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CHAPTER
32
2
Vulnerability-Stress Models
RICK E. INGRAM AND DAVID D. LUXTON
Early models of psychopathology
typically identified processes operat-
ing during the course of the disorder
as reflecting the key determinants of the
onset of psychopathology (e.g., irrational
beliefs; Ellis, 1962). Such models have led
to important advances in understanding
important features of psychopathology. For
example, in the cognitive arena, schema
models initially focused almost exclusively
on understanding cognitive variables func-
tioning in the disordered state. This con-
ceptual approach, as well as the empirical
research motivated by these models, has
led to a number of significant insights into
depression (Ingram, Miranda, & Segal,
1998), anxiety (e.g., McManus & Clark,
2002), personality disorders (Beck, 1999),
and even problematic marital interactions
(Beck, 1989). Schema models thus represent
a clear example of the power of such con-
structs as they apply to the description of
psychopathology.
Stress has also been recognized as an
important contributor to the development and
course of psychopathology, so much so that a
variety of models have featured stress as a
primary determinant of disordered functioning
(Brown & Harris, 1978, 1989). Such models
suggest that severe enough negative events
could precipitate psychological disorders even
without reference to individual psychological
or biological characteristics. For example, the
link between an adverse social environment
and the onset of depression has long been
recognized. The majority of research investi-
gating possible links consistently finds a rela-
tionship between the experience of stressful
life events and the onset of depression, with
some data suggesting that approximately
50% of individuals diagnosed with depression
have experienced severe stress before onset
(Mazure, 1998). More recent perspectives
suggest the possibility that life stress may
engender a specific subtype of depression
(Monroe & Hadjiyannakis, 2002).
Despite advancing understanding, the limi-
tations of these approaches have become
increasingly apparent. For instance, models that
place primary emphasis on stress as a key cause
of a disorder have difficulty dealing with data
showing that even extreme stress is not linked
to psychopathology in all individuals (Monroe
& Hadjiyannakis, 2002); after all, approxi-
mately 50% of individuals do not show
evidence of a disorder such as depression
02-Hankin.qxd 2/24/2005 12:20 PM Page 32
following significant life stress. Hence, although
data convincingly show that stress plays a role
in depression, they just as convincingly show
that other factors also play a critical role.
The fact that not all individuals who expe-
rience significant stress develop a disorder has
led, in part, to the recognition that vulnerabil-
ity processes are important components of psy-
chopathology; such factors predispose some
individuals to psychopathology when stress is
encountered. Notions about vulnerability have
also begun to address questions about whether
variables operating within the disordered state
are antecedents of the state, or whether they
can reasonably be considered to be conse-
quences of the state (e.g., Barnett & Gotlib,
1988). By definition, vulnerability to a disorder
must serve as an antecedent of the disorder.
Although vulnerability ideas have been a cen-
tral part of some of the earliest models of psy-
chopathology (e.g., Beck, 1967), the emphasis
on their essential nature in the onset of psy-
chopathology has seen a remarkable resur-
gence (Segal & Ingram, 1994).
Although vulnerability and stress can be
reasonably considered to be conceptually dis-
tinct constructs, separately, their power to
describe key aspects of psychopathology is
limited. Thus, most modern models of psy-
chopathology explicitly combine vulnerability
and stress in their descriptions of the func-
tional processes leading to disorder. This
chapter focuses on the interaction of vulnera-
bility and stress as essential for understand
ing the development of psychopathology. To
serve as a background for exploring their
interactive role, we briefly provide definitions
of vulnerability and stress and then briefly dis-
cuss the origins of these constructs. We then
examine general principles that characterize
most diathesis-stress models and, finally,
explore different models of vulnerability-stress
interactions. Finally, we comment on some
issues that are pertinent to conceptualizations
of stress and conceptualizations of diatheses in
the context of the diathesis-stress relationship.
DEFINITIONS
Numerous discussions of vulnerability (e.g.,
Ingram et al., 1998) and stress (e.g., Grant &
McMahon, Chapter 1 of this volume) can be
found in the literature. Detailed examination
of these ideas can be found in these sources.
For purposes of context, in this chapter we
briefly note ideas about the individual con-
structs that form diathesis-stress models. We
start with stress.
Stress
Definitions of stress encompass a number of
facets. In general, however, stress falls into a
limited number of broad categories. One major
category of stress is conceptualized as the
occurrence of significant life events that are
interpreted by the person as undesirable
(Lazarus & Folkman, 1984; Luthar & Zigler,
1991; Monroe & Peterman, 1988; Monroe
& Simons, 1991). The accumulation of minor
events or hassles represents another kind of
stress (Dohrenwend & Shrout, 1985; Lazarus,
1990). Socioeconomic factors have also been
implicated in stress, in that variables such as
low maternal educational status or membership
in an ethnic minority group may reflect stress-
ful living circumstances (Luthar & Zigler).
Although it is clear from these descrip-
tions that the definitions of stress are many,
we can view stress in the context of this chap-
ter as the life events (major or minor) that
disrupt those mechanisms that maintain the
stability of individuals’ physiology, emotion,
and cognition. Indeed, Selye’s (1963) classic
description of stress notes that such events
represent a strain on the person’s adaptive
capability that cause an interruption of the
person’s routine or habitual functioning.
Stress thus reflects those factors that interfere
with the system’s physiological and psycho-
logical homeostasis.
Even though stress is frequently conceptu-
alized as the occurrence of “externally”
Vulnerability-Stress Models 33
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ordained processes, two sets of factors suggest
an important role for “internal” forces in the
occurrence of stress. First, although some
stressful events may simply befall people, sev-
eral researchers have persuasively argued, and
empirically demonstrated, that other events
are the results of individuals’ own actions
(Depue & Monroe, 1986; Hammen, 1991;
Monroe & Simons, 1991; Rutter, 1986). For
instance, a person with social skills deficits
(e.g., inappropriately critical of others) may
engender tumultuous relationships with
acquaintances, coworkers, and romantic part-
ners that result in the generation of significant
stress. Vulnerable individuals, or those in a
disordered state, may therefore play a role in
creating their own stresses (Ingram et al.,
1998). Later in this chapter, we expand on the
implications of this idea as it pertains to
diathesis-stress models.
A second factor is the influence of appraisal
processes on what is perceived to be stressful
(Monroe, 1989; Monroe & Simons, 1991).
That is, stress is not independent of the indi-
vidual’s appraisals of events. Even though
there are a number of events that are undoubt-
edly universally appraised as stressful (e.g., the
death of a loved one), even in these cases indi-
vidual differences may determine the degree of
stress that is perceived and experienced. In
other cases, events that are perceived as stress-
ful by some individuals may be perceived and
experienced as not stressful, or at the least
as minimally stressful, by other individuals.
Indeed, a multitude of other factors can affect
the determination and degree of stress.
Diatheses
We employ the terms diathesis and
vulnerability interchangeably. A diathesis, or
vulnerability, is typically conceptualized as a
predispositional factor, or set of factors, that
makes possible a disordered state. The earliest
psychopathology models featuring vulnera-
bility suggested that these redispositional
factors constituted genetic or biological
factors. In more recent years, the term has
been broadened to include psychological
factors, such as cognitive and interpersonal
variables, that make a person susceptible to
psychopathology (Monroe & Simons, 1991).
Intuitive ideas about vulnerability imply
an increased susceptibility to emotional pain
and to the occurrence of psychopathology of
some type. Yet, as intuitively straightforward
as this concept has been, and despite exten-
sive discussion in the literature about vulner-
ability, few precise definitions are available
in the scientific literature. Ingram et al.
(1998) noted several core features of vulner-
ability that appear to constitute the common
themes that emerge in discussions of vulner-
ability and that can thus help establish a
working definition of the construct. These
ideas suggest that vulnerability is a trait, is
stable but can change, is endogenous to indi-
viduals, and is usually latent.
Most discussions regard vulnerability as
an enduring trait. For example, Zubin and
Spring (1977) argued that “we regard [vul-
nerability] as a relatively permanent, endur-
ing trait” (p. 109). They continue, “The one
feature that all schizophrenics have . . . is the
everpresence of their vulnerability” (p. 122).
Such assumptions of permanence seem likely
to be rooted in the genetic level of analysis
employed by researchers who pioneered this
concept, as can be seen among schizophrenia
researchers who point to the genetic endow-
ment of individuals who are at risk for this
disorder. Meehl’s (1962) idea of schizotaxia
represents an inherited neural deficit,
whereas other researchers, such as Zubin and
Spring, Nicholson and Neufeld (1992), and
McGue and Gottesman (1989), explicitly
argue that genetic endowment determines
one’s level of vulnerability (at least to
schizophrenia). Hence, little change is theo-
retically possible.
Although vulnerability may in many cases
be permanent and enduring, this need not
OVERVIEW AND FOUNDATIONS34
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always be true. For example, when the level
of vulnerability analysis is psychological
rather than genetic in nature, change may be
possible. Even though assumptions of genetic
vulnerability offer little possibility for modi-
fication of vulnerability, most psychological
approaches rely on assumptions of dysfunc-
tional learning as the genesis of vulnerability.
Given such assumptions, vulnerability levels
may fluctuate as a function of new learning
experiences.
The traitlike nature of vulnerability sug-
gests that vulnerability tends to be, at the
least, stable. It is important to note, however,
that stability does not necessarily mean per-
manence. That is, even though the idea of
stability suggests a resistance to change, it
does not presume that change is never possi-
ble. Under some circumstances, positive
changes in an otherwise stable variable may
very well occur. Indeed, the notion of ther-
apy is based on just this premise. It is also the
case, however, that some experiences (e.g.,
trauma) might serve to strengthen vulnerabil-
ity. It thus seems reasonable to conceptualize
vulnerability as stable but not immutable.
