Research on poor eating habits among individuals recovering from substance use disorders (SUD) is limited. This study examines the relationship between poor eating habits, delay discounting (DD), quality of life (QOL), and remission status, in addition to examining DD as a mediator of the relationship between poor eating and QOL.

Participants (n = 257) in recovery from SUD, completed the Health Behaviors Questionnaire (poor eating was measured using the food domain), a DD task, the World Health Organization QOL questionnaire, demographics, and SUD-related questions. Multivariate linear regression was used to test associations between poor eating and DD, as well as each QOL domain. Mediation analyses were conducted to evaluate the role of DD in the relationship between poor eating and QOL. A binary logistic regression was used to test associations between poor eating and remission status, as well as DD and remission status.

Poor eating habits were significantly associated with higher rates of DD (β = 0.08, p < .001) and lower QOL across psychological (β = -0.88, p < .001, only for those in remission), physical (β = -0.58, p < .001), and environmental (β = -0.75, p < .001) domains. Additionally, DD significantly mediated the relationship between poor eating habits and reduced QOL in these domains (ꞵs < -0.08, ps < 0.003). Poor eating (ꞵ = 0.05, p = .014; OR = 1.05, p = .012) and high DD rates (ꞵ = 0.12, p = .049; OR = 1.12, p = .038) were associated with a lower likelihood of remission from SUD.

Our findings highlight the integral role of dietary habits in the recovery trajectory of individuals with SUD. The study supports the need for holistic treatment approaches that consider the impacts of nutrition on both psychological and physiological aspects of recovery.

Mental illnesses and psychotropic drug use are associated with an increased risk of weight gain and metabolic disorders. Growing evidence suggests that agonists of the glucagon-like peptide-1 receptor (GLP-1RAs) might be safe and effective weight loss medications. However, the current evidence for the use of GLP-1RAs in individuals with obesity and mental illness is limited.

Evaluation of the safety and the impact of GLP-1RAs on mental health and psychotropics-induced metabolic disorders such as obesity and type 2 diabetes (T2D).

A literature search from January 1st, 2010 to August 31st, 2024 was conducted using PubMed and Cochrane Library online databases. Studies comprising adults with obesity or/and T2D and mental illness were included. Studies that examined individuals with obesity or/and T2D without mental illness and completed psychiatric questionnaires before and after GLP-1RAs treatment were also included.

From the 36 included studies 18 examined the weight-reducing effect of GLP-1RAs in patients with mental disorders and the other studies examined patients without mental illness. GLP-1RAs lead to a significant weight loss and improvement of glycemic control in patients with mental illness on psychotropics. They showed a beneficial effect on mental health in patients with and without mental disorders and were not associated with a worsening of mental state, suicidality, new-onset mental illness, or increased psychiatric admissions.

GLP-1RAs are safe and effective weight loss treatments for individuals with obesity and mental illness exerting a positive effect on mental state and quality of life. There is a need for RCTs with larger sample sizes, a longer treatment duration and longer follow-up periods to evaluate the long-term effect of GLP-1RAs. It would be of great interest to conduct studies investigating the use of GLP-1RAs with the purpose to treat mental illness in order to directly assess their use in improving mental health.

Following bariatric surgery (BS) patients have an increased risk of alcohol misuse.

This 1-year cross-sectional study in potential BS candidates had several objectives: (a) assess the prevalence of risky drinking, alcohol use disorder (AUD), and other substance use/disorder; (b) compare the prevalence of these behaviors to that of the general Spanish population; (c) determine the proportion of patients with positive results in toxicology tests; and (d) study the predictive factors of risky drinking.

tertiary university hospital.

Alcohol and other substance use were evaluated with the AUDIT-C and ASSIST questionnaires. Urine tests analyzed several markers (ethyl-glucoronide [EtG] ≥ 500 ng/ml, amphetamine, benzodiazepine, cannabinoid, cocaine, and opioid). The Mini-International-Neuropsychiatric-Interview (5.0.0) was employed to assess psychiatric diagnoses.

Among 308 candidates for BS, 196 were accepted to participate (69% women; mean age 46.7 ± 10.9 years; mean body mass index 45.6 ± 5.9). AUDIT-C and ASSIST identified 7% and 5% of risky drinkers, respectively. Men were more frequently risky drinkers compared to women (18% vs. 2%) and compared to the general population (18% vs. 8%). Six percent of individuals had AUD, being men the most affected, and 2% met criteria for other substance disorder. Fifteen percent of the sample presented risky tobacco use. Cannabis was self-reported only by males (3%). EtG ≥ 500 ng/ml was present in 15% of the sample, being a risk factor for risky drinking together with the male sex.

Identification of candidates at risk for risky drinking can help to prevent any alcohol misuse after BS. The combination of subjective and objective measures improves the validity of the assessment of substance use.

Obesity is an increasing public health problem because of its high prevalence and associated morbidity and mortality. Two weight-loss strategies are currently used, either bariatric surgery or pharmacological therapy with glucagon-like peptide-1 receptor agonists (GLP-1RAs). Preclinical studies in rodents suggested an increased risk of additive disorders after bariatric surgery contrasting with a reduced risk with GLP-1RAs.

An extensive literature search to detect clinical studies that investigated the prevalence of addictive disorders (food addiction, alcohol abuse, smoking, cannabis, cocaine, opioid use) following bariatric surgery or GLP-1RA therapy in obese patients.

In observational cohort studies, the prevalence of alcohol use disorder was twofold higher after > 2 years following surgery (eleven studies, mainly with gastric bypass) whereas it was reduced roughly by half with GLP-1RA therapy (five studies, mainly with semaglutide). Similar findings were reported with other addictive disorders. An addiction transfer from food addiction to other addictive disorders is hypothesized to explain the increased risk after bariatric surgery. Several mechanisms are proposed to explain the favorable findings reported with GLP-1RAs, i.e. effects on the dopamine reward pathway, central GABA (gamma-aminobutyric acid) release, negative emotional stress associated with food/drug restriction and/or neuronal inflammation.

Available data from observational cohort studies confirm an increased risk of addictive disorders following bariatric surgery, contrasting with a reduced risk with GLP-1RA therapy. Both physicians and patients should be informed of the higher risk post-surgery whereas available promising results with GLP-1RAs should be confirmed in ongoing dedicated randomized controlled trials before any official indication.

