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Food that is rich in omega-3

NIHR Signal Omega-3 supplements do not prevent heart disease, stroke or death

Published on 6 November 2018

doi: 10.3310/signal-000670

Omega-3 fatty acid supplements from fish oils or plants have little or no effect on the risk of heart disease, stroke or overall death rates. This finding contradicts a widespread belief that omega-3 supplements are protective. Previous evidence in favour of omega-3 supplements is mainly derived from trials at high risk of bias. The better evidence identified in this review does not demonstrate any health benefit.

The review provides robust evidence confirming current guidance that omega-3 supplements should not be used to prevent cardiovascular disease. However, few of the trials included in this review looked at foodsources of omega-3. Other studies have demonstrated that intake of omega-3 is essential to human health, and it is possible that the intake of foods rich in omega-3 may have a place in a healthy balanced diet.

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Why was this study needed?

Heart disease, stroke and arterial disease, all affect blood vessels. They account for one-third of deaths and, in 2010, cost NHS England £8 billion.

There is a widespread belief that omega-3 can protect against heart disease and stroke, and capsules containing purified omega-3 are widely used. Three different types of omega-3 are metabolically important for humans. These are eicosapentaenoic acid and docosahexaenoic acid, commonly found in marine algae, krill and fish; and alpha-linolenic acid found in seeds, nuts and legumes.

This review aimed to combine all trials of omega-3 supplementation to assess outcomes for all-cause mortality, cardiovascular events (except peripheral artery disease), lipid markers, and weight.

What did this study do?

This updated Cochrane review found 79 randomised controlled trials that compared increased omega-3 intake to usual or lower intake for at least 12 months. Most of the trials used supplements, but some used foods rich in omega-3 or offered dietary advice. Overall, 112,059 adults were included; participants included adults at low and high risk or with established cardiovascular disease. The trials took place in North America, Europe, Australia and Asia, with eight from the UK.

Twenty-five of the trials had a low risk of bias and can be considered highly trustworthy. The rest had a moderate or high risk of bias. Most of the studies assessed omega-3 supplementation with capsules but few examined the effects of other dietary sources, and so it is possible the health effects available from food sources differ.

What did it find?

  • Increasing omega-3 intake showed no effect on overall risk of death (risk ratio [RR] 0.98, 95% confidence interval [CI] 0.90 to 1.03; 39 trials with 92,653 participants, high quality evidence). All-cause mortality was about 9% in both groups.
  • Increasing omega-3 showed no effect on death from heart disease or stroke (RR 0.95, 95% CI 0.87 to 1.03; 25 trials with 67,772 participants, moderate quality evidence). Mortality from these causes was about 7% in both groups.
  • Increasing omega-3 showed no effect on heart disease or stroke (RR 0.99, 95% CI 0.94 to 1.04; 38 trials with 90,378 participants, high-quality evidence). The risk of an event was about 16% in both groups.
  • There is weak evidence that omega-3 may slightly affect serum lipid markers. No effect on body weight was found.

What does current guidance say on this issue?

NICE 2016 guidance on cardiovascular disease risk assessment and reduction states that there is no evidence that omega-3 fatty acid compounds help prevent cardiovascular disease.

It says that omega-3 should not be offered for primary or secondary prevention. It does, however, say that people at high risk of or with existing cardiovascular disease should eat at least two portions of fish each week, including a portion of oily fish, and 4-5 portions of nuts, seeds and legumes.

What are the implications?

This extensive systematic review provides evidence to support current NICE guidance that omega-3 supplements do not prevent heart disease or stroke. Previous claims for benefits of omega-3 supplements appear to come from trials with a higher risk of bias.

The findings do not mean that people should stop eating foods (such as oily fish, seeds, nuts, and legumes) that are rich in omega-3. These foods form an important part of a healthy diet.

Citation and Funding

Abdelhamid AS, Brown TJ, Brainard JS, et al. Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2018;7:CD003177.

Cochrane UK and the Cochrane Heart Group are supported by NIHR infrastructure funding.

Bibliography

Alhassan A, Young J, Lean MEJ et al. Consumption of fish and vascular risk factors: A systematic review and meta-analysis of intervention studies. Atherosclerosis. 2017;266:87-94.

NICE. Cardiovascular disease: risk assessment and reduction, including lipid modification. CG181. London: National Institute for Health and Care Excellence; 2016.

Why was this study needed?

Heart disease, stroke and arterial disease, all affect blood vessels. They account for one-third of deaths and, in 2010, cost NHS England £8 billion.

There is a widespread belief that omega-3 can protect against heart disease and stroke, and capsules containing purified omega-3 are widely used. Three different types of omega-3 are metabolically important for humans. These are eicosapentaenoic acid and docosahexaenoic acid, commonly found in marine algae, krill and fish; and alpha-linolenic acid found in seeds, nuts and legumes.

