The first Australian case description of anorexia nervosa

To the best of our knowledge, H.E. Astles was the first Australian physician who, in a lecture in 1882, paid explicit attention to the illness of anorexia nervosa. We reproduce his paper because of its historical value, which we underline in our comments.     

Three cases of posttraumatic anorexia nervosa

Three patients developed anorexia nervosa after car accidents that caused physical injuries. These cases suggest that anorexia nervosa can be secondary to real or perceived figure distortion and that some cases may be caused by it.     

Entero-insular axis in children with anorexia nervosa

Entero-insular axis plays an important role in generating satiety signal. Thus disturbances in this axis may influence the course of anorexia nervosa. The aim of the study was analysis of the function of the hormonal part of the entero-insular axis in girls with anorexia nervosa. Thirteen girls with anorexia nervosa and in 10 healthy girls were studied. Each girl was subjected to oral glucose tolerance test and standard meal test. Blood was collected before stimulation and within 15, 30, 60, and 120 min thereafter. The concentrations of all peptides were determined by radioimmunoassay commercial kits. Fasted and postprandial levels of these peptides as well as integrated outputs were measured. Fasting insulin concentration was significantly higher in the group of girls with anorexia nervosa than in the control group (p<0.03). What more in girls with anorexia the integrated output of insulin was significantly lower in oral glucose tolerance test than after the meal (p<0.001). Also the integrated output of glucagon in both tests was higher in the group of girls with anorexia than in the control group. The mean output of pancreatic polypeptide and cholecystokinin in anorexia group was significantly higher (p<0.001 in both cases) than that in the control group but only after the test meal. The integrated outputs of gastric inhibitory peptide in both tests were significantly higher in anorectic girls than those in the control group (oral glucose tolerance test, p<0.02; meal test, p<0.001), However, mean values of the integrated output of glucagon-like peptide 1 in both tests were significantly higher in the control group than in the girls with anorexia (p<0.001 in each case). Highly significant correlation was found between glucose concentration and the concentrations of insulin, cholecystokinin, and gastric inhibitory peptide in both tests and for the both groups. In the anorectic girls, significant correlation between insulin concentration and the concentration of gastric inhibitory peptide was found after both stimulation tests and between insulin and cholecystokinin after oral glucose only. Conclusion: the disturbed secretion of the hormones of entero-insular axis after the meal in anorectic girls may have negative influence on the course of anorexia nervosa. This disease has no effect on the incretin function of cholecystokinin, gastric inhibitory peptide and glucagon-like peptide 1.     

Hyperactivity in anorexia nervosa: A fundamental clinical feature

Toward the goal of assessing the prevalence and chronology of heightened physical activity in primary anorexia nervosa, we reviewed the charts of 33 patients hospitalized with this illness during the past 10 years. Fifteen of these patients, or their parents, were also interviewed at least 1 year after the hospitalization. In 25 of the 33 charts, the presence of “hyperactivity” during the present illness was recorded; only one patient was specifically noted to show unremarkable physical activity. Twenty-one of the 25 patients were also described as having been unusually active physically prior to the onset of dieting and weight loss. The 15 follow-ups revealed two deaths, one patient by suicide and the other from complications of malnutrition. Among the 13 patients interviewed directly, ten described themselves as continuing to be highly active physically—this despite significant weight gain in eight and complete subsidence of both eating symptomatology and amenorrhea in three. Physical activity appeared to be more extensive, disorganized, and aimless during the acute phase of anorexia nervosa, when excessive and bizarre dieting and rapid weight loss are occurring, than during the premorbid or weight recovery phases. However, these preliminary findings suggest that “hyperactivity” is an early and enduring clinical feature of anorexia nervosa and not merely secondary to either a conscious attempt to lose weight or weight loss per se.     

Functional neuroimaging in anorexia nervosa: A clinical approach

Aims

To provide a review of the available literature about the functional neuroimaging of anorexia nervosa, and to summarize the possible role of neurobiological factors in its pathogenesis.

Methods

A systematic review of the literature was performed using PubMed and Medline electronic database (1950-September 2009). Eligible studies were restricted to those involving the main parameters of cerebral activity and functional neuroimaging techniques. Findings of the reviewed studies have been grouped on a diagnostic subtype basis, and their comparison has been interpreted in terms of concordance.

Results

We found a high level of concordance among available studies with regard to the presence of frontal, parietal and cingulate functional disturbances in both anorexia nervosa restricting and binge/purging subtypes. Concordance among studies conducted regardless of the anorexia nervosa subtypes suggests an alteration in temporal and parietal functions and striatal metabolism.

Conclusions

The most consistent alterations in anorexia nervosa cerebral activity seem to involve the dorsolateral prefrontal cortex, the inferior parietal lobule, the anterior cingulate cortex and the caudate nucleus. They may affect different neural systems such as the frontal visual system, the attention network, the arousal and emotional processing systems, the reward processing network, and the network for the body schema.     

