Orexigenic/anorexigenic signals in bulimia nervosa

Bulimia nervosa (BN) and Anorexia Nervosa (AN) are currently classified as eating disorders (ED). Both disorders are the product of complex interaction between physiological and psychological and social processes; they are characterized by abnormal eating behavior. However, patients with BN differ from AN in their nutritional state and response of treatment with serotonin-selective reuptake inhibitor (SSRI) as well as frequency of comorbidity of mood and anxiety disorders. Although biological mechanisms of both BN and AN are largely unknown, excess of both feeding-stimulatory and feeding inhibitory signaling in AN have been indicated. This report reviews data that point to the hypothesis that dysregulation of monoaminergic and new peptidergic circuitry controlling food intake and energy expenditure play a major role in the eating behavior of BN.     

Anorexia nervosa and bulimia nervosa.

No definitive therapy exists for anorexia nervosa (AN) or bulimia nervosa (BN). Nevertheless, biologic and psychologic research into these disorders has increased over the last decade. We examine the various drugs available for treatment. Advances in pharmacotherapy for AN have been modest and have reflected efforts either to stimulate hunger and weight gain or to control complications of the starvation process. Food remains the "drug" of choice. Antidepressants have been found to be beneficial in the treatment of BN. The meaning of this in the context of a relation between BN and mood disorders remains unclear, since coexistent depression does not predict a positive response to these drugs. Pharmacotherapy represents a single but important dimension of the management of patients with eating disorders. The optimal integration of drug therapy and psychotherapy and the identification of predictors of a positive response to drugs have yet to be addressed by clinical research.     

The role of leptin and orexins in the dysfunction of hypothalamo-pituitary-gonadal regulation and in the mechanism of hyperactivity in patients with anorexia nervosa

Anorexia nervosa (AN) belongs to a group of eating disorders and is characterized by extreme body weight loss. AN patients show combination of physical, psychological and behavioral disturbances. Neuropeptides partly control energy homeostasis and modulate hormone release. Leptin, a peptide secreted by adipocytes, may influence the interactions between central and peripheral signals. Hypoleptinaemia found in AN is connected with disturbed control of appetite and hormonal dysfunction as well as has implications for the hypothalamo-pituitary-gonadal axis, bone mineral density and physical hyperactivity. Low leptin levels are increased with refeeding. However, the prolonged hypoleptinaemia in weight recovered AN patients may result in persistent hypothalamic amenorrhoea. The hyperactivity has been observed in 31-80 % of AN cases. The mechanisms underlying the hyperactivity found in patients with anorexia nervosa seem to be more complicated as many factors including neuropeptides may be involved. Orexins may affect not only appetite but also behavior and psychophysical activity as they may regulate reproductive and stress hormone secretion, stimulate a variety of stereotypic behaviors including eating and stress reaction, and affect the hypothalamo-pituitary-adrenal (HPA) axis, alter glucocorticoid and catecholamine secretion and activate the sympathetic nervous system. Orexins influence the mechanism regulating arousal and sleep, cardiovascular function, temperature, metabolic rate and locomotive activity. It is worth considering how abnormal activity of hypothalamic neuropeptides or their receptors may play a role in the mechanisms of hyperactivity, disturbed control of appetite and hormonal dysfunction in patients with anorexia nervosa.     

Changes of plasma obestatin, ghrelin and NPY in anorexia and bulimia nervosa patients before and after a high-carbohydrate breakfast

Peptides ghrelin, obestatin and neuropeptide Y (NPY) play an important role in regulation of energy homeostasis, the imbalance of which is associated with eating disorders anorexia (AN) and bulimia nervosa (BN). The changes in ghrelin, obestatin and NPY plasma levels were investigated in AN and BN patients after administration of a high-carbohydrate breakfast (1604 kJ). Eight AN women (aged 25.4+/-1.9, BMI: 15.8+/-0.5), thirteen BN women (aged 22.0+/-1.05, BMI: 20.1+/-0.41) and eleven healthy women (aged 25.1+/-1.16, BMI: 20.9+/-0.40) were recruited for the study. We demonstrated increased fasting ghrelin in AN, but not in BN patients, while fasting obestatin and NPY were increased in both AN and BN patients compared to the controls. Administration of high-carbohydrate breakfast induced a similar relative decrease in ghrelin and obestatin plasma levels in all groups, while NPY remained increased in postprandial period in both patient groups. Ghrelin/obestatin ratio was lower in AN and BN compared to the controls. In conclusions, increased plasma levels of fasting NPY and its unchanged levels after breakfast indicate that NPY is an important marker of eating disorders AN and BN. Different fasting ghrelin and obestatin levels in AN and BN could demonstrate their diverse functions in appetite and eating suppression.     