Following from the traitlike characteris-
tics of vulnerability, another core feature of
the construct is that vulnerability is an endoge-
nous process. In particular, whether stem-
ming from genetically or biologically acquired
characteristics or acquired through psycho-
logical or learning processes, vulnerability
resides within the person. This serves to
explicitly distinguish vulnerability from
“external” stress or life events. Finally,
because diatheses are often not easily recog-
nized, they are frequently considered to be
latent, requiring activation in some fashion
before psychopathology can occur. Although
not all researchers agree with this position
(e.g., Just, Abramson, & Alloy, 2001), there
is widespread consensus among many
researchers concerning the latent nature of
many vulnerability characteristics. This is
particularly the case with “unseen” genetic
or biological factors that may predispose to
disorder, but it also includes more psycho-
logically based vulnerability processes.
Risk and Diatheses/Vulnerability
Terms such as risk and vulnerability (or
diatheses) are often used interchangeably, and
in fact there is little doubt that these con-
structs overlap substantially. However, it is
important to note that although we use the
terms diathesis and vulnerability interchange-
ably, we do not view vulnerability and risk as
interchangeable. As several investigators have
argued (e.g., Ingram et al., 1998; Luthar &
Zigler, 1991; Rutter, 1987), risk describes
factors that are associated, or correlated, with
an increased likelihood of experiencing a dis-
order. Nevertheless, the presence of risk sug-
gests only an increased probability of the
occurrence of a disorder; it does not specify
what causes the disorder. Risk factors are
thus not informative about the actual mecha-
nisms that bring about a state of psy-
chopathology. For example, female gender is
a well-established risk factor for many disor-
ders, but this knowledge alone is uninforma-
tive about why women are more likely to
experience a range of disorders. Alternatively,
vulnerability is usually defined in such a way
that it reflects statements about causal mech-
anisms.1Risk is certainly an important pre-
dictive variable that can be seen as acting in
concert with vulnerability (Rutter, 1988), but
these constructs are not synonymous.
DIATHESIS-STRESS
ORIGINS CONSIDERED
To understand fully diathesis-stress interac-
tions, it is useful to briefly consider the his-
torical context in which these ideas emerged.
Monroe and Simons (1991) note that the
diathesis concept has a long history in medi-
cal terminology. The concept dates back to
Vulnerability-Stress Models 35
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the ancient Greeks; the word diathesis
derives from the ancient Greek idea of dispo-
sition, which is related to the humoral (body
fluids) theory of temperament and disease
(Zuckerman, 1999). By the 1800s, the term
had become part of the psychiatric language
of the day (e.g., Beard, 1881). Likewise,
although the role of stress had long been con-
sidered an important factor in the develop-
ment of mental disorders, it was theories
of schizophrenia proposed during the 1960s
(e.g., Meehl, 1962) that highlighted stress
and brought the diathesis and stress concepts
together. More specifically, the particular
terminology of the diathesis-stress interac-
tions was developed by Bleuler (1963) and
Rosenthal (1963).
Beyond these pioneering approaches,
somewhat more contemporary and detailed
conceptualizations of the nature of vulnera-
bility and the role of stress have been pro-
posed that specify under what circumstances
a disorder will ensue. For example, Audy
(1971) suggested that the preservation of
health requires the maintenance of a dynamic
equilibrium against insults coming from
chemical, physical, infectious, psychological,
and social environment factors. A disorder
occurs when the equilibrium is disturbed
by an inability to maintain homeostasis.
Vulnerability factors influence the ease and
frequency with which these factors will chal-
lenge homeostasis; such factors therefore
determine the probability that the disorder
will occur. Thus, the highly vulnerable per-
son is one in whom numerous circumstances
can elicit an episode.
GENERAL PRINCIPLES OF
DIATHESIS-STRESS MODELS
According to Monroe and Simons (1991) and
Monroe and Hadjiyannakis (2002), most
diathesis-stress models of psychopathology
suggest that all people have some level of
predisposing factors (diatheses) for any given
mental disorder. However, individuals have
their own point at which they will develop
a given disorder, a point that depends on
the interaction between the degree to which
these risk factors exist and the degree of
stress experienced by the individual. Because
diathesis-stress models address the interac-
tions between premorbid risk factors and
situational stressors, they are useful for
describing who will develop a disorder and
who will not. Many—perhaps most—psy-
chopathologists have recognized the concep-
tual and empirical utility of combining
diathesis and stress constructs, and accord-
ingly, models of psychopathology tend to be
explicit diathesis-stress models.
A variety of diathesis-stress models have
been proposed for various types of psy-
chopathology (see Ingram & Price, 2001).
Depending upon the particular theory, these
models suggest specific variables that com-
bine in some fashion to produce the disorder.
Beyond the description of particular vari-
ables in particular disorders, however, these
ideas about psychopathology also illustrate
different ways that the structure of a diathesis-
stress interaction can be conceptualized.
Examination of these models suggests several
general principles that characterize hypothe-
sized diathesis-stress interactions.
Additivity
On the surface, diathesis-stress models
represent straightforward, linear, dose-
response–type relationships, or additive rela-
tionships. Hence, at the most basic level,
many models suggest that whether or not a
disorder will develop depends on the com-
bined effects of stress and the loading of the
diathesis. One model, for example, may sug-
gest that relatively minor stressors may pre-
cipitate the onset of the disorder for a person
who is highly vulnerable, whereas another
model might suggest that a major stressful
OVERVIEW AND FOUNDATIONS36
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event might cause a similar reaction in a
person low in vulnerability. Although vari-
ous models may accord a stronger role for
one component over the other, this idea pre-
supposes additivity, that is, the idea that
diatheses and stress add together in some
way to produce the disorder.
Ipsative Models
Monroe and Hadjiyannakis (2002) note
that many diathesis-stress models reflect
an ipsative approach to the relationship
between the constructs. Ipsative models posit
an inverse relationship between factors such
that the greater the presence of one factor,
the less of the other factor is needed to bring
about the disorder. Ipsative models are not
necessarily distinct from additive approaches
and can thus be considered an additional
quality of many diathesis-stress models of
psychopathology. More specifically, these
models suggest that the diathesis and stress
sum together to cause psychopathology, and
that whatever this sum is, it reflects an
inverse relationship. Thus, the degree of
effect of diathesis or stress can be offset or
compensated by the other in the summation
that is needed for psychopathology.
Mega Diathesis-Stress Models
Although ipsative (and additive) models
are prevalent, Monroe and Hadjiyannakis
(2002) also note that other possibilities exist.
One such possibility is a model that suggests
that disorder results from the combination of
significant life stress and a heightened vul-
nerability. For the sake of simplicity, we refer
to this as a mega diathesis-stress model to
denote that both the diathesis and the stress
must be considerable before a disorder
occurs. Thus, cognitive models of depression
that conceptually rely on diathesis-stress
interactions would suggest that not only is
the presence of a depressogenic schema
needed, but substantial life stress must also
occur before the process eventuates in
depression. This differs from an ipsative
model, which suggests that minimal stress is
needed for depression to occur in individuals
with a strongly depressogenic schema.
Static Versus Dynamic
Diathesis-Stress Relationships
Comparison of ipsative and mega models
reveals a neglected aspect of many diathesis-
stress models of psychopathology, specifi-
cally the idea that the relationship between
the diathesis and stress can change over time.
This changing interaction can be illustrated
by reference to the idea of kindling. In
response to data showing that repeated
episodes of depression within some individu-
als begin to appear with decreasing stress,
Post (1992) proposed the idea of kindling.
Kindling suggests that repeated instances of a
disorder cause neuronal changes that result
in more sensitivity to stress. With heightened
sensitivity, less stress becomes necessary to
activate the requisite processes that lead
to psychopathology. Applying these ideas to
diathesis-stress models suggests that the pre-
cise relationship between these constructs is
not necessarily static. More specifically, this
also suggests that as the relationship changes
with recurrence or relapse, mega processes
may become more ipsative. That is, whereas
the mega model suggests that high levels of
both stress and diatheses are needed, the kin-
dling theory suggests that at some point
diatheses are changed (and presumably
strengthened) so that less stress becomes nec-
essary to activate the vulnerability factors.
Of course, other changes are also possible.
Recall that we noted that in at least some
models, diatheses are viewed as stable
although not necessarily immutable. It is
therefore possible that the relationship
between diatheses and stress may change if
the diathesis becomes weaker.
Vulnerability-Stress Models 37
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We believe that consideration of the static
versus dynamic relationship between diatheses
and stress has potentially important implica-
tions for the conceptualization of diathesis-
stress ideas. In general, varying relations
between diatheses and stress models over time
may affect the accuracy of the model at any
given moment, but they may also have con-
siderable implications for models that seek to
understand the function of these processes in
remission, recovery, relapse, and recurrence.
As we have noted, few contemporary models,
at least explicitly, take into theoretical account
potential changes over time of the relationship
between diatheses and stress, but clearly the
nature of the relationship over time is an
important factor to consider.
DIATHESIS-STRESS MODELS
With the caveat that dynamic relationships
may be quite significant, our focus is on more
“static” models of the diathesis-stress pro-
cesses. At present, most diathesis-stress mod-
els are ipsative, although several permutations
are possible. Hence, different investigators
have described these models in somewhat
varying terms. The models we describe here
illustrate these different terms. In particular,
we discuss the interactive model with dichoto-
mous diatheses, the quasi-continuous diathesis
models, threshold models, and risk-resilience
continuum models. Before doing so, it is
important to acknowledge that these models
tend to vary in emphasis rather than in basic
structure. Thus, there is considerable overlap
in how these approaches view the relationship
between diatheses and stress.
Interactive Model With
Dichotomous Diatheses
As noted, vulnerability-stress models
originated from schizophrenia theory and
research, starting with Meehl’s (1962)
groundbreaking ideas. In his first model of
schizophrenia, Meehl described the diathesis
as a single dominant “schizogene,” which
produces a schizotaxic brain pathology (e.g.,
neural integrative defect) that eventuates in a
schizotypic personality. According to Meehl,
however, only some people with schizotypic
personality will develop clinical schizophre-
nia. Most at-risk individuals will not,
because the schizotypic personality, although
necessary for the development of schizophre-
nia, is not sufficient in and of itself for the
development of schizophrenia. Instead, an
environmental stressor is required to produce
schizophrenia. Meehl suggested that the
stress produced by a schizophrenogenic-type
mother who is “ambivalent and inconsis-
tently aversive to the schizotypic” is the most
important type of stress that may produce
the disorder. Alternatively, if the schizogene
is absent, no amount of stress or type of rear-
ing will produce schizophrenia. In sum,
Meehl’s theory suggested that the onset of
schizophrenia is a joint function of both
biological and psychological factors.
Meehl’s (1962) first model for schizophre-
nia, which arguably launched the idea of
diatheses and stress, can thus be described
as an interactive model with dichotomous
diatheses (see Figure 2.1). Dichotomous diathe-
sis suggests that one either has the diathesis or
OVERVIEW AND FOUNDATIONS38
Present
Stress
Level
Low
High
Disorder
Not
Present
High
Diathesis
(Individual A)
Low
Diathesis
(Individual B)
Figure 2.1 Additive Model of Diathesis-
Stress Interaction With a
Dichotomous Diathesis for
Disorder
02-Hankin.qxd 2/24/2005 12:20 PM Page 38
does not; if the diathesis is absent, there is no
effect for stress. Hence, even severe stress will
not lead to the development of the disorder.
On the other hand, when the diathesis is pre-
sent, the expression of disorder will be con-
ditional on the degree of stress. That is, as
stress increases, so does the risk for the dis-
order in those who possess the diathesis.
We note Meehl’s (1962) original model for
historical context, but it is also important to
note that this model has been updated to the
extent that it no longer resembles the earlier
model. Hence, to better clarify the interac-
tion between diathetic characteristics and
environmental stressors, Meehl (1989, 1990)
revised his original model to describe another
pathway that could lead to schizophrenia,
called the SHAITU genophenocopy (Meehl,
1989, 1990). SHAI stands for personality
trait extremes—submissive, hypohedonic,
anxious, and introverted—of polygenic ori-
gins, which may increase the potential for
schizotaxia to develop into schizotypic per-
sonality and subsequently lead to clinical
schizophrenia. TU stands for environmental
risk factors; T stands for major or frequent
minor traumas during development, whereas
U stands for unlucky events in adult life,
which also increase the risk for schizophrenia.
In Meehl’s original 1962 model, the domi-
nant schizogene and the resulting schizotaxic
brain pathology were necessary but not suffi-
cient causes of schizophrenia. In contrast, the
SHAITU genophenocopy not only plays a
role in the schizotaxic type of schizophrenia,
but it can produce a schizophrenic disorder
even in the absence of the schizogene. As
such, however, the revised diathesis-stress
model is no longer an example of an
interactive model with dichotomous diathesis
conceptualization.
Although Meehl’s (1962) original model
of schizophrenia illustrates the idea of an
interactive model with dichotomous diathesis,
a more contemporary example can be seen
in the posttraumatic stress disorder (PTSD)
theory proposed by McKeever and Huff
(2003). They suggest two types of diatheses:
One type consists of ecological variables
and revolves around factors such as child
abuse and cognitive distortions. Another
type is biological and includes variables
such as neurophysiological dysregulation.
Individuals with higher degrees of these
premorbid vulnerability factors (diatheses)
would not need to experience as severe a
stressor to reach the threshold and develop
PTSD symptomatology. In contrast, indi-
viduals without the diatheses might not dis-
play any signs or symptoms of PTSD even
after experiencing a traumatic event. Even
to the extent that signs or symptoms are
experienced, however, they would not be
indicative of a clinical disorder.
Quasi-Continuous Diathesis Models
Dichotomous models suggest that when the
diathesis is absent, there is no effect for stress.
That is, regardless of the amount of stress expe-
rienced by the individual, the disorder will not
occur if the individual does not have the diathe-
sis. However, many disorders suggest polygenic
models that allow for varying degrees of diathe-
ses (such as the level of a particular neurotrans-
mitter) (Zuckerman, 1999). Thus, instead of
being dichotomous, the diathesis is “quasi-con-
tinuous” (Monroe & Simons, 1991). As illus-
trated in Figure 2.2, in the quasi-continuous
model there is a point beyond which a disorder
Vulnerability-Stress Models 39
High
Degree of
Disorder
Low
Low Stress Level High
Minimal Loading
No Loading
Diathesis
Present
(Low to High
Loading)
High Loading
Figure 2.2 Interactive Model of Diathesis-
Stress Interaction With Quasi-
Continuous Diathesis
02-Hankin.qxd 2/24/2005 12:20 PM Page 39
will occur, but there is also a continuous effect
of the diathesis once the threshold is passed. In
other words, a very minimal level of diathesis
may be insufficient to produce the disorder
even under high stress, but the probability of
disorder increases as a function of both level of
stress and strength of the diathesis beyond a
minimal level (Zuckerman).
Few models of psychopathology are explic-
itly framed in terms of a continuous or quasi-
continuous vulnerability model, but it is easy
to see how this diathesis-stress conceptualization
could be applied to psychopathology models.
Moreover, this idea could also help clarify or
refine these models. For example, schema
models of depression are typically conceptu-
ally stated as dichotomous models; if the indi-
vidual possesses a depressogenic schema, then
he or she is at risk for depression when events
occur that activate this schema (see Beck,
1967, for the original description of the role
of depressogenic schemata in depression).
However, various discussions of the proper-
ties of schemata suggest how schemata could
be conceptualized in more continuous terms
(e.g., the relative density and strength of nega-
tive connections; see Segal, 1988). Some
descriptions of these processes have been
implicitly, but rarely explicitly, suggested (see
Ingram et al., 1998). To the extent that
schemata could explicitly be considered to
represent a more continuous variable, such
that some individuals may possess schemata
that are “strongly” depressogenic, whereas
others may possess only “weak” or mild
depressive schemata, then a more continuous
diathesis-stress model may not only be appli-
cable to depression, but may also suggest
refinement of key elements of the theory that
were not previously considered.
Threshold Models
Some models suggest that the synergism
between the diathesis and stress yields an
effect beyond their combined separate effects
(Monroe & Simons, 1991; Rothman, 1976).
Moreover, complex diathesis-stress models
that represent additive and interactional rela-
tionships between variables, as well as
threshold effects for the diathesis, have also
been proposed (Monroe & Simons). These
ideas can be illustrated by what we would
term a threshold model.
To illustrate a threshold model, consider
the integrative model of schizophrenia
proposed by Zubin and Spring (1977).
Zubin and Spring suggest that every person
has a degree of vulnerability that represents a
threshold for the development of schizophre-
nia. At the most basic level, this model sug-
gests that as the intensity of the trauma
(stressor) increases, so too do the risks for
psychopathology. The diathetic threshold is
the point at which the people who fall below
the threshold will not develop the disorder,
whereas those above this level cross the
threshold into disorder (see Bebbington,
1987; Monroe & Simons, 1991). Thus, the
threshold for triggering schizophrenia may
vary from one person to the next depending
on the degree of vulnerability and the level of
stress experienced. For a person who is
highly vulnerable, relatively minor stressors
may cause the threshold to be crossed. On
the other hand, a major stressful event might
cause a similar reaction even for a person low
in vulnerability.
Risk-Resilience Continuum Models
Invulnerability, competence, protective
factors, and resilience are terms often used
to describe the opposite of vulnerability
(Ingram & Price, 2001). Resilience can be
thought of as factors that make a person
resistant to the deleterious effects of stres-
sors. Examples of resilience features could
include particular personality traits, social
skills, and coping responses. Resilience and
vulnerability represent, therefore, opposite
ends of a vulnerability continuum, although
models typically do not specify if resilience
simply reflects the lack of vulnerability
OVERVIEW AND FOUNDATIONS40
02-Hankin.qxd 2/24/2005 12:20 PM Page 40
factors or instead encompasses specific
factors that confer resilience.
As in other models, the diathesis contin-
uum interacts with a continuum of stress to
produce the possibility that a disordered state
will occur. At the most extreme vulnerability
end of the spectrum, little life stress is neces-
sary to trigger disorder. At the resilient end,
however, a great deal of stress is needed before
psychopathology develops. A vulnerability-
resilience relationship is presented in Figure
2.3. As this figure illustrates, with decreasing
resilience, and hence increasing vulnerability,
the probability that stress will result in a dis-
order increases. Conversely, when resilience
increases, the risk of disorder goes down but
does not vanish entirely. That is, resilience
may be the opposite of vulnerability, suggest-
ing a resistance to disorder but not immunity
from it entirely (Ingram et al., 1998). Of
course, although not specified by most mod-
els, the idea of resilience can easily be incor-
porated into diathesis-stress interactions.
