The Development of Obsessive-Compulsive Disorder (OCD)

 

Abstract

Obsessive-compulsive disorder (OCD) is a complex and debilitating disorder that will affect 2.5% of individuals across their lifespan (American Psychiatric Association, 2000).  Despite a great deal of research on this disorder, no one knows exactly how OCD develops.  Current theories on the development of this disorder lack an appropriate developmental context, examining the disorder from an adult perspective then speculating about which factors in childhood might have led to the current presentation.  Researchers hypothesize that a combination of biological, genetic, environmental and cognitive factors contribute to the disorder (Abramowitz, Khandker, Nelson, Deacon, & Rygwall, 2006).  Biological factors implicated in OCD include genes, neurotransmitters, immunology (physiological diseases impacting OCD), neurophysiology, and sex hormones.  Aspects of an individual’s environment potentially impacting OCD development include perinatal factors, temperament, parenting styles, and traumatic experiences.  Cognitive factors, which involve the way an individual interprets information, include responsibility, thought-action fusion, intolerance for ambiguity, perfectionism, need for control, and threat overestimation.  This paper will review and critique the literature on the biological, environmental, and cognitive factors potentially related to OCD’s development and attempt to locate this research within a developmental framework, hopefully providing a better understanding of OCD’s development, including measurement considerations and directions for future research.

Obsessive-Compulsive Disorder Construct

Obsessive-Compulsive Disorder, Obsessive-Compulsive Personality Disorder, Obsessive-Compulsive Spectrum Disorders

Before examining the factors and processes that may contribute to OCD development, a clarification of what OCD is, and is not, is necessary.  Obsessive-compulsive disorder is a complex and heterogeneous disorder that has been conceptualized as part of a cluster of disorders that is both complex and controversial.  Obsessive-compulsive disorder (OCD) is characterized by: (1) obsessions, which are unwanted, intrusive thoughts and (2) compulsions, which are repetitive behaviors or various types of mental acts such as counting or other strategies that, in the short term, serve to reduce obsessions and the anxiety or distress caused by the obsessions. 

In OCD, the obsessive and compulsive phenomena are inextricably linked through their functions.  Compulsive behavior in OCD functions as a negative reinforcer of obsessions, to alleviate anxiety, obtain reassurance to reduce distress, to prevent catastrophe, and escape from feared outcomes (Abramowitz & Deacon, 2005).  This is distinct from compulsive behavior that causes pleasurable feelings, such as that seen in addictions (McElroy, Harrison, Keck, & Hudson, 1995).  Despite the qualitative differences between OCD-specific and non-OCD obsessions and compulsions, obsessions and compulsions have become mislabeled to represent any sort of fixation (e.g., infatuation), or repetitive or impulsive behavior (e.g., tics, compulsive gambling; Abramowitz & Deacon).      

OCD is also often confused with OCPD or obsessive-compulsive personality disorder (Mancebo, Eisen, Grant, & Rasmussen, 2005).  OCPD is a pervasive part of an individual’s personality, hence is labeled a “personality disorder”, but most importantly, it does not involve obsessions and compulsions, as in OCD. Rather, OCPD involves a high level of concern with control, order, rules, and perfection (American Psychiatric Association, 2000).  These distinctions are important in the conceptualization, assessment, study, and treatment of OCD because OCPD is a qualitatively different disorder than OCD.   

In addition to the disorders formally labeled as “obsessive-compulsive” in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), individuals have proposed the existence of obsessive-compulsive spectrum disorders (OCSDs), further complicating the conceptualization of OCD.  The OCSDs are thought to include disorders from a variety of categories that appear to share features, familial history, comorbidity, neurobiological systems, course, and response to treatment in common with OCD.  OCSDs include some of the eating disorders (e.g., anorexia, bulimia), impulse control disorders (e.g., pathological gambling, kleptomania, trichotillomania, sexually impulsive behavior), movement disorders (e.g., Tourette’s Syndrome), and somatoform disorders (e.g., hypochondriasis, body dysmorphic disorder; (Hollander, Friedberg, Wasserman, Yeh, & Iyengar, 2005; Turner, Beidel, Stanley, & Heiser, 2004), spanning the gamut from truly compulsive (e.g., OCD, body dysmorphic disorder) to impulsive (e.g., pathological gambling, kleptomania; Hollander & Cohen, 1996).

Although development of the OCSD construct was based upon similarities among disorders, researchers have begun to examine the differences between OCD and some of its OCSD counterparts.  As mentioned, the function of the compulsive behavior is an important way to distinguish obsessive compulsions from compulsions in other disorders.  In this vein, one distinction between OCD and one type of OCSD, the impulse control disorders, is the function of their respective compulsive behaviors: In OCD, the function is to remove something negative from one’s environment, whereas in the impulse control disorders, the purpose is to add something positive (e.g., pleasurable feelings).  Indeed, individuals with impulse control disorders, including behaviors such as kleptomania or compulsive gambling, report a “rush”, “high”, or pleasurable feelings following these behaviors (McElroy et al., 1995).  Further underscoring a difference in the function of compulsions between OCD and the impulse control disorders is evidence that compulsive behavior activates different neurological pathways, depending on disorder type: anxiolytic and serotonergic for OCD versus opioid/pleasure pathways for impulse control disorders (Romach et al., 2002). 

The function of “compulsive” behavior within another disorder type, movement disorders, also provides an example of the functional differences between OCD and some OCSDs.  In the case of Tourette’s syndrome, tics are unprompted and serve to reduce sensory discomfort, whereas OCD compulsions are purposeful and function as avoidance from the feared obsession (Miguel et al., 1995).  Although both sets of compulsive behaviors are negatively reinforcing, the behavioral functions are qualitatively different.  Tourette’s involves reduction of sensory discomfort of a nonspecific origin whereas OCD’s compulsions target the reduction of distress or anxiety caused by a specific feared obsession.  For example, a Tourette’s presentation may involve sudden eye blinking or barking, not tied to a specific fear, rather a general discomfort, and an OCD presentation may involve an obsessive fear of contamination and compulsive hand washing to reduce the perceived likelihood of contamination.    

The impulse control, movement, eating, and somatoform disorders appear to have several features in common with OCD.  Research comparing impulsive control and movement disorders with OCD, however, leads to concerns over whether the differences occur at such a fundamental level that comparison, and more importantly, inclusion within the same construct is contraindicated.  For the other disorder categories (i.e., eating disorders, somatoform disorders), further examination is needed to determine whether their inclusion within the same construct as OCD is also contraindicated.  Regardless, the construct as it currently exists is problematic, and unless future research indicates otherwise, it should not be used in the conceptualization of OCD.  Further, in a disorder that is already complex and heterogeneous, the lack of consensus on what should be part of the OCD construct makes the study of the development of this disorder even more problematic.

Lifetime Prevalence, Age of Onset, and Comorbidity

A brief review of the current classification systems, prevalence, and phenomenology of this disorder is also warranted before examining its development in more detail.  Unfortunately, obsessive-compulsive disorder is one of the most disabling anxiety disorders, often worsening when left untreated, rather than remitting with the passing of time (Turner et al., 2004).  OCD affects 2.5% of the population across the lifespan (American Psychiatric Association, 2000), and although boys have higher rates in childhood, this discrepancy levels off and flips, so that by adulthood, women have a slightly higher prevalence rate (Steketee & Barlow, 2002).  OCD typically appears around age 19 (Kessler et al., 2005), though one third to one half of all OCD cases are thought to have early onset, between ages 10-12.5 (Leonard & Rapoport, 1991; Wewetzer et al., 2001).   

OCD’s comorbidity with other disorders, especially major depressive disorder, is quite high.  According to a Johns Hopkins OCD study, the rates were 51.4% with recurrent major depressive disorder, 8% with dysthymia, 36% with social phobia, 30.7% with specific phobia, 29% with hoarding, 20.8% with panic disorder, 16.7% with agoraphobia, 13% with generalized anxiety disorder, 25% with pathologic nail biting, 24% with pathologic skin picking, 16% with body dysmorphic disorder, 15% with hypochondriasis, 9% with anorexia, 4% with bulimia, 4% with trichotillomania, and 3% for kleptomania (Bienvenu et al., 2000; Nestadt et al., 2001; Samuels et al., 2002).  For individuals with an already debilitating disorder, these comorbid conditions make their experience especially distressing.  The realities of the disorder’s debilitating effects, course, and comorbidity increase the urgency of answering the questions of how the disorder develops, and how it is best conceptualized, studied and treated.   

Developmental Considerations in OCD Diagnosis

According to the DSM-IV-TR, individuals must be able to identify the intrusive and inappropriate nature of thoughts to meet the criteria for OCD (American Psychiatric Association, 2000); this task requires metacognitive ability.  Children do not typically gain these abilities until around age 9-10, so they are unable to make such attributions prior to this time period (Berk, 2006).  The DSM attempts to make concessions for children by noting that children do not have to identify the excessive or unreasonable nature of thoughts, but this concession, ostensibly for children, applies to adults with low insight too (American Psychiatric Association, 2000).  The DSM then, really does not make any special accommodations for developmental limitations.  And, despite the fact that it addresses children’s limitations in identifying the excessive and unreasonable nature of thoughts, it says nothing of the fact that metacognitive abilities are needed to classify thoughts as intrusive and inappropriate.             

Research on OCD, and many other psychological disorders, tends to approach the disorder from an adult psychopathology framework, even when conceptualizing childhood onset of a disorder.  Taking an adult perspective on OCD and working backwards to childhood is problematic.  In childhood, actual “problem” behaviors or emotional issues are generally not indicative of disorders in and of themselves.  Some suggest that when the behaviors or emotional issues become severe, frequent, persistent and/or age inappropriate, diagnosis is warranted (Carter & Pollock, 2000; Mash & Dozois, 2003).  In the case of OCD, many children engage in rituals, such as rigid bedtime routines, but around age  9, the “normal” behavioral rituals tend to cease (Leonard, Goldberger, Rapoport, Cheslow, & Swedo, 1990), with early-onset OCD typically diagnosed around ages 10-12.5 (Leonard & Rapoport, 1991; Wewetzer et al., 2001).  In children, then, onset of full-blown OCD is difficult to differentiate from normal behavior prior to age 9-10, which is an important consideration for studying or diagnosing the disorder. 

Given these developmental considerations, diagnosis really should not be made prior to age 9-10, but children are still being diagnosed with OCD.  If diagnosis cannot be made for developmental reasons using DSM, what criteria are people using?  Some suggest that when thoughts become distressing, take up significant portions of time and/or interfere with functioning, they can be considered “obsessions”  (Carter & Pollock, 2000; Flament, Koby, Rapoport, & Berg, 1990); this is similar to the proposed differentiation between normal and compulsive behavior; that is, if preventing a ritual causes distress, the ritual takes a significant amount of time and/or interferes with functioning, the ritual is purportedly an OCD compulsion (Albano, Chorpita, & Barlow, 2003; Carter & Pollock, 2000).  This practice is a problem because individuals are making assumptions about what OCD symptoms should look like in children without researching these symptoms or using formalized new criteria.  If distress and time truly differentiate normal thoughts and behaviors from obsessions and compulsions, then those diagnosed with OCD prior to age 9 should continue to evidence OCD-positive thoughts and behaviors after this age, and, the metacognitive features of OCD should also appear.  This does not appear to have been addressed empirically in children yet, though studies of intrusive thoughts in adults indicate that the only differences between normal and OCD-intrusive thoughts were distress experienced, duration of thoughts, and difficulty dismissing thoughts (Rachman & De Silva, 1978). 

Biological Factors in OCD

Genetic Factors

Among the earliest and most basic work on genes in psychopathology are family studies.  These studies measure prevalence rates of OCD within families, notably in families with a member who has OCD.  Prevalence rates for first-degree relatives of individuals with OCD were higher than what would be expected in the general population, ranging from 6.4-22.5% (Grabe et al., 2006; Hanna, Himle, Curtis, & Gillespie, 2005; Nestadt et al., 2000), with a 2.5% lifetime prevalence for the general population (American Psychiatric Association, 2000).  Meta-analytic results of overall OCD risk present aggregate rates of risk at 8.2% for first-degree relatives of an individual with OCD (Hettema, Neale, & Kendler, 2001); for first-degree relatives of controls, risk rates are only 2%.  Taken together, these results indicate a familial, and possibly, genetic component of OCD.  The results presented are aggregate risk and prevalence rates for OCD, so further examination is necessary to examine the nuances of genetic propensity for OCD. 