Alcohol use disorder (AUD) is a massive burden for the individual, relatives and society. Despite this, the treatment gap is wide compared with other mental health disorders. Treatment options are sparse, with only three Food and Drug Administration (FDA)-approved pharmacotherapies. Glucagon-like peptide-1 (GLP-1) receptor agonists have shown promising effects in reducing alcohol consumption in preclinical experiments, and clinical trials are in high demand to investigate these potentially beneficial effects in patients diagnosed with AUD.

The effects of the once-weekly GLP-1 receptor agonist semaglutide will be investigated in a 26-week, randomised, placebo-controlled, double-blinded clinical trial. 108 patients diagnosed with AUD and comorbid obesity (body mass index (BMI)≥30 kg/m2)) will be randomised to treatment with either semaglutide or placebo in combination with cognitive behavioural therapy. A subgroup of the patients will have structural, functional and neurochemical brain imaging performed at baseline and after 26 weeks of treatment. The primary endpoint is the reduction in heavy drinking days, defined as days with excess consumption of 48/60 g of alcohol per day (women and men, respectively). Secondary endpoints include changes from baseline to week 26 in alcohol consumption, smoking status, quality of life, fibrosis-4 score, plasma concentration of phosphatidylethanol, brain gamma-aminobutyric acid (GABA) levels, alcohol cue reactivity, functional connectivity and white matter tract integrity.

Recruitment started in June 2023.

The study is approved by the Ethics Committee of the Capital Region of Denmark, the Danish Board of Health and the Danish Data Protection Agency. All patients will sign the written consent form before being included in the trial. Results will be disseminated through peer-reviewed publications and conference presentations. After the results are published, all de-identified data will be available in the Mendeley database.

NCT05895643.

Considering the increasing consumption of soft drinks and their adverse health effects, identifying addiction to these drinks in the population is significant. Accordingly, this study aimed to evaluate the reliability and validity of the Turkish version of the Soft Drink Addiction Scale.

For this purpose, we included 669 participants and distributed them homogeneously for exploratory and confirmatory factor analyses. To assess the psychometric properties of the scale, we used the Soft Drink Addiction Scale, the Beverage Intake Questionnaire-15, and a questionnaire that included questions assessing self-efficacy regarding soft drinks and attitudes toward alternatives.

The mean age of 669 participants was 34.05 ± 9.26 years. A total of 93.72% were female and 6.28% were male. The scale's Cronbach's alpha coefficient was 0.942. An exploratory factor analysis revealed the following three-factor structure: withdrawal syndrome symptoms, persistent desire, and decrease in social and recreational activities, which explained 29.1%, 16%, and 16.9% of the total variance, respectively. A confirmatory factor analysis also confirmed this construct. Moreover, soft drink addiction was associated with self-efficacy and total calories from beverages questioned in the beverage consumption questionnaire.

In conclusion, the Turkish version of the Soft Drink Addiction Scale is a reliable and valid tool.

The cerebellum is one of the major central nervous structures consistently altered in obesity. Its role in higher cognitive function, parts of which are affected by obesity, is mediated through projections to and from the cerebral cortex. We therefore investigated the relationship between body mass index (BMI) and cerebellocerebral connectivity.

We utilized the Human Connectome Project's Young Adults dataset, including functional magnetic resonance imaging (fMRI) and behavioral data, to perform connectome-based predictive modeling (CPM) restricted to cerebellocerebral connectivity of resting-state fMRI and task-based fMRI. We developed a Python-based open-source framework to perform CPM, a data-driven technique with built-in cross-validation to establish brain-behavior relationships. Significance was assessed with permutation analysis.

We found that (i) cerebellocerebral connectivity predicted BMI, (ii) task-general cerebellocerebral connectivity predicted BMI more reliably than resting-state fMRI and individual task-based fMRI separately, (iii) predictive networks derived this way overlapped with established functional brain networks (namely, frontoparietal networks, the somatomotor network, the salience network, and the default mode network), and (iv) we found there was an inverse overlap between networks predictive of BMI and networks predictive of cognitive measures adversely affected by overweight/obesity.

Our results suggest obesity-specific alterations in cerebellocerebral connectivity, specifically with regard to task execution. With brain areas and brain networks relevant to task performance implicated, these alterations seem to reflect a neurobiological substrate for task performance adversely affected by obesity.

Previous literature suggests a link between insomnia symptoms and eating disorders (EDs), yet empirical data on the temporal associations between these two variables are lacking. This study aimed to explore the bidirectional associations between insomnia symptoms and EDs in a population of college students. A total of 11,010 college students were assessed initially from October 17 to 29, 2023, and again 6 months later from April 15 to 24, 2024. EDs were assessed using the Short Form of the Eating Disorder Examination Questionnaire (EDE-QS), while insomnia symptoms were measured through a three-item questionnaire addressing difficulty initiating sleep, difficulty maintaining sleep, and early morning awakening. Our findings indicated that insomnia symptoms at baseline was significantly associated with increased odds of EDs six months later. Moreover, EDs at baseline were significantly predict insomnia symptoms at the six-month follow-up. This study identifies prospective bidirectional relationships between insomnia symptoms and EDs among college students, offering insights that may inform educational and clinical approaches to preventing and treating insomnia symptoms and EDs.

Does it matter how many hours we spend scrolling through Instagram? This article examines the neurobiological impact of prolonged social media use, focusing on how it affects the brain's reward, attention, and emotional regulation systems. Frequent engagement with social media platforms alters dopamine pathways, a critical component in reward processing, fostering dependency analogous to substance addiction. Furthermore, changes in brain activity within the prefrontal cortex and amygdala suggest increased emotional sensitivity and compromised decision-making abilities. The role of artificial intelligence (AI) in this process is significant. AI-driven social media algorithms are designed solely to capture our attention for profit without prioritizing ethical concerns, personalizing content, and enhancing user engagement by continuously tailoring feeds to individual preferences. These adaptive algorithms are designed to maximize screen time, thereby deepening the activation of the brain's reward centers. This cycle of optimized content and heightened engagement accelerates the development of addictive behaviors. The interplay between altered brain physiology and AI-driven content optimization creates a feedback loop that promotes social media addiction among teenagers. This raises significant ethical concerns regarding privacy and the promotion of personalized content. This review article offers a comprehensive and in-depth analysis of the neurophysiological impact of social media on adolescents and the moral concerns governing them. It also provides solutions for ethical social media use and preventing addiction among teenagers.

