Poor set-shifting has been implicated as a risk marker, maintenance factor and candidate endophenotype of eating disorders (ED). This study aimed to add clarity to the cognitive profile of set-shifting by examining the trait across ED subtypes, assessing whether it is a state or trait marker, and whether it runs in families. A battery of neuropsychological tasks was administered to 270 women with current anorexia (AN) and bulimia nervosa (BN), women recovered from AN, unaffected sisters of AN and BN probands, and healthy control women. Set-shifting was examined using both individual task scores and a composite variable (poor/intact/superior shifting) calculated from four neuropsychological tasks. Poor set-shifting was found at a higher rate in those with an ED particularly binge/purging subtypes. Some evidence for poor set-shifting was also present in those recovered from AN and in unaffected sisters of AN and BN. Clinically, poor set-shifting was associated with a longer duration of illness and more severe ED rituals but not body mass index. In sum, poor set-shifting is a transdiagnostic feature related to aspects of the illness but not to malnutrition. In part it is a familial trait, and is likely involved in the maintenance of the illness.
Psychiatric illnesses are complex both in terms of aetiology and presentation, making research based on overt clinical symptoms particularly challenging. An alternative strategy is to focus on underlying mechanisms such as maintaining factors and biological markers. The search for such markers is particularly applicable to the eating disorders (ED) given their unstable diagnostic categories (Anderluh et al., 2009) and the current lack of targeted and effective treatment (Bulik et al., 2007, Shapiro et al., 2007, Steinhausen, 2009 and Treasure et al., 2009). One medium used to explore such mechanisms is that of neuropsychology (Gottesman and Gould, 2003 and Ritsner and Gottesman, 2009), where standardised and systematic assessment allows for detailed exploration of altered cognitive functioning.
Cognitive flexibility or set-shifting is an aspect of executive functioning that has been implicated as a risk marker (Tchanturia et al., 2002), maintenance factor (Steinglass et al., 2006), biomarker (Lopez et al., 2008a) and candidate endophenotype of ED (Holliday et al., 2005). Difficulties shifting set have been found in women with current and past ED across a number neuropsychological tasks (Roberts et al., 2007 and Tchanturia et al., 2005). Poor set-shifting has been found in unaffected sisters of women with anorexia nervosa (AN) (Holliday et al., 2005), providing some evidence for this cognitive feature as an endophenotype. Recent theoretical models of AN have highlighted the role of set-shifting in the illness, one implicating rigidity (poor set-shifting) as a maintenance factor (Schmidt and Treasure, 2006) and another suggesting that the presence of poor set-shifting provides evidence for disturbed neural pathways in the brain (Steinglass et al., 2006). Recent work in neuroimaging demonstrated the neural correlates of poor set-shifting in AN, with less activation of the ventral anterior cingulated striato thalamic network and greater activation of the fronto parietal circuits (Zastrow et al., 2009). One interpretation is that people with ED recruit more top down, effortful control in this type of task.
The aim of this study was to further explore and understand the cognitive profile of poor set-shifting using a battery of neuropsychological tasks investigating this concept in women with a current or past ED, their unaffected sisters, and a healthy comparison group. The specific primary aims were to explore set-shifting 1) across ED subtypes, 2) in the recovered state, and 3) within the family of the affected individuals. A secondary aim was to examine the relationship between set-shifting ability and clinical features.
It is therefore possible that a predisposition to set-shifting difficulties is a familial vulnerability factor, which acts in a general way to either predispose to or perpetuate forms of psychopathology including anorexia and bulimia nervosa.
