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Blood eicosapentaenoic and docosahexaenoic acids predict all-cause mortality in patients with stable coronary heart disease: the Heart and Soul study.

ABSTRACT: Omega-3 fatty acid (n-3 FA) blood levels and intake have been inversely associated with risk for sudden cardiac death, but their relationship with all-cause mortality is unclear. The purpose of this study was to determine the extent to which baseline blood n-3 FA levels are associated with reduced risk for all-cause mortality in patients with stable coronary heart disease.The Heart and Soul study used a prospective cohort design with a median follow-up of 5.9 years. Patients were recruited between 2000 and 2002 from 12 outpatient facilities in the San Francisco Bay Area. Standard cardiovascular risk factors, demographics, socioeconomic status, health behaviors, and inflammatory markers were collected at baseline. Fasting blood levels of eicosapentaenoic and docosahexaenoic acids were measured and expressed as a percent of total blood FAs. Vital status was assessed with annual telephone interviews and confirmed by review of death certificates. There were 237 deaths among 956 patients. Cox proportional hazards models were used to evaluate the extent to which blood eicosapentaenoic and docosahexaenoic acids were independently associated with all cause mortality. Compared with patients having baseline eicosapentaenoic and docosahexaenoic acids levels below the median (<3.6%), those at or above the median had a 27% decreased risk of death (hazard ratio, 0.73; 95% confidence interval, 0.56-0.94). This association was unaffected by adjustment for age, sex, ethnicity, center, socioeconomic status, traditional cardiovascular risk factors, and inflammatory markers (hazard ratio, 0.74; 95% confidence interval, 0.55-1.00, P<0.05).In these outpatients with stable coronary heart disease, blood n-3 FA levels were inversely associated with total mortality independent of standard and emerging risk factors, suggesting that reduced tissue n-3 FA levels may adversely impact metabolism.

SUBMITTER: Pottala JV

PROVIDER: S-EPMC3058601 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature

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Blood eicosapentaenoic and docosahexaenoic acids predict all-cause mortality in patients with stable coronary heart disease: the Heart and Soul study.

Pottala James V JV Garg Sachin S Cohen Beth E BE Whooley Mary A MA Harris William S WS

Circulation. Cardiovascular quality and outcomes 20100615 4

<h4>Background</h4>Omega-3 fatty acid (n-3 FA) blood levels and intake have been inversely associated with risk for sudden cardiac death, but their relationship with all-cause mortality is unclear. The purpose of this study was to determine the extent to which baseline blood n-3 FA levels are associated with reduced risk for all-cause mortality in patients with stable coronary heart disease.<h4>Methods and results</h4>The Heart and Soul study used a prospective cohort design with a median follow ...[more]

PMID: 20551373

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Project description:Mass changes in the incorporation of linoleic (C18:2), eicosapentaenoic (C20:5) and docosahexaenoic (C22:6) acids in human blood platelet phospholipids were induced by incubating the cells and these fatty acids complexed to albumin. The remodelling of [14C]C18:2, [14C]C20:5 and [14C]C22:6 in classes, subclasses and molecular species of platelet phospholipids was studied in resting and thrombin-stimulated cells. More than 85% of the incorporation was located in phospholipids, representing 5-fold and 2.5-fold increases in the phospholipid C20:5 and C22:6 endogenous content respectively. Thrombin stimulation induced a 30% degradation of 1-acyl-2-C20:5-glycerophosphocholine (GPC) and 1-acyl-2-C22:6-GPC, but did not induce significant release of C18:2 from 1-acyl-2-C18:2-GPC. There was no change in the [14C]fatty acid composition of 1-alkyl-2-acyl-GPC. Thrombin-dependent increases in 1-alkenyl-2-C20:5-glycerophosphoethanolamine (GPE) and 1-alkenyl-2-C22:6-GPE of 2.1-fold and 2.5-fold respectively accounted for the rise in GPE radioactivity and partly compensated for the loss of these fatty acids from 1,2-diacyl-GPC: transfer to 1-alkenyl-2-acyl-GPE was 0.4 and 1.5 nmol/10(9) platelets for C20:5 and C22:6 respectively. [14C]C20:5 and [14C]C22:6 were incorporated into six different species of 1,2-diacyl-GPC, with acylation in the major endogenous forms (C18:1 +C16:0 and C18:0 species) representing 76% and 66% respectively of the total radioactivity present in 1,2-diacyl-GPC. Stimulation by thrombin induced significant release of these fatty acids from the main molecular species of 1,2-diacyl-GPC, but significantly stimulated the synthesis of alkenyl forms of GPE containing C18:1/C22:6 +C16:0/C22:6, C18:0/C22:6 and C18:0/C20:5. C18:0/C18:2, the major endogenous C18:2 molecular species, represented only 10.5% of the incorporation; none of the [14C]C18:2 molecular species was a substrate for transfer towards 1-alkenyl-2-acyl-GPE. It is concluded that when C20:5 and C22:6, but not C18:2, are acylated in 1,2-diacyl-GPC, they participate in thrombin-dependent phospholipid remodelling, and might compete with the turnover and release of arachidonic acid from platelet phospholipids and the subsequent activation of the cells.

Project description:BackgroundEicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have been suggested to prevent the development of metabolic disorders. However, their individual role in treating hyperglycemia and the mechanism of action regarding gut microbiome and metabolome in the context of diabetes remain unclear.ResultsSupplementation of DHA and EPA attenuated hyperglycemia and insulin resistance without changing body weight in db/db mice while the ameliorative effect appeared to be more pronounced for EPA. DHA/EPA supplementation reduced the abundance of the lipopolysaccharide-containing Enterobacteriaceae whereas elevated the family Coriobacteriaceae negatively correlated with glutamate level, genera Barnesiella and Clostridium XlVa associated with bile acids production, beneficial Bifidobacterium and Lactobacillus, and SCFA-producing species. The gut microbiome alterations co-occurred with the shifts in the metabolome, including glutamate, bile acids, propionic/butyric acid, and lipopolysaccharide, which subsequently relieved β cell apoptosis, suppressed hepatic gluconeogenesis, and promoted GLP-1 secretion, white adipose beiging, and insulin signaling. All these changes appeared to be more evident for EPA. Furthermore, transplantation with DHA/EPA-mediated gut microbiota mimicked the ameliorative effect of DHA/EPA on glucose homeostasis in db/db mice, together with similar changes in gut metabolites. In vitro, DHA/EPA treatment directly inhibited the growth of Escherichia coli (Family Enterobacteriaceae) while promoted Coriobacterium glomerans (Family Coriobacteriaceae), demonstrating a causal effect of DHA/EPA on featured gut microbiota.ConclusionsDHA and EPA dramatically attenuated hyperglycemia and insulin resistance in db/db mice, which was mediated by alterations in gut microbiome and metabolites linking gut to adipose, liver and pancreas. These findings shed light into the gut-organs axis as a promising target for restoring glucose homeostasis and also suggest a better therapeutic effect of EPA for treating diabetes. Video abstract.

Dataset Information

Blood eicosapentaenoic and docosahexaenoic acids predict all-cause mortality in patients with stable coronary heart disease: the Heart and Soul study.

Publications

Blood eicosapentaenoic and docosahexaenoic acids predict all-cause mortality in patients with stable coronary heart disease: the Heart and Soul study.

Similar Datasets

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