Eating disorders are severe mental disorders with a high mortality rate - suicidality - and a high incidence in adolescence and early adulthood, especially in women. The course of these disorders is uncertain and treatment outcomes are limited, with successful outcomes in 50-75% of cases. For bulimia nervosa (BN) and binge eating disorder (BED), several factors, such as duration of the disorder, eating and general psychopathology, dysfunctional personality traits and cognitive impairment, have been found to be associated with treatment adherence and response. In anorexia nervosa (AN) and atypical ED (OSFED), treatment response is poorer, with higher dropout rates and longer duration and chronicity. In this presentation, we will describe recent prospective observational studies in large samples of EDs analysing clinical, personality and cognitive predictors of treatment response in eating disorders, as well as potential associated neurobiomarkers. Optimisation of health care resources and transitions, as well as early and effective personalised treatments, can change the trajectory of EDs.

F. Fernandez-Aranda Grant / Research support from: We thank CERCA Programme/Generalitat de Catalunya for institutional support. We also want to thank the Institut d’Investigació Biomèdica de Bellvitge (IDIBELL) and ISCIII (CIBERobn is its initiative). This research was supported by grants from Instituto de Salud Carlos III (ISCIII) (FIS PI20/00132) and co-funded by FEDER funds/European Regional Development Fund (ERDF), a way to build Europe.Additional support was received from the Delegación del Gobierno para el Plan Nacional sobre Drogas (2021I031) and Ministerio de Ciencia e Innovación (grant PID2021-124887OB-I00), but also AGAUR-Generalitat de Catalunya (2021-SGR-00824), European Union’s Horizon 2020 research and innovation program under Grant agreement no. 847879 (PRIME/H2020, Prevention and Remediation of Insulin Multimorbidity in Europe) and the European Union’s Horizon Europe research and innovation program under grant agreement No 101080219 (eprObes)., Consultant of: FFA received consultancy and speakers honoraria from Novo Nordisk.

Extreme eating and weight conditions (EWC) are a construct that emerges as a dimensional and theoretical model that identifies individuals who exhibit inappropriate eating behaviours and abrupt weight fluctuations. According to this spectrum of EWC, one extreme can be represented by individuals with anorexia nervosa (AN), characterised by excessive food restriction and an extremely low body mass index (BMI), whereas the other end of this continuum is represented by individuals with obesity (OB), characterised by a BMI above 30. In addition to AN and OB, some eating disorders (EDs), namely bulimia nervosa and binge eating disorder, are also part of this continuum, given the high risk of falling into one of the extremes, especially that of higher BMI. Studies have described similar changes at the psychological and neurobiological levels associated with their abnormal eating patterns, delineating vulnerability pathways related to the neurobiological basis.

Based on previous literature, individuals suffering from EWC would show dysfunctional brain activity in regions associated with emotional reward processing and cognitive control compared to healthy controls (HC). Similarly, neuroendocrine alterations in EWC are expected to influence clinical symptomatology. It will also be discussed how impairments in executive function and differential brain activity observed in individuals with EWC may negatively impact their clinical course and treatment outcome.

F. Fernandez-Aranda: None Declared, S. Jimenez- Murcia Grant / Research support from: We thank CERCA Programme/Generalitat de Catalunya for institutional support. This research was supported by grants from Instituto de Salud Carlos III (ISCIII) (FIS PI20/00132) and co-funded by FEDER funds/European Regional Development Fund (ERDF), a way to build Europe. CIBERObn is an initiative of ISCIII. Additional support was received from the Delegación del Gobierno para el Plan Nacional sobre Drogas (2021I031) and Ministerio de Ciencia e Innovación (grant PID2021-124887OB-I00). Additional funding was received by AGAUR-Generalitat de Catalunya (2021-SGR- 00824), European Union’s Horizon 2020 research and innovation program under Grant agreement no. 847879 (PRIME/H2020, Prevention and Remediation of Insulin Multimorbidity in Europe) and the European Union’s Horizon Europe research and innovation program under grant agreement No 101080219 (eprObes)., Consultant of: FFA and SJM received consultancy and speakers honoraria from Novo Nordisk.

