Current dietary guidelines have focused on the reduction of dietary saturated fatty acid (SFA) intake as a means of reducing cardiovascular disease risk (CVD). Questions still remain as to whether monounsaturated (MUFA) or n-6 polyunsaturated (n-6 PUFA) fatty acids are the optimal macronutrient to replace dietary SFA. The aim of DIVAS (Dietary Intervention and VAscular function Study; ClinicalTrials.gov NCT01478958) was to determine the impact of substitution of dietary SFA with either MUFA or n-6 PUFA on plasma lipids and markers of insulin resistance in adults at an increased risk of developing CVD.

Men and women (n=195, mean (sd) age 44 (10) years and BMI 26.9 (4.0) kg/m²) participated in a 16-week, parallel, randomised, controlled, single-blinded intervention study. Volunteers were randomly assigned (minimised by gender, age, BMI and CVD risk score) to one of three isoenergetic diets: SFA-rich (target composition: 36% of total energy (%E) as total fat, 17%E SFA, 11%E MUFA, 4%E n-6 PUFA), MUFA-rich (36% E total fat, 9%E SFA, 19%E MUFA, 4%E n-6 PUFA), or n-6 PUFA-rich (36% E total fat, 9%E SFA, 13%E MUFA, 10%E n-6 PUFA). For the successful delivery of the dietary targets, a flexible dietary exchange model was developed in which exchangeable fats in the habitual diet were replaced by study foods (spreads, oils, snacks) with a specific fatty acid profile. Fasting blood total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), triacylglycerol (TAG), glucose, insulin and non-esterified fatty acids (NEFA) concentrations were measured at baseline and week 16. Low-density lipoprotein cholesterol (LDL-C) concentrations were estimated by using the Friedewald formula⁽ Reference Friedewald, Levy and Fredrickson ^{1 )}. Homeostasis model assessment (HOMA) was calculated as an index of insulin resistance⁽ Reference Matthews, Hosker and Rudenski ^{2 )}.

There was a significant effect of diet on fasting TC, LDL-C and TC:HDL-C ratio with significantly lower concentrations observed after the MUFA-and PUFA-diets compared with the SFA-rich diet. No differences were evident between the PUFA-rich and MUFA-rich diets. Dietary fatty acid intake did not significantly influence HOMA, blood glucose, insulin or NEFA levels (data not shown).

¹Derived by Univariate Analysis for between diet comparison with baseline, BMI and age as covariates followed by the LSD post-hoc test; * significantly different from the SFA-rich diet (P<0.05).

In conclusion, replacement of dietary SFA for 16 weeks with either MUFA or n-6 PUFA resulted in a shift towards a beneficial lipid profile in men and women at increased CVD risk.