Binge eating

pattern of disordered eating which consists of episodes of uncontrollable eating

Binge eating (often used interchangeably with Binge Eating Disorder) is overeating, followed by feelings of shame and guilt.

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  • 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.
  • Studies comparing PSH with GSH found no significant differences between treatment groups at end of treatment or follow-up. Comparison between different types of PSH/GSH found significant differences on eating disorder symptoms but not on bingeing/purging abstinence rates.
  • PSH/GSH may have some utility as a first step in treatment and may have potential as an alternative to formal therapist-delivered psychological therapy. Future research should focus on producing large well-conducted studies of self-help treatments in eating disorders including health economic evaluations, different types and modes of delivering self-help (e.g. computerised versus manual-based) and different populations and settings.
  • Personality traits have been implicated in the onset, symptomatic expression, and maintenance of eating disorders (EDs). The present article reviews literature examining the link between personality and EDs published within the past decade, and presents a meta-analysis evaluating the prevalence of personality disorders (PDs) in anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) as assessed by self-report instruments versus diagnostic interviews. AN and BN are both consistently characterized by perfectionism, obsessive-compulsiveness, neuroticism, negative emotionality, harm avoidance, low self-directedness, low cooperativeness, and traits associated with avoidant PD. Consistent differences that emerge between ED groups are high constraint and persistence and low novelty seeking in AN and high impulsivity, sensation seeking, novelty seeking, and traits associated with borderline PD in BN. The meta-analysis, which found PD rates of 0 to 58% among individuals with AN and BN, documented that self-report instruments greatly overestimate the prevalence of every PD.
  • Eating disorders, such as anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorders (BED), are described as abnormal eating habits that usually involve insufficient or excessive food intake. Animal models have been developed that provide insight into certain aspects of eating disorders. Several drugs have been found efficacious in these animal models and some of them have eventually proven useful in the treatment of eating disorders. This review will cover the role of monoaminergic neurotransmitters in eating disorders and their pharmacological manipulations in animal models and humans. Dopamine, 5-HT (serotonin) and noradrenaline in hypothalamic and striatal regions regulate food intake by affecting hunger and satiety and by affecting rewarding and motivational aspects of feeding. Reduced neurotransmission by dopamine, 5-HT and noradrenaline and compensatory changes, at least in dopamine D2 and 5-HT(2C/2A) receptors, have been related to the pathophysiology of AN in humans and animal models. Also, in disorders and animal models of BN and BED, monoaminergic neurotransmission is down-regulated but receptor level changes are different from those seen in AN. A hypofunctional dopamine system or overactive α2-adrenoceptors may contribute to an attenuated response to (palatable) food and result in hedonic binge eating. Evidence for the efficacy of monoaminergic treatments for AN is limited, while more support exists for the treatment of BN or BED with monoaminergic drugs.
  • While abnormalities in central norepinephrine regulation may contribute to abnormal eating patterns in bulimia nervosa, alterations in function of the peripheral sympathetic nervous system could contribute to the decreased metabolic rate and increased anxiety responses previously reported in these patients. To assess beta-adrenergic receptor sensitivity in bulimic patients, we studied cardiovascular and hormonal responses to acute pharmacological challenge with intravenously administered isoproterenol. In comparison to healthy controls, binge-abstinent bulimic patients had significantly reduced mean baseline plasma norepinephrine level, pulse rate, and systolic blood pressure, and significantly increased chronotropic responses to isoproterenol infusion. Decreased sympathoneural activity may contribute to a tendency for bulimic patients to maintain body weight despite low caloric intake.
  • There is no one sign of an eating disorder, however there are red flags. These can include excessive “fat, weight or calorie talk,” a pattern of eating a limited choice of low-calorie food or a pattern of occasional binge eating of calorie-dense foods.
    • Angela Guarda, M.D. "Eating Disorders". American Psychiatric Association. Archived from the original on 21 December 2014. Retrieved 4 December 2014.
  • Eating disorders occur in men too. An estimated 10 percent of people with anorexia nervosa and bulimia and a third or more of people with binge eating disorder are male.
