People with type 2 diabetes are known to be at increased risk of cardiovascular disease (such as heart attack or stroke). Type 2 diabetes mellitus is the fourth leading cause of death in developed countries with a two fold excess mortality and a two to four fold increased risk of coronary heart disease and stroke. The typical dyslipidemia (abnormality in blood lipids) associated with type 2 diabetes is a combination of hypertriglyceridemia (high levels of fats (triglycerides) in the blood), low levels of HDL (high density lipoprotein) cholesterol and abnormal LDL (low density lipoprotein) composition. Low levels of HDL cholesterol and high levels of LDL cholesterol are associated with an increased risk of cardiovascular disease, while the raised levels of triglycerides are less clearly linked to an increased risk of cardiovascular disease. Several pharmacologic approaches have been used to treat diabetic dyslipidemia and standard dietary approaches focus on restriction of saturated fat and limitation of simple carbohydrate and alcohol intake. In the late 1980s, several investigators reported on the use of dietary supplementation with fish oil as a means of treating diabetic dyslipidemia. Dietary fats and oils from different sources differ considerably in their fatty acid composition. Animal fat is rich in saturated fatty acids, vegetable and marine oils are rich in polyunsaturated fatty acids. Most fish oils are of the so-called omega-3 variety (omega-3 polyunsaturated fatty acids (PUFAs)).
We identified 23 randomised trials (maximum duration of eight months) including 1075 people in which omega-3 PUFA was compared to a vegetable oil or placebo. None of the trials looked at cardiovascular endpoints in cardiovascular disease or death as an outcome measure.
The review shows that although some types of fat in the blood are reduced through omega-3 supplementation, others including LDL cholesterol (which may promote heart disease) were increased. Control of blood sugar levels was not affected by the treatment. There were no other adverse effects of the interventions noted. Clinical outcome trials of sufficient duration are required to establish conclusively the role of omega-3 PUFA in type 2 diabetes but our results do not suggest a major harmful effect on the balance of blood fats and confirm that it has no adverse affect on blood sugar control.
Omega-3 PUFA supplementation in type 2 diabetes lowers triglycerides and VLDL cholesterol, but may raise LDL cholesterol (although results were non-significant in subgroups) and has no statistically significant effect on glycemic control or fasting insulin. Trials with vascular events or mortality defined endpoints are needed.
People with type 2 diabetes mellitus are at increased risk from cardiovascular disease. Dietary omega-3 polyunsaturated fatty acids (PUFAs) are known to reduce triglyceride levels, but their impact on cholesterol levels, glycemic control and vascular outcomes are not well known.
To determine the effects of omega-3 PUFA supplementation on cardiovascular outcomes, cholesterol levels and glycemic control in people with type 2 diabetes mellitus.
We carried out a comprehensive search of The Cochrane Library, MEDLINE, EMBASE, bibliographies of relevant papers and contacted experts for identifying additional trials.
All randomised controlled trials were included where omega-3 PUFA supplementation or dietary intake was randomly allocated and unconfounded in people with type 2 diabetes. Authors of large trials were contacted for missing information.
Trials were assessed for inclusion. Authors were contacted for missing information. Data was extracted and quality assessed independently in duplicate. Fixed-effect meta-analysis was carried out.
Twenty three randomised controlled trials (1075 participants) were included with a mean treatment duration of 8.9 weeks. The mean dose of omega-3 PUFA used in the trials was 3.5 g/d. No trials with vascular events or mortality endpoints were identified. Among those taking omega-3 PUFA triglyceride levels were significantly lowered by 0.45 mmol/L (95% confidence interval (CI) -0.58 to -0.32, P < 0.00001) and VLDL cholesterol lowered by -0.07 mmol/L (95% CI -0.13 to 0.00, P = 0.04). LDL cholesterol levels were raised by 0.11 mmol/L (95% CI 0.00 to 0.22, P = 0.05). No significant change in or total or HDL cholesterol, HbA1c, fasting glucose, fasting insulin or body weight was observed. The increase in VLDL remained significant only in trials of longer duration and in hypertriglyceridemic patients. The elevation in LDL cholesterol was non-significant in subgroup analyses. No adverse effects of the intervention were reported.