This article aims to study the different dietary fat types associated with obesity and coronary indices. A sample of 491 healthy adults was included in a cross-sectional manner. Dietary fats intake, obesity indices (conicity index (CI), body adiposity index (BAI), abdominal volume index (AVI), body roundness index (BRI), and weight-adjusted-waist index (WWI)), and cardiovascular indices (cardiometabolic index (CMI), lipid accumulation product (LAP), and atherogenic index of plasma (AIP)) were calculated and studied. Participants with an acceptable intake of omega-3 had a higher BRI score (1⋅90 ± 0⋅06 v. 1⋅70 ± 0⋅06). Participants with an unacceptable intake of cholesterol had a higher CI (1⋅31 ± 0⋅11 v. 1⋅28 ± 0⋅12; P = 0⋅011), AVI (20⋅24 ± 5⋅8 v. 18⋅33 ± 6⋅0; P < 0⋅001), BRI (2⋅00 ± 1⋅01 v. 1⋅70 ± 1⋅00; P = 0⋅003), WWI (11⋅00 ± 0⋅91 v. 10⋅80 ± 0⋅97; P = 0⋅032), and lower AIP (0⋅46 ± 0⋅33 v. 0⋅53 ± 0⋅33; P = 0⋅024). Total fat, saturated fat (SFA), and polyunsaturated fat (PUFA) intake had a significant moderate correlation with AVI and BRI. The monounsaturated fat (MUFA) intake had a significantly weak correlation with CI, AVI, BRI, WWI, and AIP. Cholesterol and omega-6 had weak correlations with all indices. Similar correlations were seen among male and female participants. The different types of fat intake significantly affected obesity and coronary indices, especially SFA and PUFA, as well as omega-3 and cholesterol. Gender and the dietary type of fat intake have a relationship to influence the indicators of both obesity and coronary indices.

Diets varying in SFA and MUFA content can impact glycaemic control; however, whether underlying differences in genetic make-up can influence blood glucose responses to these dietary fatty acids is unknown. We examined the impact of dietary oils varying in SFA/MUFA content on changes in blood glucose levels (primary outcome) and whether these changes were modified by variants in the stearoyl-CoA desaturase (SCD) gene (secondary outcome). Obese men and women participating in the randomised, crossover, isoenergetic, controlled-feeding Canola Oil Multicenter Intervention Trial II consumed three dietary oils for 6 weeks, with washout periods of ˜6 weeks between each treatment. Diets studied included a high SFA/low MUFA Control oil (36·6 % SFA/28·2 % MUFA), a conventional canola oil (6·2 % SFA/63·1 % MUFA) and a high-oleic acid canola oil (5·8 % SFA/74·7 % MUFA). No differences in fasting blood glucose were observed following the consumption of the dietary oils. However, when stratified by SCD genotypes, significant SNP-by-treatment interactions on blood glucose response were found with additive models for rs1502593 (P = 0·01), rs3071 (P = 0·02) and rs522951 (P = 0·03). The interaction for rs3071 remained significant (P = 0·005) when analysed with a recessive model, where individuals carrying the CC genotype showed an increase (0·14 (sem 0·09) mmol/l) in blood glucose levels with the Control oil diet, but reductions in blood glucose with both MUFA oil diets. Individuals carrying the AA and AC genotypes experienced reductions in blood glucose in response to all three oils. These findings identify a potential new target for personalised nutrition approaches aimed at improving glycaemic control.

