Developing and Testing a Novel Neuroscience Hypothesis of Anorexia Nervosa
Thesis or dissertation
University of Exeter
Eating disorders are difficult to treat: there is still no NICE-approved first-line treatment for anorexia nervosa. In part this could be due to a lack of a compelling theoretical model to account for the development and dogged persistence of the illness. Sociocultural factors implicating western preoccupation with thinness and attractiveness are likely to play a contributory role, but cannot be by themselves causal in societies where such ideals are dominant. Recent theoretical models in neuroscience predict that predisposing neurobiological factors in early brain development may render some young people more vulnerable than others to universal psychosocial pressures, especially during adolescence. This dissertation reviews the existing evidence for abnormal neurobiological functioning in eating disorders, acknowledging that it is difficult to distinguish between the acute effects of starvation on the brain and possibly pre-existing underlying factors. Nevertheless, such empirical studies do support the development of a novel hypothesis implicating abnormal functioning of a neural network centred on the insula cortex in anorexia nervosa. The insula hypothesis is tested in a series of functional imaging studies using Single Positron Emission Computed Tomography (SPECT) indicating focal abnormalities in the temporal region that persist following weight restoration treatment and correlate with neuropsychological deficits. A subsequent study using higher resolution functional Magnetic Resonance Imaging (fMRI) lends further partial support to the insula hypothesis (in three out of four tasks) and also implicates additional brain structures in the basal ganglia. These findings, if replicated, could contribute to the development of novel therapeutic approaches to the treatment of anorexia nervosa, including realtime fMRI and mindfulness-based approaches, both of which have been shown to modulate insula activation. The studies presented here could hopefully also help to reduce the stigma and shame so often associated with eating disorders, for the benefit of sufferers and their families.
Helse Sør Øst, Norway.
Frampton, I., & Rose, M. (2013). Eating disorders and the brain. in B.Lask & R.Bryant-Waugh (Eds.), Eating disorders in childhood and adolescence (pp.125-147). London: Wiley
Fuglset, T., & Frampton, I. (2011). Neuroimaging. in B.Lask & I.Frampton (Eds). Eating disorders and the brain (pp. 56-105). London: Wiley
Nunn, K.P., Frampton, I., Gordon, I., & Lask, B. (2008). The fault is not in her parents but in her insula – a neurobiological hypothesis of anorexia nervosa. European Eating Disorders Review, 16, 355–360
Nunn, K., Frampton, I., Fuglset, T., Törzsök-Sonnevend, M., & Lask, B. (2011). Anorexia nervosa and the insula. Medical Hypotheses. 76. 353-357
Frampton. I., Wisting, L., Øverås, M., Midstund, M., & Lask, B. (2011). Reliability and validity of the Norwegian translation of the Child Eating Disorder Examination (ChEDE). Scandinavian Journal of Psychology, 52, 196-9
Frampton I., Watkins E., Gordon I., & Lask B. (2011). Do abnormalities in regional cerebral blood flow in anorexia nervosa resolve after weight restoration? European Eating Disorders Review, 19. 55-58
Frampton, I., Hutchinson, A., Watkins, E., & Lask, B. (2012). Neurobiological status at initial presentation predicts neuropsychological functioning in early onset anorexia nervosa at four-year follow-up. Developmental Neuropsychology, 37, 1–8.
Frampton, I., & Lask, B. (2011). Future directions. In B.Lask & I.Frampton (Eds.), Eating disorders and the brain (pp.208-218). London: Wiley.
PhD in Psychology