Food Addiction and Bulimia Nervosa

In individuals with obesity and binge eating disorder (BED), eating patterns can show addictive qualities, with similarities to substance use disorders on behavioural and neurobiological levels. Bulimia nervosa (BN) has received less attention in this regard, despite their regular binge eating symptoms. The Yale Food Addiction Scale (YFAS) was developed according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, diagnostic criteria for substance use disorders, and food addiction can be diagnosed when at least three addiction symptoms are endorsed and a clinically significant impairment or distress is present. Although the prevalence of food addiction diagnoses is increased in individuals with obesity and BED, recent studies which used the YFAS showed that there are also individuals with normal weight who can be classified as being ‘food addicted’. Based on self‐reported eating disorder symptoms, women with current (n = 26) or remitted (n = 20) BN, and a control group of women matched for age and body mass index (n = 63) completed the YFAS and other measures. Results revealed that all patients with current BN received a food addiction diagnosis according to the YFAS while only six (30%) women with remitted BN did. None of the women in the control group received a food addiction diagnosis. Results provide support for the notion that BN can be described as addiction‐like eating behaviour and suggest that food addiction most likely improves when BN symptoms remit. Copyright © 2014 John Wiley & Sons, Ltd and Eating Disorders Association.     

Obesity and Its Relationship to Addictions: Is Overeating a Form of Addictive Behavior?

Obesity is a major public health problem and notoriously difficult to treat. There are many parallels between obesity/overeating and addictions to alcohol and drugs. This paper discusses similarities between obesity and addictive disorders, including common personality characteristics, disruptive behavior syndromes, and brain mechanisms. Although there are important differences between overeating and other addictive behaviors, an addiction model of overeating may effectively inform prevention and treatment of obesity     

Are trans diagnostic models of eating disorders fit for purpose? A consideration of the evidence for food addiction

Explanatory models for eating disorders have changed over time to account for changing clinical presentations. The transdiagnostic model evolved from the maintenance model, which provided the framework for cognitive behavioural therapy for bulimia nervosa. However, for many individuals (especially those at the extreme ends of the weight spectrum), this account does not fully fit. New evidence generated from research framed within the food addiction hypothesis is synthesized here into a model that can explain recurrent binge eating behaviour. New interventions that target core maintenance elements identified within the model may be useful additions to a complex model of treatment for eating disorders.     

Assessment and treatment of co-occurring eating disorders in privately funded addiction treatment programs

Privately funded addiction treatment programs were surveyed to increase understanding of assessment and current treatment options for patients with co-occurring substance use and eating disorders. Data were collected from face-to-face interviews with program administrators of a nationally representative sample of 345 private addiction treatment programs. Although the majority of programs reported screening for eating disorders, programs varied in screening instruments used. Sixty-seven percent reported admitting cases of low severity. Twenty-one percent of programs attempt to treat eating disorders. These results highlight the need for education of addiction treatment professionals in assessment, referral, and treatment of eating disorders.     

Obesity and addiction: can a complication of surgery help us understand the connection?

Obesity is a multifactorial, chronic disease that has proven difficult to treat. An increased understanding of aetiological mechanisms is critical to the development of more effective obesity prevention and treatment strategies. A growing body of empirical evidence has demonstrated parallels between obesity, overeating and substance abuse, including shared behavioural, psychological and neurophysiological factors implicated in the excessive intake of both food and substances of abuse. Several different lines of research have recently emerged that hold the potential to shed light on the connection between obesity, food reward and addiction, with studies examining changes in alcohol use/misuse after weight loss surgery providing a particularly interesting perspective on these interrelationships. However, these lines of investigation have proceeded in relative isolation, and relevant research findings have yet to be integrated in a synthesized, comprehensive manner. To provide an opportunity to achieve such a synthesis, a scientific symposium was convened at the Radcliffe Institute in Cambridge, Massachusetts. Invited participants were researchers working in diverse domains related to the intersection between obesity and addiction. Extensive discussion was generated suggesting novel research directions. In this article, we summarize and synthesize the symposium participants' ongoing research in this area, incorporating additional relevant research holding potential clues regarding the connections between obesity, weight loss surgery and addiction.     

