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Plasma phospholipid long-chain ω-3 fatty acids and total and cause-specific mortality in older adults: a cohort study.
Tuesday,2013-10-01 09:06 America/Los_Angeles — poolea2
| Title | Plasma phospholipid long-chain ω-3 fatty acids and total and cause-specific mortality in older adults: a cohort study. |
| Publication Type | Journal Article |
| Year of Publication | 2013 |
| Authors | Mozaffarian, D, Lemaitre, RN, King, IB, Song, X, Huang, H, Sacks, FM, Rimm, EB, Wang, M, Siscovick, DS |
| Journal | Ann Intern Med |
| Volume | 158 |
| Issue | 7 |
| Pagination | 515-25 |
| Date Published | 2013 Apr 02 |
| ISSN | 1539-3704 |
| Keywords | Aged, Biomarkers, Cause of Death, Coronary Disease, Diet Records, Docosahexaenoic Acids, Eicosapentaenoic Acid, Fatty Acids, Omega-3, Fatty Acids, Unsaturated, Feeding Behavior, Female, Humans, Male, Prospective Studies, Risk Assessment, Stroke |
| Abstract | <p><b>BACKGROUND: </b>Long-chain ω-3 polyunsaturated fatty acids (ω3-PUFAs), including eicosapentaenoic acid (EPA) (20:5ω-3), docosapentaenoic acid (DPA) (22:5ω-3), and docosahexaenoic acid (DHA) (22:6ω-3), have been shown to reduce cardiovascular risk, but effects on cause-specific and total mortality and potential dose-responses remain controversial. Most observational studies have assessed self-reported dietary intake and most randomized trials have tested effects of adding supplements to dietary intake and evaluated secondary prevention, thus limiting inference for dietary ω3-PUFAs or primary prevention.</p><p><b>OBJECTIVE: </b>To investigate associations of plasma phospholipid EPA, DPA, DHA, and total ω3-PUFA levels with total and cause-specific mortality among healthy older adults not receiving supplements.</p><p><b>DESIGN: </b>Prospective cohort study.</p><p><b>SETTING: </b>4 U.S. communities.</p><p><b>PARTICIPANTS: </b>2692 U.S. adults aged 74 years (±5 years) without prevalent coronary heart disease (CHD), stroke, or heart failure at baseline.</p><p><b>MEASUREMENTS: </b>Phospholipid fatty acid levels and cardiovascular risk factors were measured in 1992. Relationships with total and cause-specific mortality and incident fatal or nonfatal CHD and stroke through 2008 were assessed.</p><p><b>RESULTS: </b>During 30 829 person-years, 1625 deaths (including 570 cardiovascular deaths), 359 fatal and 371 nonfatal CHD events, and 130 fatal and 276 nonfatal strokes occurred. After adjustment, higher plasma levels of ω3-PUFA biomarkers were associated with lower total mortality, with extreme-quintile hazard ratios of 0.83 for EPA (95% CI, 0.71 to 0.98; P for trend = 0.005), 0.77 for DPA (CI, 0.66 to 0.90; P for trend = 0.008), 0.80 for DHA (CI, 0.67 to 0.94; P for trend = 0.006), and 0.73 for total ω3-PUFAs (CI, 0.61 to 0.86; P for trend < 0.001). Lower risk was largely attributable to fewer cardiovascular than noncardiovascular deaths. Individuals in the highest quintile of phospholipid ω3-PUFA level lived an average of 2.22 more years (CI, 0.75 to 3.13 years) after age 65 years than did those in the lowest quintile.</p><p><b>LIMITATION: </b>Temporal changes in fatty acid levels and misclassification of causes of death may have resulted in underestimated associations, and unmeasured or imperfectly measured covariates may have caused residual confounding.</p><p><b>CONCLUSION: </b>Higher circulating individual and total ω3-PUFA levels are associated with lower total mortality, especially CHD death, in older adults.</p><p><b>PRIMARY FUNDING SOURCE: </b>National Institutes of Health.</p> |
| DOI | 10.7326/0003-4819-158-7-201304020-00003 |
| Alternate Journal | Ann. Intern. Med. |
| PubMed ID | 23546563 |
| PubMed Central ID | PMC3698844 |
| Grant List | N01-HC-85085 / HC / NHLBI NIH HHS / United States R01 AG015928 / AG / NIA NIH HHS / United States R01 HL085710 / HL / NHLBI NIH HHS / United States R01-HL-085710 / HL / NHLBI NIH HHS / United States U01 HL080295 / HL / NHLBI NIH HHS / United States N01-HC-85081 / HC / NHLBI NIH HHS / United States N01 HC015103 / HC / NHLBI NIH HHS / United States R56 AG020098 / AG / NIA NIH HHS / United States AG-20098 / AG / NIA NIH HHS / United States N01HC55222 / HL / NHLBI NIH HHS / United States N01-HC-85086 / HC / NHLBI NIH HHS / United States N01HC85086 / HL / NHLBI NIH HHS / United States AG-027058 / AG / NIA NIH HHS / United States N01-HC-85082 / HC / NHLBI NIH HHS / United States N01 HC-55222 / HC / NHLBI NIH HHS / United States HHSN268201200036C / HL / NHLBI NIH HHS / United States N01-HC-85083 / HC / NHLBI NIH HHS / United States N01-HC-75150 / HC / NHLBI NIH HHS / United States N01-HC-85080 / HC / NHLBI NIH HHS / United States R01 HL080295 / HL / NHLBI NIH HHS / United States R01 AG020098 / AG / NIA NIH HHS / United States N01HC75150 / HL / NHLBI NIH HHS / United States N01-HC-85079 / HC / NHLBI NIH HHS / United States HL080295 / HL / NHLBI NIH HHS / United States N01-HC-85239 / HC / NHLBI NIH HHS / United States AG-023629 / AG / NIA NIH HHS / United States N01HC85079 / HL / NHLBI NIH HHS / United States R01 AG023629 / AG / NIA NIH HHS / United States R01 AG027058 / AG / NIA NIH HHS / United States N01 HC045133 / HC / NHLBI NIH HHS / United States N01 HC035129 / HC / NHLBI NIH HHS / United States R56 AG023629 / AG / NIA NIH HHS / United States N01-HC-85084 / HC / NHLBI NIH HHS / United States |