Pathological eating and addictive processes are linked to obesity. Food addiction (FA) involves hedonic eating of highly palatable foods, accompanied by addictive symptoms like craving, loss-of-control (LOC) eating, and withdrawal. The main objectives of this study were to assess FA prevalence and symptoms in bariatric surgery candidates, and its relationship with depression, dysregulated eating, and 1- year postoperative weight loss (WL).

Data from 69 bariatric surgery patients (74% female, 26% male, ) were analysed. Self-report measures including Yale Food Addiction Scale (YFAS) 2.0, Eating Disorder Examination-Questionnaire (EDE-Q), Repetitive Eating Questionnaire [Rep(eat)-Q] and Hospital Anxiety and Depression Scale (HADS) were administered pre-surgery and at 1-year follow-up.

The mean preoperative YFAS symptom score was 2.2. (SD = 2.59). 16% of the sample met YFAS diagnostic criteria for FA. Top reported FA criteria were "substance taken in larger amount than intended" (33%), "persisted desire or repeated unsuccessful attempts to quit" (29%), and "use in physically hazardous situations" (23%). The YFAS symptom scores correlated significantly with the frequency of LOC binge eating, depression and repetitive eating scores, but showed no correlation with age or BMI. Preoperative YFAS symptom scores did not significantly predict % WL at 1-year follow-up.

Our findings align with previous research, indicating that preoperative FA symptoms is unrelated to preoperative BMI and total %WL, but linked to eating pathology, such as LOC binge eating and grazing, as well as depression in bariatric surgery candidates.

Incretin-based treatments, such as glucagon-like peptide-1 receptor (GLP-1R) agonists (eg liraglutide and semaglutide), have rapidly transformed obesity treatment. The well-documented weight loss effect from these agents is considered to be primarily a result of their actions on food intake, but frequent anecdotal reports from varied sources have suggested that they might also broadly affect consummatory behavior, including alcohol and drugs of abuse, suggesting a potential modulatory effect on reward behavior. Herein, we critically review the extant literature on the behavioral effects of GLP-1R agonists in humans, including their impact on feeding behavior, alcohol/drug intake, and overall reward response. We also consider the physiological and neurobiological underpinnings of GLP-1 actions, with a focus on its distinct central and peripheral roles, as well as its relationships with the broader energy homeostasis network. We conclude with a discussion on the implications of this line of research on how behavior is conceptualized, and the potential future directions for research.

Ultra-processed foods (UPFs) are harmful to health but ubiquitous in the modern food environment, comprising almost 60% of the average American diet. This study assessed the feasibility, acceptability, and preliminary efficacy of a novel behavioral intervention designed to reduce UPF intake.

Fourteen adults participated in an 8-week pilot intervention, which consisted of weekly group sessions, individual meal planning sessions, and financial support. Dietary intake was assessed using three Automated Self-Administered 24-h Dietary Recalls (ASA24) at both baseline and post-treatment.

The intervention was highly feasible and acceptable. Qualitative data demonstrated that participants were enthusiastic about the benefits of reducing UPF intake and found the intervention highly valuable. Participants reduced average daily calories from UPF by 48.9%, number of UPFs consumed by almost half, total daily calorie intake by 612 calories/day, sodium consumption by 37% and sugar consumption by 50%. There were no significant changes in fruit or vegetable intake. Participants lost an average of 3.5 kg (SD = 3.0 kg).

This pilot data suggests that behavioral interventions to reduce UPF intake will be well-received and are capable of success despite the barriers of the United States food environment. Future research should prioritize behavioral interventions targeting UPF consumption alongside policy changes.

This study aimed to assess the association between emotional attitudes towards diabetes, eating behaviour styles and glycaemic control in outpatients with type 2 diabetes.

Observational study.

Endocrinology Division of Hospital de Clínicas de Porto Alegre, Brazil.

Ninety-one outpatients diagnosed with type 2 diabetes. Baseline assessments included data on clinical parameters, lifestyle factors, laboratory results, eating behaviour styles and emotional attitudes. All patients received nutritional counseling following diabetes recommendations. A follow-up visit was scheduled approximately 90 days later to evaluate changes in weight, medication dosages and glycated Hb (HbA1c) values. Patients were categorised based on their emotional attitude scores towards diabetes (positive or negative), and their characteristics were compared using appropriate statistical tests.

At baseline, no differences were observed in the proportion of patients with good glycaemic control, eating behaviour styles and emotional attitudes. However, patients with a positive attitude towards the disease exhibited a significantly better response in glycaemic control compared with the reference group (OR = 3·47; 95 % CI = 1·12, 10·75), after adjusting for diabetes duration, sex and medication effect score. However, when BMI was included in the model, the association did not reach statistical significance. Therefore, these results should be interpreted with caution.

Patients with a positive attitude towards diabetes showed a greater reduction in HbA1c levels following nutritional counseling. However, baseline BMI could be a potential confounding factor.

Food addiction is a multifactorial disorder characterised by a loss of control over food intake that may promote obesity and alter gut microbiota composition. We have investigated the potential involvement of the gut microbiota in the mechanisms underlying food addiction.

We used the Yale Food Addiction Scale (YFAS) 2.0 criteria to classify extreme food addiction in mouse and human subpopulations to identify gut microbiota signatures associated with vulnerability to this disorder.

Both animal and human cohorts showed important similarities in the gut microbiota signatures linked to food addiction. The signatures suggested possible non-beneficial effects of bacteria belonging to the Proteobacteria phylum and potential protective effects of Actinobacteria against the development of food addiction in both cohorts of humans and mice. A decreased relative abundance of the species Blautia wexlerae was observed in addicted humans and of Blautia genus in addicted mice. Administration of the non-digestible carbohydrates, lactulose and rhamnose, known to favour Blautia growth, led to increased relative abundance of Blautia in mice faeces in parallel with dramatic improvements in food addiction. A similar improvement was revealed after oral administration of Blautia wexlerae as a beneficial microbe.

By understanding the crosstalk between this behavioural alteration and gut microbiota, these findings constitute a step forward to future treatments for food addiction and related eating disorders.

