Psychological Bulletin |
© 1991 by the American
Psychological Association |
November 1991 Vol. 110, No. 3, 406-425 |
For personal use only--not
for distribution. |
Scott M. Monroe
Department of Psychology University of Oregon
Anne D. Simons
Department of Psychology University of Oregon
ABSTRACT
Advances in the conceptualization and measurement of life stress in the past 2
decades raise several questions concerning traditional diathesis—stress
theories of psychopathology. First, comprehensive measures of life stress force
investigators to become more precise about the particular stressful
circumstances hypothesized to interact with diatheses. Second, the influence of
the diathesis on a person's life is typically ignored, which results in several
types of possible bias in the assessment of life stress. Finally, information
is available on diatheses and stress for specific disorders to provide a
foundation for more empirically based hypotheses about diathesis—stress
interactions. This possibility is outlined for depression. Such an approach
provides the basis for developing broader, yet more specific, frameworks for
investigating diathesis—stress theories of psychopathology in general and of
depression in particular.
This work was supported in part by National Institute of Mental Health Research
Grants MH39139 (to Scott M. Monroe) and MH41884(to Anne D. Simons).
We wish to thank George Brown, Sheldon Cohen, Tirril Harris, Joel Greenhouse,
Peter Lewinsohn, John McQuaid, Michael Pogue-Geile, John Roberts, and anonymous
reviewers for very helpful comments on drafts of the article or discussion of
the ideas involved.
Correspondence may be addressed to Scott M. Monroe, Department of Psychology,
University of Oregon, Eugene, Oregon, 97403-1227.
Received: January 18, 1990
Revised: February 28, 1991
Accepted: April 30, 1991
In attempting to understand
the antecedents of psychopathology, theorists historically have sought
explanations from two spheres. On the one hand, the belief has long been held
that people who develop a psychiatric disorder differ premorbidly from those
who do not. Such differences were thought to be constitutional in origin. Well
over 100 years ago, for example, the terminology of a diathesis for mental
disease was quite active in the psychiatric vocabulary (e.g., Beard, 1881 ).
1 On the other hand, the belief also has long
been held that stress is an important factor in the development of
psychological disturbances ( Hawkes, 1857 ;
Hinkle, 1977 ; Rees, 1976 ;
Rosen, 1959 ). Yet, it has been recognized that not all
people, even when exposed to the most dire of environmental conditions,
necessarily break down ( B. P. Dohrenwend & Dohrenwend,
1979 ; Grinker & Spiegel, 1963 ). Among the first to bring these two spheres
together in a more unified fashion ( Meehl, 1962 )
and to develop the specific terminology of diathesis—stress interactions ( Bleuler, 1963 ;
Rosenthal, 1963 ) were theories of schizophrenia proposed
during the 1960s. Most recently, theories of depression have explicitly adopted
such models (e.g., Abramson, Metalsky, & Alloy,
1989 ; Bebbington, 1987 ; Beck, 1987 ; McGuffin, Katz, & Bebbington, 1988 ; Robins & Block, 1989 ). The basic premise is that stress activates a diathesis, transforming
the potential of predisposition into the presence of psychopathology.
Recent efforts to
incorporate diathesis—stress premises in theories of depression appear
promising. However, invoking new domains of predisposition other than
constitutional (e.g., cognitive or social vulnerability) and applying them to
other forms of psychopathology (e.g., depression) require a reevaluation of
several premises involving diathesis—stress interactions. Three topics
consequently constitute the foci of the present article. First, over the past
20 years, the conceptualization and measurement of life stress have become more
detailed and sophisticated. Definitions and operational procedures adopted by
different investigators vary in terms of the qualities and dimensions of
experience that are included, the importance assigned to these qualities and
dimensions, and the manner in which these different components of stress are
combined. Ironically, depending on how these advances are used, they may
obscure rather than reveal the nature of specific diathesis—stress interactions
for particular disorders.
The second topic concerns
the diathesis and its implications for stress. As noted previously, early
formulations of the diathesis—stress model were predicated on biological
factors (e.g., Beard, 1881 ; Meehl, 1962 ).
Owing to the inferred temporal precedence and assumed quiescent nature of the
diathesis in the developmental scheme, the interpretation of a significant
interaction seemed straightforward: Stress activated the diathesis, which in
turn brought about onset of disorder. The complementary influence, that of the
diathesis on stress, was typically ignored. The recent incarnations of the diathesis—stress
model for depression have suggested that other domains of predisposition can be
conceptualized as a diathesis (e.g., cognitive or social factors; Abramson et al., 1989 ; Alloy, Hartlage, & Abramson, 1988 ; Bebbington, 1987 ; Beck, 1987 ; Brown & Harris, 1978 ; Perris, 1987 ; Robins & Block, 1989 ). Such possibilities stimulate important questions about the
diathesis's potential effects on stress. For instance, there are cogent reasons
to suspect that diatheses influence the reporting and the generation of life
stress.
The third section of the
article builds on these insights deduced from examining diathesis—stress models
from the perspective of life stress theory and research. We outline several
considerations for understanding diathesis—stress interactions. For example,
the types of stressors and diatheses, the prevalence of these factors in the general
population, and other characteristics of these constructs require elaboration.
Instead of general, nonspecific interactive principles, more empirically based
hypotheses about diathesis—stress interactions can be developed for specific
disorders. In particular, we use information about the epidemiology of
depression and of stress to outline interactive pathways through which people
may become depressed. This provides the basis for developing a broader, yet
more detailed, framework for understanding diathesis—stress interactions in
depression.
After each of these
sections we provide recommendations for theory and research specific to the
issues raised. We conclude the article with a general discussion of limitations
concerning stress and diathesis concepts separately, of models built on these
two concepts, and of the implications for theory and research that essays to
develop multifactorial models of psychopathology.
A person's life comprises
multifacted circumstances and dynamic processes. The basic task for stress
theory is to abstract the characteristics of the concept that lead to disorder
from the background turmoil of life's ongoing vicissitudes. Since the creative,
but understandably crude, initial efforts at quantifying life stress using life
event checklists ( Holmes & Rahe, 1967 ), a great deal of effort has gone
into comprehensively specifying the characteristics of life experiences that
are believed relevant for precipitating disorder ( Alloy et al., 1988 ; Brown & Harris, 1986 ; B. P. Dohrenwend, Krasnoff, Askenasy, & Dohrenwend, 1978 ; Katschnig, 1986 ; Lazarus & Folkman, 1984 ; Monroe & Roberts, 1990 ; Sarason, Johnson, & Siegel, 1978
). Much attention
also has been devoted to including forms of stress other than major life events,
such as chronic stressors ( Brown & Harris, 1978 , 1986 ; Pearlin, 1982 )
or daily hassles ( Kanner, Coyne, Schaefer, &
Lazarus, 1981 ; Lazarus & Folkman, 1984 ). Most investigators have availed themselves
of such advances in theory and method. For example, a recent extensive
discussion of issues involving diathesis—stress research suggests "an
adequate test of these theories would require as comprehensive or
exhaustive an assessment as possible of potential stressors" ( Alloy et al., 1988 , p. 49).
A comprehensive approach to
measuring stress appears both thorough and rigorous. Such approaches, though,
may lead to unintended problems as well. Whereas many of life's circumstances
may be deemed stressful in one way or another, not all of these uncomfortable
conditions necessarily lead to the development of pathology. The central
question is whether all forms of life stress are important for activating a
diathesis and precipitating disorder. What has not been appreciated is that a
comprehensive measurement approach to stress may lead to confusion about the
particular diathesis—stress model held by the investigator. Within the current
literature, four aspects of life stress are useful for illustrating this
potential problem: (a) temporal factors (e.g., acute vs. chronic stressors),
(b) dimensional issues (e.g., major vs. minor stressors), (c) qualitative
characteristics (e.g., desirable vs. undesirable stressors), and (d) the rules
for combining temporal, dimensional, and qualitative aspects of life stress ( Elliot & Eisdorfer, 1982 ).
Qualities
of Life Stress
Not all life experiences
lead to disorder. Although the founding fathers of life event research
conceptualized increased "readjustment" as the feature responsible
for promoting nonspecific vulnerability to virtually any form of illness,
recent research indicates that more specific qualities of life experiences are
of particular importance for bringing about illness in general, or specific
forms of illness ( Brown & Harris, 1986 ; Monroe & Peterman, 1988 ). Not only is the magnitude of events
critical, but so may be the particular qualities of events. For example, severe
major events that signify loss or exits from one's social field have been found
to predict the onset of depression, whereas events that signify danger (but not
loss) have been reported to precede episodes of anxiety disorders ( Finlay-Jones & Brown, 1981 ; Paykel, 1982 ).
Even within experiences
designated as major and undesirable, then, only a subset are likely to be
relevant for vulnerability to a particular form of disorder. The importance of
these distinctions becomes clear when examining the manner in which the
different components of stress can be united in the operational scheme. For
example, cognitive theories of depression single out affiliative and
achievement events as being most theoretically relevant ( Abramson et al., 1989 ; Beck, 1987 ; Hammen, Ellicott, Gitlin, & Jaimison, 1989 ; Robins & Block, 1988 ). However, the frequency of major types of these events (i.e., severe
interpersonal losses or achievement failures; see Hammen et al., 1989 ) is relatively low compared with the other types of events (e.g., more
minor interpersonal or achievement events, or other types of events; Brown & Harris, 1986 ), and even lower compared with the other facets of stress (e.g., chronic
stressors or daily hassles). Consequently, if one were to aggregate all forms
of stress, or to aggregate major, minor, and chronic forms of interpersonal (or
achievement) stress, the importance of the major events would be obscured by
the more common components of stress.
The general concern is that
as thinking on stress becomes more differentiated and intricate, the
implications for diathesi—stress theories must be thought through in consonant
ways. In place of generic stress concepts and measures, more specific forms and
qualities of the construct should be evaluated. Whereas recent discussions
commendably focus on properties of stress that are consonant with specific
theory (e.g., Abramson et al., 1989 ), such discussions tend to overlook
more general issues involving properties of stress that transcend the
particular theory involved. As we illustrate next, specific forms and qualities
of stress also have important implications for clarifying how stress might
interact with diatheses to produce disorder.