Possible involvement of brain-derived neurotrophic factor in eating disorders

Eating disorders (EDs) manifest as abnormal patterns of eating behavior and weight regulation driven by low self-esteem due to weight preoccupation and perceptions toward body weight and shape. Two major groups of such disorders are anorexia nervosa (AN) and bulimia nervosa (BN). The etiology of EDs is complex and evidence indicates that both biological/genetic and psychosocial factors are involved. Several lines of evidence indicate that brain-derived neurotrophic factor (BDNF) plays a critical role in regulating eating behaviors and cognitive impairments in the EDs. BDNF is involved in neuronal proliferation, differentiation, and survival during development. BDNF and its tyrosine kinase receptor (TrkB) are expressed in hypothalamic nuclei associated with eating behaviors. A series of studies using BDNF knockout mice and the human BDNF gene indicate an association of BDNF and EDs with predisposition and vulnerability. In the previous studies, serum BDNF levels in subjects with EDs are reduced significantly compared with healthy controls, hence, we proposed that levels of serum BDNF would be a useful diagnostic indicator for EDs.     

Ghrelin concentrations and cardiac vagal tone are decreased after pharmacologic and cognitive-behavioral treatment in patients with bulimia nervosa

Patients with bulimia nervosa (BN) have bulimic and depressive symptoms, which have been associated with abnormalities in the neuroendocrine and vagal systems. Subjects included twenty-four female drug-free outpatients with BN that were selected from patients seeking treatment for eating behavior in our hospital along with twenty-five age-matched healthy females who served as controls. We investigated ghrelin and leptin levels, cardiac vagal tone and sympathovagal balance, frequency of sets of binge-eating and vomiting episodes per week and the Profile of Mood States (POMS) depression scale in BN before and after a 16-week administration of the serotonin selective reuptake inhibitor (SSRI) paroxetine combined with cognitive-behavioral therapy. Compared to controls, the BN group had higher ghrelin levels and resting cardiac vagal tone, and lower leptin levels and resting cardiac sympathovagal balance before treatment, although there was a significant difference between the two groups for the body mass index (BMI). The elevated ghrelin levels (301.7 +/- 18.9 pmol/l, mean +/- SEM vs. 202.8 +/- 15.6 pmol/l, P < 0.01), cardiac vagal tone (2246.4 +/- 335.5 ms(2) vs. 1128.5 +/- 193.3 ms(2), P < 0.01), frequency of sets of binge-eating and purging episodes and T scores for the POMS depression scale were all significantly decreased after treatment despite similar BMI, percent body fat and leptin levels. In close association with cardiac vagal function and ghrelin recoveries, abnormal eating behavior and depressive symptoms improved, indicating the usefulness of these indexes in the assessment of clinical condition and therapeutic efficacy in BN.     

Characteristics of suicide attempts in anorexia and bulimia nervosa: a case-control study

Objective

Compared to other eating disorders, anorexia nervosa (AN) has the highest rates of completed suicide whereas suicide attempt rates are similar or lower than in bulimia nervosa (BN). Attempted suicide is a key predictor of suicide, thus this mismatch is intriguing. We sought to explore whether the clinical characteristics of suicidal acts differ between suicide attempters with AN, BN or without an eating disorders (ED).

Method

Case-control study in a cohort of suicide attempters (n = 1563). Forty-four patients with AN and 71 with BN were compared with 235 non-ED attempters matched for sex, age and education, using interview measures of suicidal intent and severity.

Results

AN patients were more likely to have made a serious attempt (OR = 3.4, 95% CI 1.4–7.9), with a higher expectation of dying (OR = 3.7,95% CI 1.1–13.5), and an increased risk of severity (OR = 3.4,95% CI 1.2–9.6). BN patients did not differ from the control group. Clinical markers of the severity of ED were associated with the seriousness of the attempt.

Conclusion

There are distinct features of suicide attempts in AN. This may explain the higher suicide rates in AN. Higher completed suicide rates in AN may be partially explained by AN patients'' higher desire to die and their more severe and lethal attempts.     

