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Abstract

Similarities and differences between obesity and addiction are a prominent topic of ongoing research. We conducted an activation likelihood estimation meta-analysis on 87 studies in order to map the functional magnetic resonance imaging (fMRI) response to reward in participants with obesity, substance addiction and non-substance (or behavioural) addiction, and to identify commonalities and differences between them. Our study confirms the existence of alterations during reward processing in obesity, non-substance addiction and substance addiction. Specifically, participants with obesity or with addictions differed from controls in several brain regions including prefrontal areas, subcortical structures and sensory areas. Additionally, participants with obesity and substance addictions exhibited similar blood-oxygen-level-dependent fMRI hyperactivity in the amygdala and striatum when processing either general rewarding stimuli or the problematic stimuli (food and drug-related stimuli, respectively). We propose that these similarities may be associated with an enhanced focus on reward – especially with regard to food or drug-related stimuli – in obesity and substance addiction. Ultimately, this enhancement of reward processes may facilitate the presence of compulsive-like behaviour in some individuals or under some specific circumstances. We hope that increasing knowledge about the neurobehavioural correlates of obesity and addictions will lead to practical strategies that target the high prevalence of these central public health challenges.

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... Unexpectedly, greater BMI was associated with increased activity in cerebellar Lobule VI, a region associated with hunger and satiety regulation. Our results overlap with previous meta-analyses showing that greater BMI is associated with greater insula activity in response to sweet stimuli [2,[55][56][57]. Greater BMI is associated with higher activity in regions associated with reward processing, including the caudate and postcentral gyrus [2,[55][56][57]. ...
... Our results overlap with previous meta-analyses showing that greater BMI is associated with greater insula activity in response to sweet stimuli [2,[55][56][57]. Greater BMI is associated with higher activity in regions associated with reward processing, including the caudate and postcentral gyrus [2,[55][56][57]. Observed differences from previous reviews could be due to: (a) only including studies reporting fasting and hunger measures, or (b) the use of categorical contrasts rather than meta-regression. ...
... Unfortunately, we could not dissociate cue-only from cued and uncued sweet stimulus presentation, which may account for different findings from meta-analyses using food pictures as stimuli [56,57]. Stimulus modality may be important in comparisons of overweight and lean individuals. ...
Article
Consuming sweet foods, even when sated, can lead to unwanted weight gain. Contextual factors, such as longer time fasting, subjective hunger, and body mass index (BMI), may increase the likelihood of overeating. Nevertheless, the neural mechanisms underlying these moderating influences on energy intake are poorly understood. We conducted both categorical meta-analysis and meta-regression of factors modulating neural responses to sweet stimuli, using data from 30 functional magnetic resonance imaging (fMRI) articles incorporating 39 experiments (N = 995) carried out between 2006 and 2019. Responses to sweet stimuli were associated with increased activity in regions associated with taste, sensory integration, and reward processing. These taste-evoked responses were modulated by context. Longer fasts were associated with higher posterior cerebellar, thalamic, and striatal activity. Greater self-reported hunger was associated with higher medial orbitofrontal cortex (OFC), dorsal striatum, and amygdala activity and lower posterior cerebellar activity. Higher BMI was associated with higher posterior cerebellar and insular activity. Variations in fasting time, self-reported hunger, and BMI are contexts associated with differential sweet stimulus responses in regions associated with reward processing and homeostatic regulation. These results are broadly consistent with a hierarchical model of taste processing. Hunger, but not fasting or BMI, was associated with sweet stimulus-related OFC activity. Our findings extend existing models of taste processing to include posterior cerebellar regions that are associated with moderating effects of both state (fast length and self-reported hunger) and trait (BMI) variables.
... In the current longitudinal study resting-state functional magnetic resonance imaging (rs-fMRI) and seed-based functional connectivity (FC) analysis were used to examine associations between caudaterelated FC and BMI change in adolescents. We hypothesized that increased BMI or BMI change would be associated with reduced caudate-related FC in the inhibitory region and increased caudate-related FC in reward processing or motivation regions, which were associated with food reward processing and weight gain (e.g., striatum, midbrain, amygdala, insula, pre-/postcentral gyrus, and orbitofrontal cortex) (García-García et al., 2014;Stice and Yokum, 2016). ...
... Contrary to the study hypothesis, BMI was not significantly associated with caudate-related FC in reward regions, such as the striatum, midbrain, amygdala, insula, and orbitofrontal cortex (García-García et al., 2014;Stice and Yokum, 2016). Reward regions are related to weight gain and obesity (Stice and Yokum, 2016) and people with obesity reportedly have different caudate-related FC in reward-related regions (Lips et al., 2014). ...
Article
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Background: Childhood obesity has become a global epidemic and the etiology of maladaptive ingestive behavior in children warrants further research. Mounting evidence suggests that the caudate is associated with body weight gain and obesity in adults. In adolescents, however, how caudate-related neural networks are associated with body weight gain is unclear because their central nervous systems are still developing. Objectives: The current longitudinal resting-state functional magnetic resonance imaging (rs-fMRI) study was conducted to investigate the hypothesis that caudate-related neural networks have a role in weight gain in adolescents. Methods: The study included 20 healthy adolescents with a mean age of 17.5 ± 2.0 years and a mean body mass index of 20.6 ± 2.1 who underwent baseline rs-fMRI then follow-up rs-fMRI approximately 1 year later. Body mass index (BMI) was measured at both timepoints. Seed-based functional connectivity analysis was utilized to analyze caudate-related functional connectivity (FC) using the caudate as a seed. Associations between caudate-related FC and BMI at baseline were assessed, as were associations between change in BMI and caudate-related FC between baseline and follow-up. Results: At baseline, greater caudate-lateral prefrontal cortex FC was correlated with lower BMI (family wise error-corrected p < 0.05). Compared to the baseline, increased FC in the caudate-lateral prefrontal cortex at follow up were negatively associated with increased BMI (p < 0.05). Conclusion: Given that the lateral prefrontal cortex and caudate are associated with inhibitory control, the caudate-lateral prefrontal cortex FC may have a preventive effect on weight gain in adolescents. The results of the current study suggest that developing inhibitory control would lead to the prevention of childhood obesity.
... Indeed, the construct of FA refers to the idea that high calories (and/or highly processed foods) should activate an addiction-like response in individuals [7] that may lead to excessive food consumption [8]. Therefore, FA seems to share clinical characteristics of some eating disorders (EDs, e.g., bulimia nervosa, binge eating disorder) [7,9] but also of substance-related and addictive disorders (SRAD) [10][11][12] as well as behavioral addictions [3,13]. ...
... According to Gearhardt et al. [8], FA relies on the evidence that some foods may be potentially addictive [20][21][22][32][33][34][35]. Indeed, several studies highlighted that the neural reward response triggered by high palatable food (e.g., chocolate, pizza, etc.) is observed also in SRAD (e.g., drug and/or alcohol) [4,13,27,[126][127][128][129][130] as well as in certain EDs (e.g., bulimia nervosa, BED) [12,39,131,132]. Based on this parallelism and in light of the DSM-5 SRAD criteria, the YFAS 2.0 [8] rapidly became the instrument of choice for the assessment of FA [6,18,39]. ...
Article
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Purpose To examine the structural validity, measurement invariance, reliability, and some other psychometrical properties of the Italian version of the Yale Food Addiction Scale 2 (I-YFAS 2.0) in patients with severe obesity and the general population. Methods 704 participants—400 inpatients with severe obesity and 304 participants enrolled from the general population—completed the I-YFAS 2.0 and questionnaires measuring eating disorder symptoms. A first confirmatory factor analysis (CFA) tested a hierarchical structure in which each item of the I-YFAS 2.0 loaded onto one of the twelve latent symptoms/criteria which loaded onto a general dimension of Food Addiction (FA). The second CFA tested a first-order structure in which symptoms/criteria of FA simply loaded onto a latent dimension. Measurement invariance (MI) between the group of inpatients with severe obesity and the sample from the general population was also tested. Finally, convergent validity, test–retest reliability, internal consistency, and prevalence analyses were performed. Results CFAs confirmed the structure for the I-YFAS 2.0 for both the hierarchical structure and the first-order structure. Configural MI and strong MI were reached for hierarchical and the first-order structure, respectively. Internal consistencies were shown to be acceptable. Prevalence of FA was 24% in the group of inpatients with severe obesity and 3.6% in the sample from the general population. Conclusions The I-YFAS 2.0 represents a valid and reliable questionnaire for the assessment of FA in both Italian adult inpatients with severe obesity and the general population, and is a psychometrically sound tool for clinical as well as research purposes. Level of evidence Level V, descriptive study.
... FA is associated with low self-esteem, high psychological distress, lower quality of life and depressive symptoms (Gearhardt et al., 2012;Burmeister et al., 2013;Minhas et al., 2021;Vidmar et al., 2021). From a psychobiological perspective, there is the assumption that similar processes in FA and other addiction disorders may be operating, which might explain the similarities and the high comorbidity of FA with substance-related disorders and behavioural addictions (Davis and Carter, 2009;García-García et al., 2014;Marmet et al., 2019). ...
... FA severity was associated with increased BMI, which is in line with findings of previous studies (Pedram et al., 2013;Gearhardt et al., 2014). A variety of studies reports associations between FA and SUDs (Davis and Carter, 2009;García-García et al., 2014;Tinghino et al., 2020). In our study, AUD severity was not associated with FA. ...
