In contrast to the interest that has been shown in understanding and treatment of the behaviours, physical consequences and thoughts, emotions have been somewhat neglected. Perhaps, this neglect mirrors the emotional avoidance and attachment difficulties that are characteristic of people with eating disorders and that can distort introspection and self-report. Figure 1 is a schematic representation of the emotional brain based on Panksepp's model (Panksepp, 2011) of three interacting processes. The primary process lies within the evolutionary oldest parts of the brain and represents the affective consciousness from sensory, homeostatic and emotional inputs. The secondary process involves learning and memory that contribute to emotional habits. Finally, there is the tertiary process of cognitive control. How does what we know about eating disorder fit within this model? I selectively look at the literature in order to set the scene for the papers in this edition that follow.


Figure 1. This figure schematically represents Panksepp's model of emotions with three interacting processes

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Eating disorders may result from abnormal functioning in each of these three processes. First, there appears to be enhanced sensitivity to punishment in the primary process whereas the response to reward is attenuated in anorexia nervosa and exaggerated in bulimic disorders (Harrison, Treasure, & Smillie, 2011). Anxiety, internalising traits and threat sensitivity can emerge before the onset of the eating disorder (Adambegan et al., 2012) in particular social anxiety (Swinbourne et al., 2012). These traits are also seen in family members (Lilenfeld et al., 1998), which suggest that they may in part be genetically or epigenetically determined. Anomalies in the secondary process may arise from particular experiences that account for how and why negative emotional reactions to food weight and social stimuli are learned (Treasure, Cardi and Kan, 2012; Treasure, Corfield, & Cardi, 2012). Many eating disorder behaviours represent cognitive control of the tertiary system. Functional differences in the dorsal cognitive system (dorsal caudate, hippocampus, parietal dorsolateral prefrontal and anterior cingulate) are present in both the ill and recovered state in anorexia nervosa (Wagner et al., 2007; Zastrow et al., 2009). These are associated with altered dopamine and serotonin function (Bailer & Kaye, 2011).

In this edition, anomalies between the top down control and the experiential bottom level in eating disorders are described. Emotional inhibition suggestive of high levels of control are reported in anorexia nervosa (Claes et al., 2012; Davies, Swan, Schmidt, & Tchanturia, 2011; Espeset, Gulliksen, Nordbo, Skarderud, & Holte, 2012; Joos et al., 2012), whereas in binge eating disorder, top down control is reduced (Danner, Evers, Stok, van Elburg, & de Ridder, 2012). At the experiential level, cues relating to food and shape are associated with increased activation in limbic and cortical areas in people with eating disorders, whereas activation to more standard emotional cues is similar to what is found in healthy controls. Eating disorder behaviours are linked with emotional experiences. Unlike healthy controls, fasting improved mood in people with bulimia nervosa (Moreno-Dominguez, Rodriguez-Ruiz, Fernandez-Santaella, Ortega-Roldan, & Cepeda-Benito, 2012). In a subclinical group, decreased emotional expression mediated the relationship between an invalidating early environment and eating disorder symptoms (Haslam, Arcelus, Farrow, & Meyer, 2012). Treatments focused on improving emotional regulation can produce change (Abbate-Daga et al., 2012), but after recovery, a tendency to hold attitudes consistent with low-ranking, negative judgments of self compared with others persisted (Oldershaw et al., 2012).

In conclusion, the emotional life of people with eating disorders centres upon food, weight and shape. However, questions remain as to how, why and when this anomalous pattern was learned. Perhaps, there are some clues within this work as anomalies in social emotional functioning both precede and persist outside of the eating disorder itself. Thus, issues relating to attachment, competition/co-operation, theory of mind and self-representation may be key to understanding eating disorders. Can this be translated into new brain-directed treatments that focus on the experiential first level of experiences such as deep brain stimulation (Wu et al., 2012) and pharmacological approaches acting on dopamine, opiate and oxytocin receptors or on cognitive control through transmagnetic stimulation (Downar, Sankar, Giacobbe, Woodside, & Colton, 2012; Van den Eynde et al., 2010)? Certainly, our current talking treatments that focus mainly on tertiary processes do not provide sufficient help for a large proportion of people with eating disorders. Treatments that focus on intensive new learning of emotional habits such as playmancer (Claes et al., 2012; Fernandez-Aranda et al., 2012), self-directed exposure (Cardi et al., 2012) and attentional bias training may also need to be considered.


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