Cristian Arturo Abia-Meashima

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a highly prevalent metabolic disorder characterized by substantial clinical heterogeneity and frequent association with obesity, insulin resistance, type 2 diabetes mellitus, dyslipidemia, visceral adiposity, and alterations in body composition. This study analyzed the principal clinical phenotypes of MASLD and their relationship with personalized nutritional interventions through a structured analytical review of clinical guidelines, systematic reviews, meta-analyses, randomized controlled trials, and observational studies. The evidence showed marked differences in disease prevalence and metabolic characteristics across lean, overweight, obese, and diabetic populations. Sustained weight loss was associated with progressive hepatic improvement, with reductions of approximately 5% linked to decreased liver fat, 7–10% to improvement in inflammatory activity, and reductions of 10% or greater to greater probability of fibrosis improvement. Dietary quality was also relevant independently of absolute weight reduction, particularly through Mediterranean-style patterns, reduced intake of added sugars and ultra-processed foods, and replacement of saturated fats with unsaturated sources. Lean MASLD represented a distinct phenotype in which metabolic dysfunction may persist despite normal body mass index, requiring greater emphasis on body composition, visceral adiposity, physical activity, and preservation of lean mass rather than aggressive caloric restriction. Overall, the findings support a phenotype-oriented model of nutritional management in which common evidence-based lifestyle principles are maintained while the intensity and priority of specific interventions are adapted to individual metabolic, hepatic, anthropometric, and behavioral characteristics. Further prospective studies are required to determine whether personalized nutritional strategies improve long-term fibrosis progression, cardiovascular outcomes, liver-related complications, and mortality.

The gut microbiota has emerged as a fundamental regulator of systemic human physiology, extending its influence far beyond the gastrointestinal tract. Recent advances in microbiome research have demonstrated that intestinal microorganisms participate actively in metabolic regulation, immune homeostasis, neuroimmune communication, inflammatory signaling, and chronic disease progression. The present review aimed to analyze current scientific evidence regarding the relationship between gut microbiota and systemic diseases, with special emphasis on immunological and neurological implications beyond digestive pathology. A structured narrative review methodology based on the Scientific Method was employed through analysis of peer-reviewed literature indexed in internationally recognized scientific databases including PubMed, Scopus, ScienceDirect, and SpringerLink. The review integrated multidisciplinary evidence involving gastroenterology, neurology, immunology, microbiology, metabolism, and translational medicine. The selected studies evaluated mechanisms associated with intestinal dysbiosis, systemic inflammation, gut–brain axis signaling, immune dysregulation, microbial metabolites, and microbiota-targeted therapeutic strategies. The analyzed evidence demonstrated that alterations in gut microbial diversity are strongly associated with chronic inflammatory diseases, obesity, type 2 diabetes mellitus, cardiovascular disease, autoimmune disorders, neurodegenerative pathology, and psychiatric conditions. Key mechanisms identified included increased intestinal permeability, chronic low-grade inflammation, abnormal immune activation, altered short-chain fatty acid production, and neuroimmune dysregulation mediated through the gut–brain axis. Furthermore, microbiota-targeted interventions such as probiotics, prebiotics, dietary modulation, postbiotics, and fecal microbiota transplantation demonstrated promising therapeutic potential in restoring microbial balance and reducing inflammatory activity.

Neuroimmune interactions have emerged as a central framework for understanding the complexity of gastrointestinal diseases, integrating immune regulation, neural signaling, and microbiota-driven mechanisms within the gut–brain axis. This review synthesizes current evidence on the role of neuroimmune pathways in both inflammatory and functional gastrointestinal disorders, with particular emphasis on inflammatory bowel disease and irritable bowel syndrome. The analyzed literature demonstrates that gastrointestinal symptom generation and disease expression result from dynamic interactions among immune cells, enteric and autonomic neural circuits, microbial signaling, and stress-related modulation rather than from isolated pathological processes. In inflammatory conditions, immune dysregulation and macrophage-mediated pathways predominate, while neural and autonomic mechanisms contribute to symptom persistence and variability. In functional disorders, immune–neural coupling, mast cell–nerve interactions, and visceral sensory sensitization emerge as key drivers of pain and altered bowel habits despite minimal structural abnormalities. Across both disease categories, the intestinal microbiota acts as a cross-cutting regulator influencing immune tone, barrier integrity, and neural responsiveness. From a clinical and diagnostic perspective, these findings support a mechanism-based approach that complements traditional inflammatory and structural assessments with neuroimmune-informed reasoning. This integrative framework has particular relevance for medical education and clinical practice in diverse healthcare settings, including Latin America, where resource variability necessitates strong pathophysiological interpretation. Overall, neuroimmune models provide a coherent and biologically grounded perspective for advancing diagnosis, teaching, and future translational strategies in gastroenterology.

