Purpose of review
Studies increasingly show the importance of reward processing in binge eating and provide evidence of associated changes in the neurobiological reward system. This review gives an ...up-to-date overview of the neurobiological substrates of reward processing subconstructs in binge eating. Neural findings are linked to different behavioral theories and the clinical relevance is discussed.
Recent findings
Increased neural responses in the orbitofrontal cortex, anterior cingulate cortex as well as striatum during anticipation and receipt of food rewards are found in association to binge eating. Increased model-free learning is also found and associated with altered brain reward reactivity. Data in rest report reduced striatal dopamine release and lower frontostriatal connectivity. Mechanisms of onset of binge eating are less clear, but specific personality traits, related to frontostriatal dysconnectivity, probably increase the risk of binge eating onset.
Summary
Both structural and task-based imaging studies show differences in the neurobiological reward system in binge eating. These changes are linked to specific reward processing, such as altered reward responsiveness to food cues, reinforcement learning, and habitual behavior. Findings are lined with different behavioral theories of binge eating, and a staging model is described, from onset to full illness development. Understanding the specific underlying aberrant reward mechanism in binge eating, associated with different stages of the illness, enables caregivers to focus their treatment more precisely.
Recent research shows that the effects of oxytocin are more diverse than initially thought and that in some cases oxytocin can directly influence the response to drugs and alcohol. Large individual ...differences in basal oxytocin levels and reactivity of the oxytocin system exist. This paper will review the literature to explore how individual differences in the oxytocin system arise and examine the hypothesis that this may mediate some of the individual differences in susceptibility to addiction and relapse.
Differences in the oxytocin system can be based on individual factors, e.g. genetic variation especially in the oxytocin receptor, age or gender, or be the result of early environmental influences such as social experiences, stress or trauma. The paper addresses the factors that cause individual differences in the oxytocin system and the environmental factors that have been identified to induce long-term changes in the developing oxytocin system during different life phases.
Individual differences in the oxytocin system can influence effects of drugs and alcohol directly or indirectly. The oxytocin system has bidirectional interactions with the stress-axis, autonomic nervous system, neurotransmitter systems (e.g. dopamine, serotonin and GABA/glutamate) and the immune system. These systems are all important, even vital, in different phases of addiction.
It is suggested that early life adversity can change the development of the oxytocin system and the way it modulates other systems. This in turn could minimise the negative feedback loops that would normally exist. Individuals may show only minor differences in behaviour and function unless subsequent stressors or drug use challenges the system. It is postulated that at that time individual differences in oxytocin levels, reactivity of the system or interactions with other systems can influence general resilience, drug effects and the susceptibility to develop problematic drug and alcohol use.
Suggested model: individual factors and (early) environment shape the development of the oxytocin system affecting susceptibility to addiction and resilience.
Substantial individual differences exist in basal oxytocin levels and reactivity of the system. The endogenous oxytocin system changes and matures over time as part of normal development. This paper postulates that individual factors and early external influences (i.e. parenting, stress and illness) affect the developing endogenous oxytocin system and its connectivity with other systems affecting oxytocin levels and alter responsiveness of the oxytocin system. When an individual is exposed to alcohol and drugs in adolescence, these individual differences in the endogenous oxytocin system can affect reward seeking and drug use behaviour. It is postulated that for example drug use may be more rewarding resulting in an escalation of use; an imbalance between natural and drug rewards could affect the attractiveness of excessive drug use; individuals may be more susceptible to stress-induced relapse to drug use. Display omitted
•Individual differences exist in the endogenous oxytocin system.•These differences can arise from individual and environmental factors.•Oxytocin can (in)directly influence biological systems involved in addiction.•Differences in endogenous oxytocin system may affect susceptibility to addiction.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Assessment and Treatment of Eating Disorders YOSHIUCHI, Kazuhiro; YAMADA, Hisashi; TAKAKURA, Shu ...
