Journal of Personality Disorders, 7(3), 255-264, 1993

1993 The Guilford Press

PERSONALITY DISORDERS:
A BIOPSYCHOSOCIAL MODEL

Joel Paris, MD

The biopsychosocial model of mental disorders is particularly

appropriate to the personality disorders. Theoretical
considerations and available empirical evidence suggest that
only a combination of biological, psychological, and social risk
factors is a sufficient condition for the
development of these
disorders. Personality disorders can best be conceptualized as
exaggerations of personality traits to dysfunctional levels.
Biological predispositions are reflected in heritable personality
traits, which can then be amplified by psychosocial factors.
The present state of the evidence for biological, psychological,
and social risk factors in these disorders is reviewed.

THE BASIC MODEL

The biopsychosocial model (Engel, 1980) is an attempt to conceptualize the

multiple causes of mental disorders. This theoretical model implies that
many etiological factors could be necessary but that none by themselves
would be sufficient conditions for the development of a psychiatric disorder.
The influences on any disorder may function as risk factors or
etiological
protective factors. These factors could include biological vulnerability, the

psychological impact of life experiences, and the influence of the social

environment. The biopsychosocial approach contrasts with more linear
etiological models in medicine(McHugh & Slavney, 1983), such as the germ
of disease the one gene one enzyme theory of hereditary illnesses,
theory or

in that only the cumulative and interactive effects of multiple causal factors
can produce overt disorder. The model is consistent with modern
epidemiological theory in viewing the etiology of disease as resulting from
the interactions of multiple risk factors, each of which accounts for only a
certain percentage of a pathological outcome (Mausner & Kramer, 1986).
The biopsychosocial model has been applied most consistently to schizo

phrenia, whose etiology involves a combination of biological, psychological,

From the Department of Psychiatry. McGill University: and the Institute of Community and
Family Psychiatry, Sir Mortimer B. Davis-Jewish General Hospital. Address correspondence to
the author at the Institute of Community and Family Psychiatry. Sir Mortimer B. Davis-
Jewish General Hospital, 4333 Chemin de la Cote Ste. Catherine, Montreal QC, H3T1E4.
Canada.

255
256 PARIS

and social factors (Carpenter, Kirkpatrick, & Buchanan, 1990). Biological

vulnerability by itself does not
necessarily lead to the full disorder but may
express itself in various ways, on a continuum from personality traits to
psychosis (Meehl, 1990). The example of schizophrenia influenced the de
velopment of the neo-Kraepelinian school of psychiatry, whose theoretical
point of view has become the predominant paradigm of modern psychiatry
(Klerman, 1986). This theory can be considered as a variant of the biopsy
chosocial model in which biological and psychosocial factors are differen

tially weighted. Neo-Kraepelinian theorists favor a predisposition stress

model, in which genetic vulnerability explains why patients faced with the
same stressors develop different mental disorders
(Cloninger, Martin, Guze,
& Clayton, 1990). The model considers psychological and social factors as
precipitants that are not necessarily specific to diagnosis.
This paper reviews evidence supporting the neo-Kraepelinian version of
the biopsychosocial model in understanding the personality disorders.
Since research into these disorders is still in its early stages, much of the
discussion is necessarily theoretical and somewhat speculative. However,
the complex etiology of the personality disorders requires some form of

biopsychosocial theory.

PERSONALITY TRAITS AND PERSONALITY DISORDERS

All individuals can be characterized by personality traits, which are pat

terns of behavior, thought, and emotion that are consistent in many con

texts. There is an important difference between temperament and traits

(Rutter, Temperament reflects behavioral dispositions that are

1987).
observable early in life and are primarily determined by biological factors.
Traits are complex dispositions that involve both behavioral and cognitive
factors and reflect an important degree of environmental input.
Personality traits can best be understood developing from the interac
as

tion of temperament and social learning. Temperament corresponds to the

biological roots ofpersonality, and consists of behavioral factors such as
emotionality, sociability, and activity (Buss & Plomin, 1984). Measures of
temperament in infancy show discontinuities over time, probably because
of environmental shaping. In a major follow-up study of children who were
initially scored for temperamental variation in the first weeks of life, only
the broadest factor (a "difficult" temperament) was predictive of levels of

functioning in young adulthood (Chess & Thomas, 1990). Nevertheless,

given the strong heritability of adult personality traits (Plomin, DeFries, &
McClearn, 1990), temperament must play a crucial role in the development
of personality.
Personality traits in adulthood show continuous variation in community
populations (Livesley, Jackson, & Schroeder, 1992). Within a wide range,
variations in the dimensions of personality are compatible with normal

functioning (Meehl, 1990). Like anatomical and physiological variability,

individual differences in personality represent alternate behavioral pro

grams which can be more or less adaptive depending on the environment.

