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Reward processing in obesity, substance addiction and non-substance addiction
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.
... Additionally, there is evidence for aberrant neural reward processing in numerous substance use disorders compared to healthy controls [24]. In another meta-analysis, an enhanced brain activation in the reward system pointed towards hypersensitivity, especially regarding drug-related stimuli [25]. A similar pattern has been observed in non-substance-related rewards [25]. ...
... In another meta-analysis, an enhanced brain activation in the reward system pointed towards hypersensitivity, especially regarding drug-related stimuli [25]. A similar pattern has been observed in non-substance-related rewards [25]. ...
... It is noteworthy that alcohol consumption was not strongly associated with reward sensitivity, a possible explanation for why there were no significant results in the first crosslagged panel (T1, T2, T3). These results are in contrast to prior research that demonstrated aberrant reward processing in substance use disorders [11,24,25,69]. However, this work mostly considered clinical samples with chronic conditions. ...
Background
Reward sensitivity constitutes a potential key mechanism regarding the etiology and maintenance of mental disorders, especially depression. However, due to a lack of longitudinal studies, the temporal dynamics are not clear yet. Although some evidence indicates that reward processing could be a transdiagnostic mechanism of disorders, these observations could be also a product of comorbidity with depression. This study aimed at investigating the temporal dynamics of reward sensitivity and the course of psychopathological symptoms in a longitudinal investigation, while taking a possible mediating role of depression into account.
Methods
We conducted a three-wave longitudinal online survey with a 4-week interval. A total of N = 453 participants filled out all three questionnaires. Reward sensitivity was assessed with the Positive Valence System Scale-21 (PVSS-21), depression with the Patient Health Questionnaire (PHQ-9), eating disorder symptoms with the Eating Disorder Examination-Questionnaire-8 (EDE-Q-8), social anxiety with the Mini-social phobia inventory (Mini-SPIN) and alcohol consumption with the Alcohol Use Disorders Identification Test-Consumption (AUDIT-C). Cross-lagged panels and mediation analyses were calculated using path analyses.
Results
Depressive and eating disorder symptoms predicted reward insensitivity at later points in time. Effects were larger from T2 to T3. A bidirectional relationship concerning social anxiety was found. Higher alcohol consumption predicted higher reward sensitivity. Depression at T2 fully mediated the association between psychopathological symptoms at T1 and reward sensitivity at T3 for social anxiety and eating disorder symptoms.
Conclusions
Our findings imply that reduced reward sensitivity seems to be a consequence rather than an antecedent of psychopathological symptoms. Comorbid depression plays a crucial role in other mental disorders regarding observed hyposensitivity towards rewards. Therefore, our results do not support a transdiagnostic notion of reward sensitivity, but they indicate a potential role of reward sensitivity for symptom persistence.
Trial registration
The study was preregistered at the Open Science Framework (OSF) (https://archive.org/details/osf-registrations-6n3s8-v1; registration DOI https://doi.org/10.17605/OSF.IO/6N3S8).
... Obesity is a widespread cause of disability with severe public health implications (Mathers & Loncar, 2015). While diminished impulse control and altered valuation of rewarding food cues have been associated with dysfunctional eating behavior and obesity on a behavioral level (Maxwell et al., 2020), research also points toward aberrant neurobiological mechanisms underlying weight gain and obesity during reward processing (Donofry et al., 2020;García-García et al., 2014). ...
... Overweight and obesity have repeatedly been linked to brain functional aberrations in response to reward cues (García-García et al., 2014;Opel et al., 2015). The insula, orbitofrontal cortex (OFC), and striatum have consistently been identified as key regions implicated in reward processing and obesity (Burger & Berner, 2014;Volkow et al., 2011;Wang et al., 2004). ...
... Most previous research on the relationship between body weight and neural reward processing has investigated small sample sizes (García-García et al., 2014;Han et al., 2021) and typically either compared individuals with obesity with a normal weight control group (Han et al., 2021;Opel et al., 2015) or made no distinction between overweight and obese weight groups (García-García et al., 2014;Meng et al., 2020). Studies that consider the entire BMI range in larger samples do not typically investigate whether the effects occur as a function of higher body weight, or whether they are driven by a particular weight group (Beyer et al., 2021;Bhutani et al., 2021). ...
Obesity is associated with alterations in brain structure and function, particularly in areas related to reward processing. Although brain structural investigations have demonstrated a continuous association between higher body weight and reduced gray matter in well-powered samples, functional neuroimaging studies have typically only contrasted individuals from the normal weight and obese body mass index (BMI) ranges with modest sample sizes. It remains unclear, whether the commonly found hyperresponsiveness of the reward circuit can (a) be replicated in well-powered studies and (b) be found as a function of higher body weight even below the threshold of clinical obesity. 383 adults across the weight spectrum underwent functional magnetic resonance imaging during a common card-guessing paradigm simulating monetary reward. Multiple regression was used to investigate the association of BMI and neural activation in the reward circuit. In addition, a one-way ANOVA model comparing three weight groups (normal weight, overweight, obese) was calculated. Higher BMI was associated with higher reward response in the bilateral insula. This association could no longer be found when participants with obesity were excluded from the analysis. The ANOVA revealed higher activation in obese vs. lean, but no difference between lean and overweight participants. The overactivation of reward-related brain areas in obesity is a consistent finding that can be replicated in large samples. In contrast to brain structural aberrations associated with higher body weight, the neurofunctional underpinnings of reward processing in the insula appear to be more pronounced in the higher body weight range.
... Reward-related disorders such as addiction, binge-eating disorder and obesity, are characterized by altered responses to reward cues related to the target of abuse (1)(2)(3). Mesolimbic regions in the brain, including the striatum and the midbrain-with its dopaminergic projections to the striatum (4, 5)-respond to increases in appetitive motivation induced by reward cues (6). Responses of these subcortical reward regions have been related to eating behavior. ...
... The EC program was based on the Dutch healthy food-based dietary guidelines. 1 To establish similar (active) group activities as in the ME, participants were enrolled in cooking workshops during the group meetings of the EC. Sessions focused on healthy eating, healthy cooking of vegetables and fruit, use of different types of fat and salt for cooking, reading of nutrition labels on food products, healthy snacking, guidelines for making healthy choices when eating in restaurants, and how to incorporate healthy eating and cooking in daily life. ...
Introduction
Accumulating evidence suggests that increased neural responses during the anticipation of high-calorie food play an important role in the tendency to overeat. A promising method for counteracting enhanced food anticipation in overeating might be mindfulness-based interventions (MBIs). However, the neural mechanisms by which MBIs can affect food reward anticipation are unclear. In this randomized, actively controlled study, the primary objective was to investigate the effect of an 8-week mindful eating intervention on reward anticipation. We hypothesized that mindful eating would decrease striatal reward anticipation responses. Additionally, responses in the midbrain—from which the reward pathways originate—were explored.
Methods
Using functional magnetic resonance imaging (fMRI), we tested 58 healthy participants with a wide body mass index range (BMI: 19–35 kg/m²), motivated to change their eating behavior. During scanning they performed an incentive delay task, measuring neural reward anticipation responses to caloric and monetary cues before and after 8 weeks of mindful eating or educational cooking (active control).
Results
Compared with the educational cooking intervention, mindful eating affected neural reward anticipation responses, with reduced caloric relative to monetary reward responses. This effect was, however, not seen in the striatum, but only in the midbrain. The secondary objective was to assess temporary and long-lasting (1 year follow-up) intervention effects on self-reported eating behavior and anthropometric measures [BMI, waist circumference, waist-to-hip-ratio (WHR)]. We did not observe effects of the mindful eating intervention on eating behavior. Instead, the control intervention showed temporary beneficial effects on BMI, waist circumference, and diet quality, but not on WHR or self-reported eating behavior, as well as long-lasting increases in knowledge about healthy eating.
Discussion
These results suggest that an 8-week mindful eating intervention may have decreased the relative salience of food cues by affecting midbrain but not striatal reward responses, without necessarily affecting regular eating behavior. However, these exploratory results should be verified in confirmatory research.
The primary and secondary objectives of the study were registered in the Dutch Trial Register (NTR): NL4923 (NTR5025).
... Furthermore, amygdala activity has been associated with scores on the Yale Food Addiction Scale, 35,36 and both the amygdala and the orbitofrontal cortex have been shown to be more highly activated in obese than lean individuals when anticipating the receipt of food. 35 There is evidence that both patients with obesity and those with addictions exhibit augmented activity in the amygdala and ventral striatum in response to reward, 59 thus supporting an overlap between food-related and salience-related circuits. ...
... Our study demonstrated increased activation of the right amygdala in response to a food-related odour in patients with PWS, similar to the increased activation seen in subjects with obesity or substance addiction. 59 Individuals with PWS also showed greater activation in the right amygdala, compared to the controls, to high-calorie foods compared to non-foods. 66 It is possible that the activations were higher than they would have been for a different food odour with lower sugar content. ...
Prader-Willi syndrome is a rare neurodevelopmental genetic disorder characterized by various endocrine, cognitive, and behavioral problems. The symptoms include an obsession for food and reduced satiety, which leads to hyperphagia and morbid obesity. Neuropsychological studies have reported that Prader-Willi patients display altered social interactions with a specific weakness in interpreting social information and responding to them, a symptom close to that observed in autism spectrum disorders.
In the present case-control study, we hypothesized that brain regions associated with compulsive eating behavior would be abnormally activated by food-related odors in Prader-Willi syndrome, as these can stimulate the appetite and induce hunger-related behavior. We conducted a brain imaging study using the olfactory modality because odors have a high hedonic valence and can cause stronger emotional reactions than other modalities. Further, the olfactory system is also intimately associated with the endocrine regulation of energy balance and is the most appropriate modality for studies of Prader-Willi syndrome.
A total of 16 Prader-Willi participants were recruited for this study, which is a significant achievement given the low incidence rate of this rare disease. The second group of 11 control age-matched subjects also participated in the brain imaging study. In the MRI scanner, using an MRI-compatible olfactometer during 56 block sessions, we randomly presented two odors (tulip and caramel), which have different hedonic valence and a different capacity to arouse hunger-related behavior.
Our results demonstrate that Prader-Willi participants have abnormal activity in the brain reward system that regulates eating behavior. Indeed, we found that these patients had the right amygdala activity up to five times higher in response to a food odor (caramel) compared with the tulip odor. In contrast, age-matched control participants had similar activity levels in response to both odors. The amygdala activity levels were found to be associated with the severity of the hyperphagia in Prader-Willi patients.
Our results provide evidence for functional alteration of the right amygdala in Prader-Willi syndrome, which is part of the brain network involved in food addiction modulated by the ghrelin and oxytocin systems, which may drive the hyperphagia. Our study provides important new insights into the functioning of emotion-related brain circuits and pathology, and it is one of the few to explore the dysfunction of the neural circuits involved in emotion and addiction in Prader-Willi syndrome. It suggests new directions for the exploration and remediation of addictive behaviors.
... 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). ...
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.
... 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. ...
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; MBMI=33.35kg/m², SDBMI=3.79kg/m²) 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.
... The EEG/ERPs technique is well-known for its high temporal resolution in characterizing information processing. However, while this technique has been widely employed to examine reward processing in association with other forms of psychopathology (e.g., depression, Keren et al. 2018;anxiety, Sequeira et al. 2022;substance use;García-García et al. 2014), surprisingly little work has used the ERPs to study reward processing in relation to eating pathology. Forester et al. (2024) for the first time applied the ERPs to a reward task in adults with BED. ...
Objective
Early adolescence is marked by elevated psychopathology, including disrupted eating attitudes and behaviors. Reward processing is an identified mechanism in portending eating pathology, that is, aberrant reward responsivity may contribute to disrupted reward‐seeking behaviors (e.g., food consuming). This literature has focused on adults or mid‐to‐late adolescents, with little work done on early adolescence. We examined the linkages between reward feedback processing, indexed by event‐related potentials (ERPs), and changes of emerging disordered eating in community‐dwelling early adolescents.
Method
At T1, 115 youths (66 girls, mean/SD age = 11.00/1.16 years) completed an EEG monetary reward Doors task. Youths completed the Eating Disorder Examination‐Questionnaire Short at T1 and ~6 months (T2) and ~12 months (T3) after T1. In the ERP data, we isolated a reward positivity (RewP) and a late positive potential (LPP) via principal component analysis. We applied multilevel modeling to examine whether baseline ERPs interacted with Time in predicting disordered eating and whether these interactions varied by sex.
Results
We found a significant Time × LPP interaction in girls but not boys. Among girls, only those with a smaller LPP toward the losses (versus wins), which might reflect suboptimal evaluation and regulatory processes in undesired situations, showed increases in disordered eating from T1 to T3.
Discussion
We provided preliminary yet novel evidence concerning the prospective associations between reward processing and changes of disordered eating in early adolescents. Future studies along this line will be critical for understanding the early mechanisms of eating pathology, identifying youths at risk, and developing prevention strategies.
... Similar to drug addiction, gambling disorder, and other addiction disorders, there are also some symptoms of concentration, tolerance and withdrawal in IGD (Petry et al., 2014). At the same time, IGD and other types of addiction disorder all cause cognitive dysfunction, including abnormal reward function, impaired decision-making function and inhibitory control behaviors (Antons et al., 2020;Balconi et al., 2014;Cabedo-Peris et al., 2022;García-García et al., 2014;Luke & Goudriaan, 2018;Wang et al., 2023;Zheng et al., 2022). These cognitive dysfunctions are manifested in several brain regions and system activation abnormalities shown in both substance addiction and behavioral addiction, including the prefrontal cortex, amygdala, hippocampus and mesolimbic dopamine system (Lu et al., 2005;Mantsch et al., 2016;Siciliano et al., 2019). ...
Reward processing dysfunction and inhibition control deficiency have been observed in Internet gaming disorder (IGD). However, it is still unclear whether the previous reinforcement learning depends on reward/punishment feedback influences on the cognitive inhibitory control of IGD. This study compared the differences between an IGD group and healthy people without game experiences in the probability selection task and the subsequent stop signal task by the method of behavioral experiments, in order to explore whether the reward learning ability is impaired in the IGD group. We also discuss the influence of previous reward learning on subsequent inhibition control. The results showed that (1) during the reward learning phase, the IGD group's accuracy was significantly lower than that of the control group; (2) compared with the control group, the IGD group's reaction times were longer in the transfer phase; (3) for no‐go trials of the inhibitory control phase after reward learning, the accuracy of the reward‐related stimulation in the IGD group was lower than that of punishment‐related or neutral stimulation, but there was no significant difference among the three conditions in the control group. These findings indicated that the reinforcement learning ability of the IGD group was impaired, which further caused the abnormal response to reinforcement stimuli.
... Specifically, being driven by unhealthy eating patterns [25][26][27][28][29][30], the ease of access to highly processed foods (HPFs) [31-33]-which are highly palatable and psychologically rewarding [34-38]-may predispose people to develop an addiction. These foods have the potential to activate neural reward systems [34][35][36][37][38], requiring the individual to seek the same feelings of well-being and pleasure. If these cravings are not satisfied, this could lead to the appearance of withdrawal symptoms [39][40][41]. ...
Background: Among the dysfunctional eating behaviors associated with excessive food intake, a construct that is gaining increasing attention is grazing—the constant, continuous, compulsive, and repetitive consumption of small/moderate amounts of food. Furthermore, in some cases, grazing seems to indicate a dependence on food and/or eating. Currently, the Repetitive Eating Questionnaire (Rep(Eat)-Q) appears to be the only questionnaire that comprehensively measures grazing, including its repetitive and compulsive eating component. Therefore, in a sample of individuals with severe obesity, the objective of this study was twofold: (A) to evaluate the psychometric properties of the Italian version of the Rep(Eat)-Q, and (B) to analyze the association between grazing and food addiction (FA). Method: A cross-sectional research design was used. A total of 402 inpatients with severe obesity (BMI > 35) were recruited. Participants underwent a series of questionnaires to investigate structural validity and convergent validity and association with FA criteria. Results: The factorial structure of the Rep(Eat)-Q is robust and showed fit indexes: CFI = 0.973; RMSEA = 0.074; 90%CI [0.056–0.091]; and SRMR = 0.029. Also, it exhibited good internal consistency and convergent validity. Furthermore, logistic regression analysis highlights a specific association between certain FA criteria and grazing. Conclusions: The Rep(Eat)-Q can be considered to be a concise, robust, reliable, and statistically sound tool to assess repetitive eating, specifically grazing. Its strong psychometric properties offer significant advantages for both research and clinical applications. Furthermore, in a sample of individuals with severe obesity, the results suggest that individuals with problematic grazing exhibit a typical behavioral profile of subjects with FA, indicating that FA can manifest through problematic grazing as well.
... Abnormal addictive behaviors toward food in patients with an ED are related to reward circuitry, which is also responsible for substance and non-substance addiction [52]. By assessing and modulating abnormal brain functions involved in appetite control and reward, we might help patients with obesity control their eating behaviors. ...
Neuroimaging has great potential to provide insight into the neural response to food stimuli. Remarkable advances have been made in understanding the neural activity underlying food perception, not only in normal eating but also in obesity, eating disorders, and disorders of gut-brain interaction in recent decades. In addition to the abnormal brain function in patients with eating disorders compared to healthy controls, new therapies, such as neurofeedback and neurostimulation techniques, have been developed that target the malfunctioning brain regions in patients with eating disorders based on the results of neuroimaging studies. In this review, we present an overview of early and more recent research on the central processing and regulation of eating behavior in healthy and patient populations. In order to better understand the relationship between the gut and the brain as well as the neural mechanisms underlying abnormal ingestive behaviors, we also provide suggestions for future directions to enhance our current methods used in food-related neuroimaging studies.
... Then, evidence from studies shows that there are common brain processes between obesity and various addictions. Both obesity and addiction illnesses may be associated with impairments in inhibitory control, as well as elevated reward sensitivity and heightened attention to signals (foods or substances) [268]. However, despite the similarities highlighted, there is evidence that obesity and other addictive behaviors are distinct and may only partially overlap [269]. ...
This comprehensive narrative review explores the concept of neuro-vulnerability in energy metabolism regulation and its implications for metabolic disorders. The review highlights the complex interactions among the neural, hormonal, and metabolic pathways involved in the regulation of energy metabolism. The key topics discussed include the role of organs, hormones, and neural circuits in maintaining metabolic balance. The review investigates the association between neuro-vulnerability and metabolic disorders, such as obesity, insulin resistance, and eating disorders, considering genetic, epigenetic, and environmental factors that influence neuro-vulnerability and subsequent metabolic dysregulation. Neuroendocrine interactions and the neural regulation of food intake and energy expenditure are examined, with a focus on the impact of neuro-vulnerability on appetite dysregulation and altered energy expenditure. The role of neuroinflammation in metabolic health and neuro-vulnerability is discussed, emphasizing the bidirectional relationship between metabolic dysregulation and neuroinflammatory processes. This review also evaluates the use of neuroimaging techniques in studying neuro-vulnerability and their potential applications in clinical settings. Furthermore, the association between neuro-vulnerability and eating disorders, as well as its contribution to obesity, is examined. Potential therapeutic interventions targeting neuro-vulnerability, including pharmacological treatments and lifestyle modifications, are reviewed. In conclusion, understanding the concept of neuro-vulnerability in energy metabolism regulation is crucial for addressing metabolic disorders. This review provides valuable insights into the underlying neurobiological mechanisms and their implications for metabolic health. Targeting neuro-vulnerability holds promise for developing innovative strategies in the prevention and treatment of metabolic disorders, ultimately improving metabolic health outcomes.
... In addition, many people with T2D (over 40%) also have a comorbid SUD (Wu et al., 2018;Feldman et al., 2019). The brain regions primarily responsible for food-seeking behaviors include the hypothalamus (e.g., arcuate nucleus, median eminence, lateral hypothalamus), hippocampus (Martin and Davidson, 2014;Parent et al., 2014), and PFC (Garcia-Garcia et al., 2014). Obesogenic diets have been reported to result in inflammation and alterations in synaptic plasticity and bloodbrain barrier regulation, all of which are regulated in part by the ECM (Gustafson et al., 2007;Guillemot-Legris and Muccioli, 2017;Matikainen-Ankney and Kravitz, 2018;Brown and Sorg, 2023). ...
Substance use disorders are a global health problem with increasing prevalence resulting in significant socioeconomic burden and increased mortality. Converging lines of evidence point to a critical role of brain extracellular matrix (ECM) molecules in the pathophysiology of substance use disorders. An increasing number of preclinical studies highlight the ECM as a promising target for development of novel cessation pharmacotherapies. The brain ECM is dynamically regulated during learning and memory processes, thus the time course of ECM alterations in substance use disorders is a critical factor that may impact interpretation of the current studies and development of pharmacological therapies. This review highlights the evidence for the involvement of ECM molecules in reward learning, including drug reward and natural reward such as food, as well as evidence regarding the pathophysiological state of the brain's ECM in substance use disorders and metabolic disorders. We focus on the information regarding time-course and substance specific changes in ECM molecules and how this information can be leveraged for the development of therapeutic strategies.
... Our results also suggest a lateralization effect of the caudate and amygdala with the MetS severity, which persisted even after adjusting for handedness. However, the evidence for lateralization in the food appetite network is inconclusive, with some studies indicating a left preference [51,52] and others pointing to a right tendency [53,54]. Given only two subcortical regions exhibited a significant lateralization effect related to the MetS severity in our study, we advise against drawing strong conclusions regarding the lateralization effect in the context of MetS. ...
s
Metabolic syndrome (MetS) is characterized by a constellation of metabolic risk factors, including obesity, hypertriglyceridemia, low high-density lipoprotein (HDL) levels, hypertension, and hyperglycemia, and is associated with stroke and neurodegenerative diseases. This study capitalized on brain structural images and clinical data from the UK Biobank and explored the associations of brain morphology with MetS and brain aging due to MetS. Cortical surface area, thickness, and subcortical volumes were assessed using FreeSurfer. Linear regression was used to examine associations of brain morphology with five MetS components and the MetS severity in a metabolic aging group (N = 23,676, age 62.8 ± 7.5 years). Partial least squares (PLS) were employed to predict brain age using MetS-associated brain morphology. The five MetS components and MetS severity were associated with increased cortical surface area and decreased thickness, particularly in the frontal, temporal, and sensorimotor cortex, and reduced volumes in the basal ganglia. Obesity best explained the variation of brain morphology. Moreover, participants with the most severe MetS had brain age 1-year older than those without MetS. Brain age in patients with stroke (N = 1042), dementia (N = 83), Parkinson’s (N = 107), and multiple sclerosis (N = 235) was greater than that in the metabolic aging group. The obesity-related brain morphology had the leading discriminative power. Therefore, the MetS-related brain morphological model can be used for risk assessment of stroke and neurodegenerative diseases. Our findings suggested that prioritizing adjusting obesity among the five metabolic components may be more helpful for improving brain health in aging populations.
... The anterior and posterior midline DMN have distinct roles in self-referential processing, with the anterior DMN implicated in the attribution of personal value and the posterior DMN implicated in internally directed attention (38). Finally, the subcortical network comprises all subcortical structures, including reward regions (e.g., amygdala, thalamus, striatum), and typically differences in subcortical connectivity between control subjects and individuals with substance use disorders or obesity are interpreted as differences in reward processing (32,39). Furthermore, functional connectivity in the salience, motor-sensory, and subcortical networks has been related to reward responsiveness in a model of cocaine abstinence derived using a similar CPM approach (19). ...
Objective:
Craving is a central construct in the study of motivation and human behavior and is also a clinical symptom of substance and non-substance-related addictive disorders. Thus, craving represents a target for transdiagnostic modeling.
Methods:
The authors applied connectome-based predictive modeling (CPM) to functional connectivity data in a large (N=274) transdiagnostic sample of individuals with and without substance use-related conditions, to predict self-reported craving. Functional connectomes derived from three guided imagery conditions of personalized appetitive, stress, and neutral-relaxing experiences were used to predict craving rated before and after each imagery condition. The generalizability of the "craving network" was tested in an independent sample using functional connectomes derived from a cue-induced craving task collected before and after fasting to predict craving rated during fasting.
Results:
CPM successfully predicted craving, thereby identifying a transdiagnostic "craving network." Anatomical localization of model contribution suggested that the strongest predictors of craving were regions of the salience, subcortical, and default mode networks. As external validation, in an independent sample, the "craving network" predicted food craving during fasting using data from a cue-induced craving task.
Conclusions:
These data provide a transdiagnostic perspective to a key phenomenological feature of addictive disorders-craving-and identify a common "craving network" across individuals with and without substance use-related disorders, thereby suggesting a neural signature for craving or urge for motivated behaviors.
... The mechanism of this effect has been debated. One possibility relates to inhibitory processes that restrain impulsive decision-making ( Eshel et al., 2007 ;Morein-Zamir and Robbins 2015 ), as indicated by involvement of this area in pathological gambling (e.g., Van Holst et al., 2010 ;Miedl et al., 2015 ) and substance addiction ( García -García et al., 2014 ). Another option involves the facilitation of risk valuation through attentional control and plan programming processes ( Wearne 2018 ;Poudel et al., 2020 ). ...
The right inferior frontal gyrus (rIFG) is a region involved in the neural underpinning of cognitive control across several domains such as inhibitory control and attentional allocation process. Therefore, it constitutes a desirable neural target for brain-guided interventions such as neurofeedback (NF). To date, rIFG-NF has shown beneficial ability to rehabilitate or enhance cognitive functions using functional Magnetic Resonance Imaging (fMRI-NF). However, the utilization of fMRI-NF for clinical purposes is severely limited, due to its poor scalability. The present study aimed to overcome the limited applicability of fMRI-NF by developing and validating an EEG model of fMRI-defined rIFG activity (hereby termed "Electrical FingerPrint of rIFG"; rIFG-EFP). To validate the computational model, we employed two experiments in healthy individuals. The first experiment (n=14) aimed to test the target engagement of the model by employing rIFG-EFP-NF training while simultaneously acquiring fMRI. The second experiment (n = 41) aimed to test the functional outcome of two sessions of rIFG-EFP-NF using a risk preference task (known to depict cognitive control processes), employed before and after the training. Results from the first experiment demonstrated neural target engagement as expected, showing associated rIFG-BOLD signal changing during simultaneous rIFG-EFP-NF training. Target anatomical specificity was verified by showing a more precise prediction of the rIFG-BOLD by the rIFG-EFP model compared to other EFP models. Results of the second experiment suggested that successful learning to up-regulate the rIFG-EFP signal through NF can reduce one's tendency for risk taking, indicating improved cognitive control after two sessions of rIFG-EFP-NF. Overall, our results confirm the validity of a scalable NF method for targeting rIFG activity by using an EEG probe.
... 21 These findings provide support for an overlapping neural model of addiction and high BMI. García-García et al. 22 conducted a meta-analysis on functional magnetic resonance imaging (fMRI) neural response to reward in participants with obesity, substance addiction and non-substance addiction. Their findings confirm changes in reward processing across all groups as opposed to healthy controls. ...