Food Addiction and Bulimia Nervosa: New Data Based on the Yale Food Addiction Scale 2.0

Previous research on ‘food addiction’ as measured with the Yale Food Addiction Scale (YFAS) showed a large overlap between addiction‐like eating and bulimia nervosa. Most recently, a revised version of the YFAS has been developed according to the changes made in the diagnostic criteria for substance use disorder in the Diagnostic and Statistical Manual of Mental Disorders fifth edition. The current study examined prevalence and correlates of the YFAS2.0 in individuals with bulimia (n = 115) and controls (n = 341). Ninety‐six per cent of participants with bulimia and 14% of controls received a YFAS2.0 diagnosis. A higher number of YFAS2.0 symptoms was associated with lower interoceptive awareness, higher depressiveness, and higher impulsivity in both groups. However, a higher number of YFAS2.0 symptoms was associated with higher body mass and weight suppression in controls only and not in participants with bulimia. The current study is the first to show a large overlap between bulimia and ‘food addiction’ as measured with the YFAS2.0, replicating and extending findings from studies, which used the previous version of the YFAS. Compensatory weight control behaviours in individuals with bulimia likely alleviate the association between addiction‐like eating and higher body mass. Thus, the large overlap between bulimia and ‘food addiction’ should be taken into consideration when examining the role of addiction‐like eating in weight gain and obesity. Copyright © 2016 John Wiley & Sons, Ltd and Eating Disorders Association.     

Functional neuroimaging: a new generation of human brain studies in obesity research

Obesity is predominantly caused by overeating, an abnormal behaviour for which there is no unequivocal neurophysiological explanation. Functional neuroimaging techniques, such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), have recently emerged as new tools to search for regions of the brain that are involved in the regulation of eating behaviours and those that are involved in the pathophysiology of obesity. Using these techniques, a limited number of studies have provided the first in vivo images of the human hypothalamic response to nutritional stimuli and revealed the complexity of the human brain response to hunger, taste, and satiation. Selective differences have been reported in the functional architecture of the brain of obese and lean individuals. We discuss current use and possible future developments of functional neuroimaging applied to obesity research. We conclude that functional neuroimaging provides an increasingly important tool for investigating how different regions of the brain work in concert to orchestrate normal eating behaviours and how they conspire to produce obesity and other eating disorders.     

Obesity and addiction: neurobiological overlaps

Drug addiction and obesity appear to share several properties. Both can be defined as disorders in which the saliency of a specific type of reward (food or drug) becomes exaggerated relative to, and at the expense of others rewards. Both drugs and food have powerful reinforcing effects, which are in part mediated by abrupt dopamine increases in the brain reward centres. The abrupt dopamine increases, in vulnerable individuals, can override the brain's homeostatic control mechanisms. These parallels have generated interest in understanding the shared vulnerabilities between addiction and obesity. Predictably, they also engendered a heated debate. Specifically, brain imaging studies are beginning to uncover common features between these two conditions and delineate some of the overlapping brain circuits whose dysfunctions may underlie the observed deficits. The combined results suggest that both obese and drug‐addicted individuals suffer from impairments in dopaminergic pathways that regulate neuronal systems associated not only with reward sensitivity and incentive motivation, but also with conditioning, self‐control, stress reactivity and interoceptive awareness. In parallel, studies are also delineating differences between them that centre on the key role that peripheral signals involved with homeostatic control exert on food intake. Here, we focus on the shared neurobiological substrates of obesity and addiction.     

