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Evolutionary Perspectives on Obsessive Compulsive Disorder

Background

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Obsessive compulsive disorder (OCD) is formed by persistent obsessions and repetitive compulsions which are ego-dystonic with individual’s self. Having such symptoms lead to help-seeking behaviors in suffering patients.[1]. OCD has a heterogenous manifestations in clinical situations. Based on developmental and dimensional perspectives, obsessive compulsive disorder is a part of broader spectrum such as tic disorders, trichotillomania, body dysmorphic disorders, and compulsive hoarding[2]. Several case reports and epidemiological cross-cultural studies show the similar outbreak in rate of obsessive compulsive disorders; however, some cultural differences are reported by several countries which are attributed to the role of religion on contamination fears and obsessions. Indeed, anthropological studies mention that OCD symptoms are consistent cross-culturally, because basis of many religious and civil rituals are the same in diverse cultures. As neural/brain circuitry and culture are mediating on the underlying abnormal behaviors, there are the same themes of OCD symptoms for both children and adults[3]. Based on Darwin’s theory, natural selection has saved developmental mechanisms which have survival value for human beings. However, there are some negotiations around persistence of vulnerability to certain mental disease. So, the evolutionary approach is looking for the benefits of OCD like symptoms for human species. Evidences from scientific studies on obsessive compulsive disorder manifest that having obsessive-compulsive symptoms have had reproductive and survival benefits in the evolution of human. Besides, some themes of OCD are similar to normal mental states and behaviors, such as rituals and religious experiences. But the diagnosis of OCD is based on the dominance of such patterns in emotional, intellectual, and behavioral aspects of life[1]. There are three benefits or advantages for evolutionary viewpoint: (1) explanation of normal and abnormal by considering normal functions of the range of emotions, (2) considering the effect of individual differences associated with pathogenesis factors on expression of disorder, and (3) constructing an evaluation framework to better comprehension of emotion regulation, motivation, and social conflicts[4].

Evolutionary origins

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Epidemiological Evidence

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Dysfunction vs. Defense Mechanism

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Evolutionary perspective has highlighted not only reasons behind the vulnerability to OCD, but also limitations, inconformity, and compromises in such descriptions. Although obsessive-compulsive disorder is defined as a malfunction, proponents of this view emphasized on useful functions of such symptoms. In another words, they are looking for the sustainability of symptoms through natural selection. In this view, OCD is considered as a dysregulation of adaptive trait[4]. There are two main mechanisms behind the biological description of obsessive-compulsive disorder: proximal and distal. The proximal mechanism can explain the neurobiological basis of OCD, and the distal mechanism demonstrates the state (how) formation of neurobiological mechanisms. These mechanisms posit between scientism which insisted on strict criteria of diagnosis in psychiatric approach, and skepticism which consider mental disorders as a social structure. These two mechanisms not only facilitate grouping (categorizing) OCRDs and related disorders but, help to discriminate the deviance of such disorders from each other and abnormality[4]. The malfunction of cortico-striatal-thalamic-cortical neurocircuitry (CSTC) is emphasized as a neuroanatomical model for obsessive compulsive and related disorder[4][2]. Based on this assumption, the impairment in this circuitry lead to OCD (responsibility of this circuitry is in threat detection and harm avoidance)[1][4]. Long duration, high frequency and intensity, wide-spreading, and incommensurate with context are the diagnostic criteria of dysfunction OC symptom in comparison to OC behaviors as adaptive defense. In this view, chronic and severe obsessive-compulsive disorder is considered as a dysfunction and there is an evidence about peculiar variations in CSTC[4].

OC behaviors as a response to threat

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There are four main classes of threat responding for obsessive-compulsive behaviors which are aggressive threat, physical security threat, environmental cleanliness threat, and privation threat. Fears about well-being of one-self and loved ones pertain to the aggressive threat scope. This threat consists of obsessive thoughts about images of separation or loss and urgent responsibility to inhibit such happenings. For example, a child, who suffers from separation, makes sure about closeness of mother by requesting for a bedtime story in a ritualistic manner. Also, parents make sure about safety of a child by checking (compulsion) his or her during night in determined intervals. Asymmetry and inaccuracy of objects or their positions stimulate checking behaviors which belong to physical security threat. Such obsessions and compulsions are mostly observed when babies look for daily routines at home in order to be familiar with their surrounding environment during childhood. Obsessive thoughts about cleanliness, individual hygiene, and associated compulsions (such as checking the environment, not touching nasty objects, and extreme washing) constitute environmental cleanliness threat domain. For example, as parents concern about protecting their kids to be safe from pathogens, they themselves prefer to select food and drink for them. Privation threat domain includes obsessive intrusive images about catastrophic happenings for oneself or loved ones are in accordance with collecting and hoarding compulsions of unnecessary objects or availability of food supplies. As an example, parents collect their personal items to make sure about safety and sufficient provisions for their infants. In summary, biological life crisis such as childbirth, puberty, and early parenthood raise the frequency and intensity of threats and their associated avoidant rituals[1].

Ontological Evidence

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Some OC-like symptoms are accepted as stereotypical functions of non-patient individuals, for example, checking of a locked door when leaving house or wiping the floor without any spots before party. In another words, diagnosis of OCD from normal behaviors is mostly based on frequency, intensity, and malfunction of intrusive thoughts rather than their contents. This view consider OCD-like symptoms as a dysregulation of adaptive trait[4] which can happen during normal life span, such as early childhood, early adulthood, and adulthood[1][2]. There are several reports about repetitive behaviors, rightness of behaviors, and specific clusters of fears (such as fear of strangers, bedtime fears, separation, death fears, city fears, contamination, and animal fears) as prevalent OC symptoms during early childhood. Associated thoughts and behaviors with romantic love in early adulthood are similar to preoccupation of thoughts with other in OCD. Phantasies around pregnancy and childbirth during adulthood are categorized as normal OCD-like thoughts and behaviors, because they are vital for human survival. Besides, religious beliefs and practices in general influence on themes and expressions of OCD symptoms[1].

Ethological Evidence

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Rituals have an essential role during life crisis of most species. However, there are some differences between animal and human rituals. For example, animal rituals transfer signals for sexual or social bonding, whereas human rituals transfer rich linguistic and cultural meaning[1]. Based on classic neuropathologic studies there are some similarities between rituals associated with OCD symptoms and stereotypical behaviors in animals. The OCD model for gnawers is based on the execution of dopamine agonist to make ritual like behaviors respondent to clomipramine treatment[5].

Neurobiological Evidence

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Biological Evidence

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Twins’ and families’ studies recommend that genetic factors have an influence on manifestation of obsessive-compulsive disorder. Chromosome 9p24 is suggested as one of the most influential genetic factors on expression of OCD symptoms. Besides, loci of genetic susceptibility to symmetry/ordering and hoarding symptoms are proved by measuring quantitative and qualitative traits through tracking symptoms in multigenerational families, genome scans, and twin and cross-fostering studies[1]. Based on serotonin hypothesis, serotonergic drugs have the significant influence on OC symptoms, because they block the reuptake of serotonin by brain neurons. The efficacy of this hypothesis lead to the medical usage of selective serotonin reuptake inhibitors (SSRIs) for the treatment of obsessive compulsive disorder. However, some investigations revealed that SSSRIs have an effect on other neurotransmitters and this is the reason of delayed action of these drugs in the treatment of OCD symptoms[3]. Besides, one of the famous medical findings about vulnerability to obsessive-compulsive disorder comes from Streptococcal (PANDAS) infectious[4][2].

Neuroimaging studies (neuroethology and human brain evolution)

