Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0268596 (EMA)
 2,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eating disorders (EDs) are characterized by marked cognitive distortions and maladaptive schemas. Cognitive models of EDs highlight the direct impact of cognitive dysfunctions on eating-related disturbances, insofar as specific cognitive contents such as thoughts about diet rules and food or loss of control may trigger disturbed eating behavior. Moreover, early maladaptive schemas that reflect perfectionist standards and relate to achievement and performance seem to be associated with disturbed eating, e.g., via their impact on situation-specific appraisals. However, so far, no study has investigated these assumptions. Hence, the present study sought to demonstrate whether and how cognitive content exerts an impact on eating behavior in daily life, and whether maladaptive core schemas impact the occurrence of binge eating via dysfunctional ED cognitions in eating-related contexts. N = 29 females with bulimia nervosa (BN), n = 31 females with binge eating disorder (BED) and n = 30 female controls without EDs (NC) participated in the study. All participants received a handheld computer for a 48-h period to capture antecedents of disturbed eating behavior in daily life. Event-sampling (meals, binge eating, purging, stressful situations) and signal-sampling (five times a day) methods were applied. EMA included a short questionnaire to assess dysfunctional cognitions and level of craving and to capture information about situational contexts. Early maladaptive schemas were assessed using a short version of the Young Schema Questionnaire at baseline. The main results showed specific patterns of dysfunctional eating-related cognitions for BED and BN. Binge eating was predicted by thoughts about loss of control (positively) and dietary restraint (negatively). For meal situations, no significant differences between the two ED groups emerged. All three domains exerted indirect effects on craving via thoughts about 'eating/loss of control,' whereas neither a direct nor an indirect effect emerged regarding thoughts about 'dietary restraint.' These results fit well with previous studies and support cognitive models of EDs; schema therapeutic approaches may be a valuable contribution to enhance treatment of EDs. Further studies should explore whether the findings from emerging adulthood can be generalized to younger age groups.
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PMID:Power of Cognition: How Dysfunctional Cognitions and Schemas Influence Eating Behavior in Daily Life Among Individuals With Eating Disorders. 3048 75

The core phenotype of anorexia nervosa (AN) comprises the age and stage dependent intertwining of both its primary and secondary (i.e., starvation induced) somatic and mental symptoms. Hypoleptinemia acts as a key trigger for the adaptation to starvation by affecting diverse brain regions including the reward system and by induction of alterations of the hypothalamus-pituitary-"target-organ" axes, e.g., resulting in amenorrhea as a characteristic symptom of AN. Particularly, the rat model activity-based anorexia (ABA) convincingly demonstrates the pivotal role of hypoleptinemia in the development of starvation-induced hyperactivity. STAT3 signaling in dopaminergic neurons in the ventral tegmental area (VTA) plays a crucial role in the transmission of the leptin signal in ABA. In patients with AN, an inverted U-shaped relationship has been observed between their serum leptin levels and physical activity. Albeit obese and therewith of a very different phenotype, humans diagnosed with rare congenital leptin deficiency have starvation like symptoms including hypothalamic amenorrhea in females. Over the past 20 years, such patients have been successfully treated with recombinant human (rh) leptin (metreleptin) within a compassionate use program. The extreme hunger of these patients subsides within hours upon initiation of treatment; substantial weight loss and menarche in females ensue after medium term treatment. In contrast, metreleptin had little effect in patients with multifactorial obesity. Small clinical trials have been conducted for hypothalamic amenorrhea and to increase bone mineral density, in which metreleptin proved beneficial. Up to now, metreleptin has not yet been used to treat patients with AN. Metreleptin has been approved by the FDA under strict regulations solely for the treatment of generalized lipodystrophy. The recent approval by the EMA may offer, for the first time, the possibility to treat extremely hyperactive patients with AN off-label. Furthermore, a potential dissection of hypoleptinemia-induced AN symptoms from the primary cognitions and behaviors of these patients could ensue. Accordingly, the aim of this article is to review the current state of the art of leptin in relation to AN to provide the theoretical basis for the initiation of clinical trials for treatment of this eating disorder.
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PMID:Clinical Trials Required to Assess Potential Benefits and Side Effects of Treatment of Patients With Anorexia Nervosa With Recombinant Human Leptin. 3115 89