Temporal
Characteristics of Stress
Time is another dimension
along which life stressors can be conceptualized. Some experiences are
relatively acute, circumscribed events that occur at a particular point (e.g.,
deaths, job loss). Others are more chronic or intermittent and defy precise
temporal specification (e.g., chronic financial or marital difficulties). Most
important, acute and chronic stressors might play different roles in relation to
diatheses and the etiology of the disorder.
For acute major events, it
is relatively clear why the diathesis is activated and the disorder develops at
a particular point (i.e., the event accounts for both the diathesis activation
and the timing of disorder onset). For chronic stressors, however, this issue
is more problematic: Why, at one particular time, does the diathesis activate
and the person succumb? Instead of acute breaking effects of stress, there may
be a more gradual, chronic attrition that eventually brings about disorder. One
implication of a chronic stress model, then, is that additional components are
necessary to account for the timing of breakdown. Another implication parallels
the temporal characteristics of the particular disorder under study. For
example, chronic forms of adversity may be of particular relevance for chronic
forms of disorder (e.g., dysthymia; Brown, Bifulco, Harris, & Bridge, 1986 ), or for disorders with a prolonged
developmental course (e.g., coronary heart disease; Monroe, 1989 ;
Neilson, Brown, & Marmot, 1989 ).
By virtue of being
parsimonious, the acute major event model may be implicit in many views of
diathesis—stress interactions. Yet the issue of the type of stress involved
remains an empirical question. Most discussions of diathesis—stress theories,
though, are simply unclear with respect to the implications of these
distinctions between types of stress for disorder onset ( Abramson et al., 1989 ; Alloy et al., 1988 ; Hammen, 1988 ;
Robins & Block, 1989 ). Lack of theoretical attention to
such differences in the nature of stress leads to imprecision in the assessment
of acute and chronic stressors (see below, Perspectives on Perspectives of
Stress Measurement section). At least at the present stage of knowledge, these
different types of adversity should not be indiscriminately merged.
Major
and Minor Dimensions of Events
Another aspect of life
stress currently attracting interest is major versus minor events ( B. P. Dowhrenwend & Shrout, 1985 ; B. S. Dohrenwend, Dohrenwend, Dodson, & Shrout, 1984 ; Kanner et al., 1981 ; Lazarus, 1990 ; Monroe, 1983 ).
The latter forms of stress, often referred to as daily hassles, have a high
frequency of occurrence as compared with major events and have been found to
predict a variety of psychological and physical health outcomes. Some
investigators suggest that these forms of stress are better indexes of
vulnerability than major life events ( Kanner et al., 1981 ; Lazarus, 1990 ).
Many of the minor events
included in existing inventories reflect experiences that also tend to be
intermittent or chronic. Although these events can be characterized as
low-level intensity, they often represent consistently recurrent problems
(e.g., ongoing financial problems) or background chronic conditions (e.g., job
dissatisfactions). Again, the issue is raised of how these fit into the
operational approach adopted and into the stress model of the process involved.
For instance, if hassles are recurrent and chronic (as the test—retest
correlations strongly suggest; see Kanner et al., 1981 ; Monroe, 1983 ), the timing of onset is again an
issue. Both by definition and recent evidence, daily hassles are a common and
recurring component of everyday life. Why at any one point in time might they
activate the diathesis as opposed to any other point in time?
In parallel with the
previous discussion involving chronic and acute forms of stress, the minor
dimensions of life stress appear to be at variance with the implicit major
acute event model of stress. Furthermore, there are many challenging
considerations involving the measurement of daily hassles, particularly when
studied in relation to psychological disturbances (see below; also Brown, 1990 ;
B. P. Dohrenwend & Shrout, 1985 ; B. S. Dohrenwend et al., 1984 ; Lazarus, 1990 ;
Monroe, 1983 ). Again, merging such stressors with other
types of stress may result in an insensitive or misleading operational scheme.
Summary:
The Conceptualization of Life Stress
The essence of the
foregoing discussion is how different facets of life stress should be
integrated or differentiated in theory with respect to disorder. In summarizing
this issue, we address two major considerations. First is a question of
additivity: Do diverse dimensions and qualities of stressful life experiences
summate in their impact? Second is a more complex issue pertaining to the
association between different forms or qualities of stress over time in the
production of disorder: Do different dimensions or qualities of stress interact
in ways to increase overall vulnerability?
The issue of additivity
traditionally has been restricted to whether disparate types of events are
cumulative in their effects or whether any specific subsets of events are
significant for disorder. With the inclusion of new dimensions and severities
in more recent formulations of stress, this topic may be expanded from totals
of major life events to totals of diverse major events, chronic difficulties,
and minor stressors. Using the additive approach, people can attain comparable
stress scores through exposure to very different psychosocial circumstances.
For example, someone experiencing a variety of minor annoyances can be equated
in a summary additive operational scheme with a person experiencing one major,
devastating experience. Furthermore, in a probabilistic sense, the minor events
and chronic stressor–so frequent and prevalent–typically account for the
majority of the variance in any person's stress score (as noted before, the
major life events occur relatively infrequently; Brown & Harris, 1986 ; Depue & Monroe, 1986 ; Miller et al., 1986 ). Thus, it would seem unwise at the present state of knowledge to equate
people reporting many minor difficulties with those reporting but one major
life crisis.
The question of
interactions between types of stress raises relatively novel questions. It
suggests that particular combinations of different stressors may prove especially
noxious, above and beyond their independent additive effects. For instance, an
increased frequency of minor hassles in the presence of a major life event
might produce especially high risk. Alternatively, major life events that
"match" severe chronic stressors have been found to be particularly
likely to bring about depression (i.e., acute events that arise from or have
direct implications for an ongoing difficulty; see Brown & Harris, 1989 ). Interestingly, such possible interactions among stressors indicate
ways in which these factors impact over time in the development of disorder.
For example, daily hassles in the context of major acute stress may represent
one mechanism through which extreme stress impacts on a daily basis (cf. Monroe, 1983 ).
Or major events that match a preexisting, ongoing difficulty may be
particularly powerful in producing a hopeless cognitive set ( Abramson et al., 1989 ; Brown & Harris, 1986 ). These expanded models of stress
effects, too, require evaluation within diathesis—stress formulations.
Ultimately such questions
must be anchored within theory for specific disorders. It is unlikely that
stress or different components of stress possess uniform consequences across
different psychobiologic mechanisms and different forms of disorder ( Depue & Monroe, 1986 ). Thus, different forms of stress may eventually prove to be important
for the development of a particular disorder, or for different forms of
disorder. This appears particularly true for depression. For example, Brown and Harris (1986) have shown that severe types of events involving loss are highly
associated with risk for this disorder. In contrast, these investigators have not
found that other types of major life events, or any types of minor life events,
contribute to the likelihood of depression. At least for clinical forms of
depression, many types of stress may not be etiologically relevant. (This is a
point of considerable importance to which we return.) Overall, in light of
these studies, one can conclude that conceptual approaches insensitive to
distinguishing these different forms and qualities of stress, and insensitive
to the interrelations between these forms of stress in creating vulnerability,
will most likely provide diluted and weak tests of diathesis—stress theories.
Conclusions
and Recommendations
Recent conceptualizations
of stress proposed for research on the diathesis—stress theories tend to be
vague about the nature of stress involved and the types of interactions between
stressful circumstances that may be of particular importance in creating
vulnerability. Some types of stress represent relatively major events
circumscribed in time. Other types of stress represent minor hassles, and still
others represent chronic problems. If the stress score is a composite of all of
these, it is difficult to pull apart the essential elements. This is especially
problematic, in that the majority of items that will be endorsed repeatedly
over time are likely to be the chronic and minor events. These facets of stress
obscure the types of experiences on which the diathesis—stress theory most
parsimoniously rests: the major events or large-scale adverse changes in one's
life circumstances.
It could be contended that
(a) recent conceptualizations of stress do not preclude a subsequent, more
fine-grained analysis or (b) diverse forms of stress many be relevant for
depression onset. Although these points have merit, we believe that they miss a
central concern. Namely, the conceptualization of stress–its dimensions and
qualities–should guide the definition of the construct and consequent
measurement practices. The nature of the particular stressors, and the role
that they play with other forms of stress, requires greater theoretical
emphasis in relation to specific diatheses as one enters into the empirical
arena. Existing research on life stress has not attended to these distinctions
in dimensions of stress. For instance, recent studies and reviews do not
distinguish adequately among types of stress at a conceptual level (e.g., Barnett & Gotlib, 1990 ; Holahan & Moos, 1990 ; Neitzl & Harris, 1990 ; Smith, Smoll, & Ptacek, 1990 ), and virtually all such research
has not attended to critical measurement issues for adequately defining and
distinguishing between different forms of stress (e.g., Lazarus, 1990 ;
Needles & Abramson, 1990 ; Smith et al., 1990 ; see below, Perspectives on Perspectives of Stress Measurement
section).
Overall, a comprehensive
conceptualization of stress can lead to a vague definition of the construct,
which lacks the requisite theoretical specificity for powerful prediction. The
propensity to experience the syndrome of depression may have evolved as a
response to relatively specific forms of adversity and privation, not as a
response to a haphazard assemblage of abrasive and annoying circumstances.
Activation of the diathesis, then, may be confined to certain classes of major,
biologically meaningful, stimuli or chronic conditions. For other forms of
disorder and the respective mechanisms involved, similar specificities of
environmental demands are likely to be of importance. Careful attention is
required to avoid diluting the stress construct by overinclusion of intuitively
appealing, yet theoretically disjointed, aspects of life stress.
Without evidence to the
contrary, to assume that a diathesis is entirely latent before its activation
would be shortsighted. Indeed, a diathesis may influence (a) the measurement of
life stress or (b) the generation of life stress. Before addressing these
specific concerns, preliminary discussion of assessment and measurement issues
in life stress research is required. This lays the groundwork for understanding
particular problems concerning diathesis—stress theories when viewed in the
context of contemporary life stress research.