If OCD is broken down into early and late onset groups, results reveal that first-degree relatives of individuals diagnosed with OCD onset prior to age 16 or 17 are much more likely to also develop OCD at some point in their lives, 16.1-22.5 % prevalence rates (Chabane et al., 2005; Hanna et al., 2005).  Conversely, relatives of those with late-onset OCD (after age 16) were much less likely to develop OCD (Chabane et al., 2005; Hanna et al., 2005), exhibiting a lifetime prevalence rate similar to that of general population, 2.9%.  This would suggest that OCD is somewhat genetically based and the genetic component is strongest when onset is early.  Additional studies support this hypothesis: Sibling pairs with OCD were much more likely to report early onset of symptoms than late onset; 57% versus 15%, respectively (Chacon et al., 2007).  Finally, although not specifically examining early versus late onset, a review of twin studies comparing OCD rates in children versus adults suggests heritability rates of OCD symptoms that are much higher in children: from 45-65% in children versus 27-47% in adults (Van Grootheest, Cath, Beekman, & Boomsma, 2005). These findings highlight the heightened genetic propensity for OCD symptomatology in childhood cases of OCD, but the actual heritability rates are confusing because the study did not tease out which portion of the adults with OCD exhibited childhood onset.  Given previously discussed study data, it is possible that if these early-onset individuals were factored out, the heritability rates in the adult group would drop. 

Other work on genes and psychopathology has gone beyond basic heritability and prevalence rates, conducting much more complex analyses of genetic involvement by isolating specific genes in disorders, including OCD.  Using a genome scan on individuals with OCD and their relatives, two studies found evidence implicating a region of chromosome 9p24 in OCD (Hanna et al., 2002; Willour et al., 2004); these findings were more robust when early-onset OCD probands were utilized.  Another study identified gene(s) on chromosome 1 as potentially liable for an increased risk of early-onset OCD (Shugart et al., 2006).  Taken together, these findings are in line with the more general studies of genetic heritability and risk rates, suggesting that early-onset OCD may be more genetically based than late-onset OCD.

Studies have used different methodology for measuring genetic propensity for OCD (e.g., prevalence rates in first-degree family members, twin studies, etc.), so actual prevalence rates appear to differ, but overall, the evidence points to heightened genetic involvement for early-onset OCD versus late-onset OCD.  The fact that research has begun to examine early and late onset separately indicates recognition of the fundamental differences between children and adults. However, the involvement of genes in OCD is also likely to be much more complex than studies have been able to assess with current methods; that is, more complex than the black-and-white distinction that early-onset OCD is genetic and late-onset OCD is nongenetic.  Indeed, one study of specific genes identified gene(s) on chromosome 7 as potentially responsible for increasing risk of late-onset OCD (Shugart et al., 2006), again indicating the need for additional study to uncover the intricacies of genetic influence on OCD development. 

Although findings have identified an increased genetic propensity for early-onset OCD, the heritability rates are not 100%, indicating that other factors are involved both in increasing risk for OCD development and in protecting against OCD development.  The current literature also assumes a linear model of OCD development; that is, genes either contribute to OCD or they do not.  Recent work with another disorder, depression, reveals a much more complex pathway from genes to disorder development.  Specifically, that certain genes contribute to the development of depression, but only in the presence of stressful life experiences; that is, certain negative life events (e.g., trauma) “switch on” depressive genes (Beck, 2008).  Support for a nonlinear model of genetic involvement in depression indicates that genetic research in OCD should begin to address nonlinear pathways, examining the impact of other risk and protective factors.     

Immunological

A unique disorder with many symptoms in common with OCD has emerged in recent years: pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS).  According to Swedo et al. (1998), a PANDAS diagnosis indicates that an individual a) meets criteria for OCD and/or a tic disorder, b) has symptoms that appear unexpectedly and/or have symptom severity that is intermittent, c) experiences symptom onset and increases in severity after Group-A beta-hemolytic streptococcal (GABHS) infection, d) develops symptoms prior to the onset of puberty, and e) experiences neurological abnormalities when symptoms worsen (e.g., choreiform movements). 

PANDAS is currently conceptualized as a subgroup of OCD or of a tic disorder, sharing diagnostic criteria with OCD or a tic disorder plus characteristics unique to PANDAS such as symptom onset or increase following GABHS infection.  By the very nature of the diagnostic process, then, OCD and PANDAS share in common a large portion of symptomatology.  In addition, PANDAS appears to exhibit some neurobiological markers of OCD: abnormalities in basal ganglia regions, including the putamen, globus pallidus, and caudate (Giedd, Rapoport, Garvey, Perlmutter, & Swedo, 2000).  Further, the genetic influences on the development of OCD or a tic disorder appear similar in the development of PANDAS, evidenced by higher OCD and tic disorder prevalence rates in first-degree relatives of  individuals with a PANDAS diagnosis than the general population (Lougee, Perlmutter, Nicolson, Garvey, & Swedo, 2000). 

PANDAS is thought to make up 10% of the pediatric OCD sample (Trifiletti & Packard, 1999), so the decision to include PANDAS as a subgroup of OCD has profound diagnostic implications.  And, the continued practice of including PANDAS as an OCD subgroup should be considered in light of the many differences between the two disorders.  One basic but very notable difference is that PANDAS is predominantly diagnosed in males (Swedo et al., 1998), with some estimates indicating that 75% of PANDAS cases are male (Swedo et al., 1998).  And although more males are diagnosed with non-PANDAS OCD in childhood than females, around 66%, the sex difference is not quite as profound as that in PANDAS (Steketee & Barlow, 2002).  Additionally, individuals with PANDAS and OCD both exhibit neurobiological abnormalities in basal gangliar regions (Giedd et al., 2000; Luxenberg et al., 1988; Robinson et al., 1995; Rosenberg et al., 1997; Whiteside, Port, & Abramowitz, 2004). The difference, however, is that those with OCD exhibited reductions in basal ganglia volume (Luxenberg et al., 1988; Robinson et al., 1995; Rosenberg et al., 1997; Whiteside et al., 2004)whereas those with PANDAS exhibited enlargements (Giedd et al., 2000), which may reflect different neurobiological etiologies in the two disorders.  Another difference is that the pattern of relapse and remitting symptoms in PANDAS, apparently associated with GABHS infection, is not seen in OCD; OCD is generally characterized by a gradual onset and worsening of symptoms until intervention (Swedo et al., 1998; Turner et al., 2004).  Further, the choreiform movements of hands and fingers that appear to be specific to the PANDAS subgroup, such that they can be used to reliably recognize children within this group, do not appear in OCD (Garvey, Giedd, & Swedo, 1998; Snider & Swedo, 2004).  Common comorbid symptoms in PANDAS, including inattentiveness, hyperactivity, separation anxiety, enuresis (Swedo et al., 1998), and handwriting deteriorations (Swedo et al., 1998), also are not typically comorbid with OCD.              

Another difference between OCD and PANDAS is age of onset.  For pediatric OCD, onset occurs between 10-12.5 years of age (Leonard & Rapoport, 1991; Wewetzer et al., 2001) and research suggests that diagnosis cannot be reliably made until age 9 because many children engage in OCD-like rituals (Leonard et al., 1990) and experience intrusive thoughts (Flament et al., 1990).  Around this time, these “normal” behaviors tend to stop and the residual rituals are associated with distress and impairment, indicating presence of a disorder (Albano et al., 2003).  Further, the metacognitive assessment of thoughts as intrusive and inappropriate necessary to meet criteria for OCD is not developmentally possible in children prior to age 9-10 (Berk, 2006).  Any diagnosis made prior to this age range, then, should raise concerns regarding accuracy of diagnosis.  In order to diagnose PANDAS, full criteria for OCD or a tic disorder must be met, so the issues with diagnosing OCD symptoms prior to age 9 should also apply to diagnosis of PANDAS.  In practice, however, PANDAS is usually diagnosed before age 9.  In fact, the mean age of onset PANDAS with OCD symptoms is 7.4 (Swedo et al., 1998), ranging from 3-12 (Swedo, Leonard, & Rapoport, 2004).  If OCD-like behavior is normal in children up to age 9 and metacognitive abilities do not develop until age 9-10, how can clinicians differentiate OCD symptoms in PANDAS (or in any presentation) from normal behavior prior to that age? 

Such a question applies directly to accuracy of PANDAS diagnosis but becomes salient to OCD when considering that an estimated 10% of the pediatric OCD sample is made up of PANDAS.  Therefore, including PANDAS as part of OCD may be problematic because PANDAS may include individuals who really don’t meet criteria for OCD. Further, after comparing OCD and PANDAS, it appears that the causes, course, and features of the two disorders differ markedly.  These distinctions raise concerns about inclusion within the same construct, especially when considering the implications for conceptualization, assessment, research, and treatment; PANDAS appears to confound an already complex disorder construct. 

Overview of Basic Neurophysiology: Basal Ganglia, Orbitofrontal Cortex, Neurotransmitters, Sex Hormones

Primary Brain Structures Involved in OCD: Basal Ganglia and Orbitofrontal Cortex

From a developmental perspective, examining brain structures and functioning in a brain that is not fully developed is problematic.  Even more problematic is making determinations about what constitutes normal/abnormal brain structures and functioning.  Although rough determinations could theoretically be made, a large amount of individual variation would be expected, with the most mature, deeper subcortical brain regions exhibiting more stability than the upper, cortical regions, namely the frontal lobe, which is last to mature (Berk, 2006).  In OCD, both cortical and subcortical brain structures are involved.  Specifically, the basal ganglia and orbitofrontal cortex, as well as two brain pathways are thought to be involved in OCD. 

The basal ganglia is involved in movement, namely, selection of which action to execute at a given time and in the ability to inhibit movement (Bear, Connors, & Paradiso, 2001).  In obsessive-compulsive disorder, reports suggest dysfunction in the basal ganglia and bilateral reductions in basal ganglia volume (Luxenberg et al., 1988; Robinson et al., 1995; Rosenberg et al., 1997; Whiteside et al., 2004).  These abnormalities are thought to influence the overt behavioral component of many OCD cases, compulsions, leading to an increase in compulsive behavior. There is evidence that those with the more genetically based, early-onset OCD exhibit more basal gangliar abnormality (Kim, 2003) and report more compulsions than later onset OCD (Butwicka & Gmitrowicz, 2010; Geller et al., 1998; Okino, 2007; Rettew, Swedo, Leonard, Lenane, & Rapoport, 1992).  It is unclear whether the early-onset type of OCD is more prone to basal gangliar abnormalities and thus, overt behavioral compulsions, if the cortical regions are simply not developed enough to make clear neurophysiological determinations about functioning, or whether developing OCD at such an early age leads to abnormal brain development.      

As discussed earlier, not all individuals with OCD experience overt behavioral compulsions.  Some exhibit covert mental compulsions (e.g., counting, picturing the image of a deity in response to a blasphemous obsession), so the logic for basal gangliar involvement in these cases is problematic.  Indeed, not all individuals with OCD show such basal gangliar abnormalities compared to controls (Robinson et al., 1995; Rosenberg et al., 1997); these studies did not examine the nature of individuals’ compulsions, so conclusions cannot be drawn regarding specificity of basal gangliar abnormalities to only those with overt behavioral compulsions.  Abnormalities in basal ganglia physiology lead to questions about the nature of its involvement and whether differences are indicative of different subtypes. 

In OCD, evidence points to dysfunction in the frontal lobe, and specifically, the orbitofrontal cortex (Chamberlain et al., 2008; Whiteside et al., 2004) and reduced bilateral cortex volume compared to controls (Szeszko et al., 1999).  The frontal lobe is involved in executive functioning, which includes inhibition, social appropriateness, planned behavior, metacognition, confirmation of previous behaviors, and emotional valence of reinforcers (Abramowitz, Taylor, & McKay, 2009; Bechara, 2004; Bechara, Damasio, Damasio, & Anderson, 1994; Bechara, Damasio, & Damasio, 2000; Kringelbach, 2005; Rauch & Jenike, 1993).  More specifically, this area controls the type of planned behaviors and emotional valence related to operant conditioning (i.e., punishers and reinforcers; Bechara, 2004; Bechara et al., 1994; Kringelbach, 2005). If this brain region is not functioning properly, normal operant conditioning may become frenetic.  Linkages between stimuli and response could become less logical so that obsessions become the stimuli and compulsions become the actions necessary to prevent the stimuli (obsessions) from coming true.  This process may lead to the perception that thoughts hold great power and facilitates the development of strong emotional ties between obsessions and the methods used to reduce the distress they produce.  Further, if the area of the brain responsible for confirming whether an action is performed is dysfunctional, one would expect to see repetitive behaviors and uncertainty; indeed, these are exhibited in OCD.  Preschool and school age children do exhibit the capacity to experience similar processes, assigning power to certain beliefs and perceiving control over those beliefs through their actions, such as in the case of superstition and magical thinking (Bolton, 1996; Bolton, Dearsley, Madronal-Luque, & Baron-Cohen, 2002).  At some point in normal development, though, individuals recognize that certain beliefs are illogical and recognize that they lack the power to control certain aspects of their environment.  Why this process persists (or develops again later) as related to obsessional thought is unclear.  Understanding this developmental process and the involvement of this brain region is imperative in a disorder with significant components of planned behavior, operant conditioning (the negatively reinforcing nature of compulsions on obsessions), confirmation of behavior, and high emotional valence of the operant conditioning process.

