Binge Eating Disorder Mediates Links between Symptoms of Depression, Anxiety, and Caloric Intake in Overweight and Obese Women

Despite considerable comorbidity between mood disorders, binge eating disorder (BED), and obesity, the underlying mechanisms remain unresolved. Therefore, the purpose of this study was to examine models by which internalizing behaviors of depression and anxiety influence food intake in overweight/obese women. Thirty-two women (15 BED, 17 controls) participated in a laboratory eating-episode and completed questionnaires assessing symptoms of anxiety and depression. Path analysis was used to test mediation and moderation models to determine the mechanisms by which internalizing symptoms influenced kilocalorie (kcal) intake. The BED group endorsed significantly more symptoms of depression (10.1 versus 4.8,P=0.005) and anxiety (8.5 versus 2.7,P=0.003). Linear regression indicated that BED diagnosis and internalizing symptoms accounted for 30% of the variance in kcal intake. Results from path analysis suggested that BED mediates the influence of internalizing symptoms on total kcal intake (empiricalP<0.001). The associations between internalizing symptoms and food intake are best described as operating indirectly through a BED diagnosis. This suggests that symptoms of depression and anxiety influence whether one engages in binge eating, which influences kcal intake. Greater understanding of the mechanisms underlying the associations between mood, binge eating, and food intake will facilitate the development of more effective prevention and treatment strategies for both BED and obesity.

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Recorded food intake of obese women with binge eating disorder before and after weight loss

International Journal of Eating Disorders ◽

10.1002/1098-108x(199403)15:2<135::aid-eat2260150205>3.0.co;2-i ◽

1994 ◽

Vol 15 (2) ◽

pp. 135-150 ◽

Cited By ~ 74

Author(s):

Susan Zelitch Yanovski ◽

Nancy G. Sebring

Keyword(s):

Weight Loss ◽

Eating Disorder ◽

Food Intake ◽

Binge Eating ◽

Binge Eating Disorder ◽

Obese Women ◽

Before And After

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Binge Eating Disorder, Depression and Anxiety, and Weight Gain and Increased BMI After Five Years of Bariatric Surgery

10.21203/rs.3.rs-999292/v1 ◽

2021 ◽

Author(s):

Heitor Bernardes Pereira Delfino ◽

Marcela Augusta Souza Pinhel ◽

Flávia Campos Ferreira ◽

Carolina Ferreira Nicoletti ◽

Sofia Teixeira Prates Oliveira ◽

...

Keyword(s):

Bariatric Surgery ◽

Body Composition ◽

Eating Disorder ◽

Weight Gain ◽

Binge Eating ◽

Binge Eating Disorder ◽

Severe Depression ◽

Depression And Anxiety ◽

Level Of Evidence ◽

Symptoms Of Depression

Abstract ObjectivesAnalyze the influence of Binge Eating Disorder (BED) and symptoms of depression and anxiety on anthropometric and body composition changes over five years after bariatric surgery in patients with obesity.MethodsEvaluation of 118 individuals undergoing bariatric surgery, divided into two groups: Group 1: individuals with BED; Group 2: individuals without BED. The individuals were submitted to anthropometric and body composition evaluation, and analysis of the presence of BED, depression, and anxiety according to the DSM-V and using validated questionnaires. The Kolmogorovi-Smirnov, t-test, Fisher’s, chi-square, and ANOVA were used for statistical analysis.ResultsThe groups with BED (N=61, 51,7%) and without BED (N=57, 48,3%) did not differ from each other for all sociodemographic assessed variables (p>0.05) and had similar changes in waist circumference and body composition over five years after bariatric surgery (p>0.05). On the other hand, only patients with BED had severe depression (13,11%, p=0.0079) and had a higher frequency of moderate (22.95%, p=0.0022) and severe (14.75%, p=0.0022) anxiety in the preoperative period of bariatric surgery. In addition, only the group with BED had increased weight and increased BMI in the fifth year after bariatric surgery (p<0.05).ConclusionPatients with BED had more intense symptoms of depression and anxiety, and this disorder may reappear in the postoperative period of bariatric surgery and contribute to weight gain and an increase in BMI.Level of evidence: III (evidence obtained from case-control analytic study).

