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A Heuristic for Developing Transdiagnostic Models of Psychopathology

Explaining Multifinality and Divergent Trajectories

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A Heuristic for Developing Transdiagnostic Models of Psychopathology : Explaining Multifinality and

Divergent Trajectories
Susan Nolen-Hoeksema and Edward R. Watkins
Perspectives on Psychological Science 2011 6: 589
DOI: 10.1177/1745691611419672

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 Perspectives on Psychological Science

A Heuristic for Developing Transdiagnostic 6(6) 589­–609

© The Author(s) 2011
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DOI: 10.1177/1745691611419672

Multifinality and Divergent Trajectories http://pps.sagepub.com

Susan Nolen-Hoeksema1 and Edward R. Watkins2

1
Yale University and 2University of Exeter

Abstract
Transdiagnostic models of psychopathology are increasingly prominent because they focus on fundamental processes underlying
multiple disorders, help to explain comorbidity among disorders, and may lead to more effective assessment and treatment
of disorders. Current transdiagnostic models, however, have difficulty simultaneously explaining the mechanisms by which a
transdiagnostic risk factor leads to multiple disorders (i.e., multifinality) and why one individual with a particular transdiagnostic
risk factor develops one set of symptoms while another with the same transdiagnostic risk factor develops another set of
symptoms (i.e., divergent trajectories). In this article, we propose a heuristic for developing transdiagnostic models that can guide
theorists in explicating how a transdiagnostic risk factor results in both multifinality and divergent trajectories. We also (a)
describe different levels of transdiagnostic factors and their relative theoretical and clinical usefulness, (b) suggest the types
of mechanisms by which factors at 1 level may be related to factors at other levels, and (c) suggest the types of moderating
factors that may determine whether a transdiagnostic factor leads to certain specific disorders or symptoms and not others.
We illustrate this heuristic using research on rumination, a process for which there is evidence it is a transdiagnostic risk factor.

Keywords
transdiagnostic, multifinality, trajectories, comorbidity, psychopathology

Transdiagnostic models of psychopathology, which seek to
identify fundamental processes underlying multiple, usually
comorbid, psychopathologies, are increasingly prominent
(Barlow, Allen, & Choate, 2004; Ehring & Watkins, 2008;
Harvey, Watkins, Mansell, & Shafran, 2004; Kring & Sloan,
2010; Mansell, Harvey, Watkins, & Shafran, 2009). Transdi-
agnostic models hold several theoretical and clinical advan-
tages over disorder-specific models (e.g., see Mansell et al.,
2009). Current transdiagnostic models, however, have diffi-
culty simultaneously explaining the mechanisms by which a
transdiagnostic risk factor leads to multiple disorders (i.e.,
multifinality) and why one individual with a particular transdi-
agnostic risk factor develops one set of symptoms while
another with the same transdiagnostic risk factor develops
another set of symptoms (i.e., divergent trajectories). For
example, current models of stress as a risk factor (e.g., Meyer,
2003; Monroe, 2008) tend not to address how stress both is
related to many different disorders, including depression, anx-
iety, and alcohol abuse (i.e., multifinality), and leads to depres-
sion in some people, anxiety in others, and alcohol abuse in
others (i.e., divergent trajectories).
In this article, we propose a heuristic for developing transdi-
agnostic models that can guide theorists in explicating how a
transdiagnostic risk factor results in both multiple symptom
presentations or disorders and particular symptom presentations
or disorders in particular people. We also (a) specify different
levels of transdiagnostic factors and their relative theoretical
and clinical usefulness, (b) suggest the types of mechanisms by
which factors at one level may be related to factors at other lev-
els, and (c) suggest the types of moderating factors that may
determine whether a transdiagnostic factor leads to certain spe-
cific disorders or symptoms and not others. We then apply this
heuristic to develop a transdiagnostic model of rumination, a
cognitive emotion-regulation process that has been linked to
multiple psychopathologies (Aldao, Nolen-Hoeksema, & Sch-
weizer, 2010; Ehring & Watkins, 2008; Watkins, 2011).
Existing Transdiagnostic Models: Advantages
and Disadvantages
In the early and mid-20th century, psychology was dominated
by broad models that described processes thought to underlie
most forms of psychopathology. Processes such as repression
Corresponding Author:
Susan Nolen-Hoeksema, Department of Psychology,Yale University, P.O. Box
208205, New Haven, CT 06520
E-mail: susan.nolen-hoeksema@yale.edu