Article
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Background and Aims: It is assumed that a relevant subgroup of individuals experiences an addiction-like eating behaviour (Food Addiction), characterized by an impaired control over eating behaviour, emotional eating and food craving. Individuals experiencing Food Addiction partially share common symptomatology with Binge-Eating-Disorder and Bulimia Nervosa. The aim of this study was to investigate the prevalence of Food Addiction, general psychopathology, and associations with weight- and addiction-related constructs in individuals with overweight and obesity, who did not suffer from Binge-Eating-Disorder or Bulimia Nervosa. Methods: N =213 (67.1% female; M BMI =33.35kg/m ² , SD BMI =3.79kg/m ² ) participants who were included in a weight loss program (I-GENDO project) reported BMI and completed questionnaires before the start of the treatment. Food Addiction severity, depressive symptoms, alcohol use disorder, internet use disorder, psychological distress, impulsivity personality trait, impulsive and emotional eating behaviour, food related inhibitory control, weight bias internalization, and self-efficacy were assessed. Results: The prevalence of Food Addiction was 15% with higher, although not statistically significant, prevalence in female (18.2%) compared to male (8.6%) participants. Food Addiction was associated with higher BMI at baseline assessment, low self-esteem, impulsive and emotional eating behaviour, weight bias internalization, and deficits in food-related inhibitory control. In addition, correlations were found between Food Addiction and severity of depressive symptoms, internet use disorder, and psychological distress. Conclusion: A relevant subgroup of participants experiences Food Addiction even when controlling for Binge-Eating-Disorder and Bulimia Nervosa. Future studies are warranted that investigate whether Food Addiction affects treatment success.
... Boutelle and colleagues similarly observed greater activation in the amygdala (i.e., an area associated with impulsive decision-making) [6] and bilateral insula to both sucrose and water among children with obesity, compared to controls [22]. In addition, children with obesity had greater responses to sucrose compared to water in areas such as the right amygdala and paracingulate gyrus (i.e., associated with general reward processing among individuals with substance dependence) [26], whereas in controls these areas responded more to water than to sucrose. The authors also found that children with obesity recruited the right putamen (i.e., associated with processing of reward) [26] more than controls; however, they did not have increased responses in the striatum as the authors had hypothesized. ...
... In addition, children with obesity had greater responses to sucrose compared to water in areas such as the right amygdala and paracingulate gyrus (i.e., associated with general reward processing among individuals with substance dependence) [26], whereas in controls these areas responded more to water than to sucrose. The authors also found that children with obesity recruited the right putamen (i.e., associated with processing of reward) [26] more than controls; however, they did not have increased responses in the striatum as the authors had hypothesized. In an adolescent sample, Feldstein Ewing and associates also found greater BOLD responses to high-calorie beverages in the nucleus accumbens (i.e., another area associated with pleasure) [25] and right amygdala compared to a low-calorie beverage [21]. ...
Article
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Purpose of review: Controversy surrounds the construct of food addiction. The current review examines neurobiological evidence for the existence of food addiction as a valid diagnosis. Recent findings: Recent neuroimaging studies suggest significant overlap in the areas of the brain that are activated in relation to both food and drug addiction. Specifically, areas of the brain implicated in executive functioning (e.g., attention, planning, decision-making, inhibition), pleasure and the experience of reward, and sensory input and motor functioning display increased activation among individuals with symptoms of both food and drug addiction. Proposed symptoms of food addiction mirror those comprising other substance use disorder diagnoses, with similar psychological and behavioral sequelae. Results of neuroimaging studies suggest significant overlap in the areas of the brain that are activated in relation to both food and drug addiction, providing support for continued research into the construct of food addiction.
... In obesity research, several theories argue that obesity is characterized by an increased responsivity to rewarding food cues (Berridge et al., 2010;Chen et al., 2018;Stice and Burger, 2018). In support of this, multiple studies have consistently found increased neural activation to palatable food cues (Stice et al., 2008;García-García et al., 2014;Feldstein Ewing et al., 2017) as well as a potentially stronger reinforcing efficacy (Saelens and Epstein, 1996). This increased responsiveness to cues of reward may similarly affect the execution of goaldirected behavior. ...
... Participants were asked to learn correct approach (Go) or inhibitory (NoGo) responses to cues that predicted reward or punishment. Monetary reinforcement stimuli (gains and losses) were used as they show obesity-related brain activity alterations that are similar to those found for food-stimuli in other studies (e.g., Balodis et al., 2013;García-García et al., 2014;Opel et al., 2015), and may be less prone to momentary evaluation fluctuations than food cues (Field et al., 2016). In addition to the primary task, two brief control experiments were carried out. ...
Article
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Overeating in individuals with obesity is hypothesized to be partly caused by automatic action tendencies to food cues that have the potential to override goal-directed dietary restriction. Individuals with obesity are often characterized by alterations in the processing of such rewarding food, but also of non-food stimuli, and previous research has suggested a stronger impact on the execution of goal-directed actions in obesity. Here, we investigated whether Pavlovian cues can also corrupt the learning of new approach or withdrawal behavior in individuals with obesity. We employed a probabilistic Pavlovian-instrumental learning paradigm in which participants (29 normal-weight and 29 obese) learned to actively respond (Go learning) or withhold a response (NoGo learning) in order to gain monetary rewards or avoid losses. Participants were better at learning active approach responses (Go) in the light of anticipated rewards and at learning to withhold a response (NoGo) in the light of imminent punishments. Importantly, there was no evidence for a stronger corruption of instrumental learning in individuals with obesity. Instead, they showed better learning across conditions than normal-weight participants. Using a computational reinforcement learning model, we additionally found an increased learning rate in individuals with obesity. Previous studies have mostly reported a lower reinforcement learning performance in individuals with obesity. Our results contradict this and suggest that their performance is not universally impaired: Instead, while previous studies found reduced stimulus-value learning, individuals with obesity may show better action-value learning. Our findings highlight the need for a broader investigation of behavioral adaptation in obesity across different task designs and types of reinforcement learning.
... Other reinforcers, such as psychoactive drugs, elicit similar neural reward responses (e.g., [6]). This has led some researchers to hypothesize a common neural basis of FA and other types of addiction (e.g., [7,8]). ...
... This has led some researchers to hypothesize a common neural basis of FA and other types of addiction (e.g., [7,8]). Garcia-Garcia et al. [6] conducted a meta-analysis on reward processing in obesity and addiction. Both patient groups showed altered brain activation in several brain regions including prefrontal areas (e.g., inferior frontal gyrus), subcortical structures (e.g., basal ganglia) and sensory areas compared to control subjects. ...
Article
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Background: The concept of 'food addiction' (FA) posits that highly processed food with added fat and/or refined carbohydrates is capable of triggering addictive-like eating behavior. FA may be one possible phenotype in obesity. Methods: The present voxel-based morphometry (VBM) study compared data from three groups of women. One group scored high on the Yale Food Addiction Scale (YFAS) and was overweight (n = 21), whereas the two other groups had low YFAS scores and were either overweight (n = 21) or normal-weight (n = 21). Results: Overweight women with high YFAS scores had less grey matter volume (GMV) in the inferior frontal gyrus (IFG) than overweight women with low FA tendency, who in turn had less GMV in the IFG than the normal-weight group. The IFG is involved in response inhibition, which is relevant for the control of appetite and food intake. In the group with high FA tendency, the frequency of binge episodes was substantially correlated with the YFAS scores, and 11 women of this group were diagnosed with binge-eating disorder (BED). The association between IFG volume and YFAS scores was not statistically significant anymore when controlling for the effect of binge frequency as revealed by partial correlation analysis. Conclusion: This VBM study revealed an association between reported FA tendency and a neural correlate of disinhibited eating. Future studies with bigger sample sizes are needed in order to demonstrate that FA is sufficiently different from existing conditions (e.g., BED) to warrant classification as a distinct disease phenotype.
... Moreover, research has already demonstrated that affective mechanisms such as reward processing and cognitive control (e.g., the inhibition of impulses) are altered in both SRAs and NSRAs. Specifically, altered (anticipatory) signaling in the amygdala and striatum seems to underlie aberrant reward processing in addictive disorders (in NSRAs as well as SRAs; Balodis & Potenza, 2015;García-García et al., 2014;Luijten et al., 2017). During inhibitory control tasks, individuals with addictive disorders show reduced activity in the ACC as well as prefrontal regions, including the DLPFC (Luijten et al., 2014). ...
... Increased OFC/vmPFC as well as striatal activation in addictive disorders are in line with the general notion of an increased reward sensitivity (Balodis & Potenza, 2015;García-García et al., 2014;Luijten et al., 2017) and an overvaluation of rewarding stimuli in addiction (Schultz, 2011). Recently, the OFC has been conceptualized as providing a cognitive map of task/state space that enables inference of relationships that are not directly observed (Murray & Rudebeck, 2018;Stalnaker et al., 2015;Wilson et al., 2014;Yu et al., 2020). ...
Article
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Both substance-related as well as non-substance-related addictions may include recurrent engagement in risky actions despite adverse outcomes. We here apply a unified approach and review task-based neuroimaging studies on substance-related (SRAs) and non-substance related addictions (NSRAs) to examine commonalities and differences in neural correlates of risk-taking in these two addiction types. To this end, we conducted a systematic review adhering to the PRISMA guidelines. Two databases were searched with predefined search terms to identify neuroimaging studies on risk-taking tasks in individuals with addiction disorders. In total, 19 studies on SRAs (comprising a total of 648 individuals with SRAs) and 10 studies on NSRAs (comprising a total of 187 individuals with NSRAs) were included. Risk-related brain activation in SRAs and NSRAs was summarized individually and subsequently compared to each other. Results suggest convergent altered risk-related neural processes, including hyperactivity in the OFC and the striatum. As characteristic for both addiction types, these brain regions may represent an underlying mechanism of suboptimal decision-making. In contrast, decreased DLPFC activity may be specific to SRAs and decreased IFG activity could only be identified for NSRAs. The precuneus and posterior cingulate show elevated activity in SRAs, while findings regarding these areas were mixed in NSRAs. Additional scarce evidence suggests decreased ventral ACC activity and increased dorsal ACC activity in both addiction types. Associations between identified activation patterns with drug use severity underpin the clinical relevance of these findings. However, this exploratory evidence should be interpreted with caution and should be regarded as preliminary. Future research is needed to evaluate the findings gathered by this review.
