232 research outputs found

    Increased colonic propionate reduces anticipatory reward responses in the human striatum to high-energy foods

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    Background: Short-chain fatty acids (SCFAs), metabolites produced through the microbial fermentation of nondigestible dietary components, have key roles in energy homeostasis. Animal research suggests that colon-derived SCFAs modulate feeding behavior via central mechanisms. In humans, increased colonic production of the SCFA propionate acutely reduces energy intake. However, evidence of an effect of colonic propionate on the human brain or reward-based eating behavior is currently unavailable. Objectives: We investigated the effect of increased colonic propionate production on brain anticipatory reward responses during food picture evaluation. We hypothesized that elevated colonic propionate would reduce both reward responses and ad libitum energy intake via stimulation of anorexigenic gut hormone secretion. Design: In a randomized crossover design, 20 healthy nonobese men completed a functional magnetic resonance imaging (fMRI) food picture evaluation task after consumption of control inulin or inulin-propionate ester, a unique dietary compound that selectively augments colonic propionate production. The blood oxygen level–dependent (BOLD) signal was measured in a priori brain regions involved in reward processing, including the caudate, nucleus accumbens, amygdala, anterior insula, and orbitofrontal cortex (n = 18 had analyzable fMRI data). Results: Increasing colonic propionate production reduced BOLD signal during food picture evaluation in the caudate and nucleus accumbens. In the caudate, the reduction in BOLD signal was driven specifically by a lowering of the response to high-energy food. These central effects were partnered with a decrease in subjective appeal of high-energy food pictures and reduced energy intake during an ad libitum meal. These observations were not related to changes in blood peptide YY (PYY), glucagon-like peptide 1 (GLP-1), glucose, or insulin concentrations. Conclusion: Our results suggest that colonic propionate production may play an important role in attenuating reward-based eating behavior via striatal pathways, independent of changes in plasma PYY and GLP-1. This trial was registered at clinicaltrials.gov as NCT00750438

    Training motor responses to food: A novel treatment for obesity targeting implicit processes.

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    PublishedREVIEWJOURNAL ARTICLEThis is the author accepted manuscript. The final version is available from Elsevier via the DOI in this record.The present review first summarizes results from prospective brain imaging studies focused on identifying neural vulnerability factors that predict excessive weight gain. Next, findings from cognitive psychology experiments evaluating various interventions involving food response inhibition training or food response facilitation training are reviewed that appear to target these neural vulnerability factors and that have produced encouraging weight loss effects. Findings from both of these reviewed research fields suggest that interventions that reduce reward and attention region responses to high calorie food cues and increase inhibitory region responses to high calorie food cues could prove useful in the treatment of obesity. Based on this review, a new conceptual model is presented to describe how different cognitive training procedures may contribute to modifying eating behavior and important directions for future research are offered. It is concluded that there is a need for evaluating the effectiveness of more intensive food response training interventions and testing whether adding such training to extant weight loss interventions increases their efficacy

    Obesity is associated with insufficient behavioral adaptation

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    Obesity is one of the major health concerns nowadays according to the World Health Organisation (WHO global status report on noncommunicable diseases 2010). Thus, there is an urgent need for understanding obesity-associated alterations in food-related and general cognition and their underlying structural and functional correlates within the central nervous system (CNS). Neuroscientific research of the past decade has mainly focussed on obesity-related differences within homeostatic and hedonic processing of food stimuli. Therein, alterations during anticipation and consumption of food-reward stimuli in obese compared with lean subjects have been highlighted. This points at an altered adaptation of eating behavior in obese individuals. This thesis investigates if adaptation of behavior is attenuated in obese compared to lean individuals in learning-related processes beyond the food domain. In five consecutive experimental studies, we show that obese participants reveal reduced adaptation of behavior within and outside the food context. With the help of MRI, we relate these behavioral findings to alterations in structure and function of the fronto-striatal dopaminergic system in obesity. In more detail, reduced behavioral adaptation seems to be associated with attenuated utilization of negative prediction errors in obese individuals. Within the brain, this relates to reduced functional coupling between subcortical dopaminergic target regions (ventral striatum) and executive cortical structures (supplementary motor area) in obesity, as revealed by fMRI analysis

    A core eating network and its modulations underlie diverse eating phenomena

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    We propose that a core eating network and its modulations account for much of what is currently known about the neural activity underlying a wide range of eating phenomena in humans (excluding homeostasis and related phenomena). The core eating network is closely adapted from a network that Kaye, Fudge, and Paulus (2009) proposed to explain the neurocircuitry of eating, including a ventral reward pathway and a dorsal control pathway. In a review across multiple literatures that focuses on experiments using functional Magnetic Resonance Imaging (fMRI), we first show that neural responses to food cues, such as food pictures, utilize the same core eating network as eating. Consistent with the theoretical perspective of grounded cognition, food cues activate eating simulations that produce reward predictions about a perceived food and potentially motivate its consumption. Reviewing additional literatures, we then illustrate how various factors modulate the core eating network, increasing and/or decreasing activity in subsets of its neural areas. These modulating factors include food significance (palatability, hunger), body mass index (BMI, overweight/obesity), eating disorders (anorexia nervosa, bulimia nervosa, binge eating), and various eating goals (losing weight, hedonic pleasure, healthy living). By viewing all these phenomena as modulating a core eating network, it becomes possible to understand how they are related to one another within this common theoretical framework. Finally, we discuss future directions for better establishing the core eating network, its modulations, and their implications for behavior