As mentioned, the frontal lobe also controls metacognition.  Thinking about thoughts and making the determination that they are intrusive and inappropriate is part of the definition of obsessions in OCD.  But, as discussed, this metacognitive ability is not fully developed in children and thus, these attributions cannot be made at an early age (Berk, 2006).  Interestingly, early-onset cases of OCD do not appear to exhibit the executive functioning deficits,indicative of poor frontal lobe functioning that late-onset individuals evidence (Hwang et al., 2007; Lomax, Oldfield, & Salkovskis, 2009; Roth, Milovan, Baribeau, & O'Connor, 2005).  It is unclear whether developing OCD early in life impacts brain development, protecting some areas and impairing others, or whether different manifestations of the disorder, one with more compulsions, the other with more metacognitive dysfunction, lead to brain abnormalities.  For example, does the processing of OCD-related metacognitive information overwhelm the cognitive processing system, leaving fewer cognitive resources to perform other executive functions?  The DSM-IV indicates that it might (American Psychiatric Association, 2000).

In addition to reduced activation in the basal ganglia and orbitofrontal cortex, some believe that certain brain pathways also exhibit dysfunction.  Researchers hypothesize that a disinhibition in the direct pathway from the orbitofrontal cortex to the basal ganglia to the thalamus (and back to the cortex) results in overactivity, specifically in the thalamic system.  This problem is further compounded by a dysfunctional indirect pathway between the cortex, basal ganglia, and thalamus (and back to the cortex) which typically provides negative feedback, damping down hyperactivity in the direct pathway.  The direct pathway becomes overactive and is not kept in check by the indirect pathway (Saxena & Rauch, 2000).  As a result, it is proposed that in individuals with neurological difficulties in inhibiting, the bizarre and perverse thoughts common in all humans but readily dismissed, progress to obsessional thoughts about danger, violence, sex, hygiene, contamination, and order (Hollander et al., 2005). 

The basal ganglia, important in overt, behavioral components of OCD; the orbitofrontal cortex, involved in executive functioning; and at least two related brain pathways, important in inhibition, appear implicated in OCD.  A better understanding of how these brain areas and pathways function in OCD in both adults and children, and ultimately, whether neurophysiological abnormalities lead to OCD or result from it, is essential to understand disorder development. 

Neurotransmitters

As with many other psychological disorders (e.g., schizophrenia), research findings indicate the involvement of serotonin and dopamine in OCD.  The primary evidence for the role of serotonin in human OCD comes from the results of drug trials.  Overall, 40-60% of individuals taking serotonin uptake inhibitors (SUIs) experience an improvement in OCD symptoms (Jenike, Baer, & Minichiello, 1998; Pigott & Seay, 1999).  A review of pediatric OCD treatment studies also highlights the utility of serotonergic drugs in reducing OCD symptoms (Mancuso, Faro, Joshi, & Geller, 2010).  Further, a meta-analysis examining a dosage effect of selective serotonin reuptake inhibitors (SSRIs) found that greater dosage predicts greater reductions in OCD symptoms and higher rates of treatment response (Bloch, McGuire, Landeros-Weisenberger, Leckman, & Pittenger, 2010).  These response rates are evidence that taking drugs designed to manipulate serotonin reduces OCD symptomatology in a portion of OCD sufferers; and more specifically, that increasing serotonin helps reduce the symptoms of OCD. 

Animal studies provide additional support for serotonin’s role in OCD.  In particular, many of these studies have used an animal model of OCD, stereotypy, to approximate OCD.  Repetitive, functionless, and consistent, stereotypic behaviors have been used as an animal model for OCD because they appear similar to human compulsions.  Observed frequently in caged animals, stereotypic behaviors such as pacing in zoo animals, cribbing in domestic horses (i.e., swallowing air), and excessive grooming behaviors, such as acral lick dermatitis in canines (i.e., excessive licking that causes skin lesions), often develop in response to lack of environmental stimuli (Garner, Meehan, & Mench, 2003; Mason, 1991) and may also be the result of anxiety.  Stereotypy’s link to anxiety comes from research findings illustrating that the prevention of stereotypy seems to increase anxiety levels (Dodman & Shuster, 2005).  The observation that these behaviors are similar in appearance to compulsions, the belief that they appear to occur in response to anxiety, and findings that the prevention of these behaviors results in increases in anxiety, suggest that they could be useful models for human anxiety and OCD.  Indeed, differential responses of acral lick dermatitis to SSRIs but not noradrenergic substances provide preliminary support for the efficacy of SSRIs in the treatment of stereotypic behavior and for the specificity of the role of serotonin in stereotypic behavior (Rapoport, Ryland, & Kriete, 1992). 

Research suggests that another neurotransmitter, dopamine, may also be involved in OCD, serving to increasecompulsive behavior.  The primary work on dopamine’s involvement in OCD has been conducted within animal studies of OCD: Rats developed compulsive checking and ritualistic behavior after repeated administration of quinpirole, a dopamine D2/D4 receptor agonist (Jithendra & Murthy, 2010; Szechtman, Sulis, & Eilam, 1998; Tizabi et al., 2002).  This induced checking behavior was lower if rats were given the SSRI, clomipramine (Szechtman et al., 1998), providing evidence for the role of dopamine in contributing to compulsive behavior and additional evidence for the role of serotonin in reducing it.  Other work suggests that the effects of dopamine on OCD might include an interaction with hormones, specifically estrogen.  In an animal study of OCD, estrogen deficiency led to a reduction in production of catechol-O-methyltransferase (COMT), an enzyme that breaks down dopamine.  As a result, compulsive behaviors increased, and a restoration of estrogen levels brought COMT back to a normal level and reduced compulsive behaviors (Hill et al., 2007).  

Evidence to support the role of serotonin and dopamine in OCD is met with evidence that questions the role of these neurotransmitters in OCD.  Although a portion of individuals taking serotonin uptake inhibitors see improvements in OCD symptoms (40-60%), a similar portion (i.e., 40-60%) does not see clinically significant improvements, and those who do only see an average improvement in symptoms of 20-40% (Jenike, 2004).  Further, prospective studies suggest that although improvements are seen with drugs that increase serotonin levels, at follow-up, very few individuals were in full remission (only 6%) and a large portion continued to meet full OCD criteria (Leonard et al., 1993). The large nonresponse rate suggests that the neurobiology and treatment of OCD probably involves more than just increasing serotonin (McDougle, Barr, Goodman, & Price, 1999).  Indeed, animal studies suggest that the neurobiology of OCD also involves dopamine (Hill et al., 2007; Jithendra & Murthy, 2010; Szechtman et al., 1998; Tizabi et al., 2002) and possibly neuropeptides in both animals and humans (McDougle et al., 1999).  Even so, given the complexity of the disorder and the brain itself, it is still unlikely that serotonin, dopamine, and neuropeptides explain the entirety of neurochemical involvement in OCD.   

Animal studies have been useful in both psychology and medicine, uncovering important biological underpinnings and treatments for disorders that would have gone undiscovered with current methodological limitations on using human subjects.  Although important, in this case for uncovering neurotransmitter involvement in OCD, these studies are not without limitations.  The main problem with studying human mental disorders in animals is that the disorders cannot be conceptualized in the same ways.  This is especially problematic for a disorder in which much of the symptomatology is accessible only through client report (i.e., obsessions, neutralization strategies, and other covert compulsions such as counting).  Because animals cannot tell humans what they are thinking, the only piece of OCD that researchers can measure is overt compulsive behavior.  Unfortunately, even if compulsive behavior is evident in animals, the key difference between true obsessive compulsions and other types of compulsive behavior is the behavior’s function, and behavioral function is difficult to assess without asking the individual.  Therefore, the behaviors conceptualized as “compulsive” in the animal study of neurotransmitters in OCD may not be tapping the same construct in the human study of OCD, and thus, may not be utilizing the same neurotransmitters.   

Serotonin and dopamine appear linked to compulsive behavior in animals, but their roles in human compulsive behavior, and more importantly, OCD are much less clear.  Specifically, the current methods of studying neurotransmitters in human OCD are not optimal and animal models of OCD are problematic.  Clinical trials of serotonergic and dopaminergic drugs indicate that groups taking these drugs experience either reductions or increases in OCD symptomatology, respectively.  Researchers assume that because these drugs are designed to increase levels of serotonin and dopamine that this is how they impact OCD.  Although this is a logical assumption, no one knows for sure that this is why they impact OCD symptomatology because neurotransmitters have not been studied at a micro level in humans. Further, although mechanisms of action in many of the serotonergic and dopaminergic drugs are fairly well understood, there are still questions that remain unanswered.  For example, although the serotonergic drugs impact serotonin levels immediately, symptom reductions typically are not seen for several weeks.  Why does this happen?  Additionally, although one neurotransmitter, serotonin, has been studied and appears to be implicated in children with OCD, prospective studies are needed to determine directionality of neurotransmitter involvement and how neurotransmitter levels change over the course of development.  Further examination of neurotransmitter involvement, using more sophisticated methodology may help uncover important insights into OCD’s neurobiology, development, and hopefully, will provide much more specific information on not only which neurotransmitters are involved, but how they are involved, and how their involvement differs in OCD compared to other disorders.

Sex Differences in OCD

In addition to neurophysiology and neurotransmitters, another potential biological influence on OCD is sex hormones.  The presence of sex differences within a disorder can be indicative of the role of sex hormones in the disorder.  In OCD, males exhibit higher prevalence rates in childhood, around 66%, but the rates even out and then flip in puberty, so that women exhibit slightly higher rates in adulthood (Albano et al., 2003; Geller et al., 1998; Steketee & Barlow, 2002).  Exactly why this occurs is unclear, but given that this occurs after puberty, one hypothesis is that sex hormones are involved.  One sex hormone in particular has been implicated in anxiety disorders, estrogen, but only appears problematic in anxiety if there is an excess (Morgan & Pfaff, 2002) or shortage (Hill et al., 2007; Österlund, Witt, & Gustafsson, 2005).  If the evidence for the role of estrogen in anxiety is generalizable to OCD, estrogen would not be expected to impact OCD unless estrogen rates were above or below a certain level.

Animal studies support the generalizability of the low estrogen hypothesis in anxiety to OCD, with low estrogen levels increasing OCD symptomatology.  In one animal study, estrogen deficiencies led to increases in compulsive behavior: Pre-pubertal rats experiencing estradiol withdrawal exhibit a rise in compulsive lever pressing (Flaisher-Grinberg et al.).  Alternatively, restoration of estrogen levels led to decreases in compulsive behaviors in rats (Hill et al., 2007) and actually alleviated anxiety in perimenopausal humans (Nathorst-Boos, Von Schoultz, & Carlstrom, 1993). 

Males naturally have lower levels of estrogen.  Females have low levels of estrogen in childhood than in adulthood, but their levels are still higher than males throughout the lifespan (Klein, Baron, Colli, McDonnell, & Cutler, 1994).  If the hypothesis that low levels of estrogen lead to higher levels of anxiety, and specifically, OCD symptoms, is true, then the effects would be most apparent during a period in development when estrogen is lowest (childhood) and in individuals with the lowest levels of estrogen (males).   Indeed, prevalence data indicate that males do display a higher propensity for OCD in childhood (Steketee & Barlow, 2002). 

More complex examinations in animals may shed some light on a potential mechanism by which estrogen deficiencies serve to increase OCD development—through the effects of estrogen on dopamine breakdown.  As previously discussed, dopamine is important in understanding OCD because it has been shown to increase compulsive behavior in animals (Szechtman et al., 1998; Tizabi et al., 2002).  Further, low levels of the enzyme, catechol-O-methyltransferase (COMT), which is implicated in the breaking down of dopamine, have been associated with an elevated risk for OCD development in humans (Karayiorgou et al., 1997).  One innovative study utilized aromatase knockout mice (ArKO) to examine the effects of estrogen deficiency on COMT and OCD behaviors.  Aromatase knockout mice are a useful vehicle for studying the effects of estrogen, because without aromatase, the conversion of androgens to estrogen is impaired.  Male knockout mice exhibited increases in compulsive behavior such as wheel running activity and increased grooming, in addition to other changes such as facial hair loss, decreased ambulatory behavior, and decreases in hypothalamic COMT protein expression, indicating that dopamine was not broken down normally.  Estrogen replacement returned COMT, wheel running activity, and grooming to levels observed in control, wild male mice (Hill et al., 2007).  Estrogen deficiency appears to lead to compulsive behaviors by indirectly increasing dopamine levels through a reduction in the production of the enzyme, COMT, which normally breaks it down. 

