(PS2-71) Early Life Adversity and Inhibitory Control Among Individuals with OCD

Introduction: Inhibitory control (i.e., the ability to stop an initiated action given changes in goals, context, or task demands) is impaired among people with OCD and this might contribute to the etiology of compulsive behaviors. Early life adversity (ELA) is also associated with poorer inhibitory control and can increase the likelihood of developing OCD later in life. However, the relationship between ELA and inhibitory control in OCD remains unclear. 

Methods: Participants were 78 adults (56.4% male, 43.6% female; Mage = 36.4) with a lifetime diagnosis of OCD, recruited from the OCD Collaborative Genetic Association Study. Participants completed a 9-item self-report measure of ELA wherein the total number of endorsed items approximated ELA. A clinical interview (the Yale-Brown Obsessive Compulsive Scale; Y-BOCS) assessed peak lifetime OCD symptom severity and a self-report measure assessed perceived behavioral regulation ability (the Behavioral Regulation Index of the Behavior Rating Inventory of Executive Function; BRIEF-BRI). Participants also completed a computerized stop-signal task requiring rapid responses to stimuli and cessation of initiated responses following an auditory cue. The stop-signal reaction time (SSRT) during this task indexed inhibitory control, wherein greater SSRTs indicate longer times required to inhibit response, and therefore poorer inhibitory control.

Hierarchical linear regressions were performed to test whether ELA, peak OCD severity, and age predict SSRT and BRIEF-BRI scores. We also tested associations between ELA and subscale scores of BRIEF-BRI. ELA was entered into step one and OCD severity and age were added in step two.

Results: ELA in step one predicted SSRT, b = 0.287, SE = 5.127, t = 2.260, p = 0.028, but not when the other variables were added to the model, b = 0.162, SE = 4.924, t = 1.330, p = 0.189. OCD severity did not predict SSRT, b = 0.125, SE = 0.796, t = 1.080, p = 0.285. Age predicted SSRT, b = 0.426, SE = 0.411, t = 3.492, p = 0.001. 

ELA in step one predicted self-reported behavioral regulation, b = 0.383, SE = 1.401, t = 2.749, p = 0.009. This relationship remained when other variables were added to the model, b = 0.365, SE = 1.488, t = 2.465, p = 0.018. OCD severity did not predict self-reported behavioral regulation, b = 0.011, SE = 0.273, t = 0.075, p = 0.940, nor did age, b = 0.069, SE = 0.128, t = 0.462, p = 0.647. In subscale analyses, ELA predicted inhibition, b = 0.327, SE = 0.413, t = 2.350, p = 0.023, and self-monitoring, b = 0.375, SE = 0.303, t = 2.773, p = 0.008. These associations remained significant after the addition of age and OCD severity in step two.

Conclusion: These results suggest that greater ELA among people with OCD is associated with poorer inhibitory control, but that age accounts for a greater portion of the variance in inhibitory control. These results also suggest that, among people with OCD, greater ELA is associated with poorer perceptions of behavioral regulation ability, particularly of inhibition and self-monitoring ability. Limitations of this study include the use of a noncomprehensive ELA measure and a lack of data on OCD severity at the time of the stop-signal task. Future studies should work to clarify the effect that ELA can have on inhibitory control among people with OCD.