1.
The plasma level of retinol, vitamins A, C and α-tocopherol could reduce breast cancer risk? A meta-analysis and meta-regression.
Hu, F, Wu, Z, Li, G, Teng, C, Liu, Y, Wang, F, Zhao, Y, Pang, D
Journal of cancer research and clinical oncology. 2015;(4):601-14
Abstract
PURPOSE Plasma antioxidants are supposed to be directly related to breast cancer risk. However, the results remain inconsistent. Herein, we carried this meta-analysis to comprehensively summarize the associations between plasma retinol, vitamins A, C and α-tocopherol and breast cancer risk. METHODS We searched PubMed, Embase and the Cochrane Databases (through September 24, 2014) and the reference lists of the retrieved articles in English with sufficient information to estimate relative risk or odds ratio and the 95% confidence intervals (CIs), or with mean serum/plasma level of vitamins and SD/SEM/p value in breast cancer and controls. Two reviewers independently extracted data using a standardized form, with any discrepancy adjudicated by the third reviewer. RESULTS Forty studies entered this meta-analysis. For the pooled OR, no significant association between plasma retinol and breast cancer was observed (p = 0.13). Significant association was observed between plasma α-tocopherol and breast cancer (pooled OR 0.42, 95% CI 0.25, 0.72, p = 0.00) in the subgroup with the median lowest level of 5.74-9.16 μmol/L. For the weighted mean difference (WMD), the plasma α-tocopherol and vitamin C level between breast cancer and controls were significantly different [WMD = -0.93 μmol/L (95% CI -1.26, -0.61, p = 0.00) and -2.51 μmol/L (95% CI -4.00, -1.02, p = 0.00), respectively]. No significant association between plasma retinol and vitamin A and breast cancer was observed. CONCLUSIONS Severe α-tocopherol deficiency could increase breast cancer risk. The association between plasma vitamin C and breast cancer was only significant in case-control studies. There was no significant association between other vitamins and breast cancer risk.
2.
Effect of vitamin E supplementation on serum C-reactive protein level: a meta-analysis of randomized controlled trials.
Saboori, S, Shab-Bidar, S, Speakman, JR, Yousefi Rad, E, Djafarian, K
European journal of clinical nutrition. 2015;(8):867-73
Abstract
C-reactive protein (CRP), a marker of chronic inflammation, has a major role in the etiology of chronic disease. Vitamin E may have anti-inflammatory effects. However, there is no consensus on the effects of vitamin E supplementation on CRP levels in clinical trials. The aim of this study was to systematically review randomized controlled trials (RCTs) that report on the effects of vitamin E supplementation (α- and γ-tocopherols) on CRP levels. A systematic search of RCTs was conducted on Medline and EMBASE through PubMed, Scopus, Ovid and Science Direct, and completed by a manual review of the literature up to May 2014. Pooled effects were estimated by using random-effects models and heterogeneity was assessed by Cochran's Q and I(2) tests. Subgroup analyses and meta-regression analyses were also performed according to intervention duration, dose of supplementation and baseline level of CRP. Of 4734 potentially relevant studies, only 12 trials met the inclusion criteria with 246 participants in the intervention arms and 249 participants in control arms. Pooled analysis showed a significant reduction in CRP levels of 0.62 mg/l (95% confidence interval = -0.92, -0.31; P < 0.001) in vitamin E-treated individuals, with the evidence of heterogeneity across studies. This significant effect was maintained in all subgroups, although the univariate meta-regression analysis showed that the vitamin E supplementation dose, baseline level of CRP and duration of intervention were not the sources of the observed heterogeneity. The results of this meta-analysis suggest that supplementation with vitamin E in the form of either α-tocopherol or γ-tocopherol would reduce serum CRP levels.
3.
Blood α-tocopherol, γ-tocopherol levels and risk of prostate cancer: a meta-analysis of prospective studies.
Cui, R, Liu, ZQ, Xu, Q
PloS one. 2014;(3):e93044
Abstract
BACKGROUND Epidemiological studies that have examined the association of blood α-tocopherol and γ-tocopherol (the principal bioactive form of vitamin E) levels with the risk of prostate cancer have yielded inconsistent results. In addition, a quantitative assessment of published studies is not available. METHODS AND FINDINGS In this meta-analysis, relevant studies were sought by a search of the PubMed and Embase databases for articles published up to October 2013, with no restrictions. Bibliographies from retrieved articles also were scoured to find further eligible studies. Prospective studies that reported adjusted relative risk (RR) estimates with 95% confidence intervals (CIs) for the association between blood tocopherol levels and the risk of prostate cancer were included. Nine nested case-control studies involving approximately 370,000 participants from several countries were eligible. The pooled RRs of prostate cancer for the highest versus lowest category of blood α-tocopherol levels were 0.79 (95% CI: 0.68-0.91), and those for γ-tocopherol levels were 0.89 (95% CI: 0.71-1.12), respectively. Significant heterogeneity was present among the studies in terms of blood γ-tocopherol levels (p = 0.008) but not in terms of blood α-tocopherol levels (p = 0.33). The risk of prostate cancer decreased by 21% for every 25-mg/L increase in blood α-tocopherol levels (RR: 0.79; 95% CI: 0.69-0.91). CONCLUSIONS Blood α-tocopherol levels, but not γ-tocopherol levels, were inversely associated with the risk of prostate cancer in this meta-analysis.
4.
Use of antioxidant vitamins for the prevention of cardiovascular disease: meta-analysis of randomised trials.
Vivekananthan, DP, Penn, MS, Sapp, SK, Hsu, A, Topol, EJ
Lancet (London, England). 2003;(9374):2017-23
Abstract
INTRODUCTION Oxidised LDL is thought to play an important part in the pathogenesis of atherosclerosis. Observational studies have associated alpha tocopherol (vitamin E), beta carotene, or both, with reductions in cardiovascular events, but not clinical trials. We did a meta-analysis to assess the effect of these compounds on long-term cardiovascular mortality and morbidity. METHODS We analysed seven randomised trials of vitamin E treatment and, separately, eight of beta carotene treatment; all trials included 1000 or more patients. The dose range for vitamin E was 50-800 IU, and for beta carotene was 15-50 mg. Follow-up ranged from 1.4 to 12.0 years. FINDINGS The vitamin E trials involved a total of 81788 patients and the beta carotene trials 138113 in the all-cause mortality analyses. Vitamin E did not provide benefit in mortality compared with control treatment (11.3 vs 11.1%, odds ratio 1.02 [95% CI 0.98-1.06] p=0.42) or significantly decrease risk of cardiovascular death (6.0 vs 6.0%, p=0.86) or cerebrovascular accident (3.6 vs 3.5%, p=0.31). Beta carotene led to a small but significant increase in all-cause mortality (7.4 vs 7.0%, 1.07 [1.02-1.11] p=0.003) and with a slight increase in cardiovascular death (3.4 vs 3.1%, 1.1 [1.03-1.17] p=0.003). No significant heterogeneity was noted for any analysis. INTERPRETATION The lack of a salutary effect was seen consistently for various doses of vitamins in diverse populations. Our results, combined with the lack of mechanistic data for efficacy of vitamin E, do not support the routine use of vitamin E.