Of course, but the kind of fats still proven most effective for long term health, thus far, are MUFAs.
Do you have any evidence for this?
What is the effect of dietary intake of MUFA on health and intermediate health outcomes?
Conclusion
Strong evidence indicates that dietary monounsaturated fatty acids (MUFA) are associated with improved blood lipids related to both cardiovascular disease (CVD) and type 2 diabetes (T2D), when they are a replacement for dietary saturated fatty acids (SFA). The evidence shows that five percent energy replacement of SFA with MUFA decreases intermediate markers and the risk of CVD and T2D in healthy adults and improves insulin responsiveness in insulin resistant and T2D subjects.
Grade: Strong
Overall strength of the available supporting evidence: Strong; Moderate; Limited; Expert Opinion Only; Grade not assignable For additional information regarding how to interpret grades, click here.
Evidence Summary Overview
Thirteen studies published since 2004 and conducted in the US, Europe and Australia were reviewed to determine the effect of monounsaturated fat (MUFA) on health outcomes. These included one methodologically strong meta-analysis evaluating 11 prospective cohort studies (Jakobsen, 2009) and 11 randomized controlled trials (RCTs) ranging from 14 to 162 subjects, including six methodologically strong studies (Appel, 2005; Berglund, 2007; Due, 2008; Lopez, 2008; Thijssen and Mensink, 2005; and Thijssen, 2005) and five methodologically neutral studies (Allman-Farinelli, 2005; Binkoski, 2005; Clifton, 2004; Paniagua, 2007; and Rasmussen, 2006). The reviewed studies also included one methodologically strong prospective cohort study of 5,672 subjects from the Nurses’ Health Study who reported a diagnosis of type 2 diabetes (T2D) (Tanasescu, 2004).
Overall, MUFA replacing saturated fat (SFA) in the diet as percent of energy leads to a decrease in low-density lipoprotein cholesterol (LDL-C) (Allman-Farinelli, 2005; Appel, 2005; Berglund, 2007), a decrease in serum triglycerides (TG) (Allman-Farinelli, 2005), a decrease in markers of inflammation (Allman-Farinelli, 2005), and a decrease in cardiovascular disease (CVD) risk (Appel, 2005; Rasmussen, 2006). Increasing MUFA intake, rather than replacing SFA with MUFA, also leads to a decrease in total cholesterol (TC) (Haban, 2004), LDL-C (Haban, 2004), LDL-C to high-density lipoprotein cholesterol (HDL-C) ratio (Due, 2008), serum TG (Brunerova, 2007), inflammatory markers (Brunerova, 2007) and fasting insulin and Homeostasis Model Assessment-Insulin Resistance (HOMA-IR) scores (Brunerova, 2007; Due, 2008). However, Clifton et al, (2004) found a greater decrease in TC and HDL-C in women who consumed a very low-fat diet, compared with a high MUFA diet and no difference in the LDL:HDL ratio between the two diets (Clifton, 2004). Replacing SFA with MUFA, compared to replacement with carbohydrates (CHO), decreased serum TG (Appel, 2005) and increased HDL-C (Appel, 2005; Berglund, 2007). Lastly, a prospective cohort study involving a T2D subpopulation within the Nurses’ Health Study found that replacing 5% energy from SFA with equivalent energy from MUFA was associated with a 27% lower risk of CVD. The authors conclude that replacing SFA with MUFA may be more protective against CVD than replacement with CHO (Tanasescu, 2004).
Comparing substitution of SFA with MUFA vs. polyunsaturated fat (PUFA) showed a greater decrease in TC and LDL-C with PUFA substitution (Binkoski, 2005). Furthermore, a pooled analysis of 11 prospective cohort studies showed that risk of coronary events and coronary death was lowest with 5% energy substitution of SFA with PUFA; PUFA substitution resulted in the greatest decrease, with MUFA showing somewhat less, and CHO showing the least improvement when substituted for SFA (Jakobsen, 2009). In a comparison of individual fatty acids, oleic acid was no different than stearic or linoleic acid in its effect on measures of serum lipids or lipoproteins and markers of inflammation (Thijssen and Mensink, 2005; Thijssen, 2005).
Evidence Summary Paragraphs
Allman-Farinelli et al, 2005 (neutral quality) This was a randomized, extra-period crossover trial, conducted in Australia. The study compared the effect of a SFA-rich diet with a MUFA-rich diet on the concentrations of factor VII coagulant activity factor, fibrinogen, plasminogen, activator inhibitor-1 and blood lipids. Subjects consumed either the SFA-rich diet (20.8% energy as fat) for five weeks and crossed over to the MUFA-rich diet (20.3% energy as fat) for 10 weeks or the opposite diets with no washout period between diets. Fifteen of the 18 initial subjects (five males, 10 females; aged 35-69 years) completed the study. Subjects completed three-day food diaries on two occasions during each intervention. Weight was maintained throughout the study. Dietary compliance was confirmed by a significant increase in both plasma phospholipids and neutral lipid oleic acid (P<0.0001) on the MUFA diet. Factor VIIc was lower (97±1%) on the MUFA diet (P<0.05) compared to the SFA diet (99±1). Low-density lipoprotein cholesterol (3.47±0.06mmol per L) was lower (P<0.001) compared to SFA (4.01±0.07mmol per L) and TG levels were also lower (P<0.01) on the MUFA -rich diet (144.0±4.6mmol per L) compared to the SFA diet (145.1±4.9mmol per L). There were no differences between diets for fibrinogen and insulin concentrations or plasminogen activator inhibitor-1 activity.
Appel et al, 2005 (positive quality) This was the Omni Heart randomized, three-period crossover trial conducted in the US. The study compared the effect of three reduced SFA, on blood pressure (BP) and serum lipids in 191 healthy adults with stage I hypertension (HTN) or pre-hypertension (PHTN). The three six-week interventions included a diet rich in CHO, a diet rich in protein (about half from plant sources) and a diet rich in unsaturated fat (predominantly MUFA); all were reduced in SFA, cholesterol and sodium, and rich in fruits, vegetables, fiber, potassium and other minerals at the recommended levels. One hundred sixty one subjects were included in this analysis (45% women, mean age 53.6±10.9 years). Blood pressure, LDL-C and estimated CHD risk were lower on each diet compared to baseline. Compared with the CHO-rich diet, the unsaturated fat diet decreased systolic blood pressure (SBP) by 1.3mmHg (P=0.005) and by 2.9mmHg among those with HTN (P=0.02), had no effect on LDL-C, increased HDL-C by 1.1mg per dL (0.03mmol per L, P=0.03) and lowered TG by 9.6mg per dL (0.11mmol per L, P=0.02).
Berglund et al, 2007 (positive quality) This was a randomized crossover trial conducted in the US. The study compared MUFA with CHO as a replacement for SFA in subjects with a high metabolic risk profile. Three diets were fed in a double-blind, three-way crossover with each lasting seven-weeks with a rest period of four to six weeks between each intervention. The three diets reflected the typical pattern of the US population. Two were modified to replace 7% of energy from SFA with either CHO (primarily complex) on the CHO-replacement diet or with MUFA on the MUFA-replacement diet. All food was provided except for a self-selected meal [following the NCEP Step I guidelines] on Saturday evenings. Blood samples were drawn at weeks five, six and seven of each intervention. Eighty five of the initial 110 subjects completed all three interventions (33 females, 52 males and mean age 35.5±9.2 years, range 21-61 years). Relative to the average American diet, LDL-C was lower with both the CHO-replacement diet (-7.0%) and MUFA-replacement diet (-6.3%), whereas the difference in HDL-C was smaller during the MUFA-replacement diet (-4.3%) than during the CHO-replacement diet (-7.2%). Lipoprotein (a) concentrations increased with both the CHO-replacement diet (20%) and MUFA-replacement diet (11%) relative to the average American diet.
