Dr Andrea Phillipou is a Postdoctoral Research Fellow at Swinburne University and St Vincent’s Hospital. Her research has focused on uncovering the neurobiological mechanisms involved in anorexia nervosa, with an aim to improve treatment outcomes in the future.
Anorexia nervosa is considered a biopsychosocial condition, meaning biological, psychological and sociocultural factors are likely contributors to the development of the illness. Although psychological and sociocultural factors are likely to play a role in anorexia nervosa, most individuals exposed to these factors do not develop the condition. For example, most people exposed to the ‘thin ideal’ portrayed in the media will not develop anorexia nervosa. Therefore, an individual’s biology is an important factor to consider, in regards to predisposition. Specifically, a person’s neurobiology, or the way their brain is structured and functions may predispose them to developing anorexia nervosa.
Research to date has not identified a specific brain area or neurotransmitter (‘brain chemical’) that is responsible for anorexia nervosa. A lot of research has been undertaken in how people with anorexia nervosa’s brains look (the ‘structure’ of the brain) compared to people without the condition. This research has shown that some parts of the brain are smaller in people with anorexia nervosa, but these return to a comparable size to people without the condition during recovery (Castro-Fornieles, et al., 2009). These findings can mean one of two things: either, the size of brain regions ‘normalise’ when someone no longer has anorexia nervosa showing that their brain is also recovering from the condition; or that the difference in brain size when unwell was due to the effects of starvation experienced by someone with anorexia nervosa.
Although the structure of the brain is important, the way that an individual’s brain functions can provide insight into the mechanisms behind disordered behaviours and distorted thoughts. There are a few different ways to observe how someone’s brain is functioning. Two of the most informative ways are to look at which brain areas are ‘activated’ when completing different tasks, and the other is to look at the concentrations of different neurotransmitters.
In terms of brain activity, a number of brain imaging methods can be used, the most common being functional magnetic resonance imaging or fMRI. This scan looks at the amount of blood flow to a brain area when presented with different stimuli, for example when looking at an image of high-calorie food. Similarly to other organs in the human body, blood rushes to regions that are in use or ‘active’, and an fMRI scan highlights the brain areas activating to stimuli. Research in anorexia nervosa has found that some brain areas are not as active and some areas are more active in response to different stimuli. For example, when presented with bodies depicting an underweight state, an area of the brain involved in reward processing, called the ventral striatum, has been found to be more active in individuals with anorexia nervosa (Fladung, et al., 2009). This suggests that looking at an underweight body may be more rewarding to someone with anorexia nervosa, compared to someone without the condition. Another example is when individuals with anorexia nervosa are presented with images of their own face. Research findings have suggested increased activity in regions of the brain involved in the processing of fine details (i.e. the inferior and middle temporal gyri, and the lingual gyrus) in anorexia nervosa, compared to healthy individuals; which may help explain why some individuals with anorexia nervosa have a tendency to focus on the fine details of their physical appearance (Phillipou, et al., 2015).
Levels of different types of neurotransmitters have also been of interest in anorexia nervosa. Neurotransmitters are the chemical messengers that enable the brain to function. The greatest research interest has been in the neurotransmitters dopamine and serotonin because of their roles in regulating eating behaviours and reward. Although these neurotransmitters have been found to be reduced in individuals with anorexia nervosa, similarly to the structural brain findings described earlier, they tend to ‘normalise’ when recovered, suggesting that the reduced levels may be due to the low body weight experienced in anorexia nervosa (Phillipou, et al., 2014a). Recent findings have, however, suggested that a neurotransmitter called gamma-Aminobutyric acid or GABA may be involved in anorexia nervosa, though the exact nature of its involvement is still unclear (Phillipou, et al., 2014b; Phillipou, et al., 2016). Levels of GABA are closely related to anxiety levels, which is why GABA-ergic medications are sometimes used to treat anxiety (Nemeroff, 2002). High levels of anxiety are often characteristic of someone with anorexia nervosa (Swinbourne & Touyz, 2007), and it is thought that altered GABA levels and increased anxiety may be related to some of the behaviours seen in someone with anorexia nervosa, including anxiety around body image and food.