Journal of Nutritional Science and Vitaminology,
2022/11/30, 2022-11-30, Volume:
68, Issue:
Supplement
Journal Article
Peer reviewed
Open access
Eating disorders are serious psychiatric conditions in terms of chronicity and have the highest mortality rate among psychiatric disorders. The assessment and treatment of eating disorders are also ...challenging, due to patients’ denial of their illness and reluctance for change. Despite a large number of previous assessment and treatment studies, new strategies to overcome these difficulties are still needed. This study casts light on four aspects; involvement of the brain’s reward system, stages of change in relationship with motivation, refeeding syndrome during renourishment, and gut microbiota changes relating to chronicity. Further studies relating to these aspects are encouraged.
Sexually explicit material (SEM) is increasingly used in western societies. One reason for this high usage might be the rewarding property of SEM demonstrated in many brain imaging studies showing an ...activation of the reward system during the presentation of SEM. It is not yet well understood why women use SEM to a remarkably lesser extent than men. Maybe men react stronger to stimuli – so called SEM cues –, which signal the presentation of SEM and are therefore more vulnerable to use SEM than women. Therefore, the present study aimed at investigating the sex specific neural correlates towards SEM and SEM cues. We were further interested in whether person characteristics as trait sexual motivation, extent of SEM use in the last month, and age at onset of goal-oriented SEM use affect the neural responses to SEM and SEM cues. The trials of the fMRI experiment consisted of an expectation phase with SEM or neutral cues and a presentation phase with SEM or neutral stimuli, respectively. Analyses showed that the reward circuitry was activated by SEM, but also by SEM cues. There were some sex differences in hemodynamic responses to SEM during the presentation phase, but not during the expectation phase to SEM cues in any of the regions of interest. The influence of the investigated person characteristics was only small if existent. The results suggest that sex specific cue processing cannot explain sex differences in the use of SEM.
•SEM cues resulted in similar neural activations as the presentation of SEM.•The neural responses towards cues did not differ between men and women.•There were some sex differences in the neural responses towards SEM.•The nucleus accumbens response was unaffected by person characteristics.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZRSKP
Background:
Fatigue is one of the most frequent and disabling symptoms in multiple sclerosis, but its pathophysiological mechanisms are poorly understood. It is in particular unclear whether and how ...fatigue relates to structural and functional brain changes.
Objective:
We aimed to analyse the association of fatigue severity with basal ganglia functional connectivity, basal ganglia volumes, white matter integrity and grey matter density.
Methods:
In 44 patients with relapsing–remitting multiple sclerosis and 20 age- and gender-matched healthy controls, resting-state fMRI, diffusion tensor imaging and voxel-based morphometry was performed.
Results:
In comparison with healthy controls, patients showed alteration of grey matter density, white matter integrity, basal ganglia volumes and basal ganglia functional connectivity. No association of fatigue severity with grey matter density, white matter integrity and basal ganglia volumes was observed within patients. In contrast, fatigue severity was negatively correlated with functional connectivity of basal ganglia nuclei with medial prefrontal cortex, precuneus and posterior cingulate cortex in patients. Furthermore, fatigue severity was positively correlated with functional connectivity between caudate nucleus and motor cortex.
Conclusion:
Fatigue is associated with distinct alterations of basal ganglia functional connectivity independent of overall disability. The pattern of connectivity changes suggests that disruption of motor and non-motor basal ganglia functions, including motivation and reward processing, contributes to fatigue pathophysiology in multiple sclerosis.
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NUK, OILJ, SAZU, UKNU, UL, UM, UPUK
Social rewards (e.g., social feedback, praise, and social interactions) are fundamental to social learning and relationships across the life span. Exposure to social rewards is linked to activation ...in key brain regions, that are impaired in major depression. This is the first summary of neuroimaging literature on social reward processing in depressed and healthy individuals.
