Compulsive Eating Behavior Research Articles

Measuring Motivations to Eat Palatable Foods: Adaptation and Psychometric Properties of the Italian Version of the Palatable Eating Motives Scale (PEMS-IT).

Gaining knowledge of the various reasons behind people's consumption of highly processed foods has the potential to enhance obesity prevention initiatives and open avenues to tailor treatment approaches for obesity and binge eating at a more personalized level. This contribution aimed to test the psychometric properties and factor structure of the Palatable Eating Motives Scale (PEMS-IT) in a community sample of Italian adults. A confirmatory factor analysis was performed to test the factor structure of the Italian version of the PEMS (PEMS-IT) on a total of 616 respondents. Furthermore, the reliability and convergent validity analysis of the tool were evaluated. The analysis confirmed the four-factor structure of PEMS-IT [(YBχ2 (164) = 537.901; p < 0.001, the CFI = 0.918, RMSEA = 0.072; 90%CI [0.065-0.078]; p(RMSEA < 0.05) < 0.001, and SRMR = 0.080] and satisfactory reliability on its subscales (Cronbach's α: 0.745-0.917). Positive correlations were also found with food addiction and binge-eating symptoms, compulsive eating behavior, and uncontrolled and emotional eating. The PEMS-IT appears to be an instrument with promising psychometric properties and potential applications in clinical settings. However, it also has some limitations, and future studies could focus on improving the semantic content of the elements to increase the overall utility and precision of the instrument.

O-16 Never too late: Delayed diagnosis of Prader-Willi syndrome

Abstract Introduction Prader-Willi syndrome (PWS) is the leading inherited cause of severe childhood obesity. The aim of this case report is to describe a case of delayed diagnosis of PWS and to emphasize the importance of early diagnosis of PWS. Clinical Case A 24-year-old young woman with a history of hyperphagia, severe obesity, and cognitive impairment was admitted to our department for glycemic control due to newly diagnosed type 2 diabetes mellitus. She also had obstructive sleep apnea, daytime sleepiness, scoliosis, short stature (148 cm), and impaired speech articulation. Central obesity (BMI:54.7 kg/m2, waist circumference 147 cm), cognitive impairment, and characteristic body and facial features (narrow bifrontal diameter, almond-shaped palpebral fissures, small hands and feet, strabismus) suggested a genetic disorder. Test results showed growth hormone 0.07 ng/mL (0-3.5) and IGF-1 46 ng/mL (191-478). Cytogenetic analysis was performed on GTG-banded metaphases obtained from peripheral blood lymphocyte culture. t(3;16)(p21;p13) was observed in the patient. Cytogenetic analysis of the parents showed that this translocation was of paternal origin. The SNRPN gene was amplified from the patient's genomic DNA by PCR using methylation-specific primers after bisulfite modification. PCR products were visualized by agarose gel electrophoresis. The methylation pattern was found to be consistent with PWS. Hypocaloric diet (1400 Kcal/day) metformin 2 g/day, liraglutide (dose gradually increased to 2.4 mg/day), and dapagliflozin 10 mg/day were started. During hospitalization, glycemic regulation was achieved and 5.4 kilograms of weight loss occurred. Conclusion Obesity-related complications (e.g. sleep apnea, type 2 diabetes) and behavioral problems contribute significantly to morbidity and mortality in individuals with PWS. Prevention and treatment of morbid obesity and related conditions in individuals with PWS and management of maladaptive behaviors are key goals that require long-term follow-up and attention to managing the process. In these adults with compulsive eating behaviors who lack the ability to make informed decisions, it is very challenging to ensure compliance with treatments such as obesity treatment and the use of assistive devices for sleep apnea, which require the patient's consent and compliance. The complexity of this multisystemic disease increases with age, and we emphasize the need for early diagnosis to reduce the morbidity and mortality associated with PWS.Figure 1.Used with the patient's and family's consent.

