Omega 6 intake to prevent cardiovascular disease

Review question

We reviewed randomised controlled trials examining the effect of either increased or decreased omega 6 fatty acids for the primary prevention of CVD in healthy adults or adults at high risk of CVD. Four RCTs met the inclusion criteria for this Cochrane review.

Background

Omega 6 is an essential fatty acid because humans cannot make it in their bodies and must obtain it in their diet. Omega 6 can be obtained from a variety of dietary sources, such as vegetable oil and nuts. Omega 6 fatty acids play a vital role in many physiological functions. They are particularly important for maintaining bone health, regulating metabolism, and in stimulating skin and hair growth. Some evidence suggests that a proportionally higher intake of omega 6 fatty acids along with a low intake of saturated fat is associated with significant reductions in coronary heart disease. In contrast, there is concern that high levels of omega 6 fatty acids may worsen cardiovascular risk. There appears to be inconclusive evidence from observational studies and meta-analyses on the benefits of omega 6 intake on CVD outcomes.

Study characteristics

The evidence is current to 23 September 2014. In this Cochrane review, four trials met the inclusion criteria and we examined these trials (660 participants) that assessed the effects of either increased or decreased omega 6 intake on lipid levels and blood pressure (major risk factors for cardiovascular disease (CVD)). The diets were followed for 24 weeks. All four trials recruited both male and female participants but varied in the type of participants recruited. Two trials recruited overweight or obese but otherwise healthy adults. One trial recruited older men and post menopausal women, and the remaining trial recruited younger adults with hypercholesterolaemia. Two trials were conducted in the UK, one in the Netherlands, and the remaining trial was conducted in Finland. Trials included a relatively small number of participants and were at some risk of bias.

Two studies were supported by funding from the UK Food Standards Agency and Medical Research Council. One study was supported by Lipid Nutrition, a commercial company in the Netherlands and the Dutch Ministry of Economic Affairs. The final study was supported by grants from the Finnish Food Research Foundation, Finnish Heart Research Foundation, Aarne and Aili Turnen Foundation, and the Research Council for Health, Academy of Finland.

Key results

No differences in effects of increased or decreased omega 6 intake were seen on blood lipids and blood pressure, but this is based on very few studies. No included trials reported CVD events. There is insufficient evidence to date from randomised controlled trials to recommend increasing or reducing omega 6 for the prevention of CVD.

Quality of the evidence

There are very few included studies and therefore the results have to be interpreted with caution. Overall we regarded the trials were at unclear risk of bias.

Authors' conclusions: 

We found no studies examining the effects of either increased or decreased omega 6 on our primary outcome CVD clinical endpoints and insufficient evidence to show an effect of increased or decreased omega 6 intake on CVD risk factors such as blood lipids and blood pressure. Very few trials were identified with a relatively small number of participants randomised. There is a need for larger well conducted RCTs assessing cardiovascular events as well as cardiovascular risk factors.

Read the full abstract...
Background: 

Omega 6 plays a vital role in many physiological functions but there is controversy concerning its effect on cardiovascular disease (CVD) risk. There is conflicting evidence whether increasing or decreasing omega 6 intake results in beneficial effects.

Objectives: 

The two primary objectives of this Cochrane review were to determine the effectiveness of:
1. Increasing omega 6 (Linoleic acid (LA), Gamma-linolenic acid (GLA), Dihomo-gamma-linolenic acid (DGLA), Arachidonic acid (AA), or any combination) intake in place of saturated or monounsaturated fats or carbohydrates for the primary prevention of CVD.
2. Decreasing omega 6 (LA, GLA, DGLA, AA, or any combination) intake in place of carbohydrates or protein (or both) for the primary prevention of CVD.

Search strategy: 

We searched the following electronic databases up to 23 September 2014: the Cochrane Central Register of Controlled Trials (CENTRAL) on the Cochrane Library (Issue 8 of 12, 2014); MEDLINE (Ovid) (1946 to September week 2, 2014); EMBASE Classic and EMBASE (Ovid) (1947 to September 2014); Web of Science Core Collection (Thomson Reuters) (1990 to September 2014); Database of Abstracts of Reviews of Effects (DARE) and Health Technology Assessment Database, and Health Economics Evaluations Database on the Cochrane Library (Issue 3 of 4, 2014). We searched trial registers and reference lists of reviews for further studies. We applied no language restrictions.

Selection criteria: 

Randomised controlled trials (RCTs) of interventions stating an intention to increase or decrease omega 6 fatty acids, lasting at least six months, and including healthy adults or adults at high risk of CVD. The comparison group was given no advice, no supplementation, a placebo, a control diet, or continued with their usual diet. The outcomes of interest were CVD clinical events (all-cause mortality, cardiovascular mortality, non-fatal end points) and CVD risk factors (changes in blood pressure, changes in blood lipids, occurrence of type 2 diabetes). We excluded trials involving exercise or multifactorial interventions to avoid confounding.

Data collection and analysis: 

Two review authors independently selected trials for inclusion, extracted the data, and assessed the risk of bias in the included trials.

Main results: 

We included four RCTs (five papers) that randomised 660 participants. No ongoing trials were identified. All included trials had at least one domain with an unclear risk of bias. There were no RCTs of omega 6 intake reporting CVD clinical events. Three trials investigated the effect of increased omega 6 intake on lipid levels (total cholesterol, low density lipoprotein (LDL-cholesterol), and high density lipoprotein (HDL-cholesterol)), two trials reported triglycerides, and two trials reported blood pressure (diastolic and systolic blood pressure). Two trials, one with two relevant intervention arms, investigated the effect of decreased omega 6 intake on blood pressure parameters and lipid levels (total cholesterol, LDL-cholesterol, and HDL-cholesterol) and one trial reported triglycerides. Our analyses found no statistically significant effects of either increased or decreased omega 6 intake on CVD risk factors.

Two studies were supported by funding from the UK Food Standards Agency and Medical Research Council. One study was supported by Lipid Nutrition, a commercial company in the Netherlands and the Dutch Ministry of Economic Affairs. The final study was supported by grants from the Finnish Food Research Foundation, Finnish Heart Research Foundation, Aarne and Aili Turnen Foundation, and the Research Council for Health, Academy of Finland.

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