Psychophysiological Predictors of Gastrointestinal Symptomatology in Autism Spectrum Disorder
Objectives: The present investigation examined the relationship between GI symptomatology and heart rate variability (HRV), a measure of stress reactivity, in those with ASD. Given the relationship between stress and GI symptoms, we hypothesized that a negative relationship would exist between HRV and GI symptomatology.
Methods: Children and adolescents from Missouri and Vanderbilt ATN sites (n = 101, Mean Age =12.2, SD =3.8, Range = 6-18) with an ASD diagnosis were outfitted with a 2-lead ECG apparatus. Initial baseline reactivity to the testing environment was taken for a period of 3 minutes. Next, to examine stress reactivity, participants engaged in independent trials of unilateral cold pressor and vibrotactile stimulation to the hands for 30 seconds in a counterbalanced fashion. After artifacts in the data were removed, the R-R interval data (average pulse interval) were processed, and the percentage of normal R-R intervals during each trial were calculated for each stimulus condition, and for each hand. Baseline and cold pressor stress reactivity are reported here. To assess GI symptomatology over the past 2 months, the participant’s caretaker completed the QPGS Rome-III, and a continuous severity score was calculated with higher scores indicating greater GI severity.
Results: Results indicate that a significant positive correlation was found between lower GI symptomatology and baseline heart rate variability (Pearson correlation r = 0.23, p=0.024). Furthermore, a significant negative correlation was found between lower GI symptomatology and the change in heart rate variability from baseline under cold pressor stimulation (Pearson correlation r = -0.32, p=0.002). Similar but slightly weaker associations were observed with upper GI symptomatology (baseline: r = 0.18, p=0.08; cold pressor change: r = -0.26, p=0.01).
Conclusions: These findings suggest that altered autonomic function and reactivity may co-occur with lower GI symptoms in ASD. From these correlational data, it is unclear whether stress and stress reactivity may trigger GI symptoms, whether GI symptoms could exacerbate stress or stress reactivity, or whether abnormalities in both domains might reflect a common underlying pathophysiology that spans these systems in ASD. Future treatment work may be necessary to understand the directionality of this association.