In this study, we determined the rate of current and lifetime SUDs in 176 consecutive individuals with DSM-IV BDD. To our knowledge, this is the first study to report rates of abuse and dependence for specific substances and the first to examine clinical correlates of SUD comorbidity in BDD (e.g., demographic characteristics, BDD severity, psychosocial functioning, and quality of life). To our knowledge, this is also the broadest sample of individuals with BDD that has been studied (our study had very broad inclusion/exclusion criteria, and one third of subjects were not currently receiving psychiatric treatment), which may increase the generalizability of the results.
Nearly half of BDD subjects in this study had a lifetime SUD, with a majority of subjects (68%) reporting that BDD symptoms contributed to their substance use. BDD subjects with a lifetime SUD had poorer scores on variables assessing various aspects of morbidity (); however, differences were statistically significant only for suicide attempts, but effect sizes were in the medium range for variables assessing social and occupational functioning. These findings do not appear to be accounted for by comorbid disorders other than SUDs, as rates of comorbid disorders did not differ between groups; this finding is consistent with data from other disorders.32
The high lifetime rate of SUDs and the very high rate of suicide attempts in subjects with an SUD suggests that clinicians should carefully screen BDD patients for an SUD, as the presence of a lifetime SUD may have treatment implications.
Regarding current SUDs, subjects with BDD and a current SUD were not more severely ill or functionally impaired than subjects without a current SUD. Although power was somewhat limited for these analyses, the effect sizes were generally small. Both groups of BDD subjects had such severe current BDD symptoms and poor overall functioning that the presence of a current SUD appears to have had little effect on these measures. For example, on the SAS, the mean ± SD score for all subjects (2.4 ± 0.5) was 2.8 standard deviation units poorer than the published community norm of 1.59 ± 0.33,25
regardless of the presence of a current SUD. Mean scores on the SF-36 mental health subscales for both groups were 1.8 to 2.0 standard deviation units poorer than norms for the general U.S. population.27,28
On the Q-LES-Q Short Form, the mean scores for both groups were 2.2 standard deviation units poorer than a nonclinical community sample mean ± SD converted score of 78.1 ± 13.7 (N = 89) (J. Endicott, Ph.D., written communication, Oct. 2004).
The lifetime SUD rate in subjects with BDD in this study (48.9%) is notably higher than reported rates in the general population (26.6−%29.0%)33,34
and higher than rates reported for many other psychiatric disorders. For example, the Epidemiologic Catchment Area (ECA) study34
found that among persons with any affective disorder, the lifetime prevalence of alcohol use disorders was 21.8%, which is notably lower than the lifetime rate of 42.6% found in our study. In individuals with social phobia, epidemiological studies (the ECA, National Comorbidity Survey, and an epidemiologic study in Edmonton, Alberta, Canada) have reported lifetime rates of 18.8% to 35.0% for alcohol use disorders and 13.0% to 24.0% for nonalcohol substance use disorders,35-40
which are also lower than the rates we found for BDD. Additionally, the ECA study found that 47.0% of persons with schizophrenia had a lifetime SUD.34
Only in the case of bipolar I disorder did the ECA study find a lifetime SUD comorbidity rate (60.7%) that was higher than the rate found in this sample of BDD subjects.34
The rates of lifetime comorbid SUDs found in our study are also higher than those in previous BDD studies.2,3,5-7
The reasons for this are unclear, although most previous studies had small samples; our finding is most similar to that of the largest previous study. It is interesting that we found similar lifetime SUD rates in subjects who were currently receiving psychiatric treatment and in those who were not receiving treatment. Studies done in clinical settings tend to be biased toward finding higher comorbidity rates (due to Berkson bias and clinical bias) than studies done in nonclinical settings.41
Although our study was not epidemiologic in nature and may have various biases, our finding of a high lifetime SUD rate among individuals who were not under psychiatric care suggests that our results may be reasonably generalizable to community settings, although large epidemiologic surveys are needed to confirm this.
