This study aimed to evaluate the impact of GAD comorbidity on OCD. Only Abramowitz and Foa have performed a study on OCD with and without GAD comorbidity, mainly focused on worries and obsessions (
18). In contrast, we investigated the effects of GAD on the clinical course and prognosis of OCD. The differentiation of GAD from OCD is a seemingly straightforward task when compulsions are easily identifiable; however, in the cases presenting little to no compulsive behaviors, this differentiation becomes a formidable endeavor (
18,
29,
30). Health-related GAD is associated with symptoms such as excessive cleaning and fear of contamination, which are not readily distinguishable from the compulsions associated with OCD. Consequently, thorough evaluations are required to minimize the hardships of arriving at a definitive diagnosis. In the current study, participants were not only assessed by standardized tests and scales, but they were also individually interviewed to increase the accuracy of the final diagnosis.
Our study found no difference in demographic features and clinical variables between the OCD and OCD-GAD groups. Most notably, our results indicated that medical treatment significantly decreased obsessive thoughts in both groups. It should be mentioned that the severity of OCD was lower in the OCD-GAD group than in the OCD group, which remained unchanged throughout the course of treatment. In comparison, other studies reported that the presence of a comorbid disorder was often accompanied by a higher severity of OCD (
7,
31). Our findings suggest that GAD comorbidity with OCD does not necessarily result in the disorder's intensification nor affect the total response to the treatment. Furthermore, our results signify that comorbidities do not necessarily intensify the disorders. Similarly, Abramowitz and Foa (
18) reported that the severity of OCD symptoms is not increased when GAD is present, which does not contradict our results.
It has been demonstrated that one out of ten OCD patients attempts suicide (
32). Studies also suggest that a GAD diagnosis leads to a higher rate of suicidal behavior (
33) and aggression (
34) in these patients than in the normal population. The risk of suicidality in individuals with OCD has been shown to vary greatly in terms of prevalence (
35). This is not surprising, as studies have found that the risk of suicide is associated with more severe obsessions and less intense compulsions (
32). As a result, the risk of suicide can vary depending on the specific symptoms of OCD in each case. It is also commonly believed that either depression or bipolar disorder comorbidity with OCD might commence a higher incidence of suicide (
32). Contrary to this belief, our results showed that suicide and aggression rates are not higher in GAD-OCD patients than in OCD patients. Even so, it is apparent that GAD may increase suicidality and aggression in the normal population, but as OCD-GAD reduces compulsions in OCD patients, the interaction of these effects does not lead to an over-intensification of suicidality and aggression in OCD-GAD patients. Furthermore, some reports suggest that comorbid anxiety in OCD patients is a possible protective factor against suicidal thoughts and attempts (
32). This occurrence could potentially be associated with the harm avoidance by-product of anxiety symptoms, ultimately improving OCD prognosis regarding suicidality.
We found that the aggression, taboo, and ordering-counting symptoms were notably more intense in the OCD group than in the OCD-GAD group. Different studies have reported other aspects of this comorbidity, such as indecisiveness, extreme pathological responsibility, and excessive worries in OCD-GAD patients (
18). Nonetheless, similar to our findings, a large-scale report has also shown that symptoms such as ordering are more frequent and intense in OCD patients without comorbidities (
9). Even so, there are major inconsistencies between the reported results in comorbid studies (
18,
36,
37), indicating a large gap in the current understanding of the complexities of OCD comorbidities.
Nonetheless, it is known that in almost all cases, comorbidity of more than two disorders usually results in an impeded response to medical treatment and hence, the need for a multidrug regimen. Interestingly, however, our results are inconsistent with this belief. In other words, we found that GAD does not deteriorate the course of treatment in OCD patients and does not necessitate more discrete medications. Furthermore, we found that the response rate was much higher in the GAD-OCD group at the beginning of the treatment; this difference gradually decreased with time. This inconsistency might have been due to the lower severity of obsessive-compulsive symptoms in the OCD-GAD group than in the OCD group; additionally, SSRIs are the first treatment choice for both GAD and OCD groups. The alignment of the treatment plans for both parts of the OCD-GAD comorbidity and the lessened symptoms may have had a pivotal role in the observed medication results, such that OCD-GAD does not appear to impact the course of treatment negatively. In contrast, some comorbidities with counteractive medications (i.e., psychotic and bipolar disorders) result in a diminished response to treatment (
38,
39).
Our results indicated that following therapies, obsession, and anxiety levels significantly decreased with time; however, the rate of decline was not consistent at all time frames (Y-BOCS scores declined more at the first follow-up while HAM-A anxiety declined more at the second follow-up). Interestingly, however, we anecdotally found that some OCD-GAD patients who had improved obsessive symptoms following therapy were dissatisfied with the effects of therapy on their anxiety. This may hint at the presence of a GAD subtype, accompanied by OCD, with distinct clinical presentations and minimal response to treatments; consequently, further studies might aid in evaluating such possibilities.
As a chronic disorder, OCD begins in adolescence, and patients seek treatment at different time intervals from the onset of the disease and receive different treatments. Due to the large variety of treatments, we could not find a suitable model to compare previous treatments and limited ourselves to not receiving the standard treatment three months before admission and the moderate severity of the disorder. Based on the standard treatment protocols, SSRIs are the first-line treatment of OCD. They can be augmented with SADs. The third agent is a glutamatergic drug. Therefore, the number of medications shows the number of augmentation strategies. All patients received a standard dosage of SSRIs for the treatment of OCD. As the effect size of SSRIs was similar in review studies, the types of SSRIs were not considered.
A limiting factor of our study was the lack of a GAD-only group, which hindered further evaluations on the impacts of OCD-GAD comorbidity. Furthermore, our study group only consisted of outpatients seeking long-term treatment plans. Therefore, the results cannot be easily generalized to all individuals affected by the condition. Lastly, very few studies have reported on the same variables of the OCD-GAD comorbidity, which limited the extent of comparative consideration of our results. Future longitudinal studies are recommended instead of our cross-sectional method to fully appreciate the clinical significance of OCD-GAD comorbidity.
5.1. Conclusions
Our study demonstrated no negative effect of GAD comorbidity on the prognosis of OCD patients. Nonetheless, our findings do not suggest that an OCD-GAD diagnosis is a distinct subcategory of clinical disorders, and it may not be beneficial to treat it as such. Further investigations are indicated to evaluate the clinical significance of OCD-GAD comorbidity.