Like a threshold model, a risk-resilience
model also notes a threshold at which a
particular disorder will be encountered.
However, this model can also take into
account the severity of psychopathology that
is experienced. Hence, even the most resilient
people can be at risk for developing significant
symptomatology with enough stress, although
the symptomatology will likely be less severe
than that experienced by individuals who
experience stress and who are vulnerable. On
the other hand, highly vulnerable people who
encounter significant stress are proposed to
experience a more severely disordered state.
This model therefore takes into account not
only the continuum of vulnerability, ranging
from vulnerable to resilient, but also a contin-
uum of disorder severity.
SOME ISSUES FOR CONSIDERATION
IN DIATHESIS-STRESS MODELS
While maintaining the same basic structure,
the models we have described reflect the
different approaches that investigators have
taken to understanding psychopathology.
Beyond these basic models, there are, however,
a number of issues that need to be considered
as efforts continue to more fully understand
how diatheses and stress interact to produce
psychopathology. Although artificial in some
respects, for discussion purposes we divide
these into diathesis issues and stress issues.
Diathesis Issues in Diathesis-
Stress Models: Single Versus
Multiple Diatheses Factors
For models suggesting genetic diatheses,
evidence of the polygenic aspect of psy-
chopathological disorders suggests a combina-
tion of genes that may be required for
disorder. Thus, individuals inheriting any par-
ticular gene defect will be normal if they do
not possess the other gene defects needed to
produce a disorder such as schizophrenia. Of
course, genetic diatheses are not the only
approach to understanding psychopathology.
Hence, models featuring psychosocial factors
may also need to highlight more than one dia-
thetic factor. For example, an interpersonal
and cognitive model of depression (Gotlib &
Hammen, 1992) extended to vulnerability
would need to specify the multiple diathesis
factors that fall into their respective cognitive
and interpersonal categories, and the link
Vulnerability-Stress Models 41
Vulnerability
Continuum
Extreme
Stress
Low
Vulnerable Resilient
Threshold
Mild
Disorder
Mild
Disorder
Severe
Figure 2.3 The Vulnerability-Resilience
Model
02-Hankin.qxd 2/24/2005 12:20 PM Page 41
between them, to provide a more complete
model. Likewise, models that highlight biolog-
ical and psychological factors (e.g., Goodman
& Gotlib, 1999) would also need to specify
the link between various processes and how
they would work in concert to produce the
disorder when life stress is encountered.
Development and Stress Issues
in Diathesis-Stress Models
The nature of the diathesis-stress interaction
described in various models is often ambiguous
(Monroe & Hadjiyannakis, 2002). As we have
noted in our description of schema models of
depression, diatheses are often portrayed as
discontinuous and categorical (people either
have a given diathesis or they do not).
Alternatively, stress is frequently portrayed
as nonspecific and continuous, varying only
in degree but not in type. However, diatheses
can often become continuous once a certain
threshold has been reached. Moreover,
because diatheses and stress are rarely com-
pletely independent of each other, the inter-
actions between the diathesis and stress can
be quite complex (Monroe & Simons, 1991).
Early formulations of the diathesis-stress
model were based on biological factors (e.g.,
Meehl, 1962) that inferred temporal prece-
dence and assumed that the diathesis was
inactive in the developmental scheme of
things. Thus, the interpretation of a signifi-
cant interaction seemed relatively clear-cut:
Stress activated the diathesis, which in turn
brought about the onset of disorder. This
interpretation suggests that until the diathe-
sis is activated by stress, the diathesis is
inconsequential. The complementary influ-
ence of the diathesis on stress was typically
disregarded in these early models (Monroe
& Simons, 1991).
The influence of diatheses on stress also
received little attention in early formulations
of this relationship, but there are several
ways in which the constructs may not be as
independent as they seem at first glance. For
example, it may be that likelihood of incurring
a stressor increases with the loading of the
diathesis. To the extent that the diathesis
influences the incidence of the requisite forms
of stress, the more likely it is that highly
predisposed people will develop a disorder.
For a young person in the early stages of
schizophrenia onset, for example, abnormal
or socially withdrawn behavior that results
from diathesis may create tension in the
young person’s interpersonal life at home
and at school. The additional interpersonal
stress, which is directly influenced by the
diathesis, may exacerbate stress and subse-
quently increase the likelihood of the onset of
full-blown schizophrenia.
This idea is similar to proposals regarding
stress generation. As we have previously
noted, stress is typically seen as operating
externally to the individual, although it does
appear that at least some people may also play
a part in creating the stressful environment
that acts to trigger pathology. That is, the
diathesis may influence the manner in which a
person deals with life and thus the nature of
the stressors to which he or she is exposed.