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OCD symptoms due to rupture at different levels of cortico-subcortical human brain[5]. Functional neuroimaging studies demonstrate underlying neural mechanisms in obsessive-compulsive symptoms[1] which are activation of the orbitofrontal cortex with lesser assistance of anterior cingulate gyrus, the striatum (particularly the caudate nucleus), the thalamus, the lateral frontal and temporal cortices, and the insula[3]. The role of comparatively different parts of frontostriatothalamic circuits in cognitive and emotional processes of threat detection and harm avoidance in OCD is confirmed by fMRI studies. Indeed, the involved brain circuitry and neurochemical systems in OCD have a role in executive functions such as self-monitoring, error detection, and selection among competing responses[1]. Dysfunction of cortical-basal ganglia circuitry underlies the expression of obsessive compulsive symptoms. Several neuroimaging studies revealed that the basal ganglia involve in OCD and motor control disorders. So, there are a significant comorbidity between obsessive compulsive disorders and movement disorders (degenerative disorders) such as Huntington’s disease, Parkinson’s disease, and Tourette’s syndrome[3]. Besides, some infectious disorders such as encephalitis lethargica (von Economo), chorea minor (Sydenham), or toxoplasmosis are associated with obsessive compulsive symptoms, too[5]. Besides, the over-stimulation of two threat assessment regions in brain amygdala, which evaluates immediate threat, and cingulate cortex, which evaluates for potential threat, produce obsessive compulsive disorder symptoms[6].

Evolutionary psychological origins

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Evolutionary psychology states that the evolution of human mind is similar to the evolution of physical characteristics. Based on this approach, current environmental situation has led to different variation, inheritance, and selection in comparison to the classic adaptation theory. This means that some premature cognitive, emotional, and behavioral adaptations have been formed through human history, and they are not only provide efficient solutions to current adaptive problems but, have contradictory functions toward other adaptations. Because biological etiology describes OCD symptoms in a bottom-up pathway and psychological etiology explain them in a top-down route, there are different methods of pharmacotherapy and cognitive psychotherapy for the treatment of OCD symptoms[5]. There are two main hypotheses about evolutionary psychology of obsessive compulsive disorders: involuntary risk scenario generating system, and theory of mind and episodic memory.

‘Involuntary Risk Scenario Generating System’ (IRSGS)

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Most social sciences assumed that human mind is a domain-free and general-purpose problem-solving instrument; however, based on modular configuration, human brain includes domain-specific and adjusted system which can perform determined tasks. Based on ‘Involuntary Risk Scenario Generating System’ (IRSGS), although there is no real-life crisis, a patient who suffers from OCD may represent harm-avoidance behaviors. Normal harm-avoidance behaviors happen during risky activities and certain life crisis such as childbirth and pregnancy. This explanation about obsession’s function based on IRSGS is similar to the function of antibodies of the immune system[7]. Bickerton considers two types of thinking; on-line thinking in which mental activity is focused on problem solving of current issue, and off-line thinking, which is language-based and unique for human beings, involves in problem solving of probable future situation. By considering these definitions, obsessional thinking is a type of off-line thinking process which develop risk avoidance process for a probable danger in future; however, anxiety and panic are evolved as on-line emotional states which have harm avoidance behavior toward near and possible threat. The overactivation and dysregulation of IRSGS may lead to obsessive compulsive symptoms. This model formulates obsessional phenomena evolved by natural selection and provides cognitive explanation for obsessive compulsive symptoms[7].

Theory of mind (ToM) and Episodic Memory

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The overactivation of metacognitive mechanisms is another assumption about cognitive basis of symptoms of obsessive compulsive disorder. In another words, both episodic memory (the ability to cognitive representation of further events) and ‘theory of mind’ (capability to form metarepresentation) have crucial roles in cognitive pathology of obsessive compulsive disorder. Formation of episodic memory is dependent to evolving the ability to make distinction between imagined and real mental states. And acquiring theory of mind is related to evolving the capability to distinguish between one’s and others’ mental states. It is assumed that the overactivation of these two metacognitive mechanisms lead to the manifestation of OCD[5].