Downloaded from pps.sagepub.com by Susan Nolen-Hoeksema on October 18, 2011

590 Nolen-Hoeksema and Watkins
and defense mechanisms (Freud, 1937/1966), on the one hand,
and operant and classical conditioning (Mowrer, 1939; Skin-
ner, 1957; Wolpe, 1969), on the other, were thought to account
for disorders ranging from phobias and depression to
schizophrenia.
Then, particularly with the introduction in 1980 of the third
edition of the Diagnostic and Statistical Manual of Mental
Disorders (DSM-III; American Psychiatric Association, 1980),
there was a shift toward distinguishing between disorders both
in their characteristics and causes. The authors of the DSM-III
rejected old classification systems based on the assumption
that certain neuroses underpinned broadly defined disorders
and carved psychopathology into a much larger number of
individual disorders, with attempts to define these disorders by
specific, observable behaviors when possible. Many research-
ers then turned their attention to identifying risk factors and
causes specific to a given disorder, and the specificity of a
putative risk or etiological factor became an important stan-
dard for its acceptance.
Now, in the early 21st century, the focus has shifted again
toward processes that may play a causal role in multiple disor-
ders, often referred to as transdiagnostic processes (Barlow et
al., 2004; Ehring & Watkins, 2008; Harvey et al., 2004; Kring &
Sloan, 2010; Mansell et al., 2009). Approaches focused on
transdiagnostic processes have a number of theoretical and clin-
ical advantages over disorder-specific approaches. First, there is
growing agreement that the heterogeneous disorders in our cur-
rent diagnostic system are each made up of dysfunctional ver-
sions of processes that vary along continua in the general
population (Cannon & Keller, 2006; Insel et al., 2010; Regier,
Narrow, Kuhl, & Kupfer, 2009). Moreover, these dysfunctional
processes are seen in a number of different disorders. For exam-
ple, an attentional bias toward negative information is a com-
mon finding in healthy samples, and extreme attentional bias is
seen in patients with a variety of psychological disorders (e.g.,
Rozin & Royzman, 2001). A transdiagnostic approach focuses
on these fundamental dysfunctional processes and thus brings
us closer to understanding the true nature of psychopathology in
a more parsimonious way.
Second, transdiagnostic approaches can help us understand
the comorbidity between disorders. Over half of individuals
with one diagnosis meet criteria for at least one other diagno-
sis (Kessler, Chiu, Demler, & Walters, 2005). In addition, the
stability of diagnoses within individuals is low; instead, over
time individuals may meet criteria for a variety of different
disorders (Forrester, Owens, & Johnstone, 2001). Certain dis-
orders cluster together reliably, however, suggesting that there
are commonalities within groups of disorders (Krueger &
Markon, 2006; Watson, 2009). For example, major depression
is highly comorbid with particular anxiety disorders, such as
generalized anxiety disorder and social anxiety (T. A. Brown
& Barlow, 2009). Transdiagnostic approaches hold promise in
explaining comorbidities such as these by focusing on pro-
cesses that are common to comorbid disorders and that caus-
ally contribute to symptoms.
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Third, if a transdiagnostic factor is causally related to
two or more disorders, then assessment and training could
more parsimoniously focus on these factors than on the large
number of discrete disorders currently in the DSM (Mansell
et al., 2009). Moreover, treatments that remediate a transdi-
agnostic factor could have effects on all the disorders it is
related to.
The concept of transdiagnostic processes has similarities
to the concepts of intermediate phenotypes and endopheno-
types in psychiatric research (Cannon & Keller, 2006; Insel
& Cuthbert, 2009). Whereas mental disorders are heteroge-
neous clusters of symptoms, intermediate phenotypes are
conceived as neurocognitive and affective processes, such as
learning, memory, attention, stress sensitivity, and emotional
reactivity that are causally linked to the development of
symptoms (Cannon & Keller, 2006). The recent Research
Domain Criteria (RDoC) initiative is specifically focused on
intermediate phenotypes that can be linked to problems of
neural circuitry and functioning, such as excessive fear, dis-
ruptions in working memory, and poor impulse control (Insel
& Cuthbert, 2009; Sanislow et al., 2010). Endophenotypes
are intermediate phenotypes that are heritable (Gottesman &
Gould, 2003).
Psychologists have focused on a broader array of cognitive,
behavioral, and emotional processes thought to underlie
comorbid disorders. Indeed, developmental psychopatholo-
gists highlighted the phenomenon of multifinality decades ago
(Cicchetti, 1984; Egeland, Pianta, & Ogawa, 1996). Multifi-
nality refers to the process by which certain environments,
experiences, or characteristics increase risk for a number of
different types of psychopathology in children or adults—for
example, stress is associated with multiple disorders (Cic-
chetti & Rogosch, 1996).
The list of putative transdiagnostic processes or risk factors
is quite long (e.g., see D. A. Clark & Taylor, 2009; Dudley,
Kuyken, & Padesky, 2010; Mansell et al., 2009). There are a
number of environments or experiences that have been reli-
ably linked to many different psychopathologies, including
sexual and physical abuse, particularly in childhood (Mani-
glio, 2009); inconsistent, harsh, or neglectful parenting
(Dozois, Seeds, & Collins, 2009); and parental psychopathol-
ogy (Avenevoli & Merikangas, 2006; Beidel & Turner, 1997;
Johnson, Cohen, Kasen, & Brook, 2006). Then there are sev-
eral intrapersonal factors that are related to a range of psycho-
pathologies. Harvey and colleagues (2004) identified a number
of cognitive processes reliably associated with multiple disor-
ders, including selective attention and memory, recurrent
memories, overgeneral memory, interpretation and expectancy
biases, emotional reasoning, recurrent negative thinking such
as worry and rumination, certain metacognitive beliefs,
thought suppression, attentional avoidance, and safety behav-
iors. Executive control deficits, particularly in working mem-
ory, cognitive and behavioral inhibitory processes, and
attentional control, have been associated with both emotional
and behavioral disorders and some psychotic disorders (Barch,
Transdiagnostic Processes 591
2005; Gotlib & Joormann, 2010; Mathews & MacLeod, 2005).
Two personality characteristics that have been associated with
many types of psychopathology are neuroticism and negative
affectivity (Kotov, Gamez, Schmidt, & Watson, 2010). Diffi-
culties in regulating emotion have also been identified as
transdiagnostic factors (Aldao et al., 2010; Kring & Sloan,
2010).
Psychobiological factors may also serve as intermediate
transdiagnostic factors (Cannon & Keller, 2006; Sanislow
et al., 2010). A dysregulated stress response is evident in sev-
eral emotional and behavioral disorders (Cicchetti & Toth,
2005). Similarly, Harvey and colleagues (Harvey, Murray,
Chandler, & Soehner, 2010) have shown that sleep distur-
bances are common across a wide range of disorders and pre-
dict onset and relapse of psychopathology.
Several transdiagnostic therapies have been proposed based
on the evidence just reviewed (see Mansell et al., 2009). Bar-
low and colleagues (2004) designed a transdiagnostic cogni-
tive behavioral therapy to address faulty appraisals, avoidance,
and maladaptive action tendencies (e.g., withdrawal) associ-
ated with a wide range of emotional disorders. Similarly,
Hayes et al. (2004) argued that experiential avoidance is a
common causal factor across many disorders and developed
treatments to overcome such avoidance. Fairburn, Cooper, and
Shafran (2003) introduced a transdiagnostic therapy for vari-
ous eating disorders focused on concerns over weight and
shape and related behavioral tendencies. Therapies to address
deficits in emotion regulation are also emerging (Greenberg,
2002; Mennin & Fresco, 2010; Roemer, Erisman, & Orsillo,
2009). Finally, given evidence that sleep disturbances occur
across many disorders, Harvey and colleagues (2010) have
proposed cognitive and behavioral interventions for these
disturbances.
Several limitations exist in current transdiagnostic models,
however. First, transdiagnostic models generally do a better
job explaining multifinality than divergent trajectories of
symptom expression across individuals or across time. For
example, why is it that one person with attentional biases
develops obsessive–compulsive disorder and another devel-
ops primary insomnia? Or why is it that an individual who
carries a risk factor that leads him to experience both sub-
stance abuse and depression is depressed but not abusing some
of the time and abusing but not depressed at other times? Har-
vey et al. (2004) suggested that cognitive behavioral processes
could be common across disorders and still produce disorder-
specific presentations because the exact clinical presentation
would depend upon the interaction between processes and cur-
rent concerns (Klinger, 1996), defined as a nonconscious pro-
cessing state initiated when a person commits to pursue a
specific goal. Current concerns sensitize emotional responses
to, and cognitive processing of, cues associated with that goal.
Thus, a person with an attentional bias may develop obses-
sive–compulsive disorder if her concerns focus on germs and
contamination, or she may develop primary insomnia if her
concerns focus on difficulties with sleeping (Harvey et al.,
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2004; Mansell et al., 2009). However, this account leaves open
the question of where the current concerns come from.
Similarly, transdiagnostic processes generally have not
addressed phenotypic plasticity, wherein the pattern of symp-
toms morphs across the life course, often unpredictably, espe-
cially during the transitions through childhood and adolescence
into adulthood (e.g., childhood anxiety frequently being a pre-
cursor for depression in adulthood; Pine, Cohen, Gurley,
Brook, & Ma, 1998). Thus, a key question is why the same
transdiagnostic risk factor results in divergent trajectories of
symptom expression across individuals or across time.
In addition, more work is needed to specify the mecha-
nisms linking some more distal transdiagnostic factors to the
disorders they predict. For example, childhood sexual abuse is
a global risk factor for mood disorders, anxiety disorders, eat-
ing disorders, sexual disorders, dissociative disorders, sub-
stance use disorders, and most personality disorders (Maniglio,
2009). In order for childhood sexual abuse to be theoretically
useful as a transdiagnostic factor, it is important to know how
it could be linked to so many disorders. Some theorists have
suggested mediators that link childhood sexual abuse to spe-
cific disorders, such as problems in attachment, poor emotion
regulation, and hypervigilance for threat (e.g., Roche, Runtz,
& Hunter, 1999; Sarin & Nolen-Hoeksema, 2010; Spasojevic
& Alloy, 2002). In general, little work has been done to deter-
mine how distal transdiagnostic factors lead to intermediate
transdiagnostic factors, which then lead to a group of disor-
ders, and, in turn, how other factors come into play to deter-
mine which specific cluster of disorders or symptoms
individuals will manifest.
Thus, in summary, for transdiagnostic models to be of theo-
retical and practical value and for them to have meaningful
explanatory power, they need to be able to explain (a) the
mechanisms by which a transdiagnostic factor causes all the
different disorders it is associated with (i.e., the mechanisms
underpinning multifinality), and (b) why a given transdiagnos-
tic factor leads to different disorders in different people or to
different disorders within the same person over time (i.e.,
divergent trajectories). Transdiagnostic models also need to
be able to explain the mechanisms linking distal and more
proximal risk factors to each other and to psychopathologies.
We offer herein a heuristic for the development of transdi-
agnostic models, with a particular focus on guidelines for
identifying factors explaining multifinality and divergent tra-
jectories. We (a) specify different levels of transdiagnostic
factors and their relative theoretical and clinical usefulness,
(b) suggest the types of mechanisms by which factors at one
level may be related to factors at other levels, and (c) suggest
the types of moderating factors that may determine whether a
transdiagnostic factor leads to certain specific disorders or
symptoms and not others. We then apply this heuristic to
develop a transdiagnostic model of rumination, a risk factor
for multiple disorders that has been relatively well researched
(see Ehring & Watkins, 2008; Nolen-Hoeksema, Wisco, &
Lyubomirsky, 2008).
592 Nolen-Hoeksema and Watkins

A Heuristic for Developing Transdiagnostic
Models of Psychopathology
Our heuristic for developing models of transdiagnostic pro-
cesses, illustrated in Figure 1, organizes variables that have
been proposed to be transdiagnostic and suggests what
needs to be specified about transdiagnostic processes to
illuminate how they work to create a general risk for psy-
chopathology (multifinality) and a specific risk for certain
disorders (divergent trajectories). In brief, we argue that
transdiagnostic factors can be organized into those that are
more distal to psychopathology (setting conditions with a
number of causal mechanisms intervening between the con-
ditions and the psychopathology) and those that are more
proximal (processes with relatively few causal mechanisms
intervening between these process and the psychopathol-
ogy). We suggest the types of mechanisms that may link the
distal transdiagnostic risk factors with the more proximal
transdiagnostic risk factors. We further suggest the types of
mechanisms that may link proximal transdiagnostic risk

Distal Risk Factors

- Environmental context
- Congenital biological
abnormalities

Possible mechanisms
- Shape responses to environment
- Shape negative beliefs/self-image
- Condition specific behaviors

Proximal Risk Factors

- Biological factors leading to emotional,
cognitive, or behavioral tendencies
- Basic cognitive factors
- Stable psychological individual difference
factors

Moderators
- Conditions that raise concerns
or themes
- Conditions that shape
responses
- Conditions that change the
reward value of stimuli

Disorder A Disorder B Disorder C

Fig. 1.  A heuristic for developing transdiagnostic models of psychopathology.

Distal risk factors contribute to disorders only through mediating proximal risk factors. Proximal risk factors
directly influence symptoms relative to distal risk factors. Distal and proximal risk factors lead to multiple disorders
(i.e., multifinality), which are comorbid (indicated by dashed lines). Moderators interact with proximal risk factors to
determine which specific disorder individuals will experience (i.e., to determine divergent trajectories).

