Personality and Temperament

Jeffrey R Gagne, University of Texas, Arlington, Texas, USA

Based in part on the previous version of this eLS article Personality and Temperament (2005) by Joel T Nigg and H Hill Goldsmith.

Introductory article
Article Contents
. Introduction . Advances in the Field of Behavior-Genetic Research on Temperament/Personality . Established Behavioural Genetic Findings . Recent Developments and Findings in Quantitative Temperament Research . Molecular Genetic Work on Temperament and Personality . Summary and Conclusion

Online posting date: 15th March 2013

Temperament is an early developing set of characteristics related to later personality. Commonly studied dimensions of temperament include activity level, anger/frustration, behavioural inhibition/fear, effortful control and positive affect. Personality includes a range of traits, including major traits of extraversion, neuroticism and impulsivity/sensation-seeking. Different aspects of personality and temperament are related to important developmental outcomes such as behavioural problems and psychopathology. Both behavioural genetic and molecular genetic research have contributed to the understanding of major traits of temperament and personality. Behavioural genetic approaches use twin and adoption study designs to estimate genetic and environmental contributions to individual differences in traits. Most behavioural genetic studies have found substantial heritability for personality and temperament. Molecular genetic investigations focus on the effects of specific genes (primarily dopamine- and serotonin-related genes in studies of temperament and personality).

psychopathology (e.g. psychiatric disorders and behaviour problems), which may be related in part to extremes of temperament or, later, personality in children and adults. Personality traits and by extension of early temperament dimensions, may also moderate important health outcomes (e.g. cancer, heart disease and smoking). Perhaps because of these important ramications, the literature on behavioural and molecular genetics of temperament and personality has recently increased markedly. A eld that could be summarised by several twin and adoption samples in decades past is now addressed by hundreds of studies that either link personality or temperament traits with specic genes, promote temperament dimensions and personality traits as genetic risk factors, point to the genetic commonalities in temperament and personality and health problems (such as smoking and heart disease) and psychopathology or to neural mechanisms related to genetic and personality ndings. Throughout this introductory article, the author points to: (1) well-established or classic ndings; (2) recent developments, noting that the latter may change rapidly and (3) conceptual and methodological issues and complications that the new student should bear in mind.

Introduction
That there should be genetic contribution to personality and temperament should come as no surprise. The social context of human evolution suggests that, from an evolutionary framework, fairly wide individual variation in personality and temperament would confer group reproductive advantage. One reason for which advances in this area are important is that they provide understanding not only of the sources of individual dierences, but also of routes to development of human problems and human
eLS subject area: Neuroscience How to cite: Gagne, Jeffrey R (March 2013) Personality and Temperament. In: eLS. John Wiley & Sons, Ltd: Chichester. DOI: 10.1002/9780470015902.a0005244.pub2

Personality and temperament

Several theoretical traditions guide temperament and personality research. Of these, trait models have been the main focus of behavioural genetic research on temperament and personality. Temperamental dimensions can be conceptualised as fairly stable behavioural traits that develop early, are constitutionally based (Goldsmith et al., 1987) and refer to aective or emotional aspects of personality (Goldsmith and Campos, 1982). Temperament traits have also been dened as biologically based individual dierences in reactivity and self-regulation (Posner et al., 2007; Rothbart, 2007; Rothbart and Derryberry, 1981). Rothbarts (2007) model proposes that reactive emotional, attentional and motor behaviours in addition to the self-regulatory process of eortful control form the structure of early temperament. Although there are several major traditional theories/conceptions of temperament (Goldsmith et al., 1987), Rothbarts (2007) (see Table 1) is a
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Table 1 Selected models of personality and temperament showing phenotypic parallels across models Models Three-factor models Tellegen Watson and Clark Eysenck Cloninger Rothbart Five-factor models Big-Five Zuckerman
Adapted from Nigg (2000).

Reactivity factor (negative aect) Negative emotionality Negative temperament Neuroticism Harm avoidance Negative aectivity Neuroticism Neuroticismanxiety

Sociability factor (positive aect) Positive emotionality Positive temperament Extraversion Reward dependence Surgency Extraversion Sociability

Control factor Constraint Disinhibition Psychoticism Novelty-seeking Eortful control Conscientiousness Impulsive sensationseeking

contemporary model that is empirically related to models of adult personality structure. Relations between early temperament dimensions and later personality have become an area of intense study within the eld over the last two decades (Caspi et al., 2005). Individual dierences in early temperament tend to change over development and combine with environmental factors to give rise to personality traits in adulthood (Caspi, 2000; Rothbart and Bates, 1998). Like temperamental traits, most personality traits also show modest genetic inuence (Bouchard and Loehlin, 2001). Table 1 lists several major models of personality (including Rothbarts (2007) temperament model). The authors review of genetic research on personality focuses on major higher-order traits featured in leading models of personality as shown in Table 1, because these are the most well studied, tend to have replicated ndings and have the broadest interpretive reach. Personality traits are generally understood as governing behaviour under a limited set of incentive contexts. Most of the time, behaviour is activated under the inuence of several traits. The classic Big Five personality traits are openness, conscientiousness, extraversion, agreeableness and neuroticism. Trait theorists such as Eysenck, Tellegen and Zuckerman agree that neuroticism and extraversion are two of the major traits in adults (Table 1). Most models agree that there are one to three additional major traits that are needed for even the most concise description of personality structure. One of these remaining traits concerns impulsive sensation-seeking, sometimes referred to by its opposite pole of constraint or conscientiousness. In the interests of space, the author emphasises these major traits of personality. The current generation of research concerning the continuity of traits over development owes much to pioneering studies of temperament begun in the 1950s and 1960s by Thomas and Chess in New York, among others. Since then, several longitudinal studies, many with genetically informative samples, have obtained results supporting at least moderate continuity of these core personality traits as well as dimensions of temperament.
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Commonly researched temperament dimensions

Commonly researched dimensions of temperament include activity level, anger/frustration, behavioural inhibition/ fear, eortful control and positive aect. A relative consensus has emerged among temperament scholars about the importance of these dimensions within the structure of temperament and these dimensions have been extensively studied with genetically informative designs. As a temperament trait, activity level refers to individual dierences in proneness to higher versus lower characteristic degrees, or vigour of movement. Anger/frustration describes the individuals propensity toward experiencing an approachrelated type of negative aect within a challenging context, where goals may be blocked or attack may be perceived. Behavioural inhibition/fear can be dened as the individuals tendency to react with distress or wariness toward novel or threatening objects, persons, or situations. Eortful control refers to ones ability to inhibit a dominant response and instead activate and execute a subdominant response (Murray and Kochanska, 2002; Posner and Rothbart, 2003; Rothbart and Bates, 1998). Positive aect refers to a propensity to experience and express enjoyment (Bates, 1989) and to be responsive to reward.

Personality traits of neuroticism, extraversion and impulsivity and sensation-seeking

Neuroticism, sometimes labelled negative aect, connotes vulnerability to anxiety and depression, worry and poor coping with stress. Extraversion, sometimes labelled positive aect, but also connoting sociability and energy, implicates activity level, interest in socialising with others and interpersonal warmth. Impulsive sensation-seeking (or low constraint) generally refers to a response style that pursues reward without due reection. Although these major traits have long been theorised to have biogenetic

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underpinnings, similar to conceptions of temperament in children, the extent to which this is true has received ongoing empirical investigation. Trait researchers also agree that personality is hierarchically organised. That is, broadband, higher-order factors such as neuroticism and extraversion each comprise several narrower, more homogenous traits. Child temperament has an organisation that, while not necessarily the same as adult personality, may parallel it in many ways. Thus, researchers studying early childhood identify traits such as anger and reactive fear (strength of emotional distress), positive aect or approach and later in infancy, ability to regulate attention or eortful control (both possible precursors to constraint).

Developmental relation of personality and temperament

Conceptual understanding of the relation between temperament and personality trait models continues to evolve. Classically, temperament has been viewed as a set of narrower, biologically based characteristics, for which the inuence of genetic factors has been assumed. Personality, in contrast, represents later elaboration of experience and development and presumably more socially determined characteristics. Yet, the main dimensions of temperament identied in current research may map at least partially onto domains of adult personality. For example, recent conceptual reviews suggest that the temperamental construct approach may map onto personality trait extraversion, negative aectivity to neuroticism, and inhibitory control to constraint or conscientiousness. One exciting trend comprises empirical attempts to link temperament and personality from a developmental perspective, mapping the heterotypic continuity of early temperament in its development to mature personality. Empirical eorts have begun to support these conceptual links with modest but reliable associations over time. Rothbart (2007) has identied the three broad extraversion/surgency, negative aectivity and eortful control dimensions of temperament through factor analysis of scales from her questionnaires. These broad dimensions or factors are related to the Big Five personality factors of extraversion (extraversion/surgency), neuroticism (negative aectivity) and conscientiousness (eortful control). Similar broad temperament factors have also emerged from factor analyses of laboratory assessments of temperament (e.g. Dyson et al., 2012).

measured directly in many behaviour genetic studies, genetic (and environmental) variance is inferred statistically using family, twin and adoption designs by testing for similarity across dierent types of relatives. Recent work often emphasises tting multivariate twin, longitudinal and other biometric models to test competing aetiological theories. In general, these models recognise that multiple genes contribute to variation in temperament and personality. It is now possible (and very aordable) to genotype specic genes and incorporate this information into investigations of temperament and personality. Currently, molecular genetic techniques are being integrated into many behavioural studies. Because the molecular eld is developing rapidly, only the major outlines emerging to date are pointed out. Most behavioural researchers are using either candidate gene studies or genome-wide association studies (GWAS). Candidate gene approaches are based on prevalent theories and the selection of specic genes based on underlying biology associated with behaviours. In GWAS, the entire genome is scanned for eects (Dick et al., 2011). A range of other methodological and conceptual issues in genetic research are beyond the scope of this brief review, including such important issues as nonMendelizing eects, theoretical considerations in genotypeenvironment (G E) correlations and empirical examinations of the assumptions of behaviourgenetic research. Discussion of such issues in regard to developmental psychopathology is provided in the Further Reading listings and in other entries in this volume. See also: Behaviour Genetics Human; Genome-wide Association Studies

Established Behavioural Genetic Findings

Much of the current quantitative data arises from twin studies. Twin research in the United States and Europe has provided an intriguing suggestion of minimal heritability for traits in the neonatal period along with fairly established ndings of: (1) increasing heritability of traits through infancy into childhood; (2) heritability of major traits approximating 0.5 for childhood temperament and young- to middle-adult personality traits, with stability or slight increase in heritability in later life; (3) environmental variance generally is of the nonshared (within family) type and (4) shared experience (between family variance) contributes little to variation in these traits. An additional nding that is increasingly established is that the role of cultural transmission or within-family experiential eects may be notable for social attitudes (e.g. conservativism), but not so for personality. These patterns are seen across all major dimensions of temperament and personality lending support to the assumption that personality/temperament traits are biologically based and genetically inuenced. A larger issue has been that the available adoption data, tend to yield signicantly smaller estimates of heritability
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Advances in the Field of BehaviorGenetic Research on Temperament/ Personality

Whereas early twin adoption and family studies have emphasised magnitudes of genetic contribution to variability in a trait or disorder, the eld has steadily moved beyond that question. Genetic factors are not typically

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than do twin studies. Perhaps the twin data overestimate heritability due to violations of the equal-environments assumption of twin studies or to undetected biases in rating data such as rater contrast eects. Contrast eects take place when raters (typically parents) inate dierences between family members. Or perhaps the adoption studies underestimate heritability due to the lack of control for developmental stage (individuals compared in adoption studies are typically of dierent ages) or to nonadditive gene eects not being detected in adoption studies. Studies underway with twin and adoption data using laboratory measures of temperament should clarify the picture. So far, recent studies seem to indicate that contrast eects are a factor in parent ratings of twins only, leading to underestimates of nonidentical twin similarities in child-temperament studies that rely on parent report (Saudino et al., 2004). Of the replicated ndings, perhaps the most unexpected was the importance of nonshared environment to individual dierences in development. This nding was provocative because it suggested that many theories of how families inuence child development must be revised. Families apparently do not function to make siblings similar to one another. Yet systematic empirical investigation of nonshared environmental inuences is quite recent. One issue is that many twin samples assess an incomplete range of developmentally relevant environments (e.g. portions of the socioeconomic spectrum are often underrepresented). As a result, heritability estimates may be too high and estimates of the role of shared (between family) environment eects may be too low. In addition, it has proven dicult to account for nonshared-environment eects by specic environmental measures. Perhaps specic environmental eects are difcult to detect because they depend on many genotype (or phenotype) by environment interactions, each of modest eect. However, methodological factors such as those noted earlier also continue to receive investigation. For instance, when rater or sibling contrast eects are controlled, shared-environment eects emerge for some temperamental traits. Also, laboratory or observer ratings of temperament sometimes show patterns of shared environmental eects in certain cases (e.g. inhibitory control and activity level in preschoolers) even though there are no shared environmental eects for parent ratings at the same age. Measures of environmental eects therefore continue to be incorporated into genetically informative designs.

Recent Developments and Findings in Quantitative Temperament Research

Developmental and methodological explorations
Contemporary quantitative genetic research has sought to understand (1) developmental variation in heritability and (2) genetic and environmental contributions to
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developmental change in temperament expression. Results from a major longitudinal twin investigation sponsored by the MacArthur Foundation are illustrative. Temperament data were obtained by observer and parent report for a large sample of some 800 twins assessed at 14, 20, 24 and 36 months of age. Heritability of the major temperament domains assessed (inhibition, shyness, activity and task orientation) was approximately 0.3 for observational data and approximately 0.5 for parent ratings at both 14 and 20 months, although some traits reected a slight increase in heritability whereas others revealed a slight decrease in heritability. Notably, correlations between scores at the dierent time points were modest, indicating considerable developmental change during the time periods assessed. This change was analysed for several temperament measures. In general, stability over time was due to genetic factors, and change over time to nonshared-environment factors, but there were exceptions. See also: Quantitative Genetics As an example, ndings for laboratory-rated behavioural inhibition, a major trait possibly related to later neuroticism as well as to anxiety disorders is considered. Stability of inhibition over time was due entirely to genetic stability. However, a portion of the change over time was due to genetic factors as well, suggesting that genes may exert dierent inuences over time as the context for their expression the developing child itself changes dramatically. The remainder of the change over time was due to nonshared-environment (and measurement error) eects. Notably, a closely related construct, shyness, revealed extensive inuence of shared environment but no signicant genetic inuence on change over time. This highlights the importance of careful phenotypic denition when drawing conclusions about genetic eects on development. Other trait domains besides inhibition revealed either genetic or nonshared-environment explanations for developmental change, with some interesting dierences for parent versus laboratory ratings of temperament. These ndings underscore the dynamic nature of genetic inuence across development. Another example that exemplies an objective rating perspective on temperament measurement was a twin study that employed motion recorders (actometers) to assess activity level at 7 months of age. Intraclass monozygotic twin correlations exceeded dizygotic twin correlations, supporting evidence of genetic inuences (Saudino and Eaton, 1991). Longitudinally, genetic factors continued to be present in activity level assessed with motion recorders at 35 months of age (Saudino and Eaton, 1995) and twin concordance patterns from 7 to 35 months reected genetic inuences on developmental change (Saudino and Eaton, 1995). A more recent investigation of actometer-assessed activity level used 7- to 9-year-old twins. Model-tting analyses of a test and a break-from-testing situation showed heritability estimates of 24% and 30% respectively, with shared environment contributing 27% and 42% of the variance (Wood et al., 2007). The genetic correlation between the test and break situation scores was 1.0,

