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Eating Disorders (ED) are a syndrome characterized by persistent alteration of eating behavior and the conditions that cause insufficient ingestion and/or adsorption of foods. There are three different ED diseases: Anorexia Nervosa (AN), Bulimia Nervosa (BN) and Binge Eating Disorders (BED). ED are complex conditions that arise from a combination of long-standing behavioral, emotional, psychological, interpersonal, and social factors. A common trait to all EDs is the incongruous diet, often based on arbitrary parameters, disconnected from physiological needs, with a strong alteration of the sensations of hunger and satiety, to which variations in weight, body composition, health status and quality of life of patients occur. Although EDs are relatively frequent psychiatric disorders in the general population, especially in adolescent and juvenile age groups, evidence based on the scientific evidence of the efficacy of the pharmacological treatment of EDAs remains modest. The currently available international guidelines related to the pharmacological treatment of EDs are currently few and not always adequately informative, as they are affected by the lack of studies on the subject. As a further consequence of this it is not surprising that, with the sole exception of fluoxetine for the treatment of Bulimia Nervosa (BN) symptoms, no psychopharmaceutical has been authorized by national and international regulators for the treatment of ED. This narrative review focuses on the advantages and limitations of drugs used in the treatment of ED.

Eating Disorders (ED) are associated with multiple physical complications that strongly affect the physical health of these young and fragile patients and can also cause significant mortality, the highest among psychiatric pathologies. Among the various organic complications, albeit still little known, the gynecological implications, up to infertility, are very widespread. Both among adolescent and adult patients, gynecological symptoms can be very widespread and range from menstrual irregularities to amenorrhea, from vaginitis to ovarian polycystosis, up to complications during the gestational phase and in postpartum, in addition to the possible consequences on the unborn child. Among the most frequent and significant gynecological disorders in women with ED, there are menstrual irregularities that may occur with oligomenorrhea or even amenorrhea. This symptom, although no longer part of the DSM-5 diagnostic criteria for defining Anorexia Nervosa (AN), must be considered a very relevant event in the overall evaluation of young women and adolescents with eating disorders. Functional Hypothalamic Amenorrhea in ED patients is related to psychological distress, excessive exercise, disordered eating, or a combination of these factors which results in suppression of the hypothalamic- pituitary-ovarian axis, resulting in hypoestrogenism. The objective of this paper is to summarize the causes and the mechanism underlying the menstrual disorders and to provide a better understanding of the correlation between the reproductive system and the mechanisms that regulate food intake and eating habits. In addition, early recognition of risk factors for eating disorders for gynecological implications can help put more accurate assessments of patients to prevent potentially fatal complications. The importance of the involvement of specialist gynecologists in the multidisciplinary team that has to follow patients with eating disorders is also discussed.

Depression and obesity are very common pathologies. Both cause significant problems of both morbidity and mortality and have decisive impacts not only on the health and well-being of patients, but also on socioeconomic and health expenditure aspects. Many epidemiological studies, clinical studies and meta-analyses support the association between mood disorders and obesity in relationships to different conditions such as the severity of depression, the severity of obesity, gender, socioeconomic status, genetic susceptibility, environmental influences and adverse experiences of childhood. Currently, both depression and obesity are considered pathologies with a high-inflammatory impact; it is believed that several overlapping factors, such as the activation of the cortico-adrenal axis, the exaggerated and prolonged response of the innate immune system and proinflammatory cytokines to stress factors and pathogens—as well as alterations of the intestinal microbiota which promote intestinal permeability—can favor the expression of an increasingly proinflammatory phenotype that can be considered a key and common phenomenon between these two widespread pathologies. The purpose of this literature review is to evaluate the common and interacting mechanisms between depression and obesity.

Anorexia nervosa is a psychiatric disorder, the etiopathogenesis of which is still not fully understood. Currently, the most accredited model is a multifactorial model, which involves interaction between predisposing factors of biological nature, partly genetically determined, and psychological/personological and environmental socio-cultural factors. The last 20 years have led to the advancement in our knowledge on the mechanisms of energy homeostasis maintenance. There has been a veritable explosion of studies aimed at investigating anorexia nervosa and the functionality of associated neurotransmitters and neuromodulators in both central and peripheral systems. They play a key role in the regulation of eating behavior. We provide a brief review of the current knowledge on the neurochemical system involved in anorexia nervosa.

