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Incidental findings from animal experiments involving administration of exogenous opioid agonists indicate that there are close links between the endogenous opioid system and feeding behaviour. Subsequent investigations aimed at elucidating the nature of the opioid-feeding relationship led to a wide variety of findings, some of them apparently contradictory. This paper examines the effects of opioid agonists and antagonists on feeding behaviour, and considers the evidence relating levels of endogenous opioids to feeding states, with particular reference to certain eating disorders, including anorexia nervosa, bulimia nervosa, Prader-Willi syndrome, and eating-induced obesity. The receptors which may be involved in opioid-feeding relationships are discussed. Relationships between the endogenous opioid system and other systems, such as the dopaminergic, noradrenergic and hormonal systems, are considered insofar as they may have bearing on the modulation of feeding behaviour. Finally, three theories are briefly outlined which attempt to link the endogenous opioid system with feeding modulation and the pathogenesis of certain eating disorders. The suggestion is put forward that anorexia nervosa may represent a pathological consequence of the triggering of a primitive mechanism for coping with unforeseen food shortages which may have short-term advantages, e.g., for masking or temporarily alleviating a depressed state.
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PMID:Opioid involvement in feeding behaviour and the pathogenesis of certain eating disorders. 874 94

This cross-sectional survey used a self-report questionnaire to measure the prevalence and correlates of bulimia nervosa and bulimic behaviors in a sample of undergraduate students enrolled in two state-supported universities in Texas in 1990. In one university, the student population was predominantly white; in the other, it was predominantly nonwhite. Bulimia status was assessed using criteria from the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised (DSM-III-R), of the American Psychiatric Association and was operationalized using the Revised Bulimia Test. Overall, 0.9% of the sample, 1.3% of the females, and 0.2% of the males were classified as having bulimia nervosa. The prevalence of bulimic behaviors was 5.4% overall, 6.6% for females, and 3.6% for males. There was no racial/ethnic difference in the prevalence of bulimia nervosa or bulimic behaviors; 1.5% of the whites (n = 459) and 0.4% of the nonwhites (n = 693) were classified as having bulimia nervosa, while 5.5% of the whites and 5.3% of the nonwhites reported bulimic behaviors. In univariate analysis, female sex, obesity, dieting behavior, and a family history of alcoholism, drug abuse, and depression were statistically associated with bulimic behaviors. After adjustment for covariates, only obesity and dieting behavior were statistically significant. We concluded that the sex difference in bulimic behaviors reported in other studies may be due to the failure to control for confounding factors.
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PMID:Prevalence and correlates of bulimia nervosa and bulimic behaviors in a racially diverse sample of undergraduate students in two universities in southeast Texas. 878 59

Research in obesity has generally not demonstrated an association with increased rates of psychopathology compared to normal-weight comparison groups. However, studies of obese individuals from clinical samples with recurrent binge eating or binge eating disorder (BED) have generally revealed increased rates of psychiatric comorbidity compared to non-binge eating obese individuals. Also, several studies have reported finding an association between BED and elevated rates of psychological distress, social problems, and impaired self-esteem. This report provides an overview of research findings regarding psychiatric comorbidity among individuals with BED, and it presents suggestion for future research.
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PMID:Comorbidity and binge eating disorder. 882 May 25

In this study we examined whether obese women with binge eating disorder (BED) reporting earlier onset binge eating differed from those with later onset binge eating on salient clinical parameters. Subjects were 112 women who sought treatment for BED. Subjects with early (< or = age 18) and later onset (> age 18) did not differ in age, weight, body mass index, or severity of binge eating. Participants were interviewed using the Eating Disorder Examination (EDE) and the Structured Clinical Interview for DSM-III-R, and completed a weight and diet history questionnaire. Early-onset binge eaters were more likely than those with later-onset to binge-eat before dieting, to have early onset of obesity and dieting, to have longer binge-free periods, and more paternal obesity and binge eating. Early-onset binge eaters also reported more eating-disorders psychopathology, and they were more likely to report a lifetime history of bulimia nervosa and DSM-III-R mood disorder. These data suggest that there are marked differences among BED patients presenting for treatment. Further research is needed to determine whether these differences reflect a different etiology or have implications for treatment.
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PMID:Binge eating onset in obese patients with binge eating disorder. 882 May 27