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Stress-induced laboratory eating behavior in obese women with binge eating disorder

Appetite ◽

10.1016/j.appet.2011.12.007 ◽

2012 ◽

Vol 58 (2) ◽

pp. 457-461 ◽

Cited By ~ 42

Author(s):

S. Schulz ◽

R.G. Laessle

Keyword(s):

Eating Disorder ◽

Binge Eating ◽

Eating Behavior ◽

Binge Eating Disorder ◽

Obese Women

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A comparison of energy intake and food selection during laboratory binge eating episodes in obese women with and without a binge eating disorder diagnosis

International Journal of Eating Disorders ◽

10.1002/eat.20312 ◽

2006 ◽

Vol 40 (1) ◽

pp. 67-71 ◽

Cited By ~ 37

Author(s):

Nancy C. Raymond ◽

Lindsay T. Bartholome ◽

Susanne S. Lee ◽

Roseann E. Peterson ◽

Susan K. Raatz

Keyword(s):

Eating Disorder ◽

Binge Eating ◽

Energy Intake ◽

Binge Eating Disorder ◽

Food Selection ◽

Obese Women

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Oleoylethanolamide decreases frustration stress-induced binge-like eating in female rats: a novel potential treatment for binge eating disorder

Neuropsychopharmacology ◽

10.1038/s41386-020-0686-z ◽

2020 ◽

Vol 45 (11) ◽

pp. 1931-1941 ◽

Cited By ~ 5

Author(s):

Adele Romano ◽

Maria Vittoria Micioni Di Bonaventura ◽

Cristina Anna Gallelli ◽

Justyna Barbara Koczwara ◽

Dorien Smeets ◽

...

Keyword(s):

Eating Disorder ◽

Nucleus Accumbens ◽

Food Intake ◽

Binge Eating ◽

Binge Eating Disorder ◽

Female Rats ◽

Early Gene ◽

Mrna Levels ◽

Palatable Food ◽

Brain Areas

Abstract Binge eating disorder (BED) is the most frequent eating disorder, for which current pharmacotherapies show poor response rates and safety concerns, thus highlighting the need for novel treatment options. The lipid-derived messenger oleoylethanolamide (OEA) acts as a satiety signal inhibiting food intake through the involvement of central noradrenergic and oxytocinergic neurons. We investigated the anti-binge effects of OEA in a rat model of binge-like eating, in which, after cycles of intermittent food restrictions/refeeding and palatable food consumptions, female rats show a binge-like intake of palatable food, following a 15-min exposure to their sight and smell (“frustration stress”). Systemically administered OEA dose-dependently (2.5, 5, and 10 mg kg−1) prevented binge-like eating. This behavioral effect was associated with a decreased activation (measured by mapping the expression of c-fos, an early gene widely used as a marker of cellular activation) of brain areas responding to stress (such as the nucleus accumbens and amygdala) and to a stimulation of areas involved in the control of food intake, such as the VTA and the PVN. These effects were paralleled, also, to the modulation of monoamine transmission in key brain areas involved in both homeostatic and hedonic control of eating. In particular, a decreased dopaminergic response to stress was observed by measuring dopamine extracellular concentrations in microdialysates from the nucleus accumbens shell, whereas an increased serotonergic and noradrenergic tone was detected in tissue homogenates of selected brain areas. Finally, a decrease in corticotropin-releasing factor (CRF) mRNA levels was induced by OEA in the central amygdala, while an increase in oxytocin mRNA levels was induced in the PVN. The restoration of a normal oxytocin receptor density in the striatum paralleled the oxytocinergic stimulation produced by OEA. In conclusion, we provide evidence suggesting that OEA might represent a novel potential pharmacological target for the treatment of binge-like eating behavior.

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