Downloaded from pps.sagepub.com by Susan Nolen-Hoeksema on October 18, 2011

Transdiagnostic Processes 593
factors to psychopathology. We argue that identifying the
mechanisms linking distal risk factors to proximal risk fac-
tors and proximal risk factors to psychopathology is critical
to a useful understanding of transdiagnostic processes. Finally,
we suggest two types of moderators that lead individuals with
transdiagnostic risk factors to develop specific types of
symptoms.
Distal and proximal transdiagnostic risk factors
The variables that have been argued to be transdiagnostic risk
factors vary in their causal distance to the psychopathology
they predict. We can organize them roughly into two catego-
ries: (a) environmental and congenital biological variables
relatively distal to observable symptoms of disorders and (b)
within-person variables that are more proximal to symptoms
of disorders. The critical distinction between distal and proxi-
mal risk factors is in how close the causal connection is
between the risk factor and psychopathology; distal risk fac-
tors lead to psychopathology only via mediating proximal risk
factors, whereas proximal risk factors more directly cause
psychopathology.
Distal transdiagnostic factors. The distal transdiagnostic
risk factors predict many disorders but it seems likely that a
number of processes at various levels intervene between these
distal risk factors and the psychopathologies they predict.
Thus, within this operationalization, a distal risk factor does
not directly cause symptoms but only influences symptoms
via mediating proximal factors (see Table 1). As such, a distal
risk factor is distant from the expression of symptoms both in
probability and mechanism. It is important to note that expo-
sure to a distal risk factor does not necessarily mean that sub-
sequent psychopathology will follow.
We conceive of distal transdiagnostic risk factors as experi-
ences or characteristics that are usually independent of
any actions of the individual—basically they “happen” to an
individual—and they set the stage for proximal risk factors (or
mediators) that more directly lead to psychopathology. This
characterization draws attention to the independent conditions
that may create more proximal vulnerability factors; it also
distinguishes between “setting conditions” that are less modi-
fiable and factors that may be more modifiable. However, the
nonmodifiability of a risk factor is not the critical characteris-
tic making it a distal risk factor; instead the critical character-
istic of distal risk factors is that they influence symptoms only
via mediating proximal factors.
We suggest that it is useful to confine distal risk factors to
two categories. The first is environmental context factors, such
as parental psychopathology, a history of sexual or physical
abuse, and other traumatic events. These are what Hammen
(1991, 2005) labels independent stressors because they are
not caused by the individual experiencing them (e.g., the death
of a spouse), and dependent stressors, which the individual may
have played a role in creating (e.g., interpersonal conflict). The
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Table 1.  Primary Characteristics of Components of the Heuristic
Component Characteristics
Distal risk Environmental context factors or congenital bio-
factors logical characteristics that cause psychopathol-
ogy only via mediating proximal risk factors
Tend to be distant in time from psychopatholo-
gies they predict but are not always temporally
distant
Tend to be difficult to control or modify
Proximal risk Within-person variables that mediate the
factors relationships between distal risk factors and
symptoms
Directly influence symptoms relative to distal
risk factors
Follow distal risk factors in time; precede psy-
chopathology in time
Tend to be more modifiable or controllable than
distal risk factors
Moderators Environmental context factors or biological
characteristics that
(a)  raise concerns or themes that the proximal
risk factors then act upon,
(b)  shape responses through conditioning, or
(c)  determine the reinforcement value of
certain stimuli (i.e., both how rewarding
certain stimuli are and how aversive they
are and thus how much negative reinforce-
ment value occurs at their removal)
Closer in time and causal effect to outcomes
than are distal risk factors; are concurrent
with, or follow, proximal risk factors in time;
precede psychopathology in time
Interact with proximal risk factors to produce
specific disorders or symptom expressions
experience of severe independent stressors, particularly during
childhood, is a clear risk factor for a large number of mental
disorders (Monroe, 2008), but several processes must inter-
vene to determine whether an individual who experienced
adversity as a child develops any type of psychopathology
and, if so, what specific symptoms he or she will develop.
The second category of distal risk factors consists of con-
genital biological abnormalities, principally genetic abnormal-
ities and congenital abnormalities in brain function or structure
(caused by genetic abnormalities or early brain injuries). These
biological characteristics shape the individual’s development
from birth, but multiple processes can intervene to determine
whether individuals born with these characteristics go on to
develop psychopathology. As an example, abnormalities in
certain genes, including G72/G30, the brain-derived neuro-
trophic factor (BDNF) gene, DISC1, COMT, neuregulin1, and
dysbindin, seem to confer risk for both schizophrenia and
bipolar disorder (Hill, Harris, Herbener, Pavuluri, & Sweeney,
2008), although only a subset of individuals with these abnor-
malities develop psychopathology. These genes do not have a
direct effect on symptoms of schizophrenia or bipolar disorder
594 Nolen-Hoeksema and Watkins
but instead appear linked to deficits in neurocognitive factors
such as attention regulation, working memory, episodic mem-
ory, and emotion processing (which we view as more proximal
risk factors), that may lead to the development of psychotic
symptoms (Barch, 2005; Hill et al., 2008).
Note that in most of the examples given here, the distal risk
factors are not only causally distant from the psychopathology
they produce but temporally distant as well (e.g., childhood
abuse contributing to adult psychopathology). Distal risk fac-
tors need not always be temporally distant from the symptoms
they produce. Posttraumatic stress disorder (PTSD) or acute
stress disorder can result soon after the experience of a major
trauma (American Psychiatric Association, 2000). In both
cases, we would consider the trauma a distal risk factor
because it sets the conditions for the development of symp-
toms, but not everyone who experiences the trauma will
develop PTSD or acute stress disorder, and a number of proxi-
mal risk factors appear to intervene to determine who will
develop symptoms (Keane, Marshall, & Taft, 2006).
Proximal transdiagnostic factors. We define proximal
transdiagnostic risk factors as within-person variables that
have been linked more directly to disorders via specific mech-
anisms; these are akin to what many theorists have dubbed
intermediate phenotypes (Cannon & Keller, 2006; Insel &
Cuthbert, 2009; Sanislow et al., 2010). Thus, proximal risk
factors are operationalized as those intrapersonal risk factors
that (a) directly precede symptoms (relative to distal risk fac-
tors), and/or (b) directly influence symptoms. Proximal risk
factors are more often modifiable than distal risk factors, but
being modifiable is not a criterion for proximal risk factors.
We suggest that proximal risk factors fall into three catego-
ries, which can be interrelated. The first category is biological
factors leading to potentially maladaptive emotional, cogni-
tive, or behavioral tendencies. Some examples include hyper-
activity in the amygdala associated with excessive emotional
reactivity (Davidson, Pizzagalli, & Nitschke, 2009), dysfunc-
tion in the hypothalamic-pituitary-adrenal axis associated with
a dysregulated stress response (Belmaker & Agam, 2008), or
hypoactivity in the prefrontal cortex that impairs impulse con-
trol and emotion regulation (Davidson et al., 2009; Potenza et
al., 2003). These biological factors are more proximal to psy-
chopathology than those we have categorized as distal factors
because they can lead more directly to symptoms (e.g., each of
the conditions just listed have been linked to depressive and
anxiety reactions to events; see Davidson et al., 2009; Konar-
ski et al., 2008; Southwick, Vythilingam, & Charney, 2005).
Also, although some of these biological characteristics may be
due to congenital factors such as genetic abnormalities, they
may also result from experiences; for example, some individu-
als with a childhood history of neglect or abuse develop a dys-
regulated stress response (Cicchetti & Toth, 2005; Heim &
Nemeroff, 2001).
The second category of proximal transdiagnostic risk factors
is basic cognitive deficits or biases in information processing,
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such as attentional biases or working memory deficits, which
are consistently and strongly linked to several psychopatholo-
gies (for comprehensive reviews of this large literature, see
Harvey et al., 2004; Mathews & MacLeod, 2005). Again, we
place these in the proximal risk factors class because they have
been linked through specific mechanisms to psychopathology
(e.g., working memory deficits contribute to symptoms of
schizophrenia; Barch, 2005) but probably result from more
distal factors such as genetic polymorphisms or early life
experiences (e.g., MacLeod, 1999).
A third category of proximal transdiagnostic risk factors is
stable psychological individual difference factors reflecting
the tendency to adopt particular styles of responding to situa-
tions, such as a pessimistic attributional style, emotion regula-
tion tendencies like chronic suppression, or personality
characteristics such as neuroticism or negative affectivity.
Again, these individual differences have been directly linked
to psychopathology—for example, greater negative emotional
reactivity (neuroticism) is associated with increased negative
emotional states and depression (e.g., Boyce, Parker, Barnett,
Cooney, & Smith, 1991; Kotov et al., 2010; Roberts & Kendler,
1999). The mechanisms linking some individual difference fac-
tors to psychopathology have been extensively studied; in sev-
eral cases, these mechanisms involve other proximal risk
factors. For example, the personality construct of neuroticism is
associated with a number of even more proximal risk factors,
including increased attention toward threat (Rusting, 1998),
increased accessibility of negative information (Martin, Ward,
& Clark, 1983), and increased amygdala reactivity to negative
stimuli (Hariri, Tessitore, Mattay, Fera, & Weinberger, 2002),
which in turn are associated with symptoms of depression and
anxiety (Charbonneau, Mezulis, & Hyde, 2009).
Although there is the possibility of causal relationships
among proximal risk factors, as just described, we group them
together because they share the characteristics of relative
closeness to psychopathology (compared with distal risk fac-
tors) and causal mechanisms linking them to psychopathology.
Future models of the transdiagnostic factors leading to spe-
cific disorders may delineate a larger number of levels of risk
factors than our distal and proximal levels; we believe our
heuristic is a good starting point for the development of mod-
els with more levels.
Mechanisms linking distal and proximal transdiagnostic
risk factors. Distal risk factors may lead to proximal risk fac-
tors via at least three mechanisms or processes. First, distal risk
factors may shape responses to the environment. For example,
MacLeod (1999) has argued that prolonged exposure to an
extended stressor, such as an abusive or neglectful environ-
ment, may lead to attentional biases to negative stimuli, because
under such circumstances it may be temporarily adaptive to
attend to threat. Attending to threat would be instrumentally
reinforced, increasing the tendency to attend to threat in future
situations. Consistent with this analysis, experimental exposure
to contingencies that make it adaptive to attend toward
Transdiagnostic Processes 595
threatening stimuli, or prolonged exposure to mild stressors,
can induce attentional bias toward threat (Clarke, MacLeod, &
Shirazee, 2008; MacLeod, Rutherford, Campbell, Ebsworthy,
& Holker, 2002).
Congenital biological abnormalities may also shape indi-
viduals’ responses to the environment, creating proximal risk
