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Eating disorders (anorexia nervosa, bulimia nervosa, binge-eating disorder, and other specified eating or feeding disorders) have a combined prevalence of 13% and are associated with severe physical and psychosocial problems. Early diagnosis, which is important for effective treatment and prevention of undesirable long-term health consequences, imposes problems among non-specialist clinicians unfamiliar with these patients, such as those working in primary care. Early, accurate diagnosis, particularly in primary care, allows expert interventions early enough in the disorder to facilitate positive treatment outcomes. Computer-assisted diagnostic procedures offer a possible solution to this problem by providing expertise via an algorithm that has been developed from a large number of cases that have been diagnosed in person by expert diagnosticians and expert caregivers. A web-based system for determining an accurate diagnosis for patients suspected to suffer from an eating disorder was developed based on these data. The process is automated using an algorithm that estimates the respondent's probability of having an eating disorder and the type of eating disorder the individual has. The system provides a report that works as an aid for clinicians during the diagnostic process and serves as an educational tool for new clinicians.

Background: Individuals with Anorexia Nervosa are often described as restless, hyperactive and having disturbed sleep. The result reproducibility and generalisability of these results are low due to the use of unreliable methods, different measurement methods and outcome measures. A reliable method to measure both physical activity and sleep is through accelerometry. The main purpose of the study was to quantify the physical activity and sleeping behaviour of anorexia nervosa patients. Another purpose was to increase result reproducibility and generalisability of the study., Material and Methods: Accelerometer data were collected from the first week of treatment of anorexia nervosa at an inpatient ward. Raw data from the Axivity AX3© accelerometer was used with the open-source package GGIR for analysis, in the free statistical software R. Accelerometer measurements were transformed into euclidean norm minus one with negative values rounded to zero (ENMO). Physical activity measurements of interest were 24h average ENMO, daytime average ENMO, inactivity, light activity, moderate activity, and vigorous activity. Sleep parameters of interest were sleep duration, sleep efficiency, awakenings, and wake after sleep onset. The sleep duration of different age groups was compared to recommendations by the National Sleep Foundation using a Fisher's exact test., Results: Of 67 patients, due to data quality 58 (93% female) were included in the analysis. Average age of participants was 17.8 (±6.9) years and body mass index was 15.5 (±1.9) kg/m2. Daytime average ENMO was 17.4 (±5.1) mg. Participants spent 862.6 (±66.2) min per day inactive, 88.4 (±22.6) min with light activities, 25.8 (±16.7) min with moderate activities and 0.5 (±1.8) min with vigorous activities. Participants slept for 461.0 (±68.4) min, waking up 1.45 (±1.25) times per night for 54.6 (±35.8) min, having an average sleep quality of 0.88 (±0.10). 31% of participants met sleep recommendations, with a significantly higher number of 6-13 year old patients failing to reach recommendations compared to 14-25 year old patients., Conclusion: The patient group spent most of their time inactive at the beginning of treatment. Most patients failed to reach sleep recommendations. The use of raw data and opensource software should ensure result reproducibility, enable comparison across points in treatment and comparison with healthy individuals., Competing Interests: I have read the journal’s policy and the authors of this manuscript have the following competing interests: JS and CB received their salaries from the Mandometer clinic during the study. PS and CB own Mandometer Group AB stocks. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

We have suggested that reduced food intake increases the risk for anorexia nervosa by engaging mesolimbic dopamine neurons, thereby initially rewarding dieting. Recent fMRI studies have confirmed that dopamine neurons are activated in anorexia nervosa, but it is not clear whether this response is due to the disorder or to its resulting nutritional deficit. When the body senses the shortage of nutrients, it rapidly shifts behavior toward foraging for food as a normal physiological response and the mesolimbic dopamine neurons may be involved in that process. On the other hand, the altered dopamine status of anorexics has been suggested to result from a brain abnormality that underlies their complex emotional disorder. We suggest that the outcomes of the treatments that emerge from that perspective remain poor because they target the mental symptoms that are actually the consequences of the food deprivation that accompanies anorexia. On the other hand, a method that normalizes the disordered eating behavior of anorexics results in much better physiological, behavioral, and emotional outcomes., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Any healthy person can develop anorexia nervosa. Prolonged dieting causes reversible endocrine changes that emerge to combat starvation, the main threat to survival. Animals have evolved to develop strategies to cope with this challenge, assisted by hormonal systems that facilitate food hoarding but which can also inhibit eating, reinforcing the anorexic state. However, a simple machine that provides feedback on how to eat can allow patients to escape from anorexia and restore their health., (© 2014 The Authors Journal of Neuroendocrinology published by John Wiley & Sons Ltd on behalf of British Society for Neuroendocrinology.)

