Scandinavian Journal of Psychology, 2009, 50, 624632

DOI: 10.1111/j.1467-9450.2009.00788.x

Personality and Individual Differences

The nature (and nurture) of personality disorders
SVENN TORGERSEN
University of Oslo and Regional Center for Child and Adolescent Mental Health East and South Norway, Norway

Torgersen, S. (2009). The nature (and nurture) of personality disorders. Scandinavian Journal of Psychology, 50, 624632.
Personality disorders have a long history in the literature but a short scientic history. The point prevalence of personality disorders is 10%, but the
lifetime prevalence is probably 3040%. Genetic factors contribute to around 4050% of the variation in the development of personality disorders.
The effect of shared environment is very small or non-existent. Some researchers have tried to promote gene-environment interaction. However, in
reality, the studies investigated gene-situation interaction, as the environment may in reality be partly of a genetic nature. Thus, we are dealing with
an unknown part of gene-gene interaction. Gene-experience (not gene-environment) correlations are the rule in human life. Personality disorders
co-occur (are comorbid) with symptom disorders (Axis I) and correlate with common personality dimensions. Possibly, the concept of personality disorder could merge with dysfunctional personality types. But it is likely that the concept will survive on its own.
Key words: Personality disorder, prevalence, genetic, gene-environment interaction, gene-environment correlation, personality types.
Dr Svenn Torgersen, Department of Psychology, University of Oslo, Postbox 1094 Blindern, N-0317 Oslo, Norway. E-mail: svenn.torgersen@
psykologi.uio.no

INTRODUCTION
Personality disorder is an old concept that includes labels
such as choleric, melancholic, hysteric, libidinal types, character neuroses, neurotic personality, neurotic styles, and many
others.
However, it was when the American system for the classication of mental disorders, DSM-III (Diagnostic and Statistical
Manual of Mental Disorders, 3rd edition) invented one axis for
symptom disorders (Axis I) and one axis for personality disorders (Axis II) that interest in personality disorders rst took off
(American Psychiatric Association [APA], 1980). Later editions
of the manual, DSM-III-R (APA, 1987) and DSM-IV (APA,
1994), and the modern international classication system for
mental disorders (International Classication of Diseases, 10th
Revision [ICD-10], Classication of Mental and Behavioural
Disorders) (World Health Organization [WHO], 1993) only
increased the interest in personality disorders. One reason was
that it was not necessary to choose between a symptom disorder
and a personality disorder when diagnosing a person. Both sets
of diagnoses could be applied at the same time. Another reason
was the creation of clear and specic criteria for the disorders; a
number of criteria, usually between seven and nine, were stated.
If four or ve criteria were fullled, the disorder was present.
Later, the number of criteria fullled (from zero to seven or
nine) was usually used in research, as a scaled semi-continual
concept of personality disorders.
First and foremost, it was important in the research and clinical communities to establish the prevalence of personality disorders in the population. The causes of the disorders were of
course of central importance. Finally, there has been a focus on
disentangling personality disorders from symptom disorders and

normal personality dimensions in order to establish the status

and legitimacy of the concept.

PREVALENCE
For a long time clinicians had had the impression that personality disorders were prevalent in clinical populations seeking treatment for psychological problems. This was conrmed in a study
of patients treated in an out-patient clinic: More than 80% of the
patients had a personality disorder (Alns & Torgersen, 1988a).
The patients usually sought treatment for depression and
anxiety, but structured clinical interviews revealed that they
almost always had a personality disorder in addition.
Most of the studies on the prevalence of personality disorders
in the common population are far from representative (Black,
Noyes, Pfohl, Goldstein & Blum, 1993; Crawford, Cohen, Johnson et al., 2005; Coid, Yang, Tyrer, Roberts & Ullrich, 2006;
Grant, Hasin, Stinson et al., 2004; Klein, Riso, Donaldson
et al., 1995; Lenzenweger, Lane, Loranger & Kessler, 2007;
Lenzenweger, Loranger, Korne & Neff, 1997; Maier, Lichtermann, Klingler, Heun & Hallmayer, 1992; Moldin, Rice, Erlenmeyer-Kimling & Squires-Wheeler, 1994; Samuels, Eaton,
Bienvenu, Brown, Costa & Nestadt, 2002; Torgersen, Kringlen
& Cramer, 2001; Zimmerman & Coryell, 1989). Almost all
studies were conducted in the United States (see Table 1). Most
investigated a city rather than the whole country. One study
included relatives of patients with schizophrenia and depression
(Zimmerman & Coryell, 1989). Another study did not include
all of the personality disorders (Grant et al., 2004). Some had
rather small samples. Some applied complex weighting methods
to arrive at the prevalence estimates. Even so, all except three
studies showed a similar prevalence for any personality