Recent theories about evolutionary origins of OCD

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Security Motivation System

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Security motivation system is defined as an independent brain module for evaluating potential danger and responding by probing or manipulating of an environment. The major characteristics of this system are special perceptual processing, sensitive activation model, probing and manipulating behaviors, internal control over termination of security motivation, and independent from ‘fear module’ and ‘safety systems’. Disturbances in each stage of initiation, maintenance, and termination of security motivation system may lead to pathologies in risk assessment and risk management[8]. This system is described by a conceptual neurobiological-circuit model with four major functional components: appraisal of potential danger, security motivation, security-related program, and motor and visceral component. The first component (appraisal of potential danger) determines the potential threat for self or others by assessing stimuli in current environment. Personal learning history and goals are used as criteria of such evaluation. An excitatory signal is sent to second component (security motivation) if a threat is discovered. In response, a supporting motivational state is activated for a prolonged time even if the primal external stimuli are faded. The activation of second component have two outputs: feedbacking to previous component in order to continue assessment because of the existence of potential danger (anxiety awareness) and sending excitatory signal to third component (security-related program) which is a reservoir of protection plans. Motor and visceral responses, such as washing and checking, are the final outcome of the chain of activation in this model. However, through performing on precautionary acts, two negative feedback signals are sending to appraisal of potential danger (first component), and security motivation (second component). In fact, the inhibitory signal to security motivation has a mediatory element which is named ‘Yedasentience’[8]. The neural circuit model of the security motivation system is structured based on both interconnections of functional units and cortico-striato-pallido-thalamo-cortical connections. In this model, different subcortical and cortical regions are categorized under four distinct loops which perform as the four major functional components of conceptual model[8]. They are respectively categorized in appraisal of potential danger loop (amygdala, bed nucleus of the stria terminalis, and hippocampus), security motivation and affect loop (mediodorsal thalamic nucleus, ventral pallidum, external segment of the globus pallidus/ subthalamic nucleus, limbic striatum, and ventral tegmental area), security-related programs loop (supplementary motor area/ premotor cortex/ motor cortex, ventroanterior thalamic nucleus- ventrolateral thalamic nucleus, internal segment of the globus pallidus- substantia nigra pars reticulata, external segment of the globus pallidus/ subthalamic nucleus, motor striatum, and substantia nigra pars compacta), and brainstem output network. In addition, some physiological changes facilitate neural networking between components of security motivation system; they are relaxing psychological tension, parasympathetic nervous system, and hypothalamic-pituitary-adrenocortical (HPA) axis[9]. Obsessive-compulsive disorder is a kind of dysfunction in security motivation system. There are two patterns in explanation of intensity and persistence of OCD symptoms: a starting and stopping problems. In a starting problem, the system is over-excited by stimuli, and in a stopping problem, the system’s components cannot terminate the normal process of activation which leads to behavioral profile of OCD. Indeed, OCD cognitive disabilities come from the malfunctions in the mechanisms of the security motivation system, for example obstruction in signaling from the motor and visceral output component to Yedasentience, or obstruction in signaling from the security-related programs component to the Motor and Visceral Output component (this is a pure-obsessional type of OCD). Basic hypothesis based on this model is about inability of brainstem output network to terminate the activation of Security motivation and affect loop, and Appraisal of potential danger loop[8].

Threat-detection System

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Fear is formed based on a real threat; however, anxiety is formed because of an abstract threat. Freezing (not being detected from danger’s attention), fleeing (escaping from the danger), and fighting (battling with the danger source) are different defensive behavioral responses to real threat. Nevertheless, anxiety does not have any specific external signal to solace tension and relieving from such feeling is subjective and individual based. Ritual is specifically devoted to decrease anxiety and it has considerable power, accuracy, and attention[10]. Based on neurobiological studies, amygdala and cingulate cortex are responsible for both immediate and potential threat detection. Basis of threat evaluation is fear conditioning which is influenced by amygdala. Defensive behaviors respond to near or remote real life-threat, while obsessive-compulsive behaviors respond to persistence illusionary threat[6]. In another word, obsessive compulsive disorder is cause by dysfunction of threat-detection system[11].

Sex differences

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Evolutionary perspective explains sex differences in both phenomenology and manifestation of obsessive compulsive disorder. In another words, sex differences in OCD consider not only onset of symptoms are different for each sex but, distribution of obsessions and compulsions are diverse within sexes[12]

Phenomenology

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OC symptoms begins for men in earlier ages rather than women.[12]. Also, different challenges of males and females during their life span can be a reason of this difference between them[1]. There are two hypotheses in this realm: over-activation of warning systems leads to OCD, and symptoms of OCD are related to universally meaningful rituals such as benefits of having contamination obsessions and hygiene compulsions for a group rather than for a person[12]