We report the results of a study based on 1,428 patients with eating disorders treated at 6 clinics. These patients were consecutively referred over 18 years and used inpatient and outpatient treatment. The subjects were diagnosed with anorexia nervosa, bulimia nervosa, or an eating disorder not otherwise specified. Patients practiced a normal eating pattern with computerized feedback technology, they were supplied with external heat, their physical activity was reduced, and their social habits restored to allow them to return to their normal life. The estimated rate of remission for this therapy was 75% after a median of 12.5 months of treatment. A competing event such as the termination of insurance coverage, or failure of the treatment, interfered with outcomes in 16% of the patients, and the other patients remained in treatment. Of those who went in remission, the estimated rate of relapse was 10% over 5 years of follow-up and there was no mortality. These data replicate the outcomes reported in our previous studies and they compare favorably with the poor long-term remission rates, the high rate of relapse, and the high mortality rate reported with standard treatments for eating disorders.

Restricted food intake is associated with increased physical activity, very likely an evolutionary advantage, initially both functional and rewarding. The hyperactivity of patients with anorexia nervosa, however, is a main problem for recovery. This seemingly paradoxical reward of hyperactivity in anorexia nervosa is one of the main aspects in our framework for the neurobiological changes that may underlie the development of the disorder. Here, we focus on the neurobiological basis of hyperactivity and reward in both animals and humans suggesting that the mesolimbic dopamine and hypothalamic orexin neurons play central roles. The paper represents an invited review by a symposium, award winner or keynote speaker at the Society for the Study of Ingestive Behavior [SSIB] Annual Meeting in Portland, July 2009., (2010 Elsevier Inc. All rights reserved.)

Outcome in anorexia nervosa remains poor and a new way of looking at this condition is therefore needed. To this aim, we review the effects of food restriction and starvation in humans. It is suggested that body weight remains stable and relatively low when the access to food requires a considerable amount of physical activity. In this condition, the human homeostatic phenotype, body fat content is also low and as a consequence, the synthesis and release of brain neurotransmitters are modified. As an example, the role of neuropeptide Y is analyzed in rat models of this state. It is suggested that the normal behavioral role of neuropeptide Y is to facilitate the search for food and switch attention from sexual stimuli to food. Descriptive neuroendocrine studies on patients with anorexia nervosa have not contributed to the management of the patients and the few studies in which hormones have been administered have, at best, reversed an endocrine consequence secondary to starvation. In a modified framework for understanding the etiology and treatment of anorexia nervosa it is suggested that the condition emerges because neural mechanisms of reward and attention are engaged. The neural neuropeptide Y receptor system may be involved in the maintenance of the behavior of eating disorder patients because the localization of these receptors overlaps with the neural systems engaged in cue-conditioned eating in limbic and cortical areas. The eating behavior of patients with anorexia nervosa, and other eating disorders as well, is viewed as a cause of the psychological changes of the patients. Patients are trained to re-learn normal eating habits using external support and as they do, their symptoms, including the psychological symptoms, dissolve.

