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Omega 6 fatty acids such as pumpkin seeds, sunflower seeds, etc

NIHR Signal A high omega-6 fatty acid diet is unlikely to prevent cardiovascular disease or deaths

Published on 19 February 2019

doi: 10.3310/signal-000736

Diets or supplements that aim to increase omega-6 fatty acids have no clear effect on the risk of cardiovascular events like heart attacks or stroke, overall deaths or deaths from cardiovascular disease. Omega-6 fatty acids are poly-unsaturated oils largely derived from seeds and nuts such as sunflower oil, corn oil, soybean oil, walnuts and pumpkin seeds.

The results of this Cochrane review can be looked at alongside another recent Cochrane review, which found no benefits of fish oil in omega-3 fatty acid supplements in reducing cardiovascular events or deaths.

These findings highlight the limited benefits of modifying one dietary component at a time. A balanced diet includes a variety of foods, any or all of which can affect health, meaning that studying the effects of diet on health is complex. The results of this review are unlikely to change guideline recommendations.

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Why was this study needed?

Cardiovascular disease describes a range of conditions caused by atherosclerosis (stiffening and furring of the arteries) including coronary heart disease and strokes. It is responsible for a quarter of deaths in the UK. Cardiovascular disease is estimated to cost the NHS almost £9 billion and £4 billion in costs to society.

A diet high in omega-6 polyunsaturated fatty acids is believed by some to protect against heart disease and stroke, although evidence is inconsistent. The most important type of omega-6 fatty acid is linoleic acid, an essential fatty acid that is obtained from food.  

This review aimed to address this inconsistency by pooling the evidence to assess the effect of increasing omega-6 fatty acid intake by dietary modification or supplementation on mortality, cardiovascular events and weight.

What did this study do?

This updated Cochrane review found 19 randomised controlled trials that compared interventions to increase omega-6 fatty acids in diets to usual or lower omega-6 fatty acids diets for at least 12 months. Overall, 6,461 adults were included. Participants included people without cardiovascular disease (primary prevention) and people already diagnosed with cardiovascular disease (secondary prevention). The trials took place in North America, Europe, Australia and Asia, with nine from the UK.

Three trials had a low risk of bias; the rest had a moderate to high risk of bias. Many studies were published more than 30 years ago, with one over 50 years old. Worldwide public-health campaigns since that time to lower consumption of saturated fats may have increased the baseline level of omega-6 fatty acids consumption. This means that more recent studies may have been less likely to show an effect than older studies.

What did it find?

  • Higher omega-6 fatty acids intake showed no effect on overall risk of death (risk ratio [RR] 1.00, 95% confidence interval [CI] 0.88 to 1.12; 10 trials with 4,506 participants,). In both groups about 17% of people died, during follow-up of up to eight years and some studies included only people older than 65 years. The lack of effect was consistent across trials.
  • Higher omega-6 fatty acids intake had no effect on deaths from cardiovascular disease (RR 1.09, 95% CI 0.76 to 1.55; 7 trials with 4,019 participants. About 13% of people on a higher omega-6 fatty acids diet and about 11% of people on lower omega-6 fatty acid diets died from cardiovascular diseases.
  • Higher omega-6 fatty acids intake had no effect on cardiovascular events (RR 0.97, 95% CI 0.81 to 1.15; 7 trials with 4,962 participants). About 30% of people on each diet had a cardiovascular event such as myocardial infarction or stroke.
  • There was no effect on weight, and inconsistent effects on cholesterol, with total blood cholesterol lower with high omega-6 fatty acid intake in 10 trials but no effect on blood levels of high-density lipoprotein (‘good’ cholesterol) or low-density lipoprotein (‘bad’ cholesterol).

What does current guidance say on this issue?

NICE’s 2016 guideline on risk assessment and reduction for cardiovascular disease has no recommendations on the omega-6 fatty acids content of the diet. However, it recommends replacing saturated fats with mono-unsaturated or polyunsaturated fats. It also recommends consumption of some foods high in omega-6 fatty acids such as nuts, seeds and rapeseed oil, or spreads based on rapeseed oil.

An update of this guideline is planned, which will look at the wording of recommendations on dietary advice.

What are the implications?

The results of this systematic review provide little if any evidence that a higher intake of omega-6 fatty acids improves cardiovascular disease risks. Though this review set out to settle the debate, it was hampered by small studies of short duration with insufficient cases of deaths or cardiovascular events.

This limits the precision in the results. Any biases might be expected to increase any effect of diet so are unlikely to explain the lack of benefit seen here.

As foods high in omega-6 fatty acids are important parts of a balanced, healthy diet. Dietary advice is unlikely to change as a result of this study.

Citation and Funding

Hooper L, Al-Khudairy L, Abdelhamid AS et al. Omega-6 fats for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2018;(11):CD011094.

Cochrane UK and the Cochrane Heart Group are supported by NIHR infrastructure funding. WHO provided funding to the University of East Anglia to support this Cochrane review.

Bibliography

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.

NHS website. Cardiovascular disease. London: Department of Health and Social Care; updated 2018.

NICE Cardiovascular disease: risk assessment and reduction, including lipid modification. CG181. London: National Institute for Health and Care Excellence; 2014.

Public Health England. Action plan for cardiovascular disease prevention, 2017 to 2018. London: Public Health England; 2017.

Why was this study needed?

Cardiovascular disease describes a range of conditions caused by atherosclerosis (stiffening and furring of the arteries) including coronary heart disease and strokes. It is responsible for a quarter of deaths in the UK. Cardiovascular disease is estimated to cost the NHS almost £9 billion and £4 billion in costs to society.

A diet high in omega-6 polyunsaturated fatty acids is believed by some to protect against heart disease and stroke, although evidence is inconsistent. The most important type of omega-6 fatty acid is linoleic acid, an essential fatty acid that is obtained from food.  

This review aimed to address this inconsistency by pooling the evidence to assess the effect of increasing omega-6 fatty acid intake by dietary modification or supplementation on mortality, cardiovascular events and weight.

What did this study do?

This updated Cochrane review found 19 randomised controlled trials that compared interventions to increase omega-6 fatty acids in diets to usual or lower omega-6 fatty acids diets for at least 12 months. Overall, 6,461 adults were included. Participants included people without cardiovascular disease (primary prevention) and people already diagnosed with cardiovascular disease (secondary prevention). The trials took place in North America, Europe, Australia and Asia, with nine from the UK.

Three trials had a low risk of bias; the rest had a moderate to high risk of bias. Many studies were published more than 30 years ago, with one over 50 years old. Worldwide public-health campaigns since that time to lower consumption of saturated fats may have increased the baseline level of omega-6 fatty acids consumption. This means that more recent studies may have been less likely to show an effect than older studies.

What did it find?

  • Higher omega-6 fatty acids intake showed no effect on overall risk of death (risk ratio [RR] 1.00, 95% confidence interval [CI] 0.88 to 1.12; 10 trials with 4,506 participants,). In both groups about 17% of people died, during follow-up of up to eight years and some studies included only people older than 65 years. The lack of effect was consistent across trials.
  • Higher omega-6 fatty acids intake had no effect on deaths from cardiovascular disease (RR 1.09, 95% CI 0.76 to 1.55; 7 trials with 4,019 participants. About 13% of people on a higher omega-6 fatty acids diet and about 11% of people on lower omega-6 fatty acid diets died from cardiovascular diseases.
  • Higher omega-6 fatty acids intake had no effect on cardiovascular events (RR 0.97, 95% CI 0.81 to 1.15; 7 trials with 4,962 participants). About 30% of people on each diet had a cardiovascular event such as myocardial infarction or stroke.
  • There was no effect on weight, and inconsistent effects on cholesterol, with total blood cholesterol lower with high omega-6 fatty acid intake in 10 trials but no effect on blood levels of high-density lipoprotein (‘good’ cholesterol) or low-density lipoprotein (‘bad’ cholesterol).

