The Evolutionary Psychology of Obsessive-Compulsive Disorder:

the role of cognitive metarepresentation

Brune, Martin.

Perspectives in Biology and Medicine, Volume 49, Number 3, Summer

2006, pp. 317-329 (Article)

Published by The Johns Hopkins University Press

DOI: 10.1353/pbm.2006.0037

For additional information about this article

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 The Evolutionary
Psychology of Obsessive-
Compulsive Disorder

the role of cognitive metarepresentation

Martin Brüne

ABSTRACT Repetitive unpleasant thoughts and ritualized behaviors are the key
features of obsessive-compulsive disorder (OCD).The classical neuroethological mod-
els of OCD rely largely on behavioral similarities between animal stereotypies and
human compulsive rituals and are unable to account for the cognitive component of
OCD.The cognitive symptoms of OCD need to be addressed in an evolutionary psy-
chological context that incorporates information about human brain evolution. OCD
can be understood as an extreme on a continuum of evolved harm-avoidance strate-
gies.A pathological exaggeration of our evolved capacity to cognitively represent future
scenarios, including imagined consequences of our own thoughts and actions (meta-
representation), may be part of the set of evolved psychological mechanisms contribut-
ing to the psychopathology of OCD. The costly side of the adaptive ability to antici-
pate future needs or threats could be that etiologically heterogeneous affections of the
underlying striatal-frontal brain circuits may render an individual vulnerable to develop
OCD.

Center for Psychiatry, Psychotherapy and Psychosomatics, University of Bochum, Alexandrinenstr.

1-3, 44791 Bochum, Germany.
E-mail: Martin.Bruene@rub.de.

The author is grateful to Dr. Thomas Suddendorf, Department of Psychology, University of Bris-
bane, Australia, for helpful comments on an earlier draft of this paper.

Perspectives in Biology and Medicine, volume 49, number 3 (summer 2006):317–29

© 2006 by The Johns Hopkins University Press

317
Martin Brüne

BSESSIVE-COMPULSIVE DISORDER (OCD) is characterized by repetitive

O thoughts, feelings, and patterns of behavior that are usually perceived as
unwanted and unpleasant. In contrast to people with delusional disorder, indi-
viduals with OCD usually perceive such thoughts and behaviors as ego-dystonic,
although some overlap between the two syndromes may exist (Fear and Healy
1997; O’Dwyer and Marks 2000). Obsessions often involve the cognitive antic-
ipation of situations that are perceived as dangerous and as needing to be con-
trolled, whereas compulsive behavior is enacted to reduce fear and anxiety.
Individuals with OCD have a strong tendency to keep their rituals secret before
their social environment. This often leads to a substantial delay of diagnosis and
treatment (Rapoport and Fiske 1998).
In addition to idiopathic forms of OCD, OCD-related symptoms may ac-
company disorders involving dysfunction of the basal ganglia, including infec-
tious disorders such as encephalitis lethargica (von Economo), chorea minor
(Sydenham), or toxoplasmosis; degenerative disorders such as Huntington’s dis-
ease or Parkinson’s disease; and other idiopathic disorders such as Tourette’s syn-
drome (Alegret et al. 2001; Cummings and Cunningham 1992; Frankel et al.
1986; Swedo et al. 1989a). The lifetime prevalence rate of OCD has been esti-
mated between 1.9 and 3.1% (Bebbington 1998). Both biological and psy-
chosocial factors are thought to contribute to the manifestations and the exac-
erbations of OCD (Abed and de Pauw 1998; Maina et al. 2001; Williams and
Koran 1997). Cross-cultural studies suggest that OCD exists in every culture
(Horwath and Weissman 2000).The content of OCD is not independent of cul-
ture, since the manifestations of OCD sometimes strikingly resemble culture-
bound rituals (Fiske and Haslam 1997). Twin and family aggregation studies
indicate that genetic factors are involved in OCD, yet the complex inheritance
patterns have not been fully elucidated (Pato, Schindler, and Pato 2001; Pauls and
Alsobrook 1999).
Animal studies have been useful to explain aspects of the behavioral subrou-
tines associated with human OCD (Insel 1988; Szechtman, Sulis, and Eilam
1998). However, animal models are necessarily constrained in their capacity to
fully explain OCD, simply because their explanatory power regarding the cog-
nitive component of OCD is weak.
Evolutionary psychological accounts of OCD have described such factors as
the resemblance of compulsive behavior to human rituals and the difficulties of
patients with OCD in set shifting and decision making, and have offered a num-
ber of hypotheses about the origins of OCD, including the possibility that OCD
may arise as the result of an “evolutionary arms race” between streptococci and
the human immune system; that OCD symptoms represent exaggerated motiva-
tional mechanisms that normally prioritize behavioral routines; that OCD may
be preserved in the human gene pool by group selection; and that OCD repre-
sents an extreme of an evolved “involuntary risk scenario generating system”
(Abed and de Pauw 1998; Marks and Nesse 1994; Nesse and Williams 1994;

318 Perspectives in Biology and Medicine

 Evolutionary Psychology of Obsessive-Compulsive Disorder

Polimeni, Reiss, and Sareen 2005; Rapoport and Fiske 1998; Saxena and Rauch
2000). None of these hypotheses, however, fully account for the evolved psy-
chological mechanisms necessary to make patients with OCD overly ruminate
about their own thoughts and actions to control potentially dangerous situations
in the future (Myers and Wells, 2005). In this article, I suggest that OCD may in-
volve a pathological exaggeration of the evolved psychological mechanism to
cognitively represent the consequences of one’s own thoughts and actions. This
article summarizes the behavior associated with OCD in a (neuro)ethological
perspective, outlines some of the crucial cognitive aspects of OCD with empha-
sis on an evolutionary psychological perspective, and suggests potential CNS
correlates of the psychological mechanisms contributing to OCD in relation to
human brain evolution.

Ethology
Classical neuroethology has drawn parallels between OCD-associated rituals and
displacement activities and stereotypies in animals (Insel 1988). Displacement
activities occur when two opposing motivational drives are simultaneously acti-
vated. Such displacement behavior often involves the incorporation of species-
specific feeding or locomotive behavior patterns into ritualized behaviors (Tin-
bergen 1952). Similarly, highly stereotyped behaviors, such as equine “weaving,”
have been compared with some OCD symptoms, because, like obsessive-com-
pulsive behavior, stereotypies are performed excessively, inappropriately, or both
(Insel 1988; Nurnberg, Keith, and Paxton 1997). The administration of dopa-
mine agonists to rats may produce a ritual-like set of behaviors that partly
respond to clomipramine treatment, and may serve as a rodent model of OCD
(Szechtman, Sulis, and Eilam 1998). At best, the existing neuroethological mod-
els of OCD mimic the heterogeneous behavioral aspects of the disorder, but they
fail to account for the cognitive mechanisms involved in OCD.
Culture-bound rituals are remarkably similar in form, function, and content
to some behavioral patterns found in OCD. Many rituals are characterized by
repetitive, exaggerated, and, in part, highly stereotyped behavior. Rituals may
serve social purposes and help contain fear, anxiety, or perceived threats. In con-
trast to compulsive behaviors, however, rituals are culturally accepted habits.
With respect to the similarity in content of OCD and rituals, Fiske and Haslam
(1997) reported in their comparative study in 52 cultures that OCD features
were much more likely to resemble culture-bound rituals than work-related
activities. These findings suggest that both rituals and OCD behavior could
reflect a psychological mechanism “to produce order, regularity, boundaries, and
clearly demarcated categories” that is overactive in OCD (p. 221).

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Martin Brüne

Evolutionary Psychology of OCD

Evolutionary psychology posits that variation, inheritance, and selection have
shaped the human mind in essentially the same way as the evolution of physical
characteristics. Inclusive fitness theory, the theoretical basis of evolutionary psy-
chology, holds that the primary targets of natural and sexual selection have been
individuals and their genetically related kin (Buss 1995). Evolutionary psycholo-
gists have stressed that the modern human environment is not identical or even
necessarily similar to the “environments of evolutionary adaptedness,” in which
the majority of human psychological mechanisms evolved (Bowlby 1969). In
other words, the human mind comprises a set of partially anachronistic cognitive,
emotional, and behavioral adaptations. Moreover, evolved psychological mechan-
isms need not be “optimal”: in fact, they rather represent sufficient solutions to
adaptive problems and may be balanced against other adaptations (trade-offs).
Psychopathology may therefore arise due to a mismatch of current problems with
old solutions or due to dysfunctions (both hyperactivity or hypoactivity) of
evolved mechanisms (Brüne 2002).
Evolutionary Psychological Hypotheses of OCD
A number of evolved psychological mechanisms appear to function accord-
ing to a low-threshold “smoke detector principle” (Nesse 2001). Behaviors asso-
ciated with fight-or-flight responses illustrate the adaptive significance of such
harm avoidance–oriented natural defense mechanisms (Gilbert 2001). It is bet-
ter to activate a flight mechanism even if it proves unnecessary in retrospect, than
not to activate it when it is mandatory for survival—and hence reproduction
(Nesse and Williams 1994; Stein and Bouwer 1997). Likewise, symptoms associ-
ated with OCD may be interpreted as exaggerated behavioral strategies aiming
at harm avoidance. Marks and Nesse (1994) see OCD symptoms as caricatures
of risk-minimizing motivational mechanisms. The repetition of actions until
they “feel right,” excessive orderliness, washing rituals, overconcern with the risk
of harming others, and excessive hoarding reflect pathological distortions of such
mechanisms—and come at the cost of wasting energy. Polimeni, Reiss, and Sa-
reen (2005) have hypothesized that such symptoms of OCD may reflect behav-
ioral specializations that evolved to benefit the group or tribe, rather than the
individual, but this proposal depreciates the importance of individual and kin
selection in evolution (Buss 1995).
Abed and de Pauw (1998) were the first to emphasize the role of predicting
future events in OCD. They have suggested the existence of an evolved “invol-
untary risk scenario generating system” that enables an individual to develop
harm-avoiding behavioral strategies without being subjected to real-life dangers.
Accordingly, an overactive “risk scenario generating system” could be the cogni-
tive basis of OCD.This hypothesis predicts that OCD should be rare in individ-
uals who habitually engage in risky activities, including patients with antisocial
personality disorder, that OCD patients should tend to be socially compliant and

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 Evolutionary Psychology of Obsessive-Compulsive Disorder

rule abiding in order to avoid social risks, that the severity of OCD should cor-
relate with measures of harm avoidance, and that certain life events such as preg-
nancy or childbirth should exacerbate the symptoms of OCD (Abed and de
Pauw 1998; Cloninger, Svrakic, and Przybeck 1993).
Implicitly, these hypotheses relate harm avoidance to the capacity to mentally
generate future risk scenarios. They do not, however, identify the underlying
cognitive mechanisms involved in anticipating future scenarios or explain why
they evolved in humans. While it is intuitively plausible that individuals who
were capable of “foreseeing” future threats or future needs had adaptive advan-
tages over others who were not, animals may also instinctively “anticipate”
threats. Hibernating animals, for instance, are able to anticipate future needs as
shown in behavioral patterns of collecting and storing foods, which at first sight
may resemble some forms of compulsive hoarding. The instinct-driven behavior
of hibernators, however, lacks insight. It also occurs in animals that have never
experienced the hibernating season before. Human anticipation is fundamentally
different, because it is an insightful cognitive representation of events that may
or may not happen in the future (Suddendorf and Corballis 1997).The ability to
form a cognitive representation of anticipation could play a central role in the
cognitive pathology of OCD (Myers and Wells 2005; Suddendorf and Corballis
1997).What selection pressures might have led to the evolution of this capacity?

Metarepresentation and Episodic Memory

In a seminal paper, Suddendorf and Corballis (1997) have argued that the
ability to “travel mentally in time” (which roughly equals the functions of epi-
sodic memory and of anticipating future scenarios) and what has been termed
“theory of mind” (ToM) have a common cognitive basis, because both require
the capacity to form representations about representations or “metarepresenta-
tions.” Earlier research into the cognitive capacities of our closest relatives, the
extant apes, had suggested that apes are relatively constrained in their cognitive
capacity to represent episodic memories and that they live in a rather restricted
“present” (Köhler 1921). (The arguments for or against the existence of episodic
memory in nonhuman primates have recently been discussed by Schwartz and
Evans [2001].) On the other hand, limited and not universally accepted evidence
suggests that great apes do have a rudimentary ToM (Byrne and Whiten 1988;
Suddendorf and Whiten 2001). If both ToM and episodic memory were medi-
ated by the more general ability to metarepresent one’s own and others’ mental
states, it would be plausible to assume that apes have some cognitive access to
their episodic memory.
The evolutionary scenario illuminating why metacognitive capacities have so
greatly advanced over evolutionary time in hominids and humans, might go as
follows: Primates—including humans—are essentially social animals. After cli-
mate changes forced our ancestors to leave the dense forests for open savannas,
the ability to build bigger social groups might have evolved because it provided