Frequency of Impulsive-Compulsive Behavior and Associated Psychological Factors in Parkinson's Disease: Lack of Control or Too Much of It?

Background and Objectives: Impulse Control Disorders (ICDs) including pathological gambling, hypersexuality, compulsive eating, compulsive buying, and other related behaviors are well-known distinct non-motor symptoms in Parkinson's Disease (PD). Some large-scale studies present a prevalence of at least 10%, however, there are other reports providing much higher rates. The majority of the conducted studies investigating ICDs focus mainly on pharmacological factors, however, from a psychological perspective, there is yet enough room for investigation. In order to address the above issues, we designed a two-part study. Materials and Methods: First, we aimed to identify the incidence of ICD and related behaviors in a cohort of 892 Greek PD patients. Second, we administered a comprehensive battery of psychometric tools to assess psychological factors such as personality dimensions, quality of life, defenses, coherence, and resilience as well as to screen general cognitive capacity in PD patients with ICD manifestations. Results: With regard to the first part, we identified ICD manifestations in 12.4% of the patients. Preliminary findings from the second part indicate elevated activity, rather than impulsivity, as well as interrelations between several variables, including measures of activity, coping mechanisms, and quality of life. Conclusions: We present a working hypothesis for the contribution of high activity channeled to specific behavioral patterns through specific coping mechanisms, concerning the emergence of ICDs and related behaviors in PD, and further stress the importance of compulsivity rather than impulsivity in this process.

Amygdala hyperactivation relates to eating behaviour: a potential indicator of food addiction in Prader-Willi syndrome.

Prader-Willi syndrome is a rare neurodevelopmental genetic disorder characterized by various endocrine, cognitive and behavioural problems. The symptoms include an obsession for food and reduced satiety, which leads to hyperphagia and morbid obesity. Neuropsychological studies have reported that Prader-Willi patients display altered social interactions with a specific weakness in interpreting social information and responding to them, a symptom close to that observed in autism spectrum disorders. In the present case-control study, we hypothesized that brain regions associated with compulsive eating behaviour would be abnormally activated by food-related odours in Prader-Willi syndrome, as these can stimulate the appetite and induce hunger-related behaviour. We conducted a brain imaging study using the olfactory modality because odours have a high-hedonic valence and can cause stronger emotional reactions than other modalities. Further, the olfactory system is also intimately associated with the endocrine regulation of energy balance and is the most appropriate modality for studies of Prader-Willi syndrome. A total of 16 Prader-Willi participants were recruited for this study, which is a significant achievement given the low incidence rate of this rare disease. The second group of 11 control age-matched subjects also participated in the brain imaging study. In the MRI scanner, using an MRI-compatible olfactometer during 56 block sessions, we randomly presented two odours (tulip and caramel), which have different hedonic valence and a different capacity to arouse hunger-related behaviour. Our results demonstrate that Prader-Willi participants have abnormal activity in the brain reward system that regulates eating behaviour. Indeed, we found that these patients had right amygdala activity up to five times higher in response to a food odour (caramel) compared with the tulip odour. In contrast, age-matched control participants had similar activity levels in response to both odours. The amygdala activity levels were found to be associated with the severity of the hyperphagia in Prader-Willi patients. Our results provide evidence for functional alteration of the right amygdala in Prader-Willi syndrome, which is part of the brain network involved in food addiction modulated by the ghrelin and oxytocin systems, which may drive the hyperphagia. Our study provides important new insights into the functioning of emotion-related brain circuits and pathology, and it is one of the few to explore the dysfunction of the neural circuits involved in emotion and addiction in Prader-Willi syndrome. It suggests new directions for the exploration and remediation of addictive behaviours.

Neurobiological Correlates Shared Between Obesity, BED and Food Addiction.

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.

