Cardiovascular disease

• 'Evidence is limited regarding whether replacing SFA with MUFA confers overall CVD (or CVD endpoint) benefits. One reason is that the main sources of MUFA in a typical American diet are animal fat, and because of the co-occurrence of SFA and MUFA in foods makes it difficult to tease out the independent association of MUFA with CVD'.
• 'However, evidence from RCTs and prospective studies has demonstrated benefits of plant sources of monounsaturated fats, such as olive oil and nuts on CVD risk'.

Coronary heart disease

• Insufficient evidence 'for relationships of MUFA consumption with chronic disease end points such as CHD…'

• Possible evidence for no association between MUFA intake (without trans fatty acids) and primary prevention of CHD.

• A favourable effect (via direct association) of cis-MUFA on CHD was unlikely. It should be noted however that intakes of MUFA correlate highly with intakes of SFA, except where olive oil is the main MUFA dietary source.

• When replacing partially hydrogenated oils (PHOs) that contain industrially produced TFA ' a more significant reduction in CHD risk is estimated by replacement with vegetable oils containing higher amounts of cis-unsaturated fatty acids than with those high in saturated fatty acids, but we expect a risk reduction even if iTFA is replaced with fats and oils high in saturated fatty acids'.

Blood pressure

• With the exception of n-3 LCPUFA (see Table 5.3d) there is no convincing evidence that other fatty acids affect blood pressure.

• Probable evidence that 'substitution of carbohydrates with MUFA does not affect blood pressure'
• Insufficient evidence for an association between substitution of SFA or PUFA with MUFA and risk of hypertension.

• Limited evidence (no conclusion) for 'an effect of any modification of the quality of dietary fat on blood pressure'.

Serum lipids

• 'Under iso-energetic conditions, the most favourable lipoprotein profile to lower atherosclerotic risk is achieved when a mixture of SFA and TFA is replaced by a mixture of oleic acid, linoleic acid and n-3 LCPUFA. These effects are dose-dependent'.

• 'Convincing evidence that replacing carbohydrates with MUFA increases HDL cholesterol concentrations'
• 'Convincing evidence that replacing SFA (C12:0–C16:0) with MUFA reduces LDL cholesterol concentration and total/HDL cholesterol ratio'.

• 'increasing the intake of MUFA lowers the risk of dyslipoproteinaemias, as there is convincing evidence that the plasma HDL concentration increases and the plasma triglyceride concentration and the ratios of total to HDL cholesterol and LDL to HDL cholesterol decrease'.
• Convincing evidence that MUFA, when compared with carbohydrates, prevent a decrease in the plasma concentration of HDL cholesterol, lower the plasma triglyceride concentration and lower the ratios of total to HDL cholesterol and LDL to HDL cholesterol.
• Lack of association (probable evidence) between 'MUFA intake and the plasma concentrations of total and LDL cholesterol compared to carbohydrates'.
• Lack of an association (probable evidence) between 'intake of MUFA and plasma concentration of HDL cholesterol in comparison with long-chain SFA'.
• Possible evidence that MUFA intake, when compared with long-chain SFA, has 1) a lowering effect on the plasma concentrations of total and LDL cholesterol and 2) lacks an association with plasma triglyceride concentration.
• Insufficient evidence that MUFA intake, when compared to long-chain SFA, has an association with the ratio of total to HDL cholesterol and LDL to HDL cholesterol.

• Convincing evidence that 'serum/plasma concentrations of total cholesterol and LDL-cholesterol are reduced when SFA is replaced by cis-MUFA'.
• Limited evidence (no conclusion) 'for replacing SFA by cis-MUFA […] in regard to concentrations of serum/plasma HDL-cholesterol'
• Replacing SFA by cis-MUFA in regard to concentration of serum/plasma total triglyceride levels was 'unlikely' to have any effects.
• Limited evidence (no conclusion) for effects on serum/plasma concentrations of total cholesterol, HDL-cholesterol, and total triglycerides from replacing carbo­hydrates with cis-MUFA.
• Replacing carbohydrates by cis-MUFA in regard to concentration of serum/plasma LDL-cholesterol levels was 'unlikely' to have any effects.
• Probable evidence for a ' hypotriglyceridemic effect of fish oil supplementation compared with cis-MUFA'.

• 'Strong and consistent evidence […] shows that replacing SFA with unsaturated fats, especially PUFA, significantly reduces total and LDL cholesterol'.

• Moderate evidence that in controlled feeding trials among adults, for every 1% of energy from SFA that is replaced by 1% of energy from MUFA, LDL and HDL cholesterol is lowered by 1.3mg/dL and 1.2 mg/dL respectively, while triglycerides are raised by 0.2 mg/dL.
• Moderate evidence that in controlled feeding trials among adults, for every 1% of energy from TFA that is replaced by 1% of energy from MUFA, LDL is lowered by 1.5 mg/dL, HDL cholesterol is increased by 0.4 mg/dL respectively, while triglycerides are lowered by 1.2 mg/dL.

Stroke

• 'probable evidence that intake of MUFA does not influence the risk of various types of stroke'.

Metabolic syndrome

• Insufficient evidence for a 'an association between MUFA intake and the occurrence of metabolic syndrome'.

• 'limited number of human intervention studies in non-diabetic subjects does not provide consistent evidence that fatty acids change insulin sensitivity'
• 'Epidemiological prospective cohort studies have not found consistent relationships between […] the intake of specific fatty acids […] with the risk to develop type 2 diabetes mellitus.'

• 'Possible evidence that replacing carbohydrates with MUFA improves insulin sensitivity'.
• 'insufficient evidence of a relationship between MUFA intake and risk of diabetes'.

• Probable evidence for a 'lack of an association between MUFA intake and the risk of type 2 diabetes mellitus'.

• Probable evidence for a ' favourable effect of cis-MUFA on insulin sensitivity or fasting serum/plasma insulin concentration in comparison with carbohydrates and SFA'.
• Unlikely evidence for 'an effect on blood glucose by replacing SFA with cis-MUFA'.

• 'For many specific fatty acids, results from prospective cohort studies are still too limited, and sometimes contradictory, to conclude on clear associations between their intakes and the risk of a particular type of cancer'.
• 'Evidence is not sufficient to define a DRV for […] specific fatty acids based on cancer outcome'.

• 'insufficient evidence for relationships of MUFA consumption with chronic disease end points such as […] cancer'.

• 'probable evidence of no association between the intake of MUFA and the risk of individual cancers'.

• 'insufficient evidence for relationships of MUFA consumption and body weight and percent adiposity'.

• For the primary prevention of obesity through a diet with an increased proportion of MUFA there is (a) possible evidence of no association in studies with energy adjustment and (b) insufficient evidence in studies without energy adjustment.

• 'no evidence that the quality of fat has any effect on body weight'.

• 'Overconsumption of energy related to a high-fat, high-monounsaturated fatty acid diet is one risk associated with excess monounsaturated fatty acid intake'.
• High MUFA intakes 'can also cause an increased intake of saturated fatty acids, since many animal fats that contain one have the other'.

• 'No consistent picture has emerged on the effects of […] MUFA […] on parameters related to inflammation and immune function'.