2009 The Author. Journal compilation 2009 The Scandinavian Psychological Associations. Published by Blackwell Publishing Ltd., 9600
Garsington Road, Oxford OX4 2DQ, UK and 350 Main Street, Malden, MA 02148, USA. ISSN 0036-5564.

DSM-III

Place

System

Paranoid
Schizoid
Schizotypal
Antisocial
Borderline
Histrionic
Narcissistic
Avoidant
Dependent
Obsessive-compulsive
Passive-aggressive
Self-defeating
Sadistic
Any personality disorder
Number

0.9
0.9
2.9
3.3
1.7
3.0
0.0
1.3
1.8
2.0
3.3

14.3
797

Iowa

Authors

Personality disorder

Zimmerman &
Coryell
1989

1.6
0.0
3.2
0.8
3.2
3.2
0.0
2.0
1.6
9.3
10.5

22.7
247

DSM-III

Iowa

Black
et al.
1992

0.0
0.0
0.7
2.6
2.0
0.3
0.0
0.7
1.0
0.7
1.7

7.3
303

DSM-IIIR

DSM-IIIR

1.8
0.4
0.7
0.2
1.1
1.3
0.0
1.1
1.6
2.2
1.8

10.0
452

NYC

Moldin
et al.
1994

Mainz

Maier
et al.
1992

Table 1. Prevalences of personality disorders in twelve population studies

1.8
0.9
0.0
2.6
1.8
1.8
4.4
5.7
0.4
2.6
1.8

14.8
229

DSM-IIIR

New York

Klein
et al.
1995

0.4
0.4
0.0
0.8
0.0
1.9
1.2
0.4
0.4
0.0
0.0
0.0
0.0
3.9
258

DSM-III-R

New York

Lenzenweger
et al.
1997

2.2
1.6
0.6
0.6
0.7
1.9
0.8
5.0
1.5
1.9
1.6
0.8
0.2
13.1
2,053

DSM-III-R

Oslo

Torgersen
et al.
2001

0.7
0.7
1.8
4.5
1.2
0.4
0.1
1.4
0.3
1.2

10.0
742

DSM-IV

Baltimore

Samuels
et al.
2002

2009 The Author. Journal compilation 2009 The Scandinavian Psychological Associations.
43,093

4.4
3.1

3.6

1.8

2.4
0.5
7.9

DSM-IV

USA

Grant
et al.
2004

5.1
1.7
1.1
1.2
3.9
0.9
2.2
6.4
0.8
4.7

15.7
597

DSM-IV

New York

Crawford
et al.
2005

0.7
0.8
0.1
0.6
0.7
0
0
0.8
0.1
1.3

4.4
626

DSM-IV

UK

Coid
et al.
2006

2.3
4.9
3.3
1.0
1.6
0.0
0.0
5.2
0.6
2.4

10.3
214

DSM-IV

USA

Lenzenweger
et al.
2007

1.7
0.9
0.9
1.1
1.6
1.5
0.5
1.7
0.7
2.1
1.7
0.4
0.1
10.3

Median

Scand J Psychol 50 (2009)