We screened 409 studies and identified 25 investigating task-based fMRI activation during exposure to social stimuli in depressed and healthy populations across the lifespan. We conducted a systematic review followed by an Activation Likelihood Estimation (ALE) analysis of three main contrasts: a) positive social feedback vs. neutral stimuli; b) negative social feedback vs. neutral stimuli; c) positive vs. negative social feedback. We also compared activation patterns in depressed versus healthy controls.
Systematic review revealed that social rewards elicit increased activation in subcortical reward regions (NAcc, amygdala, ventral striatum, thalamus) in healthy and depressed individuals; and decreased activation in prefrontal reward regions (medial prefrontal cortex, orbitofrontal cortex) among depressed persons. Our meta-analysis showed, in both depressed and healthy individuals, increased cluster activation of the putamen and caudate in response to negative social stimuli vs. positive stimuli. We also found increased cluster activation in the inferior frontal gyrus (IFG) and the medial frontal gyrus (MFG) in healthy controls vs. depressed individuals, in response to negative social stimuli.
Processing of social stimuli elicits activation of key brain regions involved in affective and social information processing. Interventions for depression can increase social reward responsivity to improve outcomes.
•Social rewards are highly motivating and associated with mood fluctuations in depressed and healthy individuals.•We conducted a systematic review and a coordinate-based meta-analysis of studies using fMRI social rewards tasks.•Our meta-analysis showed higher striatal activation for social rewards in both depressed and healthy individuals.•Healthy controls had increased activation in the default mode and salience networks in response to negative social stimuli.•Social reward exposure is linked to activation in key brain regions that may be promising treatment targets for depression.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Given that the search for effective pharmacotherapies for cocaine use disorder has, thus far, been fruitless, there remains a critical need for conceptually innovative approaches toward identifying ...new medications to treat this disease. A better understanding of the neurocircuits and neurobiological mechanisms underlying cocaine taking and seeking may identify molecular substrates that could serve as targets for novel pharmacotherapies to treat cocaine use disorder. Recent preclinical evidence suggests that glucagon-like peptide-1 (GLP-1) receptor agonists could be re-purposed to treat cocaine craving-induced relapse. This review endeavors to comprehensively summarize the current literature investigating the efficacy of GLP-1 receptor agonists in reducing the rewarding and reinforcing effects of cocaine in animal models of cocaine use disorder. The role of central endogenous GLP-1 circuits in voluntary cocaine taking and seeking is also discussed. Behavioral, neurochemical, electrophysiological and molecular biology studies indicate that central GLP-1 receptor activation functionally modulates the mesolimbic reward system and decreases addiction-like phenotypes in rodents. Overall, an emerging preclinical literature provides compelling evidence to advance GLP-1 receptor agonists into clinical trials testing the efficacy of these medications in preventing cocaine craving-induced relapse.
•Central GLP-1 receptors play an important role in the reinforcing effects of cocaine.•GLP-1 receptor agonists attenuate cocaine-mediated behaviors.•Cocaine dynamically alters the endogenous central GLP-1 system.•Central GLP-1 signaling may be a novel target to treat cocaine use disorder.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
•This paper explores the pathophysiology of autism spectrum disorder (ASD).•Brain cortical excitatory - inhibitory balance and alpha EEG alterations may drive ASD.•Cortical magnetic stimulation ...guided by brain electrical (EEG) activity may treat ASD.