This review aimed to combine all trials of omega-3 supplementation to assess outcomes for all-cause mortality, cardiovascular events (except peripheral artery disease), lipid markers, and weight.

What did this study do?

This updated Cochrane review found 79 randomised controlled trials that compared increased omega-3 intake to usual or lower intake for at least 12 months. Most of the trials used supplements, but some used foods rich in omega-3 or offered dietary advice. Overall, 112,059 adults were included; participants included adults at low and high risk or with established cardiovascular disease. The trials took place in North America, Europe, Australia and Asia, with eight from the UK.

Twenty-five of the trials had a low risk of bias and can be considered highly trustworthy. The rest had a moderate or high risk of bias. Most of the studies assessed omega-3 supplementation with capsules but few examined the effects of other dietary sources, and so it is possible the health effects available from food sources differ.

What did it find?

  • Increasing omega-3 intake showed no effect on overall risk of death (risk ratio [RR] 0.98, 95% confidence interval [CI] 0.90 to 1.03; 39 trials with 92,653 participants, high quality evidence). All-cause mortality was about 9% in both groups.
  • Increasing omega-3 showed no effect on death from heart disease or stroke (RR 0.95, 95% CI 0.87 to 1.03; 25 trials with 67,772 participants, moderate quality evidence). Mortality from these causes was about 7% in both groups.
  • Increasing omega-3 showed no effect on heart disease or stroke (RR 0.99, 95% CI 0.94 to 1.04; 38 trials with 90,378 participants, high-quality evidence). The risk of an event was about 16% in both groups.
  • There is weak evidence that omega-3 may slightly affect serum lipid markers. No effect on body weight was found.

What does current guidance say on this issue?

NICE 2016 guidance on cardiovascular disease risk assessment and reduction states that there is no evidence that omega-3 fatty acid compounds help prevent cardiovascular disease.

It says that omega-3 should not be offered for primary or secondary prevention. It does, however, say that people at high risk of or with existing cardiovascular disease should eat at least two portions of fish each week, including a portion of oily fish, and 4-5 portions of nuts, seeds and legumes.

What are the implications?

This extensive systematic review provides evidence to support current NICE guidance that omega-3 supplements do not prevent heart disease or stroke. Previous claims for benefits of omega-3 supplements appear to come from trials with a higher risk of bias.

The findings do not mean that people should stop eating foods (such as oily fish, seeds, nuts, and legumes) that are rich in omega-3. These foods form an important part of a healthy diet.

Citation and Funding

Abdelhamid AS, Brown TJ, Brainard JS, et al. Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2018;7:CD003177.

Cochrane UK and the Cochrane Heart Group are supported by NIHR infrastructure funding.

Bibliography

Alhassan A, Young J, Lean MEJ et al. Consumption of fish and vascular risk factors: A systematic review and meta-analysis of intervention studies. Atherosclerosis. 2017;266:87-94.

NICE. Cardiovascular disease: risk assessment and reduction, including lipid modification. CG181. London: National Institute for Health and Care Excellence; 2016.

Omega-3 fatty acids for the primary and secondary prevention of cardiovascular disease

Published on 19 July 2018

Abdelhamid, A. S.,Brown, T. J.,Brainard, J. S.,Biswas, P.,Thorpe, G. C.,Moore, H. J.,Deane, K. H.,AlAbdulghafoor, F. K.,Summerbell, C. D.,Worthington, H. V.,Song, F.,Hooper, L.

Cochrane Database Syst Rev Volume 7 , 2018

BACKGROUND: Researchers have suggested that omega-3 polyunsaturated fatty acids from oily fish (long-chain omega-3 (LCn3), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)), as well as from plants (alpha-linolenic acid (ALA)) benefit cardiovascular health. Guidelines recommend increasing omega-3-rich foods, and sometimes supplementation, but recent trials have not confirmed this. OBJECTIVES: To assess effects of increased intake of fish- and plant-based omega-3 for all-cause mortality, cardiovascular (CVD) events, adiposity and lipids. SEARCH METHODS: We searched CENTRAL, MEDLINE and Embase to April 2017, plus ClinicalTrials.gov and World Health Organization International Clinical Trials Registry to September 2016, with no language restrictions. We handsearched systematic review references and bibliographies and contacted authors. SELECTION CRITERIA: We included randomised controlled trials (RCTs) that lasted at least 12 months and compared supplementation and/or advice to increase LCn3 or ALA intake versus usual or lower intake. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed studies for inclusion, extracted data and assessed validity. We performed separate random-effects meta-analysis for ALA and LCn3 interventions, and assessed dose-response relationships through meta-regression. MAIN RESULTS: We included 79 RCTs (112,059 participants) in this review update and found that 25 were at low summary risk of bias. Trials were of 12 to 72 months' duration and included adults at varying cardiovascular risk, mainly in high-income countries. Most studies assessed LCn3 supplementation with capsules, but some used LCn3- or ALA-rich or enriched foods or dietary advice compared to placebo or usual diet.Meta-analysis and sensitivity analyses suggested little or no effect of increasing LCn3 on all-cause mortality (RR 0.98, 95% CI 0.90 to 1.03, 92,653 participants; 8189 deaths in 39 trials, high-quality evidence), cardiovascular mortality (RR 0.95, 95% CI 0.87 to 1.03, 67,772 participants; 4544 CVD deaths in 25 RCTs), cardiovascular events (RR 0.99, 95% CI 0.94 to 1.04, 90,378 participants; 14,737 people experienced events in 38 trials, high-quality evidence), coronary heart disease (CHD) mortality (RR 0.93, 95% CI 0.79 to 1.09, 73,491 participants; 1596 CHD deaths in 21 RCTs), stroke (RR 1.06, 95% CI 0.96 to 1.16, 89,358 participants; 1822 strokes in 28 trials) or arrhythmia (RR 0.97, 95% CI 0.90 to 1.05, 53,796 participants; 3788 people experienced arrhythmia in 28 RCTs). There was a suggestion that LCn3 reduced CHD events (RR 0.93, 95% CI 0.88 to 0.97, 84,301 participants; 5469 people experienced CHD events in 28 RCTs); however, this was not maintained in sensitivity analyses - LCn3 probably makes little or no difference to CHD event risk. All evidence was of moderate GRADE quality, except as noted.Increasing ALA intake probably makes little or no difference to all-cause mortality (RR 1.01, 95% CI 0.84 to 1.20, 19,327 participants; 459 deaths, 5 RCTs),cardiovascular mortality (RR 0.96, 95% CI 0.74 to 1.25, 18,619 participants; 219 cardiovascular deaths, 4 RCTs), and it may make little or no difference to CHD events (RR 1.00, 95% CI 0.80 to 1.22, 19,061 participants, 397 CHD events, 4 RCTs, low-quality evidence). However, increased ALA may slightly reduce risk of cardiovascular events (from 4.8% to 4.7%, RR 0.95, 95% CI 0.83 to 1.07, 19,327 participants; 884 CVD events, 5 RCTs, low-quality evidence), and probably reduces risk of CHD mortality (1.1% to 1.0%, RR 0.95, 95% CI 0.72 to 1.26, 18,353 participants; 193 CHD deaths, 3 RCTs), and arrhythmia (3.3% to 2.6%, RR 0.79, 95% CI 0.57 to 1.10, 4,837 participants; 141 events, 1 RCT). Effects on stroke are unclear.Sensitivity analysis retaining only trials at low summary risk of bias moved effect sizes towards the null (RR 1.0) for all LCn3 primary outcomes except arrhythmias, but for most ALA outcomes, effect sizes moved to suggest protection. LCn3 funnel plots suggested that adding in missing studies/results would move effect sizes towards null for most primary outcomes. There were no dose or duration effects in subgrouping or meta-regression.There was no evidence that increasing LCn3 or ALA altered serious adverse events, adiposity or lipids, although LCn3 slightly reduced triglycerides and increased HDL. ALA probably reduces HDL (high- or moderate-quality evidence). AUTHORS' CONCLUSIONS: This is the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date. Moderate- and high-quality evidence suggests that increasing EPA and DHA has little or no effect on mortality or cardiovascular health (evidence mainly from supplement trials). Previous suggestions of benefits from EPA and DHA supplements appear to spring from trials with higher risk of bias. Low-quality evidence suggests ALA may slightly reduce CVD event risk, CHD mortality and arrhythmia.

Expert commentary

Fatty fish contain high amounts of long chain omega-3 fatty acids that have well-established effects in protecting against often fatal coronary events such as thrombosis and cardiac arrhythmia. How then can we explain this recent meta-analysis that found they had no effects on cardiac events, mortality or other measures of cardiovascular health?

These conclusions were based almost entirely on data from high dose purified capsule supplements of long chain omega-3 fatty acids and not oily fish. Also, we know that the benefits of these fatty acids are mostly seen in people with cardio-metabolic risk factors that were not specifically included in this meta-analysis.

Patients who could be seen to benefit from the protective effects of long chain omega-3 fatty acids were outnumbered by patients who showed no effects, producing an overall negative outcome. 

Bruce A. Griffin, Professor of Nutritional Metabolism, University of Surrey