Some facts for you:
Saturated fatty acids
SFA are synthesised by the body and are not required in the diet. Therefore, no Population Reference Intake (PRI), Average Requirement (AR), Lower Threshold Intake (LTI), or Adequate Intake (AI) is set.
There is a positive, dose-dependent relationship between the intake of a mixture of saturated fatty acids and blood low density lipoprotein (LDL) cholesterol concentrations, when compared to carbohydrates. So the intake of saturated fats in your diet increases LDL
There is also evidence from dietary intervention studies that decreasing the intakes of products rich in saturated fatty acids by replacement with products rich in n-6 polyunsaturated fatty acids (without changing total fat intake) decreased the number of cardiovascular events.
As the relationship between saturated fatty acids intake and the increase in LDL cholesterol concentrations is continuous, no threshold of saturated fatty acids intake can be defined below which there is no adverse effect. Thus, also no Tolerable Upper Intake Level can be set.
The Panel concludes that saturated fatty acids intake should be as low as is possible within the context of a nutritionally adequate diet. Limiting the intake of saturated fatty acids should be considered when establishing nutrient goals and recommendations
Cis-polyunsaturated fatty acids
(cis-PUFA) In view of the different metabolic effects of the various dietary cis- polyunsaturated fatty acids, the Panel proposes not to formulate a Dietary Reference Value for the intake of total cis- polyunsaturated fatty acids.
Also, the Panel proposes not to set specific values for the n-3/n-6 ratio as there are insufficient data on clinical and biochemical endpoints in humans to recommend a ratio independent of absolute levels of intake (*this is the omega 3 / omega 6 issue)
n-6 polyunsaturated fatty acids
(n-6 PUFA) Linoleic acid (LA) cannot be synthesised by the body, is required to maintain “metabolic integrity”, and is therefore an EFA. (essential fatty acid )
However, there are not sufficient scientific data to derive an Average Requirement, a Lower Threshold Intake or a Population Reference Intake.
There is a negative (beneficial), dose-dependent relationship between the intake of linoleic acid and blood LDL cholesterol concentrations, while this relationship is positive for HDL cholesterol concentrations (* so omega 6 decrease LDL and raises HDL)
In addition, linoleic acid (LA) lowers fasting blood triacylglycerol concentrations when compared to carbohydrates.
There is also evidence that replacement of saturated fatty acids by n-6 polyunsaturated fatty acids (without changing total fat intake) decreases the number of cardiovascular events in the population
.As the relationship between linoleic acid intake and the blood lipid profile is continuous, no threshold value of linoleic acid intake can be identified below which the risk for cardiovascular events increases.
The Panel proposes to set an Adequate Intake for linoleic acid of 4 E%, based on the lowest estimated mean intakes of the various population groups from a number of European countries, where overt LA deficiency symptoms are not present.
n-3 polyunsaturated fatty acids
(n-3 PUFA) Alpha-linolenic acid (ALA) cannot be synthesised by the body, is required to maintain “metabolic integrity”, and is therefore considered to be an EFA.
However, there are not sufficient scientific data to derive an Average Requirement, a Lower Threshold Intake or a Population Reference Intake.. The Panel proposes to set an Adequate Intake for alpha-linolenic acid of 0.5 E%, based on the lowest estimated mean intakes of the various population groups from a number of European countries, where overt alpha-linolenic acid deficiency symptoms are not present.
There is no convincing evidence that the intake of alpha-linolenic acid has detrimental effects on health (e.g. in promoting diet-related diseases). The Panel, therefore, proposes not to set a Tolerable Upper Intake Level for alpha-linolenic acid.
The human body can synthesise eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from alpha-linolenic acid.
The fish oil question
Intervention studies have demonstrated beneficial effects of preformed n-3 long-chain polyunsaturated fatty acids on recognised cardiovascular risk factors, such as a reduction of plasma triacylglycerol concentrations, platelet aggregation, and blood pressure
Trans fatty acids
(TFA) Trans fatty acids are not synthesised by the human body and are not required in the diet. Therefore, no Population Reference Intake, Average Requirement, or Adequate Intake is set.
Consumption of diets containing trans-monounsaturated fatty acids, like diets containing mixtures of saturated fatty acids, increases blood total and LDL cholesterol concentrations in a dose-dependent manner, compared with consumption of diets containing cis-monounsaturated fatty acids or cis-polyunsaturated fatty acids.
Consumption of diets containing trans-monounsaturated fatty acids also results in reduced blood HDL cholesterol concentrations and increases the total cholesterol to HDL cholesterol ratio. The available evidence indicates that trans fatty acids from ruminant sources have adverse effects on blood lipids and lipoproteins similar to those from industrial sources when consumed in equal amounts.
Prospective cohort studies show a consistent relationship between higher intakes of trans fatty acids and increased risk of coronary heart disease. The available evidence is insufficient to establish whether there is a difference between ruminant and industrial trans fatty acids consumed in equivalent amounts on the risk of coronary heart disease.
Dietary trans fatty acids are provided by several fats and oils that are also important sources of essential fatty acids and other nutrients. Thus, there is a limit to which the intake of trans fatty acids can be lowered without compromising adequacy of intake of essential nutrients. Therefore, the Panel concludes that trans fatty acids intake should be as low as is possible within the context of a nutritionally adequate diet.
Limiting the intake of trans fatty acids should be considered when establishing nutrient goals and recommendations.
Cholesterol
Cholesterol is synthesised by the body and is not required in the diet. Therefore, no Population Reference Intake, Average Requirