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PubMed2006

Clinical, psychological, and personality correlates of asceticism in anorexia nervosa: from saint anorexia to pathologic perfectionism.

This study investigated the personality and clinical correlates of asceticism in 154 anorectic patients. Multiple linear regression models showed that asceticism was related to angry temperament, high control over anger, perfectionism, maturity fears, and number of vomiting episodes per week. These results suggest that the self-discipline and hypercontrol of anorectic patients are related to a temperament prone to angry feelings in subjects with a fear of becoming adult and with a trait of pathologic perfectionism.

Adolescent↗
PubMed1978

[Dysperception of body image and dysmorphophobias in mental anorexia. Apropos of 115 cases involving both sexes. II. Dysmorphophobias in mental anorexia].

Study of DPP extended over 2 groups selected as following: It was prospective in every patient seen between July 1976 and May 1977 (systematic study: SS: 35 girls and 2 boys). It was retrospective in another group before selected for importance of DPP (no systematic study: NSS: 34 girls and 6 boys). DPP were distributed into Dalpha (fear of any weight recovery), Dbeta (obsessing repercussion of a real defect, amplified in its perception) and Dgamma (delirious and obsessing conviction of a physical anomaly). We researched correlations with the type of AN (fixity or recession to childhood), premorbid weight-height ratio, overweight of the same-sex parent, important problems towards sexuality (ASC = Absolute sexual conflict = An entirely caused by a sexual difficulty, or PSC = Partial Sexual Conflict = difficulty towards sexuality when insuffisant to explain AN, or no sexual conflict), attitude towards pregnancy in cases of big-belly DPP. Every DPP were DPP of localized or generalized obesity. Dalpha is constant and pathognomonic. In females of SS, 37% presented Dbeta and 5% Dgamma before AN, 25% Dbeta and 11% Dgamma during AN. Among the 8 boys of the 2 studies, 3 presented Dgamma before AN, and everyone expressed their obsessing fear of "ugly grease". In 20% girls and 50% boys, explained aim of loss of weight was to "wipe out" the anomally DPP emphasized. We did not find any correlation between generalized DPP and studied elements, particularly with sexual conflicts (22% of our cases). The more frequent localized DPP was "big-belly"-DPP, always associated with overweight of the same sex parent, but as for other localized DPP, without any correlation with sexual conflicts, problems towards the father, neither reject of pregnancy.

Adolescent↗
PubMedDate not supplied

[Hyperactivity and anorexia nervosa: behavioural and biological perspective].

Anorexia nervosa is an eating disorder defined by a symptomatic triad, anorexia, emaciation and amenorrhoea. This disease mainly affects young women. Besides these three symptoms, hyperactivity is often associated with anorexia nervosa. Hyperactivity can be considered as a strategy to lose weight, but studies on animal models have shown that it could be explained by more complicated mechanisms. Hyperactivity is defined by an excess of physical activity, which can induce social, professional and family consequences. Hyperactivity can take different forms, most striking is the restless one. Patients with anorexia nervosa are not all hyperactive. Brewerton et al. have compared patients with anorexia nervosa and hyperactivity to patients without hyperactivity. Hyperactive patients are more dissatisfied by their body image, they use less means of purging (laxatives, vomiting), and they start starving earlier than patients without hyperactivity. Many factors can promote the emergence and maintenance of hyperactivity, especially social and cultural requirements, sports environment, family influences. Various models can explain the links between excessive exercise and anorexia nervosa. Epling and Pierce have exposed a behavioural model which shows how hyperactivity can lead to starvation, creating a self-maintained cycle. Eisler and Le Grande have described four models to explain the links between hyperactivity and anorexia nervosa. First, excessive exercise can be considered as a symptom of anorexia nervosa. It can also promote the development of eating disorders. Anorexia nervosa and hyperactivity can be a manifestation of an other psychiatric disorder. At least, hyperactivity can be a variant of anorexia nervosa, which has the same effects, as weight loss. Hyperactivity can also be considered as a kind of obsessive compulsive disorder. Hyperactivity and obsessive compulsive disorders actually share some clinical and neurochemical characteristics. An other model consists in comparing excessive exercise in anorexia nervosa to an addictive behaviour. Self-starvation exacerbated by hyperactivity can be considered as an addiction to endogenous opioid. Few studies are carried out in order to estimate the prevalence of high level exercise in the eating disorders. Davis et al. have achieved a prevalence study. The results indicate that a large majority of patients with anorexia nervosa (80,8%) were exercising excessively during an acute phase of the disorder. Research on animals, specially on rats, brings us an interesting model explaining interactions between anorexia nervosa and hyperactivity. With animal models, we have noticed that, when rats with access to a running wheel, are restricted in their food intake, they become excessively active, and paradoxically reduce food consumption. Many searchers have tried to explain this phenomenon. Morse et al. have pointed from animal models that the level of hyperactivity was linked to the severity of food restriction. This result can be explained by a failure of a part of the brain involved in rest and activity regulation. Animal research brings us explanations about the effects of starvation on the endocrine system and the neurotransmitters. Broocks et al. have shown that corticosterone concentration in plasma was synergistically increased by semi starvation and exercise, and the reduction of triiodothyronine by semi starvation was significantly greater in the running wheel group. An other study of Broocks et al. has revealed an increased hypothalamic serotonin metabolism with the combined effect of hyperactivity and food restriction. Tryptophan, an amid acid involved in serotonin synthesis, can also play a role in the maintenance of anorexia nervosa. In starvation conditions, opioid releasing caused by physical exercise would decrease food intake. Exner's study and Adan's one have shown that leptin would be involved in semi starvation induced hyperactivity mechanisms. In spite of animal models can not be entirely generalized to human, they are useful to try to explain biological supports of hyperactivity. Hyperactivity is not only a strategy to lose weight, but also a specific symptom which completes the clinical triad. Animal studies have led to promising results; we might use medicine, such as serotonin reuptake inhibitors or opioid antagonists in the treatment of hyperactivity in anorexia nervosa.

Anorexia Nervosa↗
PubMed1996

Anorexia during acute and chronic disease.

Anorexia is associated with disorders of all systems. Anorexia represents a consistent clinical manifestation during acute and chronic pathophysiological processes (infection, inflammation, injury, toxins, immunological reactions, malignancy and necrosis). Anorexia during disease can be beneficial or deleterious depending on the timing and duration. Temporary anorexia during acute disease may be beneficial to an organism since a restriction in the intake of micro- and macro-nutrients will inhibit bacterial growth. Long-term anorexia during chronic disease, however, is deleterious to an organism and may be associated with cachexia, which can ultimately result in death. Various mechanisms participate in the anorexia observed during disease, including cytokine action. Anorexia induced by cytokines is proposed to involve modulation of hypothalamic-feeding associated sites, prostaglandin-dependent mechanisms, modifications of neurotransmitter systems, gastrointestinal, metabolic, and endocrine factors. In addition, the anorexia-cachexia syndrome is multifactorial and may involve chronic pain, depression or anxiety, hypogeusia and hyposmia, chronic nausea, early satiety, malfunction of the gastrointestinal system, metabolic alterations, cytokine action, production of other anorexigenic substances and/or iatrogenic causes (chemotherapy, radiotherapy). Cachexia may result not only from anorexia and a decreased caloric intake, but also from malabsorption and losses from the body (ulcers, hemorrhage, effusions), or a change in body metabolism. Research has focused on potential interventions to modify anorexia during disease and the anorexia-cachexia syndrome. Nutritional modifications and the use of specific steroids (such as megestrol acetate) are being tested in the clinical setting. Understanding the specific mechanisms responsible for anorexia during disease as well as their interactions is essential to develop interventions for the control of anorexia (during a critical time in a specific disease), and to devise less toxic immunotherapeutic regimens using cytokines.

Acute Disease↗
PubMed2006

Follow-up of cardiac abnormalities in female adolescents with anorexia nervosa after refeeding.

OBJECTIVES: Anorexia nervosa is a life-threatening eating disorder, with significant risk for sudden death due to severe cardiac complications. The aim of this prospective study was to evaluate the cardiac abnormalities in female adolescents with anorexia nervosa and to examine the long-term results and reversibility of the detected cardiac abnormalities. METHODS: We prospectively studied eleven female adolescents (13.5-17 years old) with anorexia nervosa diagnosed according to DSM IV criteria. On admission they were all on a weight-losing course with a mean body mass index of 13.71 +/- 1.54 (11.38-17.05) kg/m2. The mean follow-up duration was 2.45 +/- 1.17 (1-4.5) years. All patients reached normal weight after treatment. The control group was composed of 12 healthy, age-matched, adolescent girls of normal weight. The patients with anorexia nervosa and the control group underwent a complete clinical examination, electrocardiographic and echocardiographic evaluations. These evaluations were repeated one year after refeeding. RESULTS: Patients with anorexia nervosa had a lower heart rate and blood pressure than the control group and they increased to normal levels as found in the control group after refeeding. QT and QTc were significantly longer and R wave amplitudes in V6 were significantly lower in the patients with anorexia nervosa than in the control group. QT and QT'c dispersions were significantly greater in anorexia nervosa patients compared to the control group. Left ventricular mass and left ventricular mass index were significantly lower in the anorexia nervosa group. One year after refeeding, there was a significant decrease in QT, QTc, QTd and QTcd. Although in anorexia nervosa patients, R wave amplitudes in V6 increased after refeeding; they did not reach the levels found in the control group. Control echocardiograms of anorexia nervosa patients after refeeding showed an increase in LV diameters and cardiac mass. There was a strong correlation between QT dispersion and left ventricular mass index. CONCLUSIONS: The adolescent girls with anorexia nervosa had significant structural and functional cardiac abnormalities in comparison to the control group. All these abnormalities were reversible except low R wave amplitude in V6.

Adolescent↗