神经性厌食99mTc-ECD局部脑血流变化初探

神经性厌食(Anorexia Nervosa,AN)是一种病因未明的心理行为综合症,社会文化及生物学因素间的交互作用被认为是该病的病因,脑成像体现出一些病理相关改变,但国内尚未见针对此病的成像报道。为给临床辅助诊断AN提供依据,采用经济、易获得的脑功能显像技术——单光子发射计算机断层显像(Single Photon Emission Computed Tomography,SPECT),扫描3位典型青年女性AN患者的大脑。通过统计参数图(Statistical Parametric Mapping,SPM2),基于体素的局部脑血流灌注分析,与25名正常青年女性脑图相比较发现,患者的前扣带和前额内侧、双侧额叶背外侧、后顶叶、颞叶中上部和小脑血流灌注降低,下丘脑、双侧颞叶中下部血流灌注增高,可能与神经递质回路有关,提示社会学因素可能只是该病的诱因,而生物学人格易感性才是该病的主要原因,同时说明SPECT脑血流成像有助于AN的临床辅助诊断。     

Integrated circuits and molecular components for stress and feeding: implications for eating disorders

Eating disorders are complex brain disorders that afflict millions of individuals worldwide. The etiology of these diseases is not fully understood, but a growing body of literature suggests that stress and anxiety may play a critical role in their development. As our understanding of the genetic and environmental factors that contribute to disease in clinical populations like anorexia nervosa, bulimia nervosa and binge eating disorder continue to grow, neuroscientists are using animal models to understand the neurobiology of stress and feeding. We hypothesize that eating disorder clinical phenotypes may result from stress‐induced maladaptive alterations in neural circuits that regulate feeding, and that these circuits can be neurochemically isolated using animal model of eating disorders.     

Differential neural responses to food images in women with bulimia versus anorexia nervosa

Background

Previous fMRI studies show that women with eating disorders (ED) have differential neural activation to viewing food images. However, despite clinical differences in their responses to food, differential neural activation to thinking about eating food, between women with anorexia nervosa (AN) and bulimia nervosa (BN) is not known.

Methods

We compare 50 women (8 with BN, 18 with AN and 24 age-matched healthy controls [HC]) while they view food images during functional Magnetic Resonance Imaging (fMRI).

Results

In response to food (vs non-food) images, women with BN showed greater neural activation in the visual cortex, right dorsolateral prefrontal cortex, right insular cortex and precentral gyrus, women with AN showed greater activation in the right dorsolateral prefrontal cortex, cerebellum and right precuneus. HC women activated the cerebellum, right insular cortex, right medial temporal lobe and left caudate. Direct comparisons revealed that compared to HC, the BN group showed relative deactivation in the bilateral superior temporal gyrus/insula, and visual cortex, and compared to AN had relative deactivation in the parietal lobe and dorsal posterior cingulate cortex, but greater activation in the caudate, superior temporal gyrus, right insula and supplementary motor area.

Conclusions

Women with AN and BN activate top-down cognitive control in response to food images, yet women with BN have increased activation in reward and somatosensory regions, which might impinge on cognitive control over food consumption and binge eating.     

Selective Visual Attention during Mirror Exposure in Anorexia and Bulimia Nervosa

Objective

Cognitive theories suggest that body dissatisfaction results from the activation of maladaptive appearance schemata, which guide mental processes such as selective attention to shape and weight-related information. In line with this, the present study hypothesized that patients with anorexia nervosa (AN) and bulimia nervosa (BN) are characterized by increased visual attention for the most dissatisfying/ugly body part compared to their most satisfying/beautiful body part, while a more balanced viewing pattern was expected for controls without eating disorders (CG).

Method

Eye movements were recorded in a group of patients with AN (n = 16), BN (n = 16) and a CG (n = 16) in an ecologically valid setting, i.e., during a 3-min mirror exposure.

Results

Evidence was found that patients with AN and BN display longer and more frequent gazes towards the most dissatisfying relative to the most satisfying and towards their most ugly compared to their most beautiful body parts, whereas the CG showed a more balanced gaze pattern.

Discussion

The results converge with theoretical models that emphasize the role of information processing in the maintenance of body dissatisfaction. Given the etiological importance of body dissatisfaction in the development of eating disorders, future studies should focus on the modification of the reported patterns.     