Consumption of palatable food (PF) can alleviate anxiety, and pain in humans. Contrary, spontaneous withdrawal of long-term PF intake produces anxiogenic-like behavior and abnormal pain sensation, causing challenges to weight-loss diet and anti-obesity agents. Thus, we examined α7-nicotinic acetylcholine receptors (α7nAChR) involvement since it plays essential role in nociception and psychological behaviors.

Adult male C57BL/6 mice were placed on a Standard Chow (SC) alone or with PF on intermittent or continuous regimen for 6 weeks. Then, mice were replaced with normal SC (spontaneous withdrawal). Body weight, food intake, and calories intake with and without the obesogenic diet were measured throughout the study. During PF withdrawal, anxiety-like behaviors and pain sensitivity were measured with PNU-282987 (α7nAChR agonist) administration.

Six weeks of SC + PF-intermittent and continuous paradigms produced a significant weight gain. PF withdrawal displayed hyperalgesia and anxiety-like behaviors. During withdrawal, PNU-282987 significantly attenuated hyperalgesia and anxiety-like behaviors.

The present study shows that a PF can increase food intake and body weight. Also, enhanced pain sensitivity and anxiety-like behavior were observed during PF withdrawal. α7nAChR activation attenuated anxiolytic-like behavior and hyperalgesia in PF abstinent mice. These data suggest potential therapeutic effects of targeting α7 nAChRs for obesity-withdrawal symptoms in obese subjects.

Obesity is associated with numerous health risks and ever-increasing rates are a significant global concern. However, despite weight loss attempts many people have difficulty maintaining weight loss. Previous studies in animals have shown that chronic access to an obesogenic diet can disrupt goal-directed behavior, impairing the ability of animals to flexibly adjust food-seeking behavior following changes in the value of earned outcomes. Changes in behavioral control have been linked to disruption of glutamate transmission in the dorsal medial striatum (DMS), a region critical for the acquisition and expression of goal-directed behavior.

The goal of this study was to test whether ceftriaxone, a beta-lactam antibiotic shown elsewhere to upregulate the expression of the glutamate transporter GLT-1, would improve goal-directed control following long-term exposure to an obesogenic diet.

Male and female rats were given access to either standard chow or chow plus sweetened condensed milk (SCM) for 6 weeks. Access to SCM was ended and rats received daily injections of either ceftriaxone or saline for 6 days. Rats were then trained to press a lever to earn a novel food reward and, finally, were assessed for sensitivity to outcome devaluation. Histological analyses examined changes to GLT-1 protein levels and morphological changes to astrocytes, within the DMS.

We found that ceftriaxone robustly restored goal-directed behavior in animals following long-term exposure to SCM. While we did not observe changes in protein levels of GLT-1 in the DMS, we observed that SCM induced changes in the morphology of astrocytes in the DMS, and that ceftriaxone mitigated these changes.

These results demonstrate that long-term access to a SCM diet impairs goal-directed behavior while also altering the morphology of astrocytes in the DMS. Furthermore, these results suggest that ceftriaxone administration can reverse the impairment of goal-directed behavior potentially through its actions on astrocytes in decision-making circuitry.

Obesity has become a prominent public health concern worldwide and is associated with adverse cognitive function. Exercise, particularly aerobic exercise, is known to benefit for weight loss and cognitive function. However, whether acute aerobic exercise could yield benefits to obese individuals and the precise brain mechanisms of action remain poorly understood. The study aimed to investigate whether acute aerobic exercise could improve inhibitory control among obese individuals and what neuroelectric mechanisms are implicated. A 3 (session: control, low-intensity exercise, moderate-intensity exercise) × 2 (congruency: congruent, incongruent) within-subject design was conducted. 18 obese young male adults underwent three sessions of 30-min interventions in a counterbalanced order seperated by five days: moderate-intensity aerobic exercise (MIE), low-intensity aerobic exercise (LIE) and a control session (a sedentary period of seated rest). The Flanker task and EEG recordings (N2 and P3 amplitude) were investigated following exercise and the control treatment. Results showed that the N2 amplitude following MIE was larger than the control session, whereas a larger N2 and reduced congruent P3 amplitude was observed following MIE than LIE. However, no main effect of the session was found for reaction time and accuracy, but a significant main effect of congruency was observed. These findings suggest acute moderate-intensity aerobic exercise may modulate brain activity through enhanced recruitment of attentional resources for cognitive control and conflict monitoring in adults with obesity.

Addiction offers a framework for the understanding of eating disorders, particularly those characterized by hyperphagia, with growing interest in food addiction. However, the application of the addiction model to anorexia nervosa remains more controversial. In this commented narrative review, we examine and discuss the addictive features of anorexia nervosa.

Commented narrative review of the literature.

Anorexia nervosa could be the consequence of the loss of control of several objects of positive reinforcement: food restriction, physical hyperactivity, and food itself. Craving has been little studied in the field of eating disorders. When investigated, studies mainly focus on food cravings and tend to highlight food cravings that are inversely correlated with the restrictive nature of the disorder. This would thus be less found in anorexia nervosa, in which it is nevertheless reported. The existence of a pre-existing food craving, or its appearance secondary to food restriction, is currently under discussion. In the meantime, the question of a craving for food restriction, underpinned by the gratifying effect of fasting, is raised.

The management of eating disorders has its place within the addiction care sectors. An integrative approach should be favored, for anorexia nervosa, combining, on the one hand, classic nutritional care, and, on the other hand, care within the framework of addiction treatment. Finally, in people with an eating disorder, the search for an addiction to food, food restriction and physical activity, including a systematic assessment of craving, should be systematized.

