78 Genetic Basis of Personality Structure
these findings (Flory et al., 1999; Gelernter, Kranzler,
Coccaro, Siever, & New, 1998; Hamer et al., 1999; Herbst,
Zonderman, McCrae, & Costa, 2000). Gustavsson et al.
(1999) also failed to replicate these findings using the
Karolinska Scales of Personality.
These inconsistencies can be attributed to conceptual and
measurement issues. The early studies in particular were
often based on a conceptual model that assumed that person-
ality is influenced by relatively few genes, each accounting
for substantial variance. As noted, the evidence does not sup-
port this approach. There has also been a tendency to assume
that each trait was linked a specific neurotransmitter system.
More recently, however, attention has focused on pleiotropic
effects by investigating the possibility that a given polymor-
phism influences several traits. Work on the serotonin trans-
porter gene, for example, suggests that it is not associated
with a single trait but rather has a pleiotropic relationship
with Neuroticism and Agreeableness. Studies on humans and
primates suggest that altered serotonin activity is related to
negative emotional states such as depression, anxiety, and
hostility, and to social behaviors such as dominance, aggres-
sion, and affiliation with peers (Graeff, Guimaraes, De
Andrade, & Deakin, 1996; Knutson et al., 1998; Murphy
et al., 1998). Knutson and colleagues (1998) found that ad-
ministration of the specific serotonin reuptake inhibitor,
paroxetine, decreased negative affect and increased social af-
filiation in normal human subjects. Lesch and colleagues
(1996) reported that individuals carrying the 5-HTTLPR-S
allele had increased total scores on NEO-PI-R Neuroticism
and the facets of Anxiety, Angry Hostility, Depression, and
Impulsiveness. The allele accounted for 3 to 4% of the total
variance in these scales. Unexpectedly, the allele was also as-
sociated with a decreasedNEO-PI-R Agreeableness score.
Greenberg et al. (1999) recently replicated these findings.
Hamer et al. (1999) showed that 5-HTTLPR-S genotypes
were significantly associated with increased Harm Avoidance
(which correlates .66 with NEO-PI-R Neuroticism) and de-
creased Self-Directedness (correlated −.64 with NEO-PI-R
Neuroticism), Reward Dependence, and Cooperativeness
(shown to correlate .43 and .66 with NEO-PI-R Agreeable-
ness). These effects accounted for .80%, 1.98%, .97%, and
2.60% of the total variance in these scores, respectively.
Mazzanti et al. (1998), Peirson et al. (2000), and Benjamin
et al. (2000) have reported replications.
Measurement problems contributing to inconsistent find-
ings include the use of measures with less-than-optimal
psychometric properties and the use of relatively broad per-
sonality constructs. Comparison of the dopamine–novelty
seeking and serotonin-neuroticism studies suggests that the
serotonin-neuroticism literature is less ambiguous than the
dopamine–novelty seeking literature. These differences
appear to be related to scale properties. Inconsistent find-
ings may also be due to the confounding of genetic and en-
vironmental influences on the phenotypes. As we have tried
to show, many constructs and scales are etiologically
heterogeneous.
Twin studies estimating statistical pleiotropy could con-
tribute to molecular genetic studies by identifying traits that
are etiologically homogeneous units and etiologically re-
lated. Molecular genetic work could then be used to confirm
these associations by identifying the actual genes that ac-
count for trait covariance. This would provide the strongest
basis for revising personality models and allocating traits to
etiologically related domains.CONCLUSIONSThe thesis of this chapter is that behavioral genetic ap-
proaches promise to provide an additional perspective that
may help to resolve some of the more intractable problems in
delineating and conceptualizing personality structure. The
evidence reviewed suggests an alternative perspective on the
trait structure of personality that complements traditional
conceptions. Although trait theory has largely concentrated
on mapping personality in terms of broad global traits, the
evidence suggests that personality is inherited as a large num-
ber of genetic dimensions that have relatively specific effects
on personality phenotypes and a smaller number of genetic
dimensions that have broader effects, perhaps through a
modulating influence on related dispositions. These dimen-
sions with broader effects appear to account for some of the
observed covariation among traits. They do not appear, how-
ever, to exert these effects through higher-order phenotypic
structures, but rather through a direct influence on each basic
trait. We assume that these common features are more likely
to involve modulating functions or common mechanisms that
regulate each trait in a given cluster.
These tentative conclusions suggest the need to reconsider
traditional models of the hierarchical structure of personality
in which traits are organized into broad domains due to the ef-
fects on broad dispositions. Instead, the organization of traits
into clusters is assumed to arise from the pleiotropic effects of
genetic dimensions that affect multiple traits. Under these cir-
cumstances, it is conceivable that not all traits are organized
into clusters of covarying features, but rather remain relatively
distinct characteristics. Nor is it inevitable the traits are hierar-
chically organized in similar ways across domains. That is, it
is possible that the symmetrical hierarchical structure avidly
sought by trait theorists and students of psychopathology does