We found several significant longitudinal associations between BDD and the comorbid disorders we examined. The association was strongest for depression. Time-varying associations showed that improvement in BDD and major depression were closely linked in time, with significant associations in both directions: improvement in major depression predicted BDD remission, and improvement in BDD predicted major depression remission. This finding suggests that the same etiologic processes contribute to both BDD and major depression in some subjects. The left side of further suggests that in our sample depression may be largely secondary to BDD for many subjects, as a substantial proportion remitted from major depression (PSR = 1 or 2) following BDD remission. Conversely, after remission of depression, BDD tended to improve but less markedly (right side of ).
Our findings additionally suggest that BDD is not simply a symptom of depression. If it were, BDD would be expected to remit around the time of depression remission and during subsequent months. As shown in the right side of , during the 3 months after remission of major depression, BDD persisted for most subjects, with fewer than 30% of subjects attaining full remission from BDD (PSR of 1 or 2). This finding is consistent with clinical observations of differences between BDD and depression in terms of the disorders’ clinical features and treatment response, including BDD’s apparent response to SRIs but not to non-SRI antidepressants or electroconvulsive therapy (Hollander et al., 1999
; Hollander et al., 1994
; Phillips, 1999
). In particular, a double-blind cross-over study in BDD found that the SRI clomipramine reduced depressive symptoms more than the non-SRI antidepressant desipramine; this finding suggests that depression in this sample may have been largely secondary to BDD, as depression improved significantly more with a medication that is efficacious for BDD (clomipramine) than with a medication that is usually efficacious for depression (desipramine) (Hollander et al., 1999
). It is interesting that in the present study, a majority of subjects were not taking an SRI at the time of either remission, suggesting that the linkage we have observed between remission of BDD and major depression is not fully explained by receipt of medication. However, the relationship between treatment and remission of BDD versus that of comorbid disorders requires further investigation.
Although our results are less numerically stable for OCD, they were significant in only one direction, with improvement in OCD significantly increasing the likelihood of subsequent remission from BDD. This finding suggests that BDD and OCD symptoms may be linked – or that BDD may be secondary to OCD -- for some subjects. However, we found that full-criteria BDD (PSR of 5-7) persisted in approximately half of subjects after OCD remitted (right side of ), and that only about 10% fully remitted from BDD (PSR of 1 or 2) after OCD remitted, suggesting that BDD is not simply a symptom of OCD. If it were, BDD would be expected to remit in all subjects for whom OCD remitted. Taken together, these findings give some support to the hypothesis that BDD may be related to OCD and is an “OCD-spectrum disorder,” but that BDD and OCD are not identical. This finding is consistent with evidence suggesting that BDD and OCD have many similarities but also some differences (Frare et al., 2004
; Phillips et al., 1998
). For example, studies have found that BDD patients have poorer insight than those with OCD (Eisen et al., 2004
; Simeon et al., 1995
), that a higher proportion of BDD patients are unmarried, unemployed, and less educated (Frare et al., 2004
), and that BDD patients have a higher prevalence of major depression, social phobia, and suicidal ideation and suicide attempts attributed primarily to their disorder (i.e., BDD or OCD) (Phillips et al., 1998
). A small MRI study (n=16) found that BDD subjects had a leftward shift in caudate asymmetry and greater white matter volume than healthy controls, whereas some OCD studies have found the opposite (i.e., a rightward shift in caudate asymmetry and reduced white matter volume) (Rauch et al., 2003
). BDD and OCD both appear to respond preferentially to SRIs (Hollander et al., 1999
; Phillips, 2001
), but preliminary data suggest that unlike OCD, BDD may not respond to SRI augmentation with antipsychotics (Phillips et al., 2005a
). However, additional research is needed to further examine the nature of BDD’s relationship to OCD.
We did not find significant longitudinal associations with BDD and social phobia. However, power for these analyses was more limited and the results may be less numerically stable than those for major depression. In addition, the absence of longitudinal associations between BDD and social phobia does not rule out the possibility of other causal associations (for example, the predisposing model). Clinical observations (Phillips, 2001
) as well as Eastern conceptualizations (Kleinknecht, 1997
) suggest that BDD and social phobia may be related disorders, and their relationship deserves further study.