For example, a trait such as shyness, which has been shown to have a

genetic component (Kagan, Resnick, Snidman, Gibbons, 6k Johnson,

 BIOPSYCHOSOCIAL MODEL 257

1990), may represent variability in evolutionary programs related to attach

ment behavior (Bowlby, 1969-1980). Social avoidance could be adaptive
under conditions where strangers present a real threat. Similarly, a trait
such as impulsivity could represent variability in autonomic activation
which affects the timing of response to environmental challenge (Mednick &
Moffit, 1985). Under conditions of immediate external danger more rapid

responses can be adaptive.

A personality disorder is diagnosed only when traits demonstrably in
terfere either with the capacity to work or the ability to have interpersonal
relationships (American Psychiatric Association, 1987). Many of the criteria
for the diagnosis of personality disorders describe personality traits of
unusual intensity. By themselves, these traits are fully compatible with
normal functioning. Personality disorders differ from most Axis I diagnoses
in that they lack a clear boundary with normality (Tyrer & Ferguson, 1988).
In the Axis II diagnostic system, disorders are defined categorically, which
assumes that there is a qualitative discontinuity between traits and disord
ers. A few of the Axis II criteria, such as the self-destructiveness described in
borderline personality disorder, appear to be distinct from personality
However, the vast majority of the criteria can be understood as
traits.

exaggerations of underlying traits. Moreover, there is good evidence that

traits and disorders, when measured with standard instruments, demon
strate a continuousrelationship (Livesley et al., 1992).
Dimensional measures of personality traits could therefore be used to

diagnose personality disorders. Traits would reach the level of disorders

if
only they reach a sufficient level of intensity (Livesley et al. 1992; Walton,
,

1986). In parallel with the relationship of blood pressure to hypertension,

the cutoff point for pathology could be determined by the statistical likeli
hood of dysfunctional complications.
Dimensional models are particularly useful for studying the biological
factors in personality traits. The broadest dimensional models (Buss &
Plomin, 1984;Cloninger, 1987; Costa 6k McRae, 1988; Eysenck, 1991)seem
to describe traits that are close to temperament. The heritability of these
traits can be demonstrated by comparing them in monozygotic and dizygo
tic twins (Plomin et al., 1990), or in twins raised together and apart (Tel-

legen et al., 1988). These studies have shown that personality dimensions
have a heritability of about 4050% (Plomin et al., 1990). It has also been
found that the broadest personality dimensions are valid in different cul
tures (Eysenck, 1991). Finally, there is evidence that some dimensions are
associated with biological markers (Cloninger, 1987; Eysenck, 1991). The
strongest link identified thus far has been between impulsive personality
traits and levels of serotonin activity in the brain (Siever 6k Davis, 1991).

THE PATHWAY FROM TRAITS TO DISORDERS

Individual differences in personality traits can be understood as alternative

environmental adaptations. Personality traits in themselves are ubiquitous,
and for the most part these differences are entirely compatible with normal
when underlying traits are
ity. Trait variability becomes maladaptive only
and are used under inappropriate circumstances. To account for
amplified
258 PARIS

thedevelopment of personality disorders, one would need to understand the

causes of this amplification.
The most likely explanation would involve a combination of biological.

psychological, and social risk factors. The biological risk factors could be an
unusually high intensity for one or a group of temperamental characteris
tics. The psychological risk factors could be stressful experiences, particu
larly during childhood. Although the empirical evidence for amplification of
traits under exposure to acute stressors is unclear (Lazarus 6k Folkman,

1984), chronically stressful experiences could exaggerate customary pat

terns of coping behavior. The depend on the pres
social risk factors could
ence or absence of structures that buffer dysfunctional personality traits.
All these risk factors could be necessary, but only some combination of
them would be sufficient for the development of a personality disorder.

