ArticleBrain imaging and behavior2020
Subclinical eating disorder traits are correlated with cortical thickness in regions associated with food reward and perception.
Article in Brain imaging and behavior, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- GDF15 Is Elevated in Eating Disorders and Is Involved in the Gut-Brain Axis via Ghrelin.European eating disorders review : the journal of the Eating Disorders Association · 2026Article
- Is Interoception Deficit Linking Alexithymia and Eating Spectrum Symptoms? Study on a Non-Clinical Sample of Young Adults.Healthcare (Basel, Switzerland) · 2024Article
- Abnormalities in deep-brain morphology and orbitofrontal cortical thinning relate to reward processing and body mass in adolescent girls.International journal of obesity (2005) · 2022Article
- Volumetric Alterations of the Cerebral Cortex in Eating Disorders.Journal of clinical medicine · 2021Article
- Subcortical brain volume and cortical thickness in adolescent girls and women with binge eating.The International journal of eating disorders · 2021Article
- Cortical thinning and associated connectivity changes in patients with anorexia nervosa.Translational psychiatry · 2021Article
- Between wellness, relapse, and remission: Stages of illness in anorexia nervosa.The International journal of eating disorders · 2020Article
- Lower gray matter volumes of frontal lobes and insula in adolescents with anorexia nervosa restricting type: Findings from a Brain Morphometry Study.European psychiatry : the journal of the Association of European Psychiatrists · 2020Article
- Neuroimaging and eating disorders.Current opinion in psychiatry · 2019Review
- Review
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Authors and funding
5 authors.
Funding
Abstract
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.
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