... Excellent obesity-related reviews have focused on either DA transmission [22], or cognition with little or no emphasis on the relation with dopamine [7,11,15]. Others have argued for dopamine-mediated cognitive changes in obesity [1-3, 8, 9, 23-27] paralleling findings from addiction research, with controversial opinions towards the existence of food addiction [22,23,[28][29][30][31]. Here, we argue for a more detailed assessment on the relationship between dopamine and the variety of possibly dopamine-mediated cognitive changes in obesity. ...
... salivation, skin conductance, neural activation) and craving responses to food-related stimuli are associated with both food consumption and body weight [138]. Such food stimuli also potently activate the brain's reward system, i.e. the striatum and PFC value areas [23,25,26,93]. ...
Article
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Purpose of Review Animal and human studies suggest that diet-induced obesity and plasticity in the central dopaminergic system are linked. However, it is unclear whether observed changes depend on diet or obesity, and whether they are specific to brain regions and cognitive functions. Here, we focus on neural and cognitive changes in frontostriatal circuits. Recent Findings Both diet and obesity affect dopaminergic transmission. However, site and direction of effects are inconsistent across species and studies. Non-specific changes are observed spanning all frontostriatal loops, from sensory input to motivated behaviour. Given the impact of peripheral signals on central dopaminergic signalling and the interaction between the frontostriatal loops, modulation of dopamine likely propagates through all loops and, thus, affects behaviour on various levels of complexity. Summary To improve convergence between animal and human studies on diet-induced obesity, animal studies should include sophisticated cognitive measures and diets resembling human obesogenic diets, and human studies should adopt diet interventions and longitudinal designs.
... Another problem in the field is that it allows for any finding to be interpreted as an abnormal neurobehavioral signature of food addiction. For example, findings of enhanced activation in obesity or food addiction in response to reward are generally interpreted as supportive of the dopamine sensitization hypothesis [96]. Conversely, decreased mesolimbic engagement in obesity or food addiction has been linked to dopamine hypofunctionality, as described in severe phases of drug addiction [43]. ...
Article
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Purpose of Review The food addiction model suggests the compelling hypothesis that compulsive overeating and drug addictions share common neurobiological underpinnings. However, neuroimaging results are inconsistent, and they are difficult to integrate with each other. This mini-review provides a critical overview of the human neuroimaging literature in food addiction and binge eating symptoms. Recent Findings Neuroanatomical studies suggest the involvement of the orbitofrontal cortex in food addiction. Functional imaging studies have examined whether food addiction is associated with alterations during reward processing, cognitive control, or emotion regulation. However, these results have provided limited consistency so far. Summary To overcome the limitations of current research, we suggest that future studies on food addiction should address four main points: (a) disentangle between the effects of food addiction and obesity; (b) discriminate between causes and consequences of food addiction; (c) address the heterogeneity of food addiction; (d) prevent overinterpretation of results and facilitate replicability.
... Past meta-analyses have examined the effects of valence in reward processing (Liu et al. 2011), whether the reward is personal or vicarious (Morelli et al. 2015), and how reward processing relates to decision making (Diekhof et al. 2008), in teenagers (Silverman et al. 2015), individuals diagnosed with schizophrenia (Leroy et al. 2015;Schlagenhauf et al. 2008), obesity, and substance addiction (García-García et al. 2014). Knowledge contributions of these meta-analyses are focused mainly on monetary rewards and do not distinguish among the different reward types that motivate human behavior (i.e., monetary, erotic, and food). ...
Article
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Reward processing is a fundamental human activity. The basal ganglia are recognized for their role in reward processes; however, specific roles of the different nuclei (e.g., nucleus accumbens, caudate, putamen and globus pallidus) remain unclear. Using quantitative meta-analyses we assessed whole-brain and basal ganglia specific contributions to money, erotic, and food reward processing. We analyzed data from 190 fMRI studies which reported stereotaxic coordinates of whole-brain, within-group results from healthy adult participants. Results showed concordance in overlapping and distinct cortical and sub-cortical brain regions as a function of reward type. Common to all reward types was concordance in basal ganglia nuclei, with distinct differences in hemispheric dominance and spatial extent in response to the different reward types. Food reward processing favored the right hemisphere; erotic rewards favored the right lateral globus pallidus and left caudate body. Money rewards engaged the basal ganglia bilaterally including its most anterior part, nucleus accumbens. We conclude by proposing a model of common reward processing in the basal ganglia and separate models for money, erotic, and food rewards.
... The reward system, which consists of dopaminergic neurons originating in the ventral tegmental area (VTA) and substantia nigra (SN) in the midbrain project throughout the brain especially to key areas including the nucleus accumbens, striatum (especially the caudate), orbitofrontal cortex (OFC), and insula, has been extensively researched in relation to obesity in recent years. Numerous studies have indicated a respond of these areas to food cues during fMRI, especially in obese [25][26][27][28]. Some researchers have hypothesized that exposure to highly rewarding foods results in hyper-responsivity of the reward system to food cues, which leads individuals to seek foods more frequently and in greater quantity. ...
Article
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In recent years, plenty of researches have reported in obese individuals with abnormal brain processes implicated in homeostatic regulation, reward, emotion, memory, attention, and executive function in eating behaviors. Thus, treating obesity cannot remain “brainless.” Behavioral and psychological interventions activate the food reward, attention, and motivation system, leading to minimal weight loss and high relapse rates. Pharmacotherapy is an effective weight loss method and regulate brain activity but with concerns about its brain function safety problems. Obesity surgery, the most effective therapy currently available for obesity, shows pronounced effects on brain activity, such as deactivation of reward and attention system, and activation of inhibition control toward food cues. In this review, we present an overview of alterations in the brain after the three common weight loss methods.
... The amygdala has also been widely implicated in the processing of food and other rewarding stimuli (Sescousse, Caldu, Segura, & Dreher, 2013;Tang, Fellows, Small, & Dagher, 2012;van der Laan, de Ridder, Viergever, & Smeets, 2011). Moreover, altered amygdala activity might be clinically relevant in this context, since both individuals with obesity and patients with substance use disorders were shown to exhibit increased activity of this region in response to food and drug stimuli (García-García et al., 2014). ...
Article
Emotions can influence our eating behaviors. Facing an acute stressor or being in a positive mood are examples of situations that tend to modify appetite. However, the question of how the brain integrates these emotion-related changes in food processing remains elusive. Here, we designed an emotional priming fMRI task to test if amygdala activity during food pictures differs depending on the emotional context. Fifty-eight female participants completed a novel emotional priming task, in which emotional images of negative, neutral, or positive situations were followed by pictures of either foods or objects. After priming in each trial, participants rated how much they liked the shown foods or objects. We analyzed how brain activity during the contrast “foods > objects” changed according to the emotional context—in the whole brain and in the amygdala. We also examined the potential effect of adiposity (i.e., waist circumference). We observed a higher difference between liking scores for foods and objects after positive priming than after neutral priming. In the left amygdala, activity in the contrast “foods > objects” was higher after neutral priming relative to negative priming. Waist circumference was not significantly related to this emotional priming effect on food processing. Our results suggest that emotional context alters food and nonfood perception, both in terms of liking scores and with regard to engagement of the left amygdala. Moreover, our findings indicate that emotional context has an impact on the salience advantage of food, possibly affecting eating behavior.
... Obesity is the result of systematically consuming more energy than is expended. This can be seen as a failure of control over eating behaviour [1][2][3] and could result from altered processing of reward 4 . As a consequence, appetitive and often high-caloric foods are over-consumed despite negative consequences, such as the uncomfortable feeling of being full, feelings of regret, or long-term health risks. ...
Article
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Consuming more energy than is expended may reflect a failure of control over eating behaviour in obesity. Behavioural control arises from a balance between two dissociable strategies of reinforcement learning: model-free and model-based. We hypothesized that weight status relates to an imbalance in reliance on model-based and model-free control, and that it may do so in a linear or quadratic manner. To test this, 90 healthy participants in a wide BMI range [normal-weight (n = 31), overweight (n = 29), obese (n = 30)] performed a sequential decision-making task. The primary analysis indicated that obese participants relied less on model-based control than overweight and normal-weight participants, with no difference between overweight and normal-weight participants. In line, secondary continuous analyses revealed a negative linear, but not quadratic, relationship between BMI and model-based control. Computational modelling of choice behaviour suggested that a mixture of both strategies was shifted towards less model-based control in obese participants. Our findings suggest that obesity may indeed be related to an imbalance in behavioural control as expressed in a phenotype of less model-based control potentially resulting from enhanced reliance on model-free computations.
... One recent review found evidence to support the notion that compulsivity-related deficits were common across the spectrum of excessive eating-related disorders [17], as well as in anorexia nervosa [18]. For example, individuals with binge eating disorder generally exhibit greater compulsive symptomatology than those without, though attention must be called to the fact that not all individuals with binge eating disorder have obesity and that only a small percentage of individuals with obesity binge eat [19]. ...