Perspectives
on Perspectives on Stress Assessment
A fundamental issue in the
assessment of life stress is the reference point for defining what qualifies as
stressful. One viewpoint is that the individual (i.e., the subject or
respondent) is the person most qualified to define which circumstances are
stressful, and to indicate to what degree they are stressful, in his or her own
life. The rationale is that such information is available only to the particular
person who experiences the specific life circumstances and that he or she is
therefore the best arbiter for such determinations. For convenience and
consistency with previous discussions, we term this system of assessment as respondent
based ( Brown, 1981 ). It is the most common approach
currently used in the literature.
The alternative viewpoint
is that although the individual has the best access to information pertaining
to his or her life, other considerations render the use of the individual's
definitions and assessments scientifically problematic. First, the person's
perceptions of stress can commonly result from psychopathology. The presence of
depression virtually, by definition, ensures that the person perceives stress
(because depression goes hand in hand with a view of the world as full of
obstacles and unsolvable problems; Beck, 1967 ).
Thus, when a person is asked to report on the stress in his or her life, the
independent (i.e., stress) and dependent (i.e., depression) variables are too
easily fused ( Brown, 1974 ; Monroe & Peterman, 1988 ).
Second, irrespective of
potential confounding with depression, respondent-based procedures result in
considerable variability in the types of experiences included within ostensibly
homogeneous life event categories ( B. P. Dohrenwend, Link, Kern, Shrout, & Markowitz, 1987 ). For example, two people with very
different external circumstances could endorse "serious illness in a close
family member." For a particularly worrisome person, the response could
reflect a child's one-day bout with the flu; for another, the response may
reflect a spouse's recent heart attack. Because the perception is the basis for
the measurement, the stress score could be identical for the two people,
despite dramatically different environmental bases. In fact, the person's
interpretation of an item may be so at variance with that intended by the
investigator that the person altogether misses the essence of the question
(e.g., a woman whose husband had a heart attack 4 months previously may skip
the item, because at the time of the stress assessment he had recovered well
and was doing fine and in her view it was therefore not serious). The result is
that considerable discrepancies arise between what the respondent labels as an
event and what a more objective, or investigator-based, view would
define as an event ( Brown, 1981 ). In other words, the stress
measurement contains considerable variability because of idiosyncratic
interpretations by respondents. Recent research bears out the empirical reality
and high degree of distortion resulting from this fundamental measurement
concern ( B. P. Dohrenwend et al., 1987 ).
This issue is analogous to
problems noted previously in regard to classifying depression by self-report
methods (see Depue & Monroe, 1978a ). Self-report checklists reflect a
limited range of information on the experiences involved and on the
biographical circumstances brought to bear in making informed decisions.
Subjects reporting on their lives do not have the overall perspective of the
investigator in understanding the meaning and evaluating the applicability of
the alternative items for endorsement. They thereby bring to the assessment
situation a variety of idiosyncratic views that are often at variance with
those of the investigator. Diagnostic practices in psychopathology research
have taken firm steps toward increased standardization though the development
of clear-cut guidelines and operational criteria used by diagnosticians trained
in their use. The assessment of life stress should adopt comparable procedures
to standardize definitions and to enhance measurement reliability.
Most important for the
present discussion, when theory becomes more differentiated with respect to
types of stress, these measurement concerns are magnified. Comprehensive
approaches to assessing life stress may outstrip the available operational
technologies. When different forms of stress are involved, the investigator
must ensure reliable differentiation of the respective components. The
procedures used to define and operationalize the different forms of stress must
be quite explicit about the rules and criteria used to distinguish between
them. For instance, what is deemed major or minor, acute or chronic, clearly
cannot be left to the respondent (for the errors noted above may only be
compounded) and must be confronted in a direct, elaborate manner. At what point
do events that happen more than once become ongoing difficulties (e.g., a
serious marital argument every day, week, month, or year)? How are events that
happen within the context of an ongoing difficulty distinguished and defined
(as opposed to being simply part of the difficulty)? What are the threshold
determinants that separate major events, minor events, intermittent events, and
chronic difficulties? Extensive rules and explicit guidelines about he time
frame involved, frequency of the event, and severity of the circumstances are
required to provide an adequate system of measurement. 2
Overall, this means that the
investigator using respondent-based procedures has lost control over the
specification of component features of the diathesis—stress model: The stress
score represents an uninterpretable blend of the inputs from two correlated but
different theoretical domains (i.e., subjective perception and environmental
circumstances). In a similar manner, control over specifying the component
types of stress is also lost: The stress score represents an unknown blend of
different types of stress. Yet, there are two other major reasons why
measurement issues require greater attention in diathesis—stress research.
These are addressed next.
The
Measurement of Life Stress: Potential Diathetic Biases
Most diathesis—stress
theories assume that until stress activates the diathesis, the predisposition
is essentially inconsequential. This assumption requires critical scrutiny. For
example, the diathesis may influence the person's perception of daily life and
thereby his or her reporting of life stress. Such concerns are easily illustrated
with a cognitive diathesis (although the general argument is applicable to any
form of diathesis). People with a cognitive diathesis by definition view the
world through characteristically different perceptual filters. This point is an
extension of the previous one concerning the problems of respondent-based
(i.e., subjective) assessments of life stress yet raises a more perilous
concern. Individual differences in the reporting of life stress potentially are
directly influenced by the diathesis.
There is no assurance,
then, that the cognitive diathesis does not systematically influence the
perception of stress. This concern applies to three related levels of
measurement: (a) What experiences are recalled, (b) what experiences are
defined as stressful events, and finally (c) what stress level is associated
with the event. Specifically, if one possesses a cognitive vulnerability for
certain types of stressors, the person may recall experiences differentially,
possess a lower threshold for deeming relatively minor experiences as important
life events, and rate such events as possessing greater aversiveness. For
example, if a person is cognitively vulnerable to affiliative events, he or she
would be more likely to recall such encounters, to perceive minor encounters as
more major events, and to subjectively weight such encounters as more aversive.
At the extreme, very trivial events, fueled by a markedly potent diathesis,
could underlie the relationship to depression.
Portrayed more generally,
the situation is one in which two groups are defined on a priori grounds on the
basis of the presence or absence of the cognitive diathesis: a vulnerable group
and an invulnerable group. Comprehensive measures of life stress are taken and
compared. The vulnerable group reports higher stress, but largely because of
the elevation of more minor psychosocial conditions to major levels of personal
importance (or of inconsequential incidents to daily hassles status). The
so-called objective (or investigator-defined) environmental circumstances are
comparable for the two groups, but because of the diathetically driven
perceptual differences, the respondents' viewpoints of the conditions differ
markedly. Note that the differences between the two groups could be amplified further
if subjective weights of life events are used for the stress score. Such
double-dipping into the influences attributable to the cognitive predisposition
could dramatically inflate the perceived stress scores, without differences in
the actual stressful conditions faced by the two groups.
Overall, respondent-based
procedures possess serious limitations when investigating life stress within
diathesis—stress theories. One cannot ensure that the diathesis does not
essentially override the environmental input, to the point that external stress
is a minimized, if not meaningless, component of the model. Such confounding
may increase the likelihood of a statistical endorsement of the hypothesis
(i.e., the operational confounding of the diathesis and the stress score may
bias the design toward confirming significant interactions; see Cohen & Wills, 1985 ; Thoits, 1982 ). The measure of stress now
represents an unknown amalgam of (a) individual differences in idiosyncratic
perceptions (random error), (b) biased perceptions (systematic error), and (c)
external environmental circumstances.
Generation
of Life Stress: Potential Diathetic Influences
A diathesis could influence
a person's life stress assessment in ways other than simply producing
perceptually based differences in self-report data. A very large proportion of
life's stressors comprise experiences over which people have some degree of control.
Most people are, at least in part, the creators of the circumstances they
endure ( Monroe & Peterman, 1988 ; Rutter, 1986 ).
The possibility that a diathesis influences the manner in which the person
negotiates life's course, and consequently the nature of the stressors to which
he or she is exposed, raises penetrating questions for diathesis—stress
formulations of depression.
This point is again
illustrated most easily with respect to a cognitive diathesis. People have been
predicted to be differentially susceptible, depending on their particular
cognitive vulnerability to achievement or affiliation events. However, given
the hypothesized cognitive vulnerabilities to these types of experiences, it is
quite plausible that the person navigates a life course that promotes
differential exposure to the respective areas of vulnerability. For example,
someone with a high affiliative vulnerability may be especially sensitized to
interpersonal interactions in key relationships. Vigilant to possible signs of
impending rejection, he or she makes constant demands for assurance and
security. Relatively benign interpersonal exchanges may take on major personal
meaning; over time the behavior becomes increasingly cloying, and eventually
precipitates the very circumstances it was intended to avoid (i.e., rejection).
In terms of other forms of
predisposition, equally important examples place the concept of stress into a
more encompassing framework. For instance, people who develop major mood
disturbances often display a previous subsyndromal course of affective
symptomatology ( Akiskal, Djenderdejian, Rosenthal,
& Khani, 1977 ;
Depue et al., 1981 ; Klein, Depue, & Slater, 1985 ). The predisposition possesses biologic and
familial correlates ( Depue, Kleiman, Davis, Hutchinson,
& Krauss, 1985 ;
Depue et al., 1981 ; Klein et al., 1985 ). The behavioral manifestations of the predisposition include many of
the symptoms of depression and hypomania yet do not meet both the severity and
duration criteria to qualify as major episodes of affective disturbance.
Nonetheless, these features are sufficiently frequent and severe so as to cause
considerable turbulence in the interpersonal and employment spheres of the
person's life. For example, irritability, fatigue, lack of concentration, and
social withdrawal predispose the person to a myriad of interpersonal and
employment problems, potentially resulting in major events such as losses of
relationships or of one's occupational livelihood.