Background and objective Anorexia Nervosa (AN), Bulimia Nervosa (BN) and their variants are characterized by persistent alteration of eating behaviour, such as restricted intake or bingeing and purging, as well as excessive concerns about body shape and body weight. Purging behaviour may include self induced vomiting and/or abuse of laxatives, diuretics and physical hyperactivity. Unlike other psychiatric disorders, patients suffering from AN and BN have a high prevalence of many different medical complications, through the sequelae of undernutrition and purging, often with a serious impairment of health status and quality of life. This article describes the main diagnostic and clinical aspects of medical complications in AN and BN. Results The medical complications of ED are extremely variable and can occur with only modest biological and physical damage up to extremely serious and life-threatening conditions; the mortality rate of young subjects with AN is 4 - 11% with a risk of death about 12 times higher than that of subjects of the same age of the general population. The management of the medical-internship aspects of AN and BN is rightly placed within complex and articulated programs of interdisciplinary treatment with different levels of intensity of care (outpatient, semi-residential/residential, hospital in cases of emergency/medical and/or psychiatric emergency). Conclusion the results of the investigations carried out, describe the functions of the various organs and apparatuses and the alterations detected, the possible complications and physiological adaptations to malnutrition.

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.

Background and objective Bulimia nervosa, is an eating disorder characterized by excessive influence of weight and body shape on the levels of self-esteem, with pervasive feelings of failure and inadequacy. The eating is characterized by the presence of episodes of uncontrolled eating (Binge), during which the person ingests mass wide variety of foods and the feeling of not being able to stop eating. This review focuses on the metabolic and hormonal alterations in the in bulimia nervosa. Methods A literature search was conducted using the electronic database Medline and PubMed and with additional hand searches through the reference list obtained from the articles found. Journal were searched up to 2015. Inclusion criteria were: 1) full text available in English; 2) published in a peerreviewed journal and using the following keywords: neurotransmitters (AgRP, BDNF, αMSH, NP Y, endocannabinoids, adiponectin, CCK, ghrelin, GLP-1, insulin, leptin, PP, PYY), hormones (FSH, LH, estrogen, progesterone, testosterone) and bulimia nervosa, eating disorders. Results All data reported in the present review indicated that changes in the central and peripheral neuroendocrine equilibria may favor the onset and influence the course and prognosis of a DA. However, it is still questionable whether the alterations of the peptides and hormones regulating the mechanisms of eating behavior are the cause or consequence of a compromised diet. Conclusion The results of the present review indicate that the altered balance of the various peptides or hormones can be relevant not only for the genesis and / or maintenance of altered dietary behaviors, but also for the development of specific psychopathological aspects in eating disorders.

Schizophrenia is one of the most severe psychiatric diseases with a significant impact on the psychosocial functioning of the patients. People with schizophrenia are at risk to die prematurely because of their illness with their poor lifestyle contributing to the excess morbidity and higher mortality rate. In particular, lifestyle (e.g. poor diet, low rates of physical activity and increased likelihood to smoke cigarettes) predisposes them to poor physical health and comorbid medical diseases. In addition, the treatment of schizophrenia usually involves the long-term administration of antipsychotic drugs and some of these medications are implicated in the increased risk of metabolic and cardiovascular effects. The antipsychotic-induced hyperprolactinemia was ascertained for the first time by Kleinberg in 1971 and was considered for this treatment. Antipsychotics are the most common pharmacological agents which cause hyperprolactinemia The aim of this review is to describe PRL physiology, PRL biological effects and pathway to the diagnosis, causes, consequences of HPRL focusing on the antipsychotic effects on the PRL. We conducted a review of studies published between 1974 and December 2014. The search was performed using the following PubMed search terms: "Hyperprolactinemia" and "antipsychotic" and 827 papers were detected. The articles were examined and the overlapping or insufficiently clear works were excluded. Finally we chose 104 titles. We added to the selected articles additional articles, including 28 articles regarding the latest international guidelines, the pathophysiology of hyperprolactinemia and the various therapeutic choices.