Altered brain-derived neurotrophic factor blood levels and gene variability are associated with anorexia and bulimia

Murine models and association studies in eating disorder (ED) patients have shown a role for the brain-derived neurotrophic factor (BDNF) in eating behavior. Some studies have shown association of BDNF -270C/T single-nucleotide polymorphism (SNP) with bulimia nervosa (BN), while BDNF Val66Met variant has been shown to be associated with both BN and anorexia nervosa (AN). To further test the role of this neurotrophin in humans, we screened 36 SNPs in the BDNF gene and tested for their association with ED and plasma BDNF levels as a quantitative trait. We performed a family-based association study in 106 ED nuclear families and analyzed BDNF blood levels in 110 ED patients and in 50 sib pairs discordant for ED. The rs7124442T/rs11030102C/rs11030119G haplotype was found associated with high BDNF levels (mean BDNF TCG haplotype carriers = 43.6 ng/ml vs. mean others 23.0 ng/ml, P = 0.016) and BN (Z = 2.64; P recessive = 0.008), and the rs7934165A/270T haplotype was associated with AN (Z =-2.64; P additive = 0.008). The comparison of BDNF levels in 50 ED discordant sib pairs showed elevated plasma BDNF levels for the ED group (mean controls = 41.0 vs. mean ED = 52.7; P = 0.004). Our data strongly suggest that altered BDNF levels modulated by BDNF gene variability are associated with the susceptibility to ED, providing physiological evidence that BDNF plays a role in the development of AN and BN, and strongly arguing for its involvement in eating behavior and body weight regulation.     

Binge Eating Behavior in Patients with Eating Disorders

The purpose of this study was to determine whether the objectively observed binge eating behavior of obese subjects meeting the proposed DSM-IV criteria for binge eating disorder would be similar to that observed in patients with bulimia nervosa. Non-obese patients with bulimia nervosa (BN), obese subjects with binge eating disorder (BED), obese and non-obese women without eating disorders were each instructed to binge eat single- and multiple-item meals. In the multiple-item meal, the obese subjects with BED ate significantly more (1515 kcal) than obese subjects without BED (1115 kcal), but they ate less than the normal-weight bulimic patients (2680 kcal). The non-obese controls ate amounts similar to the obese non-binge-eating-disordered group (1093 and 1115.2 kcal, respectively). In the single-item meal, consisting of ice cream, patients with BN ate significantly more than any other group (1307 kcal), while obese subjects with or without binge-eating disorder ate significantly more (762 kcal) than non-obese controls (308 kcal). This study has demonstrated that although both BN and BED are characterized by recurrent episodes of binge eating, quantitatively there appear to be differences between the eating disturbances in the two disorders. Because single- and multiple-item meals differ in external cues, these results also suggest that the obese subjects with BED may be disinhibited by external cues, while obese subjects without BED may be inhibited by external cues.     

Association of CNR1 and FAAH endocannabinoid gene polymorphisms with anorexia nervosa and bulimia nervosa: evidence for synergistic effects

Endocannabinoids modulate eating behavior; hence, endocannabinoid genes may contribute to the biological vulnerability to eating disorders. The rs1049353 (1359 G/A) single nucleotide polymorphism (SNP) of the gene coding the endocannabinoid CB1 receptor ( CNR1 ) and the rs324420 (cDNA 385C to A) SNP of the gene coding fatty acid amide hydrolase (FAAH), the major degrading enzyme of endocannabinoids, have been suggested to have functional effects on mature proteins. Therefore, we explored the possibility that those SNPs were associated to anorexia nervosa and/or bulimia nervosa. The distributions of the CNR1 1359 G/A SNP and of the FAAH cDNA 385C to A SNP were investigated in 134 patients with anorexia nervosa, 180 patients with bulimia nervosa and 148 normal weight healthy controls. Additive effects of the two SNPs in the genetic susceptibility to anorexia nervosa and bulimia nervosa were also tested. As compared to healthy controls, anorexic and bulimic patients showed significantly higher frequencies of the AG genotype and the A allele of the CNR1 1359 G/A SNP. Similarly, the AC genotype and the A allele of the FAAH cDNA 385C to A SNP were significantly more frequent in anorexic and bulimic individuals. A synergistic effect of the two SNPs was evident in anorexia nervosa but not in bulimia nervosa. Present findings show for the first time that the CNR1 1359 G/A SNP and the FAAH cDNA 385C to A SNP are significantly associated to anorexia nervosa and bulimia nervosa, and demonstrate a synergistic effect of the two SNPs in anorexia nervosa.     

