Beyond the Surface: Mechanistic Intersections Between Obesity and UVB Exposure

Obesity, a globally prevalent metabolic disorder, and ultraviolet-B (UVB) radiation, an inherent component of solar exposure, are each independently linked to a wide range of chronic health outcomes, including cancer, metabolic dysfunction, and immune dysregulation. Although traditionally viewed as separate risk factors, metabolic and environmental, respectively, emerging evidence reveals mechanistic intersections that may amplify disease burden when both are present. Obesity promotes chronic low-grade inflammation, oxidative stress, adipokine imbalance, and impaired DNA repair capacity, while UVB radiation induces mutagenic photoproducts, reactive oxygen species, and localized immunosuppression. These overlapping pathways converge on genomic instability, altered immune tolerance, and the development of tumor-promoting microenvironments, particularly within the skin. This review synthesizes recent advances in understanding the biological mechanisms linking obesity and UVB exposure, with emphasis on synergistic effects on oxidative stress, nucleotide excision repair efficiency, and immune surveillance. It examines experimental and clinical evidence supporting these interactions and highlights emerging therapeutic strategies, including phototherapy and vitamin D modulation, clarifying their mechanistic rationale in restoring immune balance and enhancing DNA repair. Finally, the review discusses implications for integrated prevention, risk stratification, and public health policy. By framing obesity and UVB radiation as a compound risk factor, this article underscores the need for interdisciplinary approaches to mitigate their combined impact on global health. Converging Effects of Obesity and UVB Exposure on Skin Carcinogenesis: Obesity and UVB exposure converge through shared inflammatory, oxidative, and immune-modulating pathways that amplify skin cancer risk. Obesity drives chronic inflammation, oxidative stress, altered adipokine signaling, and impaired DNA repair, while UVB radiation causes direct DNA damage, reactive oxygen species, and local immunosuppression. Together, these stressors synergistically intensify oxidative injury, weaken DNA damage responses, and diminish immune surveillance, promoting the development of basal and squamous cell carcinoma. Emerging therapeutic approaches including vitamin D modulation, UVB-based phototherapy, and autophagy-targeted interventions, highlight opportunities for prevention and clinical translation.