ARIPIPRAZOLE INDUCED COMPULSIVE EATING DISORDER: A CASE REPORT

IntroductionAripiprazole is a newer atypical antipsychotic with a favorable side-effect profile, especially a low propensity to result in metabolic syndromes.It is effective at treating bipolar disorder, the positive symptoms of schizophrenia and has the potential to treat negative and cognitive symptoms.However, prior studies suggested that aripiprazole seem to be associated to a risk of inducing certain impulse control behaviors, such as uncontrollable gambling, hyper sexuality, as well as compulsive eating.ObjectivesWe proposed to assess the evidence for compulsive eating associated with the use of aripiprazole.MethodsWe report a rare case of new onset aripiprazole induced compulsive eating behavior in a patient with bipolar disorder. Then, we conducted a literature review using“PubMed” database and keywords “Aripiprazole”, “Impulse Control Behaviors”, “Compulsive Eating”.ResultsHe was a 21-year-old patient, diagnosed with bipolar 1 disorder. He was prescribed Aripiprazole, after a neuroleptic malignant syndrome induced by haloperidol (which was prescribed during the first episode psychosis).One month following the treatment initiation, the patient complained of eating excessively. He was not able to control his eating and gained 30 Kg over the period of 4 months. Metabolic assessment showed a hypercholesterolemia.ConclusionsAripiprazole is a promising novel antipsychotic in mental diseases. However current evidence associates compulsive behaviors like eating with the use of Aripiprazole, probably due to the drug affinity to 5-HT receptors. More studies are needed to confirm this rare side effect.Disclosure of InterestNone Declared

Exacerbation of Pica as a Precursor of Psychosis

Abstract Pica is a sustained, compulsive eating behavior of nonedible substances. Pica has been described as sequelae of psychosis due to its state of disorganization; however, temporal and causal relationship between the two has not been reported in the context of exacerbation of pica before psychosis. Various causes of pica have been identified including malnutrition, iron-deficiency anemia, zinc deficiency, intellectual disability, and obsessive and impulse control disorders. Here, we describe a case of worsening pica which preceded exacerbation of psychosis in an 18-year-old female which was managed with antipsychotics along with complete remission of psychosis and improvement in the severity of pica. The present case highlights the association between psychosis and pica. There has been a rising voice in academia to reclassify pica alongside obsessive–compulsive disorder (OCD) with no absolute consensus. In conclusion, our findings suggest that the exacerbation of pica preceded psychosis and can be construed as an indicator for an upcoming psychotic episode or as a prodromal aspect of psychosis and may be useful for early identification and initiation of treatment in cases of relapsing psychosis.

Disordered Eating Behaviors Related to Food Addiction/Eating Addiction in Inpatients with Obesity and the General Population: The Italian Version of the Addiction-like Eating Behaviors Scale (AEBS-IT).

The purpose of this research is to test the psychometric properties and factorial structure of the Addiction-like Eating Behaviors Scale (AEBS) in an Italian sample of adults with severe obesity seeking treatment for weight reduction and the general population, and to examine the measurement invariance of the tool by comparing a clinical and a nonclinical sample. A confirmatory factor analysis (CFA) was initially conducted to test the factorial structure of the Italian version of the AEBS (AEBS-IT) on a total of 953 participants. Following this, the measurement invariance and psychometric properties of the tool AEBS-IT were assessed on both inpatients with severe obesity (n = 502) and individuals from the general population (n = 451). Reliability and convergent validity analysis were also run. CFA revealed a bi-factor structure for the AEBS-IT, which also showed good reliability and positive correlations with food addiction (through the mYFAS2.0 symptom count), binge-eating symptoms, compulsive eating behavior, and dysfunctional eating patterns and the individuals' body mass index (BMI). Moreover, the tool was invariant across populations. This study provided evidence that the AEBS-IT is a valid and reliable measure of FA in both clinical and nonclinical samples.

