Esophageal motility and symptoms in restricting and binge-eating/purging anorexia

Background

Esophageal symptoms are common in anorexia nervosa, but it is not known whether they are associated with motility disorders, with different forms of the disease, and whether they respond to nutritional rehabilitation.

Methods

To clarify these points, 23 patients with anorexia nervosa (12 binge-eating/purging, “purgers”; 11 restricting type, “restricters”) were studied by esophageal manometry before and after 22 weeks rehabilitation. Manometric parameters of 35 age and sex-matched patients were used as controls. Patients with anorexia also filled questionnaires on eating disorder psychopathology, psychopathological distress and esophageal, gastric and colonic symptoms before and after 4 and 22 weeks of a rehabilitation program.

Results

Symptoms were more severe in patients than in controls. Gastric and colonic, but not esophageal symptoms improved with treatment. LES basal pressure was higher in restricters (restricters 32.1 ± 4.6; purgers 14.9 ± 2.2; controls 17.1 ± 1.1 mm Hg, p < 0.005), but still within normal range; this difference disappeared after treatment. Postdeglutitive body waves were normally propagated. Their amplitude was significantly higher in anorexia than in controls. No correlation was found between results of psychopathological tests (improved after treatment), esophageal symptoms and manometry.

Conclusions

In anorexia, esophageal symptoms are frequent and severe. They are not adequately explained by psychological or manometric derangements.     

认知行为疗法联合帕罗西汀治疗神经性厌食的应用

目的：评价联合应用认知行为疗法和帕罗西汀治疗神经性厌食（AN）患者的疗效。方法：将符合CCMD-3诊断标准的45例AN患者给予认知行为疗法联合帕罗西汀口服,分别于治疗前、治疗4周后各进行一次症状自评量表（SCL-90）测定。结果：SCL-90测验结果显示,治疗前后各因子变化经统计学处理均有显著意义,其中以焦虑、抑郁、人际关系和强迫因子尤为显著。结论：认知行为疗法联合帕罗西汀药物治疗AN患者效果显著,值得临床心理治疗中推广应用。     

Relationship between malnutrition and depression or anxiety in Anorexia Nervosa: a critical review of the literature

Background

Depression, anxiety and obsessive-compulsive disorder (OCD) frequently co-occur with Anorexia Nervosa (AN). Clinical consensus admits that depressive symptoms and anxiety are the sequelae of malnutrition in AN. This review presents a critical assessment of the literature that looked into the link between depression/anxiety symptoms in relation to malnutrition and their improvement throughout the treatment.

Methods

We performed a systematic search of literature in Medline and PsychInfo for all the studies done to investigate psychological factors in relation to malnutrition in AN using the keywords “Anorexia Nervosa”, “depression”, “anxiety”, “obsessive-compulsive disorder” and “malnutrition”. Only articles published between 1980 and 2010 in English or French were reviewed. From the articles on AN and depression, anxiety, and/or OCD, only the ones which investigated on the relation with malnutrition were kept. This search was complemented by a manual search. We also checked the reference lists of the articles we found.

Results

Seven papers were analyzed and critically reviewed for their methods and results. Results are contradictory and inconsistent at all levels of assessment.

Conclusions

Evidence based data is very rare. From the 7 reviewed studies, none of them draw the same conclusion. This is mainly due to the large differences in the samples' populations and the studies' protocols. Future studies are needed to focus on the relationship between depression/anxiety symptoms and malnutrition. A more critical nutritional assessment should be undertaken with multiple psychological assessment scales.     

Changes in salivary cortisol levels as a prognostic predictor in children with anorexia nervosa

This study investigated the hypothalamus-pituitary-adrenal (HPA) axis activity in children with anorexia nervosa (AN) before and after inpatient treatment. Salivary cortisol levels were measured to ascertain whether changes in the HPA axis activity following therapeutic intervention could be applicable as a prognostic predictor. This study comprised 21 females with AN and 22 control subjects. Saliva was collected at 2-hour intervals from 9 a.m. to 7 p.m. before and after inpatient treatment. The concentrations for areas under the curve (AUC) were compared with physical parameters, eating attitude score, profile of mood states (POMS), and prognostic factors. Mean salivary cortisol levels at all points and mean AUC cortisol levels in subjects with AN before therapy were significantly higher than those in controls, but returned to control levels after inpatient treatment. Higher AUC cortisol levels were associated with lower standard deviation for weight in AN. A significant positive correlation between the AUC cortisol level and POMS subscale of “Fatigue” was apparent in the control group, but not in the AN group. The increased change values of AUC cortisol level before and after inpatient treatment correlated with increased body weight gain ratio just after treatment, but not with the ratio after one year. The present study indicated that HPA axis activity could reflect severity of illness, but did not show an accurate neuroendocrine response for mood states. Changes in HPA axis activity following treatment could therefore be used to predict prognosis and particularly in the short term.     

A systematic review and meta-analysis of cognitive bias to food stimuli in people with disordered eating behaviour

Aim

Maladaptive cognitions about food, weight and shape bias attention, memory and judgment and may be linked to disordered eating behaviour. This paper reviews information processing of food stimuli (words, pictures) in people with eating disorders (ED).

Method

PubMed, Ovid, ScienceDirect, PsychInfo, Web of Science, Cochrane Library and Google Scholar were searched to December 2009. 63 studies measured attention, memory and judgment bias towards food stimuli in women with ED.

Results

Stroop tasks had sufficient sample size for a meta-analyses and effects ranged from small to medium. Other studies of attention bias had variable effects (e.g. the Dot-Probe task, distracter tasks and Startle Eyeblink Modulation). A meta-analysis of memory bias studies in ED and RE yielded insignificant effect. Effect sizes for judgment bias ranged from negligible to large.

Conclusions

People with ED have greater attentional bias to food stimuli than healthy controls (HC). Evidence for a memory and judgment bias in ED is limited.     

The epidemiology of eating disorders in six European countries: Results of the ESEMeD-WMH project

Few data are available to estimate the prevalence of eating disorders (EDs) and their correlates in the community. This paper reports data on EDs obtained in the framework of the ESEMeD project, aimed at investigating the prevalence of non-psychotic mental disorders in six European countries (Belgium, France, Germany, Italy, the Netherlands and Spain), using a new version of the Composite International Diagnostic Interview. The ESEMeD study was a general population cross-sectional household survey. In total, 21,425 respondents aged 18 or older provided data for the project between January 2001 and August 2003. A subsample (N = 4139) underwent a detailed investigation on EDs. Lifetime estimated prevalence of anorexia nervosa, bulimia nervosa, binge eating disorder, sub-threshold binge eating disorder, and any binge eating were 0.48%, 0.51%, 1.12%, 0.72%, and 2.15%, respectively, and they were 3-8 times higher among women for all EDs. However, since people under 18 were excluded from this study, our prevalence should be taken as lower-bound estimate of real frequencies. Indeed, cumulative lifetime prevalence analysis showed that the majority of eating disorders had their initial onset between 10 and 20 years of age. Role impairment and comorbidity with other mental disorders were highly common, yet only small proportions of patients with a lifetime diagnosis of EDs requested medical treatment. It still has to be proven whether early diagnostic identification and access to specialized care can reduce the burden caused by these disorders.     

Low serum BDNF and food intake regulation: A possible new explanation of the pathophysiology of eating disorders

Background

Several lines of evidence suggest that brain-derived neurotrophic factor (BDNF) plays an important role in weight regulation and eating behavior, and poorly balanced diets lead to a decrease in blood BDNF levels. However, studies regarding BDNF blood levels in eating disorders (ED) have yielded inconsistent results. We measured serum concentrations of BDNF and assessed behavior and cognition related to eating in ED patients and control subjects.

Methods

Forty female drug-free patients [19 with anorexia nervosa (AN), 21 with bulimia nervosa (BN)], who did not meet the diagnostic criteria for depressive disorder, and 24 age-matched normal control subjects were enrolled in the current study. We evaluated eating-related psychopathology and depressive symptoms using the Eating Disorder Inventory-2 (EDI-2), Eating Attitude Test-26 (EAT-26) and the Hamilton Depression Rating Scale (HDRS), and measured serum BDNF levels by an enzyme-linked immunosorbent assay.

Results

Compared to normal controls, serum levels of BDNF were significantly reduced in AN, but not in BN. There was a significant positive correlation between serum BDNF levels and BMI in both AN patients (r = .649, p = .003) and BN patients (r = .626, p = .002). However, no correlation between serum BDNF levels and BMI was detected in the controls. Furthermore, there was a significant negative correlation between serum BDNF levels and the oral control subscale scores of EAT in both AN patients (r = − .506, p = .027) and BN patients (r = − .511, p = .018); whereas, no correlation was detected in normal controls.

