Psychophysiological Predictors of Gastrointestinal Symptomatology in Autism Spectrum Disorder

Thursday, May 14, 2015: 11:30 AM-1:30 PM
Imperial Ballroom (Grand America Hotel)
B. Ferguson1, S. Marler2, E. B. Lee3, J. E. Akers4, M. O. Mazurek5, K. Sohl6, A. McLaughlin5, B. Kille5, K. Hartnett5, E. A. Macklin7, E. McDonnell8, L. Alstein9, J. Veenstra-Vander Weele10 and D. Q. Beversdorf11, (1)University of Missouri-Columbia, Columbia, MO, (2)Psychiatry, Vanderbilt University, Nashville, TN, (3)Pediatrics, Vanderbilt University, Nashville, TN, (4)Research Core, Thompson Center for Autism & Neurodevelopmental Disorders, Columbia, MO, (5)University of Missouri, Columbia, MO, (6)Child Health, University of Missouri - Thompson Center, Columbia, MO, (7)Biostatistics Center, Massachusetts General Hospital and Harvard Medical School, Boston, MA, (8)Biostatistics, Massachusetts General Hospital, Boston, MA, (9)Massachusetts General Hospital, Boston, MA, (10)Psychiatry, Columbia University / New York State Psychiatric Institute, New York, NY, (11)Radiology, Neurology, Psychological Sciences, University of Missouri, Columbia, MO
Background: Research suggests that individuals with Autism Spectrum Disorder (ASD) tend to suffer from a high rate of gastrointestinal (GI) disorders, but the underlying biology and etiology of GI disorders in ASD is not clearly understood.  In the general population, there is a strong relationship between stress and GI symptomatology, and evidence suggests an augmented stress response in ASD.  Taken together, it is possible that GI symptoms in those with ASD may vary as a function of stress reactivity.  Determining the cause of GI disorders in ASD is important given their associations with sensory over-responsivity and stress, which can exacerbate problem behaviors.  Understanding of the relationships among GI symptoms, stress, and behavior will be critical in planning future studies and better individualizing treatment.

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.