Gray matter volume and functional connectivity underlying binge eating in healthy children.

PURPOSE: As a maladaptive disordered eating behavior, binge eating (BE) onset has been reported in children as young as eight years old and is linked with a range of negative psychological consequences. However, previous neuroimaging research of BE has mainly focused on adults in clinical conditions, and little is known about the potential neurostructural and neurofunctional bases of BE in healthy children. METHODS: In this study, we examined these issues in 76 primary school students (mean age = 9.86 years) using voxel-based morphometry and resting-state functional connectivity (rsFC) approaches. RESULTS: After controlling for age, sex, and total intracranial volume/head motion, we observed that higher levels of BE were correlated with greater gray matter volumes (GMV) in the left fusiform and right insula and weaker rsFC between the right insula and following three regions: right orbital frontal cortex, left cingulate gyrus, and left superior frontal gyrus. No significant associations were observed between BE and regional white matter volume. Significant sex differences were found only in the relationship between BE and GMV in the left fusiform. Furthermore, the GMV- and rsFC-based predictive models (a machine-learning method) achieved significant correlations between the actual and predicted BE values, demonstrating the robustness of our findings. CONCLUSION: The present study provides novel evidence for the brain structural and functional substrates of children's BE, and further reveals that the weakened communication between core regions associated with negative affectivity, reward responsivity, and executive function is strongly related to dysregulated eating. LEVEL OF EVIDENCE: Level V, descriptive study.

Orbitofrontal neural dissociation of healthy and unhealthy food reward sensitivity in normal-weight binge eaters.

OBJECTIVE: The orbitofrontal cortex (OFC) has been repeatedly found to play an important role in food reward processing and binge eating (BE) episodes. However, most studies have focused mainly on reward-related neural alterations in clinical binge eating patients, with little consideration of preclinical individuals with BE that are more likely to develop from non-clinical individuals to clinical patients in the future. This study aimed to examine whether preclinical binge eaters exhibited OFC-related resting-state functional connectivity (rsFC) in the context of food reward. METHOD: Binge eaters (BE group, n = 28) and healthy controls (HCs, n = 28) matched for age and body mass index (BMI) underwent rs-fMRI scans and completed self-reported assessment of BE symptoms. Food reward sensitivity was measured using the modified food incentive delay task. Analysis of covariance was used to assess the between-group differences in the medial and lateral OFC (a priori selected regions of interest) connectivity patterns in the context of food reward, while controlling for age, sex, and BMI. RESULTS: Lower unhealthy food (UF) reward sensitivity was significantly associated with stronger inverse OFC-putamen connectivity for HCs, while the BE group showed no association between UF reward sensitivity and the OFC-putamen connectivity. Higher healthy food (HF) reward sensitivity in the BE group was significantly correlated with stronger positive OFC-middle frontal gyrus and OFC-inferior parietal gyrus connectivity, while the opposite was found for HCs. CONCLUSIONS: Binge eaters showed less functional synchrony within reward regions contributing to the UF reward sensitivity, but enhanced neural interactions between reward and inhibitory control regions correlated with the HF reward sensitivity. These novel findings may demonstrate the potential orbitofrontal neural dissociation of unhealthy and healthy food reward sensitivity in normal-weight binge eaters.

Hemodynamic responses in prefrontal cortex and personality characteristics in patients with bulimic disorders: a near-infrared spectroscopy study.

PURPOSE: This study sought to identify the prefrontal cortex hemodynamic response that is dependent on cognitive performance in patients with bulimic disorders (BD), and investigate its association with personality characteristics. METHODS: Nineteen female patients with BD and 23 healthy women were recruited. Their personality characteristics related to eating disorders were examined using a self-reporting questionnaire, namely the eating disorder inventory-2 (EDI-2). Cerebral blood flow response in the prefrontal cortex during the digit span backward task (DSBT) was measured using near-infrared spectroscopy (NIRS). Change in oxygenated hemoglobin concentration (ΔoxyHb), obtained using NIRS, were used as an index of brain activity. Further, the relationship between prefrontal cortical activity and personality characteristics was investigated in patients with BD. RESULTS: The cognitive performance of patients with BD was significantly lower in the DSBT compared with healthy subjects. There was no difference between the groups in ΔoxyHb during the task. Task scores of patients with BD correlated with asceticism and perfectionism. Moreover, the asceticism score was negatively correlated with ΔoxyHb of the bilateral prefrontal cortex in patients with BD. CONCLUSION: The results suggest that cognitive performance and brain activity induced during DSBT might be affected by asceticism in BD patients. LEVEL OF EVIDENCE: III, case-control study.

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

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.

Uncontrolled eating: a unifying heritable trait linked with obesity, overeating, personality and the brain.

Many eating-related psychological constructs have been proposed to explain obesity and overeating. However, these constructs, including food addiction, disinhibition, hedonic hunger, emotional eating, binge eating and the like all have similar definitions, emphasizing loss of control over intake. As questionnaires measuring the constructs correlate strongly (r > 0.5) with each other, we propose that these constructs should be reconsidered to be part of a single broad phenotype: uncontrolled eating. Such an approach enables reviewing and meta-analysing evidence obtained with each individual questionnaire. Here, we describe robust associations between uncontrolled eating, body mass index (BMI), food intake, personality traits and brain systems. Reviewing cross-sectional and longitudinal data, we show that uncontrolled eating is phenotypically and genetically intertwined with BMI and food intake. We also review evidence on how three psychological constructs are linked with uncontrolled eating: lower cognitive control, higher negative affect and a curvilinear association with reward sensitivity. Uncontrolled eating mediates all three constructs' associations with BMI and food intake. Finally, we review and meta-analyse brain systems possibly subserving uncontrolled eating: namely, (i) the dopamine mesolimbic circuit associated with reward sensitivity, (ii) frontal cognitive networks sustaining dietary self-control and (iii) the hypothalamus-pituitary-adrenal axis, amygdala and hippocampus supporting stress reactivity. While there are limits to the explanatory and predictive power of the uncontrolled eating phenotype, we conclude that treating different eating-related constructs as a single concept, uncontrolled eating, enables drawing robust conclusions on the relationship between food intake and BMI, psychological variables and brain structure and function.

Acute gastric dilatation after dietary violation.

Acute gastric dilatation is a rare disease for which an early diagnosis and treatment are crucial in order to avoid potential serious complications. We present the case report of a woman with acute gastric dilatation after dietary violation.

Dopamine and Opioid Neurotransmission in Behavioral Addictions: A Comparative PET Study in Pathological Gambling and Binge Eating.

Although behavioral addictions share many clinical features with drug addictions, they show strikingly large variation in their behavioral phenotypes (such as in uncontrollable gambling or eating). Neurotransmitter function in behavioral addictions is poorly understood, but has important implications in understanding its relationship with substance use disorders and underlying mechanisms of therapeutic efficacy. Here, we compare opioid and dopamine function between two behavioral addiction phenotypes: pathological gambling (PG) and binge eating disorder (BED). Thirty-nine participants (15 PG, 7 BED, and 17 controls) were scanned with [11C]carfentanil and [18F]fluorodopa positron emission tomography using a high-resolution scanner. Binding potentials relative to non-displaceable binding (BPND) for [11C]carfentanil and influx rate constant (Ki) values for [18F]fluorodopa were analyzed with region-of-interest and whole-brain voxel-by-voxel analyses. BED subjects showed widespread reductions in [11C]carfentanil BPND in multiple subcortical and cortical brain regions and in striatal [18F]fluorodopa Ki compared with controls. In PG patients, [11C]carfentanil BPND was reduced in the anterior cingulate with no differences in [18F]fluorodopa Ki compared with controls. In the nucleus accumbens, a key region involved in reward processing, [11C]Carfentanil BPND was 30-34% lower and [18F]fluorodopa Ki was 20% lower in BED compared with PG and controls (p<0.002). BED and PG are thus dissociable as a function of dopaminergic and opioidergic neurotransmission. Compared with PG, BED patients show widespread losses of mu-opioid receptor availability together with presynaptic dopaminergic defects. These findings highlight the heterogeneity underlying the subtypes of addiction and indicate differential mechanisms in the expression of pathological behaviors and responses to treatment.

