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Abstract: The ubiquity of the obesity condition in the United States, Europe and other regions with developed economies will associate to a significant adverse impact on public health. Numerous data indicate that social, behavioral, neuroendocrine, and metabolic factors may encourage compulsive eating behaviors thus increasing the risk of obesity. Several pathological conditions overlap with excess weight. Among the most common, there are binge eating disorder (BED) and food addiction (FA), which share several neurobiological and behavioral aspects with substance addictions. BED has many features in common with addictive behavior, such as loss of control and the need to frequently repeat the dysfunctional pattern despite negative consequences. The food addiction hypothesis assumes that exposure to highly palatable foods alters the reward circuits of the brain, resulting in a behavioral phenotype similar to substance addiction and facilitating dysfunctional eating behaviors, such as binge eating crises. In this review, over 100 publications, researched on MEDLINE from 2000 until march 2021, were included since they evaluate neuroendocrine changes, emotional homeostatic factors and the reward circuit, associating them with exposure to highly palatable foods, loss of control, the way we eat, the increase in impulsiveness and the inability to change eating behavior despite the negative consequences related to overweight and obesity. Finally, understanding the underlying neurobiological circuits of compulsive eating behaviors and food addiction could result in a great therapeutic potential for patients suffering from ailments nutrition and obesity.

Obesity is a chronic multifactorial disease that has become a serious health problem and is currently widespread over the world. It is, in fact, strongly associated with many other conditions, including insulin resistance, type 2 diabetes, cardiovascular and neurodegenerative diseases, the onset of different types of malignant tumors and alterations in reproductive function. According to the literature, obesity is characterized by a state of low-grade chronic inflammation, with a substantial increase in immune cells, specifically macrophage infiltrates in the adipose tissue which, in turn, secrete a succession of pro-inflammatory mediators. Furthermore, recent studies on microbiota have postulated new possible mechanisms of interaction between obesity and unbalanced nutrition with inflammation. This intestinal “superorganism” complex seems to influence not only the metabolic balance of the host but also the immune response, favoring a state of systemic inflammation and insulin resistance. This review summarizes the major evidence on the interactions between the gut microbiota, energetic metabolism and host immune system, all leading to a convergence of the fields of immunology, nutrients physiology and microbiota in the context of obesity and its possible clinical complications. Finally, possible therapeutic approaches aiming to rebalance the intestinal microbial ecosystem are evaluated to improve the alteration of inflammatory and metabolic states in obesity and related diseases.

Background:: Gender dysphoria is a clinical condition in which a state of inner suffering, stress and anxiety is detected when biological sex and a person's gender identity do not coincide. People who identify themselves as transgender people are more vulnerable and may have higher rates of dissatisfaction with their bodies which are often associated with a disorderly diet in an attempt to change the bodily characteristics of the genus of birth and, conversely, to accentuate the characteristics of the desired sexual identity. Aim:: The purpose of this work is to examine the association between dissatisfaction with one's own body and eating and weight disorders in people with gender dysphoria. Results:: Gender dysphoria and eating disorders are characterized by a serious discomfort to the body and the body suffers in both conditions. The results of our study suggest that rates of pathological eating behaviors and symptoms related to a disordered diet are high in patients with gender dysphoria and that standard screening for these symptoms must be considered in both populations at the time of evaluation and during the course of the treatment. Conclusions:: In light of this evidence, clinicians should always investigate issues related to sexuality and gender identity in patients with eating disorders, to develop more effective prevention measures and better strategies for therapeutic intervention..

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.

Adipocytes play a central role in maintaining lipid homeostasis and energy balance by storing triacylglycerols (TAGs) or releasing free fatty acids in response to changes in energy requirements. Obesity is a major risk factor for many diseases, including diabetes, hypertension, and cardiovascular disease. Besides, morbidity and mortality associated with being overweight and obese are on the rise. The development of obesity is characterized by an increase in lipid cells due to mitogenesis and differentiation, which are regulated by genetic, endocrine, metabolic, neurological, pharmacological, environmental, and nutritional factors. Therefore, understanding the mechanism by which a given nutrient affects the mitogenesis of preadipocytes and their differentiation into adipocytes could help prevent the onset and progression of obesity, along with all its consequences in humans. It has been shown that nutraceuticals such as tea catechins and BCAAs (leucine, isoleucine, and valine) could be effective in preventing obesity. Green tea catechins (CTGs) are polyphenolic flavonoids, which were previously called vitamin P. CTGs, especially EGCGs, have been shown to reduce body weight and body fat. In support of its anti-obesity effect, some in vivo data have shown that EGCG or green tea extract containing EGCG reduces the absorption of food, lipids, TAGs, cholesterol, and leptins. Furthermore, it stimulates energy expenditure and fat oxidation, and ultimately increases the level of high-density lipoproteins and fecal excretion of lipids. EGCG regulates various enzymes linked to anabolism and lipid catabolism, such as acetyl-CoA carboxylase (ACC), fatty acid synthase, pancreatic lipase, gastric lipase, and lipoxygenase; it also reduces the increase in insulin (INS) and TAG during the differentiation period of nine days. Taken together, these observations, in vivo and in vitro, suggest that the EGCG contained in green tea can modulate the mitogenic, endocrine, and metabolic functions of fat cells. In this study, we report the biochemical and biological evidence indicating the benefits of green tea in 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.

