Dietary intake of vitamins A, C, and E and the risk of colorectal adenoma: a meta-analysis of observational studies
ABSTRACT To comprehensively summarize the association between dietary intake of vitamins A, C, and E and the risk of colorectal adenoma (CRA), the precursor of colorectal cancer, relevant studies were identified in MEDLINE and EMBASE up to 31 October 2012. Summary relative risks (SRRs) with 95% confidence intervals (CIs) were pooled with a random-effects model. Between-study heterogeneity was assessed using Cochran's Q and I statistics. A total of 13 studies with 3832 CRA cases were included in this meta-analysis. On the basis of the highest versus lowest analysis, dietary intake of vitamin C reduced the risk of CRA by 22% (SRRs 0.78, 95% CIs: 0.62-0.98). Subgroup analyses showed that this relation was not modified by BMI, smoking status, and dietary energy intake. Further, dietary intake of β-carotene was also inversely associated with the risk of CRA. However, dietary intake of vitamins A and E was not associated with the risk of CRA in overall and subgroup analyses (vitamin A: SRRs 0.87, 95% CIs: 0.67-1.14; vitamin E: SRRs 0.87, 95% CIs: 0.69-1.10). Our results indicate that dietary intake of vitamin C and β-carotene, but not vitamins A and E, could reduce the risk of CRA. However, these associations seem to be limited. Further investigation using large samples and a rigorous methodology is warranted.
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ABSTRACT: Several epidemiological studies show that diets rich in fruits and vegetables reduce the risk of developing several chronic diseases, such as type 2 diabetes, atherosclerosis, and cancer. These diseases are linked with systemic, low grade chronic inflammation. Although controversy persists on the bioactive ingredients, several secondary plant metabolites have been associated with these beneficial health effects. Carotenoids represent the most abundant lipid-soluble phytochemicals, and in vitro and in vivo studies have suggested that they have anti-oxidant, anti-apoptotic, and anti-inflammatory properties. Recently, many of these properties have been linked to the effect of carotenoids on intracellular signaling cascades, thereby influencing gene-expression and protein translation. By blocking the translocation of NF-κB to the nucleus, carotenoids are able to interact with the NF-κB pathway, and thus, inhibit the downstream production of inflammatory cytokines, such as IL-8 or PGE-2. Carotenoids can also block oxidative stress by interacting with the Nrf-2 pathway, enhancing its translocation into the nucleus, and activating phase II enzymes and antioxidants, such as glutathione-S-transferases. In this review, which is organized into in vitro, animal, and human investigations, we summarized current knowledge on carotenoids and metabolites with respect to their ability to modulate inflammatory and oxidative stress pathways and discussed potential dose-health relations. While many pathways involved in the bioactivity of carotenoids have been revealed, future research should be directed on dose-response relations of carotenoids, their metabolites, and their effect on transcription factors and metabolism.Nutrition Research 11/2014; DOI:10.1016/j.nutres.2014.07.010 · 2.59 Impact Factor
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ABSTRACT: Epidemiological studies evaluating the association between the intake of vitamin C and lung cancer risk have produced inconsistent results. We conducted a meta-analysis to assess the association between them. Pertinent studies were identified by a search of PubMed, Web of Knowledge and Wan Fang Med Online through December of 2013. Random-effect model was used to combine the data for analysis. Publication bias was estimated using Begg's funnel plot and Egger's regression asymmetry test. Eighteen articles reporting 21 studies involving 8938 lung cancer cases were included in this meta-analysis. Pooled results suggested that highest vitamin C intake level versus lowest level was significantly associated with the risk of lung cancer [summary relative risk (RR) = 0.829, 95%CI = 0.734-0.937, I(2) = 57.8%], especially in the United States and in prospective studies. A linear dose-response relationship was found, with the risk of lung cancer decreasing by 7% for every 100 mg/day increase in the intake of vitamin C [summary RR = 0.93, 95%CI = 0.88-0.98]. No publication bias was found. Our analysis suggested that the higher intake of vitamin C might have a protective effect against lung cancer, especially in the United States, although this conclusion needs to be confirmed.Scientific Reports 08/2014; 4:6161. DOI:10.1038/srep06161 · 5.08 Impact Factor
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ABSTRACT: Epidemiologic studies that investigate whether vitamin C and E intake protects against bladder cancer have yielded inconsistent results. We conducted a systematic review and meta-analysis of published cohort and case-control studies to summarize the epidemiologic evidence investigating vitamin C and E intake and bladder cancer. Studies were identified through a search of PubMed and Embase databases and of references from relevant publications. Meta-analyses were conducted to estimate summary risk estimates (REs) and 95% confidence intervals (CIs) for vitamin C and E intake using fixed- or random-effects model depending on the heterogeneity of the studies. Subgroup analyses were performed according to study design, sex, geographical regions and source of vitamins intake. The summary REs of bladder cancer for all published studies was 0.90 (95% CI, 0.79-1.00) and 0.82 (95% CI, 0.72-0.90) for vitamin C and E intake, respectively, with no evidence of between-study heterogeneity for vitamin E, but some heterogeneity for vitamin C intake. Although some of the summary effects were non-significant, subgroup analyses showed that these inverse relationships were not modified by study design, sex, geographical regions and source of vitamins intake for vitamin E intake. Our results indicated that high intake of vitamin E could reduce bladder cancer risk. However, the inverse association between vitamin C and bladder cancer seemed to be limited. Further studies using larger samples and a rigorous methodology are warranted.International Journal of Clinical and Experimental Medicine 01/2014; 7(11):4154-64. · 1.42 Impact Factor