Cardiovascular disease

• 'evidence from dietary intervention studies that decreasing the intakes of products rich in SFA  by replacement with products rich in n-6 PUFA (without changing total fat intake) decreased the number of cardiovascular events'.

• '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

• '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 SFA with PUFA decreases the risk of CHD'.
• Probable evidence that 'replacing SFA with largely refined carbohydrates has no benefit on CHD, and may even increase the risk of CHD'.
• Insufficient evidence 'relating to the effect on the risk of CHD in replacing SFA with either MUFA or largely whole grain carbohydrates; however, based on indirect lines of evidence this could result in a reduced risk of CHD'.

• 'The evidence for primary prevention of CHD through a reduction in the intake of SFA in exchange for PUFA is judged as probable'.
• Possible evidence for a 'missing association between CHD risk and a reduction in the intake of SFA in exchange for MUFA or carbohydrates' and a 'missing association between CHD risk and a reduction in the intake of SFA (without specific substitution by another energy source)'.

• 'In replacing partially hydrogenated oils containing 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'.

• 'Any incremental increases in saturated […] fatty acids intakes increase CHD risk'.

Blood Pressure

• With the exception of n-3 LCPUFA, there is no convincing evidence that other fatty acids affect blood pressure.

• No association between the reduction in the proportion of SFA and prevention of hypertension (probable evidence).

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

• 'Positive, dose-dependent relationship between the intake of a mixture of SFA and blood LDL cholesterol concentrations, when compared to carbohydrates'.
• 'Consumption of […] diets containing mixtures of SFA, increases blood total and LDL cholesterol concentrations in a dose-dependent manner, compared with consumption of diets containing cis-MUFA or cis-PUFA'.
• 'The various SFA may also differ in their effects on the blood lipoprotein profile. In particular, the effects of stearic acid may be less disadvantageous than those of myristic and palmitic acids. However the available data are insufficient to set different DRVs for different SFA'.

Serum lipids

• Convincing evidence that replacing SFA (C12:0 – C16:0) with PUFA 'decreases LDL cholesterol concentration and the total/HDL cholesterol ratio'. Similar but lesser effect is achieved by replacing SFA with MUFA.
• Convincing evidence that, replacing dietary sources of SFA (C12:0-C16:0) with carbohydrates 'decreases both LDL and HDL cholesterol concentration but does not change the total/HDL cholesterol ratio'.
• Convincing evidence that 'Replacing SFA (C12:0–C16:0) with trans-fatty acids (TFA) decreases HDL cholesterol and increases the total /HDL cholesterol ratio'.

• 'The evidence is convincing that intake of dietary SFA increases the plasma concentrations of total and LDL cholesterol, while a reduction in SFA intake (except for stearic acid and MCT) reduces them'.
• 'The evidence is convincing that the substitution of SFA with PUFA lowers plasma concentrations of total and LDL cholesterol'.
• 'There is possible evidence that an increased intake of SFA increases the plasma concentration of HDL cholesterol '.
• 'The evidence for a reduction in plasma triglyceride concentration after increasing intake of SFA for a short period of time is convincing'.
• 'There is probable evidence that SFA intake has no effect on the ratio of total to HDL cholesterol'.
• 'The evidence for an association between SFA intake and the ratio of LDL to HDL cholesterol is insufficient'.

• Convincing evidence that 'serum/plasma concentrations of total cholesterol and LDL-cholesterol are reduced when SFA is replaced by cis-MUFA or PUFA'.
• Limited evidence (no conclusion) on 'replacing SFA by cis-MUFA or PUFA in regard to concentrations of serum/plasma HDL-cholesterol'.
• Replacing SFA by cis-MUFA or PUFA in regard to concentration of serum/plasma total triglyceride levels was 'unlikely' to have any effects.

• Moderate evidence that 'in controlled feeding trials among adults, for every 1% of energy from SFA that is replaced by 1% of energy from carbohydrate, MUFA, or PUFA, LDL cholesterol is lowered by 1.2, 1.3, and 1.8 mg/dL, respectively, and HDL cholesterol by 0.4, 1.2, and 0.2 mg/dL, respectively'.
• Moderate evidence that 'For every 1% of energy from SFA that is replaced by 1% of energy from carbohydrate and MUFA, triglycerides are raised by an estimated 1.9 and 0.2 mg/dL, respectively'; when replaced by PUFA, 'triglycerides are lowered by an estimated 0.4 mg/dL'.

• 'Strong and consistent evidence […] shows that replacing SFA with unsaturated fats, especially PUFA, significantly reduces total and LDL cholesterol. Replacing SFA with carbohydrates (sources not defined) also reduces total and LDL cholesterol, but significantly increases triglycerides and reduces HDL cholesterol'.

• 'positive linear trend between saturated fatty acid intake and total and LDL cholesterol levels'.

Stroke

• 'probable evidence that the intake of SFA does not influence the risk of stroke'.

Metabolic syndrome

• Probable evidence that 'replacing SFA with largely refined carbohydrates […]  may even […]  favour metabolic syndrome development'.
• Insufficient evidence that 'SFA affects the risk for alterations in indices related to the  components of the metabolic syndrome'.

• Insufficient evidence for 'an association between SFA 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'.
• 'SFA intake may impair […] insulin sensitivity […]. Clear dose-response relationships have, however, not been established'.
• '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 positive relationship between SFA intake and increased risk of diabetes'.

• Probable evidence for a lack of association between SFA intake and T2DM risk
• Insufficient evidence that the substitution of SFA with PUFA lowers T2DM risk

• 'an effect on blood glucose by replacing SFA with cis-MUFA or PUFA was unlikely'.
• 'The proportion of SFA in plasma phospholipids and cholesteryl esters might be associated with increased risk of T2DM, and the evidence for this was evaluated as suggestive'.
• 'Odd chain SFA (C15:0 and 17:0) might have an inverse association with the risk of T2DM, and the evidence for this was evaluated as suggestive'.

• '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 DRVs for […] specific fatty acids based on cancer outcome'.

• Insufficient evidence 'for establishing any relationship of SFA consumption with cancer'.

• 'There is probable evidence of no association between the level of SFA intake and the risk of individual cancers'.

• Suggestive evidence for a positive association between SFA intake and ovarian cancer.

• 'Some studies may suggest that SFA decreases energy expenditure as compared with cis-unsaturated fatty acids, but more studies – especially at lower intakes – are needed to extend these observations'.

• Insufficient evidence for an association between the proportion of SFA in the diet and the primary prevention of obesity, both in studies with and without energy adjustment.

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

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