Psilocybin is the main psychoactive compound found in hallucinogenic/magic mushrooms and can bind to both serotonergic and tropomyosin receptor kinase b (TrkB) receptors. Psilocybin has begun to show efficacy for a range of neuropsychiatric conditions, including treatment-resistant depression and anxiety disorders; however, neurobiological mechanisms are still being elucidated. Clinical research has found that psilocybin can alter functional connectivity patterns in human brains, which is often associated with therapeutic outcomes. However, preclinical research affords the opportunity to assess the potential cellular mechanisms by which psilocybin may exert its therapeutic effects. Preclinical rodent models can also facilitate a more tightly controlled experimental context and minimise placebo effects. Furthermore, where there is a rationale, preclinical researchers can investigate psilocybin administration in neuropsychiatric conditions that have not yet been researched clinically. As a result, we have systematically reviewed the knowledge base, identifying 82 preclinical studies which were screened based on specific criteria. This resulted in the exclusion of 44 articles, with 34 articles being included in the main review and another 2 articles included as Supporting Information materials. We found that psilocybin shows promise as a lead candidate molecule for treating a variety of neuropsychiatric conditions, albeit showing the most efficacy for depression. We discuss the experimental findings, and identify possible mechanisms whereby psilocybin could invoke therapeutic changes. Furthermore, we critically evaluate the between-study heterogeneity and possible future research avenues. Our review suggests that preclinical rodent models can provide valid and translatable tools for researching novel psilocybin-induced molecular and cellular mechanisms, and therapeutic outcomes.

The escalating prevalence of obesity and its related disorders represents a daunting global health challenge. Unfortunately, current pharmacological interventions for obesity remain limited and are often associated with debilitating side effects. Against this backdrop, the psychoactive aminoindane derivative 5-methoxy-2-aminoindane (MEAI) has gained considerable attention for its ability to induce a pleasurable, alcohol-like sensation while curbing alcohol consumption. Given the potential impact of MEAI on food addiction and energy homeostasis, we examined its metabolic efficacy on appetite regulation, obesity, and related comorbidities under acute and chronic settings, utilizing a mouse model of diet-induced obesity (DIO). Our results demonstrated that MEAI treatment significantly reduced DIO-induced overweight and adiposity by preserving lean mass and decreasing fat mass. Additionally, MEAI treatment exhibited positive effects on glycemic control by attenuating DIO-induced hyperglycemia, glucose intolerance, and hyperinsulinemia. Furthermore, MEAI reduced DIO-induced hepatic steatosis by decreasing hepatic lipid accumulation and lowering liver triglyceride and cholesterol levels, primarily by inhibiting de novo lipid synthesis. Metabolic phenotyping revealed that MEAI increased energy expenditure and fat utilization while maintaining food consumption similar to that of the vehicle-treated group. Lastly, MEAI normalized voluntary locomotion actions without any overstimulatory effects. These findings provide compelling evidence for the antiobesity effects of MEAI treatment and call for further preclinical testing. In conclusion, our study highlights the potential of MEAI as a novel therapeutic approach for treating obesity and its associated metabolic disorders, offering hope for the development of new treatment options for this global health challenge.

The central nucleus of the amygdala (CeA) is part of the dopaminergic reward system and controls energy balance. Recently, a cluster of neurons was identified as responsive to the orexigenic effect of ghrelin and fasting. However, the signaling pathway by which ghrelin and fasting induce feeding is unknown. AMP-activated protein kinase (AMPK) is a cellular energy sensor, and its Thr172 phosphorylation (AMPKThr172) in the mediobasal hypothalamus regulates food intake. However, whether the expression and activation of AMPK in CeA could be one of the intracellular signaling activated in response to ghrelin and fasting eliciting food intake is unknown.

To evaluate the activation of AMPK into CeA in response to ghrelin, fasting, and 2-deoxy-D-glucose (2DG) and whether feeding accompanied these changes. In addition, to investigate whether the inhibition of AMPK into CeA could decrease food intake.

On a chow diet, eight-week-old Wistar male rats were stereotaxically implanted with a cannula in the CeA to inject several modulators of AMPKα1/2Thr172 phosphorylation, and we performed physiological and molecular assays.

Fasting increased, and refeeding reduced AMPKThr172 in the CeA. Intra-CeA glucose injection decreased feeding, whereas injection of 2DG, a glucoprivation inductor, in the CeA, increased food intake and blood glucose, despite faint increases in AMPKThr172. Intra-CeA ghrelin injection increased food intake and AMPKThr172. To further confirm the role of AMPK in the CeA, chronic injection of Melanotan II (MTII) in CeA reduced body mass and food intake over seven days together with a slight decrease in AMPKThr172.

Our findings identified that AMPK might be part of the signaling machinery in the CeA, which responds to nutrients and hormones contributing to feeding control. The results can contribute to understanding the pathophysiological mechanisms of altered feeding behavior/consumption, such as binge eating of caloric-dense, palatable food.

The recurrence of weight gain is attributed to the homeostatic regulation of hunger and satiety signals, influenced by metabolic state, nutrient availability, and non-homeostatic mechanisms shaped by reinforced consequences from experiences. In response, Evelyn Tribole and Elyse Resch proposed Intuitive Eating (IE) in 1980, countering restrictive diets. IE, inversely correlated with Body Mass Index (BMI), binge eating, and anxiety/depression symptoms, fosters mind-body-food harmony by recognizing hunger and satiety cues. IE encourages meeting physiological, not emotional, needs, permitting unconditional eating, and relying on internal signals for food decisions. Amidst university students' stress, exacerbated during the COVID-19 pandemic, understanding their eating behavior, particularly intuitive eating levels, becomes crucial.

This study aimed to assess the IE level of Brazilian students during the COVID-19 pandemic.

This cross-sectional study, the first to analyze the Intuitive Eating of students in Brazil during the pandemic, was conducted using an online questionnaire.

The sample comprised 1335 students, most of whom were women (82.17%), with a mean age of 26.12 ± 7.9 years, and a healthy nutritional status (57.58%). The mean IE score was 3.2 ± 0.6. A significant association was found between the confinement situation, the type of housing unit, and the IE subscale-Unconditional Permission to Eat (p = 0.043). However, there was no association between the other subscales and the total IE scale. Regarding self-reported mental and eating disorders, the most frequent were anxiety (21.2%), depression (6.5%), and binge eating disorder (BED) (4.7%). IE was negatively associated with BED (B =  - 0.66; p < .001), bulimia nervosa (B =  - 0.58; p < .001), body mass index (BMI) (p < .001) and self-reported anxiety (B =  - .102; p = 0.16). The male sex showed a higher IE score compared with the female sex (p < .001).

While no significant association was found between IE and the confinement situation, a significant association was found between housing type and the Unconditional Permission to Eat subscale.

