Background/Objectives: Fasting has been proposed as a non-pharmacologic method of reducing chemotherapy toxicity. However, its effects across outcome domains have not been well-quantified. Methods: In line with PRISMA 2020 guidelines (PROSPERO: CRD420261296778), we searched PubMed, Embase, Web of Science, and CENTRAL from January 2015 through April 2026 for randomized or prospective comparative trials evaluating fasting during chemotherapy. Risk of bias was assessed using RoB 2 and criteria aligned with ROBINS-I. Standardized mean differences (Hedges’ g) and risk ratios (RRs) were pooled using three-level random-effects models. Results: Seven publications reporting six trials (268 participants) were included. The pooled estimate did not reach statistical significance (g = 0.21, 95% CI: −0.02–0.43, p = 0.064). Hematologic parameters (g = 0.11, 95% CI: −0.23–0.45) and quality of life (QoL) and patient-reported outcomes from one trial (g = 0.32, 95% CI: −0.03–0.66) did not differ significantly between groups. Adverse events also did not differ significantly (RR = 0.86, 95% CI: 0.55–1.36). Conclusions: Across six small trials, fasting during chemotherapy did not significantly affect hematologic parameters, QoL, or adverse events. However, it is worth nothing that point estimates generally favored fasting. Hence, a small benefit can neither be confirmed nor ruled out at this time. Adequately powered trials assessing patient-important outcomes and incorporating nutritional monitoring are needed before fasting can be recommended or ruled out.
Background: Respiratory exposure to fine particulate matter (PM2.5), including diesel exhaust particles (DEPs), is a major air pollutant associated with pulmonary inflammation and cardiovascular diseases. This study investigated the protective effects and underlying mechanisms of retinoic acid (RA) against PM2.5-induced lung injury and accelerated atherosclerosis. Methods: Differentially expressed genes (DEGs) were identified from lung tissues of five non-smokers and six patients with chronic obstructive pulmonary disease obtained from the Gene Expression Omnibus (GEO) database and analyzed using the L1000CDS2, which identified RA as a candidate therapeutic compound. The Comparative Toxicogenomics Database was subsequently used to investigate curated associations between lung and cardiovascular disorders, suggesting the endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) signaling pathway as a candidate mechanism for experimental validation. ApoE−/− mice were exposed to DEP via a nebulization chamber and treated orally with all-trans retinoic acid (1 or 5 mg/kg/day) for 8 weeks. Results: RA significantly reduced C-X-C motif chemokine ligand 1/2 (CXCL1/2) levels in bronchoalveolar lavage fluid and decreased pulmonary expression of Muc5ac, IL-1β, IL-6, and TNF-α. RA also lowered blood pressure, improved serum lipid profiles, and attenuated inflammatory cell infiltration and arterial wall thickening in the thoracic aorta. In HUVECs, RA significantly increased guanosine triphosphate (GTP) cyclohydrolase-1 (GTPCH-1) expression, eNOS phosphorylation, tetrahydrobiopterin (BH4) levels, and the BH4/BH2 ratio. Conclusion: These findings suggest that the activation of the GTPCH-1/BH4/eNOS coupling pathway contributes to the protective effects of RA against DEP-induced cardiovascular injury.
Background/Objectives: Plant-based diets are widely recommended for lowering the risk of type 2 diabetes, with the caveat that their health benefits depend on the quality of the foods consumed. This analysis examined associations between five dietary patterns and pre-existing diabetes among patients with acute pancreatitis (AP), a population in which the relationship between diet and diabetes has not been well characterized. Methods: Participants were drawn from the Diabetes RElated to Acute Pancreatitis and its Mechanisms (DREAM) study, an ongoing multicenter study of adults aged 18 to 75 years with AP in the U.S. This cross-sectional analysis evaluated five dietary patterns using food frequency questionnaires (FFQ): the reverse Empirical Dietary Index for Hyperinsulinemia (rEDIH), the reverse Empirical Dietary Inflammatory Pattern (rEDIP), the overall plant-based diet index (PDI), the healthful plant-based diet index (hPDI), and the unhealthful plant-based diet index (uPDI). We used multivariable logistic regression models to estimate odds ratios (ORs) for pre-existing diabetes (i.e., prior to the AP episode). Results: A total of 647 participants (mean age 49.1 ± 14.5 years) were included. In multivariable-adjusted analyses, participants in the highest versus lowest tertile of PDI had 55% lower odds of pre-existing diabetes (adjusted OR: 0.45; 95% CI: 0.25–0.80; p-trend = 0.005). No statistically significant associations were detected for rEDIP, rEDIH, hPDI, or uPDI. Conclusions: Higher overall PDI scores were associated with lower odds of prevalent diabetes. Among patients with AP, further studies are needed to evaluate dietary contributions to future diabetes development following AP and identify potential dietary strategies for diabetes prevention.