Numerous studies point to the comorbidity between gambling disorder (GD) and attention deficit hyperactivity disorder (ADHD). However, there is a lack of research exploring how ADHD symptoms might influence psychological treatment outcomes for GD.

Therefore, we aimed to explore differences between patients with GD with and without ADHD symptoms regarding psychopathology, personality, sociodemographic and especially treatment outcome measures.

This longitudinal study included n=170 patients with GD receiving 16 sessions of cognitive behavioral therapy (CBT) in a specialized unit of a public hospital. Multiple self-reported instruments were used to assess GD severity, personality, ADHD and other symptoms and sociodemographic measures prior to treatment.

A clinical profile characterized by greater GD severity, higher psychopathology and impulsivity, and less adaptive personality features was observed in patients with self-reported ADHD symptoms compared to those without. No significant differences in treatment response (measured by dropout and relapse rates) were reported between the two groups. However, patients with ADHD symptoms described more severe relapses (more money gambled) and GD patients who relapsed scored higher on measures of ADHD, particularly inattention.

Individuals with GD and ADHD may experience more severe relapses following treatment, suggesting a need for more vigilant follow-up and interventions for patients with this comorbidity.

C. Vintró-Alcaraz: None Declared, G. Mestre-Bach: None Declared, R. Granero: None Declared, M. Gómez-Peña: None Declared, L. Moragas: None Declared, F. Fernández-Aranda Consultant of: Novo Nordisk and editorial honoraria as EIC from Wiley, M. Potenza Consultant of: Opiant Pharmaceuticals, Idorsia Pharmaceuticals, AXA, Game Day Data, Baria-Tek and the Addiction Policy Forum; has been involved in a patent application with Yale University and Novartis; has received research support (to Yale) from Mohegan Sun Casino and Connecticut Council on Problem Gambling; and has consulted for and/or advised gambling and legal entities on issues related to impulse-control/addictive disorders, S. Jiménez-Murcia: None Declared

The neurobiology of gambling disorder (GD) is not yet fully understood. Although dysfunctional signalling involved in energy homeostasis has been studied in substance use disorders, it should be examined in detail in GD.

To compare different endocrine and neuropsychological factors between individuals with GD and healthy controls (HC), and to explore endocrine interactions with neuropsychological and clinical variables.

A case-control design was performed in 297 individuals with GD and 41 HC, assessed through a semi-structured clinical interview and a psychometric battery, adding 38 HC in the evaluation of endocrine and anthropometric variables.

Individuals with GD presented higher fasting plasma ghrelin (p<.001) and lower LEAP2 and adiponectin concentrations (p<.001) than HC adjusting for body mass index (BMI). The GD group reported higher cognitive impairment regarding cognitive flexibility and decision-making strategies, a worse psychological state, higher impulsivity levels, and a more dysfunctional personality profile. Despite failing to find significant associations between endocrine factors and either neuropsychological or clinical aspects in GD, some impaired cognitive dimensions and lower LEAP2 concentrations significantly predicted GD presence.

This study suggests distinctive neuropsychological and endocrine dysfunctions may operate in individuals with GD, predicting GD presence. Further exploration of endophenotypic vulnerability pathways in GD appear warranted, especially with respect to etiological and therapeutic potentials.

F. Fernandez-Aranda Consultant of: Novo Nordisk , Employee of: editorial honoraria as EIC from Wiley, I. Baenas: None Declared, M. Etxandi : None Declared, B. Mora-Maltas: None Declared, R. Granero : None Declared, S. Tovar : None Declared, C. Diéguez: None Declared, M. Potenza Grant / Research support from: Mohegan Sun Casino and Connecticut Council on Problem Gambling, Consultant of: Opiant Pharmaceuticals, Idorsia Pharmaceuticals, Baria-Tek, AXA, Game Day Data and the Addiction Policy Forum; has participated in surveys, mailings or telephone consultations related to drug addiction, impulse control disorders or other health topics; and has consulted for law offices and gambling entities on issues related to impulse control or addictive disorders, Employee of: patent application in Yale University and Novartis, S. Jiménez-Murcia: None Declared.