factors. Neuroticism and negative affectivity demonstrate a
heritable component (e.g., Smoller & Tsuang, 1998) and have
been linked to various genetic polymorphisms, most fre-
quently on the 5-HT promoter gene (e.g., for positive evi-
dence, see Munafo, Brown, & Hariri, 2008; for negative
evidence, see Willis-Owen et al., 2005). These genetic abnor-
malities may lead to neuroticism or negative affectivity in part
by creating chronic neural hyperreactivity to emotional and
threat stimuli (Munafo et al., 2008).
Second, distal factors could shape individuals’ beliefs,
schemas, and self-images to create proximal factors. For
example, chronic uncontrollable stress could lead a child to
develop the belief that she is helpless or deficient or to view
attachment figures as untrustworthy (Cicchetti & Toth, 2005).
These beliefs and schemas could then influence the coping
strategies adopted by individuals as well as the current con-
cerns driving their cognitive processes.
Third, classical and operant conditioning, modeling, and
observational learning are likely to play roles in linking distal
and proximal risk factors. For example, parents with psycho-
pathology may not model or teach adaptive emotion regula-
tion to their children (Eisenberg, Spinrad, & Eggum, 2010). As
another example, behaviors that reduce distress, such as an
avoidant information processing style or emotion regulation
strategy, are more likely to occur and will have greater nega-
tive reinforcing value in the context of distal risk factors such
as ongoing difficult environmental context (Hayes et al.,
2004). Thus, those individuals exposed to distal risk factors
are more at risk for conditioning processes strengthening
proximal risk factors.
Moderators of the effects of proximal risk factors. The
final major component of our heuristic is the moderators that
determine what particular symptoms proximal transdiagnostic
risk factors will lead to in a given individual. Moderators cre-
ate symptoms by (a) raising concerns or themes that proximal
risk factors then act upon, (b) shaping responses through con-
ditioning, or (c) determining the reinforcement value of cer-
tain stimuli.
The first category of moderators is conditions that raise cer-
tain themes or concerns that proximal factors then act upon.
For example, individuals prone to neuroticism may be more
likely to develop an anxiety disorder than another disorder if
their environment is chronically threatening because threat
tends to produce the emotions of fear and anxiety (LeDoux,
2000); their tendency to be emotionally overreactive and to
attend to threat (Rusting, 1998) will then exacerbate and main-
tain their anxiety. In contrast, individuals prone to neuroticism
who experience a series of important losses may be more
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likely to develop depression than anxiety or another disorder
because loss is associated with sadness and depression (G. W.
Brown & Harris, 1986); again their emotional reactivity and
attentional bias will maintain their sad emotions and aware-
ness of their losses, potentially leading to depression. Thus,
the nature of the environmental circumstances may temporar-
ily make more accessible certain current concerns relative to
others (Klinger, 1996), thereby influencing the specific ways
that proximal risk factors may manifest in symptoms.
A second category of moderators is conditions that operate
on proximal transdiagnostic risk factors to shape them into
disorder-specific responses through modeling, observational
learning, and reinforcement. For example, a teenager who car-
ries the proximal risk factor of a tendency toward stimulation
seeking will be more likely to develop aggressive or antisocial
behavior if he is exposed to environments that model and rein-
force aggression (Lynam et al., 2000). Alternatively, if that
sensation-seeking teenager is raised in an environment that
does not model or reinforce aggression or antisocial behaviors
but instead shapes that sensation seeking toward prosocial
behaviors such as sports, he may be unlikely to develop anti-
social aggression (Dishion & Patterson, 1997). Thus, these
modeling, shaping, and reinforcing processes will influence
the nature of responses and cognitive processes that individu-
als learn to use in response to particular stressors or motiva-
tions. Moreover, these processes will also influence the type of
current concerns that become more chronically important and
accessible for an individual (Klinger, 1996) and thereby influ-
ence the specific ways that proximal risk factors may manifest
in symptoms.
The third group of moderators is biological or environmen-
tal characteristics that change the sensitivity to and reinforce-
ment value of internal and external stimuli. It is important to
note that changes in reinforcement value can occur for both
the processes of positive reinforcement, which refers to
responses that are followed by the presentation of a stimulus
that increases the chance of that behavior occurring (typically
onset of a pleasant stimulus), and negative reinforcement,
which refers to the removal of a stimulus that increases the
chance of the behavior occurring (typically removal of some-
thing aversive). Thus, biological characteristics may influence
the extent to which particular appetitive stimuli such as food
or alcohol are rewarding and increase the reinforcement value
of the occurrence of these stimuli and/or the extent to which
potentially unpleasant stimuli such as negative mood states are
experienced as aversive, thereby increasing the reinforcement
value of removing these stimuli (Kalivas & Volkow, 2005).
For example, individuals vary in how rewarding they find
alcohol, and heightened reward sensitivity predicts increased
use and abuse of alcohol (Jorm et al., 1999; Newlin & Thom-
son, 1990; Pardo, Aguilar, Molinuevo, & Torrubia, 2007). A
heightened sensitivity to the rewarding effects of alcohol may
shape several of the proximal risk factors, such as emotion
dysregulation, into alcohol abuse (cf. Armeli, Carney, Tennen,
Affleck, & O’Neil, 2000; Cooper, Russel, & George, 1988).
596 Nolen-Hoeksema and Watkins
That is, people whose emotions are dysregulated who have
high reward sensitivity for alcohol will be more likely to turn
to alcohol to cope than people who are emotionally dysregu-
lated but have low reward sensitivity for alcohol. As noted ear-
lier, environmental circumstances may also change the
reinforcement value of stimuli; for example, prolonged stress
may increase the negative reinforcement occurring to the
reduction of distress; hunger will increase the positive rein-
forcement occurring in response to consummation of food.
Likewise, individual differences in the capacity to with-
stand and tolerate negative emotional states may contribute to
the extent to which the individual engages in escape behaviors
such as drinking or substance abuse in response to heightened
emotional reactivity (Leyro, Zvolensky, & Bernstein, 2010;
Zvolensky, Vujanovic, Bernstein, & Leyro, 2010). Biological
(and psychological) characteristics that increase the aversive
experience of particular emotional states would increase the
reinforcement value of avoiding distress and thereby increase
engagement in behaviors like substance abuse and binge eat-
ing. In particular, lower perceived distress tolerance for nega-
tive affect is concurrently and prospectively related to
increased risk for substance use disorders, coping-oriented
drug use, bulimic symptoms, and posttraumatic stress symp-
toms (Vujanovic, Bernstein, & Litz, in press).
Some interactive models of psychopathology focus on the
interaction between two or more factors in explaining a par-
ticular disorder or symptom expression. For example, several
theorists have argued that the interaction of maladaptive per-
sonality characteristics, such as low self-esteem, and the expe-
rience of stressors increases risk for depression (G. W. Brown,
Andrews, Bifulco, & Veiel, 1990; Kendler, Kuhn, & Prescott,
2004). Indeed, it is likely true that having more than one proxi-
mal transdiagnostic risk factor or a combination of proximal
and distal risk factors increases one’s vulnerability to a given
psychopathology more than having only one proximal risk
factor. We argue, however, that we gain more explanatory
power by confining moderators to factors that do not simply
increase overall risk but specifically shape the vulnerability
created by proximal transdiagnostic factors into particular
responses or symptoms.
Moreover, we have confined moderators to environmental
and biological factors so as to distinguish them from proximal
risk factors and avoid problems that sometimes emerge in
interactive models involving multiple proximal risk factors. In
some of these models, the proximal risk factors said to interact
with each other overlap considerably, and one could be said to
be a proxy or cause of the other. For example, Vohs et al.
(2001) suggested that disordered eating is especially likely to
result when body dissatisfaction is combined with perfection-
ism and low-self esteem. Low self-esteem may be the result of
body dissatisfaction, however, or body dissatisfaction may be
the result of perfectionism. We suggest that by confining mod-
erators to environmental and biological factors as we do, we
reduce the potential for circularity and increase the potential
explanatory power of a transdiagnostic model.
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We note that there are similarities between moderators and
distal risk factors; that is, both involve environmental and bio-
logical factors that are typically independent of the individual’s
actions. Indeed, we argue that the same types of environmental
or biological factors could act as either distal risk factors for
psychopathology or moderators of a proximal risk factor. For
example, chronically threatening environments could act as a
distal risk factor that creates an attentional bias to threat. In
individuals with attentional bias to threat, exposure to a chroni-
cally threatening environment could also act as a moderator of
their attentional bias, leading to anxiety reactions.
Critical distinctions between distal risk factors and modera-
tors are (a) their temporality relative to proximal risk factors
and psychopathology and (b) how they exert their causal
effects. Distal risk factors precede proximal risk factors and
psychopathology in time; moreover, distal risk factors are con-
ceived as causes of proximal risk factors; proximal risk fac-
tors, in turn, cause psychopathology (i.e., are mediators
between distal risk factors and psychopathology). Moderators
have their effects by interacting with and acting on existing
proximal risk factors and thus follow them in time or are con-
current with them; however, moderators precede and have
causal effects on psychopathology. For example, a history of
childhood sexual abuse can act as a distal risk factor for psy-
chopathology by creating the proximal risk factor of a dys-
regulated stress response; an incident of abuse during
adulthood can act as a moderator of this dysregulated stress
response, creating an emotional disorder that develops shortly
after the adult abuse incident.
Some moderators may produce symptoms on their own
without the additional vulnerability created by the proximal
risk factors. For example, having parents who are excessively
concerned about weight and do not model healthy eating hab-
its may be enough to lead a child to develop an eating disorder
(e.g., Stein et al., 2006). Or having parents who model inap-
propriate use of alcohol to regulate emotions may be enough
to lead a teenager to develop alcohol abuse (Zucker, Kincaid,
Fitzgerald, & Bingham, 1995). These moderators alone, how-
ever, do not explain the frequent comorbidity between eating
disorders or alcohol abuse and other psychopathologies. The
value of our heuristic is that it guides researchers to explain
both specificity and comorbidity and both multifinality and
divergent trajectories. Proximal risk factors explain comorbid-
ity and multifinality, that is, the mechanisms by which one
process leads to multiple comorbid disorders. Moderators
explain how individuals with that proximal risk factor develop
specific disorders—that is, their divergent trajectories.
Applying the Heuristic: Rumination as a
Transdiagnostic Factor
To illustrate the value of our heuristic, we turn to the literature
on rumination, the tendency to repetitively analyze one’s prob-
lems, concerns, and feelings of distress without taking action
to make positive changes (Nolen-Hoeksema, 1991; Watkins,
Transdiagnostic Processes 597