Although higher dietary intake of MUFA has been shown to improve glycaemic control and lipid profiles, whether MUFA consumption from different sources is linked to the development of type 2 diabetes (T2D) remains unclear. We aimed to prospectively assess the associations of plant-derived MUFA (P-MUFA) and animal-derived MUFA (A-MUFA) intakes with T2D risk in a nationwide oriental cohort. Overall, 15 022 Chinese adults, aged ≥20 years, from the China Health and Nutrition Survey (CHNS 1997–2011) were prospectively followed up for a median of 14 years. Consumption of MUFA from plant and animal sources was assessed using 3-d 24-h recalls in each survey, and the cumulative average of intake was calculated. Multivariable-adjusted Cox models were constructed to estimate the hazard ratios (HR) of T2D according to quartiles of MUFA intake. P-MUFA were mainly consumed from cooked vegetable oils, fried bread sticks and rice, while A-MUFA were mainly consumed from pork, lard and eggs. Intake of P-MUFA was associated with a higher risk of T2D (HRQ4 v. Q1 1·50 (95 % CI 1·18, 1·90); Ptrend = 0·0013), whereas A-MUFA showed no significant association (HRQ4 v. Q1 0·84 (95 % CI 0·59, 1·20); Ptrend = 0·30). When further considering the cooking method of food sources, consumption of P-MUFA from fried foods was positively associated with T2D risk (HRQ4 v. Q1 1·60 (95 % CI 1·26, 2·02); Ptrend = 0·0006), whereas non-fried P-MUFA were not associated. Intake of MUFA from fried plant-based foods may elevate T2D risk among the Chinese population.

The effect of modifying dietary fatty acid (FA) composition on insulin sensitivity remains unclear. We aimed to investigate whether changes in plasma phospholipid (PL) FA composition, as a result of dietary intervention, correspond with changes in insulin sensitivity. The RISCK study was a 6-month randomised controlled dietary intervention study, which assessed the effect of modifying dietary fat and the glycaemic index (GI) of carbohydrates on insulin sensitivity. Total NEFA levels, fasting plasma PL FA profiles and an insulin sensitivity index (Si), derived from intravenous glucose tolerance minimal-model analysis, were available from 533 participants, all at elevated risk of type 2 diabetes. Bivariate correlations between changes in saturated PL FA (SFA), MUFA (as a percentage of total plasma NEFA) and changes in Si were assessed according to treatment group. Age, sex, ethnicity, percentage change in body mass and change in dietary GI were controlled for. Increasing total NEFA concentration was associated with worsening Si (r −0·152; P = 0·001). In the high-MUFA/low-GI diet group, change in PL-MUFA was positively and independently associated with change in Si (r 0·297; P = 0·002). Among MUFA, change in oleic acid (18 : 1) was most strongly correlated with change in Si (r 0·266; P = 0·005), as was change in minor FA 24 : 1 (r 0·244; P = 0·011) and 17 : 1 (r 0·196; P = 0·042). In the high-SFA/high-GI group, change in SFA concentration was not significantly associated with change in Si. In conclusion, increases in the proportion of plasma PL-MUFA following a high-MUFA dietary intervention were associated with improvements in insulin sensitivity.

The consumption of food with MUFA has been associated with improvement of inflammation and oxidative stress in overweight individuals. In the present study, we evaluate the effect of high-oleic peanut intake within a hypoenergetic diet on inflammatory and oxidative status markers in overweight men. Sixty-four overweight men (BMI 26–35 kg/m2, 18–50 years old) participated in this randomised controlled study for 4 weeks, allocated into three groups: control (CT, n 22), conventional peanut (CVP, n 21) and high-oleic peanut (HOP, n 21). They followed a hypoenergetic diet (−250 kcal/d; −1045 kJ/d) with or without 56 g of high-oleic or conventional peanuts. After the intervention, the inflammatory markers did not show significant changes in fasting concentrations or postprandial response among the experimental groups (P > 0·05). The activity of oxidative status markers remained unchanged after the intervention. However, in the CT, malondialdehyde showed lower concentration in comparison with the baseline (P = 0·020) and among the groups (P = 0·002). In the present study, the daily intake of high-oleic peanuts within a hypoenergetic diet did not modify the inflammatory markers and oxidative status in overweight men. More studies are needed to better understand the effect of high-oleic peanut intake on health outcomes.