Within this example, stress
is not a random process, but rather part of a developmental sequence
systematically influenced by the diathesis. Whereas the construct of stress may
still play an important role in the evolving scheme, it is generated to a
considerable degree by the person's behavior, which in turn is likely to be
influenced by the diathesis. Essentially, this places the meaning of the
diathesis—stress interactions within a broader interpretive context and
requires supplementary information and procedures to understand the
implications of these interactions for the development of depression. (We
return to this topic below.)
Conclusions
and Recommendations
When stress scores are a
composite of an unknown mixture of individual differences in psychosocial
circumstances and in perceptual processes, little headway can be made within
the diathesis—stress model in understanding the importance of these two
contributing components. This problem is exacerbated when distinctive facets of
stress also are included in the model. Only when there is some standardization
of, or consensually derived agreement on, the definition of stress and the
distinctions between components of stress can the implications of individual
differences in perception be systematically investigated (see Brown & Harris, 1986 ; B. P. Dohrenwend et al., 1987 ; Miller et al., 1986 ).
A second tier of
uncertainty arises from the possibility that the diathesis influences the form
or frequency of stress that the individual experiences. This is a more subtle
problem that is still essential for understanding the developmental processes
through which depression emerges. Principles and procedures are being developed
to address this complex concern. For example, a risk group defined according to
some diathesis must be compared with controls before the emergence of
depression in terms of the frequency and severity of investigator-defined types
of events. If differences arise, then the model becomes more complex in
depicting the nature of these interactive processes over time. (We take this
issue up again, as well as possible solutions, in the final section of the
article.) It is clear, though, that this issue has been consistently overlooked
and that considerable work remains in understanding the pathways by which
diatheses may influence life stress.
Thus far our concern has
been with (a) the nature of stress implied by diathesis—stress models and (b)
the influence of a diathesis on stress. Theory may be more explicitly developed
and more finely adapted for particular forms of stress and may need to be
extended to accommodate how the diathesis influences diathesis—stress
interactions. As is shown next, when one moves from general models to more
specific models for particular disorders, there is information available to
refine these ideas further and to elaborate the hypothetical interactive
processes.
Despite the long-standing appeal
of diathesis—stress concepts, the manner in which diatheses and stressors
interact to produce disorder remains poorly specified. In the next sections, we
first address basic ambiguities in current diathesis—stress formulations. This
helps to establish the shortcomings of existing viewpoints and to show
concretely how characteristics of stressors and diatheses may be more directly
estimated. Next, we draw from existing research on depression to illustrate how
better information about diatheses and stressors can be acquired. Finally, we
outline the implications of this analysis for developing more detailed models
of diathesis—stress interactions for depression.
Assumptions
About Interactions, Diatheses, and Stressors
There are two levels of
ambiguity that cloud the issue of interaction in diathesis—stress theories. The
first level concerns common assumptions about the nature of the
diathesis—stress interaction. The second level is more fundamental, yet subtle.
It involves assumptions about the nature of the diatheses and stressors,
respectively, that underlie the interaction.
Assumptions
about interactions.
Although most discussions
of diathesis—stress models clearly indicate that both factors are important for
producing disorder, the unique importance of their combined impact typically is
not described. This leads to considerable ambiguity. For example, it is unclear
if such thinking implies (a) simple additivity (i.e., the degree of stress and
the loading of the diathesis summate, with virtually any complementary
combination of sufficient magnitude producing the disorder), (b) simple
interaction (i.e., a synergism between the diathesis and stress that yields an
effect beyond their combined separate effects; Rothman, 1976 );
or (c) complex interaction (i.e., various combinations of additivity and
synergism, such as postulating threshold effects for the diathesis).
This verbal vagueness can
be clarified algebraically. Assuming that the influence of stress (ST) is at
least partly conditional on the diathesis (DS) in relation to depression (DEP):
3
This general model is
illustrated in Figure 1 . The effects of stress are
dependent on the diathetic loading. Typical discussions of life stress and
diatheses, however, often imply only the additive portion of this model (i.e., b
3 = 0 ). The degree of diathetic loading can be offset or
compensated by the degree of stress (and vice versa). A simplified case,
wherein the diathesis is portrayed as dichotomous (i.e., high or low), is illustrated
in Figure 2 . People with an extreme diathetic loading
(Individuals x) require only minimal stress ( b x ) for
activation and a high probability of disorder onset ( a ). People with
low diathetic loading (Individuals y ) require more extreme levels of
stress ( b y ) for activation of the diathesis and a
comparable probability of depression onset ( a ). This interpretation
fails to distinguish between conditions under which the joint effects of the
two factors are additive versus synergistic (i.e., the joint effect exceeds the
sum of the separate effects; Rothman, 1976 ).
It does not use the diathesis—stress concept. This "titration"
interpretation of the model is compatible with earliest formulations of
"nervous diseases" (e.g., Whytt, 1765 ),
which was more recently promoted by Slater and Slater (1944) , and is congruent with many contemporary descriptions of
diathesis—stress theory ( Abramson et al., 1989 ; Davison & Neal, 1990 ; Zubin & Spring, 1977 ) and research ( Pollitt, 1972 ;
Stenstedt, 1952 ).
Even when the theory
embodies true interaction (i.e., b 3 ≠ 0 ), differing
assumptions about the diatheses and stressors influence the hypothesized form
of their interaction, which in turn leads to added ambiguity for the type of
model portrayed.
Assumptions
about diatheses and stressors.
Probably as a result of
early conceptualizations of the physiology of stress ( Selye, 1936 )
and of life event stress ( Holmes & Rahe, 1967 ), stress typically has been viewed
as nonspecific, varying only in degree (from low through high levels), and a
very common aspect of everyday life. This nonspecific conceptualization of the
construct is consonant with most early and many recent theoretical formulations
(e.g., Davison & Neale, 1990 ; Lazarus & Folkman, 1984 ; Slater & Slater, 1944 ; Zubin & Spring, 1977 ). Given such assumptions, stress
would not be a very discriminating factor in the diathesis—stress model (see Guze, 1989 ;
Heston, 1988 ).
In contrast, the diathesis
is often assumed to possess very different characteristics. First, some viewpoints
hold that a diathetic threshold exists: People who fall below the threshold
will not develop the disorder, whereas those above the threshold are vulnerable
( Bebbington, 1987 ). Second, the prevalence of above-threshold
diathetic loading is inferred to be relatively restricted in the general
population (i.e., it is believed to be present among a minority of people).
Overall, this characterization, too, is consonant with many discussions of diathesis—stress
premises ( Meehl, 1962 ; Slater & Slater, 1944 ; Zubin & Spring, 1977 ), with genetic models of liability
( Bebbington, 1987 ; Falconer, 1965 ; Slater & Cowie, 1971 ), and with many if not most current
views on biological diatheses for major psychiatric disorders (e.g., Guze, 1989 ;
Heston, 1988 ; Reich, Cloninger, & Guze, 1975 ; Whybrow, Akiskal, & McKinney, 1984 ). 4
If stress is continuous and
the diathesis is discontinuous, then more specific models of interaction are
indicated. The diathesis is a necessary, but alone insufficient, component of
the scheme. Stress is relevant only once above-threshold value of the diathesis
is met. This portrayal of the diathesis—stress interaction suggests at least
two additional models. 5
In the least complicated
case, the diathesis operates in an all-or-none manner: present or absent. The
values for b 2 in Equation 1 become
either 0 (diathesis absent) or 1 (diathesis present). This permits Equation 1 to
be rewritten in terms of these assumed values of the diathesis (DS):
The threshold effect,
however, specifies that stress is only operative conditional on the diathesis.
When the diathesis is absent, there is no main effect for stress. Thus, when
the diathesis is absent (DS = 0), b 1 in Equation 2 is
constrained to equal 0. Furthermore, given a pure interaction model (stress and
diathesis are only relevant when both are present), there are no main effects
(even when DS = 1, b 1 = b 2 = 0 ). Equation 2 then
becomes the following:
This is portrayed in Figure 3 .
Without the diathesis, disorder is not possible; with the diathesis, expression
of disorder is conditional on degree of stress. Viewing the interaction in this
manner is useful for raising a question concerning the assumed representation
of the diathesis: What proportion of the population is represented by the DS =
1 (diathesis present) condition?
The second possibility that
follows from assuming a threshold is more general. Instead of being
dichotomous, the diathesis is "quasi-continuous." There is a
threshold effect, but there is also a continuous effect of the diathesis once
the threshold is superseded. In terms of Equation 1 ,
this means that b 2 = 0 (diathesis absent) or b 2
≠ 0 (diathesis present). Rewriting Equation 1 :
Once again, imposing the
constraint following from the threshold effect that if DS = 0, b 1 =
0 and assuming pure interaction b 1 = b 2 =
0 :
Finally, because the
diathesis is continuous once the threshold is exceeded, the diathesis takes on
an infinite number of possible values. Consequently, there is an infinite
number of equations for each value of DS ≠ 0. Rewriting Equation 5 to
parallel Equation 3 and allowing DS = i ( i representing
the range of values for DS when DS ≠ 0):
A family of regression
lines describes the relationships between the diathesis and stress for
different levels of the diathesis. This is represented schematically in Figure 4 .
We can now expand on the question raised above with respect to the dichotomous
model about the proportion of the population with the diathesis (DS = 1) to
include the frequency of people possessing differing values of potency for the
diathesis (DS = i ).
Overall, the
diathesis—stress model comprises a family of possibilities that portray
different relationships between diatheses and stressors. By clarifying aspects
of the proposed diatheses and stressors, we confront important issues about
their characteristics in the population. First is the question of a threshold
and its distribution (i.e., who is vulnerable, who is not?). Second is the
question of the distribution of above-threshold loadings (i.e., who is highly
vulnerable, who is not?). Interpretations of interactions between diatheses and
stressors, though, differ depending on the particular disorder under study. For
example, the diathesis and stress for schizophrenia are almost undoubtedly
different from those for depression. The nature of the diathesis in the former
case is probably more restricted in the general population (and thereby may
represent the "rate-limiting" element in the predictive model). In
the latter case for depression, the prevalence of the diathesis may be more
common (and thereby less of a primary determinant of who develops the
disorder). For specific disorders, then, the characteristics of the particular
stressors and diatheses involved suggest how the interaction can be more
precisely conceptualized and systematically investigated.