Autism spectrum disorder (ASD) is a genetically heterogeneous group of neurodevelopmental disorders that affect 1 in 36 children (CDC data) and have recognizable core deficits in common, including repetitive stereotyped behaviors and difficulties in social interaction and communication. Pharmacological interventions moderate some ASD comorbidities, but do not alleviate core deficits and have significant side effects. While many behavioral therapies are inadequate, a very intensive form called applied behavioral analysis (ABA) is demonstrably effective. ABA is based on graded progression and immediate feedback. ABA has raised concerns over its intensive nature and has triggered unease about being too harsh. One solution may derive from a widespread hypothesis of ASD pathogenesis, which posits that the brain in ASD is overexcited, i.e., excitation dominates over inhibition, and electroencephalographic (EEG) alpha band oscillatory activity is altered, which degrades sensory input and task management. This may also disrupt the brain mesolimbic dopaminergic reward cascade causing social interactions to be unrewarding, leading to deleterious social behavior and poor communication. We hypothesize that a comprehensive, personalized form of spectral EEG guided repetitive transcranial magnetic stimulation that we term PrTMS, can normalize alpha EEG oscillations, E/I balance, and dopaminergic reward signaling, to facilitate improved psychosocial behavior. The goal is for PrTMS to synergize with behavioral interventions, so that ABA for example, could be less intensive. This may hold the promise of making self-determination more readily attainable for ASD persons, and could also democratize ASD therapy by rendering it more affordable.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
That activation of the reward system involves increased activity of dopaminergic (DA) neurons in the ventral tegmental area (VTA) is widely accepted. In contrast, the lateral habenular complex (LHb), ...which is known as the center of the anti‐reward system, directly and indirectly inhibits DA neurons in the VTA. The VTA, however, is not a homogenous entity. Instead, it displays major functional differences between its anterior (aVTA) and posterior (pVTA) regions. It is not precisely known, whether habenular input to the aVTA, pVTA, and the newly recognized rostromedial tegmental nucleus (RMTg) are similarly or differently organized. Consequently, the present investigation addressed the connections between LHb and aVTA, pVTA, and RMTg using retrograde and anterograde tracing techniques in the rat. Our experiments disclosed strictly reciprocal and conspicuously focal interconnections between LHbM (LHbMPc/LHbMC) and PN, as well as between RLi and LHbLO. In addition, we found that LHb inputs to the aVTA are dorsoventrally ordered. Dorsal parts of the aVTA receive afferents from LHbL and LHbM, whereas ventral parts of the aVTA are preferentially targeted by the LHbM. LHb afferents to the pVTA are distinct from those to the RMTg, given that the RMTg is primarily innervated from the LHbL, whereas pVTA receives afferents from LHbM and LHbL. These data indicate the existence of two separate pathways from the LHb to the VTA, a direct and an indirect one, which may subserve distinct biological functions.
The study employs retrograde and anterograde tract tracing techniques to analyze the projections of the medial (LHbM) and lateral (LHbL) divisions of the lateral habenular complex (LHb), the center of the anti‐reward system, to the anterior (aVTA) and posterior (pVTA) parts of the VTA and the rostromedial tegmental nucleus (RMTg).
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
Introduction
The reward system regulates the processes that motivate people to pursue evolutionary beneficial stimuli. Effective functioning of the reward system can protect against the development ...of anhedonia. In the daily life, the reward system can be expressed as the dynamic interplay of positive affect (liking), reward anticipation (wanting), and active behavior (engaging). Applying network analysis to daily life experience data allows us to identify such reward dynamics and use them to predict future depressive symptoms.
Objectives
We investigated whether at baseline (i) higher network positive affect in-strength, reflecting how strongly positive affect is influenced by other components and hence the level of anhedonia, and (ii) higher network connectivity, reflecting overall functioning of the reward system, are associated with fewer depressive symptoms on follow-up.
Methods
We used data from 43 participants with mild depressive symptoms from the SMARTSCAN study. The dynamic interplay between momentary positive affect, reward anticipation, and active behavior was assessed with individual vector-autoregressive models and the network analysis. Network positive affect in-strength and connectivity indices were used to predict a six-month depressive symptoms trajectory.
Results
Reward systems networks vary greatly between individuals. On the group level, higher positive affect in-strength (Beta=-3.66, p=0.05) and network connectivity (Beta=-4.06, p=0.03) at baseline were associated with fewer symptoms at follow-up.
Conclusions
Higher influences of reward anticipation and active behavior on positive affect and stronger connections between reward cycle components are associated with fewer future symptoms, suggesting the importance of daily life reward cycle dynamics in depression.
Disclosure
No significant relationships.
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