70 Genetic Basis of Personality Structure
dimensions. These conclusions are, however, based on a sin-
gle study using only a single measure of personality. Replica-
tion is clearly needed, given the results’ significance for
understanding trait structure. The conclusions are, however,
similar to those drawn from a study of personality disorder
traits (Livesley & Jang, 2000).
Personality Disorder Traits
Livesley and Jang (2000) investigated the etiological struc-
ture of personality disorder by fitting independent and com-
mon pathways models to the 18 lower-order traits of
personality disorder assessed by administering the DAPP to a
volunteer sample of 686 twin pairs. Each trait consists of two
or more specific traits so that a total of 69 specific traits define
the 18 basic traits. The 18 traits in turn define four higher-
order factors. Thus the DAPP system incorporates three lev-
els of construct (higher-order factors, lower-order traits, and
specific traits) whereas the NEO-PI-R has only two levels
(domains and facets). This makes it possible to explore the
genetic architecture of personality in more detail. For exam-
ple, the basic trait of Anxiousness is defined by four specific
traits: trait anxiety, guilt proneness, rumination, and indeci-
siveness. Each basic trait represents a single phenotypic fac-
tor. If personality is inherited as a few genetic dimensions
represented by the four higher-order factors, a single genetic
dimension should underlie each basic trait that is shared by
other traits constituting the higher-order factor. Evidence of a
genetic effect specific to each trait would be provided by
evidence that the 18 basic traits are composed of two or more
genetic dimensions.
A one-factor common pathways model did not provide a
satisfactory fit for any of the 18 basic traits. On the other hand,
an independent pathways model postulating a single genetic
dimension explained the covariation among specific traits
for 12 of the 18 basic trait scales: Anxiousness, Cognitive
Dysregulation, Compulsivity, Conduct Problems, Identity
Problems, Insecure Attachment, Intimacy Problems, Opposi-
tionality, Rejection, Stimulus Seeking, Submissiveness, and
Suspiciousness. The results of model fitting for illustrative
scales are provided in Table 3.5. For three of these scales, Inti-
macy Problems, Rejection, and Stimulus Seeking, the com-
mon genetic dimension accounted for little of the variance for
one or more of the specific trait scales, indicating that a spe-
cific genetic factor influenced these traits. Two genetic dimen-
sions were found to underlie four scales: Affective Lability,
Narcissism, Restricted Expression, and Social Avoidance.
Three common genetic dimensions contributed to Callousness
(see Table 3.5).
Multivariate analyses of normal and disordered personal-
ity traits suggest that multiple genetic and environmental fac-
tors influence the covariant structure of traits. They also
confirm the findings of the regression analyses that many
lower-order traits are influenced by one or more genetic di-
mensions specific to those traits. Finally, in both sets of
analyses, the common pathways model did not provide a bet-
ter fit to the data than did the independent pathways model.
This suggests that the general genetic dimensions found by
Livesley and colleagues (1998) and others by factor analyz-
ing matrices of genetic correlations do not influence each trait
through a latent phenotypic variable, but rather exert a direct
influence on each trait.IMPLICATIONS FOR PERSONALITY STRUCTUREThe studies described in the previous section reveal a com-
plex genetic basis for personality. Multiple genetic dimen-
sions differing in the breadth of their effects contribute to
personality phenotypes (Jang et al., 1998; Livesley et al.,
1998; Livesley & Jang, 2000). Some are relatively specific
dimensions that influence single phenotypic traits, whereas
others have broader effects influencing multiple phenotypi-
cally distinct but covarying traits. Consequently, many traits
appear to be influenced by multiple genes and gene systems.
Similarly, trait covariation seems to arise from multiple
genetic effects. Genetic effects on traits appear to be direct
rather than mediated by higher-order entities. These findings
require replication. Nevertheless they appear to challengeTABLE 3.4 Multivariate Genetic Analysis (independent pathways
model) of the NEO-PI-R Neuroticism Facets on a Sample of German
and a Sample of Canadian Twins
Common
Common Nonshared Variable-
Genetic Environmental specific
Factors Factors FactorsFacet Scale 1 2 1 2 A E
Canadian Sample
Anxiety .48 .27 .50 .30 .30 .56
Hostility .65 — .29 .21 — .67
Depression .45 .43 .59 .26 .23 .38
Self-Consciousness .42 .35 .42 .24 .37 .57
Impulsivity .36 — .78 — .50 —
Vulnerability .47 .40 .40 .21 .28 .57
German Sample
Anxiety .46 .34 .29 .46 .36 .51
Hostility .66 — .76 — — —
Depression .47 .45 .33 .46 .22 .45
Self-Consciousness .35 .44 .22 .35 .40 .60
Impulsivity .24 — .19 — .57 .77
Vulnerability .43 .42 .33 .49 .28 .46
Note. All parameters are significant at p<.05.