Burnout syndrome, chronic fatigue, and mental health disorders have become major occupational health concerns among healthcare professionals worldwide. The increasing complexity of healthcare systems, growing workloads, staffing shortages, administrative pressures, and exposure to emotionally demanding clinical environments have contributed to elevated levels of psychological distress across healthcare settings. This review aimed to analyze current scientific evidence regarding the determinants, manifestations, consequences, and intervention strategies associated with burnout, chronic fatigue, and mental health outcomes among healthcare workers from an international perspective, with particular attention to findings reported in Mexico, Colombia, and Ecuador. A structured literature review was conducted using scientific publications retrieved from major biomedical and multidisciplinary databases. The evidence consistently identified emotional exhaustion, sleep disturbances, anxiety symptoms, depressive manifestations, psychological distress, and chronic fatigue as the most frequently reported outcomes. Excessive workload, prolonged working hours, staffing shortages, administrative burden, and insufficient organizational support emerged as the principal occupational determinants associated with adverse psychological outcomes. Findings from Latin America closely paralleled international trends, demonstrating similar occupational challenges across diverse healthcare systems. The review also revealed that organizational interventions, including workload optimization, leadership development, institutional support programs, and access to mental health services, were generally more effective than isolated individual-focused approaches. These findings highlight the importance of comprehensive occupational health strategies aimed at protecting healthcare worker well-being, improving workforce sustainability, and enhancing healthcare quality. Continued efforts to address organizational stressors and promote supportive work environments are essential for strengthening the resilience of healthcare professionals and healthcare systems worldwide.

The enteric nervous system (ENS), commonly referred to as the “second brain,” has emerged as a key integrative network in clinical medicine. This review analyzes its role beyond gastrointestinal physiology, emphasizing its involvement in neurological, nephrological, and urological conditions through interconnected mechanisms such as the gut–brain, gut–kidney, and gut–bladder axes. A structured analysis of current scientific literature was conducted to identify the main pathways linking ENS dysfunction with multisystem disease, including microbiota dysbiosis, neuroimmune activation, autonomic imbalance, epithelial barrier disruption, and visceral hypersensitivity. The findings demonstrate that while gastrointestinal manifestations remain predominant, ENS-related alterations are strongly associated with systemic inflammation, neurological symptoms, and urinary dysfunction. Additionally, emerging therapeutic strategies highlight the importance of integrative approaches, including dietary interventions, microbiota modulation, neuromodulation, and anti-inflammatory treatments. These results support the concept of the ENS as a central regulator in multisystem physiology and reinforce the need for interdisciplinary clinical reasoning. Understanding the ENS from a systems-based perspective provides valuable insights for improving diagnosis, treatment, and medical education in the context of complex and chronic diseases.

The gut microbiota has emerged as a key modulator of drug metabolism, efficacy, and toxicity, adding a critical layer of complexity to pharmacological processes traditionally attributed solely to host physiology. In hepatobiliary disease, this interaction acquires particular relevance due to alterations in bile acid metabolism, intestinal barrier function, immune regulation, and enterohepatic circulation. This review synthesizes current evidence on microbiota–drug interactions within hepatobiliary contexts, integrating mechanistic, translational, and clinical data to provide a coherent pharmacological framework. The analyzed literature consistently demonstrates that intestinal microorganisms can directly biotransform xenobiotics, modify effective bioavailability, and generate metabolites with altered pharmacodynamic or toxicological properties. In parallel, microbial modulation of bile acid pools and signaling pathways indirectly influences hepatic drug-metabolizing enzymes, transporters, and inflammatory responses. The reciprocal capacity of drugs to reshape microbial composition further contributes to dynamic and time-dependent variability in drug exposure. Collectively, these mechanisms help explain interindividual differences in therapeutic response and susceptibility to adverse drug reactions that are frequently observed in hepatobiliary disease but remain insufficiently accounted for by conventional dosing paradigms. By consolidating these findings, this review highlights the gut microbiota as an integral component of hepatobiliary pharmacology and underscores its relevance for advancing more precise, individualized, and safer therapeutic strategies.

Metabolic diseases constitute a growing global health burden and increasingly demand integrative biological frameworks that transcend organ-specific perspectives. This review synthesizes evidence demonstrating that metabolic deterioration arises from the interaction of three interconnected mechanisms: NLRP3 inflammasome activation, gut microbiota dysbiosis, and cellular aging/senescence. Using a structured scientific methodology, we examined mechanistic, translational, and clinical research across immunology, microbiology, and geroscience. The results highlight that inflammasome activity exerts systemic metabolic effects, influencing insulin resistance, liver injury, vascular remodeling, and renal dysfunction. In parallel, microbiota alterations follow a graded pattern that mirrors disease severity, aging trajectories, and immune dysregulation. Cellular senescence emerges as both a consequence and amplifier of metabolic stress, contributing to chronic inflammation and multi-organ vulnerability through SASP-mediated signaling. When integrated, these mechanisms form a self-reinforcing pathogenic triad that offers a more accurate explanation for the multisystemic nature and progression of metabolic disease. The model presented underscores the need for multidimensional therapeutic strategies that target inflammation, microbial ecology, and aging biology simultaneously. This triad-based framework is particularly relevant for regions undergoing rapid epidemiologic transitions, including Mexico, Colombia, and Ecuador, where metabolic disorders continue to rise.