Findings from observational studies on the associations between vitamin E intake and stroke risk remain controversial, and the dose–response relationship between vitamin E intake and risk of stroke remains to be determined. We conducted a meta-analysis of prospective studies aiming to clarify the relationships between vitamin E intake and risk of stroke. Relevant studies were identified by searching online databases through to June 2018. We computed summary relative risks (RR) with corresponding 95 % CI. Among 3156 articles retrieved from online databases and relevant bibliographies, nine studies involving 3284 events and 220 371 participants were included in the final analyses. High dietary vitamin E intake was inversely associated with the risk of overall stroke (RR=0·83, 95 % CI 0·73, 0·94), and with the risk of stroke for individuals who were followed-up for <10 (RR=0·84, 95 % CI 0·72, 0·91). There was a non-linear association between dietary vitamin E intake and stroke risk (P=0·0249). Omission of any single study did not alter the summary result. In conclusion, this meta-analysis suggests that there is a significant inverse relationship between dietary vitamin E intake and stroke risk. This meta-analysis provides evidence that a higher dietary vitamin E intake is associated with a lower stroke risk.

Previous studies show inconsistent associations between α-linolenic acid (ALA) and risk of CHD. We aimed to examine an aggregate association between ALA intake and risk of CHD, and assess for any dose–response relationship. We searched the PubMed, EMBASE and Web of Science databases for prospective cohort studies examining associations between ALA intake and CHD, including composite CHD and fatal CHD. Data were pooled using random-effects meta-analysis models, comparing the highest category of ALA intake with the lowest across studies. Subgroup analysis was conducted based on study design, geographic region, age and sex. For dose–response analyses, we used two-stage random-effects dose–response models. In all, fourteen studies of thirteen cohorts were identified and included in the meta-analysis. The pooled results showed that higher ALA intake was associated with modest reduced risk of composite CHD (risk ratios (RR)=0·91; 95 % CI 0·85, 0·97) and fatal CHD (RR=0·85; 95 % CI 0·75, 0·96). The analysis showed a J-shaped relationship between ALA intake and relative risk of composite CHD (χ2=21·95, P<0·001). Compared with people without ALA intake, only people with ALA intake <1·4 g/d showed reduced risk of composite CHD. ALA intake was linearly associated with fatal CHD – every 1 g/d increase in ALA intake was associated with a 12 % decrease in fatal CHD risk (95 % CI −0·21, −0·04). Though a higher dietary ALA intake was associated with reduced risk of composite and fatal CHD, the excess composite CHD risk at higher ALA intakes warrants further investigation, especially through randomised controlled trials.

Dietary Zn recommendations vary widely across Europe due to the heterogeneity of approaches used by expert panels. Under the EURopean micronutrient RECommendations Aligned (EURRECA) consortium a protocol was designed to systematically review and undertake meta-analyses of research data to create a database that includes ‘best practice’ guidelines which can be used as a resource by future panels when setting micronutrient recommendations. As part of this process, the objective of the present study was to undertake a systematic review and meta-analysis of previously published data describing the relationship between Zn intake and status in adults. Searches were performed of literature published up to February 2010 using MEDLINE, Embase and the Cochrane Library. Data extracted included population characteristics, dose of Zn, duration of study, dietary intake of Zn, and mean concentration of Zn in plasma or serum at the end of the intervention period. An intake–status regression coefficient ($\circ {>\beta }$$$) was estimated for each individual study, and pooled meta-analysis undertaken. The overall pooled $\circ {>\beta }$$$ for Zn supplementation on serum/plasma Zn concentrations from randomised controlled trials and observational studies was 0·08 (95 % CI 0·05, 0·11; P < 0·0001; I2 84·5 %). An overall $\circ {>\beta }$$$ of 0·08 means that for every doubling in Zn intake, the difference in Zn serum or plasma concentration is $2^{ \circ {>\beta }}$$$ (20·08 = 1·06), which is 6 %. Whether the dose–response relationship, as provided in the present paper, could be used as either qualitative or quantitative evidence to substantiate the daily Zn intake dose necessary to achieve normal or optimal levels of biomarkers for Zn status remains a matter of discussion.

The objective of the present study was to assess the effects of Enterococcus sp. strain TN-3 isolated from deep seawater on inhibition of eosinophil accumulation, IgE production and active cutaneous anaphylaxis (ACA). We investigated the effects of viable and non-viable TN-3 on allergen-induced peritoneal eosinophil accumulation in mice. Viable (5·4 × 1010 colony-forming units per 60 mg) or non-viable TN-3 (60 mg) was orally administered to BALB/c mice that had been sensitised with the cedar pollen (Cryptomeria japonica) allergen. Oral administration of non-viable TN-3 was effective in suppressing eosinophil accumulation while viable TN-3 was ineffective. We also examined the dose–response relationship for non-viable TN-3 in regard to eosinophil accumulation, IgE production and ACA in allergen-primed mice. Non-viable TN-3 was orally administered at doses of 15 mg (low dose), 30 mg (medium dose) and 60 mg (high dose) to BALB/c mice that had been sensitised with cedar pollen allergen. The anti-allergic effects expressed as inhibition of eosinophil accumulation, IgE production and ACA were found at the low and high doses, but not at the medium dose. These results suggest that non-viable TN-3 exhibited anti-allergic effects at doses of 15 and 60 mg.