Neural Responses to Visual Food Cues According to Weight Status: A Systematic Review of Functional Magnetic Resonance Imaging Studies

Pursey, Kirrilly; Stanwell, Peter; Callister, Robert J.; Brain, Katherine; Collins, Clare E.; Burrows, Tracy

doi:10.3389/fnut.2014.00007

Cited by 189 publications

(207 citation statements)

References 130 publications

(356 reference statements)

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“…It could be argued that the effects of the weight loss may have confounded the decreasing effects of liraglutide on CNS activation after 12 weeks. However, if anything, fMRI studies investigating the effect of weight loss on CNS responses to food pictures show that weight reduction may be associated with decreased CNS activation in areas involved in food motivation and reward (19,20). As a result, an effect of weight loss on the CNS would have strengthened the decreasing effect of liraglutide on CNS activation, and weight loss therefore cannot explain the absence of an effect of liraglutide on the CNS after 12 weeks.…”

Section: Resultsmentioning

confidence: 99%

Liraglutide Reduces CNS Activation in Response to Visual Food Cues Only After Short-term Treatment in Patients With Type 2 Diabetes

et al. 2015

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OBJECTIVEGlucagon-like peptide-1 receptor agonists (GLP-1RAs) are associated with reduced appetite and body weight. We investigated whether these effects could be mediated by the central nervous system (CNS). RESEARCH DESIGN AND METHODSWe performed a randomized crossover study in obese patients with type 2 diabetes (n = 20, mean age 59.3 6 4.1 years, mean BMI 32 6 4.7 kg/m 2 ), consisting of two periods of 12-week treatment with either liraglutide 1.8 mg or insulin glargine. Using functional MRI, we determined the effects of treatment on CNS responses to viewing food pictures in the fasted condition and 30 min after meal intake. RESULTSAfter 12 weeks, the decrease in HbA 1c was larger with liraglutide versus insulin glargine (D20.7% vs. 20.2%, P < 0.001). Body weight decreased during liraglutide versus insulin glargine (D23.3 kg vs. 0.8 kg, P < 0.001). After 10 days, patients treated with liraglutide, compared with insulin glargine, showed decreased responses to food pictures in insula and putamen (P £ 0.02). In addition, liraglutide enhanced the satiating effect of meal intake on responses in putamen and amygdala (P £ 0.05). Differences between liraglutide and insulin glargine were not observed after 12 weeks. CONCLUSIONSCompared with insulin, liraglutide decreased CNS activation significantly only after short-term treatment, suggesting that these effects of GLP-1RA on the CNS may contribute to the induction of weight loss, but not necessarily to its maintenance, in view of the absence of an effect of liraglutide on CNS activation in response to food pictures after longer-term treatment.Obesity and diabetes constitute a major health burden due to their pandemic occurrence (1) and their association with adverse consequences, such as cardiovascular disease (2). Obesity is the result of a long-term excess energy intake relative to expenditure, leading to increased weight and body fat mass. The central nervous system (CNS) has a major role in the regulation of food intake and the maintenance

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Section: Resultsmentioning

confidence: 99%

Liraglutide Reduces CNS Activation in Response to Visual Food Cues Only After Short-term Treatment in Patients With Type 2 Diabetes

et al. 2015

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“…Finally, the response in the hypothalamus/ventral striatum was modulated by the expected energy content of the food. 15 More recently, Pursey et al (2014) conducted a meta-analysis of 60 different neuroimaging studies (involving a total of 1565 participants) that had assessed the neural response to visual food cues as a function of the weight of their participants. In this case, the results revealed that obese individuals exhibited a greater increase in neural activation in response to food as compared to non-food images, especially for high-calorie foods, in those brain regions that are associated with reward processing (e.g., the insula and OFC), reinforcement and adaptive learning (the amygdala, putamen, and OFC), emotional processing (the insula, amygdala, and cingulate gyrus), recollective and working memory (the amygdala, hippocampus, thalamus, posterior cingulate cortex, and caudate), executive functioning (the prefrontal cortex (PFC), caudate, and cingulate gyrus), decision making (the OFC, PFC, and thalamus), visual processing (the thalamus and fusiform gyrus), and motor learning and coordination, such as hand-to-mouth movements and swallowing (the insula, putamen, thalamus, and caudate).…”