[Acute gastric dilatation in a bulimic patient; systemic efects]. / Dilatación gástrica aguda en una paciente bulímica; repercusión sistémica.

OBJECTIVES: To demonstrate through a clinical case the systemic effetcss and complications that can arise after an acute gastric dilatation caused by an eating binge. CLINICAL CASE: A young woman diagnosed of bulimia nervosa presents to the emergency room after a massive food intake. She shows important abdominal distention and refers inability to self-induce vomit. A few hours later she commences to show signs of hemodynamic instability and oliguria. A CT scan is performed; it shows bilateral renal infarctions due to compression of the abdominal aorta and some of its visceral branches. INTERVENTIONS: The evaluation procedures included quantification of the gastric volume by CT. A decompression gastrostomy was performed; it allowed the evacuation of a large amount of gastric content and restored blood supply to the abdomen, which improved renal perfusion. CONCLUSIONS: CT is a basic diagnostic tool that not only allows us to quantify the degree of acute gastric dilatation but can also evaluate the integrity of the adjacent organs which may be suffering compression hypoperfusion.

Acute gastric dilatation and acute pancreatitis in a patient with an eating disorder: solving a chicken and egg situation.

A 26-year-old woman with an eating disorder presented to the emergency department with severe abdominal pain following binge eating. A plain film X-ray demonstrated a huge dilatation of the stomach with a high air-fluid level. Serum amylase was 2,265 IU/L, and serum lipase was 2,001 IU/L. Abdominopelvic computed tomography scan revealed a massive gastric dilatation and completely compressed duodenum. The distended right colonic loop and small bowel loops were reduced to the pelvic area and the displaced small bowel and mesenteries tightly pulled on the mesenteric vasculature. After nasogastric tube decompression and irrigation, her abdominal pain subsided. On the 15th day after admission, a follow-up abdominopelvic computed tomography scan demonstrated mild edematous changes of the pancreas compatible with pancreatitis.

[Assessment of cortical brain blood flood by brain perfusion spect in patients with a diagnosis of eating behavior disorders]. / Valoración del flujo cortical cerebral mediante SPECT de perfusión cerebral en pacientes con diagnóstico de trastornos de la conducta alimentaria.

OBJECTIVE: To evaluate cortical brain blood flow by 99mTc-HMPAO SPECT in patients with Eating Disorders (ED): restrictive anorexia (RA) and purgative bulimia (PB). MATERIAL AND METHOD: The study included 7 women with diagnostic criteria of RA and 12 with PB. The control group was made up of 12 healthy women. All subjects underwent brain 99mTc-HMPAO SPECT. The SPECT studies were quantified, yielding semiquantitative indexes relating to cerebellar activity in different regions. Body dissatisfaction was assessed by means of the BSQ (Body Shape Questionnaire). The results were analyzed with the ANOVA variance and had a statistical significance of p < 0.05. RESULTS: Mean BSQ scores were 98.28 (range 71-159) in the RA group, 145.05 (range 73-191) in the PB group, and 57.4 (range 37-88) in the control group. All patients in the sample (i.e., both RA and PB) showed global cerebral hypoperfusion versus the controls, although the difference only reached statistical significance in the RA group in the left parietal lobe (p = 0.02) and in the right (p = 0.004) and left temporal lobes (p = 0.015). In the PB group, the significantly hypoperfused regions were the right (p < 0.001) and left (p = 0.008) superior frontal lobe, the right inferior frontal lobe (p = 0.042), the right (p = 0.042) and left (p = 0.002) parietal lobes, and the right temporal lobe (p = 0.002). CONCLUSION: The results obtained showed that patients with ED had cerebral hypoperfusion compared with healthy subjects. This pattern is common in parietotemporal regions for both PB and AR although with temporal and parietal predominance in RA and PB, respectively. In addition, patients with PB had frontal region involvement.