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Mechanisms and processes

Two important processes that shape development have received some initial empirical investigation. One process is G E interactions, a situation in which the association between an environment and a phenotype is moderated by an individuals genotype. Like all statistical interactions, geneenvironment interactions can also be conceptualised conversely, that is, the environment moderates the relationship between the individuals genotype and phenotype. A second process is G E correlation; because of their genotype (and subsequent phenotype), people actively select and passively elicit, dierent niches and minienvironments for themselves. Environments thus amplify gene eects.

CCTI soothability

indicating that the same genes were operating on activity across situations (Wood et al., 2007). The results of twin studies that used objective motion recorders have thus bolstered the ndings of those that employed parent, teacher and other observational measures of activity.

4.0 3.5 3.0 2.5 2.0 Left (a)

DRD4 allele Long Short

Right

Frontal brain asymmetry DRD4 allele Long Short 3.5 3.0 2.5 2.0 Left Right

4.0 CCTI attention difficulties

G E interaction
Although studies of G E interactions for temperament and personality have been somewhat limited, a few examples exist in recent literature. Fox et al. (2005) tested whether mother-reported social support moderated the association between child genotype and behavioural inhibition in 7-year-olds. The functional polymorphism in the promoter region of the serotonin transporter gene (5HTTLPR) was selected because several serotonin functions including the regulation of transporter levels, serotonin uptake and serotonin transcription (Hariri et al., 2002) could be related to behavioural inhibition. A G E interaction was detected in which links between the genotype and behavioural inhibition were stronger at low levels of social support. Another investigation found that 5-HTTLPR allele status moderated links between overprotective parenting and behavioural inhibition in middle childhood (Burkhouse et al., 2011), and another showed that the same risk allele interacts with child adversity to predict impulsivity (Carver et al., 2011). A study examining the dopamine D4 receptor gene (DRD4) candidate gene employed resting frontal electroencephalography (EEG) asymmetry at 9 months as an environmental variable in an interaction relating to temperament outcomes at 48 months (Schmidt et al., 2009; see Figure 1). DRD4 status and EEG activity at 9 months predicted dierent patterns of temperament longitudinally. In related work focusing on childhood behavioural problems, a study showed that maltreatment and genetic risk interacted to predict conduct problem scores in 5-yearolds. The association between genetic risk and child conduct problems was stronger for those children who had been maltreated in comparison to the nonmaltreated (Jaee et al., 2005). In a similar investigation of conduct problems in young children (Button et al., 2005)

(b)

Frontal brain asymmetry

Figure 1 Mean temperament difficulties among 48-month-old children as a function of (a) dopamine D4 receptor (DRD4) gene (long versus short allele) and (b) resting frontal electroencephalogram asymmetry (left versus right) at 9 months. Reproduced with permission from Schmidt et al. (2009). & Sage Publications.

heritability of child conduct problems decreased as level of family dysfunction increased.

G E correlations
Designs to evaluate G E correlations are known but have seldom been implemented. One simple test for G E correlations is to use an adoption design and evaluate whether children at genetic risk for a disorder experience more of the environmental risks for that disorder than do children not at genetic risk. For example, two studies, one in Iowa and one in Colorado, found that adopted children at genetic risk for antisocial behaviour (due to biological parents antisocial history) were more likely to experience negative/ hostile parenting in their adoptive homes than were children not at genetic risk. The presumed mechanism for this eect is the childs own aversive behaviours that are, in part, genetically mediated. Hostile parenting is thought to amplify and maintain the childs antisocial behaviour. Parallel explorations with major temperament and personality dimensions are underway using both adoption and twin data. Parentchild mutuality (Deater-Deckard and
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OConnor, 2000) provides another example of G E correlation. Parentchild mutuality is dened as shared positive aect, responsiveness and cooperation in parentchild interactions. Twin and nontwin sibling correlations of parentchild mutuality indicate that variation in this construct is inuenced by genetics and that these genetic inuences might be linked to child temperament phenotypes. Related work has shown that dyadic mutuality is specic to each child in a family and that child behaviour problems are linked to this mutuality (Deater-Deckard and Petrill, 2004).

