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Background: Lipedema is a chronic, progressive adipose tissue disorder that almost exclusively affects women,characterized by bilateral, disproportionate subcutaneous fat accumulation in the limbs, pain, easy bruising, andresistance to conventional weight-loss interventions. Because its appearance is frequently mistaken for obesity,women with lipedema are exposed to prolonged misdiagnosis, weight stigma, and inadequate healthcareresponses. The psychological, psychosocial, and behavioral burden of the condition is increasingly recognized,but the evidence is fragmented across clinical, psychological, and eating-related research. Objective: To synthesize the available evidence on the psychological, psychosocial, and behavioralconsequences of lipedema in adult women — including psychological distress, anxiety and depression, pain andfunctional impact, delayed diagnosis, weight stigma, body image, shame, emotion regulation, quality of life, andeating-related outcomes — and to organize this evidence within an explicit biopsychosocial framework. Methods: A structured narrative review following SANRA principles and incorporating applicable PRISMA2020 elements was conducted. Databases targeted included PubMed/MEDLINE, Embase, Scopus, Web of Science, PsycINFO, and the Cochrane Library; a complete PubMed search strategy is reported. Observational,qualitative, mixed-methods, longitudinal, and relevant intervention studies and reviews of adult women withclinically diagnosed lipedema and separately identifiable lipedema data were eligible. Data were extracted intostandardized tables, appraised for methodological quality, and synthesized thematically by domain. Each findingwas classified as direct evidence (lipedema populations), indirect evidence (related populations such as obesity,chronic pain, lymphedema, or weight-stigma research), or hypothesis (theoretical mechanisms not directlydemonstrated). Results: Thirty-six sources formed the evidence base. Direct evidence documents substantially reducedhealth-related quality of life across physical, emotional, and social domains, elevated prevalence of depressivesymptoms, and frequent experiences of weight stigma, shame, and body-image disturbance. Pain and functionallimitations are nearly universal and are associated with disability, kinesiophobia, and reduced activity. Emotionregulation difficulties and coping styles characterized by depressive processing are reported. Eating-disorderscreening indicators are elevated in preliminary samples, and clinically diagnosed binge-eating disorder waspresent in 14.7% of patients in one specialist pilot cohort. Direct evidence for compensatory behaviors andcompulsive exercise in lipedema was not identified. Conclusions: Distress, stigma, body image concerns, and impaired quality of life are the relativelybetter-documented psychological consequences of lipedema. Emotion regulation, eating-disorder risk, anddysfunctional eating behaviors remain less studied and methodologically heterogeneous. A biopsychosocialmodel — in which pain, functional limitation, delayed diagnosis, and stigma converge on body image, emotionregulation, eating behavior, and quality of life — is supported by converging direct and indirect evidence,although most links remain associative rather than causal. Multidisciplinary, non-stigmatizing, individualizedcare is warranted.

Lipedema is a chronic and progressive adipose tissue disorder characterized by disproportionate fat accumulation, microvascular dysfunction, chronic inflammation, and progressive fibrosis. Despite its prevalence and significant impact on quality of life, current therapeutic approaches remain largely symptomatic and fail to address the underlying biological mechanisms of the disease. Emerging evidence suggests that lipedema should be understood as a multifactorial condition involving genetic susceptibility, endothelial alterations, immune dysregulation, and extracellular matrix remodeling. In this context, pharmacological strategies targeting these pathways have gained increasing attention. Metformin, through activation of AMP-activated protein kinase (AMPK), exerts antifibrotic and immunometabolic effects, including inhibition of TGF-β signaling, reduction of extracellular matrix deposition, and modulation of adipose tissue inflammation. In parallel, incretin-based therapies, particularly glucagon-like peptide-1 (GLP-1) receptor agonists and dual GLP-1/GIP agonists such as tirzepatide, have demonstrated pleiotropic effects that extend beyond weight reduction, including improvements in metabolic homeostasis, reduction of systemic inflammation, and enhancement of endothelial function. These therapies appear to act through complementary mechanisms, with metformin primarily targeting tissue remodeling and fibrosis, and incretin-based therapies exerting broader systemic effects on metabolism, inflammation, and vascular integrity. This review proposes a hypothesis-generating mechanistic framework, supporting a shift from weight-centric and symptomatic approaches toward disease-modifying strategies. Although current evidence in lipedema is largely indirect, the convergence of experimental and clinical data provides a strong rationale for further investigation. Future studies should focus on evaluating combined therapeutic approaches and identifying biomarkers that reflect fibrosis, inflammation, and microvascular dysfunction, with the aim of developing targeted and personalized treatments for this complex disorder.

Background: Lipedema is characterized by disproportionate gluteofemoral adiposity, often regarded as a metabolic sink, yet its relationship with systemic autoimmunity, specifically celiac disease (CD), remains unexplored. Objective: We investigated the immunometabolic profiles and body composition patterns distinguishing lipedema phenotypes from celiac disease autoimmunity. Methods: This cross-sectional analysis included 3,833 women from NHANES 2011–2014. Celiac disease was defined by strict serology (tTG-IgA+ and EMA-IgA+), while the lipedema phenotype was defined as a leg-to-trunk fat ratio >90th percentile via dual-energy X-ray absorptiometry (DXA). We assessed gynoid fat mass, HOMA-IR, and neutrophil-to-lymphocyte ratio (NLR) compared to controls. Results: CD prevalence was 0.56% (n=11). Women with CD exhibited significantly lower gynoid region percent fat compared to non-celiacs (39.5% vs. 42.6%, p=0.0007). Conversely, the lipedema phenotype was associated with a distinct anti-inflammatory and insulin-sensitive profile, characterized by 44.2% lower HOMA-IR (p<0.001) and 7.6% lower NLR (p=0.012) compared to controls. While broad lipedema criteria did not reach statistical significance for CD exclusion due to low case numbers (p=0.570), no celiac cases were observed in the highest tier of gynoid adiposity. Conclusions: Although prevalence differences did not reach statistical significance, this study of US women demonstrates a phenotypic divergence where celiac disease is associated with reduced gynoid adiposity, contrasting with the superior immunometabolic profile observed in the lipedema phenotype. These findings suggest that these conditions represent opposing physiological states regarding gynoid adipose tissue function.