Most industrialized nations in the world have established Intake Recommendations for EPA and DHA omega-3; the US and Canada have not.
This just published analysis and report from the US Agency for Healthcare Research and Quality is a positive step in the right direction.
Part of the barrier toward setting intake recommendations has rested in the uncertainty about human metabolism and conversion between the different forms of omega-3s. What we’ve learned in recent years is that the shorter form of omega-3 (derived from plants) is inadequate to support healthy blood levels of the longer chain omega-3s EPA and DHA (naturally occurring in fish and marine animals). My reference here to “healthy blood levels” is an amount sufficient to meaningfully reduce the risk of someone dropping dead from a heart attack. Truth is, about half the people who die from a heart attack have not been diagnosed with heart disease.
Here, with these findings, we can move together as a country toward consuming minimal levels of EPA and DHA omega-3. It will do us all good.
A side note: Research and the study of other healthy populations has shown us that more than 200 mg EPA and DHA is clearly beneficial. For now, to improve mortality, we can start with the basic minimum.
Volume 4: Effects of Eicosapentanoic Acid and Docosahexanoic Acid on Mortality Across Diverse Settings: Systematic Review and Meta-Analysis of Randomized Trials and Prospective Cohorts
Background: Eicosapentanoic acid (EPA) and docosahexanoic acid (DHA) intake may protect from cardiovascular or all-cause mortality.
Objective: To synthesize evidence from randomized controlled trials (RCTs) and large prospective cohorts on the effects of EPA and DHA on cardiac, cardiovascular, or all-cause mortality.
Design: We conducted a systematic review with random effects meta-analysis and mixed effects dose-response meta-regression. Included were RCTs of EPA and DHA supplementation (>4 weeks of intervention, <6 grams per day) and large prospective cohorts (>1000 people, >3 years of followup) quantifying DHA or EPA intake.
Results: In RCTs, the summary relative risks for all-cause mortality (17 trials, 51,264 patients) and cardiovascular mortality (14 trials, 48,500 patients) were 0.95 (95% confidence interval, CI: 0.89, 1.01) and 0.89 (95% CI, 0.83, 0.96), respectively, with no evidence for heterogeneity. The effect of DHA and EPA was not significantly associated with population or study characteristics or supplement dose. In dose-response meta-regressions, mean EPA and DHA intake up to 0.20 grams daily was associated with decreased risk of cardiac, cardiovascular, or sudden cardiac death (odds ratio 0.64 per 0.20 grams average daily intake, 95% CI: 0.46, 0.89—data from 7 cohorts, 123,122 participants), with no significant change in risk (positive or negative) at higher mean intakes. Dose-response analyses were not statistically significant for other intake thresholds or alternative mortality definitions.
Conclusions: The maximal positive effect of EPA and DHA appears to plateau at a mean daily intake of 0.20 grams. There is no evidence that the effect of EPA and DHA on mortality phenotypes differs across populations and settings.
Link to AHRQ webpage and announcement: http://www.ahrq.gov/clinic/tp/nutritn4tp.htm
Link to full report: http://www.ahrq.gov/downloads/pub/evidence/pdf/nutrition/nutrtp4.pdf