High levels of estrogen appear to be as problematic in anxiety as low levels.  High levels have been shown to increase anxious symptoms in animal studies (Morgan & Pfaff, 2002).  In human studies of OCD, however, support for the impact of high levels of estrogen on symptomatology is much more indirect: Support comes from examining the changing sex distribution of the disorder.  Estrogen levels in childhood are relatively low for both sexes, but during puberty, estrogen levels in females increase dramatically, so that in early adulthood, females’ estrogen levels are much higher than males.  If high levels of estrogen contribute to higher levels of anxiety, and specifically, OCD symptoms, then the effects should be most apparent during a period in development when estrogen is highest (after puberty) and in individuals with the highest levels of estrogen (females).  So, if some females experience excessive rises in estrogen (e.g., those with a genetic predisposition to produce more estrogen) they may be more likely to develop OCD.  Indeed, the 2:1 male to female OCD prevalence ratio in childhood levels out around puberty, so that slightly more females exhibit OCD than males (Albano et al., 2003; Steketee & Barlow, 2002).  Human OCD studies examining the effects of high estrogen levels on OCD are scarce, however, as are animal studies, so until additional studies are conducted, the role of excessive estrogen in OCD will remain speculative. 

Perhaps hormones do not impact sex differences in OCD as findings suggest, or do not impact sex differences to the extent suggested.  The sex differences profile in OCD may appear the way it does because it is complicated by the PANDAS profile.  Ten percent of early-onset cases of OCD have been attributed to PANDAS; 75% of individuals typically afflicted are male and quite young (Swedo et al., 1998).  Given that a portion of childhood OCD cases are thought to be PANDAS related (Trifiletti & Packard, 1999) and most of these children are male, it is possible that male PANDAS cases are skewing the sex distribution in childhood.  In adolescence and early adulthood, when this disorder no longer develops, the numbers may begin to level out. 

Conclusions

OCD appears to have several biological components, including genetic factors; the basal ganglia and orbitofrontal cortex brain regions; the neurotransmitters, dopamine and serotonin; and sex hormones, specifically, estrogen.  Definitive conclusions about the biology of human OCD development, however, must be tempered because current data comes primarily from cross-sectional and case-control designs.  Experimental data is promising but has utilized animal models of OCD, which raise concerns about equivalency in human OCD conceptualizations.  Further, correlations and heritability rates between any of these factors and OCD are not 100%, indicating that something else is contributing to the disorder. One possibility is that current measurement tools are not advanced enough to detect all aspects of biological involvement; another possibility is that other factors, such as environment, are involved. 

Environmental Factors in OCD Development

Perinatal Factors

Environmental influences on development, and most relevantly, on OCD development, do not start at birth, they start at conception.  Children are exposed to a host of stressors in utero such as viruses, edema, labor, and toxins.  It is well known that certain factors can lead to physiological problems and disorders; for example, maternal alcohol consumption can lead to fetal alcohol syndrome and folic acid deficiencies can lead to neural tube defects (Mayo Clinic, 2009, 2011).  Studies have also widely investigated the impact of perinatal factors on some mental disorders, such as schizophrenia (Brown, 2011).  Perinatal factors have been examined in regard to their contribution to OCD development but to a lesser extent than most other mental disorders (Geller et al., 2008).  Overall, studies suggest that a variety of complications including edema during pregnancy, maternal illness requiring medical attention, and birth difficulties, specifically, prolonged labor and forceps use, have been related to later OCD development (Geller et al., 2008; Sampaio et al., 2009; Vasconcelos et al., 2007).  Not only do perinatal experiences appear related to an OCD diagnosis itself,  these experiences were related to earlier OCD onset, increased OCD severity, and a variety of comorbid conditions such as ADHD, major depressive disorder, generalized anxiety disorder, and tic disorder (Geller et al., 2008).  The physiological effects of these complications are regularly assessed and monitored by the medical community but these findings indicate that adverse experiences as early as gestation could have even farther reaching effects, impacting development of OCD later in life.

These findings indicate that relationships exist between OCD and perinatal factors. However, this research is not without limitations.  First, the research has largely utilized simple case-control and cross-sectional designs, so prediction of outcomes from early experiences is impossible and prospective studies are needed.  Second, many of the study designs have not allowed for the ruling out mediating/moderating variables, so whether perinatal experiences lead to OCD, whether something else predicts both, or whether something moderates the level of the relationships is unclear.  For example, factors such as excessive maternal weight gain, premature birth, jaundice, and hyperemesis gravidarum (severe morning sickness) all appeared related to OCD, but these relationships did not persist when socioeconomic status was factored out (Vasconcelos et al., 2007).  This finding highlights the importance of measuring complex sets of interactions among perinatal and environmental factors.  Environmental factors such as socioeconomic status may influence the existence of adverse perinatal factors in some and protect against the effects of perinatal factors in others.  For example, low socioeconomic status could prevent adequate prenatal care, leading to premature birth.  Alternatively, a child born prematurely to someone of high socioeconomic status may fare better despite this risk factor because their parents can afford high quality medical care.  Further, the same factors that lead to perinatal risk factors may also negatively impact developmental later on, making an already vulnerable individual much more likely to experience problems.  For example, maternal illness during pregnancy might increase risk for OCD in and of itself, but if maternal illness persists through childhood, this can impact ability to parent, which can further impact child development.  The literature on perinatal risk factors in OCD development has yet to address these complex interactions.

Third, research has not fully addressed the specificity of perinatal experiences on OCD compared to the impact of perinatal experiences on psychological disorders in general.  One study found that an OCD group did not differ from other groups (i.e., healthy control, anxiety and depression, conduct disorder) on perinatal complications and problems (Douglass, Moffitt, Dar, McGee, & Silva, 1995).  Another indicated that adverse perinatal experiences were related to OCD with several comorbid psychological disorders (Geller et al., 2008).  Additional study is needed to determine which perinatal factors are uniquely tied to OCD development. 

Finally, work has not addressed a mechanism through which perinatal experiences might lead to OCD.  Mechanisms might include fetal distress, a suboptimal fetal environment which leads to developmental deficits, and brain damage, though the damage might not be apparent in terms of intellectual development (and thus, overlooked by traditional tests).  Although there does not appear to be empirical work addressing these mechanisms perinatally, general evidence exists for brain damage as a mechanism through which an environmental context may cause OCD.  That is, individuals with documented brain damage/deterioration have been known to engage in obsessive, compulsive, and hoarding behaviors (Hollander et al., 1990; Hugo, Van Heerden, Zungu-Dirwayi, & Stein, 1999; Silver, Kramer, Greenwald, & Weissman, 2001).  So, it may be that adverse experiences in the perinatal period lead to brain damage, which leads to a manifestation of OCD and hoarding symptomatology later in life.  The problem with this line of argument is that not all individuals with OCD report unfavorable perinatal experiences, indicating that perinatal experiences do not explain all of OCD development; perhaps only a subgroup, or less likely, that all individuals experience these events but not all are aware.  

Parenting Styles

Another environmental factor that may contribute to OCD is parenting.  The aspects of parenting that appear most related to OCD fall within the parenting style designation of authoritarianism, which refers to parenting that requires a rigidly high standard of conduct, involves parents who are controlling, punitive, forceful, unyielding, rejecting, conservative, often lack warmth, and employ high levels of structure, where autonomy is discouraged, and obedience and perfectionism demanded (Baumrind, 1966, 1968, 1971).  The aspects of the authoritarian parenting style that have been examined empirically in OCD include control, overinvolvement, perfectionism, conservativism, criticism, rejection, and low emotional warmth.  However, studies providing a comprehensive examination of this constellation as a whole are lacking, so findings addressing one or more individual factors will be discussed.

The authoritarian parenting aspects of control, overinvolvement, criticism, perfectionism, and conservativism have been documented in OCD. Using an analogue sample of adults, those who scored high on OCD symptoms reported that their parents were significantly more controlling than a comparison group (Aycicegi, Harris, & Dinn, 2002).  When sampling parents of an actual clinical sample of children with OCD, researchers found that a large portion of parents were rated as overinvolved or critical; 73% of mothers and 46% of fathers, which was larger than ratings in of parents of children without a disorder, or 31% of mothers and  22% of fathers (Hibbs et al., 1991).  Further, in a prospective study of OCD, parental criticism and/or overinvolvement significantly predicted global functioning scores at follow up (Leonard et al., 1993).  Individuals with OCD are more likely to report perfectionistic parents (Lo, 1967) and those with higher levels of OCD symptoms were also more likely to endorse parental conservatism than liberalism (Zohar, Goldman, Calamary, & Mashiah, 2005).  These findings provide partial support for the role of an authoritarian parenting style in OCD, specifically implicating control, overinvolvement, criticism, perfectionism, and conservatism. 

The authoritarian parenting aspects of lack of warmth and rejection have also been documented in parents of those with OCD.  Parents of those with OCD were rated as less emotionally warm by their adult children than parents of non-clinical controls (Aycicegi et al., 2002; Hoekstra, Visser, & Emmelkamp, 1989).  Individuals with OCD rated parents as more rejecting than non-clinical controls (Aycicegi et al., 2002; Hoekstra et al., 1989), although others have found that only fathers were more rejecting in those with OCD versus non-clinical controls (Alonso et al., 2004).  Beyond a simple relationship between OCD and parental rejection, one study found that treatment outcomes for OCD were also negatively impacted by parental rejection (Emmelkamp, Hoekstra, & Visser, 1985). 

Although features of an authoritarian parenting style have been shown to be related to OCD, studies actually examining this constellation as a whole and the impact of this style on OCD development over time appear scarce.  From a theoretical standpoint, the idea of an authoritarian parenting style contributing to OCD appears logical, considering that OCD involves many of the characteristics inherent in this style: perfectionism (e.g., in personal standards, performing rituals, mental cleanliness, etc.), rigidity (e.g., in performing rituals, in obsessive beliefs, etc.), and high need for control (e.g., of thoughts, events, etc.; Sookman, Pinard, & Beck, 2001).  Retrospective reports from adults with OCD endorsing childhood experiences with authoritarian-like parents and concurrent reports from parents of children with OCD, indicating characteristics of an authoritarian style, represent attempts to approximate causation.  However, in order to make assertions about childhood experiences leading to later disorder development, individuals need to be assessed prospectively and/or experimental (or quasi experimental) designs need to be employed.  Until this happens, we cannot rule out the possibility that retrospective reports of adults are influenced by their current life experiences more so than the actual parenting styles employed.  For example, recall of stimuli appears mood congruent; that is, individuals who were more anxious were more likely to remember anxiety-provoking stimuli (Russo et al., 2006).  If these findings extend to OCD, perhaps OCD symptomatology increases the likelihood of remembering parenting styles consistent with OCD, rather than parenting styles as they truly were.  

For the most part, parenting styles in OCD have been examined linearly (exceptions include: Coles, Schofield, & Pietrefesa, 2006), but the influence of parenting on OCD is hypothesized to be much more complex than a linear model can accommodate (Carter & Pollock, 2000).  For example, almost everyone experiences intrusive thoughts, some of which are unconventional or bizarre.  If children share their intrusive thoughts with parents, an authoritarian parent may be more likely to respond with authoritarian characteristics; that is, with criticism and by imposing rigidly high standards of conduct, especially if thoughts are unconventional.  This strong overreaction may lead to the attachment of meaning to an innocuous thought, facilitating obsessional development.  Further, if these parents continue to respond in an authoritarian manner, becoming overinvolved with their child’s internal processes, facilitating the monitoring of thoughts, they may further reinforce the salience of thoughts and importance of monitoring them.  Alternatively, if a parent responds in a warm, open way to these thoughts, helping the child to normalize them, placing little emphasis on their importance (“thoughts are just thoughts; we can’t control what pops into our heads”), they might actually prevent the development of obsessional thoughts (Carter & Pollock, 2000). 

In order to better understand how parenting styles are involved in OCD, future research needs to utilize more rigorous methodology, including a more comprehensive constellation of factors as well as clinical samples and control groups to determine specificity of parenting styles to OCD.  Further, understanding of both OCD and parenting would be enhanced by applying a developmental model to address the impact of parenting on OCD, starting with longitudinal study designs, and using nonlinear models and research methodology that address the complexity of parental influences on OCD and vice versa.

Trauma

Traumatic experiences can undoubtedly have a profound impact on victims, and in some cases, contribute to the development of psychological disorders, most notably acute stress disorder and posttraumatic stress disorder (PTSD).  There is also evidence that such events might contribute to the development of OCD (Boudreaux, Kilpatrick, Resnick, Best, & Saunders, 1998; Jordan et al., 1991; Maes, Mylle, Delmeire, & Altamura, 2000).  Reviews of existing studies estimate that 4.2-19% of those who go on to develop PTSD following a traumatic event also receive OCD diagnoses; the rates of PTSD within an OCD sample range even higher, from 1.6-75% (Huppert et al., 2005).  Theorists posit that this comorbidity may exist because of similarity in underlying disorder phenomenonology: intrusive images and thoughts causing great distress, ameliorated by functionally avoidant behavior; for example, overt avoidance through compulsions, avoidance through dissociation, avoidance through neutralization (Huppert et al., 2005; Solomon et al., 1991).  Moreover, a large portion (62%) of those with OCD, but not necessarily comorbid PTSD, reported obsessive thought content in the form of intrusive images related to memories of earlier traumatic events (Speckens, Hackmann, Ehlers, & Cuthbert, 2007), indicating an impact of earlier traumatic experiences on disorder development and/or shaping of symptomatology. 

            Experimental manipulation supports the impact of traumatic events on OCD development and reveals a potential pathway of development.  Work with non-clinical populations indicates that even imaginal exposure to nonconsensual physical contact, specifically, an unwanted kiss, can trigger perceptions of “mental pollution” (i.e., feelings of dirtiness without actual contact) and urges to wash (in some cases, actual washing occurred) not unlike the obsessions and compulsions of OCD.  This nonconsensual exposure also produced significantly more anxiety, anger, sadness, and feelings of upset than did a consensual exposure.  Interestingly, 41% of those experiencing the nonconsensual imaginal exposure reported engagement in a neutralization strategy to reduce distress caused by the exposure, whereas only 7% of those in the consensual imaginal exposure engaged in neutralization. Those in the nonconsensual condition reported a significantly greater urge to wash than did those in the consensual condition.  Further, 9% of those in the nonconsensual condition engaged in actual hand washing or mouth rinsing to reduce mental pollution; only 3% of those in the consensual group rinsed to reduce mental pollution (Fairbrother, Newth, & Rachman, 2005).  This suggests that not simply imagined physical contact, but imagined unwanted physical contact can lead to OCD-like responses.  If an imagined event can cause such thoughts and urges in an ostensibly healthy population, it is possible, then, that actual forced physical contact could lead to OCD symptoms and perhaps, full-blown OCD. 

Research on OCD and sexual assault indicates that, indeed, actual sexual assault led to “mental pollution” in 60% of a sample of victims.  Of those 60%, 70% reported an urge to wash following the assault.  Forty-nine percent washed more than once in response to washing urges and 23.6% “washed excessively” following the assault (Fairbrother & Rachman, 2004).  These findings and those of the imaginal exposure suggest a pathway to OCD characteristics following a trauma or imagined trauma that begins with feelings of mental pollution, leads to urges to wash in many, actual washing behavior in a large portion, and excessive washing in a portion of assault cases assessed.  Additionally, considering evidence that obsessional content in actual OCD reflects adverse events and evidence that experimentally administered imaginal trauma produces OCD-like responses consonant with imagined events, one would expect type of OCD symptomatology to follow from type of traumatic events.  That is, rape should lead to contamination obsessions and washing obsessions, physical abuse should lead to fears of harm and checking compulsions (e.g., checking for danger, checking door locks).  However, this hypothesis has yet to receive empirical attention.

Trauma has been examined primarily in the context of PTSD, so the influence trauma may have on other disorders, including OCD, is unclear.  However, if the previously discussed research is an accurate representation of the influence that trauma can have on OCD, future studies should further address the impact of trauma on OCD development.  Additionally, not all individuals exposed to trauma go on to develop OCD (or another psychological disorder), so future studies should also examine the impact of factors preventing development of OCD following a traumatic experience.

Temperament

Temperament is commonly conceptualized as an individual’s innate emotional response, including behavioral manifestations of emotional response, and mood characteristics (Lonigan & Phillips, 2001).  Temperament not only affects how an individual responds, but it affects how others interact with that individual, and in turn, how the individual reacts to others’ interactions with him/her; this process is called a “transaction”, which makes temperament itself a transactional variable.  (Transactions will be reviewed in more detail in the developmental section below.)  As such, temperament is innate but its transactional nature means that it is both shaped by the environment and shapes the environment, making it a hybrid between a biological and environmental variable.  It is included in the environmental section rather than the biology section because of its inextricable relationship with the environment.  In OCD, behavioral inhibition and harm avoidance have been the temperament types of primary interest, receiving the largest amount of empirical study and support.

Behavioral inhibition refers to the tendency to exercise restraint, avoid novelty, and withdraw (Coles et al., 2006; Garcia Coll, Kagan, & Reznick, 1984).  This temperament has been widely studied in anxiety (Biederman et al., 2001; Hayward, Killen, Kraemer, & Taylor, 1998; Hirshfeld et al., 1992; Kagan, 1997; Prior, Smart, Sanson, & Oberklaid, 2000; Schwartz, Snidman, & Kagan, 1999) and neuroimaging studies indicate that the area of the brain implicated in fear responses, the amygdala, shows more activation in behaviorally inhibited adults than noninhibited adults when viewing unfamiliar faces (Schwartz, Wright, Shin, Kagan, & Rauch, 2003). Children labeled as “behaviorally inhibited” were more likely to have a social anxiety disorder than those not labeled as such (Biederman et al., 2001).  Behavioral inhibition in childhood predicted social anxiety in adolescence (Prior et al., 2000; Schwartz et al., 1999).  High school students reporting behavioral inhibition in childhood were 4 times more likely to develop social phobia at follow-up(Hayward et al., 1998).  And, in a cross-sectional sample of undergraduates, retrospective ratings of behavioral inhibition were correlated with social anxiety symptoms (Mick & Telch, 1998).

As with temperament in general, the specific temperament style, behavioral inhibition, serves as a transactional variable; that is, it impacts how individuals impact their environment and in turn, how the environment impacts the individual.  In particular, behaviorally inhibited children exhibited decreased physiological arousal when paired with supportive and warm parents.  Conversely, when paired with intrusive and contemptuous parents, they became even more shy and anxious.  Additionally, a supportive parenting style increased behaviorally inhibited children’s approach toward novel stimuli whereas protective parenting increased withdrawal responses (Berk, 2006; Rubin, Burgess, & Hastings, 2002; Rubin, Hastings, Stewart, Henderson, & Chen, 1997).  These are but a few examples of the research in the area, but highlight the importance of behavioral inhibition on anxiety, as well as its transactional nature.

In OCD, children and adolescents with the disorder exhibit greater levels of behavioral inhibition than do controls, evidenced by low activity scores and high shyness scores (Ivarsson & Winge-Westholm, 2004).  Retrospective self-reports of high levels of behavioral inhibition in childhood correlated with obsessive-compulsive symptoms in a non-clinical college sample (Coles et al., 2006).  The effects of behavioral inhibition on OCD appear to be compounded by overprotective parenting such that the relationship between frequency of OCD symptoms and reported behavioral inhibition in childhood was strengthened by higher reported levels of overprotective parenting (Coles et al., 2006).  These data provide evidence for the moderating effects of parenting on the OCD-behavioral inhibition relationship.  Although the data provide preliminary evidence for the potential role of behavioral inhibition in OCD development, exactly how these characteristics might lead to OCD development has not been tested, so it is unclear whether behavioral inhibition contributes to OCD, or is simply a correlate. 

The other type of temperament of primary interest in OCD is harm avoidance.  The harm avoidance temperament includes fear of the ambiguous, anticipatory worry, fatigability, and shyness with strangers (Cloninger, Svrakic, & Przybeck, 1993).  Studies have supported the co-occurrence of harm avoidance with OCD (Ettelt et al., 2008; Gothelf, Aharonovsky, Horesh, Carty, & Apter, 2004; S. J. Kim, Kang, & Kim, 2009; Lyoo, Yoon, Kang, & Kwon, 2003).  Other research examining harm avoidance in OCD, indicates that it decreases as a function of OCD-specific treatment (Lyoo et al., 2003), indicating that it shares characteristics with OCD and that these characteristics are alterable.  Not only does research support the co-occurrence of harm avoidance and OCD, research supports the potential familial transmission of this temperament trait (Ettelt et al., 2008).  Specifically, individuals with OCD and their first degree relatives scored significantly higher on harm avoidance than controls and their first degree relatives, respectively (Ettelt et al., 2008), indicating that it could be inherited (Heath, Cloninger, & Martin, 1994), learned, or both.  As with behavioral inhibition, exactly how harm avoidance might lead to OCD development has not been examined empirically.  In OCD, individuals are highly motivated to avoid obsessional content, which often includes threat or harm (e.g., contamination, aggression, misfortune), so one possibility is that a temperament geared toward avoidance and specifically, avoidance of harm, might mature into a maladaptive avoidance of thoughts and harm.

The research on temperament in OCD is in its initial stages, and thus, relies primarily on cross-sectional and case-control designs using convenience samples without full-blown OCD.  As a result, the transactional operation of temperament not been well tested in actual OCD; that is, how an individual’s temperament impacts environment, how that environment impacts the individual, how that individual reacts, and at what point OCD develops.  Rather, only simple correlations between temperament style and OCD, moderation models, and short-term prospective treatment studies have been tested.  Given the transactional nature of temperament, future research must examine the complex, transactional processes in OCD development.

Conclusions

Potential environmental influences on OCD may begin as early as conception go on to include factors such as temperament, parenting styles, and traumatic experiences.  These environmental factors may help explain the portion of variance in OCD not accounted for by genes or biology.   Although the work has been promising, several limitations in the research exist, impacting the ability to determine factors’ contribution to OCD development.  These limitations include the use of non-clinical samples to measure clinical phenomena, lack of specificity of findings to OCD, and use of cross-sectional and case-control designs.  Despite these limitations, individuals have designed studies to approximate the impact of certain factors on development.  Particularly promising is work that examined induction of “mental contamination” through an imaginal exposure to unwanted physical contact that led individuals to engage in OCD-like behaviors to reduce distress, such as washing or neutralization.  These findings allude to how traumatic experiences might lead to OCD-like behaviors.  Future work should address these concerns to extend the work from simple relationships to more complex research designs, examining pathways of OCD development.  Instead of utilizing linear models, dynamic models are needed that take into account the interactional, reciprocal nature of development. 

Cognitive Theory of OCD

OCD is a disorder that involves a disruption of normal thought patterns, so discovering how these normal thought patterns become disordered is an essential part of the conceptualization of its development.  An estimated 90% of the general population experiences intrusive thoughts similar in content to those reported in OCD (Rachman & De Silva, 1978), but only 2.5% of the population experiences these intrusive thoughts as “obsessional” (American Psychiatric Association, 2000).  In the cognitive conceptualization of OCD, based upon Aaron Beck’s cognitive theory (1976), the intrusive thought itself is not the problem, the problem is the way in which the individual interprets or appraises the thoughts.  The appraisal or interpretation of the thought is based upon underlying beliefs systems; these belief systems filter information, including thoughts, through a biased lens to produce biased interpretations of not only “normal” intrusive thoughts, but other information as well, related to self, others, and the world (e.g., interactions with others, life events, situations, etc.).  In some individuals, the underlying beliefs are balanced or “healthy”; for example, these could include themes such as positive self-worth (“I am a worthwhile person”) and safety (“the world is generally a safe place”).  In these individuals, an intrusive thought, even a somewhat unconventional thought, would be interpreted in a balanced way through these beliefs and would be readily dismissed.   

In OCD, many of these underlying beliefs are maladaptive, so intrusive thoughts and other information would be interpreted in a maladaptive way.  The underlying belief systems commonly identified in OCD include responsibility, thought-action fusion, intolerance for ambiguity, perfectionism, need for control, and threat overestimation (Fama & Wilhelm, 2005).  There is some inconsistency in labeling these beliefs; for example, thought-action fusion is sometimes identified as “overimportance of thoughts” and intolerance for ambiguity is also called “desire for certainty”, “response to unpredictability”, “discomfort with ambiguity”, “tolerance of uncertainty”, “intolerance of uncertainty”, and “need for closure”, which can make reviewing the literature confusing.  These OCD-relevant beliefs are relevant to the study of OCD development because they are thought to contribute to the onset of the disorder and to maintain symptomatology after it develops (Biddle, 2001; Frost et al., 1997; Rachman, 1997).

 

Responsibility and Thought-Action Fusion

Responsibility and thought-action fusion are separate, but entwined, beliefs in OCD, representing two maladaptive ways of interpreting information.  According to cognitive theory, factors contribute to the development of certain beliefs, in this case, responsibility and thought-action fusion; these beliefs bias the way information is processed, ultimately contributing to OCD development and maintenance.  When individuals apply responsibility beliefs in thought appraisal, they believe that they are responsible for their thought content and its potential outcomes.  In thought-action fusion beliefs, the individual comes to believe: a) Many of my intrusive thoughts are “wrong”; having them is just as bad as carrying them out, and b) by having “bad” thoughts, I can cause bad things to happen.  Both of these components of thought-action fusion lead to a sense of responsibility to stop the thoughts.  The sense of personal responsibility for thoughts leads individuals to believe that it is their responsibility and within their power to stop these thoughts, also called magical thinking.  It is the thought-action fusion that leads individuals to believe that thoughts are immoral and injurious, and inherent in those beliefs about their thoughts is the sense of responsibility to control them.  Empirical evidence indicates that thought-action fusion is correlated with OCD symptoms in clinical samples of children and adults (Barrett & Healy, 2003; Rachman & Shafran, 1999; Shafran, Thordarson, & Rachman, 1996) as is responsibility (Biddle, 2001; Frost et al., 1997; Rector, Cassin, Richter, & Burroughs, 2009).  Evidence also indicates that though-action fusion beliefs are not only related to OCD in clinical samples of adults and children but are unique to incidences of obsessive-intrusive thoughts compared to general worry in a non-clinical sample (Belloch, Morillo, & García-Soriano, 2007; Belloch et al., 2010; Farrell & Barrett, 2006). 