Distal Risk Factors

Environmental Context: Sexual and
Emotional Abuse; Overcontrolling,
Neglectful Parenting
Congenital Biological Abnormalities:
BDNF Polymorphism

Possible Mechanisms
Shape Responses to Environment: Abuse and
Overcontrolling Parenting Lead to Vigilance,
Dysregulated Stress Response, Helplessness; Genetic
Factors Lead to Impaired Inhibitory Control and
Attention to Negative Stimuli In Environment
Shape Negative Beliefs: Abuse and Overcontrolling
Parenting Lead to Views of Self as not Able to Cope
Condition Specific Behaviors: Abusive or
Overcontrolling Parents do not Teach Efficacious
Coping Responses

Proximal Risk Factors

Rumination

Moderators Moderators Moderators Moderators

Conditions Conditions Conditions Conditions
Raising Concerns Raising Changing Changing Reward
or Themes: Loss, Concerns or Reward Value Value of Stimuli:
Rejection, Failure Themes: of Stimuli: High Reward
Events Chronic High Reward Sensitivity to Food
Uncontrollable Sensitivity to
Stress (PTSD); Substances Conditions
Social Stress Shaping Responses:
(Social Anxiety Conditions Exposure to &
Disorder); Shaping Reinforcement of
Disposition to Responses: Thin Ideal, Weight
Panic Attacks Exposure to & Concerns; Social
(PD); Basal Reinforcement Punishments for
Ganglia of Substance Substance Use
Dysfunction Use
(obsessions)

Depression Anxiety Substance Bulimia

Misuse Nervosa

Fig. 2.  Using the heuristic to develop a transdiagnostic model of rumination.

Distal risk factors for rumination may include the environmental context variables of sexual and emotional abuse and overcontrolling
parenting and the congenital biological abnormality of certain polymorphisms in the brain-derived neurotrophic factor gene.These may lead
to rumination by shaping vigilant, dysregulated, helpless, negatively focused responses to the environment; shaping negative beliefs about
one’s ability to cope; and failing to teach efficacious coping responses. Moderators may determine the divergent trajectories individuals
high on rumination take: conditions raising themes of loss lead to depression; conditions raising concerns about specific threats or about
panic symptoms or obsessions may lead to anxiety disorders; conditions leading to high reward sensitivity to substances or shaping use of
substances may lead to substance misuse; conditions leading to high reward sensitivity to food, shaping weight concerns, or preventing use
of substances may lead to eating disorders.