The nature (and nurture) of personality disorders 625

626 S. Torgersen
100%

Zanarini et al.
Grilo et al.
Ferro et al.
Paris et al.
Norway

75
62.5

50

50
37.5

37

25

25
15

12.5
2 4

12

10
18

24

30 year

Fig. 1. Mean course of a specic personality disorder

an average, or even lower, lifetime trend, but still come over the
threshold for a disorder once.
The lifetime trend for the impulsive disorder problems (antisocial, histrionic, borderline) declines on average, whereas the
lifetime trend for the withdrawn, affect-controlled disorder
problems (schizoid, avoidant, obsessive-compulsive) increases.
As will be discussed below, the causes of the lifetime trend
are genes and early physical and psychological events and conditions. The causes of the temporary elevation, going above the
threshold for a disorder for a shorter or longer time, are events
and circumstances at a specic time increasing the psychological burden of life. However, they usually do not last forever,
and the person slides back toward the lifetime trend.
The course of any disorder will be a little different, as a new
disorder may arise when one disorder disappears. Persons with
an impulsive, dramatic disorder (antisocial, borderline, histrionic), for instance, sometimes develop an introverted, affectconstricted disorder (schizoid, avoidant, obsessive-compulsive).
However, there are few studies on any personality disorders, but
we do know a little: After 2.5 years, it seems that close to 50%
of persons with a personality disorder still have a personality
disorder (any personality disorder). After 5 to 10 years, this is
around 40%. From what we know from studies on a specic
disorder, the percentage is expected to approach 30% after

Number of PD criteria

disorder: between 7.3% and 15.7%, with a median rate of

10.3%. The deviant three studies had relatively small samples
with a high standard error.
As to the specic personality disorders, the variation was
large from study to study. However, for all the personality disorders except the unofcial disorders self-defeating and sadistic,
the median prevalence was between 0.7 and 2.1. The most common personality disorder was the obsessive-compulsive personality disorder, followed by passive-aggressive, avoidant,
borderline, and histrionic personality disorder. These disorders
constitute a cluster of the most common disorders. The more
rare personality disorders were the antisocial, schizoid, dependent, and schizotypal personality disorders, and as mentioned
above, the self-defeating and sadistic personality disorders.
Of particular interest for Scandinavia is the difference in the
spectrum of disorders in Oslo, Norway, as compared to other
countries (rst and foremost the United States, but also Germany and the UK). Avoidant personality disorder is 34 times
as prevalent in Norway. Dependent personality disorder is 23
times more frequent, and schizoid personality disorder is two
times as prevalent. Borderline personality disorder, on the other
hand, is less than half as frequent and antisocial disorder half as
prevalent. Unpublished studies on the countryside in Norway
show the same pattern. This draws a picture of Norway (and
probably Scandinavia) as an area where internalization personality disorders are prevalent and externalization disorders are
rarer.
All these studies deal with point prevalence, even if people
are asked how they have been most of the time in the last two
or ve years. The assumption has been that personality disorders start early and are chronic and lifelong. That means that
point prevalence and lifetime prevalence would be the same, as
they are for infantile autism, for instance. However, some more
recently published studies have begun to question this assumption with drastic consequences for the relationship between
point prevalence and lifetime prevalence. The studies of Ferro,
Klein, Schwartz, Kasch and Leader (1998), Grilo, Sanislow,
Gunderson et al. (2004), Paris and Zweig-Frank (2001), Zanarini, Frankenburg, Hennen, Reich and Silk (2006) and unpublished data from Norway show that personality disorders
disappear. If we look at a specic disorder we nd that after
2 years, only 50% of persons with the personality disorder at
the outset still have the specic disorder (Fig. 1). The percentage is 3540 after 4 years, 25% after 6 years, 15% after
10 years, and 10% after 25 years.
If we look at the course of personality problems in an individual vulnerable to a personality disorder, we will nd that he/she
usually has a life trend of personality problems above the average in the population. Usually once in a lifetime, earlier or later
in life, the person will have problems above the level dened as
a personality disorder. After a shorter or longer period, the problems will once more come under the threshold. Usually the person will not rise above the threshold a second time, although it
happens for a few. However, the level of problems will usually
be above the average in the society. A few persons might have

Scand J Psychol 50 (2009)

Threshold for a diagnosis

5
4

Individual trend

3
2

Mean trend in the population

1
Lifetime

Fig. 2. Individual course of a personality disorder

2009 The Author. Journal compilation 2009 The Scandinavian Psychological Associations.

Scand J Psychol 50 (2009)