Biological variability could be a limiting factor for the type of disorder that
could develop (Siever 6k Davis, 1991). The three clusters of personality
disorders on Axis II (American Psychiatric Association, 1987) probably
reflect common personality dimensions. One would therefore predict that
traits would tend to produce vulnerability to disorders within the same

cluster, so that an individual with traits of introversion and social anxiety

might develop a Cluster C disorder, whereas an individual with traits of
extraversion and high emotionality might develop a Cluster B disorder.

BIOLOGICAL RISK FACTORS

Biological factors in mental disorders can be identified either

through
genetic studies through biological
or markers. Genetic factors
can be identi

fied by family history, by adoption studies, or by comparisons of monozygo

tic (MZ) and dizygotic (DZ) twins. Family history studies provide findings
that are suggestive of genetic influence, although the method fails to sepa
rate heredity from environment. Adoption studies have thus far been car
ried out on antisocial personality (Cloninger, Sigvardsson, 6k Bohman,
1982) and schizotypal personality (Kendler, Gruenberg, 6k Strauss, 1981).
There have been a number of twin studies of personality disordered patients
(Torgesen, 1991).
On the whole, although there is some evidence for
heritability in the
personality disorders (McGuffin 6k Thapar, 1992), most of the
empirical
findings relate more strongly to traits than disorders. Thus the genetic
factors in antisocial personality have been measured by criminality (Clonin

ger et al., 1982; Crowe, 1974; Mednick, Gabrieli, 6k Hutchings, 1984). in the
avoidant personality by social anxiety (Torgesen, 1983), and in the schizo
typal personality by mild forms of thought disorder (Kendler et al., 1981).
In those disorders that lack clear trait markers, no clear pattern of
heritability has been found. In a series of twin
studies, Torgersen (1980,
1983, 1984, 1991) examined personality-disordered patients who were cate
gorically diagnosedand then given a measure of their underlying personal
ity dimensions. MZ-DZ differences in concordance for disorders were not
found, but there were clearcut MZ-DZ differences for traits. These results
are in concordance with the theory that it is the
underlying dimensions of
personality that are under strong biological influence, rather than personal-
 BIOPSYCHOSOCIAL MODEL 259

ity disorders themselves. Although unusually intense traits could still be a

risk factor, the findings are most consistent with the hypothesis that it is

nongenetic psychosocial factors that determine the pathway from traits to

disorders.
There is little evidence at present for biological markers that are specific
to any Axis II Where
diagnosis. biological variability has been identified in
personality-disordered patients, it has often been related to comorbidity on

Axis I, such abnormal dexamethasone suppression and decreased REM

as

latency in depressed patients with personality disorders (Gunderson 6k

Phillips, 1991). In one study of men with Cluster B diagnoses (Coccaro et

al., 1989), decreased response to fenfluramine challenge suggested that
a

their impulsivity was related to decreased activity in the serotonergic sys

tem. However, in this report there was a much stronger relationship be
tween the neurochemical measures and traits of impulsive aggression than
with any specific diagnostic category. Although it is possible that future
advances in biotechnology will provide an increased variety of biological
markers, most of them will probably continue to be associated with traits.
The biological variability associated with unusually strong personality
traitsmight nonetheless provide useful markers for vulnerability to the
personality disorders. A psychobiological model of the personality disorders
based on this possibility has been proposed by Siever and Davis (1991). It
resembles somewhat the model of Cloninger (1987) in that it relates both

personality traits and disorders to variability in neurotransmitter activity.

The model describes four dimensions: cognitiveperceptual, impulsivity
aggression, affective instability, and anxiety inhibition. Each is mediated
by specific variations in neurotransmitter interactions, and each is associ
ated with a specific group of personality disorders with shared traits.
The Siever model is highly neo-Kraepelinian in its emphasis on the biolo
gical risk factors for personality disorders. The model is clearly heuristic for
future research but has not received thorough empirical testing. It may also
be overly simplistic, given the multiple receptor systems for each
neurotransmitter and the variable effects of the same neurotransmitter

systems at different anatomical sites and on different neurophysiological

systems. However, Siever 's model provides a theoretical link between the
Axis II diagnoses and the major Axis I disorders, which could be more severe
outcomes of the same psychobiological matrix.
In general, biological factors do not seem to account by themselves for the
development of personality disorders. Most likely they are necessary but not
sufficient conditions for the development of these disorders and are limiting
factors for the type of disorder that can develop in any individual.