    • Angela Guarda, M.D. "Eating Disorders". American Psychiatric Association. Archived from the original on 21 December 2014. Retrieved 4 December 2014.
  • Anorexia nervosa is specifically characterised by an excessive exercise engagement with fear of weight gain and aversion of fat, whereas people with bulimia nervosa present with binge eating and purging. These eating disorders are considered one of the most challenging psychiatric conditions to treat, and treatment usually comprises of cognitive–behavioural therapy and pharmacological management. Exercise is usually not recommended for patients with these conditions, mainly due to the belief that it might aggravate the progress of the disorder. However, there is evidence that exercise increases body mass index and reduce depression in people with binge eating. What is uncertain is whether physiotherapy interventions are effective in treating bulimia and anorexia nervosa.
  • Binge eating is the rapid consumption of an unusually-large amount of food in a short period of time. Unlike simple overeating, people who binge feel “out of control” during these episodes. This means that one “cannot stop the urge to eat” once it has begun, even after their stomach is full. Binging may “feel good” initially, but it quickly becomes distressing for the person who is absorbed in this behavior. Food is often eaten secretly and quickly. A binge is usually ended only with abdominal discomfort, social interruption or running out of food. When the binge is over, the person with bulimia often feels guilty and will engage in inappropriate behaviors to rid their body of the excess calories that were eaten.
  • We document here the first case of bulimia nervosa associated with primary hyperparathyroidism. The binge eating and self-induced vomiting that occurred for more than 10 years disappeared completely after the surgical cure of primary hyperparathyroidism. Depressive and anxiety symptoms also improved dramatically. The possible influence of derangement in calcium metabolism on the neurobiochemical mechanism of bulimia nervosa is discussed.
  • This study explored friendship variables in relation to body image, dietary restraint, extreme weight-loss behaviors (EWEBs), and binge eating in adolescent girls. From 523 girls, 79 friendship cliques were identified using social network analysis. Participants completed questionnaires that assessed body image concerns, eating, friendship relations, and psychological family, and media variables. Similarity was greater for within than for between friendship cliques for body image concerns, dietary restraint, and EWLBs, but not for binge eating. Cliques high in body image concerns and dieting manifested these concerns in ways consistent with a high weight/shape-preoccupied subculture. Friendship attitudes contributed significantly to the prediction of individual body image concern and eating behaviors. Use of EWLBs by friends predicted an individual's own level of use.
  • The development of eating disorders including anorexia nervosa, bulimia nervosa, binge eating disorder, and atypical eating disorders that affect many young women and even men in the productive period of their lives is complex and varied. While numbers of presumed risk factors contributing to the development of eating disorders are increasing, previous evidence for biological, psychological, developmental, and sociocultural effects on the development of eating disorders have not been conclusive. Despite the fact that a huge body of research has carefully examined the possible risk factors associated with the eating disorders, they have failed not only to uncover the exact etiology of eating disorders, but also to understand the interaction between different causes of eating disorders. This failure may be due complexities of eating disorders, limitations of the studies or combination of two factors. In this review, some risk factors including biological, psychological, developmental, and sociocultural are discussed.
  • It has been hypothesized that eating disorders have multiple and often shared etiologies including biological, psychological, developmental, and sociocultural. A tightly woven network of causes, symptoms, and outcomes of eating disorders makes the study of etiology of these disorders very challenging. Some suggested risk factors for eating disorders require to be defined as either integral parts of eating disorders syndrome such as body dissatisfaction, and perfectionism or outcome of prolonged disordered eating such as functional alterations in serotonin, and some mood disturbances. Researchers should structure their thought processes around this concept that some of currently well-known risk factors for eating disorders are concurrent symptoms of eating disorders. Hence paying special attention to the new and evolved concepts is highly recommended while studying the etiology of eating disorders.
  • The development of eating disorders including anorexia nervosa, bulimia nervosa, binge eating disorder, and atypical eating disorders that affect many young women and even men in the productive period of their lives is complex and varied. While numbers of presumed risk factors contributing to the development of eating disorders are increasing, previous evidence for biological, psychological, developmental, and sociocultural effects on the development of eating disorders have not been conclusive. Despite the fact that a huge body of research has carefully examined the possible risk factors associated with the eating disorders, they have failed not only to uncover the exact etiology of eating disorders, but also to understand the interaction between different causes of eating disorders. This failure may be due complexities of eating disorders, limitations of the studies or combination of two factors. In this review, some risk factors including biological, psychological, developmental, and sociocultural are discussed.