Taken together, these findings suggest that BDD may be etiologically linked to major depression and OCD. Although they suggest that these disorders may have shared etiologic processes, they do not necessarily imply that they are identical disorders. Indeed, this seems unlikely, given that BDD persisted in a sizable proportion of subjects who remitted from the three co-occurring disorders. More than half of subjects who remitted from depression, OCD, or social phobia continued to meet full BDD criteria, and only a minority fully remitted from BDD. While our results are consistent with a model of shared etiologic mechanisms with major depression and OCD, they do not rule out the other models noted above which may potentially explain comorbidity. It is possible that BDD and major depressive disorder are etiologically distinct but produce non-specific overlapping symptoms, such as depressed mood and low self-esteem. The statistical approach used in this report is not as well suited to examining the “predisposing,” or vulnerability, model, as our primary analyses examined the relationship between already co-occurring disorders over only weeks to months. Longer-term prospective studies that examine new onsets of disorders are needed to determine whether the presence of one disorder increases the risk for developing another disorder (for example, whether social phobia predisposes to the subsequent development of BDD—even years later—perhaps by increasing sensitivity to scrutiny by other people). In addition, if one disorder predisposes to the development of a second disorder, the two disorders would not necessarily be expected to improve together, which is a focus of the analytic approach used in this report. Most important, studies of these disorders’ underlying etiopathology are needed to clarify their etiologic relationship to one another and determine which model is most valid. This relationship may be complex. For example, it is possible that multiple mechanisms (models) contribute to the co-occurrence of BDD and certain Axis I disorders. In addition, initial etiologic mechanisms may differ from pathophysiologic factors that are currently maintaining these disorders. It is also possible that there are subtypes of BDD – for example, subtypes that are etiologically linked to major depression or OCD and others that are not.
These findings have several theoretical and clinical implications. BDD’s classification in DSM is controversial and is likely to be addressed during the DSM-V development process (Phillips & Hollander, 1996
). Should BDD be classified in a section of “OCD-spectrum” disorders, if such a section is added to DSM? Or should DSM include a category of “affective spectrum disorders” which might include BDD? Or should BDD continue to be classified as a somatoform disorder, despite little evidence that it is closely related to the other somatoform disorders (Phillips et al., 2003
)? While more research is needed to answer classification questions such as these – in particular, elucidation of disorders’ underlying etiology and pathophysiology – our results offer some support for the hypothesis that BDD is a member of both the “OCD spectrum” and the “affective spectrum” (Phillips, et al., 1995
). A clinical implication of our results is that if BDD improves, major depression tends to improve as well, and vice versa, and that improvement in OCD appears to be associated with subsequent improvement in BDD. However, while these associations are statistically significant, they do not necessarily apply to all individuals with BDD; as shown in the figures, some individuals remain ill after improvement in the comorbid disorder. From a clinical perspective, it seems important to differentiate BDD from major depression and OCD, as our findings suggest that BDD is not identical to these other disorders.
This study has a number of limitations. Because disorders in this study have been unexpectedly chronic, relatively few remissions occurred, which may result in some numerical instability for results for OCD and social phobia. In addition, with the existing sample it is possible only to detect larger effects. Additional studies with a larger sample or longer follow-up periods are needed to detect smaller effects, obtain more stable results, and examine less commonly comorbid disorders. The finding on the course of OCD relative to BDD remission is in particular need of replication because of the small sample size. Another study limitation is that because BDD was unusually chronic, we examined associations for partial or full BDD remission rather than full remission alone. Also, it is unclear how representative our sample is of individuals with BDD. Although we attempted to obtain a broad and diverse sample, it is a sample of convenience and may have unknown biases. Additional studies are needed in both clinical and epidemiologic samples. Also, although symptoms of BDD and comorbid disorders were rated for each week of the follow-up period, interviews covered the previous 12 months. Efforts were made to precisely determine the timing of symptom change, but the interviewers necessarily relied on subject’s memories of symptom changes over the previous year. Our test-retest reliability study of retrospective BDD-PSR ratings showed good agreement over a year (see above), but more frequent assessments might provide more accurate data. Finally, while changes in comorbid disorders occurring closely in time suggest that the disorders have a shared etiology (in the sense of underlying risk factors or an interaction between the disorders), they do not prove this. Family, twin, and adoption studies, and – most important -- studies of etiology and pathophysiology (e.g., underlying neurobiology) are needed to elucidate the nature of disorders’ relationship to one another (Hyman, 2003
; Phillips et al., 2003
; Lyons et al., 1997
This study also has a number of strengths. The sample is larger and more diverse than most previous BDD samples, and it is to our knowledge the first prospective study of BDD’s course and the first to examine longitudinal associations between BDD and comorbid disorders. Course of illness was assessed using a standard and widely used method, which has the advantage of tracking symptom severity at weekly intervals. Additional research is needed to address this study’s limitations. As this ongoing study continues to accrue more data, the number of remissions of BDD and comorbid disorders will increase, which will increase power for analyses of the disorders in this report and other comorbid disorders. Longer durations of follow-up will also increase power to examine time-varying associations between BDD and the recurrence and new onsets of comorbid Axis I disorders. Longer follow-up will also enable further examination of possible course-based subtypes of BDD. For example, are the course subtypes we have observed -- for example, cases for whom BDD and major depression both seem to improve together versus those that seem to change independently -- consistent over time? For example, if BDD and major depression improve together, do they also relapse together? Do these subtypes respond similarly to treatment? And do subjects who remit from BDD when their comorbid OCD or major depression remit differ (e.g., in terms of demographic and clinical characteristics) from subjects who do not remit from BDD? Longitudinal studies that examine time-varying associations are also needed in other samples. Such research will shed important light on BDD’s relationship to commonly comorbid disorders, which has important implications for BDD’s classification and for patient care.