What does current guidance say on this issue?

NICE’s 2016 guideline on risk assessment and reduction for cardiovascular disease has no recommendations on the omega-6 fatty acids content of the diet. However, it recommends replacing saturated fats with mono-unsaturated or polyunsaturated fats. It also recommends consumption of some foods high in omega-6 fatty acids such as nuts, seeds and rapeseed oil, or spreads based on rapeseed oil.

An update of this guideline is planned, which will look at the wording of recommendations on dietary advice.

What are the implications?

The results of this systematic review provide little if any evidence that a higher intake of omega-6 fatty acids improves cardiovascular disease risks. Though this review set out to settle the debate, it was hampered by small studies of short duration with insufficient cases of deaths or cardiovascular events.

This limits the precision in the results. Any biases might be expected to increase any effect of diet so are unlikely to explain the lack of benefit seen here.

As foods high in omega-6 fatty acids are important parts of a balanced, healthy diet. Dietary advice is unlikely to change as a result of this study.

Citation and Funding

Hooper L, Al-Khudairy L, Abdelhamid AS et al. Omega-6 fats for the primary and secondary prevention of cardiovascular disease. Cochrane Database Syst Rev. 2018;(11):CD011094.

Cochrane UK and the Cochrane Heart Group are supported by NIHR infrastructure funding. WHO provided funding to the University of East Anglia to support this Cochrane review.

Bibliography

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.

NHS website. Cardiovascular disease. London: Department of Health and Social Care; updated 2018.

NICE Cardiovascular disease: risk assessment and reduction, including lipid modification. CG181. London: National Institute for Health and Care Excellence; 2014.

Public Health England. Action plan for cardiovascular disease prevention, 2017 to 2018. London: Public Health England; 2017.

Omega-6 fats for the primary and secondary prevention of cardiovascular disease

Published on 30 November 2018

Hooper, L.,Al-Khudairy, L.,Abdelhamid, A. S.,Rees, K.,Brainard, J. S.,Brown, T. J.,Ajabnoor, S. M.,O'Brien, A. T.,Winstanley, L. E.,Donaldson, D. H.,Song, F.,Deane, K. H.