Weight regain is a common outcome of weight loss interventions. Mental health-related comorbidities, among other factors, can mediate weight regain regardless of the implemented treatment modality. This study explores whether postoperative psychopathological comorbidities are associated with weight regain after bariatric surgery.

This cross-sectional study recruited 90 outpatients who underwent Roux-en-Y gastric bypass surgery. Anthropometric measurements were collected retrospectively from medical charts. The Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorder-IV (DSM-IV) Axis I Disorders (SCID-I) was applied to evaluate psychiatry diagnoses. Validated self-report instruments were used to assess depression, anxiety, alcohol use, impulsivity, binge eating, and body image dissatisfaction. Weight regain was defined as a ≥20% increase from the maximum weight lost. Level of evidence: Level III, cross-sectional study based on a well-designed study.

Overall, 55.6% of participants experienced weight regain. Notably, mental disorders such as current binge-eating disorder and lifetime diagnoses including bulimia nervosa, alcohol abuse/dependence, and obsessive-compulsive disorder were significantly associated with weight regain. However, controlled analysis found that, for mental disorders, only current binge-eating disorder (odds ratio [OR] 6.3, 95% confidence interval [CI] 1.26-31.06, p = 0.024) remained associated with weight regain. Eating-related psychopathologies also associated with weight regain included binge eating (d = 0.55; p = 0.013), eating disinhibition (d = 0.76; p = 0.001), higher hunger levels (d = 0.39; p = 0.004), and non-planning trait impulsivity (d = 0.69; p = 0.0001).

Postoperative presence of psychopathological comorbidities, such as eating psychopathology and trait impulsivity, were associated with weight regain after bariatric surgery. These findings highlight the importance of addressing mental health in individuals experiencing postsurgical weight regain.

Neuroimaging studies have revealed alterations in habenular (Hb) structure and functional connectivity (FC) in psychiatric conditions. The Hb plays a particularly critical role in regulating negative emotions, which trigger excessive food intake and obesity. However, obesity and weight loss intervention (i.e., laparoscopic sleeve gastrectomy [LSG])-associated changes in Hb structure and FC have not been studied.

We used voxel-based morphometry analysis to measure changes in gray matter volume (GMV) in the Hb in 56 patients with obesity at pre-LSG and 12 months post-LSG and in 78 normal-weight (NW) control participants. Then, we conducted Hb seed-based resting-state FC (RSFC) to examine obesity-related and LSG-induced alterations in RSFC. Finally, we used mediation analysis to characterize the interrelationships among Hb GMV, RSFC, and behaviors.

Compared with NW participants, Hb GMV was smaller in patients at pre-LSG and increased at 12 months post-LSG to levels equivalent to that of NW; in addition, increases in Hb GMV were correlated with reduced body mass index (BMI). Compared with NW participants, pre-LSG patients showed greater RSFCs of the Hb-insula, Hb-precentral gyrus, and Hb-rolandic operculum and weaker RSFCs of the Hb-thalamus, Hb-hypothalamus, and Hb-caudate; LSG normalized these RSFCs. Decreased RSFC of the Hb-insula was correlated with reduced BMI, Yale Food Addiction Scale rating, and emotional eating; reduced hunger levels were correlated with increased RSFCs of the Hb-thalamus and Hb-hypothalamus; and reduced BMI and Yale Food Addiction Scale ratings were correlated with increased RSFCs of the Hb-thalamus and Hb-hypothalamus, respectively. The bidirectional relationships between Hb GMV and RSFC of the Hb-insula contributed to reduced BMI.

These findings indicate that LSG increased Hb GMV and that its related improvement in RSFC of the Hb-insula may mediate long-term benefits of LSG for eating behaviors and weight loss.

Internet Addiction (IA) refers to excessive or uncontrolled behaviors related to Internet access, causing impairment or distress. Similarly, Smartphone Addiction (SPA) involves the excessive use of smartphones, disrupting users' daily lives. Cognitive control plays a relevant role in the development of IA and SPA, with executive functions and rewards processing being particularly important.

This study aims to provide a synthesis of scientific evidence on the differential effects of IA and SPA on cognition in young adults and adolescents, using fMRI.

Relevant articles published between 2013 and May 2023 were identified following the PRISMA protocol.

Included studies (n = 21) revealed that both behavioral addictions were associated with impairments in cognitive control related to reward processing (ACC, insula, amygdala) and executive function (DLPFC, frontal, parietal lobes) in adolescents and young adults.

These findings provide evidence for neuroanatomical similarities between IA and SPA in young adults and adolescents related to executive functions and rewards processing. However, differential effects of SPA and IA on cognitive control were not found in this study. Future research should explore the relationship between these addictions with other cognitive domains to further expand our understanding within this field. While both IA and SPA involve the excessive use of online technology, SPA could involve a higher risk, given that smartphones allow internet connectivity anytime.

Alcohol use disorder (AUD) is a significant contributor to morbidity and mortality in the United States. It contributes to over 140,000 annual deaths, to over 200 related diseases and health conditions globally, and accounts for 5.1% of the global disease burden. Despite its substantial impact, AUD remains undertreated, marked by a scarcity of approved medications. This paper explores the current treatment landscape and novel strategies for both alcohol withdrawal syndrome and AUD. Promising results, including the use of psychedelics alongside psychotherapy, noninvasive neural-circuit-based interventions, phosphodiesterase-4 inhibitors, and GLP-1 receptor agonists, have emerged from recent studies. While these advancements show potential, further research is crucial for a comprehensive understanding of their effectiveness. The clear shortage of approved medications and other treatment modalities underscores the pressing need for ongoing research.

Obesity has been linked to abnormal frontal function, including the white matter fibers of anterior portion of the corpus callosum, which is crucial for information exchange within frontal cortex. However, alterations in white matter anatomical connectivity between corpus callosum and cortical regions in patients with obesity have not yet been investigated. Thus, we enrolled 72 obese and 60 age-/gender-matched normal weight participants who underwent clinical measurements and diffusion tensor imaging. Probabilistic tractography with connectivity-based classification was performed to segment the corpus callosum and quantify white matter anatomical connectivity between subregions of corpus callosum and cortical regions, and associations between corpus callosum-cortex white matter anatomical connectivity and clinical behaviors were also assessed. Relative to normal weight individuals, individuals with obesity exhibited significantly greater white matter anatomical connectivity of corpus callosum-orbitofrontal cortex, which was positively correlated with body mass index and self-reported disinhibition of eating behavior, and lower white matter anatomical connectivity of corpus callosum-prefrontal cortex, which was significantly negatively correlated with craving for high-calorie food cues. The findings show that alterations in white matter anatomical connectivity between corpus callosum and frontal regions involved in reward and executive control are associated with abnormal eating behaviors.

