Omega-3 Fatty Acid Biomarkers and Incident Atrial Fibrillation.

BACKGROUND: The relationship between omega-3 fatty acids and atrial fibrillation (AF) remains controversial. OBJECTIVES: This study aimed to determine the prospective associations of blood or adipose tissue levels of eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA) with incident AF. METHODS: We used participant-level data from a global consortium of 17 prospective cohort studies, each with baseline data on blood or adipose tissue omega-3 fatty acid levels and AF outcomes. Each participating study conducted a de novo analyses using a prespecified analytical plan with harmonized definitions for exposures, outcome, covariates, and subgroups. Associations were pooled using inverse-variance weighted meta-analysis. RESULTS: Among 54,799 participants from 17 cohorts, 7,720 incident cases of AF were ascertained after a median 13.3 years of follow-up. In multivariable analysis, EPA levels were not associated with incident AF, HR per interquintile range (ie, the difference between the 90th and 10th percentiles) was 1.00 (95% CI: 0.95-1.05). HRs for higher levels of DPA, DHA, and EPA+DHA, were 0.89 (95% CI: 0.83-0.95), 0.90 (95% CI: 0.85-0.96), and 0.93 (95% CI: 0.87-0.99), respectively. CONCLUSIONS: In vivo levels of omega-3 fatty acids including EPA, DPA, DHA, and EPA+DHA were not associated with increased risk of incident AF. Our data suggest the safety of habitual dietary intakes of omega-3 fatty acids with respect to AF risk. Coupled with the known benefits of these fatty acids in the prevention of adverse coronary events, our study suggests that current dietary guidelines recommending fish/omega-3 fatty acid consumption can be maintained.

Invited commentary: dietary polyunsaturated Fatty acids and chronic systemic inflammation--a potentially intriguing link.

It remains largely unclear whether consumption of total and individual polyunsaturated fatty acids (PUFAs) is associated with chronic systemic inflammation in healthy, free-living individuals. While available evidence (stemming principally from mechanistic studies) has indicated that greater intake of n-6 PUFAs may lead to increased levels of inflammation-for instance, by their acting as precursors to proinflammatory eicosanoids and increasing levels of oxidized linoleic acid metabolites-n-3 PUFAs are precursors to some antiinflammatory eicosanoids. New human data from a Dutch prospective study, the Rotterdam Study-as presented by Muka et al. ( Am J Epidemiol. 2015;181(11):846-856) in this issue of the Journal-now make an important contribution to the relatively scarce literature on the association of dietary n-3 and n-6 PUFAs with serum levels of C-reactive protein (CRP), a key marker of inflammation, in a general population. The study by Muka et al. benefitted from repeated CRP measurements, comprehensive correction for potential confounding, and wide-ranging sensitivity analyses. The findings show no significant trend regarding n-3 PUFAs but indicate an important inverse association between n-6 PUFAs and chronic systemic inflammation. This study provides support for existing dietary guidelines, which encourage consumption of a combination of n-3 and n-6 PUFAs in the diet.

Vitamin D and risk of future hypertension: meta-analysis of 283,537 participants.

The evidence on the association between baseline vitamin D status and risk of incident hypertension in general populations is limited and has not been reliably quantified. We conducted a systematic review and meta-analysis of published prospective studies evaluating the associations of baseline vitamin D status (circulating 25-hydroxyvitamin D [25(OH)D] levels and dietary vitamin D intake) with risk of hypertension. Eligible studies were identified in a literature search of MEDLINE, EMBASE, and Web of Science up to November 2012. Pooled relative risks (RRs) with 95% confidence intervals were calculated using random effects models. Generalized least-squares trend estimation was used to assess dose-response relationships. Of the 2,432 articles reviewed for eligibility, eight unique prospective cohorts with aggregate data on 283,537 non-overlapping participants and 55,816 incident hypertension cases were included. The RRs (95% CIs) for hypertension in a comparison of extreme thirds of baseline levels of vitamin D were 0.70 (0.58, 0.86) for seven studies that measured blood 25(OH) D levels and 1.00 (0.95, 1.05) for four studies that assessed dietary vitamin D intake. The pooled RR of incident hypertension per 10 ng/mL increment in baseline 25(OH)D levels was 0.88 (0.81, 0.97) in dose-response analysis. Evidence was lacking of heterogeneity among studies that measured blood 25(OH) D levels and those that assessed dietary vitamin D status. Studies are needed to determine whether the association of vitamin D with hypertension represents a causal association and also to determine whether vitamin D therapy may be beneficial in the prevention or the treatment of hypertension.