The effects of Animal Assisted Therapy on autonomic and endocrine activity in adults with autism spectrum disorder: A randomized controlled trial

Abstract

Objective

Stress and its sequelae are very common in adults with autism spectrum disorder (ASD) without an intellectual disability (ID). Animal-assisted therapy (AAT) has shown physiological stress-reductive effects in children with ASD. The aim of the current study was to examine the acute psychophysiological response to an AAT session, and to examine the longer-term stress-physiological effects of the intervention, up until 10 weeks post-treatment, in comparison to waiting-list controls.

Method

A randomized controlled trial with pre-intervention (T0), post-intervention (T1: 10 weeks) and follow-up (T2: 20 weeks) measurements of neuroendocrine and cardiovascular measures, was conducted in 53 adults with ASD (N = 27 in intervention arm; N = 26 in control arm). Within the intervention group, stress-physiological data were collected during the 5th therapy session (acute effects). Data were analyzed with mixed models for outcome measures cortisol, alpha-amylase, heart rate variability and sympathetic activity.

Results

The AAT interventional session was significantly associated with reduced cortisol levels (β = −0.41, p = .010), while parasympathetic and sympathetic cardiovascular activity remained unaltered. No significant changes were found for stress-physiological measures at post-treatment time points.

Conclusions

Acute stress reduction, reflected in significant reduction in cortisol levels, was found during an AAT session in adults with ASD, without ID. More research is needed to explore to what extent the specific factors of AAT have contributed to the decrease in cortisol and whether stress reduction is possible for the longer-term.

Introduction

High levels of perceived stress and stress-related problems are very common in adults with autism spectrum disorders (ASD) without an intellectual disability (ID) [17]. These high levels of stress are associated with poor life outcomes in ASD, such as depression, anxiety and cardiac diseases [7]. Difficulties in initiating and maintaining social relationships and difficulties in cognitive switching, both core deficits in ASD [2], jeopardize adequate coping with stress [6,17,59]. Adults with ASD, who experience prolonged stress exposure, are at increased risk of chronic exhaustion, loss of skills and reduced tolerance for stimuli, which is called an ‘autistic burn-out’ [41].

Receiving adequate social support is associated with improved mental health in adults with ASD [6,59]. However, bullying and social exclusion are widely experienced by individuals with ASD, resulting in poor social support networks [45]. Due to these negative social experiences in the past, people with ASD (especially the higher functioning people, without ID), often try to hide or compensate one's disabilities to increase social acceptation, behavior called social camouflaging [19,29]. The downside of social camouflaging is that it is a major source of stress. Recently, research on social camouflage showed strong associations with depression, and even suicide [8]. It has been reported as one of the main factors causing a burn-out in ASD, worsening of daily life functioning, such as loss of ability to talk, and poor executive functioning [41]. The high prevalence of stress and limited resources to reduce stress in adults with ASD without ID, puts them at risk for poor life outcomes [6,17]. Interventions targeting stress in adults with ASD, without ID thus are highly needed.

Only a limited number of studies in extant literature report on interventions that reduce stress in adults with ASD without ID, and studies using stress as outcome measure are lacking [46]. In our previous publication, an RCT on the effectiveness of Animal Assisted Therapy (AAT) in a sample of adults with ASD without ID, we showed significantly lower subjective stress levels after AAT as compared to waiting list controls [56]. To date, the effects of AAT on physiological stress in adults with ASD are unknown. However, in children with ASD, lower cortisol awakening responses (CAR) were observed during the stay of a specially trained and selected service dog in their home [52]. Furthermore, in children with ASD who participated in therapy sessions incorporating goal-directed activities with horses, significant reductions in salivary cortisol were found [49].

Given the positive effects of AAT on acute stress reduction in children with ASD, and the lack of research on physiological stress reactivity in adults with ASD without ID, we aimed to explore whether physiological indicators of stress in this latter population change across an AAT session period (1 h), and hypothesized that the AAT session would be associated with a reduction in stress parameters.

Since this is the first study exploring associations between AAT and physiological stress in the adults with ASD without ID, we included a broad range of parameters, reflecting activation of the major physiological stress response systems. We included measures of the Hypothalamic-Pituitary-Adrenal axis (HPA axis) (cortisol), and the neural and neuro-endocrine branches of the sympathetic nervous system (alpha-amylase, systolic time intervals (i.e., PEP, LVET)), as well as the parasympathetic nervous system (HRV).

To examine whether possible intervention effects remained after the therapy, we performed a randomized controlled trial (RCT) in which physiological effects of AAT were tested as secondary outcomes in by comparing post-intervention (after 10 sessions) and follow-up effects (20-week follow-up period) to pre-intervention (T0). We hypothesized that participants in the AAT condition, compared to waiting list controls, would have reduced cortisol levels at post-treatment and that this would return to pre-intervention levels when therapy was not provided anymore [52]. Based on studies on mindfulness, we expected the sympathetic measures to follow a similar, but smaller-sized course, while parasympathetic activity is expected to show small-sized increases (i.e., somewhat more variability) at post-treatment, with a similar return to pre-treatment at follow-up [38,58].