Bulimia Nervosa (BN) and Binge Eating Disorder (BED) are some of the most common eating disorders (ED) in industrialized societies, characterized by uncontrolled binge eating and self-induced purging or other compensatory behaviours aiming to prevent body weight gain. It has been suggested that reduced serotonergic and noradrenergig tone triggers some of the cognitive and mood disturbances associated with ED. In fact in the active phase of ED the concentration of serotonin and noradrenaline in cerebral fluid is reduced. For these reasons, the pharmacologic treatment of ED consists mainly of selective serotonin reuptake inhibitors (SSRIs) or selective noradrenaline reuptake inhibitors (SNRIs) . At present, the physiologic basis of this disorder are not yet completely understood. In this review we evaluate several randomized controlled trials to compare the efficacy of several SSRIs and SNRIs in patients with a diagnosis of ED as defined by the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders [DSM IV]) These findings indicate that both SSRIs and SNRIs are well tolerated and reduce effectively the bulimic crisis and purging episodes in patients with ED.

Bulimia nervosa (BN) is one of the most common eating disorders in industrialized societies. It has been suggested that reduced serotonin activity triggers some of the cognitive and mood disturbances associated with BN. For this reason, the pharmacologic treatment of BN consists mainly of selective serotonin reuptake inhibitors (SSRIs), which have been proven effective. At present, the physiologic bases of this disorder are not yet completely understood. We conducted a randomized controlled trial to verify the efficacy of the SSRI fluvoxamine in patients with a diagnosis of BN. Twelve female outpatients aged 21 to 34 years with a diagnosis of BN-binge purging (as defined by the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders [DSM IV]) were randomly assigned to 2 treatment groups: the fluvoxamine 200 mg/day group and the placebo group. The patients underwent weekly clinical assessments for 12 weeks. At the end of the observation period, there was a statistically significant reduction in the number of binge-eating crises and purging episodes in the fluvoxamine group compared with placebo. In no case was treatment interrupted because of emergent side effects. These findings support the hypothesis that fluvoxamine is well tolerated and effective in reducing binge-eating crises and purging episodes in patients with BN.

The eating disorders (DCA) are complex systemic diseases with high social impact, which tend to become chronic with significant medical and psychiatric comorbidities. The literature data showed that there is good evidence to suggest the use of SSRIs, particularly at high doses of fluoxetine, in the treatment of BN reducing both the crisis of binge that the phenomena compensates and reducing the episodes of binge in patients with BED in the short term. Also, the topiramate (an AED) showed a good effectiveness in reducing the frequency and magnitude of episodes of binge with body weight reduction, both in the BN that is in the therapy of BED. To date, modest data support the use of low doses of second-generation antipsychotics in an attempt to reduce the creation of polarized weight and body shapes, the obsessive component, and anxiety in patients with AN. Data in the literature on long-term drug treatment of eating disorders are still very modest. It is essential to remember that the pharmacotherapy has, however, a remarkable efficacy in treating psychiatric disorders that occur in comorbidity with eating disorders, such as mood disorders, anxiety, insomnia, and obsessive-compulsive personality disorders and behavior.

The NES is an emerging disease in eating behavior that combines eating disorders, sleep, mood and stress. In recent years, the NES is becoming more interested in close association with obesity and depression. In the present study we have followed for 12 weeks 5 patients (2 males and 3 females) with NES and comorbid depression treated with agomelatine (25 mg / day for the first two weeks, then 50 mg / day), an antidepressant similar of melatonin. At the end of the three months of treatment, it was found an improvement in symptoms characteristic of the NES, as assessed by a reduction an average of the NEQ (from 31 to 22.8), improved mood, mean values ​​reduced by 23, 2 to 13.2 on the HAM-D, weight reduction, an average of 3.6 kg reduction in average weekly awakenings from 12 to 6.4 and the time of snoring and motion detected polysomnography. The serum chemistry values ​​remained stable and there were no reported adverse events. The present study showed that the treatment with agomelatine has improved the symptoms of NES and mood, decrease of body weight, reduce, albeit not in an optimal manner, the number of awakenings per night with a reduction of movement time and snoring . Of course, these preliminary data need to be confirmed by controlled trials on a larger sample.

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.

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.

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.

Objectives The aim of this study was to evaluate (1) the frequency of obsessive-compulsive symptoms (OCS) in patients with schizophrenia, (2) the impact of OCS on clinical features of schizophrenia, and (3) the association between type of antipsychotic treatment and presence of OCS. Methods OCS were evaluated using the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) in 70 patients with schizophrenia. The patients were then divided into two subgroups: those with at least a moderate level of OCS and those with mild or absent OCS. The two subgroups were compared using scores on the Scale for the Assessment of Positive Symptoms (SAPS), the Scale for the Assessment of Negative Symptoms (SANS), and the Global Assessment of Functioning Scale (GAF). Results Of the 70 patients with schizophrenia who were evaluated, 36 (51.4%) had at least moderate OCS (Y-BOCS score >16). SAPS subscale scores for hallucinations and delusions and GAF scores were found to be significantly higher among patients with at least moderate OCS, compared with those with mild or absent OCS. A significant relationship between at least moderate OCS and treatment with conventional antipsychotics was also observed. Conclusions The presence of OCS seems to have the potential to affect clinical outcomes in schizophrenia and treatment with conventional antipsychotics appears to be correlated with the presence of OCS.

