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Background: Lipedema is a chronic, progressive adipose tissue disorder that affects almost exclusively women and is characterized by disproportionate limb fat accumulation, pain, edema, and resistance to conventional weight-loss strategies. Although traditionally approached as a disorder of adipose tissue expansion, emerging evidence suggests that functional impairment in advanced lipedema cannot be fully explained by fat pathology alone. Methods: This hypothesis-driven review proposes a novel conceptual framework in which advanced lipedema is accompanied by a parallel failure of skeletal muscle function, characterized by dynapenia despite preserved or increased limb volume. Results: Our findings indicate a phenotype characterized by reduced muscle strength and quality in advanced lipedema, which we term lipedemata dynapenic myosteatosis. We synthesize clinical, imaging, and mechanistic data indicating that inflammatory myosteatosis, mitochondrial dysfunction, and impaired lipid oxidation contribute to reduced muscle quality and exercise intolerance in late-stage lipedema, particularly Stage 3, while emphasizing that functional decline should be proactively investigated from Stage 2 onward. Within this context, conventional resistance exercise, while physiologically required to prevent dynapenia, may be poorly tolerated due to inflammation, edema, and pain, creating a therapeutic deadlock. To address this paradox, we present a hypothesis-generating dual-target framework that integrates metabolic modulation aimed at restoring mitochondrial fatty-acid oxidation with anabolic signaling directed toward contractile tissue, drawing mechanistic analogies from established catabolic states. Conclusions: Importantly, this model is presented as a conceptual and translational framework rather than a clinical recommendation. By shifting the focus from adipose volume to muscle quality and function, this work reframes advanced lipedema as a disorder of coupled adipose–muscle bioenergetic failure. Future clinical studies are required to validate this framework, with outcomes centered on strength, mobility, pain, and functional independence rather than weight loss alone.
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Background: Emerging evidence suggests that lipedema may share hormonal, inflammatory, and genetic mechanisms with gynecologic diseases, particularly endometriosis. However, the extent and nature of these interrelationships remain poorly characterized, supporting the need for this scoping review. Objectives: To map and synthesize the available evidence on the clinical, pathophysiological, and epidemiological interrelationships between lipedema in women, endometriosis, and other gynecologic diseases. Methods: Searches were conducted in international and regional health databases, including MEDLINE (PubMed), CINAHL, Scopus, Embase, Web of Science, the Cochrane Library, LILACS/VHL, APA PsycInfo, SciELO, Epistemonikos, and La Referencia, as well as grey literature sources and relevant institutional websites. There were no language restrictions. The search period began in 1940, the year in which lipedema was first described by Allen and Hines. Study selection followed a two-stage process conducted independently by two reviewers, consisting of title and abstract screening followed by full-text review. Data extraction was performed using a pre-developed and peer-reviewed instrument covering participants, concept, context, study methods, and main findings. The review protocol was registered in the Open Science Framework. Results: Twenty-five studies from ten countries were included. Synthesized evidence supports the characterization of lipedema as a systemic condition with metabolic and hormonal dimensions. Key findings include symptom onset linked to reproductive milestones, a high frequency of gynecologic and endocrine comorbidities, and molecular features overlapping with steroid-dependent pathologies. These patterns reflect a recent shift from a predominantly lymphovascular paradigm toward a more integrated endocrinometabolic framework. Conclusions: The findings indicate that lipedema clusters with hormone-sensitive gynecologic and endocrine features across reproductive life stages.
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Lipedema is a chronic, estrogen-sensitive adipose tissue disorder characterized by disproportionate subcutaneous fat accumulation, fibrosis, inflammation, and resistance to fat mobilization. Despite its high prevalence, lipedema remains poorly understood and frequently misdiagnosed. This narrative review proposes a novel pathophysiological model in which menopause acts as a critical turning point in the progression of lipedema, driven by estrogen receptor imbalance (ERβ predominance over ERα), intracrine estrogen excess, and adipose tissue dysfunction. We demonstrate how menopauseinduced estrogen deficiency amplifies adipose tissue dysfunction by suppressing ERα signaling, enhancing ERβ activity, and disrupting mitochondrial function, insulin sensitivity, and lipid oxidation. Concurrently, the upregulation of aromatase and 17β-HSD1, combined with the suppression of 17β-HSD2, sustains localized estradiol excess, perpetuating inflammation, fibrosis, and immune dysregulation. The molecular signature observed in lipedema closely mirrors that of other estrogen-driven gynecological disorders, such as endometriosis, adenomyosis, and uterine fibroids. Understanding these molecular mechanisms highlights the pivotal role of menopause as a catalyst for disease progression and provides a rationale for targeted therapeutic strategies, including hormonal modulation and metabolic interventions. This review reframes lipedema as an estrogen receptor– driven gynecological disorder, offering a new perspective to improve clinical recognition, diagnosis, and management of this neglected condition.
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