When active, the myelinated vagus (the tenth cranial nerve) acts as a brake that inhibits sympathetic activity by reducing heart rate and blood pressure, and thus allows for social engagement by redirecting metabolic resources. Among those with selective mutism (SM), a disorder characterized by an inability to speak in certain situations, the vagal brake is dysregulated. One consequence of this is a weakening of the middle-ear acoustic reflex (MEAR), which helps clarify human voices and filters out low-frequency background noise, including the speaker’s own voice. I tested a proposed etiological model of SM and comorbid social anxiety disorder (SAD) by investigating the relationship between MEAR dysfunction and phonophobia (fear of one’s own voice), which were hypothesized to be positively correlated. A nonclinical sample of Bard undergraduate students was recruited. MEARs were assessed using a tympanometer and a signal-to-noise ratio hearing test; phonophobia was gauged by comparing transient anxiety levels before and after reading neutral words aloud. Analyses revealed no reliable correlation between MEAR dysfunction and phonophobia. I suggest an alternative explanation that incorporates a possible compensatory mechanism for unfiltered auditory information. These findings have implications for our understanding of the impact of the vagus nerve on the auditory system, as well as our conceptualization and treatment of SM, which is currently addressed with pharmacological interventions better suited to SAD than SM