A previous highly controlled pilot study revealed that body mass index (BMI) predicts outcome of in‐patients with alcohol use disorder (AUD) in a sex‐specific manner. We here provide translational evidence from a daily clinical routine setting and investigated whether BMI and sex interact to predict 24‐month readmission risk in four naturalistic cohorts of a specialized addiction clinic (i.e., all patients admitted to the clinic from 2016 to 2020): (i) in‐patients (443 males and 197 females) and (ii) day clinic patients (241 males and 103 females) with a primary diagnosis of AUD; (iii) in‐patients (175 males and 98 females) and (iv) day clinic patients (174 males and 64 females) with a primary substance use disorder (SUD) other than alcohol. In the in‐patients with AUD, BMI interacted with sex to predict the 24‐month readmission risks (p = 0.008; after adjustment for age and liver enzyme activities: p = 0.012); with higher BMI, the risk increases significantly in males, whereas for females, the risk tends to decrease. In the group of overweight in‐patients, we found higher readmission rates in males relative to females with an odds ratio of 1.8 (p = 0.038). No such significant effects were found in the other cohorts. This study's findings support previous results, suggesting that the easily accessible BMI may serve as a predictive and sex‐sensitive biomarker for outcome in in‐patients with AUD. Future studies are necessary to elucidate the underlying aetiopathological mechanisms. Better outcome predictors are needed to improve treatments of patients with alcohol use disorder. Here, we confirmed in a clinical care setting an interaction of body mass index and sex to predict hospital readmissions; that is, higher body mass index related to higher risk in males and tended to associate with lower risk in females. The body mass index is a promising and easily accessible biomarker that might become relevant for the goals of precision medicine.
... low-value feedback is supported by virtually identical results across various demographics (Smoski et al., 2009). The postcentral gyrus shows differential activation across a range of reward presentations (from food to various drugs) and demographics (obese vs. healthy weight; substance dependent vs. healthy control) (García-García et al., 2014), whereas both the right angular gyrus and left superior parietal lobule contain greater neurite density in binge drinkers vs. healthy controls (Morris et al., 2018). Cocaine abusers undergoing withdrawal show reduced activity in the anterior cingulate gyrus (Volkow & Fowler, 2000) and activation in the anterior cingulate and precuneus in response to high-vs. ...
Research shows cognitive and neurobiological overlap between sign‐tracking (value‐modulated attentional capture [VMAC] by response‐irrelevant, discrete cues) and maladaptive behaviour (e.g., substance abuse). We investigated the neural correlates of sign‐tracking in 20 adults using an additional singleton task (AST) and functional Magnetic Resonance Imaging (fMRI). Participants responded to a target to win monetary reward, the amount of which was signalled by singleton type (reward cue: high‐value vs. low‐value). Singleton responses resulted in monetary deductions. Sign‐tracking – greater distraction by high‐value vs. low‐value singletons (H>L) – was observed, with high‐value singletons producing slower responses to the target than low‐value singletons. Controlling for age and sex, analyses revealed no differential brain activity across H>L singletons. Including sign‐tracking as a regressor of interest revealed increased activity (H>L singletons) in cortico‐subcortical loops, regions associated with Pavlovian conditioning, reward processing, attention shifts, and relative value coding. Further analyses investigated responses to reward feedback (H>L). Controlling for age and sex, increased activity (H>L reward feedback) was found in regions associated with reward anticipation, attentional control, success monitoring, and emotion regulation. Including sign‐tracking as a regressor of interest revealed increased activity in the temporal pole, a region related to value discrimination. Results suggest sign‐tracking is associated with activation of the ‘attention and salience network’ in response to reward cues but not reward feedback, suggesting parcellation between the two at the level of the brain. Results add to the literature showing considerable overlap in neural systems implicated in reward processing, learning, habit formation, emotion regulation, and substance craving.
... 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). ...
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.
... 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. ...
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]. ...
Food intake regulation in humans is a complex process controlled by the dynamic interaction of homeostatic and hedonic systems. Homeostatic regulation is controlled by appetitive signals from the gut, adipose tissue, and the vagus nerve, while conscious and unconscious reward processes orchestrate hedonic regulation. On the one hand, sight, smell, taste, and texture perception deliver potent food-related feedback to the central nervous system (CNS) and influence brain areas related to food reward. On the other hand, macronutrient composition stimulates the release of appetite signals from the gut, which are translated in the CNS into unconscious reward processes. This multi-level regulation process of food intake shapes and regulates human ingestive behavior. Identifying the interface between hormones, neurotransmitters, and brain areas is critical to advance our understanding of conditions like obesity and develop better therapeutical interventions. Neuroimaging studies allow us to take a glance into the central nervous system (CNS) while these processes take place. This review focuses on the available neuroimaging evidence to describe this interaction between the homeostatic and hedonic components in human food intake regulation.
... 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. ...
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.
... 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. ...
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]. ...
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.
... 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. ...
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.
... 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). ...
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.
... 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]. ...
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.
... 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. ...
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.
... 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). ...
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.
... 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. ...
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.
... 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. ...
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.
... 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. ...
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.
Interoception, the perception of body signals, which is crucial for maintaining metabolic homeostasis, is asserted to play a vital role in obesity. Despite conceptual assumptions that impaired insular interoceptive processing contributes to overeating behaviors predominantly through modulating motor cortices, this link has not been extensively explored. Therefore, to further investigate neural mechanisms underlying insula-based interoceptive processing, this pre-registered (PMC9003175) study assessed blood oxygenation level-dependent (BOLD) responses via functional magnetic resonance tomography (fMRI) in 45 healthy participants (31 females/14 males, age 35.78 plus-or-minus sign 10 years, BMI 29.52 plus-or-minus sign 3.5 kg/m2) during a block-designed food cue reactivity task. Region of interest (insula) and whole brain voxel-wise correlation analyses explored neural correlates of visceral interoception. Furthermore, group factor analysis (GFA) unveiled coherence patterns between neural (fMRI) and psychological/behavioral measures. At the psychological level, self-reported hunger (P < 0.01, d = 0.82) and food craving (P < 0.01, d = 0.68) significantly increased, while craving control (P = 0.04, d = 0.37) decreased after cue exposure. Voxel-wise correlation analysis identified positive correlations (P < 0.01) between visceral interoception and activation of the precentral gyrus (PrG or motor cortex), insula, inferior frontal gyrus (IFG), posterior cingulate cortex (PCC), and superior parietal lobule (SPL). Moreover, altered functional connectivity dynamics were noted within the insula-PrG-IFG network during food cue exposure, with a significant reduction of IFG-PrG connections (P = 0.05). Interestingly, GFA identified a cross-unit latent factor across neural and psychological/behavioral measures. Overall, our findings indicate that altered interoceptive processing (insula activity), motor planning (motor cortex activity), and diminished inhibitory control (negative IFG-PrG connectivity) collectively contribute to food craving generation and potentially subsequent actions toward food consumption.
Background
Alcohol use disorder (AUD) is thought to bias the neurocircuitry underlying reward processing and motivation to preferentially attend to conditioned alcohol cues over natural rewards. The present case–control pilot study evaluated this hypothesis using novel natural reward paradigms.
Methods
Twenty‐eight participants (AUD, n = 14, light drinkers, n = 14) were recruited—AUD participants reported 44.0% heavy drinking days (%HDD) and 4.67 drinks/day over the preceding 90 days. Functional magnetic resonance imaging (fMRI) data were acquired during the administration of three separate picture‐viewing paradigms of alcohol cues, food scenes, and social reward, respectively. Independent samples t‐tests were performed to compare groups' fMRI data and exploratory correlation analyses were performed to examine associations with clinical characteristics of AUD.
Results
Food scenes elicited abnormally low reward‐related activation, within the superior frontal gyrus and caudate bilaterally, among AUD participants. Lower activation to food scenes within the superior frontal gyrus was, in turn, associated with higher levels of past‐month %HDD among AUD participants, specifically, along with craving and alcohol dependence severity when examined across the full sample. Contrasting reward types (e.g., alcohol cues vs. food scenes) did not reveal “preferential” activation to differentiate groups.
Conclusions
Heavy drinking appears associated with reduced responsivity to natural rewards, specifically food rather than social cues. Neural mechanisms underlying the high prevalence of malnutrition among individuals with AUD may involve some combination of blunted approach‐related affect and reduced craving‐related motivation to eat when food is present, resulting in limited engagement of cortico‐striato‐thalamic motor circuitry supporting food acquisition. However, given the preliminary nature of this pilot study, such formulations remain tentative until larger follow‐up studies can be conducted. From a potential translational standpoint, the ability of promising therapeutics to demonstrate increased responsivity to natural rewards, specifically nutritive reward may serve as a valuable complementary efficacy indicator for future clinical neuroimaging trials in AUD.