20 years. Even if a number of individuals withdraw to a subclinical level not so far below the threshold for having a personality disorder, some improve very much, and a few do not show
any trace of a personality disorder at all after a short time. The
percentage falls more slowly for any personality disorder compared to a specic personality disorder, because as we have said,
one disorder may replace another.
As the prevalence of any personality disorder is the same in
all age groups (Torgersen et al., 2001), a large number of persons in a cohort have to have a personality disorder at some
point of time in their lives to replace those that no longer
have a personality disorder.
This is not only theory. A study following a community sample from the age of 14 to 33 and assessing the sample four times
showed that whereas the prevalence of personality disorders at a
specic time was 1315%, the cumulative (lifetime prevalence)
was as high as 28% (Johnson, Cohen, Kasen, Skodol & Oldham, 2008). Non-published studies from Norway have also
shown that combining assessments at two points of time with a
follow-up time of around 6 years increased the (lifetime) prevalence of personality disorder by 40%.
Consequently, the lifetime risk of having a personality disorder is very high, probably 30 to 40%. For many this sounds
absurd. A simple way to reduce the lifetime risk of personality
disorder would be to increase the number of criteria required for
the disorder to be present. In other words, the problems have to
be more severe to be categorized as a personality disorder. However, that will not change the difference between the prevalence
of the disorder at a specic time on the one side, and the lifetime prevalence, on the other side. One could make an effort to
try to ask how the person has been their whole life. However,
memory is short, as all follow-up studies have shown. The only
solution would be to use a diagnosis of personality disorder
only if the disorder had been assessed at more points of time
spread over a long time period. But that is very unpractical, and
the rule would be difcult if not impossible to follow. Longitudinal studies consistently show that the lifetime prevalence of
symptom disorders (Axis I) is higher in follow-up studies than
in studies based on retrospective information about lifetime.
The consequence is that few people escape a symptom disorder
in the course of their lives, even if lifetime prevalence based on
a single retrospective assessment is around 50% (Kringlen, Torgersen & Cramer, 2001).

CAUSES
That personality traits and dimensions run in families has been
known for a very long time. Twin studies have indicated that
the familial transmission is more or less only genetic (Torgersen,
2005). The heritability is around 0.400.50, with a very small
effect of shared family environment, perhaps around 0.05. It has
been argued that monozygotic (MZ) twins reared together inuence each other to such an extent that the higher similarity
among MZ twins than among dizygotic (DZ) twins is explained
by learning and identication; but adoption studies, studies of

The nature (and nurture) of personality disorders 627

twins reared apart, and molecular biological identication of
genes inuencing the development of personality, have concluded beyond doubt that the observations from the studies of
twins reared together (ordinary twin studies) are not due to artifacts and methodology limitations. It has been necessary to
study genetics from several angles, as especially among clinical
professionals, there has been a strong urge to dismiss the observations that genes inuence the development of personality.
As to the personality disorders, a number of studies applying
different methods in the eld of genetics have concluded that
the development of antisocial personality disorders is inuenced
by genes, the heritability being around 0.40, with no effect of
shared family environment (Rhee & Waldman, 2002). The rest
has to be environmental inuence not shared by family members. This environmental effect may reect pre- and perinatal
circumstances, later physical events, psychological conditions,
traumas, and not least conditions at the time of the assessment.
In addition, measurement error or lack of reliability will be
included in the non-shared in families environmental effect.
Very few genetic studies have investigated the whole range of
personality disorders. One study investigated the total national
sample of twins above 18 years treated by psychiatric institutions in Norway (Torgersen, Lygren, ien et al., 2000). There
were 442 twins, and more than half of them had a personality
disorder. Another study investigated children (and consequently
applied the word personality traits) in the age group from 4
to 15 years (Coolidge, Thede & Yang, 2001). Personality disorder traits were assessed by a not validated method that was more
or less close to the ofcial denitions of personality disorders in
the DSM-IV. A recent study was based on a Norwegian sample
of relatively unselected twins at the age of 19 to 36 (Czajkowski, Kendler, Jacobson, Tambs & Rysamb, 2008; Kendler,
Czajkowski, Tambs et al., 2006; Kendler, Aggen, Czajkowski
et al., 2008; rstavik, Kendler, Czajkowski, Tambs & Reichborn-Kjennerud, 2007; Reichborn-Kjennerud et al., 2007a;
Torgersen, Czajkowski, Jacobson et al., 2008). The number of
twins was 2,794. However, the prevalence of personality disorder was as low as 3%.
All three samples investigated showed that the effect of
shared family environmental is zero, with the exception of one
disorder in one study. The size of the genetic effects varied
extensively (see Table 2). However, the samples and methods
show very much variation. The study by Coolidge and colleagues (2001) was based on parental reports. As the same
informant reported on both twins in a pair, rating bias might
exaggerate the size of the twin correlations. The same person
interviewed both twins also in the study by Torgersen et al.
(2001). Furthermore, at least one of the twins had been treated
for psychological problems. Both aspects may have increased
the twin correlations. In the third study, the very low twin correlations may be due to the opposite source of errors, namely, differences between the interview raters in rating style (they used
different interviewers for the two twins). The extremely low
prevalence in this most recent study points also to a very low
reliability, decreasing the size of the correlation coefcients.

