and interpersonal warmth.Althoughthesemajortraits

Psychopathology. The prevailingoperationaldefinitionsof psychopa-

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are behaviorallydiagnosed and lack biological gold standardsto establish

Categories and Dimensions. As readersmightguess fromthediscussion

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disorderoccurringbeyonda particularthreshold(Gottesman1991), has been

Genetic Methods. Althoughearlytwin,adoption,and familystudiesem-

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atricgenetics[e.g.,Belmakerand Biederman(1994)]. This newphaseofwork

Empirical Findings: Personality and Temperament

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dataarisefromtwinstudies.Twinresearchhas shown(1) minimalheritability

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addressedby incorporatingmultipleraters,multipletimepoints,and multiple

RecentDevelopmentsin TemperamentResearch. Of current interest

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lips and Matheny1991), researchersneed to examinetemperamental simi-

Recent Developments in PersonalityResearch. One ironyof the first

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Empirical Findings: Developmental Psychopathology

Patternsof Effectin Child Problems

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and Stevenson1989; Stevenson1992) and attentionproblems(Gjone et al.

BroadbandChildProblemDimensions. Severalrecentstudieshave inves-

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whatlowerheritability fordelinquencyin adolescence.Gjone et al. (1996b)

Comorbidityamong Child Problems. The just-notedfindingswithre-

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The same Colorado Reading Projectdata were used to examine co-

ExtremesAnalysis. As notedearlier,the fundamental questionof dimen-

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creasedat theextremes,whereassharedenvironment effectsremainedstable

Gene-Environment Interaction. We underscorethe shortageof develop-

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using inbredstrainsof mice also reveal gene-environment interaction,al-

Gene-Environment Correlation. Genotypesand environments are corre-

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existenceof anticipationforpsychiatricsyndromesawaits rigorousdemon-

Integrating Personality or Temperament and Psychopathology:

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liabilityto majordepressionwas due to sharedgeneticvarianceand 20% was

Summary. We have attempted to illustratekey findingsin temperament,

Conclusion: The Challenges Ahead

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(third-phasemolecularresearch)best be integrated?Are both typesof re-

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4. What is transmitted in heritabletraitsand disorders,and in which

Conclusion. Behavioralgeneticsresearchin relationto temperament, per-

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of choice to answeretiologicaland geneticquestionswithregardto devel-

Achenbach, T.M.1991.Manual fortheChildBehavior Checklist/4-18

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