In order to better understand the origins of responsibility beliefs, which are ultimately thought to contribute to OCD, Salkovskis and colleagues (1999) proposed a model that considers the influences of childhood experiences on development of responsibility beliefs.  It is one of the only detailed models explaining how any OCD-relevant beliefs might develop, considering the importance of early experiences.  Five pathways are hypothesized to contribute to development of inflated responsibility, and although not explicitly stated in the model, pathway 5 details how thought-action fusion beliefs may develop:

1.     An early developed and broad sense of responsibility for averting threat that is deliberately or implicitly encouraged and promoted during childhood by significant figures and circumstances, leading to enduring and “justified” beliefs about the importance of a sense of responsibility;

2.     Rigid and extreme codes of conduct and duty;

3.     Childhood experiences in which sensitivity to ideas of responsibility develops as a result of being shielded from it; this may include over indulgence, and/or may be the consequence of the implication or declaration of incompetence by those around the child;

4.     A specific incident or series of incidents in which actions or inaction actually contributed in a significant way to a serious misfortune which affects oneself or, often more importantly, others and

5.     An incident in which it wrongly appeared that one’s thoughts and/or actions or inaction contributed to a serious misfortune. (Salkovskis et al., 1999, p. 1060)

Broadly, this model highlights the importance of early experiences on the development of responsibility beliefs, and to some extent, thought-action fusion beliefs (i.e., pathway 5), which bias the way in which an individual interprets information in their environment (internal and external).  Ultimately, this biased information processing is thought to contribute to the development of OCD and to maintain its existence (Salkovskis et al., 1999). 

In order to facilitate current and future testing of the specific pathways in Salkovskis et al.’s model (1999), Coles & Schofield (2008) developed a measure to examine these pathways empirically: the Pathways to Inflated Responsibility Scale (PIRBS).  The scale appears to have good convergent validity, with all pathways correlating with a measure of responsibility beliefs; this finding also indicates that the model’s pathways tap what they purport to: responsibility beliefs.  The scale was developed and replicated using a non-clinical college sample, however, and did not examine thought-action fusion beliefs, so additional studies are needed to determine its validity in a clinical sample and convergent validity with thought-action fusion beliefs.  At present, this study represents the only attempt at examining the model empirically.        

Broadly, the early experiences described in pathways 1-5 are thought to contribute to inflated responsibility beliefs, which are hypothesized to contribute to OCD development.  In particular, responsibility beliefs are purported to lead to both checking behaviors (e.g., hypervigilance) and obsessional thoughts (e.g., “I am responsible for controlling both my thoughts and the likelihood of misfortune”; Salkovskis et al., 1999).  Experimental designs have tested the role of responsibility in contributing to OCD symptomatology.  Specifically, experimental induction of responsibility led to increased OCD-like checking in both clinical and non-clinical samples (Arntz, Voncken, & Goosen, 2007; Bouchard, Rhéaume, & Ladouceur, 1999; Mancini, D'Olimpio, & Cieri, 2004).

Although much of model specifically highlights inflated responsibility as related to behavior, pathway 5 underscores the impact of certain events on thinking styles that might develop into not only responsibility but thought-action fusion beliefs, and these thought-action fusion beliefs are hypothesized to contribute to OCD.  As indicated by the model, thought-action fusion may develop from an early emphasis on responsibility for thoughts and behaviors; this may later develop into an inflated sense of responsibility and encourage the development of thought-action fusion.  In OCD, this early emphasis on responsibility for thoughts and behaviors may lead to an inflated sense of responsibility, then to a fusion of thoughts and actions, next to reactions of guilt or anxiety when experiencing intrusive thoughts, especially thoughts which are not “proper” (Salkovskis et al., 1999); individuals may then be motivated to reduce these negative emotional reactions; and compulsions may be employed to serve this end.  There is preliminary evidence to support the hypothesis that thought-action fusion beliefs may contribute to OCD symptomatology; experimentally induction of thought-action fusion in a non-clinical adult sample resulted in an increased frequency of intrusive thoughts and resistance to these thoughts (Rassin, Merckelbach, Muris, & Spaan, 1999). 

            Despite the 12-year existence of a developmental model of responsibility and thought-action fusion beliefs in OCD, the model itself appears to have gone virtually untested in children and appears to have been tested by only one, non-clinical study in adults (Coles & Schofield, 2008).  Further, few have attempted more generally to examine responsibility and thought-action fusion beliefs in children.  Those who have investigated these beliefs have uncovered the presence of both thought-action fusion and responsibility in childhood OCD (Barrett & Healy, 2003; Farrell & Barrett, 2006; Libby, Reynolds, Derisley, & Clark, 2004; Pietrefesa, Schofield, Whiteside, Sochting, & Coles, 2010).  Finally, with the exception of a few experimental studies of thought-action fusion and responsibility beliefs (Arntz et al., 2007; Bouchard et al., 1999; Mancini et al., 2004; Rassin et al., 1999), virtually all study designs have been cross-sectional, and many have utilized non-clinical samples, precluding the study of the development of these beliefs in actual OCD.  In order to better understand how these beliefs develop and the role they play in OCD, the research methodology needs to improve, utilizing clinical samples and designs that can capture the developmental process (e.g., longitudinal studies, experiments, quasi-experiments, utilization of at-risk samples).

Perfectionism

Perfectionistic beliefs are commonly described in OCD.  These beliefs indicate that a perfect state exists, so individuals make efforts to achieve and maintain that state (Bhar & Kyrios, 2005).  Researchers have found support for a relationship between OCD features and perfectionism (Belloch et al., 2010; Bhar & Kyrios, 2005; Rector et al., 2009; Wu & Cortesi, 2009; Zohar et al., 2005) even after controlling for trait anxiety (Moretz & McKay, 2009), which indicates that perfectionism may be specific to the unique characteristics of OCD rather than underlying anxiety.  In OCD, perfectionistic beliefs may lead to attempts to control thoughts and the outside environment through compulsions, especially if aspects of thoughts and the environment are viewed as imperfect or immoral.  Empirical support for the contribution of perfectionism to OCD development, however, has been more elusive, though attempts have been made to approximate this, such as measurement of OCD and perfectionism in family members to assess OCD development in the context of early life experiences and genetics.  Specifically, first-degree relatives’ scores on measures of perfectionism/uncertainty were similar to their relatives with early-onset OCD and significantly higher than controls (Rector et al., 2009).  Perfectionistic beliefs have been documented in children with OCD, and are related to OCD symptomatology (Libby et al., 2004).  However, in childhood, the majority of children appear to exhibit a need for things to be “just so” or “just right” (Carter & Pollock, 2000; Evans et al., 1997), which is reminiscent of these perfectionistic beliefs.  Why most children exhibit “just so” tendencies but not all develop OCD is unclear.  Does this indicate that the presence of perfectionistic beliefs in children with OCD is simply an artifact or do perfectionistic beliefs appear different in children with OCD?  Unfortunately, the nature of the study design (case-control) precludes understanding of the development of this belief and how it might contribute to OCD.  Studies could begin by comparing perfectionistic beliefs in children with and without OCD to determine whether they differ, and ultimately, present uniquely in OCD.  Further, findings appear to implicate the role of a perfectionistic home environment or a genetic propensity for perfectionism in OCD development, but the case-control nature of the study precludes definitive statements.  Prospective studies of perfectionism starting in childhood would help to better understand how these beliefs might develop and contribute to OCD symptomatology. 

Intolerance for Ambiguity

Another important belief related to OCD is intolerance for ambiguity.  Intolerance for ambiguity is a dysfunctional thinking style that has also been called response to unpredictability, discomfort with ambiguity, tolerance of uncertainty, intolerance of uncertainty, and need for closure, all which refer to the dislike for that which is uncertain.  Research supports the relationship between this particular belief and OCD (Biddle, 2001; Frost et al., 1997; Holaway, Heimberg, & Coles, 2006; Rector et al., 2009; Sookman et al., 2001; Steketee, Frost, & Cohen, 1998; Tolin, Abramowitz, Brigidi, & Foa, 2003).  Additionally, there is evidence to suggest that this belief appears specific to OCD (Sookman et al., 2001; Steketee et al., 1998), though some findings have been mixed (e.g., Holaway et al., 2006; Mancini, D'Olimpio, Del Genio, Didonna, & Prunetti, 2002).  Compared with other anxiety disorders and normal controls, those with OCD exhibited significantly higher levels of this belief (Steketee et al., 1998).  Comparisons that included depression in addition to other anxiety disorders, and normal controls also revealed that those with OCD score significantly higher on response to unpredictability (Sookman et al., 2001), indicating the potential uniqueness of intolerance for ambiguity to OCD.  These findings provide support for the hypothesis that this particular belief, involving discomfort with the uncertain, is present in and possibly unique to OCD. 

Despite support for the relationship of intolerance for ambiguity beliefs with OCD, research has not examined how this might develop in adults or children.  Additionally, only one study appears to have examined this in children, and although results trended toward a significant relationship between this belief and OCD symptomatology (Pietrefesa et al., 2010), the lack of significance precludes clear statements about a relationship and further impedes the study of this belief’s development.  Although it is unclear how this may develop, processing information through such a belief system is thought to lead to rigidity, emphasis on routine, and increased need for control, especially in ambiguous situations (Sookman et al., 2001).  When ambiguity is present, it may lead to excessive reassurance or information seeking, doubting, avoidance, checking behavior, and difficulty in decision making, all seen in OCD (Tolin et al., 2003).  Young children appear to exhibit similar behaviors when faced with uncertainty, in attempt to control their environment.  Routines, rules, rigidity, and sameness are very important in children and seem to serve to fend off the ambiguous as well as cope with it when it appears (Carter & Pollock, 2000; Evans et al., 1997).  Although these childhood behaviors have not been directly hypothesized to be related to the development of intolerance for uncertainty beliefs, it is possible that these behavioral tendencies transform into belief systems in some individuals, and subsequently, OCD.        

Need for Control

Need for control beliefs in OCD represent a strong need to control all aspects of one’s environment, including the internal environment, followed by active attempts to control surroundings, both internal and external (Sookman et al., 2001). The uncontrollability of one aspect of the internal environment specifically, obsessional thoughts, may be one of the most distressing parts of the disorder.  Unlike in other anxiety disorders (e.g., snake phobia), the feared stimulus in OCD is not easily avoided nor is it predictable.  As a result, individuals tend to exhibit a strong desire to control thoughts, but perceive little control over these thoughts, and thus, feel distressed when obsessional thoughts manifest.  Indeed, in a non-clinical population, OCD symptoms were linked with higher levels of need for control but lower levels of perceived control (Moulding & Kyrios, 2007).  The tendency of individuals with OCD to exhibit need for control, and the specificity of this tendency, is further evidenced by higher scores of individuals with OCD on need for control, compared with the scores of controls, those with an anxiety disorder or depressive disorders (Sookman & Pinard, 1995, July; Sookman et al., 2001; Steketee et al., 1998; Tolin, Worhunsky, & Maltby, 2006). 

It is unclear exactly how a need for control might contribute to OCD, but it is hypothesized that a belief that all aspects of one’s environment need to be controlled (internal and external) can impact the way an individual appraises seemingly innocuous events, including the intrusive thoughts most of the population exhibits.  Furthermore, the inability to control the environment, despite its inherently uncontrollable nature, is seen as a personal deficit. As a result, if, for example, an unwanted thought enters the head of an individual with a strong need for control, it will cause distress, and they will make attempts to get rid of it (Fergus & Wu, 2010; Frost et al., 1997; Sookman et al., 2001). 

Also unclear is how need for control beliefs might develop.  These control beliefs have been investigated and documented in children, with need for control correlated with OCD symptoms (Pietrefesa et al., 2010), so they appear present early in life, but the correlational nature of the work impedes understanding of how they develop.  Children have very little control over their environment; others structure it for them.  They are told when to get up, what to do when they get up, what to eat, where to go, how to talk, who to play with, what to do, when to go to bed, etc.  If they do not follow these externally imposed controls over their environment, they are usually punished; if they do follow them, they are positively rewarded or avoid punishment.  During this time, children are likely to perceive little control over their environments because they have little control.  It is possible that some children do not respond well to high external control and as a result, engage in compulsive behaviors in an attempt to control their environment.  But why doesn’t this happen for all children?  Do some develop higher need for control because of exposure to an overcontrolled environment?  As children grow and become more autonomous, control becomes more and more internally regulated and as a result, perceived control should also increase because actual control has increased.  Adults with higher levels of OCD symptoms, however, tend to exhibit high need for control and low perceived control (Moulding & Kyrios, 2007), despite the fact that as adults, they now have much more control over their environments.  Why do these adults exhibit need for control beliefs while other adults do not?  In order to answer these questions, research needs to examine these beliefs longitudinally, starting in childhood, examining the course of need for control beliefs, as well as other variables that may impact their expression and the expression of full-blown OCD.  

