In this pilot study, there was a significant increase in caloric intake in a test meal following four training meal sessions, which provides “proof of principle” that food exposure therapy may be a useful approach to the treatment of AN. These findings build on similar efforts to treat patients with AN using exposure-based approaches. Bergh et al.25
trained patients with AN (n
= 10) and bulimia nervosa (BN) (n
= 4) to eat at a normal rate using computerized feedback, and found that patients improved in weight and psychological measures after receiving the intervention in comparison to a waitlist control group. However, this study involved several interventions in addition to the exposure-like sessions, including intensive behavioral inpatient treatment and the medication cisapride, making it difficult to determine the specific contribution of the feedback sessions. A pilot investigation of exposure for inpatients with AN found that a form of exposure therapy for body image produced a significant effect on anxiety related to body image.26
Finally, one case report described exposure to high fat foods in an underweight male patient with AN,27
with the intervention resulting in a subsequent decrease in reported anxiety and increased variety in the patient’s diet. These three studies and the current study were all small and their approaches varied, but collectively they serve as a consistent body of preliminary data that support a role for exposure therapy in the treatment of AN.
The data from this study suggest that the exposure intervention helped patients with AN increase their consumption from baseline to the final test meal. Although the patients were receiving concurrent inpatient treatment at the time of participation, comparison with the data from a previous study done by our group () indicates that inpatient treatment and/or weight gain alone is unlikely to account for the increase in intake observed in this study. Patients with AN in the comparison group did not receive the exposure intervention and did not show a statistically significant
increase in intake from baseline to the final test meal session in spite of an average inpatient treatment duration between the two meals that was almost twice as long as that in the current study (54.2 days vs. 27.8 days) and a greater amount of weight gained (26.8 pounds vs. 12.8 pounds) between the two test meal sessions. Multiple factors have been shown to have an impact on food intake in people without eating disorders, including familiarity and palatability.28,29
Patients in this study reported liking the shake less after the final test meal; therefore, palatability is not a likely explanation for the increase in intake.
The absence of adverse events with DCS in this study was reassuring; however, DCS did not demonstrate any significant enhancing effect in this small study. However, our ability to detect a statistically significant effect of DCS was limited by the small sample size and possibly by the fact that participants assigned to receive DCS had significantly lower VAS scores on post-meal anxiety than those assigned to placebo at the baseline meal. In the study of DCS in the treatment of height phobia,14
only two exposure sessions were used, compared with the usual exposure therapy standard of 7 to 8 sessions. This “suboptimal dose” presumably allowed for detection of a medication effect that might otherwise have been masked by the effects of behavior therapy. It is notable that in the current study, subjects were able to consume approximately the amount needed for lunch during the training meals. Thus, it may be that any effect of medication during the training meals was masked. In that vein, the mean consumed in the final test meal was 445 kcal ± 175 kcal. While this amount is less than the amount consumed in the training meals, and less than the amount prescribed for lunch on the inpatient unit, it approaches the mean intake for controls reported in the eating behavior study by Sysko et al.11
This raises the possibility that the intake in the test meal was sufficiently increased by the exposure intervention to obscure any effect of medication. No participant reported medication side effects, and no medication-related laboratory abnormalities were detected, providing preliminary support for the safety of this medication in patients with AN.
The potential for exposure therapy as an adjunct in the treatment of AN is promising, but needs to be considered in the light of several limitations of the present study. The patients in the current study and the earlier study of Sysko et al.11
were enrolled separately. Thus, caution is needed in drawing conclusions about the effectiveness of the exposure intervention based on this comparison group. On the other hand, both groups of patients were recruited in the same manner, were cared for on the inpatient unit using the same treatment protocol, and completed two identical test meal sessions.
In this study, the exposure intervention used several principles of standard exposure treatment, including following anxiety ratings during the session and assisting patients in tolerating moderate levels of anxiety. However, the food exposure therapy intervention warrants further development. Over the course of the four training sessions, patients’ self-reported anxiety decreased; however, there was no statistically significant difference in VAS pre- or post-meal anxiety between the first and fourth training meal sessions. Unfortunately, anxiety and fearfulness appeared to increase between the final training session and the final test meal, suggesting that any decreases that occurred over the course of training did not generalize to the test meal and highlighting the need to refine the exposure intervention. The process of conducting this study suggested some particular areas to address in future investigations of exposure and/or D-cycloserine for the treatment of individuals with AN. Participants with AN enrolled in this study used numerous cognitive strategies to avoid anxiety while eating, suggesting that a refined exposure intervention should focus more on helping patients decrease avoidance during the training meal sessions. Further, although studies using D-cycloserine and exposure therapy for anxiety disorders are typically short in duration (2-4 sessions), a brief interventions for AN may not yield similar effects because the disorder is much more difficult to treat than either height phobia or social phobia.14,15
Thus, future studies could consider extending the length of the treatment or increasing the intensity of the exposure intervention. Additionally, an a priori power analysis should be conducted to determine the size of the sample needed to evaluate the effect of the intervention or the D-cycloserine on eating behavior and anxiety among patients with AN based on the improvements observed in the current study.
Several additional methodological limitations in the current study should be noted. The range in BMI among patients completing the protocol was wide, and there was a suggestion that patients beginning the protocol at lower weights exhibited smaller changes in intake. Also, the exposure training and testing occurred during the weight gain phase of the inpatient treatment program, a context in which there are complex incentives to motivate intake during meals. Thus, it may be useful to examine the effect of exposure treatment in patients at a more uniform level of BMI and at a stage of treatment when fewer behavioral incentives are present.
In conclusion, this study suggests that food avoidance in patients with AN, akin to phobic behavior, can be mitigated by an exposure therapy intervention, yielding an increase in food intake. Future research should include a larger sample of weight-restored patients with AN using a more robust exposure therapy intervention, and comparing exposure therapy to a control intervention in order to further investigate the potential value of exposure therapy and DCS in enhancing or accelerating the extinction of eating-related phobic avoidance behaviors.