Nonpeptide corticotropin-releasing hormone receptor type 1 antagonists and their applications in psychosomatic disorders

Overproduction of corticotropin-releasing hormone (CRH) and stress system abnormalities are seen in psychiatric diseases such as depression, anxiety, eating disorders, and addiction. Investigations of CRH type 1 receptor (CRHR1) nonpeptide antagonists suggest therapeutic potential for treatment of these and other neuropsychiatric diseases. However, overproduction of CRH in the brain and on its periphery and disruption of the hypothalamic-pituitary-adrenal axis are also found in 'somatic' disorders. Some rare forms of Cushing's disease and related pituitary/adrenal disorders are obvious applications for CRHR1 antagonists. In addition, however, these antagonists may also be effective in treating more common somatic diseases. Patients with obesity and metabolic syndrome who often have subtle, but chronic hypothalamic-pituitary-adrenal hyperactivity, which may reflect central dysregulation of CRH and consequently glucocorticoid hypersecretion, could possibly be treated by administration of CRHR1 antagonists. Hormonal, autonomic, and immune aberrations are also present in chronic inflammatory, autoimmune, and allergic diseases, with considerable evidence linking CRH with the observed abnormalities. Furthermore, autonomic dysregulation is a prominent feature of common gastrointestinal disorders, such as irritable bowel syndrome and peptic ulcer disease. Patients with irritable bowel syndrome and other gastrointestinal disorders frequently develop altered pain perception and affective symptoms. CRH acts peripherally to modulate bowel activity both directly through the autonomic system and centrally by processing viscerosensory and visceromotor neural signals. This review presents clinical and preclinical evidence for the role of CRH in the pathophysiology of these disorders and for potential diagnostic and therapeutic applications of CRHR1 antagonists. Recognition of a dysfunctional stress system in these and other diseases will alter the understanding and treatment of 'psychosomatic' disorders.     

The key to unlocking the virtual body: virtual reality in the treatment of obesity and eating disorders

Obesity and eating disorders are usually considered unrelated problems with different causes. However, various studies identify unhealthful weight-control behaviors (fasting, vomiting, or laxative abuse), induced by a negative experience of the body, as the common antecedents of both obesity and eating disorders. But how might negative body image—common to most adolescents, not only to medical patients—be behind the development of obesity and eating disorders? In this paper, I review the “allocentric lock theory” of negative body image as the possible antecedent of both obesity and eating disorders. Evidence from psychology and neuroscience indicates that our bodily experience involves the integration of different sensory inputs within two different reference frames: egocentric (first-person experience) and allocentric (third-person experience). Even though functional relations between these two frames are usually limited, they influence each other during the interaction between long- and short-term memory processes in spatial cognition. If this process is impaired either through exogenous (e.g., stress) or endogenous causes, the egocentric sensory inputs are unable to update the contents of the stored allocentric representation of the body. In other words, these patients are locked in an allocentric (observer view) negative image of their body, which their sensory inputs are no longer able to update even after a demanding diet and a significant weight loss. This article discusses the possible role of virtual reality in addressing this problem within an integrated treatment approach based on the allocentric lock theory.     

Double deletion of melanocortin 4 receptors and SAPAP3 corrects compulsive behavior and obesity in mice

Compulsive behavior is a debilitating clinical feature of many forms of neuropsychiatric disease, including Tourette syndrome, obsessive-compulsive spectrum disorders, eating disorders, and autism. Although several studies link striatal dysfunction to compulsivity, the pathophysiology remains poorly understood. Here, we show that both constitutive and induced genetic deletion of the gene encoding the melanocortin 4 receptor (MC4R), as well as pharmacologic inhibition of MC4R signaling, normalize compulsive grooming and striatal electrophysiologic impairments in synapse-associated protein 90/postsynaptic density protein 95-associated protein 3 (SAPAP3)-null mice, a model of human obsessive-compulsive disorder. Unexpectedly, genetic deletion of SAPAP3 restores normal weight and metabolic features of MC4R-null mice, a model of human obesity. Our findings offer insights into the pathophysiology and treatment of both compulsive behavior and eating disorders.     