Binge-eating behavior is often thought to be the consequence of energy restriction and dietary restraint. However, evidence is accumulating that recurrent eating binges may be one behavioral mechanism in the expression of familial obesity, and may therefore precede the onset of dieting. The profile of patients with the DSM-IV binge-eating disorder resembles that of patients with familial obesity. There is further evidence for the involvement of the endogenous opiate peptide system. Binge-type foods are often rich in fat, sugar, or both. The opiate antagonist naloxone reduced the consumption of sweet high-fat foods in obese and lean female binge-eaters, though not in nonbinging controls. In contrast, obese as opposed to lean subjects were not differentially affected by naloxone. These data provide a psychobiological validation of the DSM-IV binge eating disorder and suggest that binge eating may be triggered by physiological events. As opposed to being the outcome of dieting, binge-eating episodes should be considered as its possible cause.
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PMID:Metabolic determinants of binge eating. 882 May 26

Obese individuals with binge eating disorder (BED) differ from obese non-binge eating (NBE) individuals in a number of clinically relevant ways. This study examined attitudinal responses to various measures of body image in women seeking obesity treatment, by comparing NBE participants (n = 80) to those with BED (n = 48). It was hypothesized that women with BED would demonstrate greater attitudinal disturbance of body image compared to NBE individuals. It was further hypothesized that significant differences between groups would remain after statistically controlling for degree of depression. Consistent with the primary hypothesis, BED participants reported significantly increased attitudinal disturbance in body dissatisfaction and size perception compared to NBE participants. Although shared variance was observed between measures of depression and body image on some items, several aspects of increased body image disturbance remained after statistically controlling for depression. Treatment implications and recommendations for future research are discussed.
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PMID:Differences in body image and depression among obese women with and without binge eating disorder. 888 7

The purpose of this article is to summarize briefly potential biological pathways that are common among anorexia nervosa, bulimia nervosa, and obesity. We conclude that data on serotonergic and beta-endorphin regulatory systems provide the most promising leads for potential trait-based etiological theories. We then discuss the contribution of current data to a better understanding of the etiology and maintenance of eating disorders. Finally, we comment on how the exploration for common biological mechanisms highlights problems in nosological diagnosis (i.e., the lack of symptom specificity among disorders) and obscures the etiological significance of social stressors and cultural factors.
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PMID:Common biological pathways in eating disorders and obesity. 890 39

This paper describes a framework for involving schools in primary and secondary prevention of eating disturbances. The issues of why, what, who, and how are considered. Research on the prevalence and consequences of obesity, anorexia and bulimia nervosa, unhealthy dieting, and behaviors such as binge eating and purging indicates why prevention is necessary. Research on the etiology of eating disturbances also provided a basis for determining what factors need to be addressed. However, research has not adequately addressed the question of who should be targeted for prevention and how the topic of prevention should be approached. While different approaches to school-based prevention programs are possible, a comprehensive school-based program is recommended. Important components of a comprehensive program include staff training, classroom interventions, integration of relevant material into existing curriculum, individual counseling and small group work with high risk students, referral systems, opportunities for healthy eating, modifications within the physical education program, and outreach activities. This type of comprehensive program is based on an ecological model for health promotion and aims at the modification of both individual and environmental determinants of behavior.
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PMID:School-based programs for preventing eating disturbances. 893 12

Measures of abnormal eating behaviour in 48 women referred for psychiatric assessment following an act of deliberate self-poisoning (subjects) were compared with those in 50 women attending an accident and emergency department following minor accidental injury (controls). Disordered eating behaviour was significantly more prevalent in the subject group, even when the effect of depression was removed. Four subjects fulfilled the diagnostic criteria for bulimia nervosa, but none of the subjects met the diagnostic criteria for anorexia nervosa. The prevalence of obesity was the same in both subject and control groups. The degree of abnormal eating was very strongly correlated with a measure of inwardly directed irritability in both subjects and controls, and was strongly associated with measures of impulsiveness, outwardly directed irritability and anxiety in subjects.
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PMID:Eating disorder in women admitted to hospital following deliberate self-poisoning. 906 79

The purpose was to examine the rate of alexithymia as measured by the Toronto Alexithymia Scale in a clinical sample of obese women without Binge Eating Disorder. Subjects included 165 inpatients in an eating disorder unit and 135 normal-weight individuals (comparison group). The obese subjects also completed a series of tests including the Minnesota Multiphasic Personality Inventory, the Anxiety Scale Questionnaire, and the Eating Attitude Test. Analysis showed that the subgroups of obese persons differ in important ways and cannot necessarily be treated, studied, or understood through a single paradigm. Alexithymic behaviour, too, was not characteristic of obesity, but it was present only in the subgroup of subjects with psychopathological characteristics.
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PMID:Alexithymia in a clinical sample of obese women. 912 58


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