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598 Nolen-Hoeksema and Watkins
2008). A large literature (as reviewed in Ehring & Watkins,
2008) and a recent meta-analysis (Aldao et al., 2010) show
that rumination predicts a number of types of psychopathol-
ogy (i.e., it demonstrates multifinality). Briefly, rumination
prospectively predicts both symptoms and diagnoses of major
depression (see meta-analyses by Aldao et al., 2010; Mor &
Winquist, 2002; Rood, Bogels, Nolen-Hoeksema, & Schouten,
2009; Watkins, 2008). Rumination also predicts symptoms of
anxiety, substance abuse, alcohol abuse, and eating disorders
(see Aldao et al., 2010; Caselli et al., 2010; Nolen-Hoeksema,
Stice, Wade, & Bohon, 2007). Among the specific anxiety dis-
orders, rumination is associated with an increased risk for
social phobia (Mellings & Alden, 2000), PTSD (Ehlers,
Mayou, & Bryant, 1998; Mayou, Ehlers, & Bryant, 2002), and
symptoms of generalized anxiety (Watkins, 2009a).
We consider rumination a proximal risk factor. In this illus-
tration, we will link it back to possible distal risk factors and
suggest some mechanisms by which the distal risk factors con-
tribute to rumination (see Figure 2). We will then briefly
review studies of the mechanisms linking rumination to dis-
tress and suggest moderators that may determine whether indi-
viduals who tend toward rumination experience depression,
anxiety, substance abuse, or eating disorder symptoms (i.e.,
moderators that may explain divergent trajectories).
Distal risk factors and mechanisms linking
them to rumination
Among the environmental context factors (i.e., independent
stressors) that have been associated with the tendency to rumi-
nate are childhood sexual and emotional abuse. Studies of col-
lege students (Conway, Mendelson, Giannopoulos, Csank, &
Holm, 2004), community participants (Sarin & Nolen-Hoek-
sema, 2010), and patients (Watkins, 2009b) have found that
individuals with a history of sexual abuse score significantly
higher on a self-report measure of rumination than do those
who reported no history of sexual abuse. Similarly, Spasojevic
and Alloy (2002) found that a childhood history of sexual mal-
treatment (for females only) and emotional maltreatment (for
both sexes) were significantly related to higher levels of rumi-
nation in college students.
Experiencing sexual or emotional abuse during childhood,
particularly if the abuse is chronic, could contribute to rumina-
tion by making children vigilant for signs of threat and making
them feel they are helpless to prevent severely negative events
(Spasojevic & Alloy, 2002). In turn, this could lead children to
turn inward to cope, analyzing the problems they face passively,
in a ruminative manner (Sarin & Nolen-Hoeksema, 2010).
In addition, studies suggest that children with a history of
sexual or emotional abuse may develop dysregulated stress
responses, as measured by cortisol levels, adrenocorticotropic
hormone levels, and cardiac measures (Heim, Plotsky, &
Nemeroff, 2004; Zahn-Waxler, 2000). Children who have
more poorly regulated biological responses to stress will find
it more difficult to engage in efficacious behavioral responses
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to new stressors and thus may fall into a ruminative pattern
(Nolen-Hoeksema, 2004b).
Spasojevic and Alloy (2002) also found that participants
who reported that their parents were overcontrolling had
higher levels of rumination. Overcontrolling parenting could
foster rumination in children by undermining children’s sense
of self-efficacy or mastery and instead sending messages to
children that they are helpless and incompetent (Higgins &
Silberman, 1998; Spasojevic & Alloy, 2002). In a study of
depressed and nondepressed mothers and their 5- to 7-year-old
children, Nolen-Hoeksema, Wolfson, Mumme, and Guskin
(1995) found that the children of mothers who were more
intrusive during a puzzle task, often taking over the task from
the child in a critical manner, were more helpless and passive
and less likely to engage in problem solving both during the
puzzle task and, by teachers’ reports, in their classroom behav-
ior. Parents’ overcontrolling behaviors may also provide chil-
dren with little opportunity to learn persistence and proactive
coping strategies, contributing to a tendency to ruminate (Spa-
sojevic & Alloy, 2002).
A congenital biological abnormality that has been linked to
rumination is the Val66Met polymorphism in the BDNF gene.
An amino acid substitution (valine to methionine) at codon 66
(Val66Met) of the BDNF gene results in two alleles: val and
met. Independent studies have found that adults who carried
the met allele (val/met or met/met) showed greater levels of
rumination than did adults who did not (val/val) (Beevers,
Wells, & McGeary, 2009; Hilt, Sander, Nolen-Hoeksema, &
Simen, 2007). In turn, rumination scores mediated the rela-
tionship between the presence of the met allele and higher lev-
els of depression in both studies.
Carriers of the met allele may show more rumination
because its presence is associated with impairments in cogni-
tive functioning that could make it more difficult for individu-
als to control rumination. The met allele is associated with
decreased synaptic activity and plasticity in the hippocampus
and smaller hippocampal volumes (Frodl et al., 2007) as well
as with poorer performance on tasks tapping prefrontal corti-
cal functioning, including poorer episodic memory and execu-
tive functioning (Rybakowski et al., 2006). In turn, rumination
is associated with deficits in the ability to inhibit information,
particularly self-relevant or negative information, once it
enters working memory (Joormann, 2004, 2006; see also
Johnson, Nolen-Hoeksema, Mitchell, & Levin, 2009). Thus,
the met allele may confer risk for rumination because it results
in deficits in brain areas involved in successful inhibition of
information in working memory. Making these potential con-
nections between genetic factors, neural functioning, basic
cognitive processes, and rumination as an individual differ-
ence factor contributing to psychopathology is consistent with
the goals of the RDoC initiative (Sanislow et al., 2010).
In sum, distal risk factors for rumination appear to include
the environmental context variables of sexual and emotional
abuse and overcontrolling parenting and the congenital bio-
logical factor of a particular BDNF polymorphism. These may
Transdiagnostic Processes 599
lead to rumination by shaping vigilant, dysregulated, helpless,
negatively focused responses to the environment, shaping
negative beliefs about one’s ability to cope, and conditioning
inefficacious coping responses.
Mechanisms linking rumination to depression
The mechanisms linking rumination to depression have been
extensively studied and will be only briefly reviewed here (for
comprehensive reviews, see Lyubomirsky & Tkach, 2004;
Nolen-Hoeksema et al., 2008; Watkins, 2008, 2010). First,
rumination appears to amplify the reciprocal relationship
between cognition and mood state, wherein negative mood
increases the accessibility of negative cognition, which in turn
fuels the negative mood (Ciesla & Roberts, 2007; Nolen-Hoek-
sema, 1991; Teasdale, 1988). Specifically, experimental studies
indicate that rumination exacerbates existing dysphoric mood
(see Nolen-Hoeksema et al., 2008) and leads people in a
depressed mood to have more negative thoughts about the past,
present, and future (Lavender & Watkins, 2004; Lyubomirsky,
Caldwell, & Nolen-Hoeksema, 1998; Lyubomirsky & Nolen-
Hoeksema, 1995; Rimes & Watkins, 2005), making it more
likely that people will use these negative thoughts to understand
their current circumstances. Furthermore, experience sampling
studies have found that real world rumination predicts subse-
quent negative affect and mediates the effect of negative events
on subsequent affect (Moberly & Watkins, 2008a, 2008b).
Explicitly training individuals to adopt the thinking style char-
acteristic of rumination increases affective reactivity to a subse-
quent stressful event relative to training individuals to think in a
way inconsistent with rumination (Moberly & Watkins, 2006;
Watkins, Moberly, & Moulds, 2008).
Second, rumination interferes with effective problem solv-
ing, in part by making thinking more pessimistic and fatalistic
as well as more abstract and distanced from the specific details
of how to solve a difficulty (Donaldson & Lam, 2004; Lyu-
bomirsky & Nolen-Hoeksema, 1995; Lyubomirsky, Tucker,
Caldwell, & Berg, 1999; Watkins & Baracaia, 2002; Watkins
& Moulds, 2005). Third, rumination also interferes with
instrumental behavior (Lyubomirsky & Nolen-Hoeksema,
1993). Thus, rumination prevents the resolution of problems
and difficulties that may have led to depressed mood and may
potentially produce further increases in stressful circum-
stances. Indeed, recent prospective longitudinal studies sug-
gest that rumination predicts increased chronic stress
(McLaughlin & Nolen-Hoeksema, in press; Pearson, Watkins,
Mullan, & Moberly, 2010).
Mechanisms linking rumination to anxiety
Although most of the work on rumination has focused on its
effects on individuals with an elevated depressed mood, rumi-
nation appears to exacerbate whatever mood or theme is cur-
rently active in the individual (Blagden & Craske, 1996;
Bushman, 2002; Bushman, Bonacci, Pedersen, Vasquez, &
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Miller, 2005; Rusting & Nolen-Hoeksema, 1998). Specifi-
cally, experimentally induced rumination increases anxiety in
already-anxious participants and participants whose thoughts
are directed toward anxious themes (Blagden & Craske, 1996;
McLaughlin, Borkovec, & Sibrava, 2007). The same mecha-
nisms of (a) amplifying current mood state and mood-congru-
ent cognition, (b) impairing problem solving, and (c)
interfering with instrumental behavior are also relevant to the
development of anxiety disorders. Maladaptive cognition is a
characteristic and causal contributor to anxiety disorders (D.
M. Clark, 1999), although it tends to be focused on future
threat rather than past loss as in depression (Watkins, Moulds,
& Mackintosh, 2005; see the next section). Similarly, poor
problem solving and passive, avoidant behavior when faced
with a stressful situation will lead to exacerbation of the
stressor and increased anxiety.
Moderators of the effects of rumination on
depression versus anxiety
For moderators interacting with rumination to produce one
type of symptom over another, our heuristic points to environ-
ments and biologically based individual differences that draw
individuals’ attention to certain concerns or themes over oth-
ers. A number of environmental factors may interact with
rumination to produce major depression in some individuals
and anxiety disorders in others (or depression versus anxiety at
different times in an individual’s life). Interpersonal loss or
rejection tends to create sad moods more than other types of
moods (G. W. Brown & Harris, 1986; Eley & Stevenson,
2000; Pine, Cohen, Johnson, & Brook, 2002; Williamson, Bir-
maher, Dahl, & Ryan, 2005). This suggests that rumination
among people who have recently had loss or rejection experi-
ences will be more likely to lead to depressive symptoms than
to other types of symptoms. A longitudinal study of adults who
lost a close loved one to cancer found that those who rumi-
nated experienced more depression symptoms and were more
likely to be diagnosed with depression than those who rumi-
nated less (Nolen-Hoeksema & Larson, 1999). Further analy-
ses of this study conducted for the present article showed that
the relationships between rumination and depressive symp-