Indeed, a number of researchers have argued
that many stressors may constitute the results
of one’s own actions (Depue & Monroe,
1986; Hammen, 1991, 1992; Monroe &
Simons, 1991; Rutter, 1986). For example,
people who have doubts about their self-
worth may seek reassurance in an effort to
counter these doubts (Luxton & Wenzlaff, in
press), but repeated efforts may result in rejec-
tion from others, therefore precipitating a
depressive disorder. Beyond the exacerbation
of stress that may occur as the result of the
emergent activation of diatheses, vulnerable
individuals may thus play a role in creating
their own stresses, which may then activate
the diatheses and precipitate disorder.
Some models have proposed that the vul-
nerability factor itself affects the perception
of stress (e.g., Zubin & Spring, 1977), sug-
gesting that stress is not independent from
vulnerability. In this sense, the vulnerability
OVERVIEW AND FOUNDATIONS42
02-Hankin.qxd 2/24/2005 12:20 PM Page 42
does not “cause” the stress in this case, but
rather the vulnerability is part of the stress.
In other cases, stress may affect the devel-
opment of the diathesis. For example, there
is evidence to suggest that stress may play a
role in the etiology of schizophrenia as early
as the prenatal period, when the fetus is
exposed to a possible range of developmen-
tal insults that in turn produces the diathe-
sis (Brennan & Walker, 2001). In depression
theory and research, the “scar” hypothesis
(Rohde, Lewinsohn, & Seeley, 1990) sug-
gests that a first episode of depression may
leave cognitive scars in the form of negative
thinking patterns that may not have been
previously present. If such scars subse-
quently serve as a diathesis for additional
episodes of depression, then this may be
understood as a stress-induced diathesis.
Not only may a disorder be the result of
both diathesis and stress, but the diatheses
may precipitate stress that combines with
stress not related to the diatheses (Monroe &
Simons, 1991). For example, “external” stres-
sors (e.g., a death in the family, alcoholic
parent, socioeconomic strife) may or may not
be substantial enough to trigger the disorder.
However, if the diathesis plays a direct role in
creating “other” kinds of stress by, for
example, increasing tension in the person’s
interpersonal life, the combined state of affairs
may subsequently increase the likelihood of
the onset of a full-blown disorder.
Typically, diathesis-stress models refer to
stressful events that are proximal to the onset
of disorder. However, it should be noted that
stressors earlier in life may also influence how
later stressful events are responded to and
thus increase future susceptibility to disorder.
For example, maladaptive methods of coping
with stress in childhood and throughout
development may be detrimental to the devel-
opment of effective coping competencies;
lacking effective coping skills, in turn, can
compromise resilience and encourage vul-
nerability (Hammen, 1992). Thus, maladap-
tive cognitions about the self and others
and ineffective coping competencies may
contribute to the occurrence of stressful
events and circumstances—and these in turn
may trigger depressive reactions.
SUMMARY AND CONCLUSIONS
Individually, vulnerability and stress are
important concepts, but their real power lies
in their interaction. Diathesis-stress models
thus describe the interactions between these
constructs and are useful for understanding
the development of psychopathology. In this
chapter, we described some basic principles
that characterize diatheses-stress models, such
as the idea that models tend to be additive and
ipsative. We also noted that mega diathesis-
stress models are also possible, although
uncommon, and emphasized the importance
of considering varying relationships between
diatheses and stress over time. We also
described the interactive model with dichoto-
mous diatheses approach to diathesis-stress
conceptualizations, the quasi-continuous
diathesis model, threshold models, and risk-
resilience continuum models. In describing
these different models, however, we also
noted that these models tend to vary not in
basic structure but rater in the emphasis that
different investigators give to different com-
ponents. Finally, within the context of diathe-
sis-stress interactions, we noted some
outstanding issues that reflect on conceptual-
izations of diatheses and conceptualizations
of stress.
The development of psychopathology is
obviously complex and involves numerous
vulnerability factors and interactions between
those factors and stress. Diathesis-stress mod-
els are excellent heuristic devices (Monroe &
Simons, 1991) that enable us to potentially
understand how predispositional factors from
various domains may increase susceptibility
to psychopathology and subsequently create
the sufficient conditions for the onset of
disorder. Furthermore, diathesis-stress models
Vulnerability-Stress Models 43
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OVERVIEW AND FOUNDATIONS44
help describe how diatheses and stressors can
be better conceptualized and more precisely
measured empirically with respect to specific
forms of psychopathology. Such models are
necessary if psychopathologists ever hope to
be able to understand the multifactoral
complexity of psychopathology, including
developmental experiences, biological vulnera-
bilities, psychological susceptibilities, and
socioenvironmental variables.
NOTE
1. Because possessing vulnerability places one at higher risk for developing a
disorder, vulnerability is probably most accurately seen as a subcategory of risk.
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