Molecular Genetic Work on Temperament and Personality

Broad themes related to two neurotransmitter systems
Thousands of genes are expressed in the brain and therefore could potentially inuence personality and temperament. Multiple alleles of these genes in the population could account for substantial heritability of these traits. Searching for specic genes related to personality and temperament is not the search for one gene, in contrast to some neurological and metabolic disorders. Instead, it is the search for any of the multiple genes that share a role in shaping trait expression. Although this search is fairly recent, the relatively low cost of genotyping has contributed to a generation of psychological researchers who currently collect deoxyribonucleic acid (DNA) as part of their overall research programs. Thus far, there are as yet few well-established molecular genetic ndings. A recent meta-analysis of investigations of candidate genes and personality traits found few consistent associations (Munafo et al., 2003). Nonetheless, two trends in the available data are interesting: (1) the role of dopaminemoderating genes in impulsive personality traits such as constraint or conscientiousness and (2) the role of serotonin-related genes in anxiety-related personality traits such as neuroticism. See also: Dopamine; Molecular Genetics; Serotonin

Endophenotypes
Another conceptual approach to the genetics of personality and temperament involves endophenotypes, dened as intermediate links between a genotype and an individuals observable behaviour. Endophenotypes can be proximal to the gene (e.g. level of a protein) or more distal (e.g. level of executive functioning). Therefore, an endophenotype may be a neurochemical measure; a measure of brain structure; executive functioning or a dierent measure of behaviour than the phenotype of interest. For example, extreme levels of temperament dimensions can be considered endophenotypes for behaviour problems or psychiatric diagnoses. Gottesman and Gould (2003) criteria for identifying candidate endophenotypes include being associated with the trait under study, individual dierences in the endophenotype being at least partly due to genetic factors, being state-independent, and appearing in rst degree relatives at a rate somewhere between the rate in aected persons and the rate in the general population. See also: Gene-tobehavior Pathways Although research on personality endophenotypes is fairly limited, there are a few examples from the temperament literature. Genes related to the corticotrophin releasing hormone (CRH) were implicated in animal models of behaviour inhibition (Bakshi and Kalin, 2000), and links between CRH candidate genes and behavioural inhibition in children of a parent with panic disorder have also been established (Smoller et al., 2003, 2005). Frontal EEG asymmetry is associated with individual dierences in aective style, inhibition and liability to mood disorders and has been nominated as an endophenotype in genetic studies of temperament and mood and anxiety disorders (Anokhin et al., 2006; Goldsmith and Lemery, 2000). A potential endophenotype for eortful control is the executive attention system that involves the anterior cingulate and lateral prefrontal brain areas (Rueda et al., 2005). Several researchers have proposed dimensions of temperament as potential endophenotypes for related outcomes as well. Based on overlapping genetic aetiology, low inhibitory control was proposed as a candidate endophenotype for attention decit hyperactivity disorder (Gagne et al., 2011). In all of the above cases, traits meet some of the standards for qualication as endophenotypes, although more extensive research is required.
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Some genes under active investigation

These studies include nearly a dozen specic genes or gene markers, which complicate the picture. By far the most well studied, however, are the DRD4 receptor gene and the serotonin transporter or its associated transporterpromoter region. The majority of studies have measured personality by self-report, using either the Cloninger Tridimensional Personality Questionnaire or the Big-Five NEO Personality Inventory. A small handful of studies have examined young childrens temperament on these two major genes of interest. The results can best be summarised as mixed. Although several studies nd associations, as noted above, as many studies fail to nd the association or nd a dierent association (e.g. linking the serotonin transporter with constraint).

DRD4
Several studies have examined DRD4 and some version of sensation-seeking, novelty-seeking or low constraint. About half of the studies have found an association of the 7 repeat allele of DRD4 with increased novelty-seeking (e.g. Benjamin et al., 1996; Ebstein et al., 1996) and this has been replicated in at least one study of young children (see Figure 2). The results of a meta-analysis that includes several more recent studies suggests that the generalisability of the association may be in doubt (Wahlsten, 1999),

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40 D4DR genotype
Percent of subjects

30

S L

20

10

-36- -42- -48- -54- -60- -66- -72- -78Estimated TPQ-novelty seeking score

Figure 2 Distributions of estimated novelty seeking scores by D4DR genotype. Reproduced with permission from Benjamin et al. (1996). & Nature Publishing Group.

and subsequent studies have shown both replications and nonreplications (Strobel et al., 2003). As investigations of DRD4 polymorphisms and personality have continued, more nuanced interactions with other genes and behaviours have been considered. Molecular genetic studies of personality and temperament may also benet from molecular genetic approaches to psychopathology. To give one example, more consistent results have been found in association and linkage studies of dopamine gene alleles with child attention-decit hyperactivity disorder than with related personality traits (see Gizer et al., 2009). Yet specicity to attention-decit disorders is lacking; these alleles have also been associated with other disorders, underscoring the importance of understanding the liability to disorder in the form of basic personality or temperament traits. See also: Dopamine D4 Receptor (DRD4) Box Score; Molecular Genetics of Attention DecitHyperactivity Disorder (ADHD)

be expected to show increased serotonergic transmission, and they report higher Neuroticism scores (but are not dierent on the other factors of the Big Five personality traits). Although replications have been reported, some comprehensive failures to replicate these results have also been reported, particularly in anxiety patients (WillisOwen et al., 2005). These ndings are of theoretical importance, because of the importance of Neuroticism for the development of anxiety disorders and other adjustment problems in children and adults. Another interesting set of ndings indicate that related temperament traits in infants (e.g. Rothbarts negative emotionality; Table 1) are associated with the short allele of the serotonin transporterpromoter and the short allele of the DRD4 gene. These developmental ndings suggest genetic similarities between childhood temperament and later adult personality. However, these recent childhood ndings need to be conrmed in replication studies. For example, a second study that checked association of the 5HTTLPR short allele with temperament traits from ages 48 months to 16 years failed to nd an association at most ages with shyness and/or withdrawal or with anxiety and/or depression. The inconsistency across studies could be due to dierences in the method of assessing the traits of interest (e.g. as noted earlier, shyness shows a dierent pattern of genetic inuence from behavioural inhibition) or to other methodological issues.

