This review delved into the intricate relationship between circadian clocks and physiological processes, emphasizing their critical role in maintaining homeostasis. Orchestrated by interlocked clock genes, the circadian timekeeping system regulates fundamental processes like the sleep-wake cycle, energy metabolism, immune function, and cell proliferation. The central oscillator in the hypothalamic suprachiasmatic nucleus synchronizes with light-dark cycles, while peripheral tissue clocks are influenced by cues such as feeding times. Circadian disruption, linked to modern lifestyle factors like night shift work, correlates with adverse health outcomes, including metabolic syndrome, cardiovascular diseases, infections, and cancer. We explored the molecular mechanisms of circadian clock genes and their impact on metabolic disorders and cancer pathogenesis. Specific associations between circadian disruption and endocrine tumors, spanning breast, ovarian, testicular, prostate, thyroid, pituitary, and adrenal gland cancers, are highlighted. Shift work is associated with increased breast cancer risk, with PER genes influencing tumor progression and drug resistance. CLOCK gene expression correlates with cisplatin resistance in ovarian cancer, while factors like aging and intermittent fasting affect prostate cancer. Our review underscored the intricate interplay between circadian rhythms and cancer, involving the regulation of the cell cycle, DNA repair, metabolism, immune function, and the tumor microenvironment. We advocated for integrating biological timing into clinical considerations for personalized healthcare, proposing that understanding these connections could lead to novel therapeutic approaches. Evidence supports circadian rhythm-focused therapies, particularly chronotherapy, for treating endocrine tumors. Our review called for further research to uncover detailed connections between circadian clocks and cancer, providing essential insights for targeted treatments. We emphasized the importance of public health interventions to mitigate lifestyle-related circadian disruptions and underscored the critical role of circadian rhythms in disease mechanisms and therapeutic interventions.

Background: The interaction between HIV infection, nutrition and immune system functioning is intricate, leading, in many cases, to a cycle of poor health outcomes. Despite the widespread use of highly active antiretroviral therapy (HAART) since the late 1990s and the concomitant increase in the life expectancy of people living with HIV (PLHIV), malnutrition and HIV-associated wasting continue to pose significant challenges, particularly in developing countries. Additionally, metabolic adverse effects associated with HAART, such as alterations in bone and lipid metabolism, as well as the impact on cardiovascular health, add further complexity to patient care. Methods: We conducted a comprehensive literature review of relevant studies involving adults diagnosed with HIV. The studies, published between 2000 and 2023, were identified using the Medline/PubMed, Scopus and Google Scholar databases. Results: Accumulating evidence in the literature indicates that careful monitoring and appropriate nutritional interventions can significantly enhance clinical outcomes in malnourished HIV-positive persons. The importance of addressing the prevalent deficiencies in certain micronutrients discussed in many of the studies is clearly underlined. However, challenges remain, particularly in low-income settings, where limited resources and infrastructure can impede effective implementation. Conclusions: There are critical research gaps with regard to the interaction between ART and nutrition, as well as the development of tailored nutritional approaches that aim to improve patient outcomes. Future research directions and policy strategies should focus on the development of sustainable programmes aimed at enhancing the quality of life for PLHIV.

Background/Objectives: Recent research has focused on the study of the epigenetic role of nutrition as a tool which is expected to introduce new perspectives in the field of disease prevention and management. Although maternal nutrition is one of the best-studied mechanisms of epigenetic modifications of the fetus/newborn, less is known on the impact of childhood/adolescent nutrition on the regulation of epigenetic mecha-nisms after the first year of life. The aim of the present study was the assessment of the epigenetic role of nutrition in the health and development of children and adolescents. Methods: A systematic review was performed according to the Preferred Reported Items for Systematic Reviews and Meta-analyses guidelines in five databases (PubMed, Cochrane, Science Direct, Scopus, and Google Scholar) up to 31 October 2024, which yielded 17 eligible studies. The Newcastle–Ottawa Scale and the Cochrane Collabora-tion Risk of Bias-2 tool were used for the evaluation of risk of bias in observational studies and randomized trials, respectively. Results: Three studies investigated the epi-genetic modifications due to lifestyle interventions combining changes both in diet and physical activity; the remaining 14 studies examined the role of dietary nutrients in the regulation of epigenetic mechanisms in various health conditions, such as Angelman’s syndrome, parenteral nutrition in Intensive Care Units, attention deficit hyperactivity disorder, risk of cardiovascular diseases, asthma or food sensitization, obesity, insulin resistance, and type 2 diabetes or evaluated epigenetic markers as new tools for the comprehension and prediction of the participants’ response to nutritional interven-tions. Conclusions: The important impact of diet on the regulation of epigenetic mech-anisms and the expression of various genes and gene pathways could be utilized for personalized nutritional interventions in various pediatric health conditions.

Critical illness (CI) triggers complex disruptions in the growth hormone (GH)/insulin-like growth factor (IGF) axis, significantly affecting the dynamics of insulin-like growth-factor-binding proteins (IGFBPs). Among these, IGFBP-2 shows a sustained elevation during CI, which inversely correlates with serum levels of IGF-1, IGFBP-3, and the acid-labile subunit (ALS). Although IGFBP-2 does not directly interact with ALS, it may influence the availability of IGFs by competing with other IGFBPs for binding to IGF-1 and IGF-2. Research suggests that this persistent elevation of IGFBP-2 is largely driven by cytokine activity during CI, reflecting an adaptive response rather than a direct result of GH/IGF axis dysregulation. The clinical importance of IGFBP-2 is emphasized by its correlation with disease severity in conditions like sepsis and coronavirus disease 2019 (COVID-19), where its levels are markedly elevated compared to healthy controls and are similar to those observed in sepsis from various causes. Beyond its role in endocrine regulation, IGFBP-2 appears to play a part in metabolic and inflammatory pathways. Elevated IGFBP-2 levels have been linked to increased mortality and longer hospital stays, indicating its potential utility as a prognostic marker. Furthermore, measuring plasma IGFBP-2 may have other diagnostic applications, aiding in the assessment of CI when traditional biomarkers are inconclusive.