CVD remains the greatest cause of death globally, and with the escalating prevalence of metabolic diseases, including type-2 diabetes, CVD mortality is predicted to rise. While the replacement of SFA has been the cornerstone of effective dietary recommendations to decrease CVD risk since the 1980s, the validity of these recommendations have been recently challenged. A review of evidence for the impact of SFA reduction revealed no effect on CVD mortality, but a significant reduction in risk of CVD events (7–17%). The greatest effect was found when SFA were substituted with PUFA, resulting in 27% risk reduction in CVD events, with no effect of substitution with carbohydrate or protein. There was insufficient evidence from randomised controlled trials to conclude upon the impact of SFA replacement with MUFA on CVD and metabolic outcomes. However, there was high-quality evidence that reducing SFA lowered serum total, and specifically LDL-cholesterol, a key risk factor for CVD, with greatest benefits achieved by replacing SFA with unsaturated fats. The exchange of SFA with either PUFA or MUFA, also produced favourable effects on markers of glycaemia, reducing HbA1c, a long-term marker of glycaemic control. In conclusion, the totality of evidence supports lowering SFA intake and replacement with unsaturated fats to reduce the risk of CVD events, and to a lesser extent, cardiometabolic risk factors, which is consistent with current dietary guidelines.

Dietary fatty acid (FA) composition may influence metabolism, possibly affecting weight management. The purpose of this study was to compare the effects of a 5-d diet rich in PUFA v. MUFA. A total of fifteen normal-weight men participated in a randomised cross-over design with two feeding trials (3 d lead-in diet, pre-diet visit, 5-d PUFA- or MUFA-rich diet, post-diet visit). The 5-d diets (50 % fat) were rich in either PUFA (25 % of energy) or MUFA (25 % of energy). At pre- and post-diet visits, subjects consumed breakfast and lunch test meals, rich in the FA for that 5-d diet. Indirect calorimetry was used for 4 h after each meal. There were no treatment differences in fasting metabolism acutely or after the 5-d diet. For acute meal responses before diet, RER was higher for PUFA v. MUFA (0·86 (sem 0·01) v. 0·84 (sem 0·01), P<0·05), whereas diet-induced thermogenesis (DIT) was lower for PUFA v. MUFA (18·91 (SEM 1·46) v. 21·46 (SEM 1·34) kJ, P<0·05). After the 5-d diets, the change in RER was different for PUFA v. MUFA (−0·02 (sem 0·01) v. 0·00 (sem 0·01), P<0·05). Similarly, the change in fat oxidation was greater for PUFA v. MUFA (0·18 (sem 0·07) v. 0·04 (sem 0·06) g, P<0·05). In conclusion, acutely, a MUFA-rich meal results in lower RER and greater DIT. However, after a 5-d high-fat diet, the change in metabolic responses was greater in the PUFA diet, showing the metabolic adaptability of a PUFA-rich diet.

The present randomised parallel study assessed the impact of adding MUFA to a dietary portfolio of cholesterol-lowering foods on the intravascular kinetics of apoAI- and apoB-containing lipoproteins in subjects with dyslipidaemia. A sample of sixteen men and postmenopausal women consumed a run-in stabilisation diet for 4 weeks. Subjects were then randomly assigned to an experimental dietary portfolio either high or low in MUFA for another 4 weeks. MUFA substituted 13·0 % of total energy from carbohydrate (CHO) in the high-MUFA dietary portfolio. Lipoprotein kinetics were assessed after the run-in and portfolio diets using a primed, constant infusion of [2H3]leucine and multicompartmental modelling. The high-MUFA dietary portfolio resulted in higher apoAI pool size (PS) compared with the low-MUFA dietary portfolio (15·9 % between-diet difference, P= 0·03). This difference appeared to be mainly attributable to a reduction in apoAI fractional catabolic rate (FCR) after the high-MUFA diet ( − 5·6 %, P= 0·02 v. pre-diet values), with no significant change in production rate. The high-MUFA dietary portfolio tended to reduce LDL apoB100 PS compared with the low-MUFA dietary portfolio ( − 28·5 % between-diet difference, P= 0·09), predominantly through an increase in LDL apoB100 FCR (23·2 % between-diet difference, P= 0·04). These data suggest that adding MUFA to a dietary portfolio of cholesterol-lowering foods provides the added advantage of raising HDL primarily through a reduction in HDL clearance rate. Replacing CHO with MUFA in a dietary portfolio may also lead to reductions in LDL apoB100 concentrations primarily by increasing LDL clearance rate, thus potentiating further the well-known cholesterol-lowering effect of this diet.

