In this issue, Fullana and colleagues (1) examine obsessions and compulsions in the prospective-longitudinal Dunedin study. Members of the cohort were asked four questions about obsessions and compulsions at age 11 and then a series of questions geared to DSM-IV criteria at ages 26 and 32. The investigators explored whether obsessive-compulsive symptoms at age 11 predicted a subsequent diagnosis of obsessive-compulsive disorder (OCD) and associated comorbidity. They also inquired whether particular patterns of obsessive-compulsive symptoms were developmentally stable over time and whether they were differentially predictive of outcomes.
The Dunedin study is unique in its detailed, longitudinal assessment of mental health in a population-based birth cohort. With the original cohort consisting of 1,037 individuals and with 1-year OCD prevalences of 2.4% (23 of 974) at age 26 and 1.8% (17 of 963) at age 32, there are not a lot of people with OCD to describe. But the investigators found that 21%–25% of the cohort (including 13%–17% of those without a mental disorder) reported obsessions and/or compulsions at age 26 or 32, and these rates are consistent with findings from the National Comorbidity Survey Replication (2). They further categorized obsessive-compulsive symptoms as falling into four dimensions: contamination/washing, symmetry/ordering, shameful thoughts, and harm/checking. The first three of these four dimensions map nicely onto a meta-analytically derived obsessive-compulsive symptom factor structure (3); hoarding (which was not assessed in the present study), rather than harm/checking, arose as the fourth factor in the meta-analysis. It should be noted that the questions that would permit assignment of obsessive-compulsive dimensions were not asked at age 11; the present results must therefore be considered a very limited test of developmental stability, as the epoch spanned is from age 26 to 32.
A key finding of this study is that one or more obsessive-compulsive symptoms at age 11 are strongly predictive (odds ratio, 5.90) of diagnostic OCD at age 26 or 32. The authors do not tell us whether this prediction is specific for OCD or whether these symptoms at age 11 are equally predictive of other anxiety and/or mood disorders. This would be important for clinicians and researchers to know. If the finding is not specific, then we need to think much more broadly in terms of early identification and, likely, the scope of preventive programs.
Another critical finding is that all obsessive-compulsive symptom dimensions are associated with other anxiety and mood comorbidity. Although the authors are careful to note that any apparent differences in strengths of association between particular dimensions and comorbid disorders are unlikely to be statistically significant (probably because of the limited sample size, although it is difficult to know for sure), there are several noteworthy observations. The “shameful thoughts” dimension is as strongly associated with posttraumatic stress disorder (and panic disorder) as it is with OCD. This observation raises several questions. Might the “shameful thoughts” endorsed by the individual be intrusive thoughts about prior traumatic experiences? In other words, are these really obsessive-compulsive symptoms, or are they symptoms of posttraumatic stress disorder that are being reported by (at least some) individuals? On the other hand, if these symptoms are genuinely to be thought of as obsessive-compulsive symptoms, we can then ask, Do traumatic life experiences (e.g., childhood maltreatment) influence the expression of obsessive-compulsive symptoms? If so, is there a traumatic “subtype” of OCD in DSM’s future? There is a precedent in the literature for expecting that traumatic experiences might increase risk for or trigger onset of OCD (4, 5). A productive avenue for future research would be to build on these observations to examine the interface of genetic (6) and environmental factors in the development of OCD and related disorders.
The authors wrap up their report with a set of observations and inferences that will be controversial. They remark that subthreshold obsessive-compulsive symptoms are frequently associated with “interference,” a term by which the authors seem to conflate upset about having the symptoms (i.e., “distress”) and disruption of normal behavior (i.e., “impairment”). Yet despite difficulties in one or both spheres, most persons with obsessive-compulsive symptoms do not get treated. They conclude that this indicates a need for increased efforts at early detection of obsessive-compulsive symptoms (a sentiment echoed by other investigators ) and intervention with young people experiencing them. I am not certain that their data support either of these recommendations (although I do not discount the possibility that these might be good ideas).
Researchers may conclude that if few people with OCD are in treatment, then this is evidence of unmet need (8). Ample data show that a psychiatric diagnosis alone—much less a subthreshold diagnosis—is at best a modest predictor of perceived need for treatment (9). Some might contend that self-perceived need is misleading, as individuals with mental disorders may not be good judges of whether or not they need help. Although this could be a supportable argument in the case of psychotic disorders, its application to OCD is, at best, tenuous. Data from the National Comorbidity Survey Replication clearly show that increased severity of OCD is associated with greater role impairment and higher probability of seeking treatment (2). In this light, we must consider the very real possibility that the reason so many people with obsessive-compulsive symptoms fail to get treatment is that they manage quite well despite their symptoms.
As mental health professionals, we should do everything we can to promote awareness about and accessibility to mental health interventions. As clinicians, we have an obligation to help reduce the suffering and improve the functioning of the patients who come to us for help. But, lest we forget, most people with obsessive-compulsive symptoms in the community, whether diagnosable or subthreshold or anywhere in between, are not patients. To suggest that we do more to identify (“label”) and treat such individuals implies that we know better than they whether and when they need our help. I know of no evidence to support such a claim.
This thought-provoking article by Fullana and colleagues challenges us as clinicians to think about including a richer set of dimensional measures in our clinical assessments. The data convincingly show that all obsessive-compulsive symptoms are not alike: some are more stable than others, and some are more indicative of certain types of comorbid psychopathology than others. The presence of tics and/or attention deficit hyperactivity disorder (which this study did not address) must also be incorporated (10).
From a research perspective, these findings require that we recalibrate our notion of the OCD phenotype. It is no longer reasonable to assume that all types of obsessive-compulsive symptoms (e.g., contamination/washing versus symmetry/ordering) share a common pathophysiology. Moreover, given the fact that so many people in the community have obsessions and compulsions, maybe we are missing the forest for the trees by focusing on symptoms. Perhaps we should be asking, “What, in addition to the propensity to have obsessive-compulsive symptoms (which are common), leads to expression of OCD (which is rare)?” Maybe what defines the OCD phenotype is the inability to cope with, rebut, ignore, repress, resist, regulate, or [fill in the blank with your favorite psychological defense mechanism and its corresponding neural systems basis] obsessive-compulsive symptoms. How can we study this in a meaningful way that goes beyond psychiatric philosophizing? These are the kinds of questions that are easy to ask in an editorial. Posing them as testable hypotheses in the context of informative research designs will be more difficult.