Threat Overestimation

Another OCD belief is threat overestimation, which means than information is filtered through a system that is biased toward detecting threat, even in seemingly innocuous stimuli.  Those with OCD have higher levels of threat overestimation than do controls (Belloch et al., 2010; Rector et al., 2009; Tolin, Woods, & Abramowitz, 2006; Tolin, Worhunsky et al., 2006) and threat estimation and obsessive-compulsive features were related in non-clinical samples (Wu & Cortesi, 2009).  In OCD, the tendency to overestimate threat appears to contribute to distress, disordered thoughts, and disordered behaviors.  Attempts have been made to understand how threat overestimation might contribute to the development of OCD.  For example, family studies provide some evidence for the potential impact of home environment and genetics on OCD.  Those with OCD exhibited higher levels of overestimation of threat than their first-degree relatives without OCD and “normal” controls, but their first-degree relatives scored higher than “normal” controls on threat overestimation (Rector et al., 2009), suggesting that despite lack of an OCD diagnosis, relatives still possess OCD beliefs, specifically threat overestimation, over what would be expected from the general population.  Further, these findings highlight the possibility that threat overestimation beliefs may develop prior to OCD, rather than result from it, given that they are present in individuals without OCD, but at a higher rate than the general population.  Additionally, when children with OCD and their mothers without OCD were assessed for level of correspondence in OCD-related beliefs, threat estimation scores were moderately correlated (Pietrefesa et al., 2010), further indicating a familial role in threat overestimation.  These findings indicate that a home environment ripe with overestimation of threat or a genetic propensity toward overestimation of threat might contribute to OCD development.  As intriguing as these results appear for understanding the development of beliefs and subsequent OCD, they only provide approximations, as they are lacking in prospective and experimental design.

As discussed, threat overestimation beliefs are hypothesized to result in an information-processing bias that favors threat-related stimuli in OCD, which in turn leads to efforts to control the environment (internal and external) to reduce threats.  Research examining this hypothesis in a non-clinical sample found increased attention to, memory for, and access to threat-related stimuli in those who exhibited checking symptoms compared to those classified as “noncheckers” (Irak & Flament, 2009).  Further, information-processing biases appear specific to specific type of threat.  Individuals scoring high on obsessive-compulsive-relevant contamination concerns cited more reasons why using a public bathroom would be harmful than why it would be safe compared to those low in such concerns, demonstrating an information-accessibility bias.  When faced with noncontamination situations (i.e., reading in the library, going to a museum, and cliff diving), their scores did not differ from individuals scoring low on contamination concerns (Olatunji, Connolly, Lohr, & Elwood, 2008), suggesting that harm responses are specific to the feared stimulus, rather than global.  Additionally, overestimation of threat beliefs were correlated with the belief that the world is a controllable place in an non-clinical sample (Doron, Kyrios, Moulding, Nedeljkovic, & Bhar, 2007).  Individuals who overestimate threat do not just believe the world is controllable, they make attempts to control it: Threat overestimation beliefs were related to checking and washing behaviors in clinical samples (Calleo, Hart, Björgvinsson, & Stanley, 2010).  These findings indicate that when individuals exhibit threat overestimation beliefs, they process information through a lens that is biased toward overestimating threat, exhibit higher levels of perceived threat than others and subsequently attempt to control the threat in their environment through checking (e.g., checking door locks to prevent danger) and washing (e.g., to prevent harm from contamination). 

How does threat overestimation itself develop?  One hypothesis is that individuals who experience negative or harmful events are more likely to become hypervigilant toward threat-related cues and thus, develop a threat overestimation belief (Moritz & Jelinek, 2009).  Research has found that threat overestimation is present as early as childhood and is found in children with OCD (Pietrefesa et al., 2010), but has not examined how threat overestimation develops in children or adults.  Children are inherently vulnerable because they are dependent upon others for survival and lack the physical capabilities and knowledge needed to both prevent and defend against negative stimuli; perceiving threat, even where none actually exists, is adaptive for them.  Negative or harmful events during this period, then, should have even more impact on the way in which information is processed than they would in adults, and children would be expected to be more likely to develop threat overestimation as a response to a negative or harmful event.  In order to determine whether threat overestimation develops as hypothesized, studies could assess when threat overestimation is most likely to develop (childhood or adulthood); assess presence and number of negative events to determine if they co-occur with threat overestimation, and whether threat estimation increases as a function of number or severity of events; and ultimately, prospective studies could be utilized to follow those who have experienced these events to determine whether threat overestimation beliefs later develop. 

Conclusions

Children and adults both endorse OCD-relevant beliefs, which are hypothesized to impact the way information about self, others, and the world is processed (Barrett & Healy, 2003; Farrell & Barrett, 2006; Libby et al., 2004; Pietrefesa et al., 2010).  This information can include internal (e.g., thoughts) and external (e.g., interpersonal interactions, life events, situations) experiences.  OCD beliefs endorsed by adults with OCD include responsibility, thought-action fusion, intolerance for ambiguity, perfectionism, need for control, and threat overestimation; beliefs endorsed by both children and adults include responsibility, thought-action fusion, perfectionism, need for control, and threat overestimation.  Although children, adolescents, and adults endorse many of the same beliefs, differences exist; adults and adolescents endorsed more intrusive thoughts, perceived thoughts as more distressing, perceived thoughts as more difficult to control, and had more attempts to suppress thoughts (Farrell & Barrett, 2006).  These differences may be better understood in the context of developmental theory; specifically, by considering the role of metacognition.  As discussed, children do not exhibit metacognitive ability until the around age 9-10 (Berk, 2006), so they do not have the ability to interpret their thoughts in the same ways as adults and adolescents do.  Therefore, although children may endorse OCD-relevant beliefs, these are likely used to interpret other, noncognitive aspects of their environment (e.g., “I must complete this task perfectly”) rather than thoughts because children do not have access to this level of thought analysis yet, and if they do, the level of analysis is not as sophisticated as it is in adults.  Given this developmental consideration, it makes sense that children do not perceive thoughts as difficulty to control, distressing, or make attempts to suppress them to the degree that adults do; they may know something distressing is occurring, that they’d like it to stop, and may make some attempts to do so, but again, the level of thought analysis is not likely the same as in adults or adolescents.   

Although the presence of these beliefs in OCD has been examined extensively, few have attempted to fully understand the development of these factors and how these factors in turn, might contribute to OCD.  Salkovski’s (1999)model of the development of responsibility beliefs in OCD is one exception.  It is very important in that it aids in understanding the influences of childhood experiences on OCD beliefs’ development, specifically for responsibility and thought-action fusion.  Furthermore, it appears to be one of the only detailed models of how OCD beliefs develop, highlighting early experiences.  The pathways in the model have received some preliminary empirical support in a non-clinical adult sample (Coles & Schofield, 2008) but have not been measured in clinical samples or children.

Overall, empirical work detailing how the OCD beliefs might contribute to OCD has been limited but there is preliminary evidence to support the hypothesis that these beliefs do influence the development of OCD symptomatology. In particular, a prospective study found that a composite score of OCD beliefs, which combined responsibility, thought-action fusion (labeled “overimportance of thoughts), perfectionism, intolerance for ambiguity, need for control and threat overestimation, predicted OCD symptomatology development at follow-up in an at-risk sample (Abramowitz et al., 2006).  Further, experimental designs have tested the roles of responsibility and thought-action fusion beliefs in contributing to OCD symptomatology by experimentally inducing OCD beliefs, specifically responsibility and thought-action fusion; the induction of these OCD beliefs led to increases in OCD symptomatology in both clinical and non-clinical samples (Arntz et al., 2007; Bouchard et al., 1999; Mancini et al., 2004; Rassin et al., 1999).  

Aside from cognitive theory’s assertion that the problem is not the intrusive thought itself, but the ways in which individuals interpret their thoughts, researchers do not yet have a good understanding of how the beliefs impact OCD development, and how the beliefs themselves develop.  Models examine beliefs proposed in the adult literature, and although some have begun to study these factors in children, research needs to address the importance of the developmental context on OCD-relevant beliefs and OCD itself because children and adults are not the same.  Support for the influences of these beliefs on OCD may be lacking in part because these beliefs have primarily been conceptualized in adults, with little attention to these beliefs during the developmental period in children. For many beliefs, it is not clear whether they are uniquely related to OCD or psychopathology in general because research has not examined their specificity to OCD or has produced mixed results.  Further, with the exception of a few experimental studies, virtually all study designs have been cross-sectional, and many have utilized non-clinical samples, precluding the study of the development of these beliefs in actual OCD.  In order to better understand how these beliefs develop and the role they play in OCD, the research methodology needs to improve, utilizing clinical samples and designs that can capture the developmental process (e.g., longitudinal studies, experiments, quasi-experiments, utilization of at-risk samples).

Developmental Perspective

Developmental Considerations in OCD Development

The developmental psychopathology model offers a guide for comprehending the reasons for and mechanisms through which aberrant and normal behaviors appear; this is shaped by the child and the developmental contexts, changing as a function of time (Cicchetti & Richters, 1993; Mash & Dozois, 2003).  It is complex and dynamic, considers a comprehensive set of factors, interdependent in nature, beginning in childhood, and moving forward to adulthood, considering the nonlinear, dynamic nature of development.  Unlike adults, who are fairly stable in terms of development, children are constantly changing in complex ways, so applying a model that appreciates this process is essential.  In contrast, utilizing a linear model, as is often done in adult conceptualization of mental disorders, does not fully capture the complexity of this process, and as a result, may contribute to a lack of main effects.  For example, a particular insult or set of insults early in life may not necessarily result in maladjustment later in life; other factors can change the course of the developmental path, protect against maladjustment, or aid in recovery from insults.  On the other hand, early insults can result in maladjustment, so it is essential to understand how these pathways work, including how and which factors intervene to change their course (Mash & Dozois, 2003; Tiet et al., 1998).  This section will first present a developmental model of psychopathology, then will highlight where current conceptualizations of OCD development are lacking.

As discussed, certain insults over the course of development can result in maladjustment; these insults are called “risk factors”.  Risk factors are those that that can lead to negative outcomes, including maladjustment and pathology. These include individual characteristics as well as environmental characteristics (Mash & Dozois, 2003; Tiet et al., 1998).  Individual characteristics conceptualized as risk factors include difficult temperament, cognitive impairments, and genetic makeup (Deater-Deckhard, Dunn, & Hetherington, 1999; Ingram & Price, 2001; Mash & Dozois, 2003; Rothbart, Ahadi, & Evans, 2000).  Environmental characteristics include parent psychopathology, poverty, early traumas, familial conflict, perinatal distress, and low social support (Deater-Deckhard et al., 1999; Rutter, 1999; Tebes, Kaufman, Adnopoz, & Racusin, 2001; Walden & Smith, 1997).  Although examining risk provides a logical starting point for the study of maladjustment, risk does not explain why some children do not exhibit psychopathology or maladjustment despite these risks. Therefore, a child who is “at risk” has the potential for negative outcomes because of the presence of risk factors, but actual negative outcomes are not guaranteed (Mash & Dozois, 2003), indicating that something is missing from a risk model of psychopathology development.  Specifically, negative outcomes are not guaranteed because certain factors can modulate the impact of risk. 

Resiliency refers to the phenomenon wherein some children do not develop psychopathology despite apparent vulnerability and some individuals exhibit pathological development but recover (Cicchetti & Rogosch, 1997; Cicchetti & Toth, 2009; Masten, 2006; Masten, Powell, & Luthar, 2003).  Most believe that resilience is not a special or unusual trait, but, more accurately, the result of a normal adaptational system.  When the system is working as it should, children are able to confront insults, respond in adaptive ways, and normal development processes should proceed, relatively unaffected.  When this system is dysfunctional, children are more vulnerable to insults, and it is at this point that insults are thought to negatively impact normal development (Masten, 2001).  Termed “ordinary magic” by Masten (2001), general resiliency factors include emotion regulation, parent-child relationships, neurodevelopment, drive for learning, and cognition.  Resiliency factors specific to resilience to psychopathology include high self-esteem and self-efficacy, good communication and problem-solving skills, an engaging temperament, intellectual and academic competence, positive parenting, community role models and support, talents valued by others, and positive peer relationships (Luthar, Cicchetti, & Cohen, 2006; Mash & Dozois, 2003; Masten et al., 1999; Masten, Reed, Snyder, & Lopez, 2002).  Although some specific resiliency factors have been identified as such, it is important to bear in mind that resiliency is not static; it can vary as a function of context, area of functioning, and across time.  Factors generally identified as “resiliency factors” can become maladaptive, or even become risk factors in certain contexts (e.g., academic competence can lead to teasing in school about being a “nerd”); certain individuals may exhibit resilience in one area but not others (e.g., good peer relationships but poor parent-child relationships); and ability to demonstrate resilience may change over time (e.g., prolonged exposure to a stressor may reduce the impact of resilience; Freitas & Downey, 1998).  Resiliency, then, is the complex and dynamic result of a normal adaptational system, serving to protect against risk and facilitate normal development.

