The hysterical anorexia epidemic in the French nineteenth-century

The official birth of hysterical anorexia is attributed to the French alienist Ernest Charles Lasègue (1816-1883). Starting from his 1873 article, anorexia as a ‘new’ psychopathological picture is subjected to extensive clinical and theoreticalstudy. This paper is not an analysis about the process through which anorexia was formalized as specific psychiatric condition. Rather, it focuses on another important issue: the possibility that the ‘same’ disorder may have different meaning depending on the historical period considered. Furthermore, it is asserted that the study of every pathological form is conditioned by social, individual and cultural conditions. For example, in the same year the English Sir William Gull publishes a paper about “anorexia nervosa” which is described in a different way depending on the different perspective. Lasègue’s description is a way of seeing a kind of sufferance, that is he ‘sees’ this pathology through the hysterical paradigm. Starting from these considerations, this article discusses the construct of ‘hysterical anorexia’ trying to understand why, in late nineteenth century France, hysteria and anorexia were viewed as two aspects of the same specific disorder. Finally, it is discussed why anorexia gradually emerged as an independent mental disorder just after the death of Charcot (1893)

Recent advances in understanding anorexia nervosa.

Anorexia nervosa is a complex psychiatric illness associated with food restriction and high mortality. Recent brain research in adolescents and adults with anorexia nervosa has used larger sample sizes compared with earlier studies and tasks that test specific brain circuits. Those studies have produced more robust results and advanced our knowledge of underlying biological mechanisms that may contribute to the development and maintenance of anorexia nervosa. It is now recognized that malnutrition and dehydration lead to dynamic changes in brain structure across the brain, which normalize with weight restoration. Some structural alterations could be trait factors but require replication. Functional brain imaging and behavioral studies have implicated learning-related brain circuits that may contribute to food restriction in anorexia nervosa. Most notably, those circuits involve striatal, insular, and frontal cortical regions that drive learning from reward and punishment, as well as habit learning. Disturbances in those circuits may lead to a vicious cycle that hampers recovery. Other studies have started to explore the neurobiology of interoception or social interaction and whether the connectivity between brain regions is altered in anorexia nervosa. All together, these studies build upon earlier research that indicated neurotransmitter abnormalities in anorexia nervosa and help us develop models of a distinct neurobiology that underlies anorexia nervosa

Could dopamine agonists aid in drug development for anorexia nervosa?

Anorexia nervosa is a severe psychiatric disorder most commonly starting during the teenage-years and associated with food refusal and low body weight. Typically there is a loss of menses, intense fear of gaining weight, and an often delusional quality of altered body perception. Anorexia nervosa is also associated with a pattern of high cognitive rigidity, which may contribute to treatment resistance and relapse. The complex interplay of state and trait biological, psychological, and social factors has complicated identifying neurobiological mechanisms that contribute to the illness. The dopamine D1 and D2 neurotransmitter receptors are involved in motivational aspects of food approach, fear extinction, and cognitive flexibility. They could therefore be important targets to improve core and associated behaviors in anorexia nervosa. Treatment with dopamine antagonists has shown little benefit, and it is possible that antagonists over time increase an already hypersensitive dopamine pathway activity in anorexia nervosa. On the contrary, application of dopamine receptor agonists could reduce circuit responsiveness, facilitate fear extinction, and improve cognitive flexibility in anorexia nervosa, as they may be particularly effective during underweight and low gonadal hormone states. This article provides evidence that the dopamine receptor system could be a key factor in the pathophysiology of anorexia nervosa and dopamine agonists could be helpful in reducing core symptoms of the disorder. This review is a theoretical approach that primarily focuses on dopamine receptor function as this system has been mechanistically better described than other neurotransmitters that are altered in anorexia nervosa. However, those proposed dopamine mechanisms in anorexia nervosa also warrant further study with respect to their interaction with other neurotransmitter systems, such as serotonin pathways

The anorexic mind

Anorexia and all eating disorders alike affect fundamental relationships between individuals and their bodies. This book portrays the eternal pain of the anorexic mind. Marilyn Lawrence traces the psychological origins of anorexia and discusses the fallacy of the ideal weight, size and shape that some women in anguish may compulsively seek

Altered structural and effective connectivity in anorexia and bulimia nervosa in circuits that regulate energy and reward homeostasis.