Not Your “Typical Island Woman”: Anorexia Nervosa is Reported Only in Subcultures in Curaçao

Anorexia nervosa (AN), once thought to be a problem of wealthier, Western countries has now been documented in survey studies and case reports across geographic and economic groups; however, few epidemiological studies including interview have been done on these populations. We report on a comprehensive study on Curaçao, a Caribbean island in economic transition, where the majority of the population is of predominantly black African origin. As part of an epidemiological study on the island of Curaçao indigenous cases of AN were identified. Participants were interviewed and asked to complete standardized measures of eating behaviors and cultural attitudes. In addition, matched controls completed the same measures and were seen in a focus group to assess their knowledge of eating disorders and perceived current and future challenges to young Curaçao women. Six of the nine indigenous cases of AN were successfully traced; all were of mixed race. No cases of anorexia were found among the majority black population. The women with AN were from the high-education and high-income sectors of the society and the majority had spent time overseas. The women with a history of anorexia reported higher levels of perfectionism and anxiety than the matched controls. All of the women reported challenges to maintaining an active professional and personal life and viewed themselves as different from the norm. Women who presented with AN evidenced vulnerability to a triple threat to identity formation: (1) they were of mixed race, aspiring to fit into the mobile elite (and mostly white) subgroup while distancing themselves from the black majority; (2) they had the means for education and travel that left them caught between modern and traditional constructs of femininity; and (3) they had lived overseas, and therefore struggled upon reentry with the frustrations of what was possible within the island culture. The race, class and overseas exposures of the women with anorexia were anything but typical on the island. Cases of anorexia in other developing countries may similarly be limited to specific subgroups, which require specialized treatment and planning efforts.     

Plasma intact fibroblast growth factor 23 levels in women with bulimia nervosa: A cross-sectional pilot study

Fibroblast growth factor (FGF) 23, a circulating 26-kDa peptide produced by osteogenic cells, is a novel phosphaturic factor. In our previous study, binge-eating/purging type anorexia nervosa (AN-BP) patients had elevated plasma intact FGF23 (iFGF23) levels, while restricting type (AN-R) patients had plasma iFGF23 levels similar to healthy controls. Although bulimia nervosa (BN) patients as well as some patients with AN-BP regularly engage in binge eating, there have been no studies regarding plasma iFGF23 levels in BN patients. Therefore, this study was performed to determine plasma iFGF23 concentrations in BN patients and healthy controls. The study population consisted of 13 female BN patients and 11 healthy female controls. Blood samples were collected from all subjects after overnight fasting. Plasma iFGF23 was measured using an ELISA kit in a cross-sectional manner. The two-tailed Mann-Whitney U-test was used to assess differences between BN patients and healthy controls. In addition, BN patients were divided into two groups based on questionnaire-reported binge eating frequency immediately prior to participation in this study: high frequency of binge eating (once a week or more; HF group; n = 8) and low frequency of binge eating (less than once a week; LF group; n = 5). Two-tailed Mann-Whitney U-test with Bonferroni's correction was performed after the Kruskal-Wallis test to assess differences between HF group, LF group, and healthy controls. Median (quartiles) plasma iFGF23 levels were greater in BN patients (35.5 [14.8-65.0] pg/ml) than in controls (3.8 [not detected-5.3] pg/ml; p = 0.002). In addition, median (quartiles) plasma iFGF23 levels were greater in the HF group (62.3 [44.4-73.4] pg/ml) than in controls (p < 0.001) and in the LF group (12.9 [not detected-30.3] pg/ml; p = 0.011), while there were no differences between the LF group and controls (p = 0.441). This is the first study to show that BN patients have elevated plasma iFGF23 levels. Moreover, this study showed that BN patients with a high frequency of binge eating have elevated plasma iFGF23 levels, while iFGF23 levels are similar to healthy controls in those with a low frequency of binge eating. Plasma iFGF23 level may be a suitable indicator of binge eating in BN patients.     

Cholecystokinin, vasoactive intestinal peptide and peptide histidine methionine responses to feeding in anorexia nervosa.