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.

Weight gain induced by antipsychotics is the second most frequently given reason for noncompliance with pharmacologic therapy; excessive sedative effects rank first, with extrapyramidal side effects ranking third. Frequently, weight gain leads to inconsistent pharmacologic treatment; this exposes patients to the risk of recurrent symptoms. In fact, one of the key contributors to good clinical outcomes in schizophrenic patients is compliance with pharmacologic treatment. The goals of this study were to evaluate weight gain in a group of patients treated with olanzapine, diet modifications, and moderate physical activity and to compare the findings with those from a second group of patients who were given only olanzapine treatment. For 8 wk, investigators followed 2 groups of patients suffering from schizophrenia and hypomania in bipolar disorder, according to the nosographic criteria of The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV). The first group (A) of 18 patients (9 female, 9 male) affected by manic episodes in bipolar disorder received olanzapine (10-20 mg/d), jogged lightly for 30 min 3 times a week, and complied with a diet that consisted of 500 kcal/d less than usual. The second group (B) of 10 patients (4 female, 6 male) with schizophrenia received only olanzapine (10-20 mg/d). All patients from both groups were weighed at the beginning of the observation period and weekly thereafter for 2 mo. After 2 mo of observation, group A showed a mean weight gain of 1.47 kg, whereas group B exhibited a mean weight gain of 3.5 kg; the difference between the 2 groups was almost 2 kg (P

Binge-eating disorder, which is characterized by repeated episodes of uncontrolled eating, is common in obese patients and is often accompanied by comorbid psychiatric disorders, especially depression. In previous studies, selective serotonin reuptake inhibitors have demonstrated efficacy in reducing the frequency of binge eating and addressing comorbid psychiatric disorders, but they have not shown the ability to promote weight loss. Sibutramine, a new serotonin and norepinephrine reuptake inhibitor, has been shown in short- and long-term studies to be effective in promoting and maintaining weight loss in obese patients who have binge-eating disorder. In this randomized, double-blind, placebo-controlled study, the efficacy, safety, and tolerability of sibutramine were evaluated in the treatment of binge-eating disorder in obese patients. Twenty patients were randomly assigned in equal numbers to receive either sibutramine 10 mg/day or placebo for 12 weeks. Assessments were made at baseline and every 2 weeks throughout the study. Binge frequency, defined as the number of days during the previous week that included binge-eating episodes, was the primary outcome measure. By the end of the study, the binge frequency among patients given sibutramine was significantly lower than that among those given placebo. The main adverse events in the sibutramine group were dry mouth and constipation. The findings suggest sibutramine is an effective medication in the treatment of binge-eating disorders and is well tolerated. In addition, it addresses the 3 main goals in the treatment of binge-eating disorder: reducing the frequency of binge eating, promoting and maintaining weight loss, and treating the comorbid psychiatric conditions.

Bulimia nervosa (BN) is one of the most frequently encountered eating disorders in industrialized societies. It has been suggested that reduced serotonin activity may trigger some of the cognitive and mood disturbances associated with BN. Thus, pharmacologic treatment of BN is mainly based on the use of selective serotonin reuptake inhibitors, which have proved effective. At present, the biological basis of this disorder is not completely clear. The aim of this randomized, controlled trial was to verify the efficacy of sertraline, a selective serotonin reuptake inhibitor, in a group of patients with a diagnosis of BN. Twenty female outpatients, with an age range of 24 to 36 years and a diagnosis of purging type BN as defined by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM IV), were assigned randomly to two treatment groups. The first group received sertraline 100 mg/day for 12 weeks; the second group received placebo. The study was conducted for 12 weeks, with weekly clinical assessments. At the end of the observation period, the group treated with sertraline had a statistically significant reduction in the number of binge eating crises and purging compared with the group who received placebo. In no case was treatment interrupted because of side effects. This study confirms that sertraline is well tolerated and effective in reducing binge-eating crises and purging in patients with BN.