Other candidate genes

Of course, serotonin and dopamine genes are not the only ones that have been examined for association with personality and temperament. For example, genetic variants in noradrenergic receptors have been examined for association with irritability, hostility and impulsivity (Comings et al., 2000). However, variation in a single gene accounted for only a few percent of the phenotypic variance.

Serotonin transporter promoter gene (5HTTLPR)

Other studies have examined serotonin genes in relation to neuroticism and/or anxiety. Once again, the picture is mixed, with many but not most studies nding an association. One study found an allelic association between a polymorphism in a promoter of the serotonin transporter gene (5HTTLPR) on chromosome 17q, accounting for 3 4% of the variance in self-reported anxiety-proneness. This is one of the few ndings that have been replicated across two samples, and the allele also dierentiated aected from unaected siblings (Lesch et al., 1996). The serotonin transporter is a protein that is involved in serotonin neurotransmission in regions of the limbic system and cortex associated with anxious behaviour. The allele that leads to decreased transporter activity at least in lymphoblast cell lines occurred at a high frequency, 43%, in the samples studied (Lesch et al., 1996). Persons with this allele would

Methodological issues in molecular genetic studies

Thus, despite some very intriguing initial leads, one of the most important ndings across all molecular studies to date is that ndings are inconsistent. These inconsistent results could well be due to a number of methodological issues. One limitation of the molecular studies is that they have rarely sought replication across other measurement instruments. Lack of consistency across studies could be related to dierences in measurement instruments, which in turn may vary in their ability to capture genetic variation. For example, some studies seem to suggest that use of the Big-Five model yields dierent genetic ndings than use of the Tridimensional Personality Questionnaire (Table 1). Studies have also over-relied on self-report measures, with a relative lack of other behavioural measures in their design. Other methodological factors are also important. Most studies have relied on simple association of allele to trait,
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without including more sophisticated within-family designs. Further, few studies have examined multiple genes in an eort to identify haplotypes. However, those that did yielded interesting ndings, suggesting that interactions of multiple genes may provide a clearer picture of contributions to personality variation than single-gene associations. Finally, and perhaps crucially, sample sizes may be too small across most studies to reliably nd eects that may be quite small for the contribution of single genes to temperament or personality. One technological advance that has impacted molecular genetic approaches to the study of psychology more broadly is the increased use of GWAS. The use of GWAS techniques to examine personality and temperament has been limited to one major study of ve major dimensions of personality in 3972 individuals from a genetically homogenous population in Sardinia, Italy (Terracianno et al., 2010). On the basis of the analyses of 362 129 single nucleotide polymorphisms several strong gene signals were detected including the association of neuroticism with SNAP25, extraversion with BDNF and two cadherin genes (CDH13 and CDH23), openness with CNTNAP2, agreeableness with CLOCK and conscientiousness with DYRK1A. Unfortunately, the eect sizes were small (less than 1% of variance), and most failed to replicate in followup samples. The authors concluded that there are likely many genes that inuence personality, and that follow-up studies that use even larger samples may be necessary for success using the GWAS approach.

already begun to yield tantalising leads. Advances in molecular genetics will help to specify some of the genetic variation that has been identied by quantitative designs. However, specication of environmental activating and maintaining causes in relation to genetic aetiology is no less important and may best be accomplished through more sophisticated quantitative designs.

References
Anokhin AP, Heath AC and Myers E (2006) Genetic and environmental inuences on frontal EEG asymmetry: a twin study. Biological Psychology 71: 289295. Bakshi VP and Kalin NH (2000) Corticotropin-releasing hormone and animal models of anxiety: gene-environment interactions. Biological Psychiatry 48: 11751198. Bates JE (1989) Concepts and measures of temperament. In: Kohnstramm GA, Bates JE and Rothbart MK (eds) Temperament in Childhood, pp. 326. Chichester, UK: Wiley. Benjamin L, Li L, Patterson C et al. (1996) Population and familial association between the D4 dopamine receptor gene and measures of novelty seeking. Nature Genetics 12: 8184. Bouchard TJ Jr and Loehlin JC (2001) Genes, evolution, and personality. Behavior Genetics 31: 243273. Burkhouse KL, Gigg BE, Coles ME, Knopik VS and Mcgeary JE (2011) Serotonin transporter genotype moderates the link between childrens reports of overprotective parenting and their behavioral inhibition. Journal of Abnormal Child Psychology 39: 783790. Button TM, Scoureld J, Martin N, Purcell S and McGun P (2005) Family dysfunction interacts with genes in the causation of antisocial symptoms. Behavior Genetics 35: 115120. Carver CS, Johnson SL, Joormann J, Kim Y and Nam JY (2011) Serotonin transporter polymorphism interacts with childhood adversity to predict aspects of impulsivity. Psychological Science 22: 589595. Caspi A (2000) The child is father of the man: personality continuities from childhood to adulthood. Journal of Personality and Social Psychology 78: 158172. Caspi A, Roberts BW and Shiner RL (2005) Personality development: stability and change. Annual Review of Psychology 56: 453484. Comings DE, Johnson JP, Gonzalez NS et al. (2000) Association between the adrenergic alpha 2A receptor gene (ADRA2A) and measures of irritability, hostility, impulsivity and memory in normal subjects. Psychiatric Genetics 10: 3942. Deater-Deckard K and OConnor TG (2000) Parentchild mutuality in early childhood: two behavioral genetic studies. Developmental Psychology 36: 561570. Deater-Deckard K and Petrill SA (2004) Parentchild dyadic mutuality and child behavior problems: an investigation of geneenvironment processes. Journal of Child Psychology and Psychiatry 45: 11711179. Dick DM, Latendresse SJ and Riley B (2011) Incorporating genetics into your studies: a guide for social scientists. Frontiers in Psychiatry 2: 111. Dyson MW, Olino TM, Durbin CE, Goldsmith HH and Klein DN (2012) The structure of temperament in preschoolers: a two-stage factor analytic approach. Emotion 12: 4457.

