Journal
JOURNAL OF PERSONALIZED MEDICINE
Volume 11, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/jpm11101020
Keywords
loss of control eating; renourishment; stress hormones; appetite hormones
Funding
- National Institute of Nursing Research [T32 NR007091]
- National Institute of Mental Health [R01MH120170, R01MH124871, R01MH119084, R01MH118278, K01 MH106675, R01 MH095860]
- Brain and Behavior Research Foundation Distinguished Investigator Grant
- Swedish Research Council (Vetenskapsradet) [538-2013-8864]
- Lundbeck Foundation [R276-2018-4581]
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Binge eating is a common symptom in patients with anorexia nervosa even after weight restoration, and biological predictors such as cortisol levels have been found to be significantly associated with subjective binge eating behavior. Further research is needed to confirm the role of cortisol in predicting subjective binge eating and to uncover the underlying mechanisms to prevent its negative consequences.
Binge eating is a transdiagnostic eating disorder symptom that can occur in patients with anorexia nervosa (AN), persisting after weight restoration, and impeding their recovery. However, little is known about the biological predictors of binge eating after AN weight restoration. The goals of this exploratory study of 73 females with AN were: (1) to examine changes in cortisol, the adrenocorticotropic hormone, norepinephrine, ghrelin (total and active), and leptin levels across the admission, discharge, and 3 months post-discharge from the inpatient AN weight restoration; and (2) to determine whether the target hormones were associated with objective or subjective binge eating (OBE or SBE). The participants completed the self-reported Eating Disorder Examination Questionnaire, Beck Anxiety Inventory, and Beck Depression Inventory-II, and provided fasting whole blood samples for hormone assays. The results showed significant changes in body mass index (BMI), cortisol, total ghrelin, and leptin levels over the three time points. The cortisol levels at admission and discharge were significantly associated with the number of SBE episodes at 3 months post-discharge. Findings suggest the need to replicate and confirm the role of cortisol in predicting the emergence of SBE and uncover the mechanisms underlying SBE and cortisol to prevent SBE and its negative consequences.
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