CSF oxytocin in anorexia nervosa and bulimia nervosa: clinical and pathophysiologic considerations

Oxytocin is a hypothalamic neuropeptide with both centrally and peripherally directed pathways. Data from experimental animals indicate that oxytocin impairs consolidation of aversively conditioned behaviors and is released after feeding or experimental gastric distension. The authors report that the mean CSF oxytocin level of five underweight women with restricting anorexia, but not 12 underweight bulimic anorexic women or 35 normal-weight women with bulimia nervosa, was significantly lower than the level of 11 control subjects. Restricting anorexic patients' low CSF oxytocin levels may reflect their persistently low food intake, and this behavior may exacerbate their tendency for perseverative preoccupation with adverse consequences of food intake.     

The role of leptin in anorexia nervosa: clinical implications

Leptin is a hormone with pleiotropic functions affecting several tissues. Because leptin has a crucial role in the adaptation of an organism to semi-starvation, anorexia nervosa (AN) serves as a model disorder to elucidate the functional implications of hypoleptinaemia; vice versa, several symptoms in patients with this eating disorder are related to the low leptin levels, which are characteristic of acute AN. Weight gain in AN patients can induce relative hyperleptinaemia in comparison to controls matched for body mass index; circulating leptin concentrations in AN patients thus transverse from subnormal to supranormal levels within a few weeks. We review findings on leptin secretion in AN and focus on implications, particularly for the hypothalamus-pituitary-gonadal axis, bone mineral density and physical hyperactivity. Undoubtedly, the elucidation of leptin's function as a trigger of diverse neuroendocrine adaptations to a restricted energy intake has substantially advanced our knowledge of the pathogenesis of distinct symptoms of AN, including amenorrhoea that represents one of the four diagnostic criteria. The fact that hypoleptinaemia can induce hyperactivity in a rat model for AN has led to a series of studies in AN patients, which support the notion that application of leptin to severely hyperactive patients might prove beneficial.     

Long-term outcome of 151 cases of anorexia nervosa

ABSTRACT One hundred and fifty-one patients (140 females - 11 males) with anorexia nervosa (AN) from three departments (child psychiatry, psychiatry, and internal medicine) were re-examined 4–22 years (average 12.5 years) after their first contact with the Rigshospital in Copenhagen. During the years 1960–76 the number of referrals was on the increase, and relatively more patients were treated in the psychiatric departments at the end than at the beginning of the period. Mean age was 16.6 years at onset, 19.0 years at primary contact. Mean weight loss was 32 %. Mean duration of treatment was 12 months. Differences between the three departments concern especially age, sex, and duration of treatment. Mean age at follow-up was 31.0 years (range 16–63 years) for surviving probands. Follow-up information originated from semi-structured personal interviews (in 80 % of surviving probands) together with register data on all probands, supplemented by extensive hospital data. Nine patients (6 %), including six who committed suicide, died on the average 7.3 years after primary contact (average age 27.1 years). The mortality rate was 0.5 % per year. At follow-up one fourth of the surviving probands had AN and one fourth suffered from other psychiatric disorders, while one half were free from mental illness. There were no significant differences in outcome between the three departments. As a whole, the group experienced a social decline. It is concluded that a substantial part of this group of AN patients had a poor prognosis with a tendency towards chronicity, despite relatively long and intensive treatment, but, on the other hand, about one half of the probands seemed to be healthy and well functioning.     

Olanzapine in children and adolescents with chronic anorexia nervosa. A study of five cases

 Psychopathology in severely anorexic patients often seems to be of compulsive and delusional quality rendering therapeutic approaches extremely difficult. With conventional therapeutic regimes failing, administration of the novel antipsychotic olanzapine induced remarkable improvement in five cases reported here. Paranoid ideation concerning body image or weight gain decreased and sedative effects helped to reduce inner tensions and phobia with respect to food intake. Olanzapine, therefore, might represent an important therapeutic tool in anorexic patients who present the following characteristics: long-term history of anorexia nervosa mostly with several hospitalisations, missing perception of their severe state of illness, refusal of therapy, delusional quality of anorexic thinking, risk of discontinuation of therapy with life-threatening consequences. Accepted: 4 December 2000     

Fluoxetine treatment of anorexia nervosa: an open clinical trial

Six patients with chronic, refractory anorexia nervosa were treated with fluoxetine. Depressive symptoms diminished in all patients, and this was associated with weight gain. Subjects, despite frequent medical comorbidity, tolerated fluoxetine well, even in dosages greater than those used for depression.     

Death and relapse in anorexia nervosa: survival analysis of 151 cases

The traditional historic-prospective follow-up study of anorexia nervosa patients may be well served by recent methods of statistical analysis, the so-called models for the analysis of survival data. These models are particularly suited to the sort of incomplete observations usually produced a longitudinal studies. They include methods for estimating the probability of death and relapse as a function of time. This makes possible powerful comparisons among studies and among subsamples in single studies. In the present study, 151 patients were followed-up after 4-22 yrs. The hazard of death was on average 0.5% per year, the hazard of relapse 3% per year. With both measures, the risk declined steadily after therapeutic contact.     