Depression is Associated with Impulse-compulsive Behaviors in Parkinson’s disease

BackgroundDepression and impulse control disorders (ICDs) are both common in Parkinson’s disease (PD) patients and their coexistence is frequent. Our aim was to determine the relationship between depression and impulsive-compulsive behaviors (ICBs) in a large cohort of PD patients. MethodsPD patients recruited from 35 centers of Spain from the COPPADIS cohort from January 2016 to November 2017 were included in the study. The QUIP-RS (Questionnaire for Impulsive-Compulsive Disorders in Parkinson's Disease-Rating Scale) was used for screening ICDs (cutoff points: gambling ≥6, buying ≥8, sex≥8, eating≥7) and compulsive behaviors (CBs) (cutoff points: hobbyism-punding ≥7). Mood was assessed with the BDI-II (Beck Depression Inventory – II) and major, minor, and subthreshold depression were defined. ResultsDepression was more frequent in PD patients with ICBs than in those without: 66.3% (69/104) vs 47.5% (242/509); p<0.0001. Major depression was more frequent in this group as well: 22.1% [23/104] vs 14.5% [74/509]; p=0.041. Considering types of ICBs individually, depression was more frequent in patients with pathological gambling (88.9% [8/9] vs 50.2% [303/603]; p=0.021), compulsive eating behavior (65.9% [27/41] vs 49.7% [284/572]; p=0.032), and hobbyism-punding (69% [29/42] vs 49.4% [282/571]; p=0.010) than in those without, respectively. The presence of ICBs was also associated with depression (OR=1.831; 95%CI 1.048-3.201; p=0.034) after adjusting for age, sex, civil status, disease duration, equivalent daily levodopa dose, antidepressant treatment, Hoehn&Yahr stage, non-motor symptoms burden, autonomy for activities of daily living, and global perception of QoL. LimitationsCross-sectional design. ConclusionsDepression is associated with ICBs in PD. Specifically, with pathological gambling, compulsive eating behavior, and hobbyism-punding.

Aripiprazole induced compulsive eating in adolescent: Is this the effect of aripiprazole on Serotonin receptors?

Objective: To present a case of new onset Aripiprazole induced compulsive eating in an adolescent male. Method: We describe a case history of an adolescent male treated with Aripiprazole who developed compulsive eating behavior. Result: The compulsive eating behavior stopped once the Aripiprazole was discontinued. Conclusion: We argue that the compulsive eating behavior in the adolescent male was induced by Aripiprazole and the effect of Aripiprazole on eating behavior may be due to the effect of Aripiprazole on serotonin receptors.

Role of Dopamine D2 Receptor in the Leptin Receptor‐expressing Neurons in Modulation of Compulsive‐like Eating Behavior

Leptin, a hormone secreted by adipose tissue, is known to modulate satiety, caloric intake and body weight. There are six alternative spliced isoforms of leptin receptors (LepRa‐f). LepRb is highly expressed in the hypothalamic arcuate nucleus (ARC) which is involved in the regulation of food intake and body weight. Leptin activates pro‐opiomelanocortin‐expressing (POMC) neurons and inhibits agouti‐related peptide (AgRP)‐expressing neurons in the ARC.A recent study shows that dopamine modulates neuronal activities of arcuate POMC neurons and AgRP neurons. Dopamine inhibits arcuate POMC neurons via dopamine D2 receptor but activates AgRP neurons through dopamine D1 receptor. Dopamine is a neurotransmitter that plays a key role in mood, motivation and satiety. Dysregulation of dopamine neurotransmission is involved in the drug addiction. Food addiction is a recently proposed concept and compulsive eating behavior is shown in food addiction as well as an obesity. Negative reinforcement in drug addiction is a concept that negative affect associated with drug withdrawal promotes drug taking to ‘self‐medicate’ or remove those negative states. In the present study, we generated mice lacking D2 receptor in cells expressing LepRb (D2R flox; LepRb‐Cre; D2R cKO). Mice were provided palatable food for more than two weeks to induce food‐addiction like phenotypes in mice. To examine the role of D2 receptor in the leptin receptor‐expressing neurons in modulation of compulsive‐like eating behavior, light‐dark conflict test (LD test) was performed during the palatable food withdrawal period. In addition, palatable food withdrawal‐mediated anxiety/depression‐like behavior were measured during marble burying test (MBT), elevated plus maze (EPM), open filed test (OFT), and forced swim test (FST). No significant changes were found in palatable food (PF) intake in the light box during LD test, suggesting that D2 receptor in cells expressing LepRb would not be involved in the regulation of compulsive eating behavior. Furthermore, there was no significant changes in anxiety/depression‐like behavior measured by MBT, EPM, OPT and FST during the PF withdrawal period.Support or Funding InformationThis research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2019R1I1A1A01060007).

Stress, Food Addiction and Brain: Molecular Determinants and its Neural Networks Using Omics Platform

Obesity is a complicated metabolic malfunction linked to disconnected signaling between inter-organs, and inter-molecularly affected by impairment of the neuronal circuit, stemming from environmental stressors in children and adults. Upon environmental intoxication or change in the surrounding environmental stressors; the signaling for hunger could affect regulatory signaling in energy consumption and lead to a wide range of metabolic disruption and sensitivity, cell-to-cell and organ-to-organ. Presently, food addiction is associated with substance-based and behavioral malfunction, which reflects the alteration of molecular and genetic deficiency in animal studies and clinical studies. The prevailing food addiction hypothesis suggest that food types can alter the brain circuitry for a reward compensation which may link to compulsive eating behavior phenotype comparable to drug addiction. Like synthetic drugs, food consumption results in the release of dopamine, which relates to the feelings of being rewarded, and has shown to have similar brain activation patterns. It remains unclear what molecules could engage in the regulatory process, or what are key molecular determinants to control the hormonal secretion. Several interventions such as calorie restriction, exercise, bariatric surgery, and treatments for obesity management have been moderately successful in reducing body fat in the short term, but most fail to maintain long-term weight loss. Herein, we propose the advantage of the molecular-based risk assessment, namely the omics platform, to improve health quality by reviewing the impact of environmental stressors. Bulimia nervosa has received less attention in this regard, despite their regular binge eating symptoms.

Food reward and gut-brain signalling

Abstract The increasing availability of ultra-processed, energy dense food is contributing to the spread of the obesity pandemic, which is a serious health threat in today’s world. One possible cause for this association arises from the fact that the brain is wired to derive pleasure from eating. Specifically, food intake activates reward pathways involving dopamine receptor signalling. The reinforcing value of specific food items results from the interplay between taste and nutritional properties. Increasing evidence suggests that nutritional value is sensed in the gut by chemoreceptors in the intestinal tract and the hepatic portal vein, and conveyed to the brain through neuronal and endocrine pathways to guide food selection behaviour. Ultra-processed food is designed to potentiate the reward response through a combination of high fat and high sugar, therebye seeming highly appetizing. There is increasing evidence that overconsumption of processed food distorts normal reward signalling, leading to compulsive eating behaviour and obesity. Hence, it is essential to understand food reward and gut-brain signalling to find an effective strategy to combat the obesity pandemic.

Reward sensitivity deficits in a rat model of compulsive eating behavior.