toms shortly before (r = .58, p < .001) and shortly after (r =
.60, p < .001) the loved one’s death were significantly greater
(at p < .05) than the relationships between rumination and
anxiety symptoms (before: r = .41, p < .001; after: r = .50, p <
.001) or between rumination and anger (before: r = .33, p <
.001; after: r = .39, p < .001). Thus, rumination in the context
of an important interpersonal loss was more strongly related to
depressive symptoms than to anxiety or anger, although rumi-
nation was associated with these moods as well.
Still, some participants in this study were facing conditions
that would likely induce considerable anxiety or anger, such as
a financial instability due to the loss of the loved one’s income
or to medical bills, conflicts with relatives over the settlement
of the loved one’s estate, or beliefs that doctors did not do all
600 Nolen-Hoeksema and Watkins
that was possible to save their loved one (Nolen-Hoeksema &
Larson, 1999). Among people facing such circumstances, high
levels of rumination would likely lead to anxiety and/or anger
as well as depressive symptoms over the loss of their loved
one. Thus, the environmental context can influence the diver-
gent trajectories of relative anxiety versus depression symp-
toms in response to rumination by influencing the initial
negative mood state (sadness, anger, anxiety, or some combi-
nation thereof) that subsequent rumination amplifies and
prolongs.
Environmental circumstances, including a prior history of
exposure to particular circumstances, that raise concerns over
specific types of threats or that condition anxious reactions to
specific threats may produce anxiety disorders rather than
depression among people prone to rumination (Ehring & Wat-
kins, 2008; Mineka & Zinbarg, 2006). Further, different types
of threat concerns may lead to different types of anxiety
disorders.
People with social phobia frequently report having experi-
enced traumatic social embarrassment prior to developing
their phobias. For example, McCabe, Antony, Summerfeldt,
Liss, and Swinson (2003) reported that 92% of adults with
social phobia reported a history of severe teasing in childhood,
compared with only 50% and 35% of people with panic disor-
der or obsessive–compulsive disorder, respectively. Likewise,
Hackmann, Clark, and McManus (2000) found that the major-
ity of individuals with social phobia had intrusive images of
memories of previously embarrassing events, with these mem-
ories dated to the time of onset of the disorder. Among people
who have had socially traumatizing experiences, those prone
to ruminate will rehearse memories of the experiences, analyz-
ing what they did right and wrong and how other people
reacted to them. Indeed, studies of people with social phobia
find that they do “postmortem” analyses of social encounters,
focusing on how they performed and what others think of
them (Abbott & Rapee, 2004; Kashdan & Roberts, 2007;
Kocovski, Endler, Rector, & Flett, 2005; Mellings & Alden,
2000). Wong and Moulds (2009) found that following a social-
evaluative task, rumination maintained anxiety in both high
and low socially anxious controls relative to distraction. Fur-
thermore, Vassilopoulos and Watkins (2009) found that in
individuals high in fear of negative evaluation, a concrete
rumination condition (thinking about the concrete details of a
situation and how it occurred) decreased ratings of the self as
worthless and incompetent, pre- to postmanipulation, whereas
an abstract rumination condition (thinking about the meanings
and implications of a situation) maintained such negative self-
judgments, implicating abstract rumination in the maintenance
of negative cognition. Thus, such postevent rumination seems
likely to increase risk for the development of social phobia.
Mineka and Zinbarg (2006) suggest that PTSD develops
specifically in response to events that are both uncontrollable
and unpredictable, particularly if these events are chronic.
They further suggest that individuals who are more prepared
for trauma by knowing what might happen and having
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strategies to deal with the trauma will view the trauma as more
controllable and predictable, and they will therefore be less
likely to develop PTSD. For example, torture victims who
were political activists and understood their risk for torture,
what the torture might entail, and how to remain stoic during
the experience of torture were less likely to develop PTSD
than torture victims who were ordinary, nonpolitical citizens,
even when the degree of torture experienced was greater
among the political activists (Basoglu et al., 1997). For those
who are unprepared for a trauma, rumination may be espe-
cially likely to amplify their sense of uncontrollability and
unpredictability because rumination focuses on abstract ques-
tions about an experience rather than on concrete features of
the experience that can make it seem more controllable and
predictable (Watkins, 2008). For example, studies of patients
with PTSD have found that their ruminations tend to be
focused on analyzing long-term consequences of the traumatic
event, what life would be like if the event had not happened,
what else might have happened, how unfair it was, and the
patient’s relationship to other people (Ehlers & Clark, 2000;
Michael, Halligan, Clark, & Ehlers, 2007).
Biological factors that raise certain concerns or symptoms
may also interact with rumination to produce specific anxiety
syndromes. For example, rumination in conjunction with a
susceptibility to panic attacks (due to dysfunction in systems
regulating the fight-or-flight response; Roy-Byrne, Craske, &
Stein, 2006) could contribute to panic disorder as the individ-
ual ruminates over past episodes of panic and the possibility of
future episodes. Dysfunction in the brain regions implicated in
obsessive thoughts and compulsive behaviors (the frontal cor-
tex, basal ganglia, and thalamus; see Rauch et al., 2007; Sax-
ena & Rauch, 2000), in combination with a tendency to
ruminate over the meaning of such thoughts and behaviors
(Salkovskis, 1999), could contribute to obsessive–compulsive
disorder.
Thus, environmental conditions (loss events versus specific
threats) or biological factors (predispositions to panic attacks
or obsessive thoughts) that raise certain concerns may interact
with rumination to determine whether individuals experience
depressive symptoms or anxiety symptoms. These suggestions
are speculative and require empirical testing. They illustrate,
however, how our heuristic can be used to generate predictions
about moderators of transdiagnostic risk factors leading to the
divergent trajectories of depression or anxiety.
Mechanisms and moderators of the
relationship between rumination and alcohol
and substance abuse
Other types of environmental or biological moderators may
lead people prone to rumination to diverge onto trajectories of
alcohol or substance abuse. Heatherton and colleagues
(Abramson, Bardone-Cone, Vohs, Joiner, & Heatherton, 2006;
Heatherton & Baumeister, 1991) argue that some people who
Transdiagnostic Processes 601
are highly aware of aversive aspects of themselves and their
experiences, as are people who ruminate, turn to escapist
behaviors such as binge drinking and substance abuse to tem-
porarily quell their self-directed thoughts and related distress.
Accordingly, researchers have suggested that psychoactive
substances such as alcohol may be sought by people prone to
rumination as a way of “escaping” from, or drowning out,
their ruminations (Caselli et al., 2010; Nolen-Hoeksema et al.,
2007; Nolen-Hoeksema & Harrell, 2002). What determines
why some people turn to substances to escape their rumina-
tions (i.e., why they diverge onto this path)? We suggest that
people prone to ruminate will be more likely to turn to sub-
stances as a preferred means of escape if they experience
greater reinforcement from substances due to certain biologi-
cal characteristics and/or learning histories. Thus, both bio-
logical and environmental moderators likely play a role in
determining which ruminators diverge down the path to sub-
stances and which do not.
Substances of abuse activate the mesocorticolimbic region
of the brain, known as the reward center (Kalivas & Volkow,
2005), but as noted earlier, people differ in how rewarding
they find these substances (Newlin & Thomson, 1990; Sher,
Grekin, & Williams, 2005). Higher self-reported reward sensi-
tivity is correlated with earlier age of onset of drinking alcohol
in young adults (Pardo et al., 2007), with alcohol use and
abuse in nonclinical samples (Loxton & Dawe, 2001), and
with craving and positive affect in response to alcohol cues in
young adult hazardous drinkers (Zisserson & Palfai, 2007).
Emotional distress, which is chronically higher in people who
ruminate, appears to potentiate reward systems in the brain
(Brady & Sinha, 2005), and this potentiation may be even
greater in individuals high in reward sensitivity, increasing the
chances they will turn to substances. Thus, rumination may
interact with individuals’ sensitivity to the rewarding aspects
of substances like alcohol, determining whether they will
develop alcohol abuse (Aldao et al., 2010; Carver, Johnson, &
Joormann, 2008).
We know of no direct tests of this hypothesis, but the litera-
ture on alcohol expectancies provides some evidence that the
combination of high reward sensitivity and emotional dysreg-
ulation as seen in rumination is a strong predictor of alcohol
use. Individuals who have positive expectancies for the effects
of alcohol (including the reduction of negative mood) are
more prone to drink when distressed and to develop alcohol
abuse and dependence (Armeli et al., 2000; Cooper, Frone,
Russell, & Mudar, 1995; Cooper, Russell, Skinner, Frone, &
Mudar, 1992). Positive expectancies for the effects of alcohol
are not the same as reward sensitivity but may reflect self-
knowledge that substances have rewarding consequences
(Brunelle, Barrett, & Pihl, 2007). Moreover, because many of
these studies looked specifically at the interaction between
positive expectancies and the experience of distress (e.g.,
Armeli et al., 2000) or between positive expectancies and mal-
adaptive emotion regulation styles (e.g., Cooper et al., 1988),
their results are in line with our arguments that individuals
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who are sensitive to rewards (specifically the rewarding effects
of alcohol) and who have poorly regulated emotions because
of a tendency to ruminate are more likely to consume alcohol
and develop alcohol-related problems.
The social environment also influences how much reward
or punishment individuals receive for using alcohol. Individu-
als, particularly youth, with high levels of exposure to alcohol
use and reinforcement for alcohol use are more likely to see
alcohol use as normative and as an appropriate way to respond
to distress, including the distress caused by rumination. Ado-
lescents’ alcohol use over time is predicted by peers’ perceived
drinking, offers of alcohol, and perceived norms for drinking
(e.g., Wills & Cleary, 1999; Wood, Read, Mitchell, & Brand,
2004). Children raised in homes where parents drink exces-
sively and regard drinking as an appropriate response to stress
are more likely to have positive expectancies about the effects
of alcohol, to begin to drink earlier, and to use alcohol exces-
sively in adolescence and young adulthood (Fitzgerald &
Zucker, 2006; Zucker et al., 1995). Individuals prone to rumi-
nation who have been exposed to environments that reinforce
alcohol use may be more likely to turn to alcohol to “drown
