(1) Background: Numerous meta-analyses have shown that a high intake of dietary fiber plays a protective role in preventing the development of various types of cancer. However, previous studies have been limited by focusing on a single type of dietary fiber and variations in outcome measures, which may not be effectively applied to provide dietary guidance for the general population. (2) Object: We summarized the meta-analysis of dietary fiber and cancer, and provided references for residents to prevent cancer. (3) Methods: Systematic search of relevant meta-analyses on the association between dietary fiber and cancer occurrence in PubMed, Web of Science and other databases was conducted from the time of database construction to February 2023. The method logical and evidence quality assessments were performed by applying the criteria in the “A Measurement Tool to Assess Systematic Reviews-2” (AMSTAR2) scale and the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) Expert Report, respectively. (4) Results: Our analysis included 11 meta-analyses, and the AMSTAR 2 assessment revealed that the overall methodological quality was suboptimal, with two key items lacking sufficient information. Nonetheless, our findings indicate that a high intake of dietary fiber is associated with a reduced risk of several types of cancer, including esophageal, gastric, colon, rectal, colorectal adenoma, breast, endometrial, ovarian, renal cell, prostate, and pancreatic cancers. The majority of these associations were supported by a “probable” level of evidence. (5) Conclusions: Dietary fiber intake has different protective effects on different cancers.

Cardiovascular disease (CVD) is a major global health concern associated with modifiable risk factors including obesity, hypertension, dyslipidemia, and hyperglycemia. While various dietary patterns have demonstrated cardiovascular benefits, their comparative effectiveness remains unclear. This network meta-analysis (NMA) systematically evaluates the impact of eight dietary patterns on cardiovascular risk markers. We included randomized controlled trials (RCTs) assessing low-fat, Mediterranean, ketogenic, low-carbohydrate, high-protein, vegetarian, intermittent fasting, and DASH diets. A random-effects model analyzed mean differences (MD) in body composition (weight, BMI, waist circumference), lipid profiles (triglycerides, total cholesterol, HDL-C, LDL-C), glycemic markers (glucose), and blood pressure (systolic/diastolic). Dietary efficacy was ranked via Surface Under the Cumulative Ranking Curve (SUCRA) scores. Among 21 RCTs (1,663 participants), ketogenic (MD -10.5 kg, 95% CI -18.0 to -3.05; SUCRA 99) and high-protein diets (MD -4.49 kg, 95% CI -9.55 to 0.35; SUCRA 71) showed superior efficacy for weight reduction. For waist circumference, ketogenic (MD -11.0 cm, 95% CI -17.5 to -4.54; SUCRA 100) and low-carbohydrate diets (MD -5.13 cm, 95% CI -8.83 to -1.44; SUCRA 77) achieved greatest reductions. DASH diet most effectively lowered systolic blood pressure (MD -7.81 mmHg, 95% CI -14.2 to -0.46; SUCRA 89), while intermittent fasting also demonstrated significant blood pressure-lowering effects (MD -5.98 mmHg, 95% CI -10.4 to -0.35; SUCRA 76). Low-carbohydrate (MD 4.26 mg/dL, 95% CI 2.46–6.49; SUCRA 98) and low-fat diets (MD 2.35 mg/dL, 95% CI 0.21–4.40; SUCRA 78) optimally increased HDL-C. Diet-specific cardioprotective effects were observed: ketogenic and high-protein diets excel in weight management, DASH and intermittent fasting in blood pressure control, and carbohydrate-restricted diets in lipid modulation. These findings support personalized dietary strategies for targeted CVD risk factor management.

Background: Sucralose and benzo(a)pyrene (B[a]P) are widespread foodborne substances known to harm human health. However, the effects of their combined exposure on kidney function remain unclear. This study aimed to investigate the mechanisms by which sucralose and B[a]P induce kidney injury through P-glycoprotein (PGP/ABCB1), a crucial protein involved in cellular detoxification. Methods: C57BL/6N mice were co-treated with sucralose and B[a]P for 90 days to evaluate their impact on kidney histopathology and function. In vitro experiments assessed cell viability, reactive oxygen species (ROS) levels, and B[a]P accumulation by flow cytometry. Molecular docking and cellular thermal shift assay (CETSA) were used to determine the binding affinity of sucralose to PGP. Furthermore, PCR, Western blotting, and immunohistochemistry were performed to analyze the expression of PGP and its upstream transcription factors. Results: Ninety days of co-exposure to sucralose and B[a]P significantly exacerbated renal dysfunction in mice, as evidenced by the elevated level of serum creatinine and urea nitrogen, which could be reverted by ROS scavenger N-acetyl cysteine (NAC). In vitro, sucralose promoted cellular accumulation of B[a]P, consequently enhancing B[a]P-induced cell growth inhibition and ROS production. Consistently, B[a]P accumulation was enhanced by PGP knockdown in both HK2 and HEK-293 cells. Mechanistically, sucralose can directly bind to PGP, competitively inhibiting its efflux capacity and increasing intracellular B[a]P retention. Prolonged co-exposure further downregulated PGP expression, possibly through the reductions of its transcriptional regulators (PXR, NRF2, and NF-κB). Conclusions: Co-exposure to sucralose and B[a]P exacerbates renal injury by impairing PGP function. Mechanistically, sucralose inhibits PGP activity, resulting in the accumulation of B[a]P within renal cells. This accumulation triggers oxidative stress and inhibits cell growth, which demonstrates that sucralose potentiates B[a]P-induced nephrotoxicity by directly inhibiting PGP-mediated detoxification pathways, thus underscoring the critical need to evaluate toxicity risks associated with combined exposure to these compounds.