Bu çalışma, madde kullanımının bireylerin günlük yaşam döngülerine, sosyal ilişkilerine ve mesleki performanslarına olan etkilerini incelemeyi amaçlamıştır. Çalışma, madde kullanımının günlük yaşamdaki yeri, kullanım öncesi ve sonrası bireylerde yaşanan değişimleri ve bireylerin ideal yaşam algılarında meydana gelen değişiklikleri ortaya çıkarmayı hedeflemektedir. Nitel araştırma yöntemiyle 17 katılımcıyla yarı yapılandırılmış mülakatlar kullanılarak veriler elde edilmiştir. Katılımcılarla yapılan görüşmelerde, madde kullanımının günlük yaşam ve rutinlere etkisi, sosyal ve mesleki yaşamdaki rolü, zaman ve mekân boyutları, fiziksel ve duygusal duruma etkisi ve ideal yaşam tasavvuru şeklinde beş ana tema ortaya çıkmıştır. Bu temaların analiziyle ortaya çıkan araştırmanın sonuçlarına göre; madde kullanımının bireylerin kişisel özgünlüklerini ve toplumdaki işlevlerini ciddi şekilde kısıtladığını, madde kullanımı öncesi ve sonrasındaki duygusal geçişlerin bireyin psikolojik ve sosyal hayatında derin olumsuz etkilere neden olduğu, sosyal ve mesleki rollerinde performans düşüklüğü yaşattığı, kullanım sonrası işten ayrılmaların arttığı ve sosyal ilişkilerin zayıfladığı görülmektedir. Ayrıca sağlık durumu ve kişisel bakım ihmal edilmekte, bu durum günlük yaşamlarını, sosyal ve aile ilişkilerini derinden etkilemektedir. Genel olarak, madde kullanımının bireylerin günlük yaşam rutinlerinin merkezinde olduğu ve bunun sonucunda aile, arkadaş ve sosyal faaliyetlere katılımın azaldığı görülmektedir. Bu bağlamda, sosyal destek sistemlerinin etkinliklerinin gözden geçirilmesi ve bireylerin günlük yaşam rutinlerine uyum sağlayacak şekilde müdahalelerin tasarlanması gerekmektedir.
Objective: In this study, we aimed to compare psoriasis patients with healthy controls in terms of impaired eating attitudes and to investigate the relationship of eating attitudes with cardiometabolic and clinical parameters, anxiety, depression, and quality of life. Methods: 45 psoriasis patients and 45 healthy controls were included in the study. Personal and clinical information form, eating attitude test (EAT-40), body mass index (BMI) and MetS criteria were used for all participants. Psoriasis patients were evaluated with clinical information form, hospital anxiety and depression scale (HADS), dermatological quality of life index (DQLI), psoriasis area and severity index (PASI). Results: The data of the patient and control groups differed in terms of doing sports, impaired EAT, BMI groups, and metabolic syndrome (MetS). Abnormal eating attitudes such as negative body image, inability to control oneself in eating, overeating, and some restrictive attitudes were significantly higher in the psoriasis group. Overeating, overeating or stress-induced emotional eating, presence of MetS, weight dissatisfaction, frequent dieting to lose weight, some compensatory behaviours, and loss of self-control were significantly higher in patients with BMI>25. EAT points; showed a positive moderate correlation with BMI and HAD-Anxiety. DQLI results; showed a moderate positive correlation with HADAnxiety and PASI scores. Conclusion: Our study is the first to reveal what kind of disordered eating attitudes are at risk for cardiometabolic diseases in psoriasis patients. In psoriasis patients, the rate of not being able to control their eating behaviour is high. Our results primarily highlight the relationship that can be explained by autonomic reactivity between anxiety and difficulty resisting food cravings. Professional support including psychoeducational, cognitive behavioural therapy, and acceptance-based therapies should be provided to reduce maladaptive reactions and anxiety by improving self-regulation skills.
Reward and cognitive control play crucial roles in shaping goal-directed behavior. Yet, the behavioral and neural underpinnings of interactive effects of both processes in driving our actions towards a particular goal have remained rather unclear. Given the importance of inhibitory control, we investigated the effect of reward prospect on the modulatory influence of automatic vs. controlled processes during response inhibition. For this, a performance-contingent monetary reward for both correct response selection and response inhibition was added to a Simon NoGo task, which manipulates the relationship of automatic and controlled processes in Go and NoGo trials. A neurophysiological approach was used by combining EEG temporal signal decomposition and source localization methods. Compared to a non-rewarded control group, rewarded participants showed faster response execution and overall lower response selection and inhibition accuracy (shifted speed-accuracy tradeoff). Interestingly, the reward group displayed larger interference of the interactive effects of automatic vs. controlled processes during response inhibition (i.e., a larger Simon NoGo effect), but not during response selection. The reward-specific behavioral effect was mirrored by the P3 amplitude, underlining the importance of stimulus-response association processes in explaining variability in response inhibition performance. The selective reward-induced neurophysiological modulation was associated with lower activation differences in relevant structures spanning the inferior frontal and parietal cortex, as well as higher activation differences in the somatosensory cortex. Taken together, this study highlights relevant neuroanatomical structures underlying selective reward effects on response inhibition and extends previous reports on the possible detrimental effect of reward-triggered performance trade-offs on cognitive control processes.
Objective:
This study investigated trends in the study of phytochemical treatment of post-traumatic stress disorder (PTSD).
Methods:
The Web of Science database (2007-2022) was searched using the search terms "phytochemicals" and "PTSD," and relevant literature was compiled. Network clustering co-occurrence analysis and qualitative narrative review were conducted.
Results:
Three hundred and one articles were included in the analysis of published research, which has surged since 2015 with nearly half of all relevant articles coming from North America. The category is dominated by neuroscience and neurology, with two journals, Addictive Behaviors and Drug and Alcohol Dependence, publishing the greatest number of papers on these topics. Most studies focused on psychedelic intervention for PTSD. Three timelines show an "ebb and flow" phenomenon between "substance use/marijuana abuse" and "psychedelic medicine/medicinal cannabis." Other phytochemicals account for a small proportion of the research and focus on topics like neurosteroid turnover, serotonin levels, and brain-derived neurotrophic factor expression.
Conclusion:
Research on phytochemicals and PTSD is unevenly distributed across countries/regions, disciplines, and journals. Since 2015, the research paradigm shifted to constitute the mainstream of psychedelic research thus far, leading to the exploration of botanical active ingredients and molecular mechanisms. Other studies focus on anti-oxidative stress and anti-inflammation. Please cite this article as: Gao B, Qu YC, Cai MY, Zhang YY, Lu HT, Li HX, Tang YX, Shen H. Phytochemical interventions for post-traumatic stress disorder: A cluster co-occurrence network analysis using CiteSpace. J Integr Med. 2023; Epub ahead of print.
The objective of our research was to determine the brain changes at the molecular and elemental levels typical of early-stage obesity. Therefore a combined approach using Fourier transform infrared micro-spectroscopy (FTIR-MS) and synchrotron radiation induced X-ray fluorescence (SRXRF) was introduced to evaluate some brain macromolecular and elemental parameters in high-calorie diet (HCD)- induced obese rats (OB, n = 6) and in their lean counterparts (L, n = 6). A HCD was found to alter the lipid- and protein- related structure and elemental composition of the certain brain areas important for energy homeostasis. The increased lipid unsaturation in the frontal cortex and ventral tegmental area, the increased fatty acyl chain length in the lateral hypothalamus and substantia nigra as well as the decreased both protein α helix to protein β- sheet ratio and the percentage fraction of β-turns and β-sheets in the nucleus accumbens were revealed in the OB group reflecting obesity-related brain biomolecular aberrations. In addition, the certain brain elements including P, K and Ca were found to differentiate the lean and obese groups at the best extent. We can conclude that HCD-induced obesity triggers lipid- and protein- related structural changes as well as elemental redistribution within various brain structures important for energy homeostasis. In addition, an approach applying combined X-ray and infrared spectroscopy was shown to be a reliable tool for identifying elemental-biomolecular rat brain changes for better understanding the interplay between the chemical and structural processes involved in appetite control.
Alcohol use is an important health issue and has been suggested to contribute to the burden produced by obesity. Both alcohol use and obesity are subject to sex differences. The available studies on the relationship between alcohol use and body mass index (BMI) report inconsistent results with positive, negative, and null findings which requests a meta-analytic approach. Therefore, we conducted a meta-analysis of case–control, cohort, and cross-sectional studies. The systematic literature search and data extraction was performed by 3 independent raters. We conducted sex-separated meta-analyses and -regressions to investigate how alcohol consumption associates with BMI. Our systematic literature search resulted in 36 studies with 48 data sets (Nmen = 172,254; kmen = 30; Nwomen = 24,164; kwomen = 18; Nunknown sex = 672,344; kunknown sex = 24). Alcohol use was associated with higher BMI in men (g = 0.08 [0.07; 0.09]) and lower BMI in women (g = − 0.26 [− 0.29; − 0.22]). Moreover, we found the amount of daily alcohol intake in men (β = 0.001 [0.0008; 0.0014]) and ethnicity in women (g[Caucasians] = − 0.45 versus g[Asians] = − 0.05; z = 11.5, p < 0.0001) to moderate these effects. We here identified sex-diverging relationships between alcohol use and BMI, found daily alcohol intake and ethnicity to sex-specifically moderate these effects, and argue that sex-specific choice of beverage type and higher amount of daily alcohol use in men than in women account for these observations. Future research is needed to provide empirical evidence for the underlying mechanisms.
Cigarette smoking and obesity are the leading causes of premature morbidity and mortality and increase the risk of all-cause mortality four-fold when comorbid. Individuals with these conditions demonstrate neurobiological and behavioral differences regarding how they respond to rewarding stimuli or engage in inhibitory control. This narrative review examines the role of reward and inhibition in cigarette smoking and obesity independently, as well as recent research demonstrating an effect of increased body mass index (BMI) on neurocognitive function in individuals who smoke. It is possible that chronic smoking and overeating of highly palatable food, contributing to obesity, dysregulates reward neurocircuitry, subsequently leading to hypofunction of brain networks associated with inhibitory control. These brain changes do not appear to be specific to food or nicotine and, as a result, can potentiate continued cross-use. Changes to reward and inhibitory function due to increased BMI may also make cessation more difficult for those comorbid for obesity and smoking.