In sum, the research into the neurobiology of anorexia nervosa is still in its early days. Similar research is also being conducted in other eating disorders such as bulimia nervosa, but with less research focus than anorexia nervosa. Findings in bulimia nervosa have, however, indicated some similarities between anorexia and bulimia nervosa, such as reduced activity of the parietal cortex (a ‘spatial awareness’ area of the brain) when looking at one’s own body in both conditions, when compared to individuals without an eating disorder (Vocks, et al., 2010); whereas other research has found different neural responses to images of food in the two conditions (Brooks, et al., 2011). These findings suggest that eating disorders such as anorexia and bulimia nervosa share some similarities in brain function, but differ in other ways, which helps explain why the behaviours in the two conditions often differ.
The research findings in anorexia nervosa so far suggest these individuals may have brains that look and function differently to people without anorexia nervosa, which may predispose them to developing the illness. However, much more research is needed in this area to confirm the brain mechanisms involved in anorexia nervosa so that we are able to develop more effective treatments targeting these altered mechanisms in the future.
In addition, the findings from anorexia nervosa may be later applied to and drive additional research into the neurobiology of other DSM-5 eating disorders (including, BED and OSFED).
Brooks, S. J., Owen, G. O., Uher, R., Friederich, H. C., Giampietro, V., Brammer, M., ... & Campbell, I. C. (2011). Differential neural responses to food images in women with bulimia versus anorexia nervosa. PLoS One, 6(7), e22259.
Castro-Fornieles, J., Bargalló, N., Lázaro, L., Andrés, S., Falcon, C., Plana, M. T., & Junqué, C. (2009). A cross-sectional and follow-up voxel-based morphometric MRI study in adolescent anorexia nervosa. Journal of psychiatric research, 43(3), 331-340.
Fladung, A. K., Grön, G., Grammer, K., Herrnberger, B., Schilly, E., Grasteit, S., Wolf, R.G., Walter, H. & von Wietersheim, J. (2009). A neural signature of anorexia nervosa in the ventral striatal reward system. American Journal of Psychiatry, 167(2), 206-212.
Nemeroff, C. B. (2002). The role of GABA in the pathophysiology and treatment of anxiety disorders. Psychopharmacology bulletin, 37(4), 133-146.
Phillipou, A., Rossell, S. L., & Castle, D. J. (2014a). The neurobiology of anorexia nervosa: a systematic review. Australian and New Zealand Journal of Psychiatry, 48(2), 128-152.
Phillipou, A., Rossell, S. L., Castle, D. J., Gurvich, C., & Abel, L. A. (2014b). Square Wave Jerks and Anxiety as Distinctive Biomarkers for Anorexia Nervosa. Investigative Ophthalmology & Visual Science, 55(12), 8366-8370.
Phillipou, A., Abel, L. A., Castle, D. J., Hughes, M. E., Gurvich, C., Nibbs, R. G., & Rossell, S. L. (2015). Self perception and facial emotion perception of others in anorexia nervosa. Frontiers in Psychology, 6.
Phillipou, A., Rossell, S. L., Gurvich, C., Castle, D. J., & Abel, L. A. (2016). The eyes have it: Eye movements and anorexia nervosa. Australian and New Zealand Journal of Psychiatry, 50(8), 806-807.
Swinbourne, J. M., & Touyz, S. W. (2007). The co‐morbidity of eating disorders and anxiety disorders: a review. European Eating Disorders Review, 15(4), 253-274.
Vocks, S., Busch, M., Grönemeyer, D., & Herpertz, S. (2010). Neural correlates of viewing photographs of one's own body and another woman's body in anorexia and bulimia nervosa: an fMRI study. Journal of psychiatry & neuroscience: JPN, 35(3), 163.
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