Parameters
of Predisposition to Depression: Diatheses and Stressors
We may now ask whether
existing diathesis—stress theories fit with the available information
specifically for depression. Current evidence suggests not. Knowledge about the
incidence and prevalence of depression, as well as about the nature and
prevalence of the stressors, and diatheses found to predispose to this
disorder, delimits and more precisely specifies the range of alternative
interpretations of diathesis—stress interactions. The main purpose of this
section is to provide preliminary form to these ideas. First, with respect to
depression, sufficient information exists for developing more specific models.
Limited as current data may be, they provide an empirical foundation for
assumptions about diatheses, stressors, and their interactions. Second, we
again take up the concern that the diathesis may influence the nature or degree
of stress to which the person is exposed. This possibility enlarges the
interpretative scope for understanding diathesis—stress interactions.
Essentially, another layer of issues arises for developing working hypotheses,
research strategies, and prevention programs that are based on the nature of
the multiple interactions involved. It is of interest, then, to profile
implications that follow from each alternative position (i.e., stress and
diatheses are dependent or independent).
Before proceeding, we
should emphasize that clinical depression is commonly considered to comprise an
etiologically heterogeneous group of disturbances sharing common phenotypic
characteristics ( Depue & Monroe, 1978a , 1978b ). Any
discussion of the base rate of disorder (or diatheses) should be tempered by an
awareness that subgroup differences may alter the more general picture. For example,
the estimates for the prevalence of depression and their implications for
estimates of diatheses that we discuss next may be applicable to only a
subgroup of people currently classified as depressed. This would then modify
the particulars of our argument, whereas the logic of the analysis would remain
applicable to the designated subtypes. Despite over 60 years of published
debate on the topic, though, little consensus has been reached on the debate
between the unitary and nonunitary views of nonpsychotic unipolar depression ( Farmer & McGuffin, 1989 ; Kendell, 1976 ).
Given such controversy and lack of consistent agreement on proposed subtypes,
it seems prudent at present to develop the framework on the basis of the
general condition. From this initial reference point, modifications may be made
more readily in accord with research documenting the validity of particular
subtype distinctions.
Characterizing
the diathesis for depression.
A major question about the
diathesis for depression concerns its prevalence in the general population. Is
the susceptibility to becoming clinically depressed relatively confined to an
unfortunate few with strong diathetic loading, or is it more widely distributed
as part of the psychobiology of being human ( Monroe, 1990 )?
Unfortunately, the diatheses proposed for depression are insufficiently specified
and operationalized to confidently infer their distributions within the general
population. However, lower bound estimates of their prevalence can be tied to
estimates of that to which the person is predisposed: depression.
One common viewpoint in the
psychiatric literature is that the diathesis for depression is relatively
restricted in the general population (see Cooke, 1987 ;
Guze, 1989 ; Heston, 1988 ).
By virtue of its selectivity, it is the pivotal component (i.e., necessary and
prevalence limiting) in the arrangement of etiologic factors leading to an
episode of depression. Life stress is viewed at most as a mere precipitant of
the disorder and is thereby conceived as only a comparatively trivial element
in the etiologic process. There are several sources of indirect support for
this point of view. One of the most consistent findings in depression research
is the tendency of the disorder to run in families and for the morbidity risk
of depression to be higher in such families as compared with the general
population ( Andreasen, 1987 ; McGuffin & Katz, 1989 ). Also, many studies have noted that despite high levels of stress,
only a certain percentage of people succumb to depression ( Brown & Harris, 1978 , 1986 ; Paykel, 1982 ).
Finally, strong evidence exists for the genetic transmission for at least some
forms of bipolar disorder, which is most commonly manifested as the unipolar
phenotype within the family pedigree ( Baron et al., 1987 ; Depue & Monroe, 1978b ). On the basis of these sources of
information, one might infer that for depression (a) the diathesis is strongly
associated with genetic and familial transmission, (b) the diathesis is likely
to be relatively restricted in the general population, and (c) stress leads to
depression primarily within the population of the predisposed ( Clayton, 1986 ;
Guze, 1989 ; Heston, 1988 ;
Whybrow et al., 1984 ).
In contrast, other sources
of evidence suggest that a diathesis for depression is a more common characteristic
of the human constitution and condition. With respect to incidence and
prevalence of the disorder, virtually all epidemiologic studies cite high rates
in relation to other psychiatric disorders in the general population (e.g., Boyd & Weissman, 1981 ; Charney & Weissman, 1988 ). Furthermore, an unknown
proportion of the predisposed never manifest the disorder. For estimating the
prevalence of predisposition to depression, the indexes that are based on
lifetime risk data provide a reasonable, lower bound estimate. Worldwide, the
lifetime-expectancy estimates for major depression range from 8% to 12% for
males and from 20% to 25% for females ( Charney & Weissman, 1988 ). Additionally, recent research has documented
secular trends in the rise of depression ( Gershon, Hamovit, Guroff, & Nurnberger, 1986 ; Hagnell, Lanke, Rorsman, & Öjesjö, 1982 ; Klerman, 1988 ).
In particular, for people born since World War II, depression is more common
and occurs at an earlier age. These changes in the epidemiology of depression
cannot be explained by simple genetic theories of etiology and a shift in the
genetic diathesis (because the time periods involved clearly are not sufficient
to account for necessary changes in the gene pool). Instead, some form of
gene—environment interaction has been hypothesized, with unknown environmental
factors shifting to account for recent increases in depression in general ( Klerman, 1988 )
or in the incidence of particular subtypes of the disorder ( Giles et al., 1989 ). Overall, then (a) the high frequency of depression, (b) the increasing
incidence of the disorder, and (c) the fact that all calculations necessarily
underestimate the pool of predisposed people argue for a substantial proportion
of people who possess a diathesis for depression.
Note that this line of
reasoning is based on a nonspecific view of the diathesis. If different
diatheses exist, qualifications in the argument are introduced. For example,
biologic and cognitive diatheses may operate by means of separate mechanisms.
The high frequency of depression would then be due to the combined prevalence
of the two (or more) forms of diathesis, and either predisposing element alone
would be represented in the population at a proportionately decreased
frequency. 6 (This concern parallels in several respects
that noted previously with respect to the issue of etiologic heterogeneity.)
Unlike the situation for life stress, though, there is little firm information
yet available on which to elaborate the implications of this point. For
example, although cognitive and biological diatheses have been proposed, there
is little basis for discerning if they represent separate vulnerabilities or
different levels of the same vulnerability The existence of multiple diatheses,
though, would not negate the general framework we discuss for studying specific
diathesis—stress interactions; it would simply require differentiating the
framework in accord with the characteristics of the different diatheses.
Because there is no firm evidence yet to distinguish between multiple
diatheses, the present analysis is based conservatively on the more general
condition consonant with the existing literature.
Overall, depression–and
consequently the predisposition to depression–is not restricted to a small
segment of the population. This is to some extent in contrast to the viewpoint
that the rate-limiting factor of the diathesis—stress interaction is
predominately the diathesis ( Akiskal, 1988 ;
Clayton, 1986 ; Guze, 1989 ;
Klerman, 1983 ; Whybrow et al., 1984 ). Although there may be subgroups of people with especially potent
diatheses for depression in general or for subtypes of depression in
particular, they cannot fully account for the widespread incidence of the disorder.
A substantial proportion of people must possess a diathesis for depression. 7
Characterizing
the stressors for depression.
Concepts of stress have
most often been presented as nonspecific in form and as a continuous construct
comprising a myriad of experiences (see earlier section, Conceptualization of
Life Stress in the Context of a Diathesis). However, regarding depression, this
is at variance with the available empirical evidence. More specific qualities
and dimensions of stress tend to account for the association with clinical
depression ( Brown & Harris, 1978 , 1986 ; Cooke & Hole, 1983 ; Finlay-Joness, 1981 ; Lloyd, 1980 ;
Monroe, 1990 ; Paykel, 1982 ).
In particular, severely threatening events–especially those that involve major
loss of valued persons or roles—represent a class of circumstances that appear
to be especially effective for eliciting the psychobiologic response (see Brown & Harris, 1986 ; Cooke & Hole, 1983 ; Finlay-Joness, 1981 ; Paykel, 1982 ). The most extensive series of
inquiries on this topic has been conducted by Brown and Harris over the past 20
years. They have used sophisticated methods for assessing life stress, have
conducted investigations across different samples and cultures, and have
interpreted the findings from replications by their research unit and other
investigators using the same methods. They conclude that "it is the impact
of just one event or difficulty of a sufficient severity that appears to be
critical" ( Brown & Harris, 1986 , p. 138). Less severe forms of
stress, or hassles and low-level chronic problems, are not important (cf. Bebbington et al., 1988 ).
These findings suggest a
threshold for severity and specificity of socioenvironmental circumstances that
precede depression. Qualitatively distinct experiences, in terms of severity
and nature, appear to be essential. Lower levels of stress were not found to
summate to produce depression. Estimates of the incidence of such forms of life
stress therefore can be made. For a 38-week period preceding disorder onset or
interview, Brown and Harris (1978) found that severe events or severe
difficulties occurred for 75% of psychiatric patients, 89% of onset cases in
the community, and 30% of normal or subsyndromal women in the community. These
findings are essentially replicated in 9 subsequent studies performed by a
range of investigators using Life Events and Difficulties Schedule (LEDS)
methodology. Across these studies, one or more severe events or major
difficulties occurring before onset ranged for cases from 62% to 94% (average
82%) and for noncases from 25% to 39% (average 33%; Brown & Harris, 1989 , p. 55). 8 Eleven studies of psychiatric disorder using
other life stress assessment methods yet including only measures of events
(i.e., no difficulties) yielded comparable, albeit less dramatic, results
(e.g., and average of 54% of cases experienced major stressful events before
onset as compared with an average of 18% of noncases before interview; Brown & Harris, 1989 , p. 56). 9
Overall, people in the
general population are exposed relatively infrequently, not constantly or
inevitably, to the life stressors capable of eliciting depression. In other
words (a) relatively specific forms of life stress appear to precede
depression, (b) there is a threshold of severity for these events, and (c)
these types of events are not ubiquitous in the general population. This is in
direct contrast to one common conceptualization of life stress (cf. Guze, 1989 ;
Heston, 1988 ) and, paradoxically, is more akin to the
manner in which the diathesis has been portrayed.