Compulsive eating behavior is hypothesized to be driven in part by reward deficits likely due to neuroadaptations to the mesolimbic dopamine (DA) system. Therefore, the aim of this study was to assess deficits in reward system functioning and mesolimbic DA after alternating a standard chow with palatable diet, a model of compulsive eating. In this model, rats in the control group (Chow/Chow) are provided a standard chow diet 7 days a week, while the experimental group (Chow/Palatable) is provided chow for 5 days a week ("C Phase"), followed by 2 days of access to a highly palatable sucrose diet ("P Phase"). We first tested the sensitivity to d-Amphetamine's stimulatory, reward-enhancing, and primary rewarding effects using a locomotor activity assay, an intracranial self-stimulation (ICSS) procedure, and a conditioned place preference test, respectively. We then quantified DA release in the nucleus accumbens (NAc) shell after treatment with d-Amphetamine using in vivo microdialysis, quantified levels of tyrosine hydroxylase (TH) and dopamine transporter (DAT) mRNA using quantitative polymerase chain reaction (qPCR), and lastly, quantified baseline extracellular DA and function of DAT in vivo using quantitative "no-net-flux" microdialysis. Chow/Palatable rats displayed blunted d-Amphetamine-induced locomotor activity, insensitivity to d-Amphetamine potentiation of ICSS threshold, and decreased place preference for d-Amphetamine during the P Phase. We found that Chow/Palatable rats had blunted DA efflux following d-Amphetamine treatment. Furthermore, DAT mRNA was increased in Chow/Palatable rats during the P Phase. Finally, quantitative "no-net-flux" microdialysis revealed reduced extracellular baseline DA and DAT function in Chow/Palatable rats. Altogether, these results provide evidence of reduced reward system functioning and related neuroadaptations in the DA and DAT systems in this model of compulsive eating. Reward deficits, resulting from repeated overeating, may in turn contribute to the perpetuation of compulsive eating behavior.

Dopaminergic circuitry regulating compulsive eating behavior

Dopaminergic circuitry regulating compulsive eating behavior

Compulsive eating behaviors in Parkinson's disease.

Eating disorders are common in Parkinson's disease (PD) patients and often class in Impulse control disorders, however, little is known about their phenomenology. Specific symptoms and comorbidities were described in a group of PD patients in this preliminary study. Over a period of 6 months, 51 PD patients who experienced significant changes in eating habits following diagnosis of PD and were interviewed during regularly scheduled follow-up visits. We assessed each patient's height and weight, impulsivity, psychological distress, current eating disorder symptoms, food addiction, food habits and craving. Among the PD patients who experienced modified dietary habits following diagnosis, few exhibited binge eating disorders (BED) full criteria (3.9%). However, 21.6% of patients experienced episodes of out-of-control eating with a large quantity of food in short time and 39.2% satisfied food addiction (FA) criteria without binge eating disorder. Food cravings more than once a week were experienced in approximately half of the population including all FA patients. Regarding comorbidities, FA PD patients present impulsive features and anxiety. This study confirms the existence of FA profile in PD patients. Eating disorders even in PD are complex and have a cross-cutting criteria related to out-of-control eating, FA, and BED. The association of anxiety with PD-related food addiction, contrary to L-dopa equivalent daily dose mean score or the presence of dopamine agonists, underline the complex sustainability of the dopaminergic brainstem support. A study on their detailed prevalence in this population could be helpful to better understand unspecified feeding or eating disorder. DR-2012-007. French Committee for the Protection of Persons (CPP) & French National Commission on Computing and Liberty (CNIL). Level V, descriptive study.

Addiction à l’alimentation : un concept ancien, une mesure récente

The food addiction concept postulates that it is be possible to become addicted to some specific types of foods (i.e., foods high in sugar, fat and/or salt, especially processed foods), and that these people do share symptoms with recognized substance-related and addictive disorders: craving to and loss of control over these foods, existence of harms due to this behavior, and maintenance of this behavior despite these harms. The aim of this manuscript was to review existing scientific evidence of the “food addiction” concept: relevance of the food addiction model for some forms of compulsive eating behavior, its source, how it is currently assessed (original Yale Food Addiction Scale and Yale Food Addiction Scale 2.0, respectively based on the extrapolation of DSM-IV-TR and DSM-5 addictive disorders criteria to food), and presentation of some practical and therapeutic implications for patients, including patients in liver transplantation, obesity surgery and those with ADHD and obesity.

Overeating, Overweight, and Substance Use: What Is the Connection?