Gambling Disorder (GD) is considered a multifactorial behavioral addictive disorder, leading to severe psychological, social and economic consequences. Previous studies have investigated genetic mechanisms underlying GD. Growing literature showed a possible link between addiction-related disorders and neurotrophic factors (NTF), involved in synaptic plasticity and neuronal survival. Thus, the study of NTF genes emerged as promising targets in the field of GD.

To evaluate genetic implications of the NTF family in the pathophysiology GD. We hypothesized the involvement of some NTF genes polymorphisms in the onset and progression of GD as potential biological risk factors.

The sample was composed by 166 individuals with GD and 191 healthy controls. 36 Single nucleotide polymorphisms (SNPs) from NTF (NGF, NGFR, NTRK1, BDNF, NTRK2, NTF3, NTRK3, NTF4, CNTF and CNTFR) were selected and genotyped. Linkage disequilibrium and haplotype constructions were assessed, related to the presence of GD. Moreover, regulatory elements overlapping the identified SNPs variants associated with GD was also analyzed.

6 SNPs were potentially associated to GD after the comparisons of allele frequencies between groups. Single and multiple-marker analyses showed a strong association between both NTF3 and NTRK2 genes, and GD.

This study suggests the implication of NTF genes in the development of GD, being the altered cross-regulation of some NTF factors signalling pathways, a potential biological vulnerability factor in GD. Fundings and Acknowledgements: Ministerio de Ciencia, Innovación y Universidades (RTI2018-101837-B-100) Delegación del Gobierno para el Plan Nacional sobre Drogas (2017I067, 2019I47), Instituto Salud Carlos III (ISCIII) (PI17/01167, PI20/00132) and CIBERObn, an initiative of ISCIII.

No significant relationships.

Gambling disorder (GD) is characterized by repeated problematic gambling behavior associated with unsuccessful and uncontrollable urges to keep gambling, which leads to considerable distress and impairment. Several types of interventions exist to treat GD, with cognitive behavior therapy (CBT) being one of the most widely used approaches.

To estimate trajectories of the gambling disorder (GD) severity for 12 months following a manualized cognitive-behavior-therapy (CBT) program, and to identify the main variables associated with each trajectory.

Latent Class Growth Analysis examined the longitudinal changes of n = 603 treatment-seeking patients with GD.

Five separate empirical trajectories were identified: T1 (n = 383, 63.5%) was characterized by the most highest baseline gambling severity levels and positive progress to recovery during the follow-up period; T2 (n = 154, 25.5%) featured participants with high baseline gambling severity and good progress to recovery; T3 (n = 30, 5.0%) was made up of patients with high gambling baseline severity and slow progress to recovery; T4 (n = 13, 2.2%) and T5 (n = 23, 3.8%) contained participants with high baseline gambling severity and moderate (T4) and poor (T5) progress in GD severity during the follow-up. Psychopathology, personality traits, poor compliance and relapses discriminated between trajectories.

These results show that treatment seeking patients with GD are heterogeneous. In addition, the obtained findings could be useful in the design of more efficient interventions for this behavioral addiction. Funding oftained from RTI2018-101837B-I00

No significant relationships.

COVID19 lockdown is having a significant impact on mental health, patients with eating disorders (ED) are particularly vulnerable.

1) To explore changes in eating and other psychological features due to confinement in patients with ED from various European and Asian countries; and 2) to assess differences related to diagnostic subtypes, age and geography.

The sample comprised 829 participants, diagnosed with an ED according to DSM-5 criteria from specialized ED units in Europe and Asia. Participants were assessed using the COVID19 Isolation Scale (CIES).

On one hand, patients with Binge Eating Disorder experienced the highest impact on weight and ED symptoms due to confinement. Together with subjects diagnosed with Other Specified Feeding and Eating Disorders (OFSED), they also experienced a deterioration in general psychological state. On the other hand, there was less symptomatic impact on people with Bulimia Nervosa or Anorexia Nervosa and asian and younger individuals appeared to be more resilient in this situation.

The impact of COVID varied by cultural context and individual variation in age and form of illness. Services may need to target preventive measures and adapting therapeutic approaches for the most vulnerable patients.

No significant relationships.