Conclusion

Our study demonstrated that individuals showing more extreme food intake regulation were those with lower serum BDNF levels. This finding is contrary to that in mice where mice with reduced BDNF levels showed aberrant eating behavior. This result suggests that BDNF is no longer functioning appropriately in ED patients, which could be an important factor in the pathophysiological of ED.     

Ghrelin/obestatin ratio in two populations with low bodyweight: constitutional thinness and anorexia nervosa

Constitutional thinness (CT) and anorexia nervosa (AN) are two categories of severely underweight subjects. Some appetite-regulating hormones display opposite levels in AN and CT. While levels of ghrelin, an orexigenic hormone, fit with the normal food intake in CT, the lack of efficacy of increased ghrelin levels in AN is not clear. Obestatin is a recently described peptide derived from the preproghrelin gene, reported to inhibit appetite in contrast to ghrelin. The aim of this study was to determine whether the circadian profile of obestatin, total and acylated ghrelin levels is different in CT subjects when compared with AN patients. Six-points circadian profiles of plasma obestatin, acylated ghrelin, total ghrelin and other hormonal and nutritional parameters were evaluated in four groups of young women: 10 CT, 15 restricting-type AN, 7 restored from AN and 9 control subjects. Obestatin circadian levels were significantly higher in AN (p<0.0001) while no difference was found between CT and control subjects. Acylated and total ghrelin were found increased in AN. Acylated ghrelin/obestatin and total ghrelin/obestatin were found decreased in AN compared to CT or C subjects (p<0.05). The percentage of acylated ghrelin was found decreased in CT group (p<0.05). The decreased ghrelin/obestatin ratio found in AN might participate in the restraint in nutriment intake of these patients. In contrast, in CT a lower percentage of acylated over total ghrelin might be considered in the aetiology of this condition.     

Alterations in QT dispersion in the surface electrocardiogram of female adolescents diagnosed with restricting-type anorexia nervosa

OBJECTIVE: QT dispersion (QTd), defined as the difference between the longest interval and the shortest interval in the 12-lead electrocardiogram (ECG), is a measure of myocardial repolarization inhomogeneity. We assessed QTd in malnourished anorexia nervosa (AN) inpatients and following weight restoration. METHODS: QTd analysis, anthropometric evaluations, and laboratory tests were carried out in 30 malnourished female adolescent AN restricting-type (AN-R) inpatients and following weight restoration. RESULTS: A significant increase was found in weight/height ratio and body mass index from malnourished stage to weight restoration, paralleled by a significant decrease in QTd (70+/-16 vs. 47+/-16 ms; P<.0001). No correlations were found between ECG indices and anthropometric and laboratory measures. CONCLUSION: Elevated QTd in malnourished AN-R inpatients may indicate possible cardiac autonomic imbalance and/or myocardial damage, likely corrected following weight restoration.     

Olanzapine-induced weight gain in anorexia nervosa: Involvement of leptin and ghrelin secretion?

BACKGROUND: Olanzapine (OLA) administration has been reported to induce weight gain in experimental animals and humans, through not yet fully defined mechanisms of action. Aim of this study was to determine whether in patients with Anorexia Nervosa (AN) OLA induces weight gain through the modulation of the hunger-satiety regulatory peptides leptin and ghrelin. METHODS: Twenty anorexic probands received a 3 months course of cognitive-behavioral psychotherapy and programmed nutritional rehabilitation, combined with OLA PO (2.5 mg for 1 month and 5 mg for 2 months) in ten patients and with placebo PO (PL) in the other 10. Weight, measured as body mass index (BMI), leptin and ghrelin plasma values were monitored before starting the therapy and then monthly for 3 months. Plasma leptin was measured by ELISA, and plasma ghrelin by radioimmunoassay. RESULTS: BMI increased significantly but not differently in both treatment groups. Leptin and ghrelin secretion did not change during the course of the treatments. No correlations were observed between BMI values and leptin and ghrelin levels. CONCLUSIONS: Our data suggest that the weight gain observed in our OLA-treated patients was not linked to drug administration. Moreover, leptin and ghrelin secretions were not responsible for BMI changes.