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    Heavy Metal-Contaminated Soils and Gastric Cancer Risk: Molecular Insights and the Relevance of a One Health Perspective
    (MDPI AG, 2025-11-27)
    Claudia Reytor-González
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    Yasniel Sánchez Suárez
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    Vianey Ariadna Burboa Charis
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    Emilia Jiménez-Flores
    Heavy metal contamination in agricultural soils has emerged as a critical environmental and public health issue associated with increased gastric cancer incidence worldwide. Among the most concerning pollutants are cadmium, arsenic, and lead, which persist in the environment and enter the human body primarily through the soil–plant–food chain. This review integrates environmental, molecular, and epidemiological evidence to explain how these metals alter gastric mucosal biology and promote carcinogenesis. Mechanistically, cadmium, arsenic, and lead trigger oxidative stress, mitochondrial dysfunction, DNA damage, and epigenetic reprogramming, resulting in genomic instability, resistance to programmed cell death, and the transformation of epithelial cells into invasive phenotypes. These molecular disruptions interact with Helicobacter pylori infection, microbial imbalance, chronic inflammation, and hypoxia-driven remodeling of the gastric stroma, all of which enhance angiogenesis and tumor progression. Advanced experimental platforms, such as gastric organoids, immune co-cultures, and humanized animal models, are improving the understanding of these complex interactions. Adopting a One Health perspective reveals the continuity between environmental contamination, agricultural production, and human disease, underscoring the importance of integrative monitoring systems that combine soil and crop analysis with molecular biomarkers in exposed populations. Strengthening this interdisciplinary approach is essential to design preventive strategies, guide remediation policies, and protect human, animals, and environmental health.
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    The Molecular Mechanisms Underlying Dercum’s Disease: Exploring the Intersection of Obesity, Pain, and Inflammation
    (MDPI AG, 2025-11-18) ;
    Emilia Jiménez Flores
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    Melannie Toral-Noristz
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    Campuzano Donoso Martín
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    Obesity is increasingly recognized not only as a metabolic disorder, but also as a state of chronic low-grade inflammation that predisposes to systemic complications. Within this context, Dercum’s disease (DD), or adiposis dolorosa, emerges as a rare yet debilitating disorder characterized by painful subcutaneous lipomas, most commonly affecting middle-aged women. Despite its clinical impact, DD remains underdiagnosed and is often misclassified as lipedema, fibromyalgia, or lipomatosis, complicating prevalence estimates and hindering the development of targeted interventions. Current evidence suggests that DD represents a distinctive model of inflammatory obesity, where adipose tissue actively contributes to pain generation rather than serving as a passive fat reservoir. Histological and molecular findings point to adipose tissue dysfunction, immune cell infiltration, and elevated secretion of pro-inflammatory adipokines, signals which appear to fuel systemic low-grade inflammation, perineural immune interactions, and nociceptor sensitization. Peripheral mechanisms further shape the clinical phenotype. While familial clustering suggests possible genetic contributions, no definitive markers have been identified, and the role of obesity-induced epigenetic modifications remains unexplored. Therapeutic strategies remain largely symptomatic, including analgesics, antidepressants, physical rehabilitation, and surgical excision of lipomas, whereas molecularly targeted and diet-based interventions are still experimental. This article discusses the pathophysiology of DD, current treatments, and future perspectives, emphasizing that advancing patient registries, omics-based analyses, and interdisciplinary clinical trials will be crucial to elucidate disease mechanisms and guide novel therapies. Improved understanding of DD may not only enhance patient care, but also provide broader insights into the interplay between obesity, inflammation, and chronic pain.
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    Obesity and endometrial cancer: biological mechanisms, nutritional strategies, and clinical perspectives
    (Informa UK Limited, 2025-04-12)
    Simancas Racines Daniel
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    Campuzano Donoso Martín
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    Román-galeano Náthaly Mercedes
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    Zambrano Villacres Raynier
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    Pasqualina Memoli
    Obesity is a major modifiable risk factor for endometrial cancer, significantly increasing incidence and worsening clinical outcomes. The underlying biological mechanisms include chronic inflammation, insulin resistance, hormonal dysregulation, and microbiome alterations, all of which contribute to tumour development and progression. Nutritional strategies such as plant-based and Mediterranean diets, caloric restriction, and micronutrient-rich foods show promise in reducing cancer risk through improved metabolic health and hormonal balance. However, clinical challenges persist, including surgical complications, altered chemotherapy efficacy, and poorer long-term survival in obese patients. Personalised nutrition and multidisciplinary care integrating oncology, nutrition, and metabolic expertise are essential for improving treatment outcomes. Despite promising evidence, knowledge gaps remain in understanding microbiome interactions and the long-term efficacy of dietary interventions. Addressing these challenges through research and clinical innovation is crucial to mitigating the burden of obesity-related endometrial cancer and enhancing patient care.
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    Harnessing nutrition to combat MASLD: a comprehensive guide to food-based therapeutic strategies
    (Informa UK Limited, 2025-05-06) ; ;
    Campuzano Donoso Martín
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    Castano Jimenez Janeth C.
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    Román-galeano Náthaly Mercedes
    Metabolic dysfunction-associated steatotic liver disease is a growing global health issue linked to obesity, insulin resistance, and metabolic syndrome. Diet plays a key role in its progression and management. This narrative review highlights evidence-based nutritional strategies, including the Mediterranean diet, low-carbohydrate and ketogenic diets, and high-fiber intake, which improve insulin sensitivity, reduce hepatic fat, and lower inflammation. Nutritional deficiencies, such as low vitamin D, choline, and omega-3 levels, exacerbate metabolic dysfunction-associated steatotic liver disease, emphasizing the need for targeted supplementation. Emerging approaches, including gut microbiota modulation, precision nutrition, and nutraceuticals like resveratrol and curcumin, offer promising therapeutic potential. A multidisciplinary approach integrating dietary and lifestyle modifications is essential for effective metabolic dysfunction-associated steatotic liver disease management.