    Food addiction: Implications for the diagnosis and treatment of overeating

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    This is the final version. Available from MDPI via the DOI in this record. With the obesity epidemic being largely attributed to overeating, much research has been aimed at understanding the psychological causes of overeating and using this knowledge to develop targeted interventions. Here, we review this literature under a model of food addiction and present evidence according to the fifth edition of the Diagnostic and Statistical Manual (DSM-5) criteria for substance use disorders. We review several innovative treatments related to a food addiction model ranging from cognitive intervention tasks to neuromodulation techniques. We conclude that there is evidence to suggest that, for some individuals, food can induce addictive-type behaviours similar to those seen with other addictive substances. However, with several DSM-5 criteria having limited application to overeating, the term ‘food addiction’ is likely to apply only in a minority of cases. Nevertheless, research investigating the underlying psychological causes of overeating within the context of food addiction has led to some novel and potentially effective interventions. Understanding the similarities and differences between the addictive characteristics of food and illicit substances should prove fruitful in further developing these interventions.Biotechnology and Biological Sciences Research CouncilEuropean Research Counci

    A functional neuroimaging review of obesity, appetitive hormones and ingestive behavior

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    Adequate energy intake is vital for the survival of humans and is regulated by complex homeostatic and hedonic mechanisms. Supported by functional MRI (fMRI) studies that consistently demonstrate differences in brain response as a function of weight status during exposure to appetizing food stimuli, it has been posited that hedonically driven food intake contributes to weight gain and obesity maintenance. These food reward theories of obesity are reliant on the notion that the aberrant brain response to food stimuli relates directly to ingestive behavior, specifically, excess food intake. Importantly, functioning of homeostatic neuroendocrine regulators of food intake, such as leptin and ghrelin, are impacted by weight status. Thus, data from studies that evaluate the effect of weight status on brain response to food may be a result of differences in neuroendocrine functioning and/or behavior. In the present review, we examine the influence of weight and weight change, exogenous administration of appetitive hormones, and ingestive behavior on BOLD response to food stimuli

    The role of simulations in consumer experiences and behavior: insights from the grounded cognition theory of desire

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    What are the mechanisms by which extrinsic and environmental cues affect consumer experiences, desires, and choices? Based on the recent grounded cognition theory of desire, we argue that consumption and reward simulations constitute a central mechanism in these phenomena. Specifically, we argue that appetitive stimuli, such as specific product cues, can activate simulations of consuming and enjoying the respective products, based on previous learning experiences. These consumption and reward simulations can lead to motivated behavior, and can be modulated by state and trait individual differences, situational factors, and product-extrinsic cues. We outline the role of simulations within the grounded theory of desire, offering a theoretical framework for understanding motivational processes in consumer behavior. Then we illustrate the theory with behavioral, physiological, and neuroimaging findings on simulations in appetitive behavior and sensory marketing. Finally, we outline important issues for further research and applications for stimulating healthy, prosocial, and sustainable consumer choices

    Genetic Risk for Obesity Predicts Nucleus Accumbens Size and Responsivity to Real-World Food Cues

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    Obesity is a major public health concern that involves an interaction between genetic susceptibility and exposure to environmental cues (e.g., food marketing); however, the mechanisms that link these factors and contribute to unhealthy eating are unclear. Using a well-known obesity risk polymorphism (FTO rs9939609) in a sample of 78 children (ages 9-12 y), we observed that children at risk for obesity exhibited stronger responses to food commercials in the nucleus accumbens (NAcc) than children not at risk. Similarly, children at a higher genetic risk for obesity demonstrated larger NAcc volumes. Although a recessive model of this polymorphism best predicted body mass and adiposity, a dominant model was most predictive of NAcc size and responsivity to food cues. These findings suggest that children genetically at risk for obesity are predisposed to represent reward signals more strongly, which, in turn, may contribute to unhealthy eating behaviors later in life

    Hand-held dynamic visual noise reduces naturally occurring food cravings and craving-related consumption

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    Author version made available in accordance with the publisher's policy for non-mandated open access submission. Under Elsevier's copyright, non-mandated authors are permitted to make work available in an institutional repository.This study demonstrated the applicability of the well-established laboratory task, dynamic visual noise, as a technique for reducing naturally occurring food cravings and subsequent food intake. Dynamic visual noise was delivered on a hand-held computer device. Its effects were assessed within the context of a diary study. Over a 4-week period, 48 undergraduate women recorded their food cravings and consumption. Following a 2-week baseline, half the participants watched the dynamic visual noise display whenever they experienced a food craving. Compared to a control group, these participants reported less intense cravings. They were also less likely to eat following a craving and consequently consumed fewer total calories following craving. These findings hold promise for curbing unwanted food cravings and craving-driven consumption in real-world settings
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