Circadian rhythms coordinate sleep–wake regulation, endocrine secretion, nutrient handling and cellular energy metabolism. Circadian and sleep disturbances are associated with metabolic and cardiovascular morbidity and with neurodegenerative disorders, particularly Alzheimer’s disease (AD) and Parkinson’s disease (PD), although whether restoring circadian alignment modifies neurodegeneration remains uncertain. This narrative review examines chrononutrition within the broader context of sleep regulation, physical activity and circadian care, distinguishing evidence from cellular and animal models, observational studies and clinical trials. Meal timing and dietary composition act as signals to peripheral clocks, while NAD+, sirtuins and AMP-activated protein kinase link nutrient availability with clock regulation and mitochondrial metabolism. We appraise time-restricted eating, protein distribution, NAD+ precursors, tryptophan- and melatonin-containing foods, magnesium, omega-3 fatty acids, polyphenols and fermentable fiber. Experimental findings provide mechanistic plausibility, but metabolic improvements and target engagement have not translated into demonstrated neuroprotection. Clinical application must account for levodopa–protein interactions, undernutrition, frailty and sarcopenia. Adequately powered trials with circadian-phase assessment, controlled energy intake and clinically meaningful neurological outcomes are required before a “circadian diet” can be established as a disease-modifying intervention.
Background/Objectives: We examined whether eight obesity-associated polymorphisms and four lifestyle exposures were associated with changes in body fat percentage (BF%) in young adults. Methods: Eighty-four young adults of European ancestry (82% women; age, 20.5 ± 2.6 years) from Kazan, Russia, underwent bioelectrical impedance analysis at baseline and follow-up, 1.9 ± 0.8 years apart. A subsample was genotyped for eight obesity-associated polymorphisms (ADCY3 rs11676272, RERE rs301806, FTO rs1421085, TNRC6B rs4821940, PATJ rs12140153, TFAP2B rs734597, MMS22L rs9385223, and SLC22A3 rs9364554). Dietary intake and sleep characteristics were assessed using questionnaires, including the Pittsburgh Sleep Quality Index (PSQI). Follow-up BF% was analyzed using ANCOVA adjusted for baseline BF%, follow-up duration, age and sex, with false discovery rate (FDR) correction for multiple testing. Results: Mean BF% increased by 1.61 ± 3.97 percentage points (pp) in men (p = 0.14) and by 0.25 ± 4.43 pp in women (p = 0.65), with wide inter-individual variation. Compared with participants in the bottom quartile (BF% change ≤ −2.45 pp), those in the top quartile (BF% gain ≥ 3.38 pp), i.e., those who gained more body fat, were more likely to carry the FTO rs1421085 T allele (p = 0.02; FDR q = 0.157), consumed fewer vegetables (p = 0.004; FDR q = 0.036), and had longer sleep duration (p = 0.028; FDR q = 0.126). Furthermore, poorer subjective sleep quality was associated with higher follow-up BF% in the whole cohort (β = 1.96 pp per PSQI point; 95% CI, 0.23–3.68; p = 0.027; FDR q = 0.11). Conclusions: Given the modest sample size and relatively short follow-up, few associations were detected, most of which did not remain significant after correction for multiple comparisons. Nevertheless, vegetable intake and sleep characteristics may be relevant to changes in adiposity during young adulthood.
