Our model is based upon an interaction between environmental factors and a specific genetic profile, which is up to 11 times more likely to be present in those with anorexia nervosa than those who are unaffected. This profile is characterised by the dysfunction of various neurotransmitter systems and, specifically, noradrenaline. The chemical messenger, noradrenaline, has a number of important functions: it regulates the sympathetic nervous system (fight or flight responses), blood flow to the brain and neuroplasticity (the ability of the brain to change and adapt to environmental requirements). When the noradrenaline system is overactive, as proposed in our model, anxiety levels are very high, blood flow to specific brain structures is subtly, yet significantly, reduced and the neuroplasticity of these structures is impaired. 

One specific structure-the insula-is vital to all of the above. The insula is at the centre of many brain networks. It is so crucial to the transmission of information that it can be likened to the central hub of the brain-many crucial routes pass through it. Of particular relevance to anorexia nervosa is the insula's role in sensitivity to stimuli originating inside the body (interoception); the brain's pictorial representation or map of the body (bodily representation); regulation of the sympathetic nervous system; perception of pain; the regulation of disgust and the integration of thoughts and feelings. Since all these functions are impaired in anorexia nervosa, insula dysfunction could account for the numerous features of the disorder.

Our clinically-based genetic, neuroimaging and neuropsychological studies all support this insula model. For the moment we are intrigued by the idea that a combination of genetic and environmental influences may upset the regulation of the noradrenaline system, prompting a cascade of events that culminates in dysfunction of the insula. The latter subsequently leads to a failure of information processing, then to body-image misperception and intense body-focused anxiety, finally resulting in the condition we call anorexia nervosa. 

Should this model prove to be correct, it could revolutionise the treatment of anorexia nervosa with the potential for a far better prognosis.