The hypothesis that eating disorders are caused by an antecedent mental disorder, presently believed to be an obsessive compulsive disorder, has been clinically implemented during many years but has not improved treatment outcome. Alternatively, eating disorders are eating disorders and the symptoms of anorexic patients and probably bulimic patients as well, are epiphenomena which emerge as a consequence of starvation. This hypothesis is supported by the observations of the effects of a 6 month long period of semi-starvation on healthy human volunteers, which demonstrated not only the emergence of psychiatric symptoms but also the reduction in eating rate which is typical of anorexia nervosa patients. On this framework training anorexic patients how to eat may be a useful intervention. We report that anorexic patients, either with a body mass index<14 or >15.5 display the same pattern of eating behavior, with a low level of intake, a slow eating rate and a high level of satiety. They also have the same, high level of psychiatric symptoms, including obsessive compulsive symptoms. Training patients to eat more food at a progressively higher rate reverses these symptoms and patients remain free of symptoms during an extended period of follow-up. It is suggested that the pattern of eating behavior mediates between the starved condition and the psychopathology of anorexia nervosa.

The hypothesis that treatment with neuropeptide Y (NPY) can increase running activity and decrease food intake and body weight was tested. Female rats with a running wheel lost more weight than sedentary rats and ran progressively more as the availability of food was gradually reduced. When food was available for only 1h/day, the rats lost control over body weight. Correlatively, the level of NPY mRNA was increased in the hypothalamic arcuate nucleus. This phenomenon, activity-based-anorexia, was enhanced by intracerebroventricular infusion of NPY in rats which had food available during 2h/day. By contrast, NPY stimulated food intake but not wheel running in rats which had food available continuously. These findings are inconsistent with the prevailing theory of the role of the hypothalamus in the regulation of body weight according to which food intake is a homeostatic process controlled by "orexigenic" and "anorexigenic" neural networks. However, the finding that treatment with NPY, generally considered an "orexigen", can increase physical activity and decrease food intake and cause a loss of body weight is in line with the clinical observation that patients with anorexia nervosa are physically hyperactive and eat only little food despite having depleted body fat and up-regulated hypothalamic "orexigenic" peptides.

It is suggested that the symptoms of anorexia nervosa are physiological responses to starvation. There is no evidence of a neural or non-neural dysfunction that predisposes women for anorexia nervosa and the endocrine and psychological consequences of starvation are reversed once patients have re-learnt how to eat and regained a normal body weight. Because variability in the supply of food may be a common evolutionary condition, it is more likely that body weight is variable than constant in normal circumstances. The role of the neuroendocrine system in times of feast and famine is to allow the individual to adopt behavioral strategies as needed rather than maintaining body weight homeostasis. Treatment of anorexic patients should aim at reducing their high level of physical activity in order to facilitate eating.

We present the case of an Australian girl with severe anorexia nervosa who had previously been resistant to treatment, and who was subsequently treated successfully by an innovative programme at the Karolinska Institute in Stockholm. The programme is based on a distinctive concept of causation of eating disorders in which it is postulated that they develop as a consequence of starvation rather than a primary mental disorder. The treatment focuses on relearning how to eat and perceive satiety using a unique feed-back system, together with provision of warmth, limitation of exercise and facilitating social adaptation.

Eating disorders, i.e. anorexia and bulimia nervosa, are disorders of eating behavior and body weight regulation. Most likely because there are few, if any, effective treatments, eating disorders are considered to be chronic disorders interrupted only by intermittent periods of short-lived remission. The neurobiology of eating, most of which explores hypothalamic mechanisms, has had no influence on the treatment of eating disorders, with the exception of psychopharmacology. However, while most patients are treated with psychoactive drugs, there is no evidence that these are effective. This may be because pharmacological attempts so far have targeted the wrong symptoms. We review the symptomatology of anorexia and bulimia and the outcome of presently used interventions. Everybody agrees that outcome must improve and to attack this clinical problem, we suggest a neurobiologically plausible framework for how the disorders develop and how they are maintained and outline a method of treatment and its results.