Bone mineral density in bulimic women--influence of endocrine factors and previous anorexia.

OBJECTIVE: Data concerning bone mineral density (BMD) in bulimia nervosa are contradictory and include both low and normal values. The aim of the present study was to elucidate possible endocrine-and nutrition-related factors predicting BMD in bulimic women. DESIGN: Cross-sectional study. METHODS: Seventy-seven bulimic patients and 56 age- and body mass index (BMI)-matched healthy controls were examined with respect to BMD (dual energy X-ray absorptiometry) and to serum levels of hormones and metabolic factors. RESULTS: Bulimics had significantly lower spinal BMD and higher frequency of osteopenia in the total body than controls. Furthermore, bulimic women had significantly lower levels of estradiol-17beta and free thyroxine and significantly higher cortisol levels compared with controls. Among the bulimics, 31.2% had present menstrual disturbance, 51.9% had a history of amenorrhea and 23.4% had previous anorexia nervosa. Subgroups of bulimics with a history of amenorrhea and previous anorexia nervosa had significantly lower total and spinal BMD than controls, whereas those without such history did not differ from the controls. In univariate analysis, a history of amenorrhea, cortisol, testosterone, previous anorexia nervosa, and BMI showed significant associations with spinal BMD. Multiple regression analysis including all significant variables revealed previous anorexia nervosa to be the strongest determinant of spinal BMD, accounting for 34% of the variance, while associations between endocrine factors and BMI disappeared. CONCLUSIONS: Low bone mass in bulimics may be explained by previous anorexia nervosa, whereas endocrine variables related to BMD seem to be secondary determinants that are dependent on previous anorexia nervosa and BMI.

Massive gastric dilatation after a single binge in an anorectic woman.

OBJECTIVE: Massive gastric dilatation is a very serious condition that is extremely rare in patients with no history of gastrointestinal disease. Several cases have been reported in patients with eating disorders, particularly after a binge. We report here the case of a young woman who developed severe gastric dilatation after a single binge. METHODS: A computed tomographic (CT) scan of the abdomen was done and a psychiatric evaluation was performed. RESULTS: The diagnosis of acute gastric dilatation was confirmed and superior mesenteric artery syndrome was excluded. The patient responded to nasogastric drainage and bowel rest. She was also found to have situational anxiety and depressive symptoms as well as a nonspecified eating disorder. CONCLUSION: This case illustrates the serious sequel of even a single binge in any patient with abnormal dietary habits, and demonstrates the useful role of the CT scan in the diagnosis.

Altered brain serotonin 5-HT1A receptor binding after recovery from anorexia nervosa measured by positron emission tomography and [carbonyl11C]WAY-100635.

CONTEXT: Previous studies have shown that women with anorexia nervosa (AN), when ill and after recovery, have alterations of serotonin (5-HT) neuronal activity and core eating disorder symptoms, such as anxiety. OBJECTIVE: To further characterize the 5-HT system in AN, we investigated 5-HT1A receptor activity using positron emission tomography imaging because this receptor is implicated in anxiety and feeding behavior. DESIGN, SETTING, AND PARTICIPANTS: To avoid the confounding effects of malnutrition, we studied 13 women who had recovered from restricting-type AN (mean age, 23.3 +/- 5.2 years) and 12 women who had recovered from bulimia-type AN (mean age, 28.6 +/- 7.3 years) (>1 year normal weight, regular menstrual cycles, no bingeing or purging). These subjects were compared with 18 healthy control women (mean age, 25.1 +/- 5.8 years). Intervention The 5-HT1A receptor binding was measured using positron emission tomography imaging and a specific 5-HT1A receptor antagonist, [carbonyl-11C]WAY-100635. MAIN OUTCOME MEASURE: Specific 5-HT1A receptor binding was assessed using the binding potential measure. Binding potential values were derived using both the Logan graphical method and compartmental modeling. The binding potential in a region of interest was calculated with the formula: binding potential = distribution volume of the region of interest minus distribution volume of the cerebellum. RESULTS: Women recovered from bulimia-type AN had significantly (P<.05) increased [11C]WAY-100635 binding potential in cingulate, lateral and mesial temporal, lateral and medial orbital frontal, parietal, and prefrontal cortical regions and in the dorsal raphe compared with control women. No differences were found for women recovered from restricting-type AN relative to controls. For women recovered from restricting-type AN, the 5-HT1A postsynaptic receptor binding in mesial temporal and subgenual cingulate regions was positively correlated with harm avoidance. CONCLUSIONS: We observed increased 5-HT1A receptor binding in women who had recovered from bulimia-type AN but not restricting-type AN. However, 5-HT1A receptor binding was associated with a measure of anxiety in women recovered from restricting-type AN. These data add to a growing body of evidence showing that altered serotonergic function and anxiety symptoms persist after recovery from AN. These psychobiological alterations may be trait related and may contribute to the pathogenesis of AN.