Synthesis
and Speculation
For depression, life stress
is characterized as operating in a relatively qualitative manner with a
severity threshold. But we do not yet know if further above-threshold
gradations are important and, if so, how common such influences might be. With
regard to diatheses, a relatively large proportion of the general population
possesses the psychobiologic substrate for developing depression. But, again,
we do not know if there is a threshold; if gradations in loading of the
diathesis are relevant; and if they are relevant, the prevalence of the
differing levels in the general population. We may now return to existing
evidence to synthesize speculative conclusions regarding gradations in strength
of these factors and to derive implications for refining ideas about stressors
and diathesis in depression.
As indicated previously,
most depressions follow from one severe event ( Brown & Harris, 1986 ). From the perspective of the population of depressed persons, this
indeed appears to be true. For example, Table 1 illustrates
that the majority of depressed people in the Camberwell study of Brown and Harris (1978) experienced but one severe event before onset of their depression. 10 Relatively few women experienced more than one
event. Therefore, the frequency of depressed women with zero, one, two, or more
severe events decreases considerably and proportionately.
From the perspective of
individual depressed persons, however, an important complementary
interpretation can be drawn. Table 2 represents
the same data, rearranged according to the frequency of women depressed (or not
depressed) having experienced zero, one, two, or more severe events. The
potency of the effects of life stress clearly increases proportionately with
the higher levels of exposure. Indeed, of the 7 people who experienced more
than three severe life events, all subsequently became depressed (see Table 2 ).
Thus, whereas the majority of people who become depressed in response to life
stress do so after one major severe event ( Table 1 ),
the minority of people exposed to multiple life stressors are at even greater
risk in proportion to the number of severe events encountered ( Table 2 ).
This suggests a quasi-continuous effect for above-threshold values of life
stress.
Although these particular
findings require replication, two tentative but very important implications are
noteworthy. First and most apparent, there may be above-threshold gradations in
the severity of stress that contribute to the development of depression.
Whereas a qualitative and quantitative threshold appears to exist, the effect
is not purely dichotomous. Multiple severe stressors, although occurring
relatively infrequently in a normative sense, may be disproportionately
virulent for precipitating an episode of depression. The second point is more
speculative and tentative but theoretically provocative. Under increasingly
severe levels of these stressors, most if not all people break down. This again
implies that the capacity to become clinically depressed is widely distributed
in the general population. Although there may be important reasons to moderate
this conclusion (to be addressed shortly), the major thrust of the argument
remains the same. The ability to become clinically depressed appears quite
common and not solely the province of an unfortunate few who possess a
particularly pernicious form of the diathesis. 11
Overall, research-based
characterizations of the diatheses and stressors for depression are in marked
contrast to prevailing viewpoints. The widespread incidence of depression, the
greater prevalence of the predisposition to the disorder, and the frequency and
potency of the forms of stress found to precede the disorder all indicate that
more specific and empirically based models of diathesis—stress interactions can
be developed to guide future research. We next begin to outline such a
framework for inquiry.
Characteristics
of Diathesis—Stress Interactions in Depression
If the type of stress
required to initiate an episode is not rare yet also not common and if the
diathesis for depression is relatively common, then the characteristics of
diathesis—stress interactions in the population take on different forms. On the
basis of the reasoning just outlined, we assume for heuristic and descriptive
purposes that the form of stress initiating depression is relatively uncommon
and the diathesis for depression is relatively common. Yet one issue
complicates the interpretive matrix. If the diathesis influences the stress to
which a person is exposed, the interactions must be evaluated within a broader
conceptual framework that encompasses the developmental dynamics between the
diathesis and stress ( Koopman, 1977 ). Because the influence of the
diathesis on stress is currently based only on conjecture, we outline
interpretive premises and illustrate implications that are predicated on both
independence and dependence assumptions.
Independence
of the diathesis and stress.
The more common the
predispositional factor is in the population, the less it explains the
distribution of cases ( Rose, 1985 ). This is because the more
frequently a causal agent occurs, the less it is capable of explaining the
allocation of the particular disorder in that population. Under such
conditions, greater explanatory potential resides within the elements of the
model that are distributed in a more differentiating manner. For understanding
depression, under the presently specified diathesis—stress conditions–i.e., the
requisite stress is relatively uncommon, and diathesis is relatively
common–life stress may be the more "prevalence limiting."
This characterization of
the diathesis and stress, though, raises a somewhat counterintuitive point. To
the extent that most people possess the diathesis, the majority of people who
become depressed in the general population may be people who possess lower
levels of the diathesis. When the diathesis is common and when the activating
stress is independently distributed across people (i.e., stress is not
influenced by the diathesis), the sheer number of people at lower levels of
diathetic risk experiencing significant stressors may offset those at higher
levels of risk experiencing significant stressors. Many people at small risk
produce more cases of the disorder than few people at high risk ( Rose, 1985 ).
12
The high-risk paradigm is
frequently adopted in this area of research, wherein a predispositional factor
is chosen and people are selected for study on the basis of a high loading of
the diathetic risk variable (e.g., Alloy et al., 1988 ; Buchsbaum, Coursey, & Murphy,
1976 ). People with
the outermost scores on the diathetic variable, however, may not be
representative of the majority of people predisposed to the disorder or of the
preponderance of people who eventually develop the disorder. Although the
processes that give rise to depression in the highly predisposed may be
informative theoretically for the conditions under which the less predisposed
succumb, there also may be important differences. For example, the
constellation of etiologic forces that are sufficient to precipitate depression
in the high-diathesis risk group could be different from those required for the
lower diathesis risk people.
The practical implications
of such a possibility also merit consideration. For example, from a public
health perspective, those who give rise to the majority of cases (i.e., the
less predisposed by the diathesis) constitute the natural focus of attention
for intervention. Irrespective of theoretical commonalities between groups at
very different levels of the diathetic factor, the differing combination of
diathetic factors between people still suggests potentially important
differences in conceptualizing intervention efforts. For instance, because the
incidence of relatively specific types of stress within the current framework
operates as the more pivotal factor, targeting reduction in its incidence or
the manner in which it is diminished or resolved could be more effective
prevention strategy than attempting to alter the diathesis (cf. Guze, 1989 ).
Again, we caution that such ideas are based on our previously derived estimates
and await further clarification. These points serve to provide a very
different, yet quite plausible, perspective for diathesis—stress models, given
current information and theory.
Assuming independence of
the diathesis and stress, though, may oversimplify diathesis—stress
interactions. When the diathesis influences stress, the matrix of
interpretational issues enlarges considerably, and by necessity so do the
conceptual and research demands required.
Dependence
of the diathesis and stress.
When the diathesis influences
the relevant stressors, diathesis—stress associations become more complex. One
general conclusion is that in contrast to the case in which the diathesis and
stress are independent, the likelihood of incurring the 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 depression. Under these conditions,
proportionately more people who become depressed in the general population are
people who possess the highest risk in terms of the diathesis. 13 This point has led to divergent interpretations
of existing research and to major misunderstandings between investigators of
different theoretical inclinations concerning the relative importance of stress
and diatheses in the etiology of depression.
There are at least three
alternative viewpoints of the temporal interplay between stress and the diathesis.
First, in keeping with the spirit of the diathesis—stress principles, both the
diathesis and the stress together constitute a necessary condition for
depression onset (see Figure 5 ). Neither alone is sufficient.
Although the stress in part follows from the behavioral concomitants of the
diathesis, the stress still features as an integral element in the
developmental scheme. For example, the case portrayed previously for an
affiliative diathesis and the life event of rejection illustrates the issue
well: A person who has the cognitive vulnerability to interpersonal events may
conduct such activities in ways that increase the likelihood of severe events
occurring. The person's attempts to avoid rejection, for instance, through
continual requests for reassurance and support, promote the eventual rejection.
Both factors together–the affiliative diathesis and the particular stressor–are
sufficient. Within this scheme, the diathesis operates at two levels in the
model. It enhances the likelihood of the very conditions occurring that are
also necessary to transform it into depression (pathway a ). Note,
however, that diathesis-driven events are not necessary to produce depression,
because events that happen irrespective of the diathesis or person's actions
may also serve to activate the diathesis and promote depression (pathway b ).
A second viewpoint is that
the only necessary factor is the diathesis ( Figure 6 ).
Stress is either a minor factor, a result of the diathesis's expression
(pathway a ), or simply a consequence of the emerging depression
(pathway b or c ). Indeed, this is the radical cognitive view
summarized by Epictetus in The Enchiridion: "Men are not disturbed
by things but by the views which they take of them." Similarly, some
biologic models and classification schemes view stressors as irrelevant to the
development of at least certain subtypes of depression and define subtypes on
the basis of the absence of external stress (e.g., endogenous depression; Carney, Roth, & Garside, 1965 ). Within these perspectives, stressors are
only minor contributors to etiology or are essentially epiphenomenal. A
predisposed person may become irritable and socially withdrawn and experience
concentration difficulties, crying spells, and sleep disturbance. Although
primary relationships may be strained and arguments, fights, or even breakups occur,
the depression had already begun its insidious course. The stressors, although
distressing, were a consequence of the diathesis-influenced prodrome (pathway b
) or the onslaught of the disorder (pathway c ) and therefore are
not viewed as an important element in determining the depression's emergence
(e.g., Akiskal, 1988 ; Guze, 1989 ).
The third position posits
that the only necessary factor for depression is life stress ( Figure 7 ).