Gender incongruence, gender dysphoria, and many eating and weight disorders share a troubling body uneasiness. Gender nonconformities were considered to be diseases, in particular, mental disorders, till the last decades of the twentieth century. In this chapter the new DSM-5 diagnostic category gender dysphoria is discussed together with some recent changes in terminology and medical classifications concerning gender identity and sexual orientation.The rates of psychiatric disorders are higher among transgender patients attending specialized services than in cisgender people, with higher levels of body dissatisfaction and suicidal risk. Psychiatric morbidity tends to improve after gender confirmation treatments, often but not always. Therefore, an expert multi-disciplinary team including mental health professionals should manage the assessment and intervention procedures before and after hormone and surgical treatments. The risk of disordered eating and weight control behaviors is increased among sexual minorities, maybe more among MtF (male-to-female) transgenders and homosexual men. Transgender persons may develop unhealthy eating behaviors to accentuate the physical features of their gender identity. Stigma and violence exposure are significant risk factors, while social support is a significant protective factor. The effects of medical and surgical treatments of gender incongruence on eating and weight-related disorders are mostly unknown.

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.

Functional magnetic resonance imaging (fMRI) studies have displayed a dysregulation in the way in which the brain processes pleasant taste stimuli in patients with anorexia nervosa (AN) and bulimia nervosa (BN). However, exactly how the brain processes disgusting basic taste stimuli has never been investigated, even though disgust plays a role in food intake modulation and AN and BN patients exhibit high disgust sensitivity. Therefore, we investigated the activation of brain areas following the administration of pleasant and aversive basic taste stimuli in symptomatic AN and BN patients compared to healthy subjects. Twenty underweight AN women, 20 symptomatic BN women and 20 healthy women underwent fMRI while tasting 0.292 M sucrose solution (sweet taste), 0.5 mM quinine hydrochloride solution (bitter taste) and water as a reference taste. In symptomatic AN and BN patients the pleasant sweet stimulus induced a higher activation in several brain areas than that induced by the aversive bitter taste. The opposite occurred in healthy controls. Moreover, compared to healthy controls, AN patients showed a decreased response to the bitter stimulus in the right amygdala and left anterior cingulate cortex, while BN patients showed a decreased response to the bitter stimulus in the right amygdala and left insula. These results show an altered processing of rewarding and aversive taste stimuli in ED patients, which may be relevant for understanding the pathophysiology of AN and BN.

Eating disorders (and especially anorexia nervosa) are associated with severe disability, poor quality of life and high mortality rate. Anorexia nervosa ranks among the main causes of death among young women. Despite physical and psycho-social impairment, patients suffering from anorexia nervosa do not recognize low body weight and extreme calorie restriction as a clinical problem and are ambivalent towards treatment. Some patients with anorexia nervosa refuse treatments though presenting severe medical complications and having a high mortality risk. Hence the need to evaluate when it could be appropriate to prescribe a compulsory treatment in the more complex cases who refuse interventions, deemed necessary for them. To date, the compulsory treatment in anorexia nervosa is still under debate: some authors take into account the negative impact on the therapeutic relationship, other authors consider it as a compassionate treatment or as life-saving therapy. Indeed, compulsory treatment for eating disorders must always be weighed very carefully because it is considered by law as the highest form of restriction of personal freedom. Political Institutions must provide a clear framework for the society and for professionals, while the health care services must face the problem of the adequacy of available resources (not only in terms of hospital beds but also of skilled professionals) compared to patients' needs, considering the organization and the integration of clinical services dedicated to the treatment of 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.

Cannabis may play a causal role in the onset of some schizophrenia cases; however, the biological vulnerability that predisposes some individuals to develop schizophrenia after exposure to cannabis is not known. According to the diathesis-stress pathogenetic model, it is likely that the endogenous stress response system, including the hypothalamus–pituitary–adrenal (HPA) axis, could be involved. Therefore, we investigated the saliva cortisol awakening response (CAR) of 16 patients with schizophrenia onset after the exposure to cannabis (Can+) as compared to 12 patients with schizophrenia onset without cannabis exposure (Can−) and to 15 healthy controls. The CAR was assessed by collecting saliva samples at awakening and after 15, 30 and 60 min. As compared to healthy controls, Can+ schizophrenia patients exhibited significantly enhanced baseline saliva cortisol levels and a flattened CAR. No significant abnormality in both baseline cortisol levels and CAR was detected in Can− schizophrenia patients. These findings demonstrate a dysregulation of the HPA axis in chronic schizophrenic patients whose illness started after cannabis exposure but not in those with an illness onset without cannabis exposure. Further studies need to clarify whether this HPA dysregulation is a part of the biological background underlying the increased risk to schizophrenia after exposure to cannabis.