Although nutrition is a necessary action for the survival of individuals, it is an enjoyable situation that appeals to our various senses. However, the constant consumption of delicious foods that appeal to our senses can create addiction-like situations in some individuals. Food addiction is a concept defined as a specific adaptation to one or more foods that an individual consumes regularly. Apart from various psychological and social problems, some hormonal imbalances, anomalies in brain structures and side effects caused by the use of various drugs can constitute the pathophysiology of food addiction. Clinical studies on food addiction are increasing, but there is no specific treatment method, as it is not yet officially defined as a type of addiction by international authorities. In addition to the treatment methods generally applied to obese individuals, the underlying pathological conditions of obesity are identified and appropriate multidisciplinary treatment strategies are developed. The most commonly used treatment strategies are; medical nutrition treatments, psychotherapies, pharmacological treatments and neuromodulation treatments. The aim of this compilation study is to examine and discuss the relationship between.
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.
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.
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.
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.
Delay discounting reflects a devaluation of delayed long-term benefits but pursues immediate rewards. Higher discounting rates (h-DR) are found ubiquitous in many diseases and unhealthy conditions, particularly in addiction disorder (AD), attention-deficit/hyperactivity disorder (ADHD), and obesity. Thus, h-DR was considered to be a common benchmark across many diseases facilitating to understand one disease to relevant others, which was called trans-disease process. However, the common and specific neural biomarkers associated with this process has not yet been studied well. We performed a voxel-wise task-related neuroimaging meta-analysis to clarify the neural pattern of trans-disease process across AD, ADHD and obesity. We recruited 19 eligible papers, including 9 AD papers (154 patients), 6 ADHD papers (106 patients) and 4 obesity studies (94 patients). Neuroimaging meta-analysis demonstrated the presence of neural biomarkers of trans-disease process: these patients appeared inadequate brain response in caudate, ventromedial and dorsolateral prefrontal cortex (dlPFC) than do of healthy controls (HCs). Disease-specific neural patterns were also found, with prominent hypoactivation in parahippocampal-striatum network for AD, hyperactivation in dopamine-projection striatum network for ADHD and decreased activity of dorsal anterior cingulate cortex and dlPFC for obesity. This study provided robust evidence to reveal the neural substrates of trans-disease process, as well further promoted the triple brain network model in favor of the theoretical developments of these neuropsychiatric disorders.
Food addiction (FA) has been as a construct that is associated with childhood obesity. However, relatively little is known regarding the prevalence of FA among children and adolescents. An instrument designed to assess FA among youth, the Yale Food Addiction Scale for Children and Adolescents (YFAS-C), has been developed and used to estimate FA prevalence among pediatric populations. The present systematic review and meta-analysis aimed to synthesize the results of FA prevalence among youth. Using keywords related to FA and children to search PubMed, Embase, Scopus, and Web of Science, we identified and analyzed 22 cross-sectional studies. No longitudinal studies were identified in the search. Meta-analysis with Freeman-Tukey Double Arcsine transformation was conducted to estimate FA prevalence. Meta-regression was applied to understand whether weight status (i.e., data from community samples vs. overweight/obese samples) is associated with FA. Eligible studies (N = 22) were analyzed using 6,996 participants. The estimated FA prevalence was 15% (95% CI 11-19%) for all samples, 12% (95% CI 8-17%) for community samples, and 19% (95% CI 14-26%) for overweight/obese samples. Meta-regression indicated that weight status was associated with FA severity (p = 0.002) and marginally with FA prevalence (p = 0.056). Healthcare providers should consider and address the high FA prevalence among pediatric population. K E Y W O R D S addictive behaviors, adolescent, child, food addiction, obesity, prevalence, systematic review
A psychobiological dimension of eating behaviour is proposed, which is anchored at the low end by energy intake that is relatively well matched to energy output and is reflected by a stable body mass index (BMI) in the healthy range. Further along the continuum are increasing degrees of overeating (and BMI) characterized by more severe and more compulsive ingestive behaviours. In light of the many similarities between chronic binge eating and drug abuse, several authorities have adopted the perspective that an apparent dependence on highly palatable food-accompanied by emotional and social distress-can be best conceptualized as an addiction disorder. Therefore, this review also considers the overlapping symptoms and characteristics of binge eating disorder (BED) and models of food addiction, both in preclinical animal studies and in human research. It also presents this work in the context of the modern and "toxic" food environment and therein the ubiquitous triggers for over-consumption. We complete the review by providing evidence that what we have come to call "food addiction" may simply be a more acute and pathologically dense form of BED.
To determine if methamphetamine-dependent (MD) individuals exhibit behavioral or neural processing differences in risk-taking relative to healthy comparison participants (CTL).
This was a cross-sectional study comparing two groups' behavior on a risk-taking task and neural processing as assessed using functional magnetic resonance imaging (fMRI).
The study was conducted in an inpatient treatment center and a research fMRI facility in the United States.
Sixty-eight recently abstinent MD individuals recruited from a treatment program and forty CTL recruited from the community completed the study.
The study assessed risk-taking behavior (overall and post-loss) using the Risky Gains Task (RGT), sensation-seeking, impulsivity and blood-oxygenation level dependent activation in the brain during the decision phase of the RGT.
Relative to CTL, MD displayed decreased activation in the bilateral rostral anterior cingulate cortex (ACC) and greater activation in the left insula across risky and safe decisions (p<.05). Right mid insula activation among CTL did not vary between risky and safe decisions, but among MD it was higher during risky relative to safe decisions (p<.05). Among MD, lower activation in the right rostral ACC (r=-.39, p<.01) and higher activation in the right mid insula (r=.35, p<.01) during risky decisions were linked to a higher likelihood of choosing a risky option following a loss.
Methamphetamine-dependent individuals show disrupted risk-related processing in both anterior cingulate and insula, brain areas that have been implicated in cognitive control and interoceptive processing. Attenuated neural processing of risky options may lead to risk-taking despite experiencing negative consequences.
Dysfunctional learning systems are thought to be central to the pathogenesis of and impair recovery from addictions. The functioning of the brain circuits for episodic memory or learning that support goal-directed behavior has not been studied previously in persons with cocaine dependence (CD). Thirteen abstinent CD and 13 healthy participants underwent MRI scanning while performing a task that requires the use of spatial cues to navigate a virtual-reality environment and find monetary rewards, allowing the functional assessment of the brain systems for spatial learning, a form of episodic memory. Whereas both groups performed similarly on the reward-based spatial learning task, we identified disturbances in brain regions involved in learning and reward in CD participants. In particular, CD was associated with impaired functioning of medial temporal lobe (MTL), a brain region that is crucial for spatial learning (and episodic memory) with concomitant recruitment of striatum (which normally participates in stimulus-response, or habit, learning), and prefrontal cortex. CD was also associated with enhanced sensitivity of the ventral striatum to unexpected rewards but not to expected rewards earned during spatial learning. We provide evidence that spatial learning in CD is characterized by disturbances in functioning of an MTL-based system for episodic memory and a striatum-based system for stimulus-response learning and reward. We have found additional abnormalities in distributed cortical regions. Consistent with findings from animal studies, we provide the first evidence in humans describing the disruptive effects of cocaine on the coordinated functioning of multiple neural systems for learning and memory.Neuropsychopharmacology accepted article preview online, 6 August 2013. doi:10.1038/npp.2013.189.
In spite of evidence suggesting two possible mechanisms related to drug-seeking behavior, namely reward-seeking and harm avoidance, much of the addiction literature has focused largely on positive incentivization mechanisms associated with addiction. In this study, we examined the contributing neural mechanisms of avoidance of an aversive state to drug-seeking behavior during marijuana withdrawal. To that end, marijuana users were scanned while performing the monetary incentive delay task in order to assess positive and negative incentive processes. The results showed a group x incentive interaction, such that marijuana users had greater response in areas that underlie reward processes during positive incentives while controls showed greater response in the same areas, but to negative incentives. Furthermore, a negative correlation between withdrawal symptoms and response in the amygdala during negative incentives was found in the marijuana users. These findings suggest that although marijuana users have greater reward sensitivity and less harm avoidance than controls, that attenuated amygdala response, an area that underlies fear and avoidance, was present in marijuana users with greater marijuana withdrawal symptoms. This is concordant with models of drug addiction that involve multiple sources of reinforcement in substance use disorders, and suggests the importance of strategies that focus on respective mechanisms.
Obesity is emerging as the most significant health concern of the twenty-first century. A wealth of neuroimaging data suggest that weight gain might be related to aberrant brain function, particularly in prefrontal cortical regions modulating mesolimbic addictive responses to food. Nevertheless, food addiction is currently a model hotly debated. Here, we conduct a meta-analysis of neuroimaging data, examining the most common functional differences between normal-weight and obese participants in response to food stimuli.
We conducted a search using several journal databases and adhered to the 'Preferred Reporting Items for Systematic Reviews and Meta-analyses' (PRISMA) method. To this aim, 10 studies were found with a total of 126 obese participants, 129 healthy controls, equaling 184 foci (146 increased, 38 decreased activation) using the Activation Likelihood Estimation (ALE) technique. Out of the 10 studies, 7 investigated neural responses to food versus non-food images.