Summary and Conclusion

Established ndings indicate that there is substantial genetic inuence on major temperament and personality traits and that the nonshared variety of environmental eects may be more important than has been appreciated historically. Molecular genetic work has yielded some tantalizing suggestions, relating genes that inuence key brain neurotransmitters (e.g. dopamine and serotonin) with relevant personality traits in adults and temperament characteristics in children, but this work has not yet produced established ndings, probably due to several as yet unaddressed methodological issues including the addition of GWAS approaches. In conclusion, genetic research in relation to temperament, personality and psychopathology has entered a new phase. First, the importance of liability to disorder has focused increasing scientic attention on personality and temperament as possible diatheses or endophenotypes. Second, continuities between temperament and personality are now beginning to be mapped. Third, multivariate biometrical models and molecular studies have replaced single heritability estimates as the methods of choice to answer aetiological and/or genetic questions in regard to developmental psychopathology. Fourth, the search for specic genes that contribute to development of major temperament and personality traits is now fully underway and has
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Ebstein RP, Novick O, Umansky R, Priel B and Osher Y (1996) Dopamine D4 receptor (D4DR) exon III polymorphism associated with the human personality trait of novelty seeking. Nature Genetics 12: 7880. Fox NA, Nichols KE, Henderson HA et al. (2005) Evidence for a geneenvironment interaction in predicting behavioral inhibition in middle childhood. Psychological Science 16: 921926. Gagne JR, Saudino KJ and Asherson P (2011) The genetic etiology of inhibitory control and behavior problems at 24 months of age. Journal of Child Psychology and Psychiatry 52: 11551163. Gizer IR, Ficks C and Waldman ID (2009) Candidate gene studies of ADHD: a meta-analytic review. Human Genetics 126: 5190. Goldsmith HH and Lemery KS (2000) Linking temperamental fearfulness and anxiety symptoms: a behavior-genetic perspective. Biological Psychiatry 48: 11991209. Goldsmith HH and Campos JJ (1982) Toward a theory of infant temperament. In: Emde RN and Harmon RJ (eds) The Development Of Attachment and Aliative Systems, pp. 161193. New York: Plenum Press. Goldsmith HH, Buss AH, Plomin R et al. (1987) Roundtable: what is temperament? Four approaches. Child Development 58: 505529. Gottesman II and Gould TD (2003) The endophenotype concept in psychiatry: etymology and strategic intentions. American Journal of Psychiatry 160: 636645. Hariri AR, Mattay VS, Tessitore A et al. (2002) Serotonin transporter genetic variation and the response of the human amygdale. Science 297: 400403. Jaee SR, Caspi A, Mott TE et al. (2005) Nature nurture: Genetic vulnerabilities interact with physical maltreatment to promote conduct problems. Development and Psychopathology 17: 6784. Lesch K-P, Bengel D, Heils A et al. (1996) Association of anxietyrelated traits with a polymorphism in the serotonin transporter gene regulatory region. Science 274: 15271531. Munafo MR, Clark TG, Moore LR et al. (2003) Genetic polymorphisms and personality in healthy adults: a systematic review and meta-analysis. Molecular Psychiatry 8: 471484. Murray KT and Kochanska G (2002) Eortful control: factor structure and relation to externalizing and internalizing behaviors. Journal of Abnormal Child Psychology 30: 503514. Posner MI and Rothbart MK (eds) (2003) Developing Mechanisms of Self-Regulation. New York: Brunner-Routledge. Posner MI, Rothbart MK, Sheese BE and Tang Y (2007) The anterior cingulate gyrus and the mechanism of self-regulation. Cognitive, Aective and Behavioral Neuroscience 7: 391395. Rothbart MK and Bates JE (1998) Temperament. In: Eisenberg N (volume ed.) Handbook of Child Psychology: Social, Emotional, and Personality Development, pp. 105176. New York: Wiley. Rothbart MK (2007) Temperament, development, and personality. Current Directions in Psychological Science 16: 207212. Rothbart MK and Derryberry D (1981) Development of individual dierences in temperament. In: Lamb ME and Brown AL (eds) Advances in Developmental Psychology, vol. 1, pp. 37 86. Hillsdale, NJ: Lawrence Erlbaum Associates. Rueda MR, Rothbart MK, McCandliss BD, Saccomanno L and Posner MI (2005) Training, maturation, and genetic inuences on the development of executive attention. Proceedings of the National Academy of Sciences of the USA 102: 1493114936.

