The reported abnormalities of brain function in anorexia nervosa (AN) include impairment of neural circuits involving cortical (orbito-frontal, somatosensory and parietal) and sub-cortical (amygdala, hippocampus, thalamus, hypothalamus and striatum) structures. The insular cortex serves an integrative function for all the structures relevant to the features of AN and as such may be central to this impairment. We hypothesise that a rate limiting dysfunction of neural circuitry integrated by the insula can account for the clinical phenomena of AN. Such dysfunction could account for the known psychopathology, neuroimaging abnormalities and neuropsychological deficits. Proposals to test this hypothesis are made.
(c) 2008 John Wiley & Sons, Ltd and Eating Disorders Association.