Hepatic ones are some of the most described somatic complications in anorexia nervosa (AN) affected patients. They can be due to malnutrition, which is the more usual thing, or due to re-feeding. The first one can lead to more marked elevations of the hepatic enzymes, especially alanine-aminotransferase (ALT). It’s been also described the relation between a sharply decreased body mass index (BMI) and this kind of complications, but there are still to determine more predictors.

Identifying clinical predictors of hepatic complications in AN.

We analysed data from 71 AN affected patients hospitalized at Bellvitge Hospital from January 2016 to October 2021. We used IBM SPSS Statistics 22 to do all the statistics in this work.

The medium age of the sample was 27.66 years with 10.8 years of evolution of AN. The medium BMI was 13.88. 33.80% of them had some sort of hepatic enzymes elevation, two of them a several one. AST, ALT and ALP were significantly more elevated in those patients with lower BMI. GGT was significantly more elevated in patients with more years of disorder development. We didn’t identify correlation between any purgative method and hepatic alterations.

The elevation of ALT, AST and ALP seems to be related with the BMI of the patients, while the elevation of the GGT turns out to be related to the time of evolution of the eating disorder. Purgative methods don’t seem to be related to the development of hepatic alterations in AN.

No significant relationships.

FFA received consultancy honoraria from Novo Nordisk and editorial honoraria as EIC from Wiley. The rest of the authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of

Neuroimaging findings have reported aberrant functional connectivity in brain regions involved reward system in individuals with anorexia nervosa (AN) altering hedonic processing over food. Likewise, endocannabinoids such as Anandamide (AEA) and 2-Arachidonoylglycerol (2-AG) have been involved in rewarding aspects of food intake.

To identify nucleus accumbens (NAcc) functional connectivity with whole-brain comparing between individuals with AN and controls. Furthermore, in a sub-study, to explore the interaction between NAcc functional connectivity and peripheral AEA and 2-AG levels.

A total of 60 adult women (18 to 56 years of age) took part in the present study. Twenty-six individuals belonged to the AN group (BMI<18) and 34 to the HC group (BMI=18-24.99). All participants underwent functional magnetic resonance in resting-state, and blood samples were obtained in fasting.

Negative functional connectivity was observed in the AN group compared with the control group between the NAcc and the cerebellum (pFWE<.001), between the NAcc and the insula (pFWE<.001), between the NAcc and the supramarginal gyrus (pFWE=.019), and between the NAcc and the postcentral gyrus (pFWE=.010). Analyses exploring the association between NAcc functional connectivity and peripheral endocannabinoids levels displayed altered NAcc-cerebellum functional connectivity was negatively associated with peripheral 2-AG levels in the AN group (r= -.553; p=.011).

Understanding the interaction between the reward system and peripheral endocannabinoids in patients with AN could contribute to better elucidate the pathophysiology of this disorder. Future studies will need to further investigate the clinical and therapeutic implications of these findings in patients with AN.

No significant relationships.

Despite a wide range of proposed risk factors and theoretical models, prediction of eating disorder (ED) onset remains poor. This study undertook the first comparison of two machine learning (ML) approaches [penalised logistic regression (LASSO), and prediction rule ensembles (PREs)] to conventional logistic regression (LR) models to enhance prediction of ED onset and differential ED diagnoses from a range of putative risk factors.

Data were part of a European Project and comprised 1402 participants, 642 ED patients [52% with anorexia nervosa (AN) and 40% with bulimia nervosa (BN)] and 760 controls. The Cross-Cultural Risk Factor Questionnaire, which assesses retrospectively a range of sociocultural and psychological ED risk factors occurring before the age of 12 years (46 predictors in total), was used.

All three statistical approaches had satisfactory model accuracy, with an average area under the curve (AUC) of 86% for predicting ED onset and 70% for predicting AN v. BN. Predictive performance was greatest for the two regression methods (LR and LASSO), although the PRE technique relied on fewer predictors with comparable accuracy. The individual risk factors differed depending on the outcome classification (EDs v. non-EDs and AN v. BN).

Even though the conventional LR performed comparably to the ML approaches in terms of predictive accuracy, the ML methods produced more parsimonious predictive models. ML approaches offer a viable way to modify screening practices for ED risk that balance accuracy against participant burden.

