Recent research on behavioral characteristics displayed by anorexia nervosa (AN) and anorexia nervosa recovered (ANR) patients point strongly towards an anomalous pattern of activation of the pre-frontal cortex. Unlike in normal women, where food triggers off a reward system in the brain, AN and ANR (those who have recovered from anorexia nervosa) patients display an exaggerated startle effect, as part of an intrinsic defense reaction. In addition, they often salivate less, eat slower, and have a lower preference for fatty and sweet food, suggestive of a disruption in the central food-associated reward pathways.

Animal models of AN show that both extreme under-eating and binge eating may result in a disruption of the normal brain chemicals associated with ‘reward’, by an unregulated flooding of dopamine, opioids and cannabinoids in the brain. In a positron emission tomography (PET) study of brain scans in AN patients in 2005, a markedly reduced 5-HT receptor binding was confirmed, in the ‘punishment’ center in the cingulate region. This is thought to lead to a heightened sensitivity to ‘punishment’, and explains the basic food aversion in all types of AN. On the other hand, a variability of the sensitivity of the opposing reward systems lead to dramatic opposites in behavior – from extreme starvation to bingeing.

Current research also focuses on associations of distinct personality traits of AN/ANR patients. Weak set shifting (an ability to switch between mental tasks) is thought to be a core component of AN/ANR, and although it is seen in bipolar disorders and schizophrenia, its importance lies in its link with ‘reward’ sensitivities through variable effects on the dopaminergic pathways. In addition, AN/ANR patients show a bias towards detail in their tasks, although they display weakness in global processing, described as ‘weak central coherence’, a trait shared with autism and Asperger’s syndrome. Although they perform well in learning with effort, they are deficient in incidental or unconscious learning, which explains why AN/ANR patients are often poor at adapting to the demands of their work or social environment.

Finally, as the genetic correlates of AN/ANR are becoming clearer, population studies estimate the increase in familial risk to be by a factor of 10. The linkage to chromosome 1 is thought to determine anomalies in 5-HT genes, seen in restrictive AN subtypes (under-eaters). The other aspect of AN/ANR that has a familial clustering, is obsessive-compulsiveness (often leading to traits of perfectionism and undue concern with mistakes).

In the future, models of treatment and maintenance for the AN/ANR subtypes will depend upon a better understanding of the neurologically determined patterns of behavior, with an emphasis on treating it with broader ‘global’ behavioral emphasis than simply focusing on eating behavior.

Reference

Janet Treasure. Getting beneath the Phenotype of Anorexia Nervosa: The Search for Viable Endophenotypes and Genotypes. Canadian Journal of Psychiatry; April 2007; 52:4, pp 212-19.

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