2009 The Author. Journal compilation 2009 The Scandinavian Psychological Associations.

628 S. Torgersen

Scand J Psychol 50 (2009)

Table 2. Heritability of personality disorders (Shared Environment is

zero, the rest is Non-Shared Environment and error)
Personality
disorder

Torgersen
et al., 2000

Coolidge
et al., 2001

Research
group

Paranoid
Schizoid
Schizotypal
Antisocial
Borderline
Histrionic
Narcissistic
Avoidant
Dependent
Obsessive-compulsive
Passive-aggressive
Self-defeating
Sadistic
Depressive

0.28
0.29
0.61

0.69
0.67
0.77
0.28
0.57
0.77
0.00

0.50
0.73
0.81

0.76
0.79
0.66
0.61
0.81
0.77
0.50

0.76

0.23
0.26
0.21
0.41
0.37
0.31
0.25
0.37
0.30
0.27
*

0.38

Mean
0.34
0.43
0.54
0.41
0.61
0.59
0.56
0.42
0.56
0.60
0.25
0.54

0.57

Research Group: Kendler et al., 2006, 2008; Reichborn-Kjennerud

et al., 2007a; rstavik et al., 2007; Torgersen et al., 2008; Czajkowski
et al., 2008.
* Shared Environment was 0.28.

Possibly the average of the three studies together provides a viable estimate of the heritabilities of the personality disorders,
around 0.400.50, which is relatively similar to the heritabilities
of normal personality traits and dimensions (Torgersen, 2005).
Whereas the heritability estimates vary strongly in the three
studies, the relative size of the heritability of the different personality disorders is not so different in the three samples.
Consequently, it is fair to draw some tentative conclusions
about the relative strength of the heritability of the different personality disorders. Obsessive-compulsive, borderline, and histrionic personality disorders appear to be most strongly inuenced
by genes, and the paranoid and passive-aggressive personality
disorders the least. As to passive-aggressive personality disorder, Torgersen et al. (2000) did not nd that any models were
tting. The best model in the study by Czajkowski et al. (2008)
in fact showed no heritability, but a shared family environmental
effect of 0.28.
The reliability deciency may have depressed the heritability
estimates, as mentioned above. When both interview and questionnaire are taken into account, the heritability turned out to be
0.66 for paranoid, 0.55 for schizoid, and 0.72 for schizotypal
personality disorder (Kendler, Myers, Torgersen, Neale &
Reichborn-Kjennerud, 2007). Not yet published results for the
other personality disorders show similar estimates.
Many will be interested in the content of the environmental
inuence. What exactly is the inuence from childhood? Can
systematic research conrm theorists claims that neglect and
abuse lead to personality disorders? Persons with schizotypal
personality disorder reported that they perceived their parents as
cold and distant (Torgersen & Alns, 1992). Persons with borderline personality disorder reported a childhood without paren-

