Subclinical eating disorder traits are correlated with cortical thickness in regions associated with food reward and perception.

Journal Article (Journal Article)

Behavioral traits associated with various forms of psychopathology are conceptualized as dimensional, varying from those present in a frank disorder to subclinical expression. Demonstrating links between these behavioral traits and neurobiological indicators, such as brain structure, provides one form of validation for this view. However, unlike behavioral dimensions associated with other forms of psychopathology (e.g., autism spectrum disorder, attention deficit hyperactivity disorder, antisocial disorders), eating disorder traits have not been investigated in this manner in spite of the potential that such an approach has to elucidate etiological mechanisms. Therefore, we examined for the first time neural endophenotypes of Anorexia Nervosa and Bulimia via dimensional traits (measured using the Eating Disorders Inventory-3) in a large subclinical sample of young adults (n = 456 and n = 247, respectively; ages = 18-22 years) who each provided a structural magnetic resonance imaging scan. Cortical thickness was quantified at 81,924 vertices across the cortical surface. We found: 1) increasing eating disorder traits correlated with thinner cortex in the insula and orbitofrontal cortex, among other regions, and 2) using these regions as seeds, increasing eating disorder trait scores negatively modulated structural covariance between these seed regions and other cortical regions linked to regulatory and sensorimotor functions (e.g., frontal and temporal cortices). These findings parallel those found in the clinical literature (i.e., thinner cortex in these food-related regions in individuals with eating disorders) and therefore provide evidence supporting the dimensional view of behavioral traits associated with eating disorders. Extending this approach to genetic and neuroimaging genetics studies holds promise to inform etiology.

Full Text

Duke Authors

Cited Authors

  • Wallace, GL; Richard, E; Peng, CS; Knodt, AR; Hariri, AR

Published Date

  • April 2020

Published In

Volume / Issue

  • 14 / 2

Start / End Page

  • 346 - 352

PubMed ID

  • 30617787

Pubmed Central ID

  • PMC6893094

Electronic International Standard Serial Number (EISSN)

  • 1931-7565

International Standard Serial Number (ISSN)

  • 1931-7557

Digital Object Identifier (DOI)

  • 10.1007/s11682-018-0007-x


  • eng