out” their ruminations. Conversely, ruminative people whose
environments discourage or prohibit the use of alcohol may be
less likely to turn to alcohol (Nolen-Hoeksema, 2004a).
Thus, biological conditions leading to high reward sensitiv-
ity to substances and environmental conditions enhancing
reinforcement and modeling of substance use may interact
with rumination to send some people down the pathway to
alcohol or other substance use. Again, these predictions require
future testing but illustrate how our heuristic can be used to
generate predictions about divergent trajectories.
Mechanisms and moderators of the
relationship between rumination and eating
disorders
What will determine which people high on rumination diverge
onto a trajectory toward symptoms of eating disorders? As
with alcohol use, reward sensitivity and conditioning by the
social environment may influence which individuals prone to
rumination turn to binge eating to quell their self-aversive
thoughts (Heatherton & Baumeister, 1991) and develop symp-
toms of eating disorders. Like alcohol consumption, food acti-
vates the reward centers of the brain (Avena, Rada, & Hoebel,
2008; Di Chiara, Acquas, & Tanda, 1996). Indeed, both animal
and human research suggest that food and alcohol may serve
as substitutes for each other as rewards (see Gearhardt &
Corbin, in press). Animal studies show that rats that consumed
large amounts of sugar as adolescents later drank more alcohol
as adults (Pian, Criado, Walker, & Ehlers, 2009) and when
sugar-addicted rats are deprived of sugar they consume more
alcohol (Avena, Carillo, Needham, Leibowitz, & Hoebel,
2004). Humans recovering from alcohol dependence prefer
more intense levels of sweetness than those never dependent
602 Nolen-Hoeksema and Watkins
on alcohol (Kampov-Polevoy, Garbutt, & Janowsky, 1997),
and individuals with a family history of alcoholism prefer
sweets at higher rates than those without a family history of
alcoholism (Kampov-Polevoy, Garbutt, & Khalitov, 2003).
Further, individual differences in the activity of brain
reward centers in response to food cues are associated with
food intake: neuroimaging studies found greater reactivity in
mesocorticolimbic areas in response to food cues in obese than
in nonobese participants (Rothemund et al., 2007; Stice,
Spoor, Bohon, Veldhuizen, & Small, 2008; Stoeckel et al.,
2008), and greater reactivity in this brain area predicted future
weight gain (Stice, Yokum, Bohon, Marti, & Smolen, 2010).
Among people prone to ruminate, greater sensitivity to the
rewarding aspects of food may determine whether they turn to
binge eating to shut out ruminations and the distress that rumi-
nations create.
Again, we know of no direct test of this hypothesis, but
studies on the use of food to regulate emotions are consistent.
People who believe that binge eating will improve their mood
and who binge eat in an attempt to reduce negative affect are
at increased risk to develop eating disorders (McCarthy, 1990;
Polivy & Herman, 2002). For example, Stice, Presnell, and
Spangler (2002) followed a group of adolescent girls over
2 years and found that the girls who engaged in emotional
eating—eating when they felt distressed in an attempt to feel
better—were significantly more likely to develop chronic
binge eating over the 2 years. Thus, individuals who ruminate
and who find that binge eating quells their distressing rumina-
tions and is inherently rewarding may develop eating disorder
symptoms.
Why would some people with a high biologically deter-
mined reward sensitivity turn to food and some to alcohol or
other substances? Environmental shaping likely plays a role in
leading some individuals to focus on food-related concerns
and develop disordered eating behaviors rather than substance-
related behaviors (Gearhardt & Corbin, in press). Many theo-
rists have argued that concerns about shape and weight that
characterize and predict eating disorder symptoms (Fairburn
& Harrison, 2003; Stice, 2002; Thompson & Stice, 2001) are
influenced by social factors (Garner & Garfinkel, 1980;
McCarthy, 1990; Sobal & Stunkard, 1989). Cultural pressures
to be thin are often indicted as causes of females’ preoccupa-
tions with shape and weight (Garner & Garfinkel, 1980;
McCarthy, 1990). For example, in experimental studies, Stice
and colleagues (Stice, Maxfield, & Wells, 2003; Stice & Shaw,
1994; Stice, Spangler, & Agras, 2001) showed that even brief
exposures to fashion magazines that feature ultrathin models
or to peers talking about weight and shape lead to increases in
body dissatisfaction in young women. These effects are likely
exacerbated in young women who ruminate, because they are
more likely to rehearse and analyze their self-dissatisfaction
and the distress they experience over it. Body dissatisfaction,
in turn, is a reliable predictor of eating disorder symptoms
(Thompson & Stice, 2001). Preliminary evidence consistent
Downloaded from pps.sagepub.com by Susan Nolen-Hoeksema on October 18, 2011
with this hypothesis comes from Holm-Denoma and Hankin
(2010), who found that perceived physical appearance medi-
ated the prospective relationship between rumination and the
development of bulimic symptoms. Thus, adolescent girls for
whom rumination exacerbated concerns about their physical
appearance were more likely to develop bulimic symptoms.
This finding suggests that current concerns focused on physi-
cal appearance influence whether rumination increases bulimic
behavior.
Among ruminators with high sensitivity to reward, the
choice of food over alcohol or other substances may also be
influenced by social punishments for substance use. People in
cultures that prohibit or frown upon alcohol use are less likely
to use alcohol and develop alcohol-related problems (Sher
et al., 2005). Similarly, one factor associated with women’s
lower levels of alcohol use compared with men is social disap-
proval of excessive use in women and adoption of the female
gender role (Huselid & Cooper, 1992; White & Huselid,
1997). An interesting hypothesis for future research is that
rumination will be more strongly associated with binge eating
in cultures and groups that prohibit alcohol use than in cultures
that do not prohibit alcohol use.
Because alcohol and food may serve as reward substitutes
for each other (Gearhardt & Corbin, in press), some rumina-
tors may turn to food at some times in their lives and alcohol
at other times; thus, a tendency to ruminate may partially
explain lifetime comorbidities of substance use and excess
food intake in some people (Franko et al., 2005; Herzog et al.,
2006). In conjunction with the literatures on alcohol and food,
our heuristic therefore can generate predictions both about the
comorbidity of alcohol and food-related disorders (i.e., multi-
finality) and about why some ruminative people develop alco-
hol-related disorders and some develop food-related disorders
(i.e., divergent trajectories).
Conclusions and Future Directions
We have put forth a heuristic for developing models of trans-
diagnostic processes that (a) specifies the characteristics of
distal transdiagnostic risk factors and proximal trandiagnostic
risk factors, (b) suggests the types of mechanisms by which
distal transdiagnostic risk factors can lead to proximal transdi-
agnostic risk factors, and (c) suggests the types of moderators
that may determine whether a given proximal transdiagnostic
risk factor leads to one type of symptoms over another. We
constrain distal risk factors to independent environmental con-
texts and congenital biological abnormalities to avoid circular
arguments about which risk factors precede others; we also
specify the types of mechanisms that can link distal risk fac-
tors to proximal risk factors. We argue that moderators create
symptoms by (a) raising concerns or themes that proximal risk
factors then act upon, (b) shaping responses through condi-
tioning, or (c) determining the reinforcement value of certain
stimuli. Thus, this heuristic can guide a deeper and
Transdiagnostic Processes 603
more systematic exploration of the mechanisms by which
transdiagnostic risk factors have their effects and create
comorbidity among disorders (i.e., multifinality); the heuristic
can also guide the search for moderators that determine what
specific symptoms individuals who carry transdiagnostic risk
factors will develop (i.e., divergent trajectories).
A major limitation of this heuristic is that it is new and has
not been directly tested. Our application of the heuristic to the
rumination literature suggests it is promising, but this applica-
tion, by necessity, pieced together studies with different sam-
ples and methodologies, some of which were only indirectly
relevant to the component of the model being tested. It is
unlikely that any one study will be able to test all levels of the
model (distal factors, the mechanisms leading from distal to
proximal factors, the mechanisms leading from proximal fac-
tors to multiple outcomes, and the moderators determining
which outcomes the proximal factors lead to). Given that the
literature already has a large number of distal and proximal
risk factors that have been linked to multiple outcomes (as
reviewed in the first section of this article), we suggest that
priorities for future studies will be determining (a) the proxi-
mal risk factors mediating between established distal risk fac-
tors (e.g., stress) and outcomes, (b) the mechanisms linking
those distal and proximal risk factors, and (c) the moderators
interacting with proximal risk factors to determine divergent
trajectories to various outcomes. These three areas of research
seem to us to be underdeveloped but critical for a deeper
understanding of both multifinality and divergent trajectories.
A second limitation of our heuristic is that it is likely to be
too simplistic. In our effort to be parsimonious, we reduced
risk factors to two levels, distal and proximal, but it is highly
likely there are more levels. In our effort to avoid circularity,
we set certain conditions for designating a factor a distal risk
factor, a proximal risk factor, or a moderator, but it is likely
that some important factors will not fit neatly into our
operationalizations.
Third, the heuristic has not specified the potential role of
developmental factors in the effects of risk factors and mod-
erators, although we believe that developmental processes are
important. For example, there may be critical periods during
which some moderators have particularly strong effects in
determining the trajectory of symptoms in individuals with a
given transdiagnostic risk factor. We look forward to further
refinement and expansion of our heuristic as new research
indicates is necessary.
Understanding transdiagnostic processes in psychopathol-
ogy is critically important, both theoretically and clinically.
Greater understanding of both how individual risk factors lead
to multiple disorders (i.e., multifinality) and how specific dis-
orders emerge from that risk factor (i.e., divergent trajectories)
will help us to identify who is at most risk for what disorders,
how that risk develops and changes over the lifespan, and how
best to prevent and treat single and comorbid symptom
presentations.
Downloaded from pps.sagepub.com by Susan Nolen-Hoeksema on October 18, 2011
Acknowledgments
The authors wish to thank the members of the Yale Depression and
Cognition Lab for helpful comments on drafts of this article.
Declaration of Conflicting Interests
The authors declared that they had no conflicts of interest with
respect to their authorship or the publication of this article.
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