Diet is important for the prevention of CVD, and diets high in MUFA might be more cardioprotective than low-fat diets. We hypothesise that inflammation and endothelial cell function will be improved most favourably by a high-MUFA diet compared with a low-fat diet. This was tested in a parallel randomised intervention trial on overweight individuals (aged 28·2 (sd 4·6) years) assigned to a diet moderate in the amount of fat (35–45% of energy; >20% of fat as MUFA; MUFA diet, n 39), a low-fat (20–30% of energy) diet (LF diet, n 43) or a control diet (35 % of energy as fat, n 24) for 6 months after weight loss. Protein constituted 10–20 % of energy in all diets. Food was provided free of charge. Fasting blood samples were collected before and after the intervention and analysed for C-reactive protein (CRP), IL-6, intercellular adhesion molecule, von Willebrand factor (vWF) and tissue factor pathway inhibitor. vWF concentrations tended to fall on the LF diet (4·78 (sd 16·44) %; P = 0·07). Concentrations of IL-6 were reduced by the MUFA (0·37 (sd 0·74) pg/ml; P < 0·01) and LF (0·47 (sd 0·69) pg/ml; P < 0·001) diets, and CRP was reduced on all diets (MUFA: 0·48 (sd 1·93) mg/l (P < 0·01); LF: 1·46 (sd 2·89) mg/l (P < 0·001); control: 1·20 (sd 1·97) mg/l (P < 0·01)). No significant differences were observed between changes induced by the different diets. Our findings suggest that in overweight subjects after weight loss, the MUFA and LF diets have similar long-term effects on inflammation and endothelial cell function.

Diet is important in the prevention of CVD, and it has been suggested that a diet high in MUFA is more cardioprotective than a low-fat diet. We hypothesised that the thrombotic risk profile is improved most favourably by a high-MUFA diet compared with a low-fat diet. This was tested in a parallel randomised intervention trial on overweight individuals (aged 28·2 (sd 4·6) years) randomly assigned to a diet providing a moderate amount of fat (35–45 % of energy; >20 % of fat as MUFA) (MUFA diet; n 39), to a low-fat (LF; 20–30 % of energy) diet (n 43), or to a control diet (35 % of energy as fat; n 24) for 6 months after a weight loss of about 10 %. Protein constituted 10–20 % of energy in all three diets. All foods were provided free of charge from a purpose-built supermarket. Fasting blood samples were collected before and after intervention and analysed for factor VII coagulant activity (FVII:c), fibrinogen, prothrombin fragment 1+2 (F1+2), D-dimer and plasminogen activator inhibitor (PAI). The fibrinogen concentration was significantly lowered by the LF diet, but not by the MUFA diet. Changes in fibrinogen differed significantly between diet groups. BMI and PAI concentration increased and D-dimer concentrations were reduced irrespective of the diets. No changes were observed for FVII:c and F1+2. Our findings suggest that in overweight subjects after weight loss the thrombotic risk profile is improved most favourably by the LF diet compared with the MUFA diet based on the reduction in fibrinogen concentrations.

Discordances exist in epidemiological studies regarding the association between the intake of nutrients and death and disease. We evaluated the social and health profile of persons who consumed olive oil in a prospective population cohort investigation (Pizarra study) with a 6-year follow-up. A food frequency questionnaire and a 7 d quantitative questionnaire were administered to 538 persons. The type of oil used in food preparation was determined by direct measurement of the fatty acids in samples obtained from the kitchens of the participants at baseline and after follow-up for 6 years. The fatty acid composition of the serum phospholipids was used as an endogenous marker of the type of oil consumed. Total fat intake accounted for a mean 40 % of the energy (at baseline and after follow-up). The concordance in intake of MUFA over the study period was high. The fatty acid composition of the serum phospholipids was significantly associated with the type of oil consumed and with fish intake. The concentration of polar compounds and polymers, indicative of degradation, was greater in oils from the kitchens where sunflower oil or refined olive oil was used, in oils used for deep frying and in oils that had been reused for frying five times or more. Consumption of olive oil was directly associated with educational level. Part of the discordance found in epidemiological studies between diet and health may be due to the handling of oils during food preparation. The intake of olive oil is associated with other healthy habits.

