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The VITamin D and OmegA-3 TriaL (VITAL): Principal Results for Cardiovascular Disease and Cancer
  READ WHAT THE AUTHORS AY IF YOU ALREADY EAT 1.5 fish servings a week and racial differences, IF YOU ARE AFRICAN AMERCICAN (ETHNIC DIFFERENCES IN RESULTS) and the appendix tables I added just below before the slides. Jules
Download the PDF here
Download the PDF here
"In conclusion, supplementation with n-3 fatty acids did not result in a lower incidence than placebo of the primary end points of major cardiovascular events (a composite of myocardial infarction, stroke, or death from cardiovascular causes) and invasive cancer of any type."
Presented at the AHA meeting
American Heart Association Scientific Sessions
Chicago, Illinois
November 10, 2018
JoAnn E. Manson, MD, DrPH, FAHA
Chief, Division of Preventive Medicine
Brigham and Women's Hospital
Professor of Medicine and the
Michael and Lee Bell Professor of Women's Health
Harvard Medical School
Coauthors: J. Manson, N. Cook, I-M. Lee, W. Christen, S. Bassuk, S. Mora,
H. Gibson, C. Albert, D. Gordon, T. Copeland, D. D'Agostino,
G. Friedenberg, C. Ridge, V. Bubes, E. Giovannucci, W. Willett, J. Buring
Reported by Jules Levin
Marine n-3 Fatty Acids and Prevention of Cardiovascular Disease and Cancer - (pdfs of full article & appendix attached)......In conclusion, supplementation with n-3 fatty acids did not result in a lower incidence than placebo of the primary end points of major cardiovascular events (a composite of myocardial infarction, stroke, or death from cardiovascular causes) and invasive cancer of any type.
Given the popularity of fish oil as a strategy to reduce the incidence of chronic disease,4 clarifying the relation between supplemental n-3 fatty acids and risks of cardiovascular disease and cancer and obtaining more-definitive data on the benefit-risk balance of these supplements is a high priority. Subgroup analyses showed a possible lower incidence of the primary cardiovascular end point with n-3 supplementation than with placebo among participants with low fish consumption (Figure 2) [ from Jules: people eating >1.5 fish portions a week did NOT benefit but those eating less than 1.5 fish portions a week benefited.] Additional subgroup analyses are presented in Tables S3 and S4 and Figure S3 in the Supplementary Appendix, with a focus on exploring differences according to racial or ethnic group, diabetes status, number of traditional cardiovascular risk factors, dietary fish intake, and other variables for the primary end point of major cardiovascular events and the secondary end point of total myocardial infarction. For myocardial infarction, these analyses are presented as explanatory analyses to assess whether the effect of the intervention was similar across subgroups. The suggestion of greater differences in the risk of myocardial infarction among blacks and among those with low fish intake, comparing the n-3 group with the placebo group, is discussed in the Supplementary Appendix. For the other secondary cardiovascular end points of stroke, death from cardiovascular causes, and the expanded composite of major cardiovascular events plus coronary revascularization, no appreciable effect modification was found (data not shown).
Additional Details on Subgroup Analyses
In subgroup analyses, baseline dietary fish intake modified the n-3 intervention effect on major cardiovascular events (Fig. 2) and total myocardial infarction (Supplementary Appendix Fig. S3), with nominally significant reductions of 19% and 40%, respectively, in participants with below-median intake (<1.5 servings per week) but no reductions in those with higher intake (nominal p-interaction<0.05 for both). The HR for myocardial infarction among those who ate fish less than once per month was 0.43 (0.21-0.91). For major cardiovascular events, no other significant interactions were observed. For myocardial infarction, however, race/ethnicity also modified the treatment effect, with a 77% reduction among African Americans (HR=0.23 [0.11-0.47]) and smaller reductions in other racial/ethnic groups (nominal p-interaction by race=0.001) (Fig. S3). African Americans also had reductions in coronary revascularization (HR=0.51 [0.28-0.92]) and total coronary heart disease (HR=0.47 [0.29-0.75]) with n-3 fatty acids. For myocardial infarction, treatment-associated reductions were also observed in participants with comorbidities and a larger number of traditional risk factors (nominal pinteraction=0.047) (Fig. S3). Treatment-associated benefits were more apparent in African Americans than in non-Hispanic whites across all cardiovascular risk factor strata, including among those with diabetes (HR=0.06 [0.01-0.49] in African Americans vs. HR=0.88 [0.43-1.80] in non-Hispanic whites, nominal p-interaction=0.018) (Supplementary Appendix, Table S3). For major cardiovascular events, treatment-associated reductions were greater in those with low baseline fish intake in both racial/ethnic groups (Table S4). For myocardial infarction, treatment-associated reductions among African Americans were observed irrespective of baseline fish intake, but non-Hispanic whites benefited from supplementation only if fish consumption was low (Table S4). The plasma omega-3 index did not significantly modify the intervention's effects. Analyses that censored for nonadherence did not materially change results (HR=0.91 [0.78-1.07] for major cardiovascular events and HR=0.74 [0.58-0.95] for myocardial infarction in the overall cohort). The finding in subgroup analyses of the secondary end point of myocardial infarction that suggested possible greater cardiovascular benefits of n-3 supplementation in blacks than in non-Hispanic whites was unexpected, especially given that both these racial and ethnic groups had similar blood levels of EPA and DHA at baseline and similar fish intake. It may be a chance finding that would require corroboration in future trials. Recent observational studies have shown racial variation in associations of both marine and plant-derived n-3 biomarkers with the incidence of coronary disease.26 Gene variants influence metabolism and the bioavailability of n-3 fatty acids, as has been observed in Greenland Inuits,27 and may influence coronary risk.28 Other racial and ethnic differences in clinical, dietary, or environmental factors may also account for this finding.29 Finally, blacks have a higher prevalence of coexisting conditions such as diabetes and hypertension than do non-Hispanic whites. However, treatment-associated hazard ratios for myocardial infarction were lower across cardiovascular-risk strata among blacks, with lower hazard ratios than among non-Hispanic whites (Table S3 in the Supplementary Appendix).















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