Reward processing in obesity,substance addiction and non‐substance addiction

Similarities and differences between obesity and addiction are a prominent topic of ongoing research. We conducted an activation likelihood estimation meta‐analysis on 87 studies in order to map the functional magnetic resonance imaging (fMRI) response to reward in participants with obesity, substance addiction and non‐substance (or behavioural) addiction, and to identify commonalities and differences between them. Our study confirms the existence of alterations during reward processing in obesity, non‐substance addiction and substance addiction. Specifically, participants with obesity or with addictions differed from controls in several brain regions including prefrontal areas, subcortical structures and sensory areas. Additionally, participants with obesity and substance addictions exhibited similar blood‐oxygen‐level‐dependent fMRI hyperactivity in the amygdala and striatum when processing either general rewarding stimuli or the problematic stimuli (food and drug‐related stimuli, respectively). We propose that these similarities may be associated with an enhanced focus on reward – especially with regard to food or drug‐related stimuli – in obesity and substance addiction. Ultimately, this enhancement of reward processes may facilitate the presence of compulsive‐like behaviour in some individuals or under some specific circumstances. We hope that increasing knowledge about the neurobehavioural correlates of obesity and addictions will lead to practical strategies that target the high prevalence of these central public health challenges.     

Food Addiction in Overweight and Obese Adolescents Seeking Weight‐loss Treatment

Some forms of overeating closely resemble addictive behaviour. The Yale Food Addiction Scale (YFAS) was developed to measure such addiction‐like eating in humans and has been employed in numerous studies for examining food addiction in adults. Yet, little is known about food addiction in children and adolescents. Fifty adolescents were recruited at the beginning of treatment in a weight‐loss hospital and completed the YFAS among other questionnaires. Nineteen participants (38%) received a YFAS diagnosis, who did not differ in age, body mass and gender distribution from those not receiving a diagnosis. However, those with food addiction reported more binge days, more frequent food cravings, higher eating, weight and shape concerns, more symptoms of depression and higher attentional and motor impulsivity. Eating restraint and nonplanning impulsivity did not differ between groups. Results replicate findings from studies in obese adults such that food addiction is not related to age, gender, body mass or eating restraint, but to higher eating pathology, more symptoms of depression and higher impulsivity. Furthermore, results highlight that particularly attentional impulsivity is related to ‘food addiction’. Addiction‐like eating appears to be a valid phenotype in a substantial subset of treatment‐seeking, obese adolescents. Copyright © 2015 John Wiley & Sons, Ltd and Eating Disorders Association.     

The stomach–brain axis

The stomach has distinct functions in relation to the ingestion and handling of solids and liquids. These functions include storage of the food before it is gradually emptied into the duodenum, mechanical crushing of larger food particles to increase the surface area, secretion of an acidic enzyme rich gastric juice and mixing the ingested food with the gastric juice. In addition, the stomach ‘senses’ the composition of the gastric content and this information is passed via the vagal nerve to the lateral hypothalamus and the limbic system, most likely as palatability signals that influence eating behaviour. Other sensory qualities related to the stimulation of gastric tension receptors are satiety and fullness. Receptors that respond to macronutrient content or gastric wall tension influence appetite and meal related hormone responses.The ingestion of food – in contrast to an infusion of nutrients into the stomach – has distinct effects on the activation of specific brain regions. Brain areas such as thalamus, amygdala, putamen and praecuneus are activated by the ingestion of food. Gastric nutrient infusion evokes greater activation in the hippocampus and anterior cingulate. The brain integrates these interrelated neural and hormonal signals arising from the stomach as well as visual, olfactory and anticipatory stimuli that ultimately influence eating and other behavioural patterns. Furthermore, there is now good evidence from experimental studies that gastric afferents influence mood, and animal studies point towards the possibility that gastric dysfunction may be a risk factor for mood disorders such as anxiety and depression. The stomach is also not only colonised by Helicobacter pylori but a large array of bacteria. While there is sufficient evidence to suggest that H. pylori may alter caloric intake and mood, the role of other gastric microbiome for the brain function is unknown. To address this appropriate targeted gastric microbiome studies would be required instead of widely utilised opportunistic stool microbiome studies.In summary, it is now well established that there are important links between the brain and the stomach that have significant effects on gastric function. However, the stomach also influences the brain. Disturbances in the crosstalk between the stomach and the brain may manifest as functional GI disorders while disturbances in the stomach–brain communication may also result in an altered regulation of satiety and as a consequence may affect eating behaviour and mood. These observations may enable the identification of novel therapies targeted at the gastroduodenum that positively alter brain function and treat or prevent conditions such as obesity or functional gastrointestinal disorders.     

