Michiko Nakazato

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) nu200a=u200a171; Bulimia Nervosa (BN) nu200a=u200a82; Recovered AN nu200a=u200a90; Healthy controls (HC): nu200a=u200a199. 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.

Cognitive Flexibility and Clinical Severity in Eating Disorders

Objectives The aim of this study was to explore cognitive flexibility in a large dataset of people with Eating Disorders and Healthy Controls (HC) and to see how patient characteristics (body mass index [BMI] and length of illness) are related to this thinking style. Methods A dataset was constructed from our previous studies using a conceptual shift test - the Brixton Spatial Anticipation Test. 601 participants were included, 215 patients with Anorexia Nervosa (AN) (96 inpatients; 119 outpatients), 69 patients with Bulimia Nervosa (BN), 29 Eating Disorder Not Otherwise Specified (EDNOS), 72 in long-term recovery from AN (Rec AN) and a comparison group of 216 HC. Results The AN and EDNOS groups had significantly more errors than the other groups on the Brixton Test. In comparison to the HC group, the effect size decrement was large for AN patients receiving inpatient treatment and moderate for AN outpatients. Conclusions These findings confirm that patients with AN have poor cognitive flexibility. Severity of illness measured by length of illness does not fully explain the lack of flexibility and supports the trait nature of inflexibility in people with AN.

Brain-derived neurotrophic factor (BDNF) and set-shifting in currently ill and recovered anorexia nervosa (AN) patients

BACKGROUNDnStudies of patients with anorexia nervosa (AN) have shown that they do not perform well in set-shifting tasks but little is known about the neurobiological correlates of this aspect of executive function. The aim of this study was to measure serum brain-derived neurotrophic factor (BDNF) and to establish whether set-shifting difficulties are present in people with current AN and in those recovered from AN, and whether serum BDNF concentrations are correlated with set-shifting ability.nnnMETHODnSerum BDNF concentrations were measured in 29 women with current AN (AN group), 18 women who had recovered from AN (ANRec group) and 28 age-matched healthy controls (HC group). Set-shifting was measured using the Wisconsin Card Sorting Test (WCST). Eating-related psychopathology and depressive, anxiety and obsessive-compulsive symptomatology were evaluated using the Eating Disorder Examination Questionnaire (EDEQ), the Hospital Anxiety and Depression Scale (HADS), and the Maudsley Obsessive-Compulsive Inventory (MOCI) respectively.nnnRESULTSnSerum BDNF concentrations (mean+/-s.d.) were significantly lower in the AN group (11.7+/-4.9 ng/ml) compared to the HC group (15.1+/-5.5 ng/ml, p=0.04) and also compared to the ANRec group (17.6+/-4.8 ng/ml, p=0.001). The AN group made significantly more errors (total and perseverative) in the WCST relative to the HC group. There was no significant correlation between serum BDNF concentrations and performance on the WCST.nnnCONCLUSIONSnSerum BDNF may be a biological marker for eating-related psychopathology and of recovery in AN. Longitudinal studies are needed to explore possible associations between serum BDNF concentrations, illness and recovery and neuropsychological traits.

No change between the serum brain-derived neurotrophic factor in female patients with anorexia nervosa before and after partial weight recovery.

BACKGROUNDnBrain-derived neurotrophic factor (BDNF) is a member of the nerve growth factor family. Several lines of evidence indicate that BDNF plays a role in the pathophysiology of eating disorders (ED). We found that serum BDNF levels in patients with ED were significantly lower than in normal controls. The aim of this longitudinal study was to compare serum BDNF levels in patients with anorexia nervosa (AN) before (n=13, initial mean body mass index (BMI)=14.2 kg/m(2)+/-0.7) and after partial recovery (mean BMI=16.2 kg/m(2)+/-1.7, mean weight gain 5.0 kg+/-2.0), with age-matched normal control subjects (n=17, mean BMI=20.4 kg/m(2)+/-1.5).nnnMETHODSnEating related psychopathology and depressive symptoms were evaluated before and after partial weight recovery, using the Eating Disorder Inventory-2 (EDI-2) and the 17-item Hamilton Depression Rating Scale (HDRS). Serum BDNF levels were measured using a sandwich enzyme-linked immunosorbent assay.nnnRESULTSnSerum BDNF levels with the AN patients (14.5+/-4.4 ng/ml) were significantly (p<0.01) lower than in control subjects (22.1+/-8.9 ng/ml). There were no significant differences in serum BDNF levels between the patients with AN before (14.5+/-4.4 ng/ml) and after (17.2+/-6.9 ng/ml) partial weight recovery. In all subjects, there was a positive correlation (r=0.5, p<0.01) between the baseline BDNF levels and the EDI-2 scores (n=30). Furthermore, in all subjects there was a positive correlation (r=0.4, p<0.05) between the BDNF levels and the BMI.nnnCONCLUSIONSnSerum BDNF levels did not change after partial weight recovery in AN patients. Our results suggest that an alteration of the serum BDNF in AN patients is not due to changes in body weight. Thus, other possible mechanisms that could be related to low serum BDNF levels in AN patients should be evaluated.

Serum glutamine, set-shifting ability and anorexia nervosa

BackgroundSet-shifting is impaired in people with anorexia nervosa (AN), but the underlying physiological and biochemical processes are unclear. Animal studies have established that glutamatergic pathways in the prefrontal cortex play an important role in set-shifting ability. However, it is not yet understood whether levels of serum glutamatergic amino acids are associated with set-shifting performance in humans. The aim of this study was to determine whether serum concentrations of amino acids related to glutamatergic neurotransmission (glutamine, glutamate, glycine, l-serine, d-serine) are associated with set-shifting ability in people with acute AN and those after recovery.MethodsSerum concentrations of glutamatergic amino acids were measured in 27 women with current AN (AN group), 18 women recovered from AN (ANRec group) and 28 age-matched healthy controls (HC group). Set-shifting was measured using the Wisconsin Card Sorting Test (WCST) and the Trail Making Task (TMT). Dimensional measures of psychopathology were used, including the Eating Disorder Examination Questionnaire (EDEQ), the Maudsley Obsessive-Compulsive Inventory (MOCI) and the Hospital Anxiety and Depression Scale (HADS).ResultsSerum glutamine concentrations in the AN group (1,310.2 ± 265.6 μM, mean ± SD) were significantly higher (by approximately 20%) than those in the HC group (1,102.9 ± 152.7 μM, mean ± SD) (F(2, 70) = 6.3, P = 0.003, 95% CI 61.2 to 353.4). Concentrations of serum glutamine were positively associated with markers of the illness severity: a negative correlation was present between serum glutamine concentrations and body mass index (BMI) and lowest BMI and a positive correlation was found between duration of illness and EDEQ. The AN group showed significantly impaired set shifting in the WCST, both total errors, and perseverative errors. In the AN group, there were no correlations between serum glutamine concentrations and set shifting.ConclusionsSerum concentrations of glutamine may be a biomarker of illness severity in people with AN. It does not appear to be directly associated with changes in executive function.

Psychiatric disorders in juvenile patients with insulin-dependent diabetes mellitus

The relationships of psychiatric characteristics to metabolic control and psychosocial functioning were examined in a group of 16 patients with insulin-dependent diabetes mellitus (IDDM) (mean age: 14.3+/-5.1 years, mean duration of follow-up: 5.0+/-2.3 years) and psychiatric disorders. The comparison is also made to 69 IDDM controls (mean age: 17.0+/-6.7 years) without psychiatric disorders. Metabolic control was evaluated in terms of glycosylated hemoglobin (HbA1c). Psychosocial functioning at both psychiatric treatment entry and discharge was assessed using the global assessment of functioning (GAF) scale. Subjects were divided into three subgroups - Somatoform Type (25%), Behavioral Type (50%) or Psychotic Type (25%) - according to the Diagnostic and Statistical Manual of Mental Disorders, third edition revised (DSM-III-R), based on semi-structured interviews. Four patients (25%) were diagnosed as having schizophrenia or schizoaffective disorder (Psychotic Type), which is rather rare. The mean HbA1c level in the Behavioral Type patients was significantly higher than in the other subgroups (P<0. 01). After psychiatric treatment a significant difference (P<0.0001) in the GAF Scale was observed in the Psychotic Type compared with the other subgroups. We conclude that the Behavioral Type is associated with poor metabolic control and that for the Psychotic Type, improved psychosocial functioning can be achieved through psychiatric treatment.