  • Studies have reported that the oral health status is jeopardized in patients with eating disorders. The aim was to review the oro-facial manifestations in patients with eating disorders. The address the focused question was "What is the oro-dental health status in patients with eating disorders?" MEDLINE/PubMed and Google Scholar databases were searched from 1948 to March 2012 using the following terms in various combinations: "Anorexia nervosa", "bulimia nervosa", "eating disorders", "dental", "oral health status". Letters to the editor, unpublished data and articles published in languages other than English were excluded. Dry lips, burning tongue and parotid gland swelling are common manifestations in patients with eating disorders as compared to medically healthy controls. The association of dental caries and periodontal disease in patients with eating disorders remains debatable. Temporomandibular disorders have also been reported to be more prevalent in patients with eating disorders as compared to healthy controls. A critical oral-dental examination during routine dental check-ups may reveal valuable information regarding the presence or absence of eating disorders in routine dental patients. This may be important information, updating the medical history, supporting the role of the physician.
  • According to the Diagnostic and Statistical Manual for Mental Disorders, Fourth Edition (DSM-IV), bulimia nervosa is characterized by recurrent episodes of binge eating followed by 1 or more compensatory behaviors to eliminate the calories (vomiting, laxatives, fasting, etc.) that take place on average a minimum of twice weekly for 3 or more months.5 Patients who do not meet the frequency or length criteria may be diagnosed with DSM-IV eating disorder not otherwise specified.
    Bulimia nervosa is also delineated into 2 distinct subtypes: purging and nonpurging. With the purging subtype, patients engage in some method to remove the binged food from their bodies. This is most often accomplished by self-induced vomiting but can include the misuse of laxatives, enemas, or diuretics. Nonpurging bulimics use fasting or excessive exercise as the primary compensation for binges but do not regularly purge. Regardless of subtype, bulimic patients have negative self-evaluations, placing inappropriate importance on weight and body image.
  • Eating disorders, such as anorexia, bulimia, and binge eating disorder, commonly involve a dysregulation of behavior (e.g., a lack or excess of inhibition and impulsive eating patterns) that is suggestive of prefrontal dysfunction. Functional neuro-imaging studies show that prefrontal-subcortical systems play a role in eating behavior and appetite in healthy individuals, and that people with eating disorders have altered activity in these systems. Eating behavior is often disturbed by illnesses and injuries that impinge upon prefrontal-subcortical systems. This study examined relationships between executive functioning and eating behavior in healthy individuals using validated behavioral rating scales (Frontal Systems Behavior Scale and Eating Inventory). Correlations demonstrated that increased dysexecutive traits were associated with disinhibited eating and greater food cravings. There was also a positive association with cognitive restraint of eating, suggesting that increased compensatory behaviors follow disinhibited eating. These psychometric findings reinforce those of other methodologies, supporting a role for prefrontal systems in eating.
  • Binge eating disorder (BED) was introduced in 1994 as a provisional eating disorder diagnosis. The core symptom is recurrent binge eating in the absence of inappropriate compensatory behaviors and/or extreme dietary restraint. This review examines the status of the literature on BED according to five criteria that have been proposed to determine whether BED warrants inclusion in the psychiatric nosology as a distinct eating disorder. We conclude that each of these criteria was met. There is a commonly accepted definition of and assessment approach to BED. The clinical utility and validity of BED have been established, and BED is distinguishable from both bulimia nervosa and obesity. BED should be included in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders
    • Striegel-Moore, RH; Franko, DL (2008). "Should binge eating disorder be included in the DSM-V? A critical review of the state of the evidence". Annual Review of Clinical Psychology. 4: 305–24. doi:10.1146/annurev.clinpsy.4.022007.141149. PMID 18370619.