tal caring and with much control. Persons without personality

disorders remembered a childhood with optimal parenting,
much warmth, and little control. Persons with other personality
disorders perceived their childhood as something in between the
childhoods reported by persons with borderline personality disorder and persons without personality disorders. Studies of former patients by a youth clinic showed that persons with
borderline personality disorders reported a childhood with
abuse, neglect, environmental instability, and paternal psychopathology (Helgeland & Torgersen, 2004).
Does this mean that environmental agents in the development of personality disorders have been detected? That is not
necessarily so. The reason is gene-environment, or better geneexperience correlations. If parents treat their children badly,
and the children develop personality disorders, it does not necessarily mean that the treatment of the children is the cause of
the development. An alternative explanation may be that the
parents themselves have some personality disorder traits, partly
due to genes. These genetically inuenced traits correlate with
poor parenting, explaining the genetic inuence on parenting.
The children inherit the genes and subsequently develop personality disorders. The personality disorders might thus have
developed in any case, independent of the childhood conditions. Another explanation might be that persons who later
developed personality disorders had a way of behaving that
triggered the not-so-ideal treatment in the childhood. Studies of
twins reared apart show that MZ twins growing up in different
homes describe the warmth, or the lack of warmth, in the childhood home more similarly than DZ twins growing up in the
same home do (Plomin, McClearn, Pedersen, Nesselroads &
Bergeman, 1990).
Individuals with personality disorders usually have less education, more often live alone, look upon their physical health as
poorer, and more often live in the center of the city (Torgersen
et al., 2001). They also experience more negative life events,
are less integrated in the neighborhood, receive less social support, and have poorer relationships with friends and family (Cramer, Torgersen & Kringlen, 2006, 2007). All of these life
conditions may be causes of personality disorders, but they can
also be the consequences of the disorders (gene-experience correlations). To really gure out whether we are dealing with
causes or consequences, we need genetically informed longitudinal studies. Such studies may be able to distinguish between
the unfolding of genetic endowment and the effects of change
in the environment. If something happens to one of a pair of
MZ twins, and this changes the relationship between them (for
instance, the least anxious of the twins becomes the most anxious), the effect may be demonstrated. A longer-lasting effect is
proved if the new relationship between them prevails in a new
study wave.
Accepting that gene-experience correlations raise doubt
about the causality of childhood family experiences, traumas,
and later life conditions, there is another way to promote the
inuence of the family environment, namely, through geneenvironment interaction. We shall see that also for this concept,

2009 The Author. Journal compilation 2009 The Scandinavian Psychological Associations.

Scand J Psychol 50 (2009)

gene-experience interaction is a better name, or alternatively

gene-situation interaction (Torgersen, 2006).
Gene-experience (situation) interaction implies that genes
have more impact in one situation than in another situation, or
that in a specic situation experience is more inuential given
certain genotypes. A number of twin studies have been published recently showing that heritability effects vary according
to life situation, loss, or other adverse circumstances. Also, specic genes have been claimed to be buffers between adverse
environmental factors and dysfunctional consequences. However, the problem is that if parents give a child a good childhood
versus a poor childhood, parents may vary in the genes that
affect their behavior, as we discussed above. These genes are
inherited by the children. Hence, we are dealing with an
unknown amount of gene-gene interaction. In addition, increasing with age, an individual creates his/her own life situations
based on genetic endowment. In this way we see that geneexperience correlations lead to gene-gene interaction. What is
claimed to be (and incorrectly called) gene-environment interaction may be, at least partly, gene-gene interaction.
However, adoption studies might demonstrate gene-environment interaction. A classic study from Denmark showed that
antisocial behavior among adoptive parents did not increase the
risk of antisocial behavior in adopted children whose biological
parents were not antisocial (Mednick, Gabrielli & Hutchins,
1984). But antisocial behavior among the biological parents did,
even if there was no antisocial behavior by the adoptive parents.
However, the highest risk for antisocial behavior was observed
among children that had antisocial behavior among both the
biological and the adoptive parents. Generally, genetic studies
more often indicate gene-situation interaction, or even real
gene-environment interaction for antisocial and other externalizing behavior, in contrast to internalizing behavior. The reason
may be that concrete behavior depends on the available circumstances and situation: Opportunity makes the thief. However,
thoughts and feelings that dominate in internalization are not
dependent on concrete circumstances.
The only safe way to study gene-environmental interaction is
through having experimental control over the environment.
When the inuence of obnoxious environments is studied, only
animal research is possible. However, the results of this research
are not easy to apply to human personality disorders.
When all these objections are mentioned, it is important once
more to note that genes tell only half the story of the determination of personality disorders. It is not so rare for MZ pairs to be
discordant for personality disorders. Some of this discordance
may be due to differences in the development of the disorder.
One of the twins may start to show dissocial behavior or to feel
social unease before the other twin does. After some time, the
other twin catches up. Repeated observations of the twins thus
yield much higher heritability, partly also because more of the
unreliability is eliminated from the non-shared effect. A lifelong
observation of the twins would probably reveal very high concordance. Some of the differences between MZ twins are purely
random. Many of the other factors creating discordance among

