Feeding represents a necessary behavior for an individual’s survival, requiring a balanced interaction between innate and learned responses to inner physiological needs and external environmental conditions.
Feeding behavior can, however, become pathologic and maladaptive, unbinding from the essential physiological need function and resulting in significant and potentially life-threatening medical conditions together with dysfunctional psychosocial functioning.
According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) disturbances of eating and related behavior leading to altered food consumption/absorption fall within the Feeding and Eating Disorders (FEDs) category. FEDs differ in their clinical course, outcome, and treatment, and have the potential to exacerbate a wide range of related disorders. This constitutes an increasing healthcare burden worldwide.
The pathological symptoms of FEDs -particularly when it comes to pathologies characterized by overconsumption such as binge eating disorder or bulimia nervosa - include lack of control, impulsivity, tolerance, withdrawal, distress/dysfunction, overconsumption, and craving. These patterns mirror the behavioral manifestations also reported in substance use disorders (SUDs) patients, with whom comorbidity is reported.
According to this phenotypic overlap, two non-mutually exclusive theoretical frameworks have been proposed, highlighting the central role of either specific food stimuli (“food addiction”), or the stimuli-elicited behavioral response (“eating addiction”).
Alongside similarities in behavioral manifestations, there are some shared cognitive and emotional states accompanying FEDs and SUDs patients (Anhedonia and compulsivity), as well as common environmental precipitating factors (e.g., stressful experiences or repeated/prolonged exposure to “abused foods”). This highlights the common neurobiological substrate in brain circuits involved in motivation, learning, and control processes evolutionarily developed to mediate the response to reinforcing stimuli.
Coherently, studies report functional and structural alterations in the meso-cortico-limbic and extended amygdala structures (as dopamine, norepinephrine, acetylcholine, and opioid release as well as their receptor distribution) in both patients and animal models reproducing different FEDs features, such as overeating, obesity, binge eating, withdrawal, and food-relapse.
The constructive discussion on this topic along with developments in investigation techniques such as chemo- and optogenetic, magnetic resonance, and conditional knockout encourage the development of well-characterized animal models that could advance our understanding of etiologic factors, neural processes, and mechanisms involved in the development of FEDs, as well as to set up targeted strategies for prevention and treatment.
This Research Topic will spotlight recent advances and current knowledge of dysfunctional eating behaviors, with a particular interest in the impact of genetic and environmental interplay altering the motivational and reinforcement system and related brain circuits.
We aim to gather further insights on the latest outcomes regarding protective and risk factors in FEDs derived from animal model behavioral studies and clinical practice and supported by functional and structural neurobiological analysis of brain circuits involved in motivated behaviors.
Particular interest is aimed at contributions bridging the gap between epigenetic mechanisms (miRNAs, histone modifications, DNA methylation) responsible for gene x environment interaction at the basis of FEDs susceptibility, and potential biomarkers related to pathology and treatment efficacy.
We welcome submissions addressing, but not limited to, the following subtopics:
• Sex-specific differences associated with eating disorders: evidence from sex-specific models’ investigations
• Environmental factors inducing FED’s phenotype
• Protective and risk factors for eating disorders
• Genetic and epigenetic mechanisms related to alterations in eating behavior and eating disorders
• Functional and structural alterations in neural circuitry sustaining FED’s features
• Novel targeted prevention and treatment strategies and compounds
• In vivo or in vitro studies on signaling pathways involved in FED’s phenotype
Feeding represents a necessary behavior for an individual’s survival, requiring a balanced interaction between innate and learned responses to inner physiological needs and external environmental conditions.
Feeding behavior can, however, become pathologic and maladaptive, unbinding from the essential physiological need function and resulting in significant and potentially life-threatening medical conditions together with dysfunctional psychosocial functioning.
According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) disturbances of eating and related behavior leading to altered food consumption/absorption fall within the Feeding and Eating Disorders (FEDs) category. FEDs differ in their clinical course, outcome, and treatment, and have the potential to exacerbate a wide range of related disorders. This constitutes an increasing healthcare burden worldwide.
The pathological symptoms of FEDs -particularly when it comes to pathologies characterized by overconsumption such as binge eating disorder or bulimia nervosa - include lack of control, impulsivity, tolerance, withdrawal, distress/dysfunction, overconsumption, and craving. These patterns mirror the behavioral manifestations also reported in substance use disorders (SUDs) patients, with whom comorbidity is reported.
According to this phenotypic overlap, two non-mutually exclusive theoretical frameworks have been proposed, highlighting the central role of either specific food stimuli (“food addiction”), or the stimuli-elicited behavioral response (“eating addiction”).
Alongside similarities in behavioral manifestations, there are some shared cognitive and emotional states accompanying FEDs and SUDs patients (Anhedonia and compulsivity), as well as common environmental precipitating factors (e.g., stressful experiences or repeated/prolonged exposure to “abused foods”). This highlights the common neurobiological substrate in brain circuits involved in motivation, learning, and control processes evolutionarily developed to mediate the response to reinforcing stimuli.
Coherently, studies report functional and structural alterations in the meso-cortico-limbic and extended amygdala structures (as dopamine, norepinephrine, acetylcholine, and opioid release as well as their receptor distribution) in both patients and animal models reproducing different FEDs features, such as overeating, obesity, binge eating, withdrawal, and food-relapse.
The constructive discussion on this topic along with developments in investigation techniques such as chemo- and optogenetic, magnetic resonance, and conditional knockout encourage the development of well-characterized animal models that could advance our understanding of etiologic factors, neural processes, and mechanisms involved in the development of FEDs, as well as to set up targeted strategies for prevention and treatment.
This Research Topic will spotlight recent advances and current knowledge of dysfunctional eating behaviors, with a particular interest in the impact of genetic and environmental interplay altering the motivational and reinforcement system and related brain circuits.
We aim to gather further insights on the latest outcomes regarding protective and risk factors in FEDs derived from animal model behavioral studies and clinical practice and supported by functional and structural neurobiological analysis of brain circuits involved in motivated behaviors.
Particular interest is aimed at contributions bridging the gap between epigenetic mechanisms (miRNAs, histone modifications, DNA methylation) responsible for gene x environment interaction at the basis of FEDs susceptibility, and potential biomarkers related to pathology and treatment efficacy.
We welcome submissions addressing, but not limited to, the following subtopics:
• Sex-specific differences associated with eating disorders: evidence from sex-specific models’ investigations
• Environmental factors inducing FED’s phenotype
• Protective and risk factors for eating disorders
• Genetic and epigenetic mechanisms related to alterations in eating behavior and eating disorders
• Functional and structural alterations in neural circuitry sustaining FED’s features
• Novel targeted prevention and treatment strategies and compounds
• In vivo or in vitro studies on signaling pathways involved in FED’s phenotype