Section: Neural Substrates Underlying the Processing Of Visual Food Cuesmentioning

confidence: 99%

Eating with our eyes: From visual hunger to digital satiation

Spence

Okajima

Cheok³

et al. 2016

Brain and Cognition

336

222

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One of the brain's key roles is to facilitate foraging and feeding. It is presumably no coincidence, then, that the mouth is situated close to the brain in most animal species. However, the environments in which our brains evolved were far less plentiful in terms of the availability of food resources (i.e., nutriments) than is the case for those of us living in the Western world today. The growing obesity crisis is but one of the signs that humankind is not doing such a great job in terms of optimizing the contemporary food landscape. While the blame here is often put at the doors of the global food companies - offering addictive foods, designed to hit 'the bliss point' in terms of the pleasurable ingredients (sugar, salt, fat, etc.), and the ease of access to calorie-rich foods - we wonder whether there aren't other implicit cues in our environments that might be triggering hunger more often than is perhaps good for us. Here, we take a closer look at the potential role of vision; Specifically, we question the impact that our increasing exposure to images of desirable foods (what is often labelled 'food porn', or 'gastroporn') via digital interfaces might be having, and ask whether it might not inadvertently be exacerbating our desire for food (what we call 'visual hunger'). We review the growing body of cognitive neuroscience research demonstrating the profound effect that viewing such images can have on neural activity, physiological and psychological responses, and visual attention, especially in the 'hungry' brain.

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“…While the reviewed studies show a blunted striatal response in patients with schizophrenia (or depression) and their relatives, the picture is less clear in obesity. As explained above, while we propose to explain obesity in schizophrenia as resulting from a decreased striatal signal during reward anticipation, some obesity studies point to enhanced cue reactivity (Pursey et al, 2014), possibly reflecting a distinct pathway to obesity. However, the striking differences in the various paradigms, populations, and methods used to study obesity make it hard to generalize across studies.…”

Section: Obesity-related Changes In Striatal Reward Processingmentioning

confidence: 84%

“…Most studies of cue processing presented images of appetizing food stimuli to obese patients. These studies found an increase in striatal reactivity when participants viewed these stimuli (Pursey et al, 2014). It is hard to relate these studies to studies using MID tasks due to several methodological issues: monetary (MID) vs. food rewards, eventrelated (MID) vs. block designs, uncontrolled satiation status (MID) vs. fasting or satiated participants, operant (MID) vs. Pavlovian conditioning, images often not controlled for calorie content etc.…”

Section: Obesity-related Changes In Striatal Reward Processingmentioning

confidence: 99%

Altered reward anticipation: Potential explanation for weight gain in schizophrenia?

Grimm

Kaiser

Plichta

et al. 2017

Neuroscience & Biobehavioral Reviews

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a b s t r a c tObesity and weight gain are severe complications of mental illness, especially schizophrenia. They result from changes in lifestyle and nutrition, side effects of medication and other, less well-understood factors. Recent studies suggest that obesity and weight gain are linked to psychopathology. Specifically, severe psychopathology is associated with greater weight dysregulation, typically weight gain. However, our knowledge about the neuroscientific basis of weight gain in schizophrenia is currently limited. We propose that altered reward anticipation, which in turn is related to striatal dopaminergic dysregulation, may explain why obesity is more prevalent in individuals with mental illness. We review evidence that reward anticipation and weight change are linked by a core deficit in dopaminergic striatal circuits. Several lines of evidence, running from animal studies to preclinical and clinical studies, suggest that striatal dopaminergic neurotransmission is a major hub for the regulation of eating behavior and that dopamine links eating behavior to other motivated behavior. From this perspective, the present review outlines a unifying perspective on dopaminergic reward anticipation as a theoretical frame to link weight gain, medication effects and psychopathology. We derive important but open empirical questions and present perspectives for new therapeutic concepts.

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Neural Responses to Visual Food Cues According to Weight Status: A Systematic Review of Functional Magnetic Resonance Imaging Studies

Cited by 189 publications

References 130 publications

Liraglutide Reduces CNS Activation in Response to Visual Food Cues Only After Short-term Treatment in Patients With Type 2 Diabetes

Liraglutide Reduces CNS Activation in Response to Visual Food Cues Only After Short-term Treatment in Patients With Type 2 Diabetes

Eating with our eyes: From visual hunger to digital satiation

Altered reward anticipation: Potential explanation for weight gain in schizophrenia?

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