Specific stressors are seen as essential to the onset of depression. The
diathesis is nonessential, or less important, in the theoretical scheme. Depression
can occur irrespective of the diathetic loading (pathway b ). What is
viewed as the diathesis, however, might be reconceptualized as stress
propensity. Attributes of the person (or of his or her social context) give
rise to processes that increase the likelihood of the requisite forms of stress
occurring (pathway a ). The activation of the diathesis is essentially
irrelevant compared with the generative potential of the diathesis for
contributing to the circumstances that would give rise to depression
(irrespective of the diathesis). The cognitive or biologic propensities
previously viewed as diatheses are operative in the model only in so far as
they contribute to the incidence of the forms of stress required for
depression. Although theoretically unnecessary, the generative potential
associated with the diathesis may be an important mechanism by means of which
the necessary conditions for producing depression are fulfilled.
Each of these three
depictions of diathesis—stress associations yields a variety of theoretical and
practical implications. One common point across the different interpretations
exists. To the degree that the diathesis influences stress, the high-risk
paradigm moves toward appropriately targeting the majority of people who will
in all likelihood develop the disorder. This means that there is a tighter
correspondence between the people most often selected for study with such
procedures and the people most likely to become depressed. It also suggests
public-health-relevant approaches for targeting the most important groups for
prevention purposes. What is required is a research agenda directed toward
greater elucidation of the types and degrees of association between the
proposed diatheses and stressors. Such approaches require prospective
longitudinal designs, wherein the diatheses are assessed before stress
occurrences and the implications of the different models outlined can be
tested.
Conclusions
and Recommendations
We have outlined in a broad
manner the developmental pathways between diatheses and stressors in depression
that fit with current empirical information. But the particular concern for
diathetic influences on stress has few data at present on which to base
opinions, let alone conclusions. Indeed, methodologies for studying such
influences are only beginning to emerge. This means that in concert with the
development of concepts and basic stress measures, additional thought and
assessment should be devoted to the specific task of understanding the nature
of the temporal interplay between hypothesized diatheses and forms of stress.
Whereas much of this latter topic will be at least in part a function of the
particular diathesis of interest, the more general issue pertains to the
question of how life's stressors begin in the first place.
At one level or another,
most life events and chronic difficulties can be traced to some aspect of the
person's behavior. As indicated previously, to varying degrees most people are
in part creators and perpetrators of the circumstances they endure ( Monroe & Peterman, 1988 ). This is not to say that all stress is merely
a by-product of the person's mistakes, failings, or diatheses. But stressors,
behaviors, and social environments can work together in complex and internecine
ways to initiate, and perpetuate, adversities. At a very gross level,
distinctions can be made relatively easily. For example, the death of a close
friend because of a natural disaster would not likely be immediately related to
the subject's behavior or hypothesized diathesis. But at other levels
applicable to more common life events, such judgments become more difficult.
For example, a person may be laid off because of an industry-wide initiative.
However, only 70% of the employees may actually be dismissed, perhaps
selectively on the basis of past performance. How much of the event is
attributable to the person? In a similar vein, relationship difficulties and
breakups, which often reflect processes of many years' duration, are very hard
to ascribe cleanly to one person or another, one shortcoming or another. A very
large part of life's misfortunes are end points of such multidetermined
processes.
Procedures for handling
these concerns have begun to develop. For example, investigators have devised
rating systems to describe the degree to which an event might result from a
preexisting disorder, or the behavior, of the person ( Brown & Birley, 1968 ; Brown & Harris, 1986 , 1989 ; Miller et al., 1986 ). These systems are useful for eliminating major confounds (e.g.,
events that are an obvious consequence of depression), but as yet they
typically are not adequate to address the full array of complicated
possibilities for interplay between diatheses and stress over prolonged periods
of time. Events that result from the combination of many factors, only one of
which may be the person's behavior, possess an unclear status. Are they
epiphenomenal by-products of the diathesis, or are they integral components of
the developmental process? More differentiated systems are required to study
the influential forces in the origins of life events and to use such
information to better understand the potential interactive pathways between
diatheses, stress, and psychopathology (see Brown & Harris, 1989 ).
Recent work explicitly
addressing diathesis—stress premises strongly affirms the need for such efforts
( Bebbington, et al., 1988 ; McGuffin, Katz, Aldrich, & Bebbington, 1988 ; McGuffin, Katz, & Bebbington, 1988 ). Using the LEDS life event assessment system,
McGuffin, Katz, and Bebbington studied the relationship between life events and
depression in 83 families identified through depressed probands. In contrast to
a traditional diathesis—stress prediction, they found no support for an inverse
relationship between the presence of family loading for depression (the
diathesis) and life adversities preceding the subject's depression (the
stress). In fact, "the relatives of probands whose onset of depression
followed life events or chronic difficulties had slightly higher lifetime rates
of depression than the relatives of probands whose onset was not associated
with adversity" ( McGuffin, Katz, & Bebbington,
1988 ; p. 775).
They also found relatives of depressed probands to have significantly raised
rates of both current depression and recent threatening life stress. In other
words, both the liability to depression and the propensity to experience severe
life stress apparently were familial. 14 More refined procedures for determining the
origins of events, from the personal influence through that of the broader
social structures, and the nature of their interactive impact with the
diathesis are required.
Over 25 years ago, David Rosenthal (1963) described diathesis—stress theories as "the ones in which genuine
meaning attaches to the commonly repeated statement that heredity and
environment interact" (p. 509). These theories are heuristic devices for
developing an understanding of how predispositional factors from different
domains heighten susceptibility and, eventually, create sufficient conditions
for disorder onset. This represents the promise of such ideas. It is this
interactive aspect, we believe, that has captured the minds of investigators
and represents the guiding principle of the premise. However, with respect to
these theories, Rosenthal (1963) further noted that "the great
majority of them are also exasperatingly loose, since the nature of the
predispositions and the stressors, as well as the mechanisms of interaction,
are usually only vaguely conceived or formulated" (p. 509). It is this
disintegrative accompaniment to such thinking that has impeded progress.
The looseness associated
with these theories may be addressed in a direct manner. As illustrated
throughout the article, the diatheses and stressors can be better conceptualized
and more precisely measured with respect to specific forms of psychopathology.
For example, the generic notion of stress can give way to particular types of
stressors that are most relevant for achieving an understanding of the disorder
of depression. In a complementary vein, further specification of specific types
of diatheses will also contribute to the development of more precise and useful
models. Better determinations of the diathesis through family history ( McGuffin, Katz, & Bebbington, 1988 ), biological markers ( Monroe & Depue, 1991 ), individual differences in cognitive factors ( Abramson et al., 1989 ; Beck, 1987 ), or other domains of social and
psychological vulnerability ( Brown & Harris, 1989 ) will help to clarify these issues. Finally, through focusing on
specific qualities of stress in relation to the specific disorder of
depression, we profiled alternative models for depicting diathesis—stress
interactions. These possibilities make more explicit the pathways that future
research should address to develop a better understanding of the meaning and
importance of such interactions. In turn, research findings that are based on
such approaches will contribute to more informed programs for risk detection and
prevention. These interactive issues bring the focus of the diathesis—stress
premise back to its conceptual essence: the nature of the interaction between
elements in the etiologic process over time.
There are more subtle and
pervasive problems, though, that also give rise to the "looseness"
that accompanies diathesis—stress theories. These concerns are not so easily
eliminated through the direct methods we have advocated. Rather, they are much
broader and diffuse, involving the permissive conceptual structure that gives
rise to causal explanations in psychopathology research. The concept of life
stress can be sufficiently amorphous and can be sufficiently imprecisely
defined and measured so as to fit into virtually any explanatory scheme. We
have shown that systematic errors (e.g., confounding with diatheses or
disorder) and unsystematic errors (e.g., composite measurement procedures) can
easily yield mixed and confusing findings. The idea of a diathesis, in the
abstract and in the applied, suffers from similar susceptibilities of
imprecision in concept and measure. Together, stress (a collective
representation of exogenous considerations) and diatheses (a collective
representation of endogenous considerations) essentially cover the vistas of
explanatory concepts in contemporary psychopathology research. Left only
partially constrained in theory and measure, they can unite as powerful
co-conspirators in nonexplanation.
Present-day research on
depression has expanded the list of contributory considerations from the
two-factor diathesis—stress model to more encompassing multifactorial
representations ( Akiskal, 1985 ; Akiskal & McKinney, 1975 ; Depue, 1979 ).
The factors found to be associated with depression are quite extensive,
involving aspects of early developmental experiences, various biologic
vulnerabilities, diverse psychological susceptibilities, and other types of
socioenvironmental contributions. These ideas no doubt touch on additional
elements of potential import and can assist in developing a broader
understanding of the disorders. Yet multifactorial models simultaneously inflate
the problem inherent in the relatively simple two-factor model just reviewed.
If one of these factors, one pairing of these factors, or one complex of these
factors is not found to predict disorder, then another factor, pairing of
factors, or complex of factors is readily raised (see Meehl, 1977 ).
Ultimately, within such a broad explanatory system there can exist an expanding
array of interactive and additive alternatives to account for virtually any
arrangement of findings.
Finally, the potential for
ambiguity resides not only in the realm of these independent variables and
their interactions (i.e., stress, diatheses). Most conceptualizations of the
dependent variable, disorder, cautiously acknowledge that multiple subtypes are
likely to exist ( Weiner, 1977 ). Again, although this probably
represents a reality of such conditions, it also injects another layer of
potential looseness. The problem of interchangeable elements within the
independent variable is mirrored by interchangeable categories of the dependent
variable. If the findings are not in theoretical accord for any particular
outcome, different subtypes of the disorder are invoked, which in turn can be
explained by a different factor, pair of factors, multitude of factors, and so
on. A symmetry for misunderstanding exists between the independent and
dependent variables so that hypotheses are simultaneously elusive (difficult to
prove) and evasive (difficult to disprove).