Risk and resiliency factors impacting development do not act in a vacuum, rather in a transactional manner.  That is, factors occur within a particular context, interact with factors within an individual, and most importantly, act in a fluid and often reciprocal fashion, with all potentially changing over the course of development (Mash & Dozois, 2003). Underscoring this transactional process are the concepts of equifinality and multifinality (Cicchetti & Rogosch, 1996). Equifinality refers to the concept that an outcome can be the result of multiple pathways (Cicchetti & Rogosch, 1997; Cicchetti & Toth, 2009; Jacobvitz & Sroufe, 1987; Sroufe, 1989).  For example, one individual could have a genetic predisposition to OCD, experience perinatal stressors, and have authoritarian parents, exhibit some resiliency but may still develop OCD; another individual may not have a genetic predisposition to OCD, may not experience perinatal stressors, may not have authoritarian parents, but may experience a traumatic event to which they are not resilient, and OCD may develop.  Multifinality indicates that a variety of outcomes can result from similar pathways (Cicchetti & Toth, 2009; Richters & Cicchetti, 1993).  For example, one individual may experience a traumatic event and may subsequently develop OCD; another may experience the same event and develop PTSD; yet another individual may experience the same event, exhibit resiliency, and never develop psychopathology.  Moreover, an individual’s biological makeup, environmental influences on an individual, and their observable characterological makeup all transact (Sameroff, 2009).  More specifically, an individual’s biology impacts their characterological makeup, as does their environment, but all of these influences are bidirectional, so environment also impacts the expression of biology, which further impacts how an individual interacts with their environment as well as their characterological expression (Berk, 2006; Sameroff, 2009). Behavior, then, can be conceptualized as the result of transactions between biology, environment, and characterological expression, allowing for continuity and/or change over time (Sameroff, 2009).  The transactional process renders the study of disorder development particularly challenging, and highlights the necessity for utilizing nonlinear models in the conceptualization and study of OCD. 

Within OCD, the models reviewed thus far examine only risk factors for the disorder and have been linear in nature.  Specifically, OCD risk factors include genes, neurophysiology, neurotransmitters, hormone levels, perinatal stressors, certain parenting styles, traumatic events, temperament, and belief systems that impact the interpretation of information.  Despite the extensive examination of risk factors, the research appears to have neglected the examination of why certain individuals who exhibit risk factors for OCD do not develop the disorder.  The importance of resiliency’s role in development of normal and aberrant behavior is at the heart of the developmental model of psychopathology.  Given the importance of resiliency, models of OCD development need to begin to incorporate resiliency into existing risk models in order to better understand why certain individuals at apparent risk for OCD do not develop it and why others develop OCD but recover. 

The linear models currently used in the examination of OCD development neglect the true nature of development; that is, the transactional nature of development.  When linear methodology is imposed upon a nonlinear process, rich information is missed.  In particular, genes have been implicated in OCD development for early-onset cases; however, it appears that not everyone with a genetic propensity for OCD develops the disorder.  This finding highlights the role of multifinality in OCD development (i.e., genes contribute to OCD or not OCD).  Furthermore, late-onset OCD cases do not appear to have a strong genetic component, and researchers do not yet understand how later onset might develop, highlighting the role of equifinality in OCD development (i.e., a variety of factors/paths contribute to OCD).  Taken together, these examples indicate that other variables, aside from genes, are responsible for conferring OCD onset, and underscore the complex and transactional nature of OCD development. 

The place current conceptualizations of OCD development are lacking appears not to be in examining the wrong factors, rather, in the fact that researchers have been examining these factors too simplistically and have neglected the role of resiliency.  These factors have been examined in such a way that precludes the study of a developmental course; that is, with case control, cross-sectional approaches, examining linear relationships rather than longitudinal designs, examining transactions.  Future research should employ methodology that allows for the study of risk and resiliency in OCD across time; large-scale longitudinal designs are desirable but not always practical.  One solution is to follow individuals “at risk” for certain disorders to determine whether psychopathology develops.  To date, only one such study appears to have been conducted with individuals at risk for OCD, but it appears promising, revealing that OCD beliefs predicted OCD symptomatology at follow-up (Abramowitz et al., 2006).  Future studies of OCD could examine at-risk populations as Abramowitz et al. did as well as utilize large-scale longitudinal designs to better understand the transactional nature of OCD development.

Methodological Concerns

For adults, many well-validated measures of OCD exist.  These include self-reports (e.g., Padua Inventory, Leyton Obsessional Inventory), clinician-administered interviews (e.g., Yale-Brown Obsessive-Compulsive Scale), and newer, computer tasks (e.g., virtual reality task of checking symptoms).  Well-validated children’s versions of several of these scales also exist (e.g., Children’s Yale-Brown Obsessive-Compulsive Scale, Leyton Obsessional Inventory-Child). Although these scales demonstrate good validity and reliability, there are some considerations for measuring behaviors and symptomatology in children.  Measuring behaviors in children can be problematic because of observed differences in assessor/reporter.  For example, teachers and mothers tend to report more issues than other reporters (Achenbach, Howell, Quay, & Conners, 1991; Kaufman, Cook, Arny, Jones, & Pittinsky, 1994; Mash & Dozois, 2003) and caregiver psychopathology impacts assessment of behavior.  Specifically, dismissive and avoidant adults describe less pathology than professionals (Dozier & Lee, 1995; Mash & Dozois, 2003), whereas depressed or abusive mothers exaggerate symptoms or portray children negatively (Gartstein, Bridgett, Dishion, & Kaufman, 2009; Mash & Dozois, 2003).  These factors need to be considered when assessing for symptomatology and measuring behavior in children.

Study and measurement of psychopathology should consider the importance of cultural factors, and the differences among cultures.  Experiences of adaptation and maladaptation differ and can result in contradictory outcomes (Cicchetti & Toth, 2009).  For example, oversensitivity and shyness were related to poorer outcomes for children in Western cultures but positive outcomes for children in Chinese culture (Chen, Rubin, & Li, 1995).  Culture also influences the way behaviors are interpreted, addressed, and the outcomes that result.  Indeed, in OCD, individuals often misinterpret their symptoms as legitimate attempts to follow religious or cultural law (Greenberg & Shefler, 2008).  Further, individuals of other cultures often avoid visiting mental health professionals because of beliefs that psychology is not a credible discipline (Huppert, Siev, & Kushner, 2007) and worldviews of outsiders as morally impure (Witztum & Buchbinder, 2001), so symptoms are addressed by finding support within their culture.  If symptoms are related to religious culture, individuals prefer to address symptoms by seeking help from religious leaders and prefer medication to behavior therapy if seeking outside services (Greenberg & Shefler, 2002).  Finally, treatment outcomes appear poorer in those with symptoms related to religious culture than in those without such symptoms (Starcevic & Brakoulias, 2008).   In general, the cultural differences noted in OCD appear in symptom manifestation: Culture appears to colors OCD symptomatology, such that “cultural themes” in symptom content are often identified (de Silva, 2006; Okasha, Saad, Khalil, El Dawla, & Yehia, 1994; Shooka, Al-Haddad, & Raees, 1998; Tek & Ulug, 2001). For example, in India, Hindus with OCD report a higher prevalence of symptoms relating to preoccupation with contamination and dirt; this theme is thought to be related to high levels of purification rituals within their culture (de Silva, 2006).  Despite these differences in symptom expression, actual OCD prevalence rates do not appear to differ from culture to culture and the fundamental features of obsessions and compulsions appear the same (American Psychiatric Association, 2000; de Silva, 2006).  Even so, given the previously discussed cultural differences, measurement needs to be sensitive to the potential for cultural differences in OCD; current measures may not adequately tap all unique manifestations of OCD symptomatology, namely those that are culture specific.

Measurement of the development of psychopathology, including OCD, requires a interdisciplinary, multifactoral approach, assessing multiple levels within the individuals, in order to do justice to the complexity of normal and abnormal development (Cicchetti & Toth, 2009).  This approach would involve many disciplines, including biology, neuroscience, immunology, sociology, genetics, neuroendocrinology and psychology, and would involve measurement of factors from many different domains, like temperament, genes, hormones, cognitive processes, interpersonal functioning, intelligence, parenting styles, etc.  The examination of these domains needs to consider the transactional nature of these factors, utilizing research methodology and statistical procedures that best capture transactions.   Simpler models are much easier to examine and explain both statistically and theoretically, which may partially account for the lack of a transactional model of OCD development; as mentioned, almost all work utilizes cross-sectional or case-control designs.  Additionally, funding sources tend to view such comprehensive research designs as too expansive and venturesome to fund; and many journals are reluctant to publish articles outside their scope (Cicchetti & Toth, 2009).  Lack of a transactional stance at a theoretical level, however, more likely contributes to both the lack of transactional model and lack of empirical approaches suited to examine such a model.  Advances in the statistical capabilities of computers, advanced neuroimaging techniques, improvements in genetic testing, and increased awareness of the importance of these interactions may resolve this issue in the future.

Important is not only testing for how environmental factors may contribute to OCD but examining how and why causes have different effects at different stages of development (developmental moderation; Rutter, 2009).  These numerous constructs and idiographic trajectories can pose methodological challenges in studying development, however (Gonzalez, 2009).  Measuring transactions is complicated because new responses are influenced/limited by previous responses/interactions (e.g., by self, environment, another individual, etc. Gonzalez, 2009; Sameroff, 2009).  Despite these challenges, research needs to move beyond correlation to support causal inferences of factors (e.g., natural experiments; interventions; quasi-experiments; longitudinal designs; studies of at-risk populations).  Further, some have proposed statistical measurement for a variety of complex phenomena: trajectories, using R trajectory plots; nonindependence across many individuals, using structural equation modeling; and path dependence, using state space approach (Cicchetti & Hinshaw, 2002; Gonzalez, 2009; Poehlmann & Fiese, 2001; Rutter, 2009).  Finally, given large variety of biopsychosocial factors involved in OCD’s development, future models need to utilize, at the least, a more comprehensive approach.  Although large-scale longitudinal designs would be ideal, there are obvious financial and practical constraints to employing these.  One solution within the developmental literature has been to measure those “at risk” for certain disorders, following a smaller sample of individuals over time to measure the transactional nature of disorder development, including why certain disorders do and do not develop (Burt et al., 2005; Morris, Ciesla, & Garber, 2010; Pawlby, Hay, Sharp, Waters, & O'Keane, 2009).  Future studies of OCD could examine at-risk populations as well as utilize large-scale longitudinal designs to better understand the transactional nature of OCD development

Summary and Conclusions

OCD is a complex disorder and care must be taken to ensure proper conceptualization of the theory, research, and treatment of the disorder.  Although a great deal of research and theory exists on OCD, little is known of its development.  Certain brain regions, neurotransmitters, and neuropathways appear implicated in OCD, but how these may impact disorder development is unclear.  Genes also appear to be involved, and their impact appears more pronounced in early-onset OCD.  Additionally, environmental and cognitive factors appear to play a role.  Sex differences exist, but this distribution changes over the course of development, raising questions about the potential impact of hormones on OCD development. 

Little work has been done with children and adolescents, ostensibly the time period in which factors such as genes and environment begin to shape an individual’s overall development and this is a problem.  Few models of OCD development exist, and existing models are simplistic, omitting many of the factors thought to be involved in OCD and lacking a transactional perspective of development.  A variety of developmental and psychological factors related to OCD also occur within populations that do not develop OCD (resiliency).  Research should examine which factors protect these individuals from disorder development rather than focusing solely on risk factors. 

The logistical and financial constraints of conducting prospective research are evident as are the constraints on experimental designs in this area; thus, the rationale for utilizing retrospective and concurrent research designs is apparent.  However, in so doing, research has been unable to extend theory beyond simple relationships to predictive ability.  Research on OCD has also involved a large proportion of non-clinical samples.  And, although some have argued for the continuous nature of OCD symptomatology, suggesting that OCD samples differ quantitatively rather than qualitatively from non-clinical samples (Murray, Cooper, & Smith, 1979; Rachman & De Silva, 1978), findings can be presented with more confidence and more valid conclusions drawn if true OCD samples are used.  There are challenges in studying OCD in children, adults, and cross-culturally; research needs to be sensitive to these challenges.  Finally, many studies lack the specificity to draw strong conclusions about the involvement of certain variables in OCD development, rather than anxiety disorders, or psychopathology in general; and, some studies have found that certain factors do not appear specific to OCD (Aycicegi et al., 2002; Hibbs et al., 1991).  When well-developed, comprehensive longitudinal studies of OCD development are designed and implemented and/or researchers begin to utilize more sophisticated methodology in studying OCD (e.g., interventions, quasi experiments, naturalistic designs, experiments), the directionality of the relationship between OCD and biological, environmental, and cognitive factors discussed may finally become clear.

 

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