The nature (and nurture) of personality disorders 629

MZ twins, and hence non-shared environmental effects, are of a
physical rather than a psychological nature (events in pregnancy, events around delivery, infections, diseases, or physical
traumata). Still, some may be psychological. To this day we do
not know so much about these factors. However, studies of discordant twins give us possibilities for studying environmental
effects controlling for genes. A study of twins discordant for
abuse demonstrates that abuse is related to psychopathology
(Bulik, Prescott & Kendler, 2001; Kendler, Bulik, Silberg, Hettema, Myers & Prescott, 2000). A study by Caspi and colleagues (2004) showed that differences in mothers negative
reports about MZ twins were related to differences in disruptive
behavior reported by teachers 2 years later. A reasonable objection might be that mothers were reacting to behavior already
manifested. However, the study controlled for the twins behavior at the time of surveying the mothers. In the future, there is
reason to believe that studies of discordant MZ twins can bring
us further in nding out something about environmental factors
inuencing, or at least related to, the development of personality
disorders.
Another path in genetic work will be to study the route from
genes to behavior. In this connection, the concept of endophenotypes is important since it will be important to nd behavior,
function, or structures that are strongly heritable and at the same
time correlate with the disorder studied (Siever, Torgersen, Gunderson, Livesley & Kendler, 2002).
Taking together the studies of the course of personality disorders, the waxing and the waning of personality disorders, and
the genetics, we can state that the lifetime trend of personality
disorder features is determined by genes and early physical and
psychological factors. The moving to above the trend, perhaps
as high above the trend as to fulll the criteria for a personality
disorder, and the moving back, perhaps below the lifetime trend,
is due to environmental inuences through living conditions
and events, some of them physical and some psychological.

IS THE CONCEPT SUSTAINABLE?

The concept of personality disorders has been challenged from
two sides. One has to do with the relationship to symptom disorders (Axis I). The other is about the relationship to personality
traits and dimensions.
The frequent coexistence (comorbidity) between personality
disorders and symptom disorders is well known. A Norwegian
study demonstrated that this coexistence was more the rule than
the exception (Alns & Torgersen, 1988b). Other studies have
found the same (Grant, Hasin, Stinson et al., 2005). What is
important is that there is not a total overlap between a specic
personality disorder and a specic symptom disorder diagnosis.
And the observations of comorbidity differ from study to study.
A much discussed relationship is between schizophrenia and
schizotypal personality disorder. In the ICD-10, schizotypal personality disorder is placed among the psychoses. In DSM-III
and DSM-IV it has always been among the personality disorders. Genetic analyses are a powerful method of investigating

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630 S. Torgersen
the relationship between personality and symptom disorders. A
study of twins and other rst-degree relatives showed that there
is a genetic relationship between schizotypal personality disorders and schizophrenia (Onstad, Skre, Edvardsen, Torgersen &
Kringlen, 1991; Torgersen, Onstad, Skre, Edvardsen & Kringlen, 1993). However, there is a difference between schizotypal
disorders that are genetically related to schizophrenia and
schizotypal disorders that are not genetically related to schizophrenia. The disorders genetically related to schizophrenia are
more withdrawn and affect-constricted, whereas those that are
not genetically related to schizophrenia have more colorful and
amboyant borderline-like features (Torgersen, Edvardsen,
ien et al., 2002).
Avoidant personality disorder and social phobia are often
comorbid. A twin study demonstrated that the genetic inuence
on avoidant personality disorder was completely shared with
social phobia, whereas social phobia also had some specic
genetic inuence (Reichborn-Kjennerud et al., 2007b). Nonshared environmental effects were different for the two disorders.
Studies of the quality of life associated with personality disorders and symptom disorders show that personality disorders are
strongly associated with reduced quality of life (Cramer et al.,
2006, 2007), more so than symptom disorders. So when symptom disorders are controlled for, personality disorders still have
a strong association with reduced quality of life. The poorest
quality of life is observed among people with both a personality
and a symptom disorder. These observations imply a validation
of the concept of personality disorders.
Arguments have also been raised that the concept of personality disorders is unnecessary because the Big Five (consisting of
the dimensions Neuroticism, Extraversion, Conscientiousness,
Agreeableness, Openness) describe the complete variation in
personality, including the realm of personality disorders, as
extreme variations of personality dimensions. A meta-study of
the correlations between personality disorders and the Big Five
has in fact demonstrated high correlations (Saulsman & Page,
2004). However, the regression correlations based on the ve
dimensions are not higher than about 0.500.60. A part of the
rest may be reliability deciency. Even so, a large part of the
variance in personality disorders still has to be explained. However, the biggest problem with the Big Five as a substitute for
the concept of personality disorders is the similarity between the
patterns of the Big Five personality traits that correlate with different personality disorders. All personality disorders correlate
with Neuroticism. Only one personality disorder, dependent personality disorder, does not correlate negatively with Agreeableness. Only one personality disorder, obsessive-compulsive, does
not also correlate negatively with Conscientiousness. Openness
and Extraversion do not differentiate sufciently between the
personality disorders. The personality disorders in Cluster A
(odd or eccentric disorders: paranoid, schizoid, schizotypal personality disorders) are all non-open and introverted, and
the disorders in Cluster B (dramatic disorders: antisocial, borderline, histrionic, narcissistic personality disorders) are open
and extraverted.