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Martin Brüne

better protection from predators. In turn, however, bigger social groups—espe-

cially groups of unrelated individuals—posed the problem of coping with an in-
creasing complexity of social relationships and social interactions. This might
have created the pressure to evolve greater “social intelligence,” the ability to
manipulate others for one’s own benefit, to form coalitions, and to detect
cheaters (Byrne and Whiten 1988). According to the “social brain” hypothesis,
ToM was an adaptation that enabled individuals to adopt the mental perspective
of conspecifics in order to infer what they intend, pretend, and so forth (Dunbar
1995). Evolution of the capacity to cognitively represent previous social interac-
tions might have enabled hominoids to better predict the future behavior of oth-
ers and to anticipate the possible consequences of their own behavior. Of course,
the ability to anticipate future need conveys advantages outside the social do-
main: in contrast to a full-bellied lion, a full-bellied Homo sapiens might con-
tinue to hunt and kill other animals because he or she may anticipate future food
shortages (Suddendorf and Corballis 1997).
Thus, episodic memory, the cognitive representation of future scenarios, and
ToM involve the ability to metarepresent.To have access to episodic memories,
an individual must be able to distinguish representations of imagined mental
states from present mental states (Suddendorf and Corballis 1997). Anticipating
possible consequences of one’s own thoughts and intentions facilitates the pre-
diction of future events.ToM requires the ability to draw a distinction between
one’s own mental state and other persons’ mental states, and to infer the inten-
tions and dispositions of others.
The hypothesis that the metacognitive mechanisms involved in anticipating
possible consequences of one’s own thoughts and intentions are overactive in
OCD has recently gained empirical support. In studies of nonclinical populations
using two self-report scales that assessed beliefs about worry, as well as beliefs
about the meaning, consequences, controllability, and dangers of thoughts, Myers
and Wells (2005) found that these metacognitive variables were positively corre-
lated with the number of obsessive-compulsive symptoms, independent of the
subjective rating of inflated responsibility for future events.These findings clearly
support the idea that metacognitive mechanisms are involved in OCD, although
studies of patients with OCD are not yet available.

Brain Pathology Associated with OCD

and Its Relation to Human Brain Evolution
Neuroethological models of OCD suggest an imbalance of phylogenetic older
“habitual” systems and phylogenetic younger “flexibility” systems (Insel 1988;
Pitman 1989). Flexible responses involve the capacity for selecting the relevant
sensory input, shifting the attentional focus, making the best choice of behav-
ioral alternatives, and sometimes suppressing salient responses in favor of less
salient ones (Bradshaw and Sheppard 2000). In primates, the dorsolateral pre-

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 Evolutionary Psychology of Obsessive-Compulsive Disorder

frontal cortex, the orbitofrontal cortex, the cingulate cortex, the supplementary
motor cortex, pallidostriatal structures, and parts of the thalamus all contribute
to the execution of flexible behavior, where striatum and thalamus operate as fil-
ter stations and project back to different areas of the frontal cortex (Bradshaw
and Sheppard 2000; Pitman 1989; Saint-Cyr,Taylor, and Nicholson 1995).
Two different connections have been described: a “direct” positive feedback
loop and an “indirect,” mainly negative, feedback loop. In OCD, a hyperactivity
of unknown origin in these cortical-subcortical pathways may cause a response
bias toward stimuli relating to “socioterritorial” concerns, such that individuals
with OCD are “captured” and unable to switch tasks or behavior (Saxena and
Rauch 2000).
A recent study of structural brain abnormalities in patients with OCD
revealed reduced grey matter volumes in the medial frontal gyrus, the medial
orbitofrontal gyrus, and the left insulo-opercular region. In contrast, grey matter
volumes in the ventral striatum and anterior cerebellum were greater in OCD
patients compared with controls (Pujol et al. 2004). Consistent with these find-
ings, a substantial number of functional brain imaging studies have shown—ap-
parently contradictorily—an elevated metabolism or regional blood flow in the
orbitofrontal cortex, the anterior cingulate, the basal ganglia, and the thalamus in
patients with OCD (Saxena and Rauch 2000). In a functional brain imaging
study using a symptom-provocation paradigm in patients with OCD, Breiter et
al. (1996) found a significant bilateral activation of the anterior and posterior
orbital gyri, the superior, middle, and inferior frontal gyri, the anterior cingulate
cortices, the temporal cortices, the right caudate and left lenticulate nuclei, as
well as the left insula and bilateral amygdala. In contrast, Busatto et al. (2000)
found a reduced cerebral blood flow in the right lateral orbitofrontal cortex of
OCD patients. In this study, regional blood flow correlated positively with the
severity of the OCD symptomatology. In addition, a treatment study of patients
with OCD using the selective serotonin reuptake inhibitor (SSRI) paroxetine re-
vealed a significant decrease of glucose metabolism in the anterolateral orbito-
frontal cortex after treatment in responders, but not in non-responders (Saxena
et al. 1999).The authors suggested that SSRIs may reduce excitatory activity in
orbitofrontal-subcortical pathways.
Interestingly, the brain regions presumably associated with the pathogenesis of
OCD closely match those that are selectively involved in future action planning
and episodic memory retrieval in healthy subjects. In a study using positron
emission tomography (PET) Lepage and colleagues (2000) demonstrated that
episodic memory retrieval was associated with enhanced brain activity in the an-
terior cingulate, in the prefrontal cortex, the dorsolateral prefrontal cortex, and
dorsal prefrontal cortex.Almost identical activation patterns were found in a par-
adigm involving “prospective memory,” the ability to keep in mind something
that needs to be carried out in the future (Okuda et al. 1998). Likewise, a PET
study of anticipatory anxiety in healthy subjects found activation of the right