Regional mu-opioid receptor binding in insular cortex is decreased in bulimia nervosa and correlates inversely with fasting behavior.

UNLABELLED: The endogenous opioid system of the brain has been implicated in feeding behavior. Abnormal repeated activation of this system may constitute a neural substrate for the compulsive eating behavior observed in bulimia nervosa. This study examined the binding potential of the brain mu-opioid receptor (mu-OR) in bulimia nervosa. METHODS: Eight women with bulimia nervosa and 8 female controls underwent brain MRI followed by (11)C-carfentanil PET. Voxel-based methods were used to assess group differences in mu-OR binding between controls and bulimic subjects and to correlate mu-OR binding with the frequency of recent self-reported abnormal eating behaviors in bulimic subjects. RESULTS: mu-OR binding in the left insular cortex was less in bulimic subjects than in controls and correlated negatively with recent fasting behavior. CONCLUSION: Changes in mu-OR binding in the insula may be important in the pathogenesis or maintenance of the self-perpetuating behavioral cycle of bulimic subjects because the insula is the primary gustatory cortex and has repeatedly been implicated in the processing of the reward value of food.

Comparison of cortical 5-HT2A receptor binding in bulimia nervosa patients and healthy volunteers.

OBJECTIVE: Bulimia nervosa has been associated with alterations in central serotonergic (5-HT) function. This study investigated iodine-labeled 4-amino-N-[1-[3-(4-fluorophenoxy) propyl]-4-methyl-4-piperidinyl]-5-iodo-2-methoxybenzamide ((123)I-5-I-R91150) binding to the 5-HT(2A) receptor in the brain by using single photon emission computed tomography in acutely ill bulimia nervosa patients. METHOD: Cortical (123)I-5-I-R91150 binding in 10 normal-weight patients with bulimia nervosa, purging type, was compared with that of 11 healthy volunteers. RESULTS: The 5-HT(2A) binding index of the bulimia nervosa patients, with and without correction for age, was not significantly different from that of the comparison group. CONCLUSIONS: As a group, acutely ill bulimia nervosa patients cannot be discriminated from healthy subjects on the basis of cortical (123)I-5-I-R91150 binding to the 5-HT(2A) receptor.

Altered 5-HT(2A) receptor binding after recovery from bulimia-type anorexia nervosa: relationships to harm avoidance and drive for thinness.