This second chapter in our trilogy reviews and critically appraises the scientific evidence for the role of endogenous opioid system (EOS) activity in the onset and progression of both obesity and eating disorders. Defining features of normative eating and maladaptive eating behaviors are discussed as a foundation. We review the scientific literature pertaining to the predisposing risk factors and pathophysiology for obesity and eating disorders. Research targeting the association between obesity, disordered eating, and psychiatric comorbidities is reviewed. We conclude by discussing the involvement of endogenous opioids in neurobiological and behavior traits, and the clinical evidence for the role of the EOS in obesity and eating disorders.

In rats, eating obesogenic diets increases calcium-permeable AMPA receptor (CP-AMPAR) transmission in the nucleus accumbens (NAc) core, and enhances food-motivated behavior. Interestingly, these diet-induced alterations in NAc transmission are pronounced and sustained in obesity-prone (OP) male rats and absent in obesity-resistant (OR) populations. However, effects of diet manipulation on food motivation, and the mechanisms underlying this NAc plasticity in OPs is unknown. Using male selectively-bred OP and OR rats, we assessed food-motivated behavior following ad lib access to chow (CH), junk-food (JF), or 10d of JF followed by a return to chow diet (JF-Dep). Motivation for food was greater in OP than OR rats, as expected. However, JF-Dep only produced enhancements in food-seeking in OP groups, while continuous JF access reduced food-seeking in both OPs and ORs. Additionally, optogenetic, chemogenetic, and pharmacological approaches were used to examine NAc CP-AMPAR recruitment following diet manipulation and ex vivo treatment of brain slices. Reducing excitatory transmission in the NAc was sufficient to recruit CP-AMPARs to synapses in OPs, but not ORs. In OPs, JF-induced increases in CP-AMPARs occurred in mPFC-, but not BLA-to-NAc inputs. Together results show that diet differentially affects behavioral and neural plasticity in obesity susceptible populations. We also identify conditions for acute recruitment of NAc CP-AMPARs; these results suggest that synaptic scaling mechanisms contribute to NAc CP-AMPAR recruitment. Overall, this work helps elucidate how diet interacts with obesity susceptibility to influence food-motivated behavior and extends our fundamental understanding of NAc CP-AMPAR recruitment.

High-intensity sweet-liking has been linked to alcohol use disorder (AUD) risk. However, the neural underpinning of this association is poorly understood. To find a biomarker predictive of AUD, 140 participants (social and heavy drinkers, ages 21-26) underwent functional magnetic resonance imaging (fMRI) during a monetary incentive delay (MID) task and stimulation with high (SucroseHigh)- and low-concentration sucrose, as well as viscosity-matched water. On another day after imaging, and just before free-access intravenous alcohol self-administration, participants experienced a 30 mg% alcohol prime (10 min ascent) using the Computerized Alcohol Infusion System. Principal component analysis (PCA) of subjective responses (SR) to the prime's ascending limb generated enjoyable (SRenjoy) and sedative (SRsed) intoxication components. Another PCA created one component reflective of self-administered alcohol exposure (AE) over 90 min. Component loadings were entered as regressors in a voxel-wise general linear fMRI model, with reward type as a fixed factor. By design, peak prime breath alcohol concentration was similar across participants (29 ± 3.4 mg%). SRenjoy on the prime's ascending limb correlated positively with [SucroseHigh > Water] in the supplementary motor area and right dorsal anterior insula, implicating the salience network. Neither SR component correlated with the brain's response to MID. AE was unrelated to brain reward activation. While these findings do not support a relationship between alcohol self-administration and (1) subjective liking of or (2) regional brain response to an intensely sweet taste, they show that alcohol's enjoyable intoxicating effects on the rising limb correspond with anterior insular and supplementary motor area responses to high-concentration sucrose taste. No such associations were observed with MID despite robust activation in those regions. Insula and supplementary motor area responses to intense sensations relate to a known risk factor for AUD in a way that is not apparent with a secondary (monetary) reward.

The prevalence of food addiction among patients seeking bariatric surgery is approximately 30 %. While hyper-palatable foods (HPF) have been identified as the potential 'substance' in food addiction and a contributor to severe obesity, consumption of HPF among individuals with food addiction, including those seeking bariatric surgery, is unknown. Thus, the aim of this study was to evaluate the consumption of HPF among individuals seeking bariatric surgery with food addiction, compared to those without food addiction.

Participants were N = 54 individuals with severe obesity seeking bariatric surgery. The Yale Food Addiction Scale was used to identify individuals with food addiction (FA) (37 % of sample). Dietary recalls were used to quantify HPF intake. Analyses were conducted to characterize average HPF intake and to determine whether there were significant differences between HPF intake among those with FA compared to those without FA, and whether HFP intake was correlated with FA symptoms.

On average, 71 % of participants' daily calorie intake was from HPF. There were no significant differences in HPF items intake among individuals with and without FA (70.46 % vs 71.34; p = 0.85). A positive correlation between number of FA symptoms and the intake of HPF high in fat and sugar ([0.3]; p = 0.03) was observed.

In this pilot study, HPF consumption among individuals with and without FA seeking bariatric surgery was high overall, however there were no differences across groups. In addition, intake of HPF with fat and sugar was associated with the number of symptoms of food addiction. More studies with a larger sample are needed to confirm these preliminary findings.

Obesity and substance use are leading preventable causes of mortality, yet their origins in violence remain poorly understood. This study examined child maltreatment in relation to obesity and symptoms consistent with substance use disorder (SUD) in late adolescence, determining the roles of the child maltreatment type and timing, and gender.

The sample (N = 1,161) was drawn from the Longitudinal Studies of Child Abuse and Neglect. Obesity and SUD were measured at 18-years. Lifetime child protective services records and youth self-reports indicated physical abuse, sexual abuse, supervisory neglect, failure-to-provide neglect, and emotional maltreatment during early childhood, middle childhood, and adolescence.

