Abstract:Eating disorders are complex brain disorders that afflict millions of individuals worldwide. The etiology of these diseases is not fully understood, but a growing body of literature suggests that stress and anxiety may play a critical role in their development. As our understanding of the genetic and environmental factors that contribute to disease in clinical populations like anorexia nervosa, bulimia nervosa and binge eating disorder continue to grow, neuroscientists are using animal models to understand the… Show more
“…The extra food consumption occurred without differences in self-reported appetite, further suggesting decoupling of eating behavior from hunger. These findings support theories that neural circuits regulating appetite are disrupted by chronic anxiety or stress in a manner that could promote obesity or eating disorders (46). Alternately, heightened attentional functioning (47) or even improved visual detection among anxious women (48) might explain persistent post-meal responses to visual food cues, a question that deserves further study.…”
OBJECTIVE
To test the relationship of anxiety to caloric intake and food cue perception in women and men.
METHODS
Fifty-five twins (26 complete, 3 incomplete pairs; 51% women) underwent 2 functional magnetic resonance imaging (fMRI) scans (before and after a standardized meal) and then ate at an ad libitum buffet to objectively assess food intake. State and trait anxiety were assessed using the State-Trait Anxiety Inventory. During the fMRI scans, participants viewed blocks of fattening and non-fattening food images, and non-food objects.
RESULTS
In women, higher trait anxiety was associated with a higher body mass index (BMI) (r=0.40, P=0.010). Trait anxiety was positively associated with kilocalories consumed at the buffet (r=0.53, P=0.005) and percent kilocalories consumed from fat (r=0.30, P=0.006), adjusted for BMI. In within-pair models, which control for shared familial and genetic factors, higher trait anxiety remained associated with kilocalories consumed at the buffet (ρ=0.66, P=0.014), but not with BMI. In men, higher state anxiety was related to macronutrient choices, but not to total caloric intake or BMI. FMRI results revealed that women with high trait anxiety did not suppress activation by fattening food cues across brain regions associated with satiety perception after eating a standardized meal (mean difference low anxiety: −15.4, P<0.001; high anxiety: −1.53, P=0.82, adjusted for BMI).
CONCLUSIONS
In women, trait anxiety may promote excess caloric consumption through altered perception of high-calorie environmental food cues, placing women with genetic predispositions toward weight gain at risk of obesity.
“…The extra food consumption occurred without differences in self-reported appetite, further suggesting decoupling of eating behavior from hunger. These findings support theories that neural circuits regulating appetite are disrupted by chronic anxiety or stress in a manner that could promote obesity or eating disorders (46). Alternately, heightened attentional functioning (47) or even improved visual detection among anxious women (48) might explain persistent post-meal responses to visual food cues, a question that deserves further study.…”
OBJECTIVE
To test the relationship of anxiety to caloric intake and food cue perception in women and men.
METHODS
Fifty-five twins (26 complete, 3 incomplete pairs; 51% women) underwent 2 functional magnetic resonance imaging (fMRI) scans (before and after a standardized meal) and then ate at an ad libitum buffet to objectively assess food intake. State and trait anxiety were assessed using the State-Trait Anxiety Inventory. During the fMRI scans, participants viewed blocks of fattening and non-fattening food images, and non-food objects.
RESULTS
In women, higher trait anxiety was associated with a higher body mass index (BMI) (r=0.40, P=0.010). Trait anxiety was positively associated with kilocalories consumed at the buffet (r=0.53, P=0.005) and percent kilocalories consumed from fat (r=0.30, P=0.006), adjusted for BMI. In within-pair models, which control for shared familial and genetic factors, higher trait anxiety remained associated with kilocalories consumed at the buffet (ρ=0.66, P=0.014), but not with BMI. In men, higher state anxiety was related to macronutrient choices, but not to total caloric intake or BMI. FMRI results revealed that women with high trait anxiety did not suppress activation by fattening food cues across brain regions associated with satiety perception after eating a standardized meal (mean difference low anxiety: −15.4, P<0.001; high anxiety: −1.53, P=0.82, adjusted for BMI).
CONCLUSIONS
In women, trait anxiety may promote excess caloric consumption through altered perception of high-calorie environmental food cues, placing women with genetic predispositions toward weight gain at risk of obesity.
“…In addition, an activity‐based anorexia (ABA) rodent model highlights increased physical activity and reduced body weight in response to restricted food access in animals (Chowdhury, Chen, & Aoki, ). Using neural circuit‐level approaches that enable activation or inhibition of anatomically and genetically defined brain pathways, like optogenetics and chemogenetics, multiple pathways that regulate different patterns of feeding behaviour have been identified (Hardaway, Crowley, Bulik, & Kash, ; Sternson & Roth, ) (see Table S7 for specific regions and nuclei). This approach elevates understanding of how discrete neural circuits control feeding and metabolism and provides additional evidence of how feeding behaviour may be biologically influenced.…”
Section: Truth 4: Eating Disorders Are Not Choices But Serious Biolomentioning
Objective
In 2015, the Academy for Eating Disorders (AED) collaborated with international patient, advocacy, and parent organizations to craft the “Nine Truths About Eating Disorders.” This document has been translated into over 30 languages and has been distributed globally to replace outdated and erroneous stereotypes about eating disorders with factual information. In this paper, we review the state of the science supporting the Nine Truths.
Methods
The literature supporting each of the Nine Truths was reviewed, summarized, and richly annotated.
Results
Most of the Nine Truths arise from well-established foundations in the scientific literature. Additional evidence is required to further substantiate some of the assertions in the document. Future investigations are needed in all areas to deepen our understanding of eating disorders, their causes, and their treatments.
Conclusions
The “Nine Truths About Eating Disorders” is a guiding document to accelerate global dissemination of accurate and evidence-informed information about eating disorders.
“…For example, the orexigenic hormone ghrelin is increased following repeated social defeat stress 62,63 , and not only does it mediate the stress-induced preference for high-fat food 63 , but it also reduces forced-swim immobility 62 . Given the recent resurgence of studies characterizing the detailed circuitry involved in appetite regulation using precise molecular genetic techniques to dissect the multitude of excitatory, inhibitory, neuropeptidergic and other modulatory interactions between a variety of hypothalamic and other limbic and brainstem nuclei 64–72 , further examination of the reciprocal interactions between stress and feeding-related circuits represents an important area for ongoing research 73 .…”
Section: Stress Effects On General Motivational Processesmentioning
Exposure to stress has profound, but complex, actions on motivated behavior and decision-making. These effects are central to core symptoms of a number of psychiatric disorders that are precipitated or augmented by stress, such as depressive disorders and substance use disorders. Studying the neural substrates of stress’s effects on motivation has revealed that stress affects multiple targets on circuits throughout the brain using diverse molecular signaling processes. Moreover, stress does not have unitary effects on motivated behavior, but differences in the intensity, duration, intermittency, controllability and nature of the stressor produce qualitatively and quantitatively different behavioral endpoints. Unsurprisingly, the results of neuroscientific investigations into stress and motivation often open more questions than they resolve. Here we discuss contemporary results pertaining to the neural mechanisms by which stress alters motivation, identify points of contention and highlight integrative areas for continuing research into these multifaceted complexities.
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