Several lines of evidence suggest that a disturbance of serotonin neuronal pathways may contribute to the pathogenesis of anorexia nervosa (AN) and bulimia nervosa (BN). This study applied positron emission tomography (PET) to investigate the brain serotonin 2A (5-HT(2A)) receptor, which could contribute to disturbances of appetite and behavior in AN and BN. To avoid the confounding effects of malnutrition, we studied 10 women recovered from bulimia-type AN (REC AN-BN, > 1 year normal weight, regular menstrual cycles, no binging, or purging) compared with 16 healthy control women (CW) using PET imaging and a specific 5-HT(2A) receptor antagonist, [18F]altanserin. REC AN-BN women had significantly reduced [18F]altanserin binding potential relative to CW in the left subgenual cingulate, the left parietal cortex, and the right occipital cortex. [18F]altanserin binding potential was positively related to harm avoidance and negatively related to novelty seeking in cingulate and temporal regions only in REC AN-BN subjects. In addition, REC AN-BN had negative relationships between [18F]altanserin binding potential and drive for thinness in several cortical regions. In conclusion, this study extends research suggesting that altered 5-HT neuronal system activity persists after recovery from bulimia-type AN, particularly in subgenual cingulate regions. Altered 5-HT neurotransmission after recovery also supports the possibility that this may be a trait-related disturbance that contributes to the pathophysiology of eating disorders. It is possible that subgenual cingulate findings are not specific for AN-BN, but may be related to the high incidence of lifetime major depressive disorder diagnosis in these subjects.

Gastric electric activity assessed by electrogastrography and gastric emptying scintigraphy in adolescents with eating disorders.

BACKGROUND: Patients with eating disorders can refer to a variety of gastrointestinal symptoms, sometimes to justify reduced food intake and vomiting. The authors investigated whether adolescent patients with eating disorders and dyspeptic symptoms have altered gastric electric activity and abnormal gastric emptying as assessed respectively by electrogastrography and scintigraphy. METHODS: Twenty-eight patients (18 with anorexia and 10 with bulimia) and 16 healthy volunteers underwent electrogastrography; 20 of the 28 patients (14 with anorexia and 6 with bulimia) underwent gastric emptying scintigraphy. Electrogastrography with bipolar recording lasted 1 hour, 30 minutes before and after a standard meal. Before gastric emptying scintigraphy, patients fasted overnight; during testing, they ingested a solid meal labeled with technetium-99m sulfur colloid. The ratio of fasting to postprandial electrogastrographic variables was evaluated using the Wilcoxon matched-pair test. The Mann- Whitney test was used to compare absolute values for electrogastrographic data in each group. The Student paired t test was used to compare scintigraphic results expressed as percentage of gastric emptying at 60 minutes and as the gastric emptying time (T(1/2)). RESULTS: Patients with bulimia significantly differed from those with anorexia and control subjects regarding the amount of normal gastric electric activity and bradygastria, and from patients with anorexia only regarding tachygastria. These electrogastrographic variables did not differ significantly between patients with anorexia and control subjects. Gastric emptying time (T(1/2)) was significantly longer in patients with bulimia than in those with anorexia. CONCLUSIONS: Adolescent patients with bulimia who complain of dyspeptic symptoms have documentable abnormalities of gastric electric activity and emptying, whereas their counterparts with anorexia, probably owing to their shorter disease duration, do not.

Treatment improves serotonin transporter binding and reduces binge eating.

RATIONALE: Serotonin (5-HT) is involved in the control of eating behaviour by inhibiting food intake. Obese women with binge-eating disorder (OB-BED) were recently found to have reduced 5-HT transporter binding. OBJECTIVES: The aim of this study was to investigate the effect of a successful treatment on 5-HT transporters in OB-BED. METHODS: The 5-HT transporter binding of seven OB-BED was measured by single-photon emission computed tomography (SPECT), by using iodine-123-labelled nor-beta-CIT as a tracer, before treatment and after successful treatment, when the OB-BED were asymptomatic. Treatment consisted of group psychotherapy and fluoxetine medication. The control subjects, six obese women without eating disorders, were also studied twice by using SPECT. RESULTS: The 5-HT transporter binding of the symptomatically recovered OB-BED increased significantly (24+/-22%) after treatment, whereas in the control group, binding remained unchanged. CONCLUSIONS: The results tentatively suggest that 5-HT transporter binding in OB-BED is an adaptive mechanism, which can be affected by treatment. Furthermore, there seems to be a link between improved 5-HT transporter binding and reduced binge eating.