| Summary: | Introduction Evidence suggests that diagnosis of an eating disorder (ED) is associated with differential cognitive functioning. Whether differences are present prior to onset, possibly affecting risk status for development of an ED, or whether differences are a consequence of secondary features of the disorder such as low nutritional intake, is not conclusive. One method of investigating cognitive functioning prior to onset of a disorder is to investigate cognitive functioning in those that are at high risk of developing that disorder. Studies have shown that first-degree relatives of probands are at higher risk of developing an ED than the general population. Methods This is the first study to investigate intelligence, global cognition, executive functioning, social communication and emotion recognition of children at high risk of developing an ED, in comparison to children who are not, in a large community sample. High risk status of children was defined in two ways: (i) maternal self-report diagnosis of an ED during pregnancy; (ii) maternal lifetime ED behavioural phenotype. Results Children at high risk for ED demonstrated superior intellectual functioning and working memory; but inferior attentional capacity, social communication and emotion recognition. Profile of children at high risk differed according to type of maternal ED. There was also some evidence of maternal behavioural phenotype being a better predictor of children’s functioning than maternal self-report of ED diagnosis. Discussion Results suggest that the differences observed in children at high risk are putative intermediate phenotypes for ED, possibly affecting risk status for development. Findings are extremely important: both in relation to the identification of vulnerable individuals (and therefore preventative efforts); and in furthering our understanding of which neuropsychological profiles are linked to susceptibility for ED. Also, use of a lifetime behavioural ED phenotype may provide the homogeneity required for research investigating intermediate phenotypes and genetic correlates of ED.
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