This paper integrates recent developments in the areas of excessive eating and addictive behavior, reviewing shared and unique features with respect to topography, etiological mechanisms/risk factors, comorbidity, and related adverse consequences/correlates. Emerging literature is converging to suggest a high degree of overlap in terms of eating and addictive behavior, including common risk factors and involvement of brain reward pathways. Behavioral phenotypes involving putative addictive elements include binge eating, food addiction, nocturnal eating, grazing, and emotional eating. Emerging evidence supports that dysregulation of brain reward pathways may underlie certain forms of obesity, particularly when driven by compulsive eating behavior or binge eating disorder/food addiction, and the evidence for comparable dysregulation underlying substance use disorders (SUD) and other addictive behavior is quite robust, with a high degree of overlap in brain circuitry driving excessive eating and drug addiction. At least one form of weight loss (bariatric) surgery, Roux-en-Y gastric bypass, is associated with post-surgical SUD onset, and this body of work has greatly expanded our appreciation of the intricate gut-brain connections involved in eating and addictive behavior. Nonetheless, controversy remains regarding the extent to which and in what forms eating behavior may constitute addiction. Research productivity in the intersection of eating, obesity, and addiction has increased dramatically over the past decade, particularly within the past 5 years; it is expected that our understanding of these relationships will grow substantially in the coming years, particularly in light of recent advances in our understanding of the nuances of gut-brain communication that may shed light on new mechanisms.

Trace Amine Associated Receptor 1 (TAAR1) Modulation of Food Reward.

Eating disorders and some forms of obesity are characterized by addictive-like, compulsive eating behavior which contains numerous similarities with compulsive drug use. Food intake is in part mediated by reward and reinforcement processes that can become dysregulated in these disorders. Additionally, impairments in inhibitory control regulation of reward-related responding can cause or further exacerbate binge and compulsive eating. Dysfunctions in two neurotransmitter systems in the mesocorticolimbic pathway, dopamine and glutamate, are thought to contribute to maladaptive eating behaviors. The trace amine associated receptor 1 (TAAR1) system is a promising therapeutic target for compulsive eating behavior due to the role of TAAR1 in synaptic transmission and in the modulation of dopaminergic and glutamatergic signaling. In support of this notion, the TAAR1 agonist RO5256390 was found to decrease the reinforcing effects of palatable food-cues and to reduce binge-like and compulsive-like eating of palatable food. Additionally, prolonged, intermittent access to palatable food was shown to downregulate TAAR1 in the prefrontal cortex, suggesting a potential role for TAAR1 signaling in inhibitory control processes. Research into the role of TAAR1 in addiction, including TAAR1’s ability to modulate psychostimulant reward and reinforcement, bolsters support for TAAR1 agonism as a pharmacological treatment for compulsive eating and other addictive behaviors. This review summarizes the evidence for TAAR1 agonism as a promising therapeutic for compulsive eating behavior as well as the hypothesized mechanism responsible for these effects.

Neuropharmacology of compulsive eating.

Compulsive eating behaviour is a transdiagnostic construct observed in certain forms of obesity and eating disorders, as well as in the proposed construct of 'food addiction'. Compulsive eating can be conceptualized as comprising three elements: (i) habitual overeating, (ii) overeating to relieve a negative emotional state, and (iii) overeating despite adverse consequences. Neurobiological processes that include maladaptive habit formation, the emergence of a negative affect, and dysfunctions in inhibitory control are thought to drive the development and persistence of compulsive eating behaviour. These complex psychobehavioural processes are under the control of various neuropharmacological systems. Here, we describe the current evidence implicating these systems in compulsive eating behaviour, and contextualize them within the three elements. A better understanding of the neuropharmacological substrates of compulsive eating behaviour has the potential to significantly advance the pharmacotherapy for feeding-related pathologies.This article is part of a discussion meeting issue 'Of mice and mental health: facilitating dialogue between basic and clinical neuroscientists'.