Cognitive performance in children with acute early-onset anorexia nervosa

When anorexia nervosa (AN) occurs in children below the age of 14 years, it is referred to as early-onset AN (EO-AN). Over the last years, there has been an increased focus on the role of cognitive functioning in the development and maintenance of AN. Adults with AN show inefficiencies in cognitive functions such as flexibility and central coherence. Systematic neuropsychological examinations of patients with EO-AN are missing. Thirty children with EO-AN and 30 adolescents with AN, as well as 60 healthy controls (HC) underwent an extensive neuropsychological examination. ANOVAs with post hoc tests and explorative regression analyses were conducted. Patients with EO-AN (mean age = 2.17 ± 1.57 years) showed no significant differences in flexibility, inhibition, planning, central coherence, visuospatial short- and long-term memory or recognition in comparison to HC (mean age = 11.62 ± 1.29 years). Performance of adolescents with AN (mean age = 15.93 ± 0.70 years) was not significantly different compared to HC (mean age = 16.20 ± 1.26 years). Explorative regression analyses revealed a significant interaction of age and group for flexibility (adjusted R ²  = 0.30, F = 17.85, p = 0.013, η _p ²  = 0.32). Contrary to expectations, the current study could not confirm the presence of inefficient cognitive processing in children with EO-AN compared to HC. Nonetheless, the expected age-related improvement of flexibility might be disrupted in children and adolescents with AN. Longitudinal neuropsychological examinations are necessary to provide more information about the role of cognitive functioning in the development and maintenance of AN.     

Hepatic and pancreatic dysfunction in anorexia nervosa: a report of two cases

Two patients with anorexia nervosa with evidence of pancreas and liver injury are reported. Both showed evidence of organ dysfunction in the presence of cachexia. Serum amylase, ASAT (GOT), and ALAT (GPT) became normal parallel with body weight. On the basis of reports on the effects of malnutrition on pancreas and liver function, it is suggested that nutritional pancreas and liver dysfunction might represent hitherto unrecognized complications of anorexia nervosa.     

A search for susceptibility loci for anorexia nervosa: methods and sample description.

BACKGROUND: Eating disorders have not traditionally been viewed as heritable illnesses; however, recent family and twin studies lend credence to the potential role of genetic transmission. The Price Foundation funded an international, multisite study to identify genetic factors contributing to the pathogenesis of anorexia nervosa (AN) by recruiting affective relative pairs. This article is an overview of study methods and the clinical characteristics of the sample. METHODS: All probands met modified DSM-IV criteria for AN; all affected first, second, and third degree relatives met DSM-IV criteria for AN, bulimia nervosa (BN), or eating disorder not otherwise specified (NOS). Probands and affected relatives were assessed diagnostically with the Structured Interview for Anorexia and Bulimia. DNA was collected from probands, affected relatives and a subset of their biological parents. RESULTS: Assessments were obtained from 196 probands and 237 affected relatives, over 98% of whom are of Caucasian ancestry. Overall, there were 229 relative pairs who were informative for linkage analysis. Of the proband-relative pairs, 63% were AN-AN, 20% were AN-BN, and 16% were AN-NOS. For family-based association analyses, DNA has been collected from both biological parents of 159 eating-disordered subjects. Few significant differences in demographic characteristics were found between proband and relative groups. CONCLUSIONS: The present study represents the first large-scale molecular genetic investigation of AN. Our successful recruitment of over 500 subjects, consisting of affected probands, affected relatives, and their biological parents, will provide the basis to investigate genetic transmission of eating disorders via a genome scan and assessment of candidate genes.     

Self-forgiveness in anorexia nervosa and bulimia nervosa

This study investigated whether low levels of self-forgiveness were associated with eating disorder symptomatology. Participating women (N = 51) had diagnoses of anorexia nervosa, bulimia nervosa, or no eating disorder diagnosis. They completed 3 measures of self-forgiveness. Women with eating disorders had lower levels of self-forgiveness compared with control participants. Results suggest that incorporating self-forgiveness interventions into current eating disorder treatments should be evaluated in future research as they might enhance clinical outcomes.     

Stealing in anorexia nervosa and bulimia nervosa

Only recently stealing behaviour has been noticed as a symptom of anorexia nervosa and bulimia nervosa. Reviewing our sample of 63 patients we discuss the incidence and motivation of kleptomania. In 24% of our patients stealing behaviour was reported which is a definitely high rate compared to literature. Among the intentions for stealing behaviour we found: Stealing as conversion of revenge, self-assertiveness compensation of binge-eating or stealing as achievement. The differential motivation of stealing should be considered in legal consequences.