Article
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Impulsivity and compulsivity are multidimensional constructs that are increasingly considered determinants of obesity. Studies using functional magnetic resonance imaging (fMRI) have provided insight on how differences in brain response during tasks exploring facets of impulsivity and compulsivity relate to the ingestive behaviors that support the etiology and maintenance of obesity. In this narrative review, we provide an overview of neuroimaging studies exploring impulsivity and compulsivity factors as they relate to weight status. Special focus will be placed on studies examining the impulsivity-related dimensions of attentional bias, delayed gratification and emotion regulation. Discussions of compulsivity within the context of obesity will be restricted to fMRI studies investigating habit formation and response flexibility under shifting contingencies. Further, we will highlight neuroimaging research demonstrating how alterations in neuroendocrine functioning are linked to excessive food intake and may serve as a driver of the impulsive and compulsive behaviors observed in obesity. Research on the associations between brain response with neuroendocrine factors, such as insulin, peptide YY (PYY), leptin, ghrelin and glucagon-like peptide 1 (GLP-1), will be reviewed.
... Neuroimaging can elucidate aspects of brain structure, function, and chemistry that are associated with sex/gender differences in compulsive eating behaviors in obesity. Several groups have linked the neural mechanisms underlying obesity to those for substance use disorders (SUDs) [9][10][11]. In obesity, palatable food consumption activates the mesolimbic dopaminergic pathway, begetting its rewarding and conditioning effects, as is the case for drug consumption in SUD. ...
Article
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While the global prevalence of obesity has risen among both men and women over the past 40 years, obesity has consistently been more prevalent among women relative to men. Neuroimaging studies have highlighted several potential mechanisms underlying an individual’s propensity to become obese, including sex/gender differences. Obesity has been associated with structural, functional, and chemical alterations throughout the brain. Whereas changes in somatosensory regions appear to be associated with obesity in men, reward regions appear to have greater involvement in obesity among women than men. Sex/gender differences have also been observed in the neural response to taste among people with obesity. A more thorough understanding of these neural and behavioral differences will allow for more tailored interventions, including diet suggestions, for the prevention and treatment of obesity.
... In particular, the ventromedial and orbitofrontal cortex track food-related reward values (Goldstone et al., 2009;Hare, Camerer, & Rangel, 2009;Holland & Gallagher, 2004;Kable & Glimcher, 2007;O'Doherty, Deichmann, Critchley, & Dolan, 2002;Rolls, 2011). In line with these results, our findings support the fact that individuals with obesity show altered reward system (García-García et al., 2014; by showing higher susceptibility to gustatory and visual cues in a delay discounting paradigm (Morys, Bode, & Horstmann, 2018) and increased responsivity to passive food picture viewing tasks (Pursey et al., 2014;van den Akker, Stewart, Antoniou, Palmberg, & Jansen, 2014). Further, increased macroscale connectivity, particularly in the prefrontal, parietal, and cingulate cortices is known to be related to eating behaviors in people with obesity (Park et al., 2016;Park, Lee, et al., 2018;Park, Moon, et al., 2018). ...
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Dysregulated neural mechanisms in reward and somatosensory circuits result in an increased appetitive drive for and reduced inhibitory control of eating, which in turn causes obesity. Despite many studies investigating the brain mechanisms of obesity, the role of macroscale whole‐brain functional connectivity remains poorly understood. Here, we identified a neuroimaging‐based functional connectivity pattern associated with obesity phenotypes by using functional connectivity analysis combined with machine learning in a large‐scale (n ~ 2,400) dataset spanning four independent cohorts. We found that brain regions containing the reward circuit positively associated with obesity phenotypes, while brain regions for sensory processing showed negative associations. Our study introduces a novel perspective for understanding how the whole‐brain functional connectivity correlates with obesity phenotypes. Furthermore, we demonstrated the generalizability of our findings by correlating the functional connectivity pattern with obesity phenotypes in three independent datasets containing subjects of multiple ages and ethnicities. Our findings suggest that obesity phenotypes can be understood in terms of macroscale whole‐brain functional connectivity and have important implications for the obesity neuroimaging community.
... Higher BMI has been consistently associated with higher levels of disinhibition and hunger (Bond et al., 2001;Cappelleri et al., 2009) while a more complex relationship of BMI and cognitive restraint has been proposed (Dietrich et al., 2014). The YFAS (Gearhardt et al., 2009) is a questionnaire designed to identify addictive tendencies toward certain type of foods and eating behavior (García-García et al., 2014). Here, we use the ordinal symptom score from the YFAS. ...
... Higher BMI has been consistently associated with higher levels of disinhibition and hunger (Bond et al., 2001;Cappelleri et al., 2009) while a more complex relationship of BMI and cognitive restraint has been proposed (Dietrich et al., 2014). The YFAS (Gearhardt et al., 2009) is a questionnaire designed to identify addictive tendencies toward certain type of foods and eating behavior (García-García et al., 2014). Here, we use the ordinal symptom score from the YFAS. ...
Article
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TMEM18 is the strongest candidate for childhood obesity identified from GWASs, yet as for most GWAS-derived obesity-susceptibility genes, the functional mechanism remains elusive. We here investigate the relevance of TMEM18 for adipose tissue development and obesity. We demonstrate that adipocyte TMEM18 expression is downregulated in children with obesity. Functionally, downregulation of TMEM18 impairs adipocyte formation in zebrafish and in human preadipocytes, indicating that TMEM18 is important for adipocyte differentiation in vivo and in vitro. On the molecular level, TMEM18 activates PPARG, particularly upregulating PPARG1 promoter activity, and this activation is repressed by inflammatory stimuli. The relationship between TMEM18 and PPARG1 is also evident in adipocytes of children and is clinically associated with obesity and adipocyte hypertrophy, inflammation, and insulin resistance. Our findings indicate a role of TMEM18 as an upstream regulator of PPARG signaling driving healthy adipogenesis, which is dysregulated with adipose tissue dysfunction and obesity.
... Higher BMI has been consistently associated with higher levels of disinhibition and hunger (Bond et al., 2001;Cappelleri et al., 2009) while a more complex relationship of BMI and cognitive restraint has been proposed (Dietrich et al., 2014). The YFAS (Gearhardt et al., 2009) is a questionnaire designed to identify addictive tendencies toward certain type of foods and eating behavior (García-García et al., 2014). Here, we use the ordinal symptom score from the YFAS. ...
Article
Highlights d TMEM18 expression is essential for adipocyte formation in vitro and in vivo d TMEM18 activates PPARG by upregulating PPARG1 promoter activity d TMEM18 and PPARG1 are dysregulated with obesity and adipose tissue dysfunction In Brief Landgraf et al. show that the obesity-susceptibility gene TMEM18 is of critical functional importance for adipose tissue biology. TMEM18 promotes adipogenesis by activating PPARG1 and thereby metabolically beneficial hyperplasia. The link between TMEM18 and PPARG1 is dysregulated in obesity and related inflammatory and metabolic parameters in children. SUMMARY TMEM18 is the strongest candidate for childhood obesity identified from GWASs, yet as for most GWAS-derived obesity-susceptibility genes, the functional mechanism remains elusive. We here investigate the relevance of TMEM18 for adipose tissue development and obesity. We demonstrate that adipocyte TMEM18 expression is downregulated in children with obesity. Functionally, downregulation of TMEM18 impairs adipocyte formation in zebrafish and in human preadipocytes, indicating that TMEM18 is important for adipocyte differentiation in vivo and in vitro. On the molecular level, TMEM18 activates PPARG, particularly upregulating PPARG1 promoter activity , and this activation is repressed by inflammatory stimuli. The relationship between TMEM18 and PPARG1 is also evident in adipocytes of children and is clinically associated with obesity and adipocyte hypertrophy, inflammation , and insulin resistance. Our findings indicate a role of TMEM18 as an upstream regulator of PPARG signaling driving healthy adipogenesis, which is dysregulated with adipose tissue dysfunction and obesity.
... This is supported by a meta-analysis of functional MRI studies which has shown that food and drugs activate similar brain regions (3). Additionally, similar brain abnormalities during the presentation of stimuli in reward and salience progressing has been observed between obesity and substance addiction (4). ...
Article
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Purpose This study assessed the perception of sweetness, creaminess, and pleasantness from a sweet/fat preference test in subjects who are lean (BMI: 19–25), obese (BMI: 30–33) or very obese (BMI: 34–40) using categorical modeling. Methods Subjects tasted 16 dairy solutions consisting of 0%, 3.5%, 11.3% and 37.5% fat and each containing 0%, 5%, 10%, or 20% sugar and rated them for sweetness, creaminess and pleasantness. Results A proportional odds model described the perception of sweetness using an Emax for the effect of sugar and a linear effect for fat. Perception of creaminess was dependent on the fat and sugar content and was described with proportional odds model with linear effects of sugar and fat. Perception of pleasantness increased with sugar and fat but decreased in solutions containing 37.5% fat. A differential odds model using an Emax model for fat and sugar with a negative interaction between them allowed the sugar content to be less than proportional and the fat content to be greater than proportional for pleasantness. Conclusions Application of modeling provided understanding of these complex interactions of sugar and fat on the perception of sweetness, creaminess, and pleasantness and provides a tool to investigate obesity and pharmacological intervention.
... Such external food cues have the potential to enhance the motivation to obtain and consume food, even in a satiated state. 2 Recently, it has been shown that people with obesity outperform people with normal weight when learning and tracking the reward predicting value of cues associated with a food reward. 3 In addition, individuals with a higher body mass index (BMI) compared to a lower BMI (normal weight to obese) continue to respond to such food reward cues with the same intensity, despite their decreased motivation to consume the food rewards after devaluation 4,5 In a meta-analysis, García-García et al 6 showed that people with obesity exhibit hyperactivation in reward-related brain areas and proposed that this enhanced focus on rewards may lead to compulsive-like behaviours. In addition to motivational aspects and behavioural control, obesity is associated with altered decision making and executive functions. ...