Evidence for the effectiveness of existing treatments of patients with eating disorders is weak. Here we describe and evaluate a method of treatment in a randomized controlled trial. Sixteen patients, randomly selected out of a group composed of 19 patients with anorexia nervosa and 13 with bulimia nervosa, were trained to eat and recognize satiety by using computer support. They rested in a warm room after eating, and their physical activity was restricted. The patients in the control group (n = 16) received no treatment. Remission was defined by normal body weight (anorexia), cessation of binge eating and purging (bulimia), a normal psychiatric profile, normal laboratory test values, normal eating behavior, and resumption of social activities. Fourteen patients went into remission after a median of 14.4 months (range 4.9-26.5) of treatment, but only one patient went into remission while waiting for treatment (P = 0.0057). Relapse is considered a major problem in patients who have been treated to remission. We therefore report results on a total of 168 patients who have entered our treatment program. The estimated rate of remission was 75%, and estimated time to remission was 14.7 months (quartile range 9.6 > or = 32). Six patients (7%) of 83 who were treated to remission relapsed, but the others (93%) have remained in remission for 12 months (quartile range 6-36). Because the risk of relapse is maximal in the first year after remission, we suggest that most patients treated with this method recover.

On the standard perspective, anorexia nervosa and other eating disorders are caused by genetically determined, neurochemically mediated mental illnesses. Standard treatment, cognitive behavioral therapy (CBT), targets cognitive processes thought to maintain the disorders. Effective neurochemically based treatments are not available and the rate of remission is ≤25% 1 year after CBT, with unknown outcomes in the long-term. With starvation as the major threat in biological history, the evolutionary perspective focuses on foraging for food and eating behavior. A neural network, including hypothalamic arcuate peptide-neurons, brainstem serotonin- and dopamine-neurons and their prefrontal cortical projections, mediates (rather than controls) the behavioral adaptations to variations in food availability; activation of the network is associated with opposing behavioral outcomes depending upon external variations. In the clinic, the control of eating behavior is therefore outsourced to a machine that provides feedback on how to eat. Hundreds of eating disorders patients have recovered by practicing eating; the rate of remission is 75% in on average 1 year of treatment, the rate of relapse is 10% over 5 years of follow-up and no patient has died. A two-parameter asymptotic exponential growth curve modeled the eating behavior of 17 healthy women but not that of 17 women with anorexia nervosa. When in remission, the eating behavior of the anorexic women approached that of the healthy women. It is suggested that the treatment of eating disorders should focus on eating behavior. [ABSTRACT FROM AUTHOR]

Mental causation takes explanatory priority over evolutionary biology in most accounts of eating disorders. The evolutionary threat of starvation has produced a brain that assists us in the search for food and mental change emerges as a consequence. The major mental causation hypothesis: anxiety causes eating disorders, has been extensively tested and falsified. The subsidiary hypothesis: anxiety and eating disorders are caused by the same genotype, generates inconsistent results because the phenotypes are not traits, but vary along dimensions. Challenging the mental causation hypothesis in Feighner et al. (1972) noted that anorexic patients are physically hyperactive, hoarding for food, and they are rewarded for maintaining a low body weight. In 1996, Feighner’s hypothesis was formalized, relating the patients’ behavioral phenotype to the brain mechanisms of reward and attention (Bergh and Södersten, 1996), and in 2002, the hypothesis was clinically verified by training patients how to eat normally, thus improving outcomes (Bergh et al., 2002). Seventeen years later we provide evidence supporting Feighner’s hypothesis by demonstrating that in 2012, 20 out of 37 patients who were referred by a psychiatrist, had a psychiatric diagnosis that differed from the diagnosis indicated by the SCID-I. Out of the 174 patients who were admitted in 2012, most through self-referral, there was significant disagreement between the outcomes of the SCID-I interview and the patient’s subjective experience of a psychiatric problem in 110 of the cases. In addition, 358 anorexic patients treated to remission scored high on the Comprehensive Psychopathological Rating Scale, but an item response analysis indicated one (unknown) underlying dimension, rather than the three dimensions the scale can dissociate in patients with psychiatric disorders. These results indicate that psychiatric diagnoses, which are reliable and valid in patients with psychiatric disorders, are less well suited for patients with anorexia. The results are in accord with the hypothesis of the present Research Topic, that eating disorders are not always caused by disturbed psychological processes, and support the alternative, clinically relevant hypothesis that the behavioral phenotype of the patients should be addressed directly.