Cochrane Database Syst Rev Volume 11 , 2018

BACKGROUND: Omega-6 fats are polyunsaturated fats vital for many physiological functions, but their effect on cardiovascular disease (CVD) risk is debated. OBJECTIVES: To assess effects of increasing omega-6 fats (linoleic acid (LA), gamma-linolenic acid (GLA), dihomo-gamma-linolenic acid (DGLA) and arachidonic acid (AA)) on CVD and all-cause mortality. SEARCH METHODS: We searched CENTRAL, MEDLINE and Embase to May 2017 and clinicaltrials.gov and the World Health Organization International Clinical Trials Registry Platform to September 2016, without language restrictions. We checked trials included in relevant systematic reviews. SELECTION CRITERIA: We included randomised controlled trials (RCTs) comparing higher versus lower omega-6 fat intake in adults with or without CVD, assessing effects over at least 12 months. We included full texts, abstracts, trials registry entries and unpublished studies. Outcomes were all-cause mortality, CVD mortality, CVD events, risk factors (blood lipids, adiposity, blood pressure), and potential adverse events. We excluded trials where we could not separate omega-6 fat effects from those of other dietary, lifestyle or medication interventions. DATA COLLECTION AND ANALYSIS: Two authors independently screened titles/abstracts, assessed trials for inclusion, extracted data, and assessed risk of bias of included trials. We wrote to authors of included studies. Meta-analyses used random-effects analysis, while sensitivity analyses used fixed-effects and limited analyses to trials at low summary risk of bias. We assessed GRADE quality of evidence for 'Summary of findings' tables. MAIN RESULTS: We included 19 RCTs in 6461 participants who were followed for one to eight years. Seven trials assessed the effects of supplemental GLA and 12 of LA, none DGLA or AA; the omega-6 fats usually displaced dietary saturated or monounsaturated fats. We assessed three RCTs as being at low summary risk of bias.Primary outcomes: we found low-quality evidence that increased intake of omega-6 fats may make little or no difference to all-cause mortality (risk ratio (RR) 1.00, 95% confidence interval (CI) 0.88 to 1.12, 740 deaths, 4506 randomised, 10 trials) or CVD events (RR 0.97, 95% CI 0.81 to 1.15, 1404 people experienced events of 4962 randomised, 7 trials). We are uncertain whether increasing omega-6 fats affects CVD mortality (RR 1.09, 95% CI 0.76 to 1.55, 472 deaths, 4019 randomised, 7 trials), coronary heart disease events (RR 0.88, 95% CI 0.66 to 1.17, 1059 people with events of 3997 randomised, 7 trials), major adverse cardiac and cerebrovascular events (RR 0.84, 95% CI 0.59 to 1.20, 817 events, 2879 participants, 2 trials) or stroke (RR 1.36, 95% CI 0.45 to 4.11, 54 events, 3730 participants, 4 trials), as we assessed the evidence as being of very low quality. We found no evidence of dose-response or duration effects for any primary outcome, but there was a suggestion of greater protection in participants with lower baseline omega-6 intake across outcomes.Additional key outcomes: we found increased intake of omega-6 fats may reduce myocardial infarction (MI) risk (RR 0.88, 95% CI 0.76 to 1.02, 609 events, 4606 participants, 7 trials, low-quality evidence). High-quality evidence suggests increasing omega-6 fats reduces total serum cholesterol a little in the long term (mean difference (MD) -0.33 mmol/L, 95% CI -0.50 to -0.16, I(2) = 81%; heterogeneity partially explained by dose, 4280 participants, 10 trials). Increasing omega-6 fats probably has little or no effect on adiposity (body mass index (BMI) MD -0.20 kg/m(2), 95% CI -0.56 to 0.16, 371 participants, 1 trial, moderate-quality evidence). It may make little or no difference to serum triglycerides (MD -0.01 mmol/L, 95% CI -0.23 to 0.21, 834 participants, 5 trials), HDL (MD -0.01 mmol/L, 95% CI -0.03 to 0.02, 1995 participants, 4 trials) or low-density lipoprotein (MD -0.04 mmol/L, 95% CI -0.21 to 0.14, 244 participants, 2 trials, low-quality evidence). AUTHORS' CONCLUSIONS: This is the most extensive systematic assessment of effects of omega-6 fats on cardiovascular health, mortality, lipids and adiposity to date, using previously unpublished data. We found no evidence that increasing omega-6 fats reduces cardiovascular outcomes other than MI, where 53 people may need to increase omega-6 fat intake to prevent 1 person from experiencing MI. Although benefits of omega-6 fats remain to be proven, increasing omega-6 fats may be of benefit in people at high risk of MI. Increased omega-6 fats reduce serum total cholesterol but not other blood fat fractions or adiposity.

Expert commentary

The authors should be congratulated. Interventions to increase omega-6 fatty acids (linoleic acid or gamma-linolenic acid) achieved no useful benefits in terms of convincingly reducing total deaths or cardiovascular deaths. This analysis thus offers strong evidence not to advocate omega-6 supplements.

However, healthy diet patterns themselves are now supported by a mass of scientific evidence.

We, therefore, should be doubling our intake of healthy foods (like veg, fruit, nuts, fibre, wholemeal, olive oil, fish and seafood), and slashing our consumption of sugary drinks and junk food (heavily marketed ultra-processed snacks and ready-meals deficient in nutrients, but replete with calories, salt, sugar, saturated fats and even transfats).

Simon Capewell, Professor of Clinical Epidemiology, University of Liverpool

The commentator is an expert adviser for the UK Health Forum, Obesity Health Alliance, Action on Sugar and Consensus Action on Salt (CASH)