Anorexia Nervosa Research Articles

Common and distinct neural patterns of gray matter alterations in adults with anorexia nervosa and obsessive-compulsive disorder.

Anorexia nervosa (AN) and obsessive-compulsive disorder (OCD) often share multiple similar symptoms and are highly comorbid; however, the common and distinct brain neuroanatomy of these two diseases are unclear. The current study attempted to identify the overlapping and different gray matter volume (GMV) between AN and OCD. We conducted a voxel-wise meta-analysis of GMV using the latest Seed-based d Mapping with Permutation of Subject Images Toolbox (SDM-PSI) software. Compared to healthy controls, patients with AN showed reduced GMV in supplementary motor areas, median cingulate cortices, the left cerebellum, right Rolandic operculum (RO), right insula, right superior temporal gyrus (STG), and right precuneus, while OCD patients were characterized by low GMV in the right insula, STG, RO, and inferior frontal gyrus (IFG). The conjunctional analysis indicated that these two disorders have overlapping structural abnormalities in the right insula, STG, RO and IFG. No distinct GMV alteration was found. These common structural brain abnormalities may underlie the neuropathology of the similar neuropsychological features and highly comorbid manifestations of AN and OCD.

Causal associations between immune cells and psychiatric disorders: a bidirectional mendelian randomization analysis.

Extensive researches illuminate a potential interplay between immune traits and psychiatric disorders. However, whether there is the causal relationship between the two remains an unresolved question. We conducted a two-sample bidirectional mendelian randomization by utilizing summary data of 731 immune cell traits from genome-wide association studies (GCST90001391-GCST90002121)) and 11 psychiatric disorders including attention deficit/hyperactivity disorder (ADHD), anxiety disorder, autism spectrum disorder (ASD), bipolar disorder (BIP), anorexia nervosa (AN), major depressive disorder (MDD), obsessive-compulsive disorder (OCD), Tourette syndrome (TS), post-traumatic stress disorder (PTSD), schizophrenia (SCZ), and substance use disorders (cannabis) (SUD) from the Psychiatric Genomics Consortium (PGC). A total of four types of immune signatures (median fluorescence intensities [MFI], relative cell [RC], absolute cell [AC], and morphological parameters [MP]) were included. Effect estimates were obtained by using the inverse-variance-weighted (IVW), weighted median method, Mendelian randomization (MR)-Egger, and corrected by false discovery rate. Outliers were evaluated through the leave-one-out technique. Horizontal pleiotropy was assessed using the MR pleiotropy residual sum and outlier (MR-PRESSO) and MR-Egger intercept tests. MR analysis results suggested several immune cell subtypes were casually associated with psychiatric disorders. It was found that CD33br HLA DR + CD14 - AC (Myeloid cell, AC) may contribute to decreasing the risk of BIP (odds ratio [OR] = 0.9179, confidence interval [CI] = 0.8829-0.9542, PFDR = 7.06 × 10-3), and likewise, CD38 on transitional (B cell, MFI) also showed negative causal effect on SCZ risk (OR = 0.9551, CI = 0.9330-0.9776, PFDR = 0.0441). While IgD - CD27 - %lymphocyte (B cell, RC) has causal effect on increasing BIP risk (OR = 1.0184, CI = 1.0079-1.0291, PFDR = 0.0201). In addition, HLA DR + + monocyte %monocyte (TBNK, RC) is likely to increase AN onset (OR = 1.0746, CI = 1.0324-1.1186, PFDR = 0.0506), and CCR2 on CD14 - CD16 + monocyte (Monocyte, MFI) may contribute to PTSD (OR = 1.0591, CI = 1.0275-1.0917, PFDR = 0.0369). Sensitivity analysis revealed consistency of results. Our research elucidates there may be causal links between immune traits and the onset of psychiatric disorders, which established a groundwork for the prospective clinical utilization of immune cells as markers for the diagnosis and early intervention of psychiatric disorders.

Prevention of refeeding syndrome: Evaluation of an enteral refeeding protocol for severely undernourished children.

Refeeding syndrome (RS) defines the deleterious clinical and metabolic changes occurring during nutritional support of severely malnourished patients. Pediatric guidelines to prevent and treat RS are scarce and highly variable. This study aimed to evaluate the effectiveness and safety of an enteral refeeding protocol in severely undernourished hospitalized children with anorexia nervosa (AN) or organic diseases (OD). This ancillary study to the Preventing Malnutrition and Restoring Nutritional Status in Hospitalized Children (PREDIRE) trial (NCT01081587), included severely undernourished children hospitalized between January 2010 and June 2018 and treated with an enteral refeeding protocol drafted for the study. The effectiveness was assessed by weight gain and safety by clinical and laboratory abnormality occurrence over the initial 3-week refeeding period, which represents the most critical period for the development of RS. After 3 weeks of refeeding, the mean weight for height ratio increased from 72% to 82%, and half of the patients with severe undernutrition improved their nutritional status. The prevalence of RS was 10.4%. No clinical cardiac or neurological complication occurred. The most frequent laboratory complication was hypophosphatemia in 13.7% of patients; but symptomatic in only two patients (2.5%). Compared with patients with OD, patients with AN improved their weight-for-height ratio faster without significantly more frequent complications, except for hepatic cytolysis which was less prevalent in AN (8.3% vs. 36.8%). The proposed enteral refeeding protocol appears safe for treating severely undernourished children of different etiologies, with a low prevalence of RS and half of the patients recovered from severe malnutrition within a 3-week period.

Comparing social stigma of anorexia nervosa, bulimia nervosa, and binge-eating disorder: A quantitative experimental study

BackgroundCurrently, we know little regarding how stigma attributed to eating disorders compares to that of other psychological disorders and additionally within different types of eating disorders. In the current study, we aimed to explore the stigmatisation of eating disorders by comparing the stigma attributed to anorexia nervosa, bulimia nervosa, and binge-eating disorder, utilising depression as a comparative control.MethodsA total of 235 participants from the general population were randomly assigned to an anorexia nervosa, bulimia nervosa, binge-eating disorder, or depression condition. Participants responded to a questionnaire consisting of several adapted versions of pre-existing subscales that measured levels of stigma associated with psychological disorders generally, as well as stigma associated with eating disorders specifically. We used several one-way analyses of variance to investigate the differences in stigma attributed towards the aforementioned psychological disorders.ResultsResults suggested that all three eating disorders were significantly more stigmatised than was depression. Between the eating disorders, the three were generally equivalent except that binge-eating disorder was significantly more stigmatised than both anorexia nervosa and bulimia nervosa on a subscale measuring trivialness.ConclusionsThese findings indicate that individuals with eating disorders, including binge-eating disorder, may be at a higher risk of experiencing the negative implications of stigma when compared to other psychological disorders, such as depression. To our knowledge, this study is one of few that directly quantify and compare stigma attributed towards anorexia nervosa, bulimia nervosa, and binge-eating disorder. Through further research, a better understanding around the expression of stigma towards specific eating disorders could inform the development of targeted interventions to help reduce the stigma associated with these disorders. This knowledge could also advance the understanding of the lived experience of individuals living with eating disorders, subsequently informing treatment practices.

A Bitter Pill: The Ethics of Involuntary Treatment of Adolescents With Severe Eating Disorders.

Severe eating disorders (EDs) are a common and increasing threat to normal adolescent health and development. Major clinical challenges include longstanding malnutrition potentially complicated by emergent electrolyte disorders and cardiac dysfunction. The care of adolescents with severe EDs can lead to challenging decisions regarding the initiation of involuntary feeding with restraints. After describing a representative case, we present pertinent ethical challenges involved in the use of involuntary feeding with restraints in adolescents with severe EDs. These include the following: (1)the relationship of involuntary feeding with restraints to evolving adolescent autonomy; (2)why weak efficacy evidence should prompt individualization of involuntary treatment decisions; and (3)how unequal access to ED care complicates decision-making regarding involuntary feeding with restraints. To help clinicians characterize whether involuntary feeding with restraints is ethically permissible in a specific adolescent with severe anorexia nervosa (AN), we propose a 3-step decision-making guide that weighs case features such as magnitude of health threats, whether less invasive treatment options have been tried, patient decision-making capacity, prior response to similar therapies, caregiver support for the plan, and the availability of subsequent steps in expert ED care. Decisions to undertake involuntary feeding with restraints in adolescents with severe AN are intrinsically fraught, but this 3-step decision-making guide can help clinicians identify and weigh pertinent ethical tensions effectively and with transparency.