The interaction between eating disorders and celiac disease: an exploration of 10 cases

Celiac disease is an inflammatory disorder in which certain peptides from wheat and related grains trigger and maintain an immune reaction in the small intestine. Anorexia nervosa and bulimia nervosa are eating disorders that are morbid and, at times, life-threatening forms of psychopathology. Despite a large body of evidence describing the detrimental effects of eating disorders on the gastrointestinal system, information on the role of the gastrointestinal system in causing or mimicking eating disorders is scarce. To date, eating disorders, as a comorbid condition affecting individuals with celiac disease, has received surprisingly little attention with only a single report found in peer-reviewed literature. In this report, we describe a series of 10 individuals with both celiac disease and eating disorders. These cases demonstrate the complex ways in which celiac disease and eating disorders interact with important clinical implications for the diagnosis and treatment of both illnesses. Our findings suggest that clinicians treating patients with eating disorders or celiac disease should be aware of both conditions to provide optimum care.     

Why Do We Diagnose Different Types of Eating Disorder? Arguments for a Change in Research and Clinical Practice

It is argued that the diagnosis of different types of eating disorders lacks either scientific validity or clinical utility, and that the forthcoming elaboration of diagnostic schemes (DSM-IV) is unlikely to improve matters. The central problem with the diagnosiscentred model of the eating disorders seems to be that it is based on an inappropriate model of clinical practice, focusing on syndromes rather than symptoms. However, it would be equally invalid to assume that there is little or no similarity across eatingdisorder sufferers, as suggested by an individual-centred model. Our understanding of the psychopathology and treatment of the eating disorders would benefit from employing a more clinically-appropriate model of practice—the ‘scientist practitioner’ model. Discarding specific diagnoses and using this model would help to make clinical practice and research in the eating disorders more mutually informative.     

Psychologische Faktoren in der Entstehung und Behandlung der Adipositas

BACKGROUND: The prevalence of obesity has distinctly increased in almost all industrial countries in the past decades and is considered today to be one of the most important health problems. In Germany, between 12 and 18% of the adult population is obese. Besides the known risk factors such as arterial hypertension, lipometabolism disorders and type-2 diabetes mellitus, obesity is connected to severe psychosocial burdens. The genesis of obesity is multifactorial, besides genetic factors environmental ones such as an increase in hypercaloric food and at the same time a reduction of physical activity play a decisive role. PSYCHOGENESIS: Whereas earlier mainly psychic factors were discussed in the genesis of obesity, and here especially the question as to which personality variables are most frequently associated with obesity, the discussion in the past decades has increasingly shifted towards psychosocial consequences. It does, however, seem justified to adhere to a "psychogenesis" of obesity in a subgroup of obese people. Psychosomatic/psychiatric disorders lead to a change in eating behavior and physical exercise, the result being a sustained positive energy balance with overweight and obesity. PSYCHOSOCIAL PROBLEMS AND TREATMENT CONCEPTS: This paper describes the psychosocial problems of obese people with an emphasis on the question of psychiatric co-morbidity in general and eating disorders in particular. The results of mainly behavioral therapeutically oriented treatment concepts are presented and school-overlapping concepts discussed.     

Childhood sexual abuse and obesity

The causes of the current obesity epidemic are multifactorial and include genetic, environmental, and individual factors. One potential risk factor may be the experience of childhood sexual abuse. Childhood sexual abuse is remarkably common and is thought to affect up to one-third of women and one-eighth of men. A history of childhood sexual abuse is associated with numerous psychological sequelae including depression, anxiety, substance abuse, somatization, and eating disorders. Relatively few studies have examined the relationship between childhood sexual abuse and adult obesity. These studies suggest at least a modest relationship between the two. Potential explanations for the relationship have focused on the role of disordered eating, particularly binge eating, as well as the possible "adaptive function" of obesity in childhood sexual abuse survivors. Nevertheless, additional research on the relationship between childhood sexual abuse and obesity is clearly needed, not only to address the outstanding empirical issues but also to guide clinical care.