Neonatal malnutrition is associated with several features of the metabolic syndrome, later in life. Although the recovery of malnutrition was studied with different high-fat diets, few studies compare the effects of enriched vegetable oil diets, containing PUFA and MUFA, after weaning. Our aim was to evaluate the recovery with soya oil- or rapeseed oil-enriched diet, after malnutrition in rats whose mothers were food restricted (FR) during lactation. Dams were 50 % FR and compared to standard diet-fed dams (control, C). At 21 d, FR offspring had a lower body mass and length. After weaning C and FR offspring were fed a diet containing 7 % soya oil (7 %sC and 7 %sFR), or supplemented with 19 % soya oil (19 %sC or 19 %sFR) or 19 % rapeseed oil (19 %cC or 19 %cFR). The normal animals fed enriched vegetable oil diets had more visceral fat mass, but lower serum TAG and higher HDL-cholesterol. The 19 %FR groups showed significantly less food intake and body development compared to the 7 %sFR, and the same pattern was observed when this group was compared to the C groups. Absolute and relative mass of vital organs and body were lower in the FR groups. Visceral fat depot was lower in 19 %FR than 7 %FR and C groups. Serum glucose, albumin, TAG, cholesterol, leptin and triiodothyronine did not show significant changes. However, 19 %FR groups showed higher HDL-cholesterol and the 19 %sFR group showed lower serum thyroxine. The data suggest that a higher vegetable oil diet in the recovery of neonatal malnutrition ameliorates some features of the metabolic syndrome later in life.

Despite the acknowledged benefits of reducing SFA intake few countries within the EU meet recognised targets. Milk and dairy products represent the single largest source of dietary SFA in most countries, yet epidemiological evidence indicates that milk has cardioprotective properties such that simply reducing consumption of dairy foods to meet SFA targets may not be a sound public health approach. The present paper explores the options for replacing some of the SFA in milk fat with cis-MUFA through alteration of the diet of the dairy cow, and the evidence that such changes can improve the indicators for CHD and CVD in general for the consumer. In addition, the outcome of such changes on risk factors for CHD and CVD at the population level is examined in the light of a modelling exercise involving data for eleven EU member states. Given the current and projected costs of health care, the results indicate that urgent consideration should be given to such a strategy.

Controlled human intervention trials are required to confirm the hypothesis that dietary fat quality may influence insulin action. The aim was to develop a food-exchange model, suitable for use in free-living volunteers, to investigate the effects of four experimental diets distinct in fat quantity and quality: high SFA (HSFA); high MUFA (HMUFA) and two low-fat (LF) diets, one supplemented with 1·24 g EPA and DHA/d (LFn-3). A theoretical food-exchange model was developed. The average quantity of exchangeable fat was calculated as the sum of fat provided by added fats (spreads and oils), milk, cheese, biscuits, cakes, buns and pastries using data from the National Diet and Nutrition Survey of UK adults. Most of the exchangeable fat was replaced by specifically designed study foods. Also critical to the model was the use of carbohydrate exchanges to ensure the diets were isoenergetic. Volunteers from eight centres across Europe completed the dietary intervention. Results indicated that compositional targets were largely achieved with significant differences in fat quantity between the high-fat diets (39·9 (sem 0·6) and 38·9 (sem 0·51) percentage energy (%E) from fat for the HSFA and HMUFA diets respectively) and the low-fat diets (29·6 (sem 0·6) and 29·1 (sem 0·5) %E from fat for the LF and LFn-3 diets respectively) and fat quality (17·5 (sem 0·3) and 10·4 (sem 0·2) %E from SFA and 12·7 (sem 0·3) and 18·7 (sem 0·4) %E MUFA for the HSFA and HMUFA diets respectively). In conclusion, a robust, flexible food-exchange model was developed and implemented successfully in the LIPGENE dietary intervention trial.