Lopez et al, 2008 (positive quality) This was a randomized, single-blinded, crossover trial of 14 healthy men in Spain to determine the degree to which unsaturation of dietary fatty acids influences the postprandial control of insulin secretion and insulin sensitivity. The postprandial response to high-fat meals enriched in SFAs or MUFAs was assessed using mixed meals with common foods. The isocaloric diet interventions included 9% more fat, replacing CHO in the control NCEP diet, and were as follows:
NCEP Step I
High butter (MUFA:SFA, 0.48:1.0)
Refined olive oil (ROO) (MUFA:SFA, 5.43:1.0)
High palmitic sunflower oil (HPSO) (MUFA:SFA, 2.42:1.0)
Mixture of vegetable and fish oils (VEFO) (MUFA:SFA, 7.08:1.0).
Subjects were normo-triglyceridemic and had normal fasting blood glucose (FBG) and glucose tolerance. Results showed that high fat meals increased the postprandial concentrations of insulin, TG, and free fatty acids (FFAs), and they increased postprandial b-cell activity as assessed by the insulinogenic index (IGI), a surrogate measure of first-phase insulin secretion; IGI/HOMA-IR ratio; AUCinsulin/AUCglucose ratio; and HOMA of b-cell function (HOMA-B). High fat meals also decreased postprandial insulin sensitivity assessed by a glucose and TG tolerance test meal (GTTTM)-determined insulin sensitivity test and the postprandial Belfiore indices for glycemia and blood FFAs. These effects were significantly improved, in a linear relationship, when MUFAs were substituted for SFAs; subjects became less insulin resistant postprandially as the proportion of MUFAs, compared with SFAs, in dietary fats increased (VEFO>ROO>HPSO>butter). When the early postprandial insulin response was used as a measure of b-cell activity, it decreased as the ratio of MUFA/SFA increased. Overall the findings suggest that b-cell function and insulin sensitivity progressively improve in the postprandial state as the proportion of MUFAs, relative to SFAs, increases in the diet, suggesting that MUFAs moderate the postprandial hyperactivity of the pancreatic b-cell. The underlying mechanism likely involves different insulinotropic potentials of individual FFA (e.g., oleic acid has been reported to elicit half the insulin secretion from b-cells as palmitic or stearic acids).
Tanasescu et al, 2004 (positive quality) This study used data from the prospective cohort Nurses' Health Study conducted in the US to assess the relationship between different types of dietary fat and cholesterol and the risk of CVD among women with T2D. The Nurses' Health Study started in 1986 with follow-up questionnaires sent every two years. Dietary fat and cholesterol were assessed through semi-quantitative food-frequency questionnaire (FFQ). Five thousand six hundred seventy two female nurses (30-55 years in 1976) who had reported a physician's diagnosis of diabetes at age >30 years on any follow-up questionnaire were included in the analysis. Between 1980-1998, 619 new cases of CVD (non-fatal MI, fatal CHD and stroke) were identified. Relative risks of CVD were estimated from Cox proportional hazards analysis after adjustment for potential confounders. The relative risk of CVD for an increase of 200mg cholesterol per 1,000kcal was 1.37 (95% CI: 1.12-1.68, P=0.003). Each 5% of energy intake from SFA, as compared with equivalent energy from CHO, was associated with a 29% greater risk of CVD (RR=1.29, 95% CI: 1.02-1.63, P=0.04). The PUFA: SFA (P:S) ratio was inversely associated with risk of fatal CVD. Replacement of 5% energy from SFA with equivalent energy from CHO or MUFA was associated with a 22% or 37% lower risk of CVD, respectively. Overall, an increased intake of cholesterol and SFA and a low P:S was related to increased CVD risk in women with T2D. Among women with T2D, replacement of SFA with MUFA may be more protective against CVD than replacement with CHOs.
http://www.nel.gov/e...mmary_id=250249And that doesn't even enter the olive oil studies yet.