Eating Disorders in Athletes: From Risk Management to Therapy.

BACKGROUND: Balanced sporting activity should be considered a resource in the treatment of eating disorders (ED), in particular of the BED and in obesity and, if conducted and guided by expert preparers and rehabilitators, in some forms of anorexia and in bulimia. OBJECTIVE: To assess the role of excessive physical activity, predominantly interfering with daily activities by ultimately resulting in greater energy consumption leading to weight loss, and study the diagnostic criteria of bulimia and anorexia nervosa. METHODS: A number of literature studies also report the presence of ED among athletes. A 2004 study reported that the prevalence of eating disorders in sports would be 13.5% compared to 4.5% of the control subjects. RESULTS: In general, nutrition is used as a tool for improving performance not only of athletes but also of technicians and coaches. But in the presence of factors of vulnerability towards ED, the tendency to manipulate the weight can result in an eating disorder or the so-called athletic anorexia or the RED-S. CONCLUSION: It is important to emphasize that not only do professional athletes suffer from it, but also good-looking amateurs and laypersons.

Antipsychotic drugs opposite to metabolic risk: neurotransmitters, neurohormonal and pharmacogenetic mechanisms underlying with weight gain and metabolic syndrome.

Important sources of metabolic diseases such as obesity and metabolic syndrome are significantly more prevalent in patients treated with antipsychotic drugs than the general population and they not only reduce the quality of life but also significantly reduce the life expectancy, being important risk factors for cardiovascular disease. The pathogenic mechanisms underlying these events are not entirely clear they are complex and multi-determined or not tied to a single defining event. In this review we examine the literature on the interactions of antipsychotic drugs with neurotransmitters in the brain, with pharmacogenetics hormones and peripheral mechanisms that may induce, albeit in different ways between different molecules, not only weight gain but also 'onset of major diseases such as diabetes, dyslipidemia and hypertension that are the basis of the metabolic syndrome. Today, the possible metabolic changes induced by various antipsychotic drugs and their major physical health consequences, are among the major concerns of clinicians and it is therefore necessary to monitor the main metabolic parameters to prevent or minimize any of these patients as well as the metabolism events associated with the use of antipsychotic drugs.

Agomelatine efficacy in the night eating syndrome.

Night eating syndrome (NES) is a nosographic entity included among the forms not otherwise specified (EDNOS) in eating disorders (ED) of the DSM IV. It is characterized by a reduced food intake during the day, evening hyperphagia, and nocturnal awakenings associated with conscious episodes of compulsive ingestion of food. Frequently, NES patients show significant psychopathology comorbidity with affective disorders. This paper describes a case report of an NES patient treated with agomelatine, an antidepressant analogue of melatonin, which acts by improving not only the mood but also by regulating sleep cycles and appetite. After three months of observation, the use of Agomelatine not only improved the mood of our NES patient (assessed in the HAM-D scores) but it was also able to reduce the night eating questionnaire, by both reducing the number of nocturnal awakenings with food intake, the time of snoring, the minutes of movement during night sleep (assessed at polysomnography), and the weight (-5.5 kg) and optimizing blood glucose and lipid profile. In our clinical case report, agomelatine was able both to reduce the NES symptoms and to significantly improve the mood of our NES patient without adverse side effects during the duration of treatment. Therefore, our case report supports the rationale for further studies on the use of Agomelatine in the NES treatment.

Night eating syndrome: an overview.

OBJECTIVES: The purpose of this review is to outline the nosographic characteristics of NES and the most reliable ethiopathogenetic theories in relation to the most recent evidence in the literature. KEY FINDINGS: The night eating syndrome (NES) is a disorder occurring at the stated time, that does not meet the criteria for any specific eating disorder. NES is characterized by a reduced feeding during the day, evening hyperphagia accompanied by frequent nocturnal awakenings associated with conscious episodes of compulsive ingestion of food and abnormal circadian rhythms of food and other neuroendocrine factors. Frequently it is associated with obesity and depressed mood. We highlight the therapeutic possibilities of some drugs, especially selective serotonin re-uptake inhibitors (SSRIs), which reduce the hyperactivity of the serotonin transporter in NES and significantly improve the clinical picture of this disease. CONCLUSIONS: Night eating syndrome is of importance clinically because of its association with obesity. The recognition and effective treatment of NES may be an increasingly important way to treat a subset of the obese population. Treatment of the syndrome, however, is still in its infancy. One clinical trial has reported efficacy with the SSRI sertraline. Other treatments, such as the anticonvulsant topiramate, phototherapy, and other SSRIs, may also offer future promise. Particularly useful would be studies involving brain scans (magnetic resonance imaging or single-photon emission computed tomography) of patients with NES compared with the healthy population, to investigate more thoroughly the possible alterations involved in the pathogenesis of NES.

Recent clinical aspects of hyperprolactinemia induced by antipsychotics.

This review will address the current understanding of the relationship between hyperprolactinemia and antipsychotic drugs. Hyperprolactinemia is a frequent but often neglected side effect of typical, but also of many atypical antipsychotics. Release of PRL from lactotrope cells is influenced by several factors, such as stress, physical and sexual activity and food assumption. PRL secretion is regulated by hypothalamic-pituitary portal system and its homeostasis is the result of a complex balance between stimulating and inhibitory factors, both endogeneous and esogeneous. The main physiological control mechanism of secretion is played by the inhibitory action of dopamine. Conversely, among stimulation factors, serotonin is probably the main modulator of PRL release. An high number of drugs may cause PRL increase too, such as drugs that reduce dopaminergic functions at SNC level, or drugs with an antagonistic action towards dopaminergic receptors and those increasing serotonergic neurotransmission. Hyperprolactinemia is one of the most frequent endocrine pathologies of the hypothalamic-pituitary axis. Antipsychotics (AP) are the most common cause of druginduced hyperprolactinemia. Not all AP have the same impact on inducing hyperprolactinemia. In this review we will focus on the subdivision of AP in 'PRL-raising' (stimulators) and 'PRL-sparing' (sparers) and on their differences in inducing hyperprolactinemia. Finally we evaluated different complications in patients with antipsychotics induced hyperprolactinemia that may cause not only short-term side effects but also important systemic long-term effects. At the end of the review we finally report the possible options of treatment considering however that at present there are no ideal therapies or evaluations, and decisions have to be made on a case by case basis.