Article
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Obesity is associated with alterations in dopaminergic transmission and cognitive function. Rodent studies suggest that diets rich in saturated fat and refined sugars (HFS), as opposed to diets diets low in saturated fat and refined sugars (LFS), change the dopamine system independent of excessive body weight. However, the impact of HFS on the human brain has not been investigated. Here, we compared the effect of dietary dopamine depletion on dopamine‐dependent cognitive task performance between two groups differing in habitual intake of dietary fat and sugar. Specifically, we used a double‐blind within‐subject cross‐over design to compare the effect of acute phenylalanine/tyrosine depletion on a reinforcement learning and a working memory task, in two groups that are on opposite ends of the spectrum of self‐reported HFS intake (low vs high intake: LFS vs HFS group). We tested 31 healthy young women matched for body mass index (mostly normal weight to overweight) and IQ. Depletion of peripheral precursors of dopamine reduced the working memory specific performance on the operation span task in the LFS, but not in the HFS group (P = 0.016). Learning from positive‐ and negative‐reinforcement (probabilistic selection task) was increased in both diet groups after dopamine depletion (P = 0.049). As a secondary exploratory research question, we measured peripheral dopamine precursor availability (pDAP) at baseline as an estimate for central dopamine levels. The HFS group had a significantly higher pDAP at baseline compared to the LFS group (P = 0.025). Our data provide the first evidence indicating that the intake of HFS is associated with changes in dopamine precursor availability, which is suggestive of changes in central dopamine levels in humans. The observed associations are present in a sample of normal to overweight participants (ie, in the absence of obesity), suggesting that the consumption of a HFS might already be associated with altered behaviours. Alternatively, the effects of HFS diet and obesity might be independent.
... Many drugs of abuse, including alcohol, promote striatal dopamine release (3) and alter response to natural reward. Moreover, altered reward response is characteristic of many psychopathologies (4)(5)(6). Considering the importance of reward processing in maintaining homeostasis, identifying direct and indirect modulators of reward-related pathways has important clinical relevance. ...
Article
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2019): A role for the CD38 rs3796863 polymorphism in alcohol and monetary reward: evidence from CD38 knockout mice and alcohol self-administration, [11C]-raclopride binding, and functional MRI in humans, The American Journal of Drug and Alcohol Abuse, ABSTRACT Background: Cluster of differentiation 38 (CD38) is a transmembrane protein expressed in dopa-minergic reward pathways in the brain, including the nucleus accumbens (NAc). The GG genotype of a common single nucleotide polymorphism (SNP) within CD38, rs3796863, is associated with increased social reward. Objective: Examine whether CD38 rs3796863 and Cd38 knockout (KO) are associated with reward-related neural and behavioral phenotypes. Methods: Data from four independent human studies were used to test whether rs3796863 genotype is associated with: (1) intravenous alcohol self-administration (n = 64, 30 females), (2) alcohol-stimulated dopamine (DA) release measured using 11 C-raclopride positron emission tomography (n = 22 men), (3) ventral striatum (VS) response to positive feedback measured using a card guessing functional magnetic resonance imaging (fMRI) paradigm (n = 531, 276 females), and (4) resting state functional connectivity (rsfc) of the VS (n = 51, 26 females). In a fifth study, we used a mouse model to examine whether cd38 knockout influences stimulated DA release in the NAc core and dorsal striatum using fast-scanning cyclic voltammetry. Results: Relative to T allele carriers, G homozygotes at rs3796863 within CD38 were characterized by greater alcohol self-administration, alcohol-stimulated dopamine release, VS response to positive feedback, and rsfc between the VS and anterior cingulate cortex. High-frequency stimulation reduced DA release among Cd38 KO mice had reduced dopamine release in the NAc. Conclusion: Converging evidence suggests that CD38 rs3796863 genotype may increase DA-related reward response and alcohol consumption.
... In people with obesity, high uncontrolled eating is associated with decreased functional connectivity between the amygdala and vmPFC and increased employment of sensorimotor areas when presented with food stimuli, e.g. the bilateral cerebellum [137]. People with food addiction also show augmented amygdala and ventral striatum activity to food reward cues [138] and greater connectivity in salience and emotional regulation networks, and lower connectivity in the central executive network [98]. The amygdala has an important role in emotion regulation, salience detection, attention towards stimuli and projects to sensory cortices for information processing. ...
Article
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Bariatric surgery results in long-term weight loss and an improved metabolic phenotype due to changes in the gut-brain axis regulating appetite and glycaemia. Neuroendocrine alterations associated with bariatric surgery may also influence hedonic aspects of eating by inducing changes in taste preferences and central reward reactivity towards palatable food. However, the impact of bariatric surgery on disordered eating behaviours (e.g.: binge eating, loss-of-control eating, emotional eating and ‘addictive eating’), which are commonly present in people with obesity are not well understood. Increasing evidence suggests gut-derived signals, such as appetitive hormones, bile acid profiles, microbiota concentrations and associated neuromodulatory metabolites, can influence pathways in the brain implicated in food intake, including brain areas involved in sensorimotor, reward-motivational, emotional-arousal and executive control components of food intake. As disordered eating prevalence is a key mediator of weight-loss success and patient well-being after bariatric surgery, understanding how changes in the gut-brain axis contribute to disordered eating incidence and severity after bariatric surgery is crucial to better improve treatment outcomes in people with obesity.
... Paralleling these findings, people with substance-use disorders, compared to those without, show greater activation in reward regions of the brain to substance use cues [37,38]. In an activation likelihood estimation meta-analysis of 87 studies, participants with obesity and those with substance addictions exhibited similar blood-oxygen-level-dependent fMRI hyperactivity in the amygdala and striatum when processing general rewarding stimuli as well as problematic stimuli (i.e., food-or drug-related stimuli) [39]. ...
Article
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Purpose of Review To summarize recent neurobiological evidence for (1) the addictive potential of ultra-processed foods and (2) the utility of food addiction, defined by behavioral criteria, as a clinically meaningful type of disordered eating. Recent Findings Ultra-processed foods appear to be capable of triggering biobehavioral mechanisms associated with addiction (e.g., dopaminergic sensitization, enhanced motivation), whereas naturally occurring foods do not appear to produce addictive-like responses. Neuroimaging studies have elucidated parallel mechanisms in food addiction and substance-use disorders, including dopaminergic dysfunction, emotion dysregulation, and impulsivity. Emerging data has also suggested biological distinctions for individuals with food addiction evident by the brain-gut-microbiome connection, hormones, and genetics. Summary Existing evidence has yielded convincing findings for overlapping features of ultra-processed foods and drugs of abuse. Preliminary findings from neurobiological studies of individuals with food addiction have revealed similar neural pathways triggered by food and related stimuli as observed in prior studies of persons with substance-use disorders.
... The neurocircuitries regulating food-and alcohol-seeking behaviors share common pathways such as the mesolimbic dopaminergic pathway (Kenny, 2011). Furthermore, individuals with obesity and addictions exhibited analogous brain activation patterns in the amygdala and striatum when processing food or drug-related stimuli (Garcia-Garcia et al., 2014). Collectively this literature suggests the regulation of metabolism potentially plays a role in alcohol drinking behavior, and given the neurobiological overlaps in addiction, obesity and feeding related behaviors, these metabolic factors may also contribute to reward processing in heavy alcohol drinkers, as is seen in obesity. ...
Article
Background The relationship between alcohol use and metabolism has focused on the effects of alcohol use on metabolic factors. Metabolic factors, such as triglycerides, cholesterol, and glucose, have been shown to be associated with increased risk for heavy alcohol consumption and alcohol use disorder (AUD). It’s been suggested that changes in metabolic factors may play a role in reward seeking behaviors and pathways. Studies on feeding behavior and obesity revealed the role of triglycerides in neural response to food cues in neurocircuitry regulating reward and feeding behaviors. This study aimed to explore the relationship of peripheral metabolism, alcohol use, and reward processing in individuals that use alcohol. Methods Ninety participants from a previously collected dataset were included in the analysis. Participants were treatment seeking, detoxified individuals with AUD and healthy individuals without AUD, with the following metabolic biomarkers: triglyceride, glucose, high- and low-density cholesterol, and HbA1c levels. Participants completed a neuroimaging version of the Monetary Incentive Delay task (MID). Results Correlations on peripheral metabolic biomarkers, alcohol use, and neural activity during reward anticipation and outcome during the MID task were not significant. Mediation models revealed triglycerides and high-density cholesterol had significant effects on left anterior insula during anticipation of potential monetary loss and this effect was not mediated by alcohol use. Conclusion Limbic recruitment by anticipation of monetary rewards revealed an independent relationship with peripheral metabolism and was not affected by individual differences in alcohol use, despite the effects of alcohol use on metabolic markers and reward processing neural circuitry.
... This is surprising as the main clinical populations sampled were individuals with ADHD (Demurie et al., 2016;Desman et al., 2008;Ma et al., 2016) and SUD (Charles-Walsh et al., 2016;Chung et al., 2011). Both disorders are characterised by disrupted reward processing (García-García et al., 2014;Tenenbaum et al., 2018), and with this particular sensitivity to rewarding stimuli, we may have expected an enhanced effect of reward on IC for these sub-groups. In the case of SUD populations, the lack of effect of reward may be due to the severity of the condition, for example, harmful use or dependency (Byrne & Worthy, 2019), yet we did not have enough data to reliably investigate any differences by clinical diagnosis. ...