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Martin Brüne

superior temporal sulcus, both insulae, the left fusiform gyrus, and the left ante-
rior cingulate, which partially correlated with the score on the Spielberger State
and Trait Anxiety Inventory (Chua et al. 1999). Moreover, the anterior cingulate
cortex has also found to be activated in ToM tasks (Siegal and Varley 2002).
The brain regions associated with OCD pathology and metacognition have
undergone significant modifications in primate phylogeny. In primates, includ-
ing humans, the neocortex and thalamic and limbic structures have substantially
increased in size relative to body size (Rapoport 1990). Given that brain tissue is
extraordinarily expensive in both energetic and developmental (maturational)
terms (Aiello and Wheeler 1995), there must have been good evolutionary rea-
sons for this enlargement to occur (which, I have argued, could have been meta-
cognition). Contrary to a widely held view, the human prefrontal cortex as a
whole, relative to total brain size, has not increased in size compared to the
extant great apes (Semendeferi and Damasio 2000). On the other hand, those
structures in the prefrontal cortex that are involved in future action planning and
ToM have enlarged during human evolution. The anterior cingulate cortex in
humans is increased in size relative to other parts of the frontal lobes and is twice
the size expected for an ape of human brain and body size (Allman et al. 2001).
In addition, the number of neurons in this region is greatest in humans, while at
the same time the neuron density is lowest, indicating more space for extrinsic
and intrinsic connections (Semendeferi et al. 2001). Furthermore, the anterior
cingulate cortex contains a class of neurons called spindle cells that are unique
to the great apes and humans.The concentration of spindle cells in the anterior
cingulate cortex is greatest in humans and decreases with phylogenetic distance
in the other apes (Allman et al. 2001). Given the role of the anterior cingulate
cortex in behavior control, evolutionary pressures must have favored the emer-
gence of this novel cell type as an adaptation to the need of greater self-control
and suppression of immediate response patterns.

Discussion
The findings from neuroethology, evolutionary psychology, and human brain
evolution converge to suggest that OCD may be seen as the extreme on a con-
tinuum of harm avoidance behavioral and cognitive strategies (Abed and de
Pauw 1998; Gilbert 2001). OCD arises at the interface between the maintenance
of relatively rigid behavior patterns and flexible cognitive adaptation to novel
environmental stimuli, including anticipation of future threats or needs.
In contrast to previous neuroethological accounts of OCD, which have em-
phasized the comparison of obsessive-compulsive behavior with stereotypies or
displacement activities in animals, this account stresses the role of human
metacognitive capacities that gradually evolved in apes and humans, and that
allowed greater self-control and efficiency in social relationships. The evolution
of an episodic memory and the ability to anticipate future scenarios as conscious