Manifestations

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There are some differences in patterns of obsessions and compulsions for each sex. For example, sub-constituents of romantic jealousy are different in males and females. Men and women represent different reactions toward mate-related threats; men feel more jealousy when they think about sexual infidelity of their partners, and women have the same feelings about emotional infidelity of partners. Another example is about sex-specific social threat. “Delusional dangers” are different in males and females in the order of male strangers and known females[12]. Some OCD-like intrusive thoughts are associated with life challenges related to each sex. As an example, 95% and 80% of such symptoms are respectively reported for OCD like symptoms of mothers and fathers before childbirth.[1]

See also

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Obsessive Compulsive Disorder

Obsessive–compulsive spectrum

Cause of obsessive-compulsive disorder

Biology of obsessive–compulsive disorder

References

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  1. ^ a b c d e f g h i j k l Feygin, Diana L.; Swain, James E.; Leckman, James F. (July 2006). "The normalcy of neurosis: Evolutionary origins of obsessive–compulsive disorder and related behaviors". Progress in Neuro-Psychopharmacology and Biological Psychiatry. 30 (5): 854–864. doi:10.1016/j.pnpbp.2006.01.009.
  2. ^ a b c d Leckman, James F.; Bloch, Michael H. (October 2008). "A Developmental and Evolutionary Perspective on Obsessive-Compulsive Disorder: Whence and Whither Compulsive Hoarding?". American Journal of Psychiatry. 165 (10): 1229–1233. doi:10.1176/appi.ajp.2008.08060891.
  3. ^ a b c d Rapoport, Judith L.; Fiske, Alan (1998). "The New Biology Of Obsessive-Compulsive Disorder: Implications for Evolutionary Psychology". Perspectives in Biology and Medicine. 41 (2): 159–175. doi:10.1353/pbm.1998.0063. ISSN 1529-8795.
  4. ^ a b c d e f g h Stein, Dan J.; Hermesh, Haggai; Eilam, David; Segalas, Cosi; Zohar, Joseph; Menchon, Jose; Nesse, Randolph M. (May 2016). "Human compulsivity: A perspective from evolutionary medicine". European Neuropsychopharmacology. 26 (5): 869–876. doi:10.1016/j.euroneuro.2015.12.004. ISSN 0924-977X.
  5. ^ a b c d e Brune, Martin (27 July 2006). "The Evolutionary Psychology of Obsessive-Compulsive Disorder: the role of cognitive metarepresentation". Perspectives in Biology and Medicine. 49 (3): 317–329. doi:10.1353/pbm.2006.0037. ISSN 1529-8795.
  6. ^ a b Fiddick, Laurence (March 2011). "There is more than the amygdala: Potential threat assessment in the cingulate cortex". Neuroscience & Biobehavioral Reviews. 35 (4): 1007–1018. doi:10.1016/j.neubiorev.2010.09.014.
  7. ^ a b Abed, RT; de Pauw, KW (1998). "An evolutionary hypothesis for obsessive compulsive disorder: a~psychological immune system?". Behavioural neurology. 11 (4): 245–250. PMID 11568426.
  8. ^ a b c d Woody, Erik Z.; Szechtman, Henry (March 2011). "Adaptation to potential threat: The evolution, neurobiology, and psychopathology of the security motivation system". Neuroscience & Biobehavioral Reviews. 35 (4): 1019–1033. doi:10.1016/j.neubiorev.2010.08.003.
  9. ^ Szechtman, Henry; Woody, Erik (2004). "Obsessive-Compulsive Disorder as a Disturbance of Security Motivation". Psychological Review. 111 (1): 111–127. doi:10.1037/0033-295X.111.1.111.
  10. ^ Eilam, David; Izhar, Rony; Mort, Joel (March 2011). "Threat detection: Behavioral practices in animals and humans". Neuroscience & Biobehavioral Reviews. 35 (4): 999–1006. doi:10.1016/j.neubiorev.2010.08.002.
  11. ^ Boyer, Pascal; Bergstrom, Brian (March 2011). "Threat-detection in child development: An evolutionary perspective". Neuroscience & Biobehavioral Reviews. 35 (4): 1034–1041. doi:10.1016/j.neubiorev.2010.08.010.
  12. ^ a b c d Saad, Gad (January 2006). "Sex differences in OCD symptomatology: An evolutionary perspective". Medical Hypotheses. 67 (6): 1455–1459. doi:10.1016/j.mehy.2006.05.017.
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