  • This review summarises the results of psychopharmacological treatment studies on anorexia and, bulimia nervosa. Although several drugs have tested in patients with anorexia nervosa, the outcome of controlled studies has been disappointing. Trials of pharmacotherapy for bulimia nervosa have demonstrated that tricyclic antidepressants, monoamine oxidase inhibitors and selective serotonin reuptake inhibitors significantly reduce the frequency of binge eating and purging. In some cases, psychotherapists should accept the necessity of psychopharmacological intervention, although this does not imply a known biological cause of the eating disorder. However, the significance of antidepressant medication in the overall treatment of anorexia and bulimia nervosa remains unclear.
  • This Seminar adds to the previous Lancet Seminar about eating disorders, published in 2003, with an emphasis on the biological contributions to illness onset and maintenance. The diagnostic criteria are in the process of review, and the probable four new categories are: anorexia nervosa, bulimia nervosa, binge eating disorder, and eating disorder not otherwise specified. These categories will also be broader than they were previously, which will affect the population prevalence; the present lifetime prevalence of all eating disorders is about 5%. Eating disorders can be associated with profound and protracted physical and psychosocial morbidity. The causal factors underpinning eating disorders have been clarified by understanding about the central control of appetite. Cultural, social, and interpersonal elements can trigger onset, and changes in neural networks can sustain the illness. Overall, apart from studies reporting pharmacological treatments for binge eating disorder, advances in treatment for adults have been scarce, other than interest in new forms of treatment delivery.
  • Most people overeat from time to time, and many people believe they frequently eat more than they should. Eating large amounts of food, however, does not mean that a person has binge eating disorder. Most people with serious binge eating problems have some of the following symptoms that occur at least once a week for at least three months:
Frequent episodes of eating what others would consider an abnormally large amount of food
Frequent feelings of being unable to control what or how much is being eaten
Eating much more rapidly than usual
Eating until uncomfortably full
Eating large amounts of food, even when not physically hungry
Eating alone out of embarrassment at the quantity of food being eaten
Feelings of disgust, depression, or guilt after overeating
Fluctuations in weight
Feelings of low self-esteem
Frequent dieting
  • Binge eating disorder has been linked to other mental health disorders. Nearly half of all people with binge eating disorder have a history of depression, although the exact nature of the link is unclear. Many people report that anger, sadness, boredom, anxiety, or other negative emotions can trigger an episode of binge eating. Impulsive behavior and other psychological problems also seem to be more common in people with binge eating disorder.
  • The findings of this study raise questions about the concept of comorbidity as applied to eating disorders and suggest the likely utility for both research and clinical practice of considering eating-disordered symptoms in their characterological context (e.g., references 12, 34). The data from this study suggest that individuals who develop eating disorders who are constricted in most areas of their lives—e.g., who are passive and unassertive, emotionally constricted, and interpersonally avoidant—are likely to express this pattern with anorexic, rather than bulimic behavior. Clinically, these patients tend to be just as constricted in their sexual lives as they are with food, denying themselves pleasure, avoiding sexual relationships, feeling too ashamed or guilty to indicate to their partners what feels good, and so forth.
    Conversely, individuals with eating disorders whose ability to regulate their impulses and affects is tenuous—as expressed in spiraling emotions, tantrums, clinging to others for soothing, self-mutilation, and other impulsive acts—are likely to lose control over their eating in binges and to use self-destructive compensatory measures such as vomiting that momentarily help them regulate their affects. From this point of view, the question of whether bulimic symptoms should be regarded as impulsive behavior may be misplaced. The answer is probably that it depends on the personality configuration within which bulimic symptoms are contextualized. In low-functioning, emotionally dysregulated, type II bulimic patients, binge eating and purging may be functional equivalents of substance abuse, self-mutilation, and promiscuity. For these patients, bulimic symptoms may represent desperate efforts to regulate intense negative affects that call for immediate, and often maladaptive, responses. In contrast, high-functioning, perfectionistic, type I bulimic patients do not struggle with affects of the same intensity, and they have more adaptive coping strategies at their disposal for dealing with their distress. For these patients, binge eating is not equivalent to impulsive behaviors such as drinking or self-mutilation.

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