Pharmacological Dissection Identifies Retatrutide Overcomes the Therapeutic Barrier of Obese TNBC Treatments through Suppressing the Interplay between Glycosylation and Ubiquitylation of YAP.

Triple-negative breast cancer (TNBC) in obese patients remains challenging. Recent studies have linked obesity to an increased risk of TNBC and malignancies. Through multiomic analysis and experimental validation, a dysfunctional Eukaryotic Translation Initiation Factor 3 Subunit H (EIF3H)/Yes-associated protein (YAP) proteolytic axis is identified as a pivotal junction mediating the interplay between cancer-associated adipocytes and the response to anti-cancer drugs in TNBC. Mechanistically, cancer-associated adipocytes drive metabolic reprogramming resulting in an upregulated hexosamine biosynthetic pathway (HBP). This aberrant upregulation of HBP promotes YAP O-GlcNAcylation and the subsequent recruitment of EIF3H deubiquitinase, which stabilizes YAP, thus promoting tumor growth and chemotherapy resistance. It is found that Retatrutide, an anti-obesity agent, inhibits HBP and YAP O-GlcNAcylation leading to increased YAP degradation through the deprivation of EIF3H-mediated deubiquitylation of YAP. In preclinical models of obese TNBC, Retatrutide downregulates HBP, decreases YAP protein levels, and consequently decreases tumor size and enhances chemotherapy efficacy. This effect is particularly pronounced in obese mice bearing TNBC tumors. Overall, these findings reveal a critical interplay between adipocyte-mediated metabolic reprogramming and EIF3H-mediated YAP proteolytic control, offering promising therapeutic strategies to mitigate the adverse effects of obesity on TNBC progression.

Integrating the Patient Perspective into Healthcare and Real-World Evidence: The Multi-site, Cross-Disease, Patient-Centered Outcomes Research Project in the Medical Informatics Initiative (PCOR-MII)

Abstract This paper presents the Patient-Centered Outcomes Research within the Medical Informatics Initiative (PCOR-MII) project, focusing on the integration of patient-reported outcomes (PROs) into a large-scale national data sharing infrastructure, established in Germany by the Medical Informatics Initiative (MII). PCOR-MII aims to systematically address the interests of various stakeholders in patient-reported health data and three dimensions of clinical utility: (1) prediction, (2) monitoring, and (3) outcome assessment. The project builds upon harmonized technical, data, and compliance environments established at the participating institutions as part of the MII to deploy and roll out software solutions for capturing PROs and making them accessible within local electronic health record (EHR) systems. To overcome interoperability challenges, PCOR-MII is developing a construct-oriented PROM module for the Health Level 7 (HL7) Fast Healthcare Interoperability Resources (FHIR)–based German National Core Dataset. The project applies its approach to three patient populations with distinct characteristics: anorexia nervosa targeting risk prediction (dimension 1), kidney transplantation prioritizing health status and adherence monitoring (dimension 2), and persistent somatic symptoms primarily aimed at assessing and understanding outcomes (dimension 3). With their emphasis on different aspects of PROs, those application areas can serve as blueprints for a broader roll-out. PCOR-MII represents a structured and comprehensive effort to incorporate PROs into a national data infrastructure, promising more precise diagnostics, improved treatment decisions, and the generation of new biomedical insights. We believe that our structured approach may serve as a guiding framework for others aiming to implement PROs in diverse healthcare settings.

Exploring the Role of GLP-1 Receptor Agonists in Alzheimer’s Disease: A Review of Preclinical and Clinical Evidence

Glucagon-like peptide-1 receptor agonists (GLP-1RAs), including dulaglutide, liraglutide, semaglutide, and exenatide, are effective treatments for type 2 diabetes mellitus (T2DM) and obesity. These agents mimic the action of the endogenous incretin glucagon-like peptide-1 (GLP-1) by enhancing insulin secretion, inhibiting glucagon release, and promoting weight loss through appetite suppression. GLP-1RAs have recently been suggested to have neuroprotective effects, suggesting their potential as treatment for neurodegenerative disorders, such as Alzheimer’s disease (AD). AD and T2DM share several common pathophysiological mechanisms, including insulin resistance, chronic inflammation, oxidative stress, and mitochondrial dysfunction. These shared mechanisms suggest that therapeutic agents targeting metabolic dysfunction may also be beneficial for neurodegenerative conditions. Preclinical studies on GLP-1RAs in AD models, both in vitro and in vivo, have demonstrated promising neuroprotective effects, including reductions in amyloid-beta accumulation, decreased tau hyperphosphorylation, improved synaptic plasticity, and enhanced neuronal survival. Despite the encouraging results from preclinical models, several challenges need to be addressed before GLP-1RAs can be widely used for AD treatment. Ongoing clinical trials are investigating the potential cognitive benefits of GLP-1RAs in AD patients, aiming to establish their role as a therapeutic option for AD. This review aimed to examine the current literature on preclinical and clinical studies investigating GLP-1 receptor agonists as potential therapeutic agents for AD.

The brainstem reticular formation pivots abnormal neural transmission in the course of Anorexia Nervosa.

Anorexia nervosa (AN) represents an eating disorder, which features the highest rate of mortality among all psychiatric disorders. The disease prevalence is increasing steadily, and an effective cure is missing. The neurobiology of the disease is largely unknown, and only a few studies were designed to disclose specific brain areas, where altered neural transmission may occur. In AN behavioral alterations surpassing altered feeding are present, which often involve archaic behaviors finalized to the survival of the species. In fact, alterations of sleep and reward-driven behavior accompany the eating disorder, where a disruption of peripheral and central circadian rhythms occurs along with effortful behaviors, aberrant learning and mild cognitive impairment. Abnormal behavior often co-exists with a number of metabolic alterations in peripheral organs. The present article wishes to analyze the potential role of altered brain circuitry within the brainstem reticular formation during AN. In fact, this brain area contains neuronal nuclei and pathways, which are pivotal in connecting eating pattern with archaic behaviorsand autonomic activity within peripheral organs. A number of reticular nuclei releasing catecholamine and non-catecholamine neurotransmittersare evidenced in relationship with altered behavioral states and vegetative control to produce this psycho-metabolic disorder. The relevance of the reticular formation in sustaining the disorder is discussed in the light of developing effective therapeutic strategies.

The Ethics of Ozempic and Wegovy

Semaglutide, sold under the brand names of Ozempic, Rybelsus and Wegovy, is one of the most popular drugs on the market. Manufactured by Novo Nordisk, semaglutide is the newest in...

Changes in Circadian Rhythm in Chronically-Starved Mice Are Associated With Glial Cell Density Reduction in the Suprachiasmatic Nucleus.

Anorexia nervosa (AN) is an eating disorder characterized by severe weight loss and associated with hyperactivity and circadian rhythm disruption. However, the cellular basis of circadian rhythm disruption is poorly understood. Glial cells in the suprachiasmatic nucleus (SCN), the principal circadian pacemaker, are involved in regulating circadian rhythms. We hypothesize that the circadian rhythm disruption in AN patients is associated with glial cell changes in the SCN. In the starvation-induced hyperactivity mouse model, mice had free access to a running wheel and received a restricted amount of food once a day, until a 25% body weight loss was reached and maintained their weight loss for two weeks. This was followed by a refeeding phase. Different daily periods of running wheel activity were defined, such as food anticipatory activity up to 4 h before feeding. Circadian rhythmicity was analyzed using the cosinor method. Gene expression was evaluated using real-time polymerase chain reaction. Immunohistochemistry was used to quantify astrocytes, microglia, and oligodendrocytes. Starvation induced changes in circadian rhythm, as indicated by changes in cosinor-based characteristics. Refeeding reversed these effects. Additionally, there was an increase in cryptochrome circadian regulator 1 expression and a decrease in the density of astrocytes and oligodendrocytes in the SCN after chronic starvation. Starvation-induced alterations in circadian rhythms are associated with molecular, and cellular changes in the hypothalamus. Reduced astrocytes and oligodendrocytes in the SCN in a mouse model of AN suggest that glial pathophysiology may play a role in circadian rhythm disruption.

Navigating the Complexities of Managing Severe Anorexia Nervosa in a Medical Ward: A Case Report

Navigating the Complexities of Managing Severe Anorexia Nervosa in a Medical Ward: A Case Report

Clinicians' Experiences of Eating Disorder Focused Family Therapy With Autistic Young People.

Eating disorder focused family therapy (FT-ED) is the leading outpatient intervention for adolescents with Anorexia Nervosa. Autistic people report poorer eating disorder treatment experiences and may be at increased risk of inpatient admissions. There is a need to consider adaptions to eating disorder treatment for this population. The aim of this study is to explore the experiences of clinicians in the delivery of FT-ED for Autistic young people with Anorexia Nervosa and any adaptations currently being implemented. FT-ED trained clinicians who had experience of delivering this modality with young Autistic people and their families, were invited to take part in interviews. Transcripts were analysed using Reflexive Thematic Analysis. Eleven clinicians completed interviews and analysis generated four themes and eight subthemes: (1) Systemic context, (2) Raising potential autism, (3) Autism eating disorders crossover, (4) Manual versus adaptations. This paper is the first exploration of clinician's experience delivering FT-ED to Autistic young people and their families and highlighted unique considerations with this population. It is an initial step to consider adaptations to the FT-ED model, with the aim of making eating disorder treatments more effective, accessible and acceptable for Autistic young people and their families.

Oleanolic acid inhibits appetite through the TGR5/cAMP signaling pathway.

Inhibition of appetite is an effective approach to fight obesity. Recently, bile acids have been reported to suppress appetite and alleviate obesity via the Takeda G protein-coupled receptor 5 (TGR5). However, whether the downstream signaling molecule cyclic adenosine monophosphate (cAMP) of TGR5 is involved in this process remains unclear. Oleanolic acid (OA) is a plant analogue of bile acids. The study aimed to explore the effect of dietary OA supplementation on appetite and to examine the role of TGR5/cAMP signaling in this process. In our study, mice were divided into four treatment groups: basal diet, 50 mg/kg OA-supplemented diet, 100 mg/kg OA-supplemented diet, and 30 mg/kg tauroursodeoxycholic acid (TUDCA)-supplemented diet. Our results showed that dietary supplementation of OA and TUDCA both suppressed appetite. Additionally, OA and TUDCA downregulated the expression of appetite-stimulating factors while upregulating appetite-suppressing factors in the hypothalamus. Furthermore, OA was found to activate TGR5 signaling in the hypothalamus. Mechanistic studies using N38 cells revealed that OA reduced the expression and secretion of agouti-related peptide (AgRP), while inhibition of TGR5 and cAMP attenuated this effect of OA. In conclusion, our findings suggest that OA may suppress appetite through activation of the TGR5/cAMP signaling pathway in the hypothalamus.

Latent Trajectories of Change in Dietary Restriction During Treatment in Avoidant/Restrictive Food Intake Disorder and Anorexia Nervosa.

Outcomes for low-weight restrictive eating disorders, including anorexia nervosa, restricting type (AN-R) and avoidant/restrictive food intake disorder (ARFID), are sub-optimal. Reducing dietary restriction is a key treatment target. Understanding heterogeneity in patterns of change in dietary restriction may aid in improving outcomes. We examined latent trajectories of change in dietary restriction during treatment and follow-up in AN-R and ARFID. Adolescents and adults with R-EDs (N = 276, 18% ARFID, 90% female, Mage = 18) receiving intensive ED treatment completed assessments at five timepoints. Latent growth mixture modeling examined trajectories of change in dietary restriction, measured using the Eating Pathology Symptoms Inventory Restricting subscale. Classes were compared on clinical features at admission to determine characteristics prospectively associated with trajectory. A 3-class solution emerged: Class 1 comprising individuals with "good response" (n = 138; 33% of those with ARFID in the sample); Class 2 with "good response, rebounding" (n = 81; 41% of ARFID); and Class 3 with "gradual response, low symptoms" (n = 57; 26% of ARFID). Class 3 had lower anxiety and R-ED symptoms than Classes 1 and 2. Class 2 presented with older age than Class 1. No ARFID-specific classes emerged, underscoring similarities in response to intensive treatment between AN-R and ARFID.

Safety, Tolerability, and Pharmacokinetics of a Novel Anti-obesity Agent, S-309309, in Healthy Adults with or Without Obesity.

Anti-obesity medications are recommended for patients who do not achieve and maintain weight loss despite lifestyle interventions. S-309309 is a novel oral inhibitor of monoacylglycerol O-acyltransferase 2 being developed as a treatment for obesity. The objective of the study was to investigate the safety, clinical pharmacology, pharmacokinetics and pharmacodynamic biomarker of S-309309. A phase I, single-center, two-part, randomized, double-blind, placebo-controlled study of S-309309 following oral administration of a single-ascending dose (part 1) and a multiple dose (part 2) in healthy adults with or without obesity was conducted. We also assessed the effect of food on the pharmacokinetics of S-309309 and the effect of S-309309 on electrocardiogram parameters, the pharmacokinetics of midazolam (a cytochrome P450 3A substrate), and the pharmacodynamic biomarker of monoacylglycerol O-acyltransferase 2 inhibition. In part 1 (N = 50), a single-ascending dose of S-309309 in healthy adults demonstrated dose proportionality and comparable exposure of S-309309 between the fasted and fed states. In part 2 (N = 24), no clinically meaningful difference was observed in the pharmacokinetics of multiple doses between healthy adults with or without obesity. S-309309 did not affect the pharmacokinetics of the cytochrome P450 3A substrate. The pharmacodynamic biomarker of monoacylglycerol O-acyltransferase 2 inhibition, dicarboxylic acid (18:1), was significantly increased after S-309309 administration in healthy adults with or without obesity. Overall, S-309309 demonstrated acceptable safety and tolerability without any serious adverse events or discontinuations because of adverse events, and did not have a clinically relevant effect on the heart rate or cardiac conduction. An effect on the placebo-corrected change-from-baseline corrected QT interval, corrected for heart rate using the Fridericia method, exceeding 10 ms can be excluded. S-309309 was well tolerated as single-dose (up to 300 mg) and multiple-dose (50 mg once daily for 14 days) oral administration. The pharmacokinetic characteristics remained unaffected by obesity and food intake. S-309309 did not affect the pharmacokinetics of the cytochrome P450 3A substrate. Overall, S-309309 had an acceptable safety profile and favorable pharmacokinetic and pharmacodynamic characteristics. NCT05247970, date of registration: 8 February, 2022.

Subjective and objective stress during body exposure: a comparison of adolescents with anorexia nervosa versus high body dissatisfaction

Subjective and objective stress during body exposure: a comparison of adolescents with anorexia nervosa versus high body dissatisfaction

Translation and Adaptation of the SCOFF Questionnaire to the Greek Language (G-SCOFF) Using a Tertiary-Setting Adolescent Sample.

Feeding and eating disorders (FEDs) constitute an important mental health problem today, especially among youngsters. The Sick, Control, One, Fat, Food (SCOFF) questionnaire was developed 25 years ago and remains the most frequently applied screening tool for FEDs among adults and youngsters. The aim of the present study was to translate and adapt the SCOFF questionnaire to the Greek language, using a tertiary-setting adolescent sample. A total of 167 adolescents (86 boys, 81 girls) admitted to the pediatric outpatient clinics of the Georgios Gennimatas and Hippokration General hospitals completed the SCOFF questionnaire. Anthropometric indices were measured and dietary intake was recorded. A total of 74 adolescents (44.3% of the sample) were classified as engaging in disordered eating behaviors and as possible patients with FEDs based on the SCOFF questionnaire. No differences were noted in the dietary intake between adolescents who screened positive and those who screened negative for FEDs. The body mass index z-score and obesity status were greater among children screening positive for FEDs compared to those screening negative (p < 0.01). One patient who was later diagnosed with anorexia nervosa was detected as a possible FED case by the questionnaire. The present study revealed that more than two out of five adolescents attending a pediatric clinic exhibited disordered eating behavior. The use of the G-SCOFF questionnaire is feasible and effective for FED triage in the Greek tertiary pediatric setting.

The lipocalin saga: Insights into its role in cancer-associated cachexia.

Cancer-associated cachexia (CAC) is a debilitating condition, observed in patients with advanced stages of cancer. It is marked by ongoing weight loss, weakness, and nutritional impairment. Lower tolerance of chemotherapeutic agents and radiation therapy makes it difficult to treat CAC. Anorexia is a significant contributor to worsening CAC. Anorexia can be found in the early or advanced stages of cancer. Anorexia in cancer patients arises from a confluence of factors. Tumor-related inflammatory cytokines can directly impact the gastrointestinal tract, leading to dysphagia and compromised gut function. Additionally, increased serotonin and hormonal disruptions lead to early satiety, suppressing appetite. Due to the complexities in the pathogenesis of the disease, identifying druggable targets is a challenge. Research is ongoing to identify novel targets for the treatment of this condition. Recent research suggests a potential link between elevated levels of Lipocalin 2 (LCN2) and cachexia in cancer patients. LCN2, a glycoprotein primarily released by neutrophils, is implicated in numerous illnesses, including skin disorders, cancer, atherosclerosis, and type 2 diabetes. LCN2 suppresses hunger by binding to the melanocortin-4 receptors. Several in vitro, in vivo, and clinical studies indicate the association between LCN2 levels and appetite suppression. Further research should be explored emphasizing the significance of well-crafted clinical trials to confirm LCN2's usefulness as a therapeutic target and its ability to help cancer patients who are suffering from the fatal hallmark of cachexia. This review explores LCN2's function in the multifaceted dynamics of CAC and anorexia.

Descriptives and genetic correlates of eating disorder diagnostic transitions and presumed remission in the Danish registry.

Eating disorders (EDs) are serious psychiatric disorders with an estimated 3.3 million healthy life-years lost worldwide yearly. Understanding the course of illness, diagnostic transitions and remission, and their associated genetic correlates could inform both ED etiology and treatment. The authors investigated occurrences of ED transitions and presumed remission and their genetic correlates as captured by polygenic scores (PGSs) in a large Danish register-based cohort. The sample was compromised of 10,565 individuals with a diagnosis of anorexia nervosa (AN), bulimia nervosa (BN), or eating disorder not otherwise specified (EDNOS) with at least two registered hospital contacts between 1995 and 2018. Based on medical records, occurrence of diagnostic transitions and periods of presumed remission were identified. Associations between 422 PGS and diagnostic transitions and presumed remission were evaluated using Cox proportional hazard models. A minority of ED cases (14.1%-23.1%) experienced a diagnostic transition. Presumed remission ranged between 86.9%-89.8%. Higher (one SD increase) PGS for major depressive disorder and multisite chronic pain were positively associated with transitioning from AN to either BN or EDNOS. Higher PGS on a measure of body fat percentage and financial difficulties were positively associated with presumed remission from AN. Higher PGS for mood swings was positively associated with presumed remission from EDNOS whereas higher PGS for health rating showed the opposite. The authors found that most ED patients did not experience diagnostic transitions but were more likely to experience a period of presumed remission. Both diagnostic transitions and presumed remission have significant polygenic component.