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The association of interoceptive awareness and alexithymia with neurotransmitter concentrations in insula and
Jutta Ernst1, Heinz Böker1, Joe Hättenschwiler1
1Clinic for Affective Disorders and General Psychiatry, Department of Psychiatry, Psychotherapy, and Psychosomatics, Psychiatric University Hospital, 8029 Zurich, Switzerland, Center for Anxiety and Depression, 8008 Zurich, Switzerland, University of Ottawa, Institute of Mental Health Research, Ottawa K1Z 7K4, Canada, Department of Psychiatry, Campus Benjamin Franklin, Charité, 14050 Berlin, and Languages of Emotion Cluster of Excellence, Freie Universität Berlin, 14195 Berlin, Germany.
Abstract:
Alexithymia and increased interoceptive awareness have been associated with affective disorders as well as with altered insula and anterior cingulate cortex (ACC) function. Brain imaging studies have demonstrated an association between neurotransmitter function and affective disorders as well as personality traits. Here, we first examined the relationship between alexithymic facets as assessed with the Toronto Alexithymia Scale (TAS-20) and interoceptive awareness (assessed with the Body Perception Questionnaire) in 18 healthy subjects. Second, we investigated their association with glutamate and gamma-aminobutyric acid (GABA) concentrations in the left insula and the ACC using 3-Tesla proton magnetic resonance spectroscopy. Behaviorally, we found a close association between alexithymia and interoceptive awareness. Furthermore, glutamate levels in the left insula were positively associated with both alexithymia and awareness of autonomic nervous system reactivity, while GABA concentrations in ACC were selectively associated with alexithymia. Although preliminary, our results suggest that increased glutamate-mediated excitatory transmission-related to enhanced insula activity-reflects increased interoceptive awareness in alexithymia. Suppression of the unspecific emotional arousal evoked by increased awareness of bodily responses in alexithymics might thus be reflected in decreased neuronal activity mediated by increased GABA concentration in ACC.
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