Anorexia and bulimia nervosa are severe eating disorders that share many behaviors. Structural and functional brain circuits could provide biological links that those disorders have in common. We recruited 77 young adult women, 26 healthy controls, 26 women with anorexia and 25 women with bulimia nervosa. Probabilistic tractography was used to map white matter connectivity strength across taste and food intake regulating brain circuits. An independent multisample greedy equivalence search algorithm tested effective connectivity between those regions during sucrose tasting. Anorexia and bulimia nervosa had greater structural connectivity in pathways between insula, orbitofrontal cortex and ventral striatum, but lower connectivity from orbitofrontal cortex and amygdala to the hypothalamus (P<0.05, corrected for comorbidity, medication and multiple comparisons). Functionally, in controls the hypothalamus drove ventral striatal activity, but in anorexia and bulimia nervosa effective connectivity was directed from anterior cingulate via ventral striatum to the hypothalamus. Across all groups, sweetness perception was predicted by connectivity strength in pathways connecting to the middle orbitofrontal cortex. This study provides evidence that white matter structural as well as effective connectivity within the energy-homeostasis and food reward-regulating circuitry is fundamentally different in anorexia and bulimia nervosa compared with that in controls. In eating disorders, anterior cingulate cognitive-emotional top down control could affect food reward and eating drive, override hypothalamic inputs to the ventral striatum and enable prolonged food restriction

Uncovering anorexia nervosa in a biofeedback clinic for bowel dysfunction

Biofeedback is a conservative treatment based on behavioural techniques, which can be used in the management of bowel dysfunction. This article reports the results of a retrospective review of the clinical notes of 87 female patients attending a biofeedback service at St Mark's Hospital, Harrow. The initial review was conducted to examine the incidence of polycystic ovary syndrome (PCOS) in patients attending this service. Seven percent were found to have PCOS, which is within the normal range. However, a significant proportion of patients (11.5%) had a current history of anorexia nervosa, a higher rate than in the general population, which prompted further investigation. In this article, Sonya Chelvanayagam, Julie Duncan, Brigitte Collins and Lorraine O'Brien report on the results of this review and discuss the significance of its findings. © Copyright Terms & conditions

Complement C3 serum levels in anorexia nervosa: a potential biomarker for the severity of disease?

BackgroundAnorexia nervosa carries the highest mortality rate of any psychiatric disorder. Even the most critically ill anorexic patients may present with normal 'standard' laboratory values, underscoring the need for a new sensitive biomarker. The complement cascade, a major component of innate immunity, represents a driving force in the pathophysiology of multiple inflammatory disorders. The role of complement in anorexia nervosa remains poorly understood. The present study was designed to evaluate the role of complement C3 levels, the extent of complement activation and of complement hemolytic activity in serum, as potential new biomarkers for the severity of anorexia nervosa.Patients and methodsThis was a prospective cohort study on 14 patients with severe anorexia nervosa, as defined by a body mass index (BMI) <14 kg/m2. Serum samples were obtained in a biweekly manner until hospital discharge. A total of 17 healthy subjects with normal BMI values served as controls. The serum levels of complement C3, C3a, C5a, sC5b-9, and of the 50% hemolytic complement activity (CH50) were quantified and correlated with the BMIs of patients and control subjects.ResultsSerum C3 levels were significantly lower in patients with anorexia nervosa than in controls (median 3.7 (interquartile range (IQR) 2.5-4.9) vs 11.4 (IQR 8.9-13.7, P <0.001). In contrast, complement activation fragments and CH50 levels were not significantly different between the two groups. There was a strong correlation between index C3 levels and BMI (Spearman correlation coefficient = 0.71, P <0.001).ConclusionsComplement C3 serum levels may represent a sensitive new biomarker for monitoring the severity of disease in anorexia nervosa. The finding from this preliminary pilot study will require further investigation in future prospective large-scale multicenter trials

In Response: A Discussion of Bulimia as a Masturbatory Equivalent

My research and that of my colleagues in the psychodynamic cause, structure and treatment of patients with bulimic anorexia nervosa correlates with and confirms the hypotheses presented by Levin ( 1) that bulimic symptoms may represent a masturbatory equivalent. In our recently published book, Fear of Being Fat: The Treatment of Anorexia Nervosa and Bulimia (2) we confirmed Sperling\u27s findings (3) that unresolved preoedipal fixations to the mother contribute to difficulties in psychosexual development and that anorexic girls and boys displace sexual and masturbatory conflicts from the genitals to the mouth

‘That perfect girl is gone’:Pro-ana, Anorexia and Frozen (2013) as an ‘Eating Disorder’ Film

The study of pro-anorexia (pro-ana) sites occupies a significant place in critical feminist work on eating disorders. But pro-ana sites have been studied as particular subcultural spaces which function to produce communities, identity positions and modes of subversive/ conformist femininities. Although anorexia might often be experienced as all-encompassing, people who are anorexic/ pro-anorexic don’t just ‘do’ anorexia. They also participate in everyday activities like engaging with media and as with ‘normal’ audiences, such encounters provide important resources for identity construction. In drawing on the feminist bid to challenge the conception of anorexic voices as pathological and ‘sick’, existing only ‘outside of the true’ (Saukko 2008, 77), this article explores a sample of pro-ana responses to Frozen, undertaking an analysis of the ways in which Frozen has been understood as an ‘eating disorder’ film and used in relation to pro-anorexic/ anorexic identities