Characterizing cerebral metabolite profiles in anorexia and bulimia nervosa and their associations with habitual behavior
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jats:titleAbstract</jats:title>jats:pAnorexia nervosa (AN) and bulimia nervosa (BN) are associated with altered brain structure and function, as well as increased habitual behavior. This neurobehavioral profile may implicate neurochemical changes in the pathogenesis of these illnesses. Altered glutamate, jats:italicmyo</jats:italic>-inositol and jats:italicN-</jats:italic>acetyl aspartate (NAA) concentrations are reported in restrictive AN, yet whether these extend to binge-eating disorders, or relate to habitual traits in affected individuals, remains unknown. We therefore used single-voxel proton magnetic resonance spectroscopy to measure glutamate, jats:italicmyo</jats:italic>-inositol, and NAA in the right inferior lateral prefrontal cortex and the right occipital cortex of 85 women [jats:italicn</jats:italic> = 22 AN (binge-eating/purging subtype; AN-BP), jats:italicn</jats:italic> = 33 BN, jats:italicn</jats:italic> = 30 controls]. To index habitual behavior, participants performed an instrumental learning task and completed the Creature of Habit Scale. Women with AN-BP, but not BN, had reduced jats:italicmyo</jats:italic>-inositol and NAA concentrations relative to controls in both regions. Although patient groups had intact instrumental learning task performance, both groups reported increased routine behaviors compared to controls, and automaticity was related to reduced prefrontal glutamate and NAA participants with AN-BP. Our findings extend previous reports of reduced jats:italicmyo</jats:italic>-inositol and NAA levels in restrictive AN to AN-BP, which may reflect disrupted axonal-glial signaling. Although we found inconsistent support for increased habitual behavior in AN-BP and BN, we identified preliminary associations between prefrontal metabolites and automaticity in AN-BP. These results provide further evidence of unique neurobiological profiles across binge-eating disorders.</jats:p>
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Funder: Cambridge Overseas Trust; doi: https://doi.org/10.13039/501100003341
Funder: NIH Oxford Cambridge Scholars Program
Funder: Holt Fellowship
Funder: Bernard Wolfe Health Neuroscience Fund