The gut microbiome regulates host metabolism, barrier integrity, and immune homeostasis through microbe–host signaling and bioactive metabolites. Growing evidence suggests that dysbiosis may also influence ocular immune privilege and blood–retinal barrier stability, supporting the emerging concept of the gut–eye axis. This narrative review aimed to integrate retinal, uveal, and ocular surface disorders within a shared functional framework, with emphasis on recurring mechanistic pathways and their translational relevance rather than on single diseases or isolated taxonomic findings. The review was based on a literature search of PubMed and Scopus and primarily included English-language studies published between 2015 and 2025, with earlier seminal papers included when needed. The search was last updated in March 2026, and 101 sources were included in the final narrative synthesis. Across age-related macular degeneration, diabetic retinopathy, glaucoma, uveitis, dry eye disease, and Sjögren’s syndrome, the most consistent microbiome-related signals were functional rather than taxonomic. Recurrent mechanistic themes included Th17/Treg immune programming, barrier dysfunction with microbial product translocation, and systemic metabolite signaling, particularly involving short-chain fatty acids, bile acid receptor pathways, and tryptophan-derived metabolites. Age-related macular degeneration and diabetic retinopathy showed the strongest multi-layered support, whereas uveitis provided a compelling immune-centered biological model that remains limited by treatment-related confounding in human studies. In glaucoma and ocular surface disease, evidence supports biological plausibility, especially in relation to neuroinflammation, mucosal immune dysregulation, and metabolite-dependent anti-inflammatory pathways, although much of the available human literature remains associative. Overall, current evidence supports dysbiosis as a disease modifier that may influence ocular inflammation, angiogenesis, neurodegeneration, and barrier stability. However, clinical translation remains limited by cohort heterogeneity, methodological variability, and incomplete control of confounding factors. Further progress will depend on longitudinal multi-omics cohorts and controlled intervention trials focused on actionable microbial functions.

Research objectives: The objective of this study was to synthesise evidence on resting heart rate (RHR) and heart rate variability (HRV) as biomarkers of biological aging, with a focus on their relationships to multisystem physiological decline across cardiovascular, metabolic, autonomic, and inflammatory domains. Methods: A structured literature search was conducted. Included publications comprised population-based cohorts, mechanistic studies, biomarker analyses, and autonomic assessments evaluating associations between RHR, HRV, biological aging markers, morbidity, and mortality. Key findings: Elevated RHR consistently aligned with signatures of accelerated aging, including adverse cardiometabolic profiles, reduced autonomic flexibility, and increased inflammatory activation. Higher RHR was associated with older brain age, diminished functional resilience, and biomarker patterns characteristic of inflammaging, such as heightened interleukin-6 and tumour necrosis factor-α. Lower RHR corresponded to slower biological aging trajectories. HRV analyses complemented these findings, linking reduced parasympathetic activity and lower variability with diminished physiological adaptability and greater aging burden. Conclusions: RHR emerges as a robust, multidimensional biomarker that integrates signals of cumulative physiological decline and reliably identifies individuals exhibiting accelerated biological aging. Its consistent associations with molecular, functional, and clinical indicators of aging highlight its value as a practical, noninvasive tool for assessing multisystem health status.

Chronic low-grade inflammation contributes to the pathogenesis and progression of many chronic disorders, and inflammatory biomarkers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) are frequently used to quantify systemic inflammatory activity. Yoga, a multidimensional mind–body practice combining physical postures, breathing techniques, and meditation, has been proposed as an adjunctive strategy to modulate stress-related neuroendocrine pathways and inflammation. This narrative review summarizes and critically discusses evidence on the effects of yoga-based interventions on CRP, IL-6, and TNF-α in adults with chronic conditions. The literature was explored using targeted searches of major biomedical databases and relevant reference lists, prioritizing randomized trials and meta-analyses reporting biomarker outcomes. Across clinical contexts—including inflammatory rheumatic disease, cardiovascular risk and post–myocardial infarction rehabilitation, and inflammatory bowel disease—yoga interventions consistently improved patient-reported outcomes such as stress, anxiety, and quality of life. Biomarker findings were heterogeneous: reductions in TNF-α and IL-6 were reported in some settings and protocols, whereas CRP changes were less consistent. Differences in populations, intervention intensity and duration, comparator conditions, and biomarker assessment methods likely contribute to variability across studies. Overall, current evidence suggests yoga may have anti-inflammatory potential in selected chronic disease populations, but more standardized, adequately powered trials with longer follow-up are needed to clarify the magnitude, durability, and mechanisms of biomarker effects.

Introduction and aim. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are widely used in the treatment of type 2 diabetes and obesity. However, their effects on the visual system remain unclear. This narrative review summarizes current evidence and aims to clarify the association between GLP-1RAs and ocular outcomes. Literature search. A literature search was conducted using PubMed/MEDLINE, Embase, and ScienceDirect electronic databases. Findings were grouped into thematic categories: diabetic retinopathy, NAION, AMD and other ocular events, and glaucoma. Analysis of the literature. The available evidence is heterogeneous and sometimes conflicting. GLP-1RAs may be associated with diabetic retinopathy progression, particularly in patients with pre-existing type 2 diabetes, likely related to rapid glycemic improvement rather than direct drug toxicity. Reports of NAION remain rare, and causality has not been definitively established. The reviewed studies also indicate that GLP-1RAs may reduce AMD risk. Preclinical and observational studies suggest possible neuroprotective and intraocular pressure-lowering effects in glaucoma, while clinical evidence remain limited. Conclusion. Current evidence does not indicate a consistent increase in major ophthalmic adverse outcomes associated with GLP-1RAs use. However, evidence remains limited and largely observational. Careful ophthalmic assessment and follow-up may be considered in high-risk individuals. Further prospective studies are needed to clarify causal relationships.

The escalating global prevalence of myopia constitutes a significant public health challenge. This narrative review explores the role of dietary factors, specifically vitamin D and selected nutrients, in its development in children and young adults. Current research underscores a link between low serum vitamin D levels and increased myopia risk. While this association often reflects limited time spent outdoors, vitamin D also appears to exert a direct biological role in regulating ocular growth. The impact of other micronutrients remains ambiguous. Although vitamin A, zinc, and selenium are essential for retinal health and antioxidant defense, human studies regarding their specific capacity to prevent myopia are inconclusive. In contrast, emerging evidence suggests that omega-3 polyunsaturated fatty acids confer protective benefits against axial elongation. Conversely, diets high in refined carbohydrates are associated with an elevated risk of myopia, likely due to insulin-mediated mechanisms influencing scleral structure. Overall, vitamin D and omega-3 fatty acids demonstrate the greatest promise as modifiable protective factors. However, the roles of zinc, selenium, and vitamin A remain inconclusive. Future prevention strategies may benefit from considering nutritional optimization alongside increased outdoor activity as part of a broader strategy of reducing myopia progression.

Age-related macular degeneration (AMD) remains the leading cause of irreversible central vision loss in the elderly. Increasing attention has been directed toward lipid metabolism as a potential contributor to disease onset and progression. The overlap between AMD and atherosclerosis—particularly regarding lipid accumulation, endothelial dysfunction, and chronic inflammation—has prompted interest in lipid-lowering therapies. This narrative review synthesizes the clinical evidence published between 2020 and 2025 on the potential role of statins and fenofibrate in AMD risk modification and disease progression. A structured literature search was conducted in PubMed, Scopus, and Web of Science using combined MeSH and free-text terms related to lipid-lowering agents and AMD. Human studies evaluating clinical incidence or progression outcomes were considered alongside contextual evidence from prior evidence syntheses. Overall, findings remain heterogeneous. Most studies did not demonstrate a consistent association between statin therapy and AMD incidence or progression in unselected populations. However, selected reports suggested a potential delay in dry AMD onset or slower disease progression among patients receiving prolonged or higher-intensity statin treatment. Evidence regarding fenofibrate was more limited and heterogeneous, with only a tentative protective signal observed in adherent users, particularly for non-exudative AMD. The current literature does not support lipid-lowering therapy as a universal preventive strategy for AMD. Nonetheless, subgroup-specific benefits cannot be excluded, especially in early disease stages or metabolically high-risk populations. Further well-designed prospective and randomized studies are needed to clarify therapeutic relevance and identify the patients who are most likely to benefit.