Saudino KJ and Eaton WO (1991) Infant temperament and genetics: an objective twin study of motor activity level. Child Development 62: 11671174. Saudino KJ and Eaton WO (1995) Continuity and change in objectively assessed temperament: a longitudinal twin study of activity level. British Journal of Developmental Psychology 13: 8195. Saudino KJ, Wertz AE, Gagne JR and Chawla S (2004) Night and day: are siblings as dierent in temperament as parents say they are? Journal of Personality and Social Psychology 87: 698706. Schmidt LA, Fox NA, Perez-Edgar K and Hamer DH (2009) Linking gene, brain and behavior: DRD4, frontal asymmetry, and temperament. Psychological Science 20: 831837. Smoller JW, Rosenbaum JF, Biederman J et al. (2003) Association of a genetic marker at the corticotropin-releasing hormone locus with behavioral inhibition. Biological Psychiatry 54: 13761381. Smoller JW, Yamaki LH, Fagerness JA et al. (2005) The corticotropin-releasing hormone gene and behavioral inhibition in children at risk for panic disorder. Biological Psychiatry 57: 14851492. Strobel A, Spinath FM, Angleitner A, Riemann R and Lesch KP (2003) Lack of association between polymorphisms of the dopamine D4 receptor gene and personality. Neuropsychobiology 47: 5256. Terracianno A, Sanna S, Uda M et al. (2010) Genome-wide association scan for ve major dimensions of personality. Molecular Psychiatry 15: 647656. Wahlsten D (1999) Single-gene inuences on brain and behavior. Annual Review of Psychology 50: 599624. Willis-Owen SA, Turri MG, Munafo MR et al. (2005) The serotonin transporter length polymorphism, neuroticism, and depression: a comprehensive assessment of association. Biological Psychiatry 58: 451466. Wood AC, Saudino KJ, Rogers H, Asherson P and Kuntsi J (2007) Genetic inuences on mechanically assessed activity level in children. Journal of Child Psychology and Psychiatry 48: 695702.

Further Reading
Bates JE and Wachs TD (1994) Temperament: Individual Dierences at the Interface of Biology and Behavior. Washington, DC: American Psychological Association Press. Bouchard TJ (1994) Genes, environment, and personality. Science 264: 17001701. Gagne JR, Vendlinski MK and Goldsmith HH (2009) The genetics of childhood temperament. In: Kim Y-K (ed.) Handbook of Behavioral Genetics. New York: Springer. Halverson CF, Kohnstamm GA and Martin RP (1994) The Developing Structure of Temperament and Personality from Infancy to Adulthood. Hillsdale, NJ: Lawrence Erlbaum. Nigg JT and Goldsmith HH (1998) Developmental psychopathology, personality, and temperament: reections on recent behavior genetic research. Human Biology 70: 387412. Plomin R and Caspi A (1999) Behavioral genetics and personality. In: Pervin LE and John OP (eds) Handbook of Personality: Theory and Research, pp. 251276. New York: Guilford Press.

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Saudino KJ (1997) Moving beyond the heritability question: new directions in behavioral genetic studies of personality. Current Directions in Psychological Science 6: 8690. Scarr S and McCartney K (1983) How people make their own environments: a theory of genotypeenvironment eects. Child Development 54: 424435. Tellegen A, Lykken D, Bouchard TJ et al. (1988) Personality similarity in twins reared apart and together. Journal of Personality and Social Psychology 54: 10311039. Thomas A and Chess S (1977) Temperament and Development. New York: Brunner/Mazel.

Web Links
BDNF; http://www.ncbi.nlm.nih.gov/gene/627 CDH13; http://www.ncbi.nlm.nih.gov/gene/1012 CDH23; http://www.ncbi.nlm.nih.gov/gene/64072 CLOCK http://www.ncbi.nlm.nih.gov/gene/9575

CNTNAP2; http://www.ncbi.nlm.nih.gov/gene/26047 DRD4 (dopamine receptor D4); http://www.ncbi.nlm.nih.gov/ gene/1815 DYRK1A; http://www.ncbi.nlm.nih.gov/gene/1859 H19 (H19, imprinted maternally expressed untranslated mRNA); http://www.ncbi.nlm.nih.gov/gene/283120 IGF2 (insulin-like growth factor 2 (somatomedin A)); http:// www.ncbi.nlm.nih.gov/gene/3481 SLC6A3 (solute carrier family 6 (neurotransmitter transporter, dopamine), member 3); http://www.ncbi.nlm.nih.gov/gene/ 6531 SLC6A4 (solute carrier family 6 (neurotransmitter transporter, serotonin), member 4); http://www.ncbi.nlm.nih.gov/gene/ 6532 SNAP25; http://www.ncbi.nlm.nih.gov/gene/6616 XIST (X (inactive)-specic transcript); http://www.ncbi.nlm.nih. gov/gene/7503

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