The Diagnostic and Statistical Manual of Mental Disorders-5 (DSM-5) introduced severity indices for Eating Disorders (ED).

This study assessed in a male ED sample the DSM-5 severity indices for Anorexia Nervosa (AN), Bulimia Nervosa (BN) and Binge Eating Disorder (BED) and compared them to an alternative transdiagnostic drive for thinness (DT) severity category and a combined DSM-5/DT severity categorization

178 males with EDs were classified using: a.) a DT categorisation based on the EDI-2 DT subscale; b.) the DSM-5 severity categories for AN, BN and BED and c.) a combination of the DT and the DSM-5 severity categorisation. These severity classifications were then compared based on psychopathology and personality.

For the DSM-5 severity indices, the “mild” category was most prevalent for AN and BN, and the “moderate to extreme” group for BED. For the EDI-2 DT severity classification, the “mild” category was overrepresented in all subtypes. For the combined DSM-5/DT categorization, the “mild combined” severity group was the most prevalent for AN, while for BN and BED the “severe/extreme” combined group was most prevalent. Clinically significant findings were strongest for the DT categorization followed by the combined DSM-5/DT approach. Almost non-significant findings were revealed for the DSM-5 severity categories for all ED subtypes. These findings were most pronounced for AN and BN and almost non-existent for BED.

Our findings provide support for DT as an alternative transdiagnostic severity category for EDs in males that may be more meaningful than the DSM-5 severity indices for AN and BN, but not BED.

No significant relationships.

The DSM-5 introduced severity indicies for the first time.

We conducted a systematic review and synthesis the frequency of each DSM-5 severity categories (i.e., mild, moderate, severe and extreme severe) for Anorexia Nervosa (AN), Bulimia Nervosa (BN) and Binge Eating Disorders (BED), and to evaluate studies that assess the clinical utility of these severity specifiers for all eating disorders (ED) subtypes.

Five databases (EMBASE, MEDLINE, PsycARTICLES, PsycINFO, and ProQuest) were used to identify for both academic and grey literature published from 2013 until July 8, 2020. Twenty-five studies were retrieved for the systematic review based on the inclusion and exclusion criteria, and up to six studies were qualified for meta-analysis

We found limited support for the current DSM-5 severity ratings for all ED indices, as the majority of ED severity groups were not significantly distinguishable in overall ED psychopathology (mean effect size ranged from .02 to .5). The value of the DSM-5 severity ratings was further devalued as 56.91% to 80.52% of individuals with AN, BN, and BED were categorized into mild and moderate groups. However, there was significant heterogeneity between the studies (p< .001), and some of these heterogeneities were explained by differences in study settings and measurement of eating disorder psychopathology.

Overall, the current study provided little support for the DSM-5 severity ratings for EDs, thus it is suggested that further exploration in alternative severity classification approach is needed.

No significant relationships.

Anandamide (AEA) and 2-Arachidonoylglycerol (2-AG) play a pivotal role in food intake and reward aspects of feeding. Aberrant functioning in the endocannabinoid system has been observed in patients with eating disorders (EDs). This dysfunction may influence the incentive processes stimulating behaviors towards food acquisition or the hedonic evaluation of ingested food.

The aims of this study are to compare fasting peripheral levels of AEA and 2-AG in ED patients, obese subjects (OB) and healthy controls (HCs), and to explore their association with clinical and anthropometric variables.

The sample included a total of 63 adult women. Peripheral blood samples were collected to investigate fasting levels of AEA and 2-AG in 31 ED patients: 22 Anorexia Nervosa (AN) and 9 Binge Eating Disorder (BED), compared to 21 OB and 11 HCs. Several clinical and anthropometric variables were also assessed.

Comparing groups, significant differences in AEA levels were found (p=0.001). Specifically, individuals with AN exhibited lower AEA than OB (p<0.001) and BED (p=0.007), while OB showed higher AEA than HCs (p=0.015). 2-AG was positively correlated with hostility dimension in EDs and negatively associated with impulsive traits in OB. AEA showed a direct association with body dissatisfaction in AN, contrary to OB. Finally, in AN, AEA negatively correlated with the body mass index, while 2-AG was positively associated with the fat mass.

These results suggest an interaction between biological and clinical factors defining a vulnerability pathway that could help fitting personalized therapeutic approaches in each condition.

No significant relationships.

To examine whether drug use (DU) is higher in people with eating disorders (EDs) than in matched comparison groups and to collate, summarize and perform a meta analysis where possible on the literature related to DU in people with EDs.

We searched electronic databases including Medline, PsycINFO, Web of Science and CINAHL and reviewed studies published from 1994 to August, 2007, in English, German or Spanish against a priori inclusion/exclusion criteria. A total of 248 papers were eligible for inclusion. Only a total of 16 papers fulfilled all the inclusion criteria and were finally included in the systematic review.

The meta-analysis including all the different drugs for every sort of ED revealed a negligible albeit significant (z=2.34, p<.05), pooled standardized effect size of 0.119. The data showed a high degree of heterogeneity across the studies (X2(74)= 1267.61, p<.001). When ED subdiagnoses were assessed individually, DU was found to be higher in people with bulimia nervosa (BN) as a moderate sized increase in DU was found in this ED subtype (δ =0.462, z=6.69, p=<.001). People with binge eating disorder (BED) had a small increased risk of DU (δ =0.14, z=2.28, p<.05). In contrast, people with anorexia nervosa (AN) had a lower risk of DU (δ=-.167, z=1.81, p=.070, p=NS).

The differential risk observed in BN patients might be related to differences in temperament or might be the result of reward sensitisation as a result of the ED behaviours specifically associated with BN.

The research on the aetiology of eating disorders (EDs) has implicated many apparently disparate risk factors, which include: biochemical, genetic, familial and psychological factors. In the environmental domain, the presence of particular traits such as perfectionism, comorbidity in the family, eating patterns during childhood and exposures to adverse events have been revealed to be implicated in the aetiology of EDs. Whereas, from a biological point of view some recent new findings have suggested the important role of genetic factors, in combination with share and non-share environmental factors, developmental factors seems to have also a crucial role in the development of EDs later in life.

In order to replicate these findings in a larger sample, we performed several combined population (case-control) and family-based studies of eight independently recruited samples from several European countries participating in the European Community Framework V “Factors in Healthy Eating” project. We analyzed as well genetic as environmental factors, but also developmental factors that might be implicated.

The findings of our studies agree with the growing body of research indicating that a variety of environmental and social factors are associated with unhealthy individual and family eating patterns during childhood and early adolescence, and which if not detected early could result in the development of a subsequent eating disorder.

Explore the prevalence of lifetime suicide attempts in women with bulimia nervosa (BN), and compare eating disorder symptoms, general psychopathology, impulsivity, personality, and genetic variants in four candidate genes of the serotonin pathway: the serotonin transporter (SLC6A4), serotonin receptors 1A (HTR1A) and 2A (HTR2A) and tryptophan hydroxylase 1 (TPH1) between individuals who had and had not attempted suicide. Determine the best predictors of suicide attempts.

566 consecutively admitted BN outpatients (417 BN purging, 47 BN non-purging and 102 subthreshold BN). Patients completed a comprehensive assessment battery.

Lifetime prevalence of suicide attempts was 26.9% CI 95%: 23.2 to 30.5). BN subtype was not associated with lifetime suicide attempts (p=0.36). Compared to non-attempters, attempters exhibited higher unemployment, eating disorder symptomatology, general psychopathology, previous eating disorder treatment, impulsive behaviors, and lower educational level (p<0.004). In relation to personality traits, suicide attempters exhibited significantly (p<0.002) higher Harm Avoidance and lower Self-directedness, Reward Dependence and Cooperativeness. No significant differences in any of the genetic variants between attempters and non-attempters. The best predictors of suicide attempts were (p<0.006): lower education, minimum BMI, previous eating disorder treatment, family history of alcoholism and self-directedness.

Suicidality in BN patients appears to be within the range previously found. Our results support that internalizing personality traits combined with impulsivity may increase the probability of engaging in suicidal behaviors in these patients. Our data do not support the hypothesis that variants of SLC6A4, HTR1A, HTR2A or TPH1 are associated with suicide attempts in BN individuals.