PSYCHOLOGICAL RISK FACTORS

Since personality disorders appear early in life, the most important psycho
logical risk factors for their development could derive from childhood experi
ences, particularly problems in parent child relationships. Social-learning

theory (Bandura, 1977) tends to explain the personality traits of children by

the shaping influence of parents, either through direct reinforcement or
through modeling. However, there appear to be important limiting factors
260 PARIS

for the impact of social learning, as shown by the differences in personality

between children raised in the same
family (Dunn 6k Plomin, 1990). An
interaction between parental style and temperament, of fit"
or "goodness
(Chess 6k Thomas, 1990), could provide an explanation of these differences.
A good deal of recent research has pointed to negative childhood experi
ences as risk factors for
personality disorders. Most of this evidence applies
to borderline personality disorder, the most researched of the Axis II di

agnoses. For example, a number of studies (Herman, Perry, 6k van der Kolk,
1 989: Ogata etal., 1990; Paris, Zweig-Frank, 6k Guzder, 1992: Westen et al..
1990; Zanarini et al., 1989) have shown that traumatic experiences, such
aschildhood sexual abuse and/or childhood physical abuse, are significant
ly more common in borderline patients than in related
diagnostic categor
ies. However, these risk factors have a low
specificity to diagnosis and are
far from uncommon in nonborderline personality disorders. Moreover, most
of the traumatic experiences reported in these studies are of low severity
(Paris et al., 1992). Fewer than a quarter of adults with histories of child
hood sexual abuse have long-term sequelae, and the long-term outcome of
abuse experiences depends on the severity of trauma (Browne 6k Finkelhor,
1986). Therefore the etiological significance of trauma in the personality
disorders remains unclear. Moreover, it has not been determined to what
extent trauma is a risk factor in its own right, or an epiphenomenon of
other risk factors.
These caveats
apply to other childhood experiences that have been stu
died in the personality disorders. For example, there have been reports of
early separations or losses in the histories of borderline patients (Bradley,
1979; Paris, Nowlis, 6k Brown, 1988; Zanarini et al., 1989). These histories
are common in many Axis II diagnoses (Paris etal., 1992). But the long-term
effects of separation or loss from a parent during childhood depend on
interactions with many other factors (Rutter, 1989: Tennant, 1988).
The qualifications apply to evidence that many patients with per
same

sonality disorders have

experienced abnormal parental behavior during
childhood. For example, borderline patients have parents who are likely to
have themselves some form of psychiatric diagnosis (Links, Steiner, Offord,
6k Eppel, 1988). Assumedly disorders such as depression, substance abuse,
or personality disorder would reduce the capacity to be an effective parent.
Nevertheless many children with similar experiences do not develop major
psychopathology (Anthony 6k Cohler, 1987).
Given the possibility thatproblems in attachment could lead to psy
chopathology in adulthood (Bowlby, 19691980), patients with personality
disorders have been given instruments that measure the quality of their
parenting. These instruments derive their constructs from theories of child

development (Rowe, 1981) that define parental tasks on two dimensions:

providing affection and allowing autonomy. Most personality-disordered
patients report having had problems with their parents on both these
dimensions of parental bonding (Paris et al., 1992). However, similar find
ings have been reported for many other psychiatric diagnoses (Parker,
1983). Moreover, given the retrospective nature of the instruments, we

would need prospective studies of children developing into adulthood to feel

confident of the validity of these findings.
Research on the psychological risk factors in patients with personality
 BIOPSYCHOSOCIAL MODEL 261

disorders is at an
early stage, and it is possible that more
convincing
findings will emerge in the future. At present it is not clear to what extent
there are specific
psychological risk factors for individual personality dis
orders, or whether the same risk factors personality disorders. It
apply to all
is likely that defective
parenting has some development, but this
effect on

effect may not be specific to particular personality traits. Any experience in

childhood that is sufficiently negative has the potential to increase the
intensity of trait-related behaviors to dysfunctional levels. Therefore the
effect of psychological risk factors on the development of personality disor
ders can only be understood in interaction with specific biological vul
nerabilities.

