Sniff Check! Adults with Greater Autism Symptoms Report Odors As Being More Positive
Many have speculated that hypoactivation of the amygdala is a key feature of autism spectrum disorder (ASD) (Baron-Cohen et al., 2000). While evidence for amygdala hypoactivation is mixed, there is some support for the notion that abnormal connectivity of the amygdala and orbitofrontal cortex may be implicated in the social deficits seen in ASD (Zalla and Sperduti, 2013). Evidence indicates that the amygdala and the orbitofrontal cortex are also involved with the attribution of emotional valence to olfactory stimuli (Zald and Pardo, 1997).
A growing literature suggests the presence of aberrant olfactory processing in ASD. For example, evidence suggests that odor identification, though not detection, is impaired in ASD (Suzuki et al., 2003). Likewise, children with ASD do not adjust their sniff response time to unpleasant versus pleasant odors, an atypical pattern which correlates with social impairment (Rosenkrantz et al., 2015). Similarly, it has been speculated that children with ASD are less likely to report emotional attributions to odors (Legiša et al., 2013). However, to date, no study has assessed odor valence rating as a function of ASD symptomatology.
This study examined relationship between ASD symptomatology and bias in emotional valence to olfactory stimuli. It was hypothesized that adults with greater subclinical ASD symptoms would show a less negative response to typically aversive scents.
Thirty-one typically developing adults (21 female, 10 male; ages 18 - 47, Mage = 22.2, SDage = 6.0) completed a self-report measure of autism symptomology, the Social Responsiveness Scale-2 (SRS-2; Constantino & Gruber, 2012), as well as an olfaction task (Jin et al., 2015). The task featured 9 scents that varied by positive, negative, and neutral valence. Participants rated the valence and familiarity of each scent on a continuous scale.
There was a correlation between greater autism symptoms and rating negatively-valenced odors more positively (r = .355, p =.007), an effect which remained significant after controlling for familiarity (r = .412, p = .002). The correlation was also significant for both subscales of the SRS-2, but moreso for social communication (r = .468, p < .001) than for restricted and repetitive behavior (r = .331, p = .013).
Adults with greater levels of sub-clinical ASD symptoms subjectively reported negatively-valenced odors as more pleasant. This could explain the aberrant sniff response found by Rosenkrantz et al., as perhaps individuals with ASD do not perceive negatively-valenced scents as negatively as TD controls. Taken together, these findings converge with past studies suggesting a potential relationship between ASD symptoms, particularly in the social communication domain, and atypical olfactory processing. Given that intact amygdala and orbitofrontal cortex functioning is needed to identify the pleasantness of an odor, these findings may provide a behavioral index of abnormal amygdala and orbitofrontal cortex connectivity in ASD (Zalla and Sperduti, 2013). When presented, these results will be augmented via the inclusion of 30 adults with ASD as well.