Article
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Contemporary theories predict that Inhibitory Control (IC) can be improved when rewards are available for successfully inhibiting. In non-clinical samples empirical research has demonstrated some support, however ‘null’ findings have also been published. The aim of this meta-analysis was to clarify the magnitude of the effect of reward on IC, and identify potential moderators. Seventy-three articles (contributing k = 80 studies) were identified from Pubmed, PsychInfo and Scopus, published between 1997 – 2020, using a systematic search strategy. A random effects meta-analysis was performed on effect sizes generated from IC tasks which included rewarded and non-rewarded inhibition trials. Moderator analyses were conducted on clinical samples (vs ‘healthy controls’), task type (Go/No-Go vs Stop Signal vs Flanker vs Simon vs Stroop vs Anti-Saccade), reward type (monetary vs points vs other), and age (adults vs children). The prospect of reward for successful inhibition significantly improved IC (SMD=0.429 (95% CI= 0.288, 0.570), I2=96.7%), compared to no reward conditions/groups. This finding was robust against influential cases and outliers. The significant effect was present across all IC tasks. There was no evidence the effect was moderated by type of reward, age or clinical samples. Moderator analyses did not resolve considerable heterogeneity. Findings suggest that IC is a transient state that fluctuates in response to motivations driven by reward. Future research might examine the potential of improving inhibitory control through rewards as a behavioural intervention.
... These brain regions have been suggested to guide food valuation processes and decision-making in humans ( Bartra et al., 2013;Hare et al., 2011;Hutcherson et al., 2012;Schmidt et al., 2018). Frequently, obesity has been associated with hyperactivation of RN regions during anticipation of (high-caloric) food cues, and in contrast, reduced activation to actual taste of these foods (Devoto et al., 2018;García-García et al., 2014;Meng et al., 2020;Stoeckel et al., 2009, though see Morys et al., 2020. RsfMRI studies also showed increased local FC of reward network regions, i.e. ...
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Obesity imposes serious health risks and involves alterations in resting-state functional connectivity of brain networks involved in eating behavior. Bariatric surgery is an effective treatment, but its effects on functional connectivity are still under debate. In this pre-registered study, we aimed to determine the effects of bariatric surgery on major resting-state brain networks (reward and default mode network) in a longitudinal controlled design. 33 bariatric surgery patients and 15 obese waiting-list control patients (37 females; aged 44.15 ± 11.86 SD years (range 21-68)) underwent magnetic resonance imaging at baseline, after 6 and 12 months. We conducted a pre-registered whole-brain time-by-group interaction analysis, and a time-by-group interaction analysis on within-network connectivity (https://osf.io/f8tpn/, https://osf.io/59bh7/). In exploratory analyses, we investigated the effects of weight loss and head motion. Bariatric surgery compared to waiting did not significantly affect functional connectivity (FWE-corrected p > 0.05), neither whole-brain nor within-network. In exploratory analyses, surgery-related BMI decrease (FWE-corrected p = 0.041) and higher average head motion (FWE-corrected p = 0.021) resulted in significantly stronger connectivity of the reward network with medial posterior frontal regions. This pre-registered well-controlled study did not support a strong effect of bariatric surgery, compared to waiting, on major resting-state brain networks after 6 months. Exploratory analyses indicated that head motion might have confounded the effects. Data pooling and more rigorous control of within-scanner head motion during data acquisition are needed to substantiate effects of bariatric surgery on brain organization.
... In contrast, the polygenic score analyses showed that the genetic liability to higher BMI had stronger influence on ADHD manifestations during the childhood years. There have been an abundance of data supporting the links between obesity and neuropsychological dysfunction, including cognitive decline (Prickett et al., 2015), impaired inhibitory control (Kamijo et al., 2012) and aberrant reward processing (Garcia-Garcia et al., 2014). A recent study also showed that obesity and higher BMI were associated with diminished prefrontal cortex thickness and impaired executive function in children (Laurent et al., 2019). ...
Conference Paper
Background Attention-Deficit/Hyperactivity Disorder (ADHD) is a neurodevelopmental disorder characterised by age-inappropriate, disruptive and pervasive manifestations of inattention and/or hyperactivity/impulsivity. ADHD symptoms typically emerge in childhood and persist into later stages of life. ADHD also frequently co-occurs with a number of psychiatric disorders and medical conditions, thereby bringing a tremendous burden to affected individuals as well as society. In addition to symptom severity and chronicity, the development of ADHD also plays a determinant role in disease outcomes. However, few studies have systematically investigated different predictive factors and underlying aetiologies associated with the development of ADHD. Aims This thesis aims to examine patterns, influences and genetic underpinnings of the development of ADHD from childhood to adolescence. The first study investigates childhood factors that differentiate late-onset ADHD from childhood-onset ADHD and differences in adolescent outcomes. The second study examines genetic and environmental contributions underlying the effects of the development of inattention on academic performance. The third and the fourth studies investigate the developmental relationships between ADHD and BMI through triangulation of evidence from longitudinal statistical analyses and genetically informed causal inference approaches. Methods All of the studies adopt a development-sensitive design using data from the “Twin Early Development Study” (TEDS), a longitudinal cohort in the UK. A pluralistic statistical approach is employed for different study objectives. To strengthen causal inference, this thesis compares and contrasts findings from longitudinal statistical approaches and different genetically informed methods under a triangulation framework. Results Findings of this thesis suggest that 1) late-onset ADHD is more likely to be found in males and children who exhibit increased conduct problems and experience more childhood family adversity. Moreover, low socioeconomic status specifically predicts de novo late-onset ADHD, while additional factors predict subthreshold late-onset ADHD; 2) both the baseline level and the developmental course of inattention influence academic performance. Genetic contributions to the development of inattention also affect academic performance; 3) longitudinal statistical analyses identify unidirectional effects from ADHD symptoms to subsequent BMI, while genetic methods suggest a bidirectional causal relationship. Triangulation of evidence shows that multiple sources of confounding are involved in the relationships between ADHD and BMI, including unmeasured confounding and dynastic effects. Conclusions This thesis identifies specific childhood risk factors and genetic underpinnings associated with different developmental patterns of ADHD. Influences of the developmental course of ADHD on psychological and functional outcomes can be attributable to direct causal relationships, genetic and environmental confounding, or a combination of both. Altogether, these findings contribute to a more complete and systematic understanding of different developmental aspects of ADHD. To disentangle aetiological pathways between the development of ADHD and associated conditions, a pluralistic statistical approach to triangulate evidence regarding causal mechanisms is necessary.
... This striking hemispheric asymmetry would not have been observable in the conventional GLM analysis, and exploratory neuro-behavioral correlation tests suggest that it should not be overlooked: in the right but not the left amygdala, both weaker self-inhibition and stronger food-induced disinhibition are correlated with a higher trait food craving and greater cueinduced craving. This accords with some evidence that right amygdalar volume may be associated with BMI in overweight individuals (Orsi et al., 2011), and meta-analytical evidence that both drug and food cues activate the right amygdala (García-García et al., 2014). Multiple hypotheses have been put forward to explain observations of amygdalar asymmetry in affective neuroscience, including suggestions that the right amygdala may be more sensitive to pictorial cues (Markowitsch, 1998) and responds and habituates more quickly to emotional stimuli (Sergerie et al., 2008); or that the right amygdala is engaged more strongly by negative reward and valence, while the left amygdala is more involved in positive reward and valence processing (Lee et al., 2004). ...
Article
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Neural reactivity to food cues may play a central role in overeating and excess weight gain. Functional magnetic resonance imaging (fMRI) studies have implicated regions of the reward network in dysfunctional food cue-reactivity, but neural interactions underlying observed patterns of signal change remain poorly understood. Fifty overweight and obese participants with self-reported cue-induced food craving viewed food and neutral cues during fMRI scanning. Regions of the reward network with significantly greater food versus neutral cue-reactivity were used to specify plausible models of task-related neural interactions underlying the observed blood oxygenation level-dependent (BOLD) signal, and a bi-hemispheric winning model was identified in a dynamic causal modeling (DCM) framework. Neuro-behavioral correlations are investigated with group factor analysis (GFA) and Pearson’s correlation tests. The ventral tegmental area (VTA), amygdalae, and orbitofrontal cortices (OFC) showed significant food cue-reactivity. DCM suggests these activations are produced by largely reciprocal dynamic signaling between these regions, with food cues causing regional disinhibition and an apparent shifting of activity to the right amygdala. Intrinsic self-inhibition in the VTA and right amygdala is negatively correlated with measures of food craving and hunger and right-amygdalar disinhibition by food cues is associated with the intensity of cue-induced food craving, but no robust cross-unit latent factors were identified between the neural group and behavioral or demographic variable groups. Our results suggest a rich array of dynamic signals drive reward network cue-reactivity, with the amygdalae mediating much of the dynamic signaling between the VTA and OFCs. Neuro-behavioral correlations suggest particularly crucial roles for the VTA, right amygdala, and the right OFC-amygdala connection but the more robust GFA identified no cross-unit factors, so these correlations should be interpreted with caution. This investigation provides novel insights into dynamic circuit mechanisms with etiologic relevance to obesity, suggesting pathways in biomarker development and intervention.
... Although this finding is unexpected, it may indicate that alcohol-initiating adolescents are more strongly engaging somatosensory processes (Corkin et al., 1970) than non-alcohol drinking adolescents when losing monetary outcomes. The postcentral gyrus has been similarly recruited in clinical samples during reward processing involving visual stimuli (García-García et al., 2014). Notably, this finding is mostly driven by IQ, as this cluster did not emerge as significant when covarying for psychotropic medication alone. ...
Article
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Adolescent alcohol use is associated with adverse psychosocial outcomes, including an increased risk of alcohol use disorder in adulthood. It is therefore important to identify risk factors of alcohol initiation in adolescence. Research to date has shown that altered neural activation to reward is associated with alcohol use in adolescence; however, few studies have focused on neural activation to loss and alcohol use. The current study examined neural activation to loss and reward among 64 alcohol naive 12-14 year olds that did (n = 20) and did not initiate alcohol use by a three year follow-up period. Results showed that compared to adolescents that did not initiate alcohol use, adolescents that did initiate alcohol use by the three year follow-up period had increased activation to loss in the left striatum (i.e., putamen), right precuneus, and the brainstem/pons when they were alcohol naive at baseline. By contrast, alcohol initiation was not associated with neural activation to winning a reward. These results suggest that increased activation in brain regions implicated in salience, self-referential processing, and sensorimotor function, especially to negative outcomes, may represent an initial vulnerability factor for alcohol use in adolescence.
... Meta-analysis of function MRI studies confirm this claim, showing that food and drugs activate similar brain regions [3]. Additionally, in both obesity and substance addition, similar brain abnormalities have been observed during the presentation of stimuli in reward and salience progressing [4]. One hypothesis is that the sensory perception of food in the mouth is closely linked to hedonic reward of feed and thus related to the motivation to eat [5]. ...
Article
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The aim of this work was to develop and evaluate approaches of linked categorical models using individual predictions of probability. A model was developed using data from a study which assessed the perception of sweetness, creaminess, and pleasantness in dairy solutions containing variable concentrations of sugar and fat. Ordered categorical models were used to predict the individual sweetness and creaminess scores and these individual predictions were used as covariates in the model of pleasantness response. The model using individual predictions was compared to a previously developed model using the amount of fat and sugar as covariates driving pleasantness score. The model using the individual prediction of odds of sweetness and creaminess had a lower variability of pleasantness than the model using the content of sugar and fat in the test solutions, which indicates that the individual odds explain part of the variability in pleasantness. Additionally, simultaneous and sequential modeling approaches were compared for the linked categorical model. Parameter estimation was similar, but precision was better with sequential modeling approaches compared to the simultaneous modeling approach. The previous model characterizing the pleasantness response was improved by using individual predictions of sweetness and creaminess rather than the amount of fat and sugar in the solution. The application of this approach provides an advancement within categorical modeling showing how categorical models can be linked to enable the utilization of individual prediction. This approach is aligned with biology of taste sensory which is reflective of the individual perception of sweetness and creaminess, rather than the amount of fat and sugar in the solution.
... The direction of the observed effect is opposite from our expectations that WM related frontal activation would be higher in women than men (Cousijn et al., 2021;Hill et al., 2014) found to differ between substance users and controls during cognitive tasks. For example, previous studies showed increased activation in the right SFG in cannabis users compared to controls during WM tasks (Kanayama et al. 2004;Hatchard et al., 2020), but another study found cannabis users to display relatively lower activation in the SFG during learning (Nestor et al., 2008) and mixed directions of these effects have also been identified for other addictive behaviors (García-García et al., 2014;Hester & Garavan, 2004;Moreno-López et al., 2012). The SFG is apparently involved in cognitive functions including WM, but it is unclear in what way addictive behaviors, sex, and cognitive load affect its involvement. ...
Article
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Although cannabis use patterns differ between men and women, studies on sex differences on the effects of cannabis on the brain and cognitive control are largely lacking. Working memory (WM) is a component of cognitive control believed to be involved in the development and maintenance of addiction. In this study, we evaluated the association between cannabis use and WM (load) related brain activity in a large sample, enabling us to assess sex effects in this association. The brain activity of 104 frequent cannabis users (63% men) and 85 controls (53% men) was recorded during an N-back WM task. Behavioral results showed a significant interaction between WM load and group for both accuracy and reaction time, with cannabis users showing a relatively larger decrease in performance with increasing WM load. Cannabis users compared to controls showed a relatively smaller reduction in WM (load) related activity in the precuneus and posterior cingulate cortex at higher WM load. This WM (load) related activity was not associated with performance nor cannabis use and related problems. An exploratory analysis showed higher WM-related activity in the superior frontal gyrus in men compared to women. While cannabis users showed higher WM (load) related activity in central nodes of the default mode network, this was not directly attributable to group specific worsening of performance under higher cognitive load. Further research is necessary to assess whether observed group differences increase with higher cognitive load, how group differences relate to measures of cannabis use, and how sex affects these group differences.
... These brain regions have been suggested to guide food valuation processes and decision-making in humans (Bartra, McGuire, & Kable, 2013;Hare, Malmaud, & Rangel, 2011;Hutcherson, Plassmann, Gross, & Rangel, 2012;Schmidt et al., 2018). Frequently, obesity has been associated with hyperactivation of reward network regions during anticipation of (highcaloric) food cues, and in contrast, reduced activation to actual taste of these foods (Devoto et al., 2018;García-García et al., 2014;Meng, Huang, Ao, Wang, & Gao, 2020;Stoeckel et al., 2009), though this has recently been critically discussed (see Morys, García-García, & Dagher, 2020). RsfMRI studies also showed increased local functional connectivity of reward network regions, that is, NAcc, vmPFC, putamen, insula (Contreras-Rodríguez, Martín-Pérez, Vilar-L opez, & Verdejo-Garcia, 2017;Coveleskie et al., 2015;Hogenkamp et al., 2016), and altered connectivity with salience, homeostatic, and sensorimotor networks (Lips et al., 2014;Wijngaarden et al., 2015). ...
Article
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Obesity imposes serious health risks and involves alterations in resting-state functional connectivity of brain networks involved in eating behavior. Bariatric surgery is an effective treatment, but its effects on functional connectivity are still under debate. In this pre-registered study, we aimed to determine the effects of bariatric surgery on major resting-state brain networks (reward and default mode network) in a longitudinal controlled design. Thirty-three bariatric surgery patients and 15 obese waiting-list control patients underwent magnetic resonance imaging at baseline, after 6 and 12 months. We conducted a pre-registered whole-brain time-by-group interaction analysis, and a time-by-group interaction analysis on within-network connectivity. In exploratory analyses, we investigated the effects of weight loss and head motion. Bariatric surgery compared to waiting did not significantly affect functional connectivity of the reward network and the default mode network (FWE-corrected p > .05), neither whole-brain nor within-network. In exploratory analyses, surgery-related BMI decrease (FWE-corrected p = .041) and higher average head motion (FWE-corrected p = .021) resulted in significantly stronger connectivity of the reward network with medial posterior frontal regions. This pre-registered well-controlled study did not support a strong effect of bariatric surgery, compared to waiting, on major resting-state brain networks after 6 months. Exploratory analyses indicated that head motion might have confounded the effects. Data pooling and more rigorous control of within-scanner head motion during data acquisition are needed to substantiate effects of bariatric surgery on brain organization.
... Preliminary insights into binge-eating derive from a recent line of research according to which there would be a shared behavioral and neural substrate between overeating and substance compulsive use [4,5]; in both cases, a failure of inhibitory mechanisms and high impulsivity would play key roles in the tendency to engage in such behaviors despite the negative consequences [4,6]. Support to this argument derives from neuroimaging investigations that underscored the role of prefrontal cortex (PFC) and fronto-striatal circuits at the roots of dysfunctional self-regulation [7,8], which could underlie the lack of ability to stop overconsumption. When inhibitory control is challenged (e.g., with response inhibition tasks-see [9] for a review), differences in brain activity (functional magnetic resonance imaging, fMRI) in brain regions engaged in inhibitory control (such as PFC) seem 2 of 11 to characterize obese and BED on one side and normal-weight individuals on the other side. ...
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Binge-eating refers to episodes of uncontrolled eating accompanied by a perceived loss of control, which can be common in the general population. Given the profound negative consequences of persistent binge-eating such as weight and eating disorders, it is vital to determine what makes someone more vulnerable than others to engage in such a conduct. A total of 42 normal-weight individuals (21 with binge-eating episodes and 21 without binge-eating episodes) underwent a structural magnetic resonance imaging measurement and Voxel-based morphometry (VBM) was used to assess between-group differences in terms of gray matter volume (GMV), together with self-report impulsivity and binge-eating measures. The results showed binge-eating individuals as characterized by higher trait impulsivity and greater regional GMV in the left middle frontal gyrus: however, the GMV in this region appeared to be positively correlated only with measures of binge-eating but not with trait impulsivity measures. These findings provide novel insights on the neurobiological roots of BE in normal-weight individuals and highlight how this behavior can be associated with brain morphometric changes within prefrontal regions also in a non-clinical population. Overall, this study provides a further characterization of the neural correlates of binge-eating and novel insights into the treatment of its more severe pathological forms.
... For example, the reward positivity (RewP) is a positive fronto-central component peaking around 200 to 400 ms, reflecting reward processing (Proudfit, 2015). There is evidence that overeating and obesity are associated with an increased reward value of food stimuli, that may facilitate the presence of compulsive-like behavior (García-García et al., 2014). The development of a task involving food rewards and losses may be useful to examine food-related reward processing, with measures such as the RewP, in different populations. ...
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Electroencephalography (EEG), and the measure of event-related potentials (ERPs) in particular, are useful methods to study the cognitive and cerebral mechanisms underlying the perception and processing of food cues. Further research on these aspects is necessary to better understand how cognitive functioning may influence food choices in different populations (e.g. obese individuals, individuals with eating disorders). To help researchers in designing future studies, this article provides an overview of the methods used in the current literature on ERPs and food-related cognition. Several methodological aspects are explored to outline interesting perspectives for future research, including discussions on the main experimental tasks used, the cognitive functions assessed (e.g. inhibitory control, attentional processing), the characteristics of the participants recruited (e.g. weight status, eating behaviors), and the stimuli selected (e.g. food pictures, odors). The issues generated by some of these methodological choices are discussed, and a few guidelines are provided.
... The overlap of these two circuitries has led to the development of neurocognitive theories to explain food intake dysregulation in obesity [5,[142][143][144][145][146][148][149][150][151][152][153][154]. The neurobiological resemblance of circuitries involved in food-reward with circuitries involved in substanceabuse disorders has led to interrogate whether the dysregulation of food intake in obesity fits into an addiction model (i.e., food addiction disorder) [155][156][157][158][159][160]. However, this proposal has received contradictory and non-conclusive opinions [161,162]. ...
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Nothing more usual than to find Spanish refugees of 1939 in the French Resistance as they continued their fight against fascism. Therefore, hundreds of Spaniards where caught in the nets of the Vichy Government and the Gestapo. They are imprisoned in the French jails (Toulouse, Montluc, Fresnes, Compiègne, etc.) alongside the French Resistant women. Both will be piled up in wagons to the camps of the Third Reich. Many ended at the women’s camp in Ravensbrück. Usually, the Spaniards were labelled “F”, “French”, because they were arrested in France. This “F” was part of the “red triangle” of the “political prisoners”. Some were even classified NN (Nacht und Nebel), i.e. called to disappear without a trace. As they were recognized by nobody (neither the French nor the Spaniards), this means: no mail, no parcels. They held on for life thanks to the links they forged randomly across blocks, satellite camps, languages, affinities... However, many died. For some of them, the release arrived in April 1944, thanks to “neutral” countries initiatives: in fact, a few Spanish women were able to slip into the Red Cross convoys transiting through Switzerland, which were initially reserved for French women. Others returned by Sweden. Others, finally, faced the apocalyptic evacuation of the camps of 1945 and the “marches of death”. We propose to study “the return to life” helps through some cases – obviously return to France since there could be no possible repatriation for these Spanish anti-fascist survivors, as the victory of the Allies did not affect General Franco’s power. After returning to France, this help continued for two or three years, in particular thanks to convalescent stays in Switzerland, Sweden and somewhere else, and thanks to one-off material contributions from the Swiss Grant (“Don suisse”) or from various organizations.
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Multiple neuroimaging meta-analyses have been published concerning gustation, food and taste. A meta-evaluation of these meta-analyses was conducted to qualitatively evaluate the presented evidence. A systematic search was done using multiple databases, in which no restriction was placed on participants and nature of interventions (stimuli vs control). Twenty-three meta-analyses were identified and analyzed. All of them have met 4-9 criteria, out of 11, from the modified checklist constructed by Müller et al. (2018), which implied moderate to high quality of evidence. One of the concerns we found was that no meta-analysis surveyed had been explicitly pre-registered. Also, only three meta-analyses (13.0%) provided clear explanation of how they accounted for sample overlap. Only six meta-analyses (26.1%) explicitly described how they double checked the data. Only two of the 20 meta-analyses (10.0%) using GingerALE software used both the debugged version (v2.3.6) as well as the recommended cluster-level inference with familywise error rate correction. Overall, meta-analyses are increasingly adopting more stringent statistical thresholds, but unfortunately not larger number of studies contained in the analyses.
Chapter
Recall, food addiction (FA) was considered for inclusion in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V), although the final decision was to not include it as an official diagnosis (Adams, Nutrients 11(9):2086, 2019; Schulte, Int J Eat Disord 53:1610–22 2020) (Chap. 5). But since this determination, there have been an increasing number of clinical studies published that support the construct’s validity. Many of the behaviors that manifest in substance use disorders (SUD) in relationship to substances of abuse also exist in relation to highly palatable (HP; generally highly processed, sweet, and high fat) food, and it is increasingly evident that DSM diagnostic criteria for SUD apply to food-related behaviors, as well (Adams, Nutrients 11(9):2086, 2019; Gordon, 2018;10(4):477, Nutrients; Meule, Curr Obes Rep 8(1):11–7, 2019; Tobore, Behav Brain Res 384:112560, 2020; Morin, Front Behav Neurosci 11:19, 2017). SUD-like symptoms in relation to HP food cluster together in a variety of populations, including in normal weight, obese, eating disordered, and non-disordered individuals, which has led to the successful development of a validated and widely utilized scale in FA studies to assess for FA called the Yale Food Addiction Scale (YFAS). Further support for the validity of an FA construct includes the following: (1) higher rates of SUD are seen in people with overeating problems and vice- versa; (2) people with SUD often have preferences for sweet or even fatty food, and cross-sensitization and addiction transfer (otherwise known as cross-addiction) can occur; (3) higher rates of certain neuropsychological, emotional and personality traits, psychiatric diagnoses, and predisposing conditions (trauma, stress) are seen in both SUD and disorders associated with overeating.
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Introduction Abstaining from unwanted behaviors requires a sufficient balance between the executive and impulsive cognitive systems. Working memory (WM) is a vital component of both systems, identified in a wide range of research as the central and dominant component of executive function. WM potentially modulates the desires, tendencies, and behaviors specific to and seen in individuals with substance use disorder (SUD) and obesogenic eating (OE). Compared to healthy populations, research has shown individuals with SUD, as well as those who display OE, to have some degree of executive dysfunction, and both conditions have far-reaching health care implications. Additionally, these deficits are associated with impulsive behavior. Research has proposed that impulsive and so-called reward-driven responses could be altered through cognitive therapy and that both SUD and OE could benefit from working memory training (WMT). Method In this narrative review, we systematically align extant empirical reasoning and evidence with these assumptions. Our main aim is to ascertain and summarize the value of WMT for the treatment of both SUD and food reward consummatory behaviors. As a means to include detailed narrative accounts of all papers of potential value, our thresholds for meaningful improvements in both WM and unwanted behaviors are broad. Results The results from the eleven qualifying studies are as follows: Nine of ten studies show a significant positive training effect of WMT on one or more components of WM capacity; three of six eligible papers (two on alcohol and one on opioid addiction) deliver notable improvements in SUD in response to WMT. One of two suitable studies showed WMT to be a moderately efficacious form of therapy for OE. Conversely, WMT appears to have negligible therapeutic benefit for cognitive function deficits or psychopathology unrelated to WM, suggesting that WMT has unique treatment efficacy for impulsive human behaviors. Conclusion In conclusion, more rigorous and uniform studies on WMT and impulsive harmful behaviors are required to give proof of the benefits of this potential useful treatment.
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Smell perception plays a role in eating behavior and might be involved in the development of obesity. In fact, olfactory function is impaired in obesity and might depend on metabolic health factors. To date, the underlying neural mechanisms remain unclear. Here, we investigate neural processing of food-related odors in normal-weight, overweight and obese individuals. Fifty-three young and healthy participants (28.8 ± 4.4 years, 27 female; 24 normal-weight, 10 overweight and 19 obese) were presented with high- (chocolate, potato chips) and low-caloric (orange, cucumber) food odors during a functional magnetic resonance imaging (fMRI). We also assessed olfactory identification ability, body mass index (BMI), body fat percentage, insulin resistance and leptin. In brief, olfactory perception of food odors was linked to brain activity in the entorhinal and piriform cortex, and the insula, hippocampus, and amygdala. Insulin resistance was negatively related to olfactory identification. Additionally, perception of sweet versus savory odors was related to a higher brain activity in the right middle/superior frontal gyrus. Finally, we found no effect of obesity status, BMI, metabolic factors, or body fat percentage on neural responses to food odors. Overall, this suggests that food odor processing might depend on factors other than body weight status or associated markers of metabolic health.
Chapter
As reviewed in Chap. 1, our body has designed a complex system (the homeostatic system) to respond to energy needs, which regulates appetite and satiety and, therefore, food intake. Food consumption, especially in relation to highly palatable (HP) foods (e.g., foods high in sugar, fat, and/or ultra-processed foods) (Onaolapo and Onaolapo. Pathophysiology. 25(4):263–276, 2018) (Chap. 11), is also regulated by a second system (the hedonic system), which regulates primarily pleasure-seeking or relief-driven feeding behavior. The hedonic system operates through many of the same pathways that mediate alcohol and illicit drug use, overuse, and use disorders. Hedonic eating follows the same natural laws that underly substance use disorders (SUD), such as conditioning, cue, context and mood dependency, and withdrawal, tolerance, and loss of control (Chap. 7). Hedonically-driven eating is moderated by similar neurotransmitters acting in similar brain regions as those that drive overconsumption of illicit drugs and alcohol (Chap. 7) (Novelle and Dieguez. Nutrients 10(1):71, 2018; Jeynes and Gibson. Drug Alcohol Depend 179:229–239, 2017; Morales and Berridge. Physiol Behav 227:113152, 2020; Berridge. Physiol Behav 97(5):537–550, 2009). The hedonic eating system can override the homeostatic system during relative energy abundance, and cause animals and humans to eat more than what is needed to maintain a healthy body weight (Lutter and Nestler. J Nutr 139(3):629–632, 2009; Morin et al. Front Behav Neurosci. 11:19, 2017). In this chapter, we will review the neuroscientific evidence (mostly obtained from animal studies and neuroimaging studies in humans) that food intake is regulated through these systems and that behaviors around HP food, and related brain chemistry changes, parallel those that animals and humans develop around substances of abuse. We also refer readers to Fig. 8.1 (reproduced from Lin and Qu. Obes Surg. 30(5):1988–2002, 2020) for reference while reading this chapter.
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