SOCIAL RISK FACTORS

Social risk factors for psychiatric disorders

can be identified
through
epidemiological research. Differences in prevalence under different social
conditions, rapid changes in
or prevalence over time could suggest that
social factors play an etiological role in mental disorders. Epidemiological
methods have only recently been applied to the personality disorders. There
have been a few reports that have described the prevalence of the Axis II
disorders in the community (Reich, Yates, 6k Nduaguba, 1989), but large-
scale epidemiological studies are needed to describe the effects of social
class, culture, or cohort changes.
There are some findings that point to cohort differences in the prevalence
of the personality disorders. Antisocial personality disorder, which was
included in the Epidemiological Catchment Area (ECA) study (Robins 6k

Regier, 1991), has been found to be increasing over time. There is some
indirect evidence (Paris, 1992) that borderline personality disorder is also
becoming more common. Such increases would most likely be reflections of
changes in social risk factors.
The nature of social risk factors for the personality disorders remains
somewhat speculative. One possibility is that recent social
changes have led
to a decrease in what has been called "social integration' (Leighton, Hard
construct has been operationalized in terms of
ing, 6k Macklin, 1963). This
family disruption, weak community associations, poverty, secularization,
migration, and rapid social change itself. Social disintegration has been
shown to have a general relationship to the prevalence of psychopathology
(Leighton et al., 1963). Decreased social integration, by failing to provide
social containment for impulsivity, may-have a specific relationship to those
personality disorders characterized by this trait (Millon, 1987. 1993).
Social risk factors for personality pathology may act in interaction with
biological and psychological vulnerabilities. Personality traits that are mini
mally adaptive under stable social conditions may become maladaptive
when traditional societies undergo rapid change. For example, individuals
with schizotypal traits may be able to function in settings where social roles
are fixed, so that they are
not required to make occupational and marital

1990). Those with traits of high social anxiety

choices (Meehl, might also
better in social settings that require less individual
function autonomy.
Those with traits of impulsivity may be particularly sensitive to a loss of
262 PARIS

social role structures, which provide a buffer against impulsive actions

(Millon, 1993).
Another mechanism by which social risk factors could lead to
personality
disorders involves an interaction with the functions of the nuclear
family
(Murphy, 1982). A stressful social environment would make family dysfunc
tion more likely and could amplify the effects of existing family dysfunction.

Conversely, a supportive social environment tends to act as a buffer against

the negative effects of family pathology. In studies of "resilient children"

(Anthony and Cohler, 1987; Kaufman, Grunebaum, Cohler, 6k Gamor,

1979), even highly dysfunctional nuclear families did not produce psy
chopathology when alternative attachments and identifications were avail
able. The presence or absence of these attachments to the wider social
network could be one factor that determines whether personality traits are
amplified to disorders.

A BIOPSYCHOSOCIAL THEORY OF PERSONALITY DISORDERS

The presence of biological variability by itself leads to variability in personal

ity but not necessarily to a personality disorder. Biological factors determine

the specificity of personality disorders, and psychological and social factors
are the strongest determinants of whether an
underlying predisposition
leads to an overt disorder.
Psychological risk factors increase the likelihood
of thedevelopment of personality disorders, but they need not by themselves
produce disorders because in the absence of other risk factors, children may
be sufficiently resilient to compensate for psychological insults. Social in
fluences can act either as protective factors against personality disorder
that buffer the effects of biological and psychological risk, or as risk factors
in their own
right.
This biopsychosocial model is
admittedly speculative but is reasonably
consistent with the available empirical evidence. The model could be applied
to future research on the personality disorders. Thus far most studies on
the etiology of these disorders have been univariate. If the most powerful
effects involve multiple factors, this would explain why most individual risk
factors are not strongly associated with specific disorders. In multivariate
studies, biological markers for trait vulnerabilities could be studied along
with psychological and social factors. If the cumulative variance accounted
for by multidimensional predictive models were high, one could begin to
approach causal modeling. At the very least it must be recognized that
personality disorders are highly complex phenomena, and that any model of
their etiology must be multidimensional.

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