Scand J Psychol 50 (2009)

However, some object to the word disorder. To be classied as having a disordered personality is considered more negative than having a disordered symptom syndrome. Personality is
me, whereas symptoms happen to me. Perhaps some people would prefer to speak of potentially dysfunctional personality types. Four types close to personality disorders have been
described (Lau, Hem, Berg, Ekeberg & Torgersen, 2006; Torgersen, 2008; Torgersen & Vollrath, 2006; Vollrath & Torgersen,
2000, 2002, 2008): One is named Insecure and is a combination
of high Neuroticism, high Introversion, and low Conscientiousness. This type is characterized by being insecure, dependent,
and having a poor ability to act in ones own best interests.
Another type is named Brooder (high Neuroticism, high Introversion, and high Conscientiousness), which is characterized by
worrying, constriction, and withdrawal. A third type is named
Impulsive (high Neuroticism, high Extroversion, and low Conscientiousness), which is characterized by being impulsive, erratic, having poor control, and emotional variability. The last and
more problematic type is named Complicated (high Neuroticism, high Extroversion, high Conscientiousness) and is characterized by being ambivalent, easily overwhelmed by feeling too
much responsibility, and feeling guilty because of ones own
strong emotions.
However, inventing a new name for something unfortunately
does not help much. After a time, the same stigma will be
attached to these labels. Personality disorders are in fact dysfunctional, painful, and, not least, irritating for the surroundings.
Add a dash of prejudices, and stigma will inevitably be attached
to the labels. Only reasonable, considerate, and real tolerance
for variation in behavior will diminish some of this problem.
However, a disorder will probably forever be a disorder,
whether it is somatic, mental, or psychological in nature.

POSTSCRIPT
The basic questions in research are what, why, and how. What is
the best way to dene personality and personality disorders, and
what are the prevalences? Why does personality vary, and why
do personality disorders develop? What are the mechanisms:
How do the processes behind personality and behind personality
disorders work? The authors ambitions were to contribute to
the two rst questions. It has been a great pleasure to have at
least a small part in the development towards answering them.
As for the last question, we are still lacking the methods to nd
good answers. Today, the how question is mainly discussed theoretically. To answer it in a scientic way is the nal aim for all
researchers, and it will be achieved one day.
Much has been accomplished and much remains to be understood. Today, longitudinal studies from childhood, through
youth and up into adulthood and old age, appear particularly
appealing. In this way we will see how the genetic nature
unfolds through gene-situation, gene-occasion correlations, how
we create our life according to our nature, of course in addition
to a number of events outside our control. The overwhelming
importance of genes in the stability of personality is established;

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Scand J Psychol 50 (2009)

the future will also detect specic and stable environmental

agents. Up to now, only the effects of physical and perhaps
intense psychological traumata have been disclosed. However, it
is possible that we have to accept that not a small part of the
environmental effects are purely random. Studies of gene-situation interaction are tempting for researchers who want to avoid
genetic determinism (but are less afraid of environmental determinism). The future will disclose such effects, not least through
animal research. In the open, outside the laboratory and in the
real human life, studies on the combinations of gene-situation
correlations, gene-situation interaction, and gene-gene interaction will tell us how we create situations that interact with our
nature. These studies will nally disclose also real gene-environment interactions, which today are only possible in adoption
studies or in studies where the environment is manipulated by
the researcher, and the human being has no choice. Ethical rules
will limit the latter type of the studies, but intervention studies
are a promising alternative. The research community will nd a
way, hopefully to the benet of the challenging integration of
understanding, protection of the society, alleviation of suffering,
and tolerance of human behavior diversity.

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