OBJECTIVE: Weight regain after metabolic bariatric surgery is a common problem. Food addiction is an eating disorder that can be one of the reasons for weight regain in these patients. This study aimed to evaluate the effects of probiotic supplementation with a weight loss program and cognitive behavioral therapy (CBT) on anthropometric measures, eating behavior, food addiction, and related hormone levels, in patients with food addiction and weight regain after metabolic bariatric surgery.
METHODS: This randomized, triple-blind, placebo-controlled clinical trial was conducted on patients with food addiction and weight regain after metabolic bariatric surgery. Participants (n = 50) received a weight loss program and CBT plus probiotic, or placebo for 12 weeks. Then, anthropometric measurements, biochemical markers, eating behavior, and food addiction were assessed.
RESULTS: Weight and body mass index (BMI) decreased significantly in the probiotic group compared to placebo (p = 0.008, p = 0.001, respectively). Fat mass was significantly decreased in the probiotic group (p < 0.001). Moreover, a significant improvement was observed in the probiotic group\'s eating behavior and food addiction compared to the placebo group (p < 0.001). Serum levels of leptin decreased significantly (p = 0.02), and oxytocin serum levels increased significantly (p = 0.008) in the probiotic group compared to the placebo group.
CONCLUSIONS: Adding probiotic supplements to the weight loss program and CBT is superior to the weight loss program and CBT alone in improving weight loss, eating behavior, and food addiction in patients with food addiction and weight regain after metabolic bariatric surgery.

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UNASSIGNED: The recent global increase in obesity rates, coupled with excessive palatable food (PF) consumption, has become a serious societal concern. Literature indicates that rewarding PF, especially upon cessation, can lead to overeating, binge eating, and compulsive eating, potentially resulting in obesity. Challenges in dietary paradigms, alongside limitations in approved treatments for eating disorders and anti-obesity medications, underscore the need to explore novel targets. In this context, α7nAChR (alpha-7 nicotinic acetylcholine receptor) may serve as a promising therapeutic target in combating food dependence and obesity. The present study aims to assess the role of α7nAChR in palatable food-induced dependence-like behaviors.
UNASSIGNED: The study involved male C57BL/6J mice exposed to three different feeding paradigms over 6 weeks to induce obesity and food addiction. On day 43, palatable food was replaced with standard chow, and the mice received treatments (vehicle, PNU-282987 [α7nAChR agonist], or methyllycaconitine citrate [MLA; α7nAChR antagonist]). Addiction-like behaviors, including craving for palatable food, motivation-effort interaction tests, and compulsive eating-like behavior, were measured during abstinence with and without treatment.
UNASSIGNED: The present study shows that chronic intermittent and continuous exposure to palatable food induces craving, motivation, and effort interaction behaviors as well as compulsive eating-like behaviors in palatable food-abstinent mice. Administration of the α7nAChR agonist, PNU-282987, significantly attenuated the craving behavior only in mice continuously fed palatable food (reduced calorie intake from 63.19 % to 48.21 %; p = 0.0053). Also, PNU-282987 suppressed the effort behaviors in either intermittently or continuously fed mice (significant reduction in the Δ number of active events per minute; p-values = 0.038 and 0.0098, respectively). However, it attenuated the compulsive-like eating behavior exclusively in the continuously fed group (p = 0.0433). Active and total interaction efforts were reversed by the MLA. These findings indicate the involvement of α7nAChR in dependence-like behaviors toward palatable food in mice.
UNASSIGNED: Our findings demonstrate that dependence-like behaviors toward palatable food can emerge after prolonged exposure. Mice fed on palatable food continuously exhibited more dependence-like behaviors toward palatable food, and activation of α7nAChR signaling attenuated the vulnerability to develop such behaviors.

There are different treatments for food addiction (FA) symptomatology, but a comprehensive review with a meta-analysis to determine the most effective intervention is lacking. The aim of this review is to investigate the efficacy of pharmacological, behavioral, and bariatric-metabolic surgical interventions in reducing FA symptomatology. Meta-analyses including 15 studies in adults showed a significantly positive effect (std mean difference in FA symptoms before vs after intervention 0.72 (0.58-0.95)), with bariatric-metabolic surgical interventions showing the highest efficacy in improving FA symptoms (1.17 (0.58-1.76) before vs after intervention). The existing evidence suggests a beneficial effect of bariatric-metabolic surgical, pharmacological, and behavioral interventions, in that order, on FA symptomatology in people with overweight/obesity. Weight loss and behavioral and lifestyle changes after surgery may be determinants in improving FA symptomatology.

The dimensional Yale Food Addiction Scale for Children 2.0 (dYFAS-C 2.0) was developed to provide a reliable psychometric measure for assessing food addiction in adolescents, in accordance with the updated addiction criteria proposed in the fifth edition of the Diagnostic and Statistical Manual (DSM-5). The present study aimed to evaluate the psychometric properties of the dYFAS-C 2.0 among Portuguese adolescents and pre-adolescents and to explore the relationship between food addiction and other eating behaviors such as grazing and intuitive eating. The participants were 131 Portuguese adolescents and pre-adolescents (53.4% female and 46.6% male) aged between 10 and 15 years (Mage = 11.8) and with a BMI between 11.3 and 35.3 (MBMI z-score = 0.42). Confirmatory Factor Analysis demonstrated an adequate fit for the original one-factor model (χ2 (104) = 182; p < 0.001; CFI = 0.97; TLI = 0.97; NFI = 0.94; SRMR = 0.101; RMSEA = 0.074; 95% CI [0.056; 0.091]). Food addiction was positively correlated with higher grazing (r = 0.69, p < 0.001) and negatively correlated with lower reliance on hunger/satiety cues (r = -0.22, p = 0.015). No significant association was found between food addiction and BMI z-score, or between food addiction and age. The results support the use of dYFAS-C 2.0 as a valid and reliable measure for assessing food addiction in Portuguese adolescents and pre-adolescents. Furthermore, the findings highlight that food addiction may be part of a spectrum of disordered eating behaviors associated with control impairment. Future research with a larger sample size could further elucidate the associations between food addiction and other variables, such as psychological distress and multi-impulsive spectrum behaviors.

While the construct of food addiction has been controversial, there is growing evidence that certain foods can activate biobehavioral and neurological mechanisms consistent with addiction to other substances. Despite increased evidence and acceptance of certain foods as addictive substances amongst the scientific community, there is a paucity of interventions available that are uniquely suited for the treatment of this condition. Further, many of the addiction and disordered eating treatment models currently utilized for food addiction are seemingly at odds, with the former often recommending complete abstinence from trigger foods and the latter promoting intake of all foods in moderation. The Food Addiction Clinical Treatment (FACT) manual was created as an alternative using an empirically supported harm-reduction model specifically targeted to treat the addiction and disordered eating features of food addiction. The purpose of the current article is to expose readers to the key tenets of the FACT manual, demonstrate the feasibility of this intervention with a sample of participants with severe food addiction, and discuss future directions for the treatment of food addiction. Positive outcomes from this intervention provide preliminary evidence for the efficacy of FACT for the treatment of food addiction with minimal negative adverse effects. Future research using randomized control trials and longer follow-up is needed to validate the FACT manual as an empirically supported treatment for food addiction.

OBJECTIVE: Following vertical sleeve gastrectomy (VSG), the role of eating behaviors in weight regain remains unclear. This study aimed to examine the effects of VSG on excess weight loss (EWL) and five eating-related variables (food addiction, disinhibition, susceptibility to hunger, dietary restraint, and weight concern) while exploring their associations before and eight months post-surgery.
METHODS: A sample of 76 participants who underwent VSG was recruited from a healthcare center in Quebec, Canada. Measurements included body mass index (BMI), the Eating Disorder Examination (weight concern), the Yale Food Addiction Scale (food addiction), and the Three-Factor Eating Questionnaire (disinhibition, susceptibility to hunger, and dietary restraint). T-tests were conducted between pre-surgery (T0) and eight-month post-surgery (T8), and correlations were examined between T0 and T8, within T0, and within T8.
RESULTS: The mean EWL was 63.43% ± 13.14 at T8. Comparisons between T0 and T8 showed a significant decrease in food addiction, disinhibition, and susceptibility to hunger (p = 0.001-0.005). No significant differences were observed for dietary restraint and weight concerns. BMI at T0 was negatively correlated with EWL at T8 (r = -0.45). Within T0, a negative correlation was observed between food addiction and dietary restraint (r = -0.42), which changed from negative to positive within T8 (r = 0.35).
CONCLUSIONS: This study confirmed that VSG is effective for weight loss and associated with a reduction in maladaptive eating behaviors. Postsurgery, individuals with greater food addiction exhibited more dietary restraint, suggesting a need for restraint among those experiencing a strong drive toward food. However, weight concerns remained high even after significant weight loss, indicating that weight loss alone may not be sufficient for change. A postsurgery medical follow-up focusing on overall well-being and lifestyle adaptation would be a crucial complement.

Food addiction, or ultra-processed food addiction (UPFA), has emerged as a reliable and validated clinical entity that is especially common in individuals seeking treatment for eating disorders (EDs), substance use disorders (SUDs) and co-occurring psychiatric disorders (including mood, anxiety and trauma-related disorders). The clinical science of UPFA has relied on the development and proven reliability of the Yale Food Addiction Scale (YFAS), or subsequent versions, e.g., the modified YFAS 2.0 (mYFAS2.0), as well as neurobiological advances in understanding hedonic eating. Despite its emergence as a valid and reliable clinical entity with important clinical implications, the best treatment approaches remain elusive. To address this gap, we have developed and described a standardized assessment and treatment protocol for patients being treated in a residential program serving patients with psychiatric multi-morbidity. Patients who meet mYFAS2.0 criteria are offered one of three possible approaches: (1) treatment as usual (TAU), using standard ED treatment dietary approaches; (2) harm reduction (HR), offering support in decreasing consumption of all UPFs or particular identified UPFs; and (3) abstinence-based (AB), offering support in abstaining completely from UPFs or particular UPFs. Changes in mYFAS2.0 scores and other clinical measures of common psychiatric comorbidities are compared between admission and discharge.

Common psychiatric disorders (CPDs) and depression contribute significantly to the global epidemic of type 2 diabetes (T2D). We postulated a possible pathophysiological mechanism that through Bridge-Symptoms present in depression and CPDs, promotes the establishment of emotional eating, activation of the reward system, onset of overweight and obesity and, ultimately the increased risk of developing T2D. The plausibility of the proposed pathophysiological mechanism is supported by the mechanism of action of drugs such as naltrexone-bupropion currently approved for the treatment of both obesity/overweight with T2D and as separate active pharmaceutical ingredients in drug addiction, but also from initial evidence that is emerging regarding glucagon-like peptide 1 receptor agonists that appear to be effective in the treatment of drug addiction. We hope that our hypothesis may be useful in interpreting the higher prevalence of CPDs and depression in patients with T2D compared with the general population and may help refine the integrated psychiatric-diabetic therapy approach to improve the treatment and or remission of T2D.