Anorexia nervosa (AN) is a syndrome of unknown cause characterized by voluntary starvation. Cholecystokinin has been implicated as a neuroendocrine regulatory factor in control of satiety. Relatively little information is known about gastrointestinal hormone responses to feeding in subjects with anorexia nervosa. In the present studies, we examine fasting and postprandial levels of cholecystokinin (CCK), vasoactive intestinal peptide (VIP) and peptide histidine methionine (PHM) in anorexia nervosa subjects and in control individuals. Results of these studies indicate that plasma CCK response to a liquid meal (Ensure Plus) in untreated AN subjects was distinctly different from that observed in healthy controls, both in terms of temporal pattern of peptide released and the amount of CCK secreted into the circulation. Peak levels of CCK release occurred at 30 min following meal ingestion in AN patients and at 60 min in control subjects. Integrated CCK release in untreated AN patients was approximately twice that measured in control individuals. Renutrition therapy was associated with reversion of the pattern of CCK release to that observed in control subjects. Plasma VIP levels were unchanged following meal ingestion in both control and anorexic subjects. In contrast, PHM levels in AN subjects were significantly greater than that observed in control individuals. The pattern of PHM release following liquid meal ingestion was similar to that observed with plasma CCK; namely, peak release of peptide was observed at 30 min which was significantly greater than corresponding control values (P less than 0.05). In conclusion, these results demonstrate distinctive differences in plasma CCK and PHM levels in response to feeding in AN subjects when compared to control individuals. These findings suggest that the earlier and greater rise in plasma CCK levels in AN subjects following meal ingestion may contribute to the abnormal sensation of satiety in this condition.     

Effect of management of patients with Anorexia and Bulimia nervosa on symptoms and impulsive behavior

The aim of the study was to provide further and up to date information on the evaluation of the management of Anorexia and Bulimia nervosa at the Eating Disorders Unit (EDU) of the Ljubljana Psychiatric Clinic, based upon detailed assessment of the eating disorders specific and non specific symptoms of impulsive behaviors, highly correlated with these entities. 34 female patients with anorexia (restrictive or purgative type) and 38 female patients with Bulimia nervosa (purgative or non-purgative type) undergoing hospital treatment at the EDU were evaluated upon admission, as well as upon discharge and three and six months after discharge, using the Eating Disorder Questionnaire. Upon discharge a marked decrease in the overall symptoms was noted. The differences in symptoms incidences between the two groups were significantly specific for the individual form of eating disorder, especially upon admission, and were more pronounced in anorexia group. In later measurements, performed during the period of three and six months after discharge, a mild trend of increase in the disorder specific symptoms was detected in both groups, but was not statistically significant. In addition to binging on food, striking, quarreling and spending sprees are characteristics of patients with eating disorders, which in particular apply to the Bulimia nervosa group. Apart from the disorder specific symptoms, impulsive behavior was also reduced during study period, while the difference in its occurrence between the two groups gradually became non-significant. The management of patients with eating disorders at the EDU was successful in both groups, confirmed by an intense reduction of the disorder specific symptoms, impulsive behavior and increased stability recorded three and six months after discharge. The study strongly suggests that the effect of treatment regime for eating disorders can be predicted by careful assessment of the relevant symptoms and impulsive behavioral patterns.     

Poor cognitive flexibility in eating disorders: examining the evidence using the Wisconsin Card Sorting Task

Background

People with eating disorders (ED) frequently present with inflexible behaviours, including eating related issues which contribute to the maintenance of the illness. Small scale studies point to difficulties with cognitive set-shifting as a basis. Using larger scale studies will lend robustness to these data.

Methodology/Principal Findings

542 participants were included in the dataset as follows: Anorexia Nervosa (AN) n = 171; Bulimia Nervosa (BN) n = 82; Recovered AN n = 90; Healthy controls (HC): n = 199. All completed the Wisconsin Card Sorting Task (WCST), an assessment that integrates multiple measurement of several executive processes concerned with problem solving and cognitive flexibility. The AN and BN groups performed poorly in most domains of the WCST. Recovered AN participants showed a better performance than currently ill participants; however, the number of preservative errors was higher than for HC participants.

Conclusions/Significance

There is a growing interest in the diagnostic and treatment implications of cognitive flexibility in eating disorders. This large dataset supports previous smaller scale studies and a systematic review which indicate poor cognitive flexibility in people with ED.