Of course, if the component
concepts of the multifactorial model are reasonably well understood, if their
operationalizations represent reasonable approximations, and if the subtypes of
the disorder are amply outlined, concerns such as these are far less
compelling. Various hypotheses could be refuted because investigators would
have an acceptable hold, both in theory and in measure, on the separate
components of the model and their applicability to heterogeneous outcomes. In a
world of incomplete etiologic concepts, imperfect measures of these incomplete
etiologic concepts, and unknown boundaries between and within diagnostic
categories, the situation is quite different. And this, as we have attempted to
illustrate, is our present world. As our discussion has shown, there is a clear
and consistent danger of missing vital aspects of the concepts (e.g.,
particular qualities of life stress that are important for the disorder) and of
generating spuriously affirmative findings (e.g., through contamination of
concepts and measures), both of which preclude a meaningful analysis of
interactions between diatheses, stressors, or other predisposing factors.
We suggest that the essence
of the diathesis—stress model is its implications for interactive analysis.
This is in contrast to the complementary tendency to think in extensive terms
and comprehensive theories. Interaction implies a more restrained focus, an
in-depth probing of associations between the components of the model, often
multidirectional and transpiring over time. In contrast, comprehensive implies
a broad view of possible correlates, often sweeping and possessing functionally
interchangeable components, that can combine in nonspecific ways. The first
approach suggests an intensive study of specific factors and their integration
over time within focused, prospective studies. It describes developmental
dynamics: specific processes. The second approach suggests extensive study of
suspected etiologic influences and their respective contributions. It describes
linear, additive, and atemporal associations: nonspecific arrangements. We
suggest that both approaches have their place, but that they should be clearly
distinguished with respect to their virtues and limitations. The challenge is
to maintain a focus on the meaning of interactions between diatheses and
environment, and ultimately among other contributing factors, without falling
into the looseness that such thinking can engender. In our present world of
incomplete concepts and imperfect measures, it would seem that the intensive
rather than comprehensive focus on concepts, measures, and interactions most
closely exemplifies the spirit–and may help to realize the promise–of
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1
The concept of a diathesis
is as old as early conceptualizations of disease within naturalistic, or
physical, origins. Derived from ancient Greek, the term can be traced at least
to the writings of Galen (131—201, A. D. ) in his interpretations of
Hippocratic theories of disease ( Entralgo, 1955 ; Simpson & Weiner, 1989 ). Notions of constitutional
predisposition also dominate early theories of depression (or melancholia; Burton, 1621/1977 ; Jackson, 1986 ; Klibansky, Panofsky, & Saxl, 1979 ) and more generally of "nervous
disease" ( López Piñero, 1983 ; Whytt, 1765 ).
For present purposes, our definition is consonant with that provided in 1883 by
Stearns's chapter "The Insane Diathesis": "a nervous system so
sensitively constituted, and illy adjusted to its surroundings, that when
brought in contact with unusually exciting influences, there may occur deranged
instead of natural mental action, and it becomes more or less continuous
instead of evenascent" (cited in Grob, 1983 ,
p. 40).
2
Although several research
groups have adopted interviewer-based procedures (e.g., Alloy et al., 1988 ; Brown & Harris, 1978 ; Hammen et al., 1989 ), the actual guidelines, decision rules, and operational criteria are
not typically explicit. This is not a trivial concern and unfortunately is a
commonly ignored issue. An illuminating exception to this is the extensive and
detailed work of Brown and Harris (1989) in the development of the Beford
College Life Events and Difficulties Schedule (LEDS) and rating system. A detailed
semi-structured interview with elaborate manuals provides extensive rules and
criteria for defining events, distinguishing between related events, and
differentiating events and difficulties. Listed are some 800 categories of
experiences and over 5,000 case vignettes for standardizing stress definitions
and ratings. These manuals are for major life events and difficulties and do
not encompass the more common daily hassles or minor events. To include such
stressors and thereby study stress comprehensively, adequate technologies for
defining these latter experiences and for distinguishing them from major events
and chronic stressors need to be developed (see also B. S. Dohrenwend et al., 1984 ). As suggested by the labor-intensive LEDS
procedures for defining major events and difficulties, this would be an
extremely demanding undertaking.
3
Because we are not
concerned with the estimation of parameters, only with the properties of
interactions for illustration purposes, we have omitted error terms from the
model.
4
The existence of a
threshold is currently a debatable and ultimately an empirical issue. Certainly
not all diathesis—stress theories posit a threshold for the diathesis (e.g., Abramson, Metalsky, & Alloy, 1989 ). However, many biological theories of
depression emphasize the consistency of genetic/familial findings for
depression, and discussions of these findings often invoke biological diatheses
and genetic origins as clearly primary determinants of who develops the
disorder (e.g., Andreasen, 1987 ; Clayton, 1986 ;
Guze, 1989 ; Heston, 1988 ;
Whybrow, Akiskal, & McKinney, 1984 ). As we see later in the article,
the notion of a threshold also may be useful with respect to conceptualizing
stress. Irrespective of the ultimate validity of thresholds, their inclusion in
the present analysis is useful for simplifying issues pertaining to diathesis—stress
interactions and for setting the foundation on which we develop more elaborate
representations consonant with theories adopting a continuous view of the
diathesis.
5
Parts of the next
discussion are adapted from Cleary and Kessler (1982) . For simplicity, we have again omitted error terms from the equations.
6
The possibility of multiple
diatheses raises other intriguing questions about associations between separate
propensities to disorder and about associations of different diatheses with
different forms of stress. For example, do different diatheses create additive
or interactive risk for depression or contribute independently to separate
subtypes of the disorder? Do different diatheses require different forms of
stress for activation? Although our focus in the present article is on the
manner in which diathesis—stress models can be informed by a conceptual
analysis of stress theory and research, the complementary task of informing these
models by a conceptual analysis of different domains of predisposition and
their interactive influences could yield other valuable guidelines for theory
and research.
7
By this we do not mean to
imply that biological or genetic factors are not of importance in the genesis
of depression or of possible subtypes of the disorder. It might be useful to
think of diatheses in two senses with regard to this issue: one an active sense
and one a passive (or permissive) sense. As we have noted before, our argument
is based on the broad class of depressions and does not address hypothetical
subtypes or differences in diatheses. Consequently, we cannot infer backwards
from population estimates for depression about the frequency of specific active
diatheses. However, we can infer backwards from such evidence concerning
general passive diatheses. In other words, even if there are multiple subtypes
of depression with separate diathetic factors (e.g., biological vs. cognitive),
many people must still possess the "permissive" biologic diathesis
for incurring depression.
8
The time periods over which
life stress was assessed for these studies were 3 months (one study), 6 months
(one study), 10 months (one study), 12 months (six studies). If studies
assessing both events and difficulties that are based on a common 12-month time
period alone are examined, the comparable figures are that an average of 83%
cases experienced prior severe events or difficulties as compared with 33% of
noncases.
9
Only 7 of the 11 cited
studies included noncase comparison groups.
10
The data presented in Table 1 are
adapted and rearranged from Brown and Harris (1978, p. 108) . Only severe events unrelated to each other
are included (events that do not arise from a common source, such as a serious
marital argument, subsequent separation, and initiation of divorce
proceedings). Note also that we do not include ongoing difficulties in this
discussion. Whereas this does not affect the interpretation of the present
issue involving additivity of events, it could be misleading with respect to
more general issues of stress (i.e., events or difficulties) preceding
depression (i.e., greater proportions of women had some form of stress before
onset than is apparent from analyzing events alone; see Brown & Harris, 1986 ). Finally, for brevity, community cases and patients from this research
are combined. Similar effects hold in regard to the additive potency of
multiple severe events across both community cases of depression and the
patient sample.
11
Note that more recent
advances in clarifying the characteristics of stressors have led to even
greater precision in predicting the onset of depression in the face of
psychosocial adversity (e.g., approximating 50%; see Brown & Harris, 1989 ). These data suggest that it may be the matching of specific types of
events with specific types of psychosocial vulnerability that is especially
important in bringing about depression (see also Abramson, Metalsky, & Alloy, 1989 ). Although such findings may argue against the
idea of above-threshold additivity (because the instances of multiple events
may represent the greater probability of a match occurring rather than
additivity per se), they further support the general conclusions of this
argument: (a) There may be very specific qualities of environmental adversity
that can lead to depression for specific people, (b) under such conditions,
many people (if not all) have the capacity to become depressed, and (c) the
incidence of such specific pathogenic matching in the general population (i.e.,
stressful conditions that precipitate depression) may be even less common than
the estimates above suggest.
12
This argument assumes, we
believe reasonably, a positively skewed distribution of the diathesis (i.e.,
more people with lower loadings). It also depends in part on the percentage of
people with life stress who develop depression. The stronger the link between
severe events and subsequent depression, the more persuasive is this line of reasoning
(i.e., a lesser link leaves greater room for different loadings of the
diathesis to determine who does and does not break down). Given recent
estimates of approximately 50% of people developing depression with particular
constellations of prior life stress ( Brown & Harris, 1989 ), the implications of this point for understanding the relative
importance of diatheses merit consideration.
13
The actual degree to which
this shift occurs is again a function of several factors, including the
strength of diathetic influence on stress, the changes in the strength of this
influence at differing potencies of the diathesis, the frequency of the
differing potencies of the diathesis in the population, the incidence of stress
that is not a consequence of the diathesis, and the impact of stress at the
different potencies of the diathesis. Without more specific data on these
matters, one can only conclude that to an unspecified degree, the high-risk
people become more representative of depressed people.
14
Note that this suggests
some degree of dependency between a diathesis for depression and these forms of
life stress. It also suggests that both the diathesis and stress are important
in the predictive scheme but leaves open the question of which dependency model
cited previously is most appropriate (Model 1, in Figure 5 ,
or Model 3, in Figure 7 ).
Table 1.
Figure 1. General model of diathesis—stress interaction.
Figure 2. Additive model of diathesis—stress interaction.
Figure 3. Interactive model of diathesis—stress interaction: Dichotomous
diathesis.
Figure 4. Interactive model of diathesis—stress interaction: Quasi-continuous
diathesis.
Figure 5. Diathesis—stress interactions: Model 1. (Stress 1 = stress related to
diathesis; Stress 2 = stress unrelated to diathesis).
Figure 6. Diathesis—stress interactions: Model 2.
Figure 7. Diathesis—stress interactions: Model 3. (Stress 1 = stress related to
diathesis; Stress 2 = stress unrelated to diathesis).