In the overall sample, emotional maltreatment during adolescence was associated with obesity (OR = 2.03, 95% CI: 1.25, 3.30) and SUD (OR = 2.00, 95% CI: 1.20, 3.35), and adolescent physical abuse with obesity (OR = 2.20, 95% CI: 1.36, 3.58). In girls, early childhood physical abuse was associated with SUD (OR = 2.35, 95% CI: 1.08, 5.12), and emotional maltreatment during adolescence with obesity (OR = 2.16, 95% CI: 1.10, 4.23) and SUD (OR = 3.21, 95% CI: 1.37, 7.3 5). Adolescent physical abuse and obesity were associated in boys (OR = 3.18, 95% CI: 1.45, 6.98). Gender moderation was identified for an inverse relationship between supervisory neglect and obesity in girls (OR = .26, 95% CI: .07, .99).

Type and timing contribute to the effects of child maltreatment, contingent upon gender. Intervention focused on adolescent emotional maltreatment may reduce both SUD and obesity.

The present paper aims to provide the latest perspectives and future directions on the association between emotions and eating behavior. We discussed individual differences in the impact of negative emotions on eating, emotional eating as disinhibited eating decisions with heightened reward values of and sensitivity to palatable foods in response to negative emotions and social isolation, in addition to emotional eating as maladaptive coping strategies under negative emotion and stress, hedonic (pleasure-oriented) eating decisions mediated by the brain reward system, and self-controlled (health-oriented) eating decisions mediated by the brain control system. Perspectives on future directions were addressed, including the development of early eating phenotypes in infancy, shared neural mechanisms mediated by the ventromedial prefrontal cortex and the dorsolateral prefrontal cortex in emotion and eating decision regulation, possible roles of interoception incorporating hunger and satiety signals, gut microbiome, the insula and the orbitofrontal cortex, and emotional processing capacities in hedonic eating and weight gain.

Although studies have demonstrated the involvement of the nucleus accumbens (NAc) in the neurobiology of eating disorders, its alterations in bulimia nervosa (BN) remain largely unknown. This study investigated the structural and functional properties of NAc in patients with BN.

Based on the resting-state functional MRI and high-resolution anatomical T1-weighted imaging data acquired from 43 right-handed BN patients and 40 sex-, age- and education-matched right-handed healthy controls (HCs), the group differences in gray matter volume (GMV) and fractional amplitude of low-frequency fluctuation (fALFF) in slow-4 and -5 bands and functional connectivity (FC) of NAc subregions (core and shell) were compared. The relationships between MRI and clinical data were explored in the BN group.

Compared with HCs, BN patients showed preserved GMV, decreased fALFF in slow-5 band of the left NAc core and shell, decreased FC between left NAc core and right caudate, and increased FC between all NAc subregions and frontal regions, between all NAc subregions (except the right NAc core) and the supramarginal gyrus (SMG), and between right NAc shell and left middle temporal gyrus. FC between the NAc and SMG was correlated with emotional eating behaviors.

Our study revealed preserved GMV, local neuronal activity reduction and functional network reorganization of the NAc in BN. The functional network reorganization of the NAc mainly occurred in the frontal cortex and was correlated with emotional eating behavior. These findings may provide novel insights into the BN using NAc as an entry point.

Although studies have demonstrated the involvement of the nucleus accumbens (NAc) in the neurobiology of eating disorders, its alterations in bulimia nervosa (BN) remain largely unknown. We used a multimodal MRI technique to systematically investigate structural and functional alterations in NAc subregions of BN patients and explored the associations between such alterations and maladaptive eating behaviors, hoping to provide novel insights into BN.

University students are a vulnerable population to the development of disordered eating, such as food addiction (FA) and grazing. FA is an emerging concept characterized by an intense desire to eat hyper-palatable foods. Grazing is characterized by the repetitive and unplanned ingestion of food throughout a period of time. Both FA and grazing have been associated with increased scores of negative urgency (NU) and difficulties in emotion regulation (ER). This study aims to evaluate the frequency of FA and grazing in a university population and to test the direct, total, and indirect effects-via FA-of ER and NU on repetitive eating and compulsive grazing. A total of 338 participants responded to a set of psychological measures assessing these variables. Thirty-six (10.7%) participants met the criteria for FA diagnosis and 184 (54.4%) presented grazing. Confirmatory factor analysis showed acceptable fit indexes for the model tested (χ2(1695) = 3167.575; p < 0.001; CFI = 0.955; NFI = 0.908; TLI = 0.953; SRMR = 0.085; RMSEA = 0.051; CI 90% (0.048; 0.053); P[RMSEA ≤ 0.05] = 0.318) and suggested that FA partially mediated the effect of difficulties in ER and NU on grazing, specifically on compulsive grazing. The results indicate that individuals with difficulties in ER and impulse control under negative emotions are more likely to engage in grazing if food addiction scores are higher. These results highlight the importance of assessing these variables, particularly in at-risk populations such as university students.

Increased consumption of food that are high in energy and sugar have been pointed as a major factor in the obesity epidemic. Impaired control of food intake and the concept of food addiction has been developed as a potential contributor. Our objective was to evaluate the dimensionality and psychometric validity of diagnostic criteria for food addiction adapted from the 11 DSM-5 substance use disorder (SUD) criteria (i.e.: Food Use Disorder (FUD) criteria), and to evaluate the influence of age, gender, and body mass index (BMI).

Cross-sectional observational study including 508 participants (56.1% male; mean age 42.2) from outpatient treatment clinics for obesity or addiction disorders at time of admission. FUD diagnostic criteria were analyzed using confirmatory factor and 2-parameter item response theory analyses. Differential Item and Test Functioning analyses were performed across age, gender, and BMI.

We demonstrated the one-factor dimensionality of the criteria set. The criterion "craving" presented the strongest factor loading and discrimination parameter and the second-lowest difficulty. We found some significant uniform differential item functioning for body mass index. We found some differential test functioning for gender and BMI.

This study reports, for the first time, the validity of a potential Food Use Disorder (derived from the 11 DSM-5 SUD criteria adapted to food) in a sample of treatment seeking adults. This has great implications both at the clinical level and in terms of public health policy in the context of the global obesity epidemic.