The reasons for the elevated rate of lifetime SUDs among BDD subjects are unclear. One possibility is the very high levels of distress reported by patients with BDD. Previous studies have found that BDD patients have unusually high levels of perceived stress.42
In addition, on average, BDD patients report unusually poor quality of life, which correlates highly with BDD symptom severity.43
Use of alcohol and drugs may therefore be a means of self-medicating this distress. This self-medication hypothesis has been examined in affective and anxiety disorders as a possible explanation for the increased rates of comorbidity with SUDs.44-47
Although we cannot ascertain the extent to which this hypothesis may apply to BDD, or the causal relationship between BDD and lifetime SUDs, 68% of subjects in this study reported that their BDD symptoms contributed to substance use. In addition, 69% of subjects reported that BDD symptoms preceded the onset of their SUD. It is interesting that the substances most often abused by the BDD subjects (alcohol and cannabis), while often abused in the general population, may be more likely than other substances to alleviate social anxiety,48
which appears to be high in individuals with BDD. An alternative hypothesis, that the presence of a lifetime SUD contributes to more severe BDD symptoms, while possible, seems less plausible and is less consistent with our age at onset findings. It is also possible that the relationship between BDD and SUDs is more complex (e.g., that they share the same causal factors) or that there is not a causal relationship between them. Further research is needed to explore the relationship between BDD and SUDs, including the extent to which each disorder may contribute to the other disorder's development and maintenance.
Regardless of the specific causal relationship between BDD and SUDs, the fact that they frequently co-occur raises important clinical issues. Because SUDs appear common in individuals with BDD, it is important to screen for SUDs in these patients. Although our study did not examine the converse—the rate of BDD in patients with SUDs—the only study that to our knowledge has done this found a high rate of BDD in inpatients with an SUD (26.5%).8
This study found, however, that patients did not reveal their BDD symptoms to their clinician because of embarrassment and shame, underscoring the need for clinicians to specifically inquire about the presence of BDD symptoms.
Our results also have treatment implications. Treatment of either BDD or an SUD could be complicated or even compromised by the presence of the other untreated condition.49
Treating one disorder alone may not be effective if a comorbid disorder is exerting a causal or maintaining influence on the treated condition.18,50-52
Furthermore, subjects with both BDD and an SUD may require more intensive treatment services, not only because of the comorbidity but also because they may be at higher risk for attempting suicide or requiring hospitalization. To our knowledge, however, no research has been done on the treatment of comorbid SUDs in patients with BDD or on the treatment of BDD in patients with an SUD. Systematic BDD efficacy studies to date, which have found that serotonin reuptake inhibitors and cognitive-behavioral therapy are often efficacious,53,54
have excluded individuals with a current SUD. Research on effective treatments for individuals with BDD and an SUD is greatly needed.
This study has several limitations. Most notably, we based SUD diagnoses on subject report only and did not obtain urine toxicology screens to confirm current rates. Because substance abuse and dependence are often denied, the rates found in this study probably underestimate the actual rate of SUDs in patients with BDD.55,56
In addition, the number of subjects with certain substance use disorders (e.g., sedatives, steroids, opiates) was too small for a more detailed examination of clinical correlates of these specific SUDs. Another limitation is that it is unclear how generalizable our results are to individuals with BDD in the community. Nonetheless, our sample is broader than are those in previous BDD studies, in that the study inclusion/exclusion criteria were very broad and a substantial proportion of participants were not currently receiving psychiatric treatment. The study also used both self-report and interviewer-administered measures with strong psychometric properties and established norms.
In conclusion, these results suggest that SUDs may be common in subjects with BDD. Additional research on this topic is needed, including larger prevalence studies, studies of clinical correlates of SUDs in BDD, and studies that may shed light on the relationship between BDD and SUDs (e.g., prospective studies and studies of etiology and pathophysiology). Also greatly needed are treatment studies to identify efficacious treatments for patients with both BDD and an SUD.