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 Evolutionary Psychology of Obsessive-Compulsive Disorder

cognitive representations of past experiences evolved together with the capacity

to infer the mental states of conspecifics (ToM), possibly in the first place to bet-
ter predict other individuals’ intentions and behaviors. Comparative data on
human brain evolution strongly suggest that the brain regions mediating these
functions enlarged during hominid evolution, or represent novel adaptations that
are virtually absent in other primates. The central nervous representations of
metacognition—parts of the prefrontal cortex and the anterior cingulate cortex
that are active in healthy individuals when performing tasks involving imagina-
tion of future scenarios—correspond closely with those brain areas that are acti-
vated in OCD.
In addition to the adaptive advantage of being able to “foresee” the behavior
of other individuals, the ability to anticipate future scenarios (both social and
nonsocial) and adjust one’s behavior relatively independent of recent needs (in
the sense of “offline thinking”), and hence to make the environment more pre-
dictable and secure may also be adaptive (Abed and de Pauw 1998).
There might, however, be a costly side to the evolution of these abilities.
Overly anticipating future threats or a biased anticipation towards the negative
consequences of one’s own thoughts and intentions may lead to a constraint of
behavioral flexibility, which may become psychopathologically manifest as OCD
(Saxena and Rauch 2000). This hypothesis is in principle testable. For example,
the way OCD patients judge past and future scenarios could be measured using
the Zimbardo Time Perspective Inventory (Zimbardo and Boyd 1999). I would
predict that patients with OCD would score high on the “present-fatalistic” fac-
tor and perhaps on the “past-negative” factor, and low on the “present-hedonis-
tic” factor of this test. Zimbardo and Boyd (1999) found that the “present-hedo-
nistic” factor correlated highly with novelty seeking and sensation seeking,
which is the opposite of what would be expected in patients with OCD. On the
other hand, the “present-fatalistic” factor was highly correlated with aggression,
depression, and anxiety, which are often part of the OCD symptom spectrum or
represent comorbid disorders. Even more direct evidence comes from studies of
metacognition in nonpatient populations, where negative metacognitions about
the uncontrollability of one’s own thoughts correlated positively with the num-
ber of obsessive-compulsive symptoms (Myers and Wells 2005).
Consistent with the assumption of an overly active harm-avoidance strategy
in OCD are findings from cross-cultural studies and the existence of biological
vulnerability factors of OCD (Abed and de Pauw 1998). Similarities between
culture-bound rituals and the content of OCD underscore the importance of
“socioterritorial” issues for individuals (Fiske and Haslam 1997; Saxena and
Rauch 2000). Similarly, biologically vulnerable periods of the human life span,
such as puberty, pregnancy, or childbirth, where increased vigilance to potential
threats make biological sense, would seem to increase the risk of developing or
exacerbating obsessive-compulsive symptoms (Leckman and Mayes 1999; Loch-
ner and Stein 2001;Williams and Koran 1997).

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Martin Brüne

Phenomenological similarities between delusional disorder and may extend

into common underlying abnormal metacognitions OCD (Fear and Healy
1997; O’Dwyer and Marks 2000). The difference between the two is that in
delusional disorder, exaggerated metacognition refers to negative thoughts and
intentions of significant others (leading to paranoid ideation), whereas in OCD
exaggerated metacognition relates to one’s own negative thoughts and intentions
(Bömmer and Brüne, n.d.).This difference may be maintained at the physiolog-
ical level by a differential involvement of opposite hemispheres, with “others”
being represented in the right hemisphere and “self ” being represented in the left
(Decety and Chaminade 2005).

Future Directions
The presence of obsessive-compulsive symptoms in a variety of neurological dis-
eases suggests that OCD is etiologically heterogeneous and may result from the
disruption of cortico-subcortical pathways at different levels. OCD spectrum
disorders may range from a more “organic” (bottom-up) basal ganglia–driven
etiology to a more “psychological” (top-down) neocortical etiology, which may
respond differentially to pharmacotherapy or cognitive behavior therapy. With
respect to cognitive behavior therapy, it may be worth including the evolution-
ary psychological underpinnings of OCD as adaptive harm-avoidance strategies
and pathological exaggeration of metacognition into a multimodal therapeutic
model (Fisher and Wells 2005; Hand 1998). Assessing OCD patients’ metacogni-
tions with the Zimbardo Time Perspective Inventory and other scales could be-
come an integral part of cognitive behavior therapy (Myers and Wells 2005;Wells
and Cartwright-Hatton 2004; Zimbardo and Boyd 1999). If nothing else, a
deeper appreciation of the psychobiology of OCD might at least reduce patients’
secondary feelings of shame, embarrassment, and anxiety.
OCD is a severe and sometimes debilitating psychiatric disorder, which is
often detected only after years of suffering.An evolutionary view may open new
research perspectives and contribute to a deeper understanding of “nature” and
“nurture” in this psychopathological syndrome.

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