In response to food images, obese in comparison to healthy weight subjects had increased activation in the left dorsomedial prefrontal cortex, right parahippocampal gyrus, right precentral gyrus and right anterior cingulate cortex, and reduced activation in the left dorsolateral prefrontal cortex and left insular cortex.
Prefrontal cortex areas linked to cognitive evaluation processes, such as evaluation of rewarding stimuli, as well as explicit memory regions, appear most consistently activated in response to images of food in those who are obese. Conversely, a reduced activation in brain regions associated with cognitive control and interoceptive awareness of sensations in the body might indicate a weakened control system, combined with hypo-sensitivity to satiety and discomfort signals after eating in those who are prone to overeat.
Adolescents view thousands of food commercials annually, but the neural response to food advertising and its association with obesity is largely unknown. The current study is the first to examine how neural response to food commercials differs from other stimuli (e.g., non-food commercials, television show) and to explore how this response may differ by weight status. The blood oxygen level-dependent functional magnetic resonance imaging activation was measured in thirty adolescents ranging from lean to obese in response to food and non-food commercials imbedded in a television show. Adolescents exhibited greater activation in regions implicated in visual processing (e.g., occipital gyrus), attention (e.g., parietal lobes), cognition (e.g., temporal gyrus, posterior cerebellar lobe), movement (e.g., anterior cerebellar cortex), somatosensory response (e.g., postcentral gyrus), and reward (e.g., orbitofrontal cortex, anterior cingulate cortex (ACC)) during food commercials. Obese participants exhibited less activation during food relative to non-food commercials in neural regions implicated in visual processing (e.g., cuneus), attention (e.g., posterior cerebellar lobe), reward (e.g., ventromedial prefrontal cortex, ACC) and salience detection (e.g., precuneus). Obese participants did exhibit greater activation in a region implicated in semantic control (e.g., medial temporal gyrus). These findings may inform current policy debates regarding the impact of food advertising to minors.
We revisit our hypothesis that drug addiction can be viewed as the endpoint of a series of transitions from initial voluntarily drug use to habitual, and ultimately compulsive drug use. We especially focus on the transitions in striatal control over drug seeking behaviour that underlie these transitions since functional heterogeneity of the striatum was a key area of Ann Kelley's research interests and one in which she made enormous contributions. We also discuss the hypothesis in light of recent data that the emergence of a compulsive drug seeking habit both reflects a shift to dorsal striatal control over behaviour and impaired prefontal cortical inhibitory control mechanisms. We further discuss aspects of the vulnerability to compulsive drug use and in particular the impact of impulsivity. In writing this review we acknowledge the untimely death of an outstanding scientist and a dear personal friend.
Our brains are hardwired to respond and seek immediate rewards. Thus, it is not surprising that many people overeat, which in some can result in obesity, whereas others take drugs, which in some can result in addiction. Though food intake and body weight are under homeostatic regulation, when highly palatable food is available, the ability to resist the urge to eat hinges on self-control. There is no homeostatic regulator to check the intake of drugs (including alcohol); thus, regulation of drug consumption is mostly driven by self-control or unwanted effects (i.e., sedation for alcohol). Disruption in both the neurobiological processes that underlie sensitivity to reward and those that underlie inhibitory control can lead to compulsive food intake in some individuals and compulsive drug intake in others. There is increasing evidence that disruption of energy homeostasis can affect the reward circuitry and that overconsumption of rewarding food can lead to changes in the reward circuitry that result in compulsive food intake akin to the phenotype seen with addiction. Addiction research has produced new evidence that hints at significant commonalities between the neural substrates underlying the disease of addiction and at least some forms of obesity. This recognition has spurred a healthy debate to try and ascertain the extent to which these complex and dimensional disorders overlap and whether or not a deeper understanding of the crosstalk between the homeostatic and reward systems will usher in unique opportunities for prevention and treatment of both obesity and drug addiction.
Neuroimaging techniques are starting to reveal significant overlap in the brain circuitry underlying addiction and disorders of dyscontrol over rewarding behaviors (such as binge eating disorder and obesity). Positron emission tomography (PET) has demonstrated impaired striatal dopamine (DA) signaling (decreased D2 receptors) in drug addiction and obesity that is associated with reduced baseline glucose metabolism in medial and ventral prefrontal brain regions. Functional magnetic resonance imaging (fMRI) has documented brain activation abnormalities that also implicate DA-modulated striato-cortical pathways. In this review we map findings from recent neuroimaging studies that differentiate brain activation in drug/food addiction from those in controls within brain networks functionally connected with ventral and dorsal striatum. We show that regions found to be abnormal in addiction and obesity frequently emerge at the overlap of the dorsal and the ventral striatal networks. Medial temporal and superior frontal regions functionally connected with dorsal striatum display greater vulnerability in obesity and eating disorders than in drug addictions, indicating more widespread abnormalities for obesity and eating disorders than for addictions. This corroborates involvement of both ventral striatal (predominantly associated with reward and motivation) and dorsal striatal networks (associated with habits or stimulus response learning) in addiction and obesity but also identify distinct patterns between these two disorders.
In this paper, we consider the concept of food addiction from a clinical and neuroscientific perspective. Food addiction has an established and growing currency in the context of models of overeating and obesity, and its acceptance shapes debate and research. However, we argue that the evidence for its existence in humans is actually rather limited and, in addition, there are fundamental theoretical difficulties that require consideration.
We therefore review food addiction as a phenotypic description, one that is based on overlap between certain eating behaviours and substance dependence. To begin, we consider limitations in the general application of this concept to obesity. We share the widely held view that such a broad perspective is not sustainable and consider a more focused view: that it underlies particular eating patterns, notably binge eating. However, even with this more specific focus, there are still problems. Validation of food addiction at the neurobiological level is absolutely critical, but there are inconsistencies in the evidence from humans suggesting that caution should be exercised in accepting food addiction as a valid concept. We argue the current evidence is preliminary and suggest directions for future work that may provide more useful tests of the concept.
Pathological gambling (PG) and obsessive-compulsive disorder (OCD) are conceptualized as a behavioral addiction, with a dependency on repetitive gambling behavior and rewarding effects following compulsive behavior, respectively. However, no neuroimaging studies to date have examined reward circuitry during the anticipation phase of reward in PG compared with in OCD while considering repetitive gambling and compulsion as addictive behaviors.
To elucidate the neural activities specific to the anticipation phase of reward, we performed event-related functional magnetic resonance imaging (fMRI) in young adults with PG and compared them with those in patients with OCD and healthy controls. Fifteen male patients with PG, 13 patients with OCD, and 15 healthy controls, group-matched for age, gender, and IQ, participated in a monetary incentive delay task during fMRI scanning. Neural activation in the ventromedial caudate nucleus during anticipation of both gain and loss decreased in patients with PG compared with that in patients with OCD and healthy controls. Additionally, reduced activation in the anterior insula during anticipation of loss was observed in patients with PG compared with that in patients with OCD which was intermediate between that in OCD and healthy controls (healthy controls < PG < OCD), and a significant positive correlation between activity in the anterior insula and South Oaks Gambling Screen score was found in patients with PG.
Decreased neural activity in the ventromedial caudate nucleus during anticipation may be a specific neurobiological feature for the pathophysiology of PG, distinguishing it from OCD and healthy controls. Correlation of anterior insular activity during loss anticipation with PG symptoms suggests that patients with PG fit the features of OCD associated with harm avoidance as PG symptoms deteriorate. Our findings have identified functional disparities and similarities between patients with PG and OCD related to the neural responses associated with reward anticipation.
Drug addiction and obesity appear to share several properties. Both can be defined as disorders in which the saliency of a specific type of reward (food or drug) becomes exaggerated relative to, and at the expense of others rewards. Both drugs and food have powerful reinforcing effects, which are in part mediated by abrupt dopamine increases in the brain reward centres. The abrupt dopamine increases, in vulnerable individuals, can override the brain's homeostatic control mechanisms. These parallels have generated interest in understanding the shared vulnerabilities between addiction and obesity. Predictably, they also engendered a heated debate. Specifically, brain imaging studies are beginning to uncover common features between these two conditions and delineate some of the overlapping brain circuits whose dysfunctions may underlie the observed deficits. The combined results suggest that both obese and drug-addicted individuals suffer from impairments in dopaminergic pathways that regulate neuronal systems associated not only with reward sensitivity and incentive motivation, but also with conditioning, self-control, stress reactivity and interoceptive awareness. In parallel, studies are also delineating differences between them that centre on the key role that peripheral signals involved with homeostatic control exert on food intake. Here, we focus on the shared neurobiological substrates of obesity and addiction.
Despite a rising social relevance of pathological computer game playing, it remains unclear whether the neurobiological basics of this addiction-like behavioral disorder and substance-related addiction are comparable. In substance-related addiction, attentional bias and cue reactivity are often observed. We conducted a functional magnetic resonance study using a dot probe paradigm with short-presentation (attentional bias) and long-presentation (cue reactivity) trials in eight male pathological computer game players (PCGPs) and nine healthy controls (HCs). Computer game-related and neutral computer-generated pictures, as well as pictures from the International Affective Picture System with positive and neutral valence, served as stimuli. PCGPs showed an attentional bias toward both game-related and affective stimuli with positive valence. In contrast, HCs showed no attentional bias effect at all. PCGPs showed stronger brain responses in short-presentation trials compared with HCs in medial prefrontal cortex (MPFC) and anterior cingulate gyrus and in long-presentation trials in lingual gyrus. In an exploratory post hoc functional connectivity analyses, for long-presentation trials, connectivity strength was higher between right inferior frontal gyrus, which was associated with inhibition processing in previous studies, and cue reactivity-related regions (left orbitofrontal cortex and ventral striatum) in PCGPs. We observed behavioral and neural effects in PCGPs, which are comparable with those found in substance-related addiction. However, cue-related brain responses were depending on duration of cue presentation. Together with the connectivity result, these findings suggest that top-down inhibitory processes might suppress the cue reactivity-related neural activity in long-presentation trials.
Understanding the neurobiological mechanisms of addiction requires an integration of basic neuroscience with social psychology, experimental psychology, and psychiatry. Addiction is presented as a cycle of spiralling dysregulation of brain reward systems that progressively increases, resulting in compulsive drug use and a loss of control over drug-taking. Sensitization and counteradaptation are hypothesized to contribute to this hedonic homeostatic dysregulation, and the neurobiological mechanisms involved, such as the mesolimbic dopamine system, opioid peptidergic systems, and brain and hormonal stress systems, are beginning to be characterized. This framework provides a realistic approach to identifying the neurobiological factors that produce vulnerability to addiction and to relapse in individuals with a history of addiction.
Substance use disorder is characterized by a transition from volitional to compulsive responding for drug reward. A possible explanation for this transition may be that alcohol-dependent patients (ADP) show a general propensity for a history of rewarded instrumental responses, and these rewarded responses may boost the activation of motivational neurocircuitry for additional reward. Brain imaging studies of decision-making have demonstrated that ADP relative to controls (CON) often show altered neural activation in response to anticipating and receiving rewards, but the majority of studies have not investigated how past performance affects activation. A potential exists for ADP to show increased sensitivity to reward as a function of reward delivery history. In the current study, we used functional magnetic resonance imaging to investigate the neural correlates of risky decision-making in ADP (n = 18) and CON (n = 18) while they played a two-choice monetary risk-taking game. In addition to investigating general neural recruitment by risky decision-making, we also modeled each participant's running total of monetary earnings in order to determine areas of activation that correlated with cumulative reward. We found that ADP and CON showed few differences in behavior or in mesolimbic activation by choice for, and receipt of, risky gains. However, when including a cumulative-earnings covariate, ADP exhibited heightened striatal activation that correlated with total earnings during the choice event in the task. The heightened contextual sensitivity of striatal responses to cumulative earnings in ADP may represent a general neurobiological affective substrate for development of automatized instrumental behavior.
Pathological gambling (PG) shares clinical characteristics such as craving and loss of control with substance use disorders and is thus considered a behavioral addiction. While functional alterations in the mesolimbic reward system have been correlated with craving and relapse in substance use disorders, only a few studies have examined this brain circuit in PG, and no direct comparison has been conducted so far. Thus, we investigated the neuronal correlates of reward processing in PG in contrast to alcohol-dependent (AD) patients and healthy subjects. Eighteen PG patients, 15 AD patients and 17 controls were investigated with a monetary incentive delay task, in which visual cues predict the consequence (monetary gain, avoidance of loss, none) of a fast response to a subsequent target stimulus. Functional magnetic resonance imaging data were analyzed to account for possible confounding factors such as local gray matter volume. Activity in the right ventral striatum during loss anticipation was increased in PG patients compared with controls and AD patients. Moreover, PG patients showed decreased activation in the right ventral striatum and right medial prefrontal cortex during successful loss avoidance compared with controls, which was inversely associated with severity of gambling behavior. Thus, despite neurobiological similarities to substance use disorders in reward processing, as reported by previous studies, we found relevant differences with respect to the anticipation of loss as well as its avoidance (negative reinforcement), which further contributes to the understanding of PG.
Abstinence-based therapy (ABT) and methadone maintenance therapy (MMT) are common methods of treatment in heroin dependence as both suppress subjective feeling of drug craving. However, it is not clear whether the neural basis of craving suppression is similar in both types of treatments. In this study, we compared brain activation during pictorial presentation of heroin-related cues in ABT and MMT groups to understand the neural basis of drug craving in these groups.
Three groups of subjects (successful ABT and MMT clients and healthy control) underwent functional magnetic resonance imaging, while heroin-related cues and neutral cues were presented to them. In addition, subjective cue-elicited craving has been measured using drug drive questionnaire before and after imaging.
Self-report of craving was not different between ABT and MMT groups before and after scanning. Anterior cingulate cortex and inferior frontal gyrus showed higher activations in ABT than in healthy control. Inferior frontal gyrus and superior temporal gyrus showed higher activity in ABT than in MMT. Lingual gyrus and cerebellum showed higher activity in MMT than in healthy control.
Heroin avoidance may be achieved by MMT or ABT; however, the neural mechanism underlying these therapeutic methods differs.
Individuals with normal body weight by body mass index (BMI) and high body fat percentage show a high degree of metabolic dysregulation. This phenomenon, defined as normal weight obesity, is associated with a significantly higher risk of developing metabolic syndrome, cardiometabolic dysfunction and with higher mortality. Recently, we have also shown that coronary artery disease patients with normal BMI and central obesity have the highest mortality risk as compared to other adiposity patterns. Therefore, it is important to recognize these high-risk groups for better adiposity-based risk stratification. There is a need for an updated definition of obesity based on adiposity, not on body weight.
We evaluated neural substrates related to the loss of control in college students with internet gaming disorder (IGD). We hypothesized that deficit in response inhibition under gaming cue distraction was the possible mechanism for the loss of control internet use. Eleven cases of IGD and 11 controls performed Go/NoGo tasks with/without gaming distraction in the functional magnetic resonance imaging scanner. When the gaming picture was shown as background while individuals were performing Go/NoGo tasks, the IGD group committed more commission errors. The control group increased their brain activations more over the right dorsolateral prefrontal cortex (DLPFC) and superior parietal lobe under gaming cue distraction in comparison with the IGD group. Furthermore, brain activation of the right DLPFC and superior parietal lobe were negatively associated with performance of response inhibition among the IGD group. The results suggest that the function of response inhibition was impaired under gaming distraction among the IGD group, and individuals with IGD could not activate right DLPFC and superior parietal lobe to keep cognitive control and attention allocation for response inhibition under gaming cue distraction. This mechanism should be addressed in any intervention for IGD.
A core feature of human drug dependency is persistence in seeking and using drugs at the expense of other life goals. It has been hypothesised that addiction is associated with over-valuation of drug-related rewards and under-valuation of natural, non-drug related rewards. Humans additionally tend to persist in using drugs despite adverse consequences. This suggests that the processing of both rewarding and aversive information may be abnormal in addictions. We used fMRI to examine neural responses to reward and loss events in opiate dependent patients receiving Methadone Maintenance Treatment (MMT, n=30) and healthy controls (n=23) using non-drug related stimuli. Half of the patients were scanned after/before daily methadone intake (ADM/BDM patient groups). During reward trials, patients as a whole exhibited decreased neural discrimination between rewarding and non-rewarding outcomes in the dorsal caudate. Patients also showed reduced neural discrimination in the ventral striatum with regard to aversive and non-aversive outcomes, and failed to encode successful loss-avoidance as a reward signal in the ventral striatum. Patients additionally showed decreased insula activation during the anticipation/decision phase of loss events. ADM patients exhibited increased loss signals in the midbrain/para-hippocampal gyrus, possibly related to a disinhibition of dopamine neurons. This study suggests that patients with opiate dependency on MMT exhibit abnormal brain activations to non-drug related rewarding and loss events. Our findings add support to proposals that treatments for opiate addiction should aim to increase the reward value of non-drug related rewarding events, and highlights the importance of potential abnormalities in aversive information processing.Neuropsychopharmacology accepted article preview online, 17 October 2013. doi:10.1038/npp.2013.289.
Altered interoception, i.e., processing of stimuli from inside the body, has been considered an important component of drug-taking behavior. However, approaches to examine interoceptive sensitivity in humans have been limited. This study examined the hypothesis that adolescents with substance use disorder show altered interoceptive processing, measured by stimulating mechano-receptive C-fibers (MR-CF) via soft touch.
Adolescents with substance use disorders (SUD, n=15) and comparison youth (CON, n=17) underwent functional magnetic resonance imaging (fMRI) during anticipation or reception of a positively valenced "Soft Touch" consisting of MR-CF stimulation to the palm or forearm. Visual analog scales (VAS) indexed subjective interoceptive experience (e.g., pleasantness, intensity).
Across all conditions, SUD displayed attenuated left posterior insula activation compared to CON. Greater left anterior insula and right lentiform nucleus activation was evident during the application of soft touch for SUD but not for CON. Whereas for CON, greater left anterior insula activation was associated with higher pleasantness ratings, pleasantness was linked to less anterior insula activation in SUD. Finally, within SUD, attenuated posterior insula activation was related to more recent cannabis use.
SUD adolescents exhibit blunted somatovisceral processing of pleasant stimulation, heightened sensitivity in regions responsible for processing reward value, and altered relationships between interoceptive processing and subjective experience.
