The circadian clock regulates biological cycles across species and is crucial for physiological activities and biochemical reactions, including cancer onset and development. The interplay between the circadian rhythm and cancer involves regulating cell division, DNA repair, immune function, hormonal balance, and the potential for chronotherapy. This highlights the importance of maintaining a healthy circadian rhythm for cancer prevention and treatment. This article investigates the complex relationship between the circadian rhythm and cancer, exploring how disruptions to the internal clock may contribute to tumorigenesis and influence cancer progression. Numerous databases are utilized to conduct searches for articles, such as NCBI, MEDLINE, and Scopus. The keywords used throughout the academic archives are “circadian rhythm”, ”cancer”, and ”circadian clock”. Maintaining a healthy circadian cycle involves prioritizing healthy sleep habits and minimizing disruptions, such as consistent sleep schedules, reduced artificial light exposure, and meal timing adjustments. Dysregulation of the circadian clock gene and cell cycle can cause tumor growth, leading to the need to regulate the circadian cycle for better treatment outcomes. The circadian clock components significantly impact cellular responses to DNA damage, influencing cancer development. Understanding the circadian rhythm’s role in tumor diseases and their therapeutic targets is essential for treating and preventing cancer. Disruptions to the circadian rhythm can promote abnormal cell development and tumor metastasis, potentially due to immune system imbalances and hormonal fluctuations.

The purpose of this paper is to review the specialized literature to highlight the effects produced by energy drinks in terms of skin health. To carry out this review, we consulted previous articles with descriptive cross-sectional designs, case series, and individual case reports published between 2000 and 2023. Therefore, while caffeine acute consumption among adults can have beneficial effects, in children, it can cause health problems like overnight breaks, headaches, and dulled cognition since their organs are still developing and their endocrine system is not yet stable. Despite the antioxidant and neuroprotective effects of caffeine from energy drinks, their excessive consumption among adolescents can cause disorders like high systolic blood pressure, agitation, nausea, anxiety, osteoporosis, heart palpitations, poor sleep quality, and stomach ulcers. Among athletes, taurine supplementation has been proven to improve exercise capacity in cold weather conditions. Also, vigilance, attention, and reaction time were all improved by caffeine consumption. Caffeine administration in low doses caused a risk of cardiovascular disease. It was effective in treating migraines in children, but raised systolic blood pressure, and contributed to skin healing in adolescents. On the other side, taurine prevents obesity among children, causes positive effects on oxidative stress and inflammation in adolescents, helps shield the skin from damaging oxidative stress among students, and impacts exercise capacity in athletes. Significant increases in serum levels of uric acid, creatinine, BUN, ALT, and ALP caused by chronic intake of EDs indicated different degrees of injury to the kidneys and liver. Furthermore, the effects on the cardiovascular system could be worse if taurine and caffeine are combined. Caffeine alone does not significantly decrease sleep as much as a taurine/high caffeine ratio. On the other hand, a low ratio does.

Cancer remains a leading cause of morbidity and mortality worldwide, and effective strategies for cancer prevention are urgently needed to complement therapeutic advances. While dietary factors are known to influence cancer risk, the molecular mechanisms that mediate inter-individual responses to nutritional exposures remain poorly defined. Emerging evidence identifies long non-coding RNAs (lncRNAs) as pivotal regulators of gene expression, chromatin organization, metabolic homeostasis, immune signaling, and cellular stress responses, the core processes that drive cancer initiation and progression and are highly sensitive to nutritional status. In parallel, advances in precision nutrition have highlighted how variability in genetics, metabolism, microbiome composition, and epigenetic landscapes shape dietary influences on cancer susceptibility. This review integrates these rapidly evolving fields by positioning lncRNAs as molecular conduits that translate dietary exposures into transcriptional and epigenetic programs governing cancer development, progression, and therapeutic vulnerability. We provide mechanistic evidence demonstrating how dietary bioactive compounds and micronutrients, including polyphenols [such as curcumin, resveratrol, epigallocatechin gallate (EGCG)], flavonoids, alkaloids such as berberine, omega-3 (ω-3) fatty acids, folate, vitamin D, probiotic metabolites (such as butyrate and propionate), and trace elements (such as selenium and zinc), modulate oncogenic and tumor-suppressive lncRNAs. These nutrient–lncRNA interactions influence cancer-relevant pathways controlling proliferation, epithelial–mesenchymal transition (EMT), inflammation, oxidative stress, and metabolic rewiring. We further discuss emerging lncRNA signatures that reflect nutritional and metabolic states, their potential utility as biomarkers for individualized dietary interventions, and their integration into liquid biopsy platforms. Leveraging multi-omics datasets and systems biology, we outline AI-driven frameworks to map nutrient–lncRNA regulatory networks and identify targetable nodes for cancer chemoprevention. Finally, we address translational challenges, including compound bioavailability, inter-individual variability, and limited clinical validation, and propose future directions for incorporating lncRNA profiling into precision nutrition-guided cancer prevention trials. Together, these insights position lncRNAs at the nexus of diet and cancer biology and establish a foundation for mechanistically informed precision nutrition strategies in cancer chemoprevention.

Cancer remains a leading cause of morbidity and mortality worldwide, and effective strategies for cancer prevention are urgently needed to complement therapeutic ad-vances. While dietary factors are known to influence cancer risk, the molecular mecha-nisms that mediate inter-individual responses to nutritional exposures remain poorly defined. Emerging evidence identifies long non-coding RNAs (lncRNAs) as pivotal regulators of gene expression, chromatin organization, metabolic homeostasis, immune signaling, and cellular stress responses, core processes that drive cancer initiation and progression and are highly sensitive to nutritional status. In parallel, advances in pre-cision nutrition have highlighted how variability in genetics, metabolism, microbiome composition, and epigenetic landscapes shapes dietary influences on cancer susceptibility. This review integrates these rapidly evolving fields by positioning lncRNAs as molecular conduits that translate dietary exposures into transcriptional and epigenetic programs governing cancer development, progression, and therapeutic vulnerability. We provide mechanistic evidence demonstrating how dietary bioactive compounds and micronu-trients, including polyphenols (curcumin, resveratrol, EGCG), flavonoids, alkaloids such as berberine, omega-3 fatty acids, folate, vitamin D, probiotic metabolites (such as bu-tyrate and propionate), and trace elements (such as selenium, and zinc), modulate on-cogenic and tumor-suppressive lncRNAs. These nutrient-lncRNA interactions influence cancer-relevant pathways controlling proliferation, epithelial-mesenchymal transition, inflammation, oxidative stress, and metabolic rewiring. We further discuss emerging lncRNA signatures that reflect nutritional and metabolic states, their potential utility as biomarkers for individualized dietary interventions, and their integration into liquid biopsy platforms. Leveraging multi-omics datasets and systems biology, we outline AI-driven frameworks to map nutrient-lncRNA regulatory networks and identify tar-getable nodes for cancer chemoprevention. Finally, we address translational challenges, including compound bioavailability, inter-individual variability, and limited clinical validation, and propose future directions for incorporating lncRNA profiling into preci-sion nutrition-guided cancer prevention trials. Together, these insights position lncRNAs at the nexus of diet and cancer biology and establish a foundation for mechanistically informed precision nutrition strategies in cancer chemoprevention.