Omega-3 no protection against heart attack or strokes

Posted 19 July 2018

Omega-3 no protection against heart attack or strokes, say scientists

Supplements do not offer cardiovascular benefits, researchers conclude from trials involving 112,000 people

Sarah Boseley Health editor The Guardian 18 Jul 2018

The widespread belief that taking omega-3 capsules will help protect you from a heart attack, stroke or early death is wrong, according to a large and comprehensive review of the evidence.

Thousands of people take omega-3 supplements regularly and for years. The belief that it protects the heart has spread – and is promoted in the marketing of the supplements – because the results from early trials suggested the capsules had cardiovascular benefits.

Small amounts of omega-3 fatty acids, are essential for our health. Omega-3 fats are found in certain foods – most famously in oily fish such as salmon and cod liver oil, which contain the long chain fats called eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). Nuts and seeds, and in particular walnuts and rapeseed oil, contain another sort of omega-3, called alpha­linolenic acid (ALA).

But a major review by the respected Cochrane collaboration of all the well-conducted trials carried out internationally to test the effect of omega-3, involving more than 112,000 people, says there is no evidence that the supplements do any good.

“We can be confident in the findings of this review which go against the popular belief that long-chain omega-3 supplements protect the heart,” said Cochrane lead author, Dr Lee Hooper from the University of East Anglia. “This large systematic review included information from many thousands of people over long periods. Despite all this information, we don’t see protective effects.”

The researchers examined 79 randomised trials of omega-3 fats, of which 25 were considered highly trustworthy because they were designed and carried out well. The studies recruited men and women, some healthy and others with existing illnesses, from North America, Europe, Australia and Asia. Some of those who took part had been asked to eat their usual diet, while the rest supplemented it with extra omega-3 fats for at least a year.

In most of the trials, people in the supplement group were asked to take long chain omega-3 fats in the form of a daily capsule. Only a few trials looked at the effects of eating extra oily fish. Other trials asked people to consume more ALA – the form derived from plants – which was added to margarine or given to them in walnuts.

Fish oil supplements made no difference to the risk of death or heart attacks or strokes, the Cochrane researchers found. Eating more ALA from supplemented margarine or walnuts did convey a small benefit, but the reduction in cardiovascular events was very small.

The researchers embarked on their systematic review at the request of the World Health Organisation, which is updating its guidance on polyunsaturated fats. The belief that omega-3 supplements could protect against cardiovascular diseases came from a couple of positive results from trials in the late 1980s and early 1990s, said Lee. “We’ve all believed it for quite a long while,” she said. “But none of the trials since have shown these results. We somehow haven’t adjusted to that data.”

Lee said there was not enough trial evidence to show whether or not eating more oily fish is beneficial – although she suspected it probably is. Extra fish replaces something else in the diet, which may be less good for you, she said. “Also iodine, selenium, calcium and vitamin D are at good high levels and much less common in other foods that the fish might replace. And if you take an oily fish capsule you might think you have done the healthy thing and now you can relax,” she said.

Tim Chico, professor of cardiovascular medicine at Sheffield University, said it was unlikely any one element of the diet could alone prevent heart disease. “Previous experience has shown that although some types of diet are linked to lower risk of heart disease, when we try to identify the beneficial element of the diet and give it as a supplement it generally has little or no benefit,” he said. It happened with vitamins and now the Cochrane research had shown the same thing with omega-3.

“Such supplements come with a significant cost,” he said, “so to anyone buying them in the hope that they reduce the risk of heart disease, I’d advise them to spend their money on vegetables instead.”

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

http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD003177.pub3/full

Asmaa S Abdelhamid, Tracey J Brown, Julii S Brainard, Priti Biswas, Gabrielle C Thorpe, Helen J Moore, Katherine HO Deane, Fai K AlAbdulghafoor, Carolyn D Summerbell, Helen V Worthington, Fujian Song, Lee Hooper

First published: 18 July 2018

Editorial Group: Cochrane Heart Group

DOI: 10.1002/14651858.CD003177.pub3 

Abstract

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.

Plain language summary

Omega-3 intake for cardiovascular disease

Review question

We reviewed randomised trials (where participants have an equal chance of being assigned to either treatment) examining effects of increasing fish- and plant-based omega-3 fats on heart and circulatory disease (called cardiovascular diseases, CVD, which include heart attacks and stroke), fatness and blood fats (lipids, including cholesterol, triglycerides, high-density lipoprotein (HDL – ‘good’ cholesterol) and low-density lipoprotein (LDL – ‘bad’ cholesterol)).

Background

Omega-3 fats are essential – to stay healthy we must obtain some from food. The main types of omega-3 fats are alpha-linolenic acid (ALA), a fat found in plant foods, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), both found in fish. There is a common belief that eating more fish or taking omega-3 supplements reduces our risk of heart disease, stroke and death.

 

Study characteristics

 

The evidence is current to April 2017. The review included 79 trials involving over 112,000 people. These studies assessed effects of greater omega-3 intake versus lower or no omega-3 intake for heart and circulatory disease. Twenty-five studies were very trustworthy (well-designed so as not to give biased results). Participants were adults, some with existing illness and some healthy, living in North America, Europe, Australia and Asia. Participants increased omega-3 fats, or maintained their usual fats for at least a year. Most EPA and DHA trials provided capsules, few gave oily fish.

 

Key results

 

Increasing EPA and DHA has little or no effect on all-cause deaths and cardiovascular events (high-quality evidence) and probably makes little or no difference to cardiovascular death, coronary deaths or events, stroke, or heart irregularities (moderate-quality evidence, coronary events are illnesses of the arteries which supply the heart). EPA and DHA slightly reduce serum triglycerides and raise HDL (high-quality evidence).

 

Eating more ALA (for example, by increasing walnuts or enriched margarine) probably makes little or no difference to all-cause or cardiovascular deaths or coronary events but probably slightly reduce cardiovascular events, coronary mortality and heart irregularities (moderate/low-quality evidence). Effects of ALA on stroke are unclear as the evidence was of very low quality.

 

There is evidence that taking omega-3 capsules does not reduce heart disease, stroke or death. There is little evidence of effects of eating fish. Although EPA and DHA reduce triglycerides, supplementary omega-3 fats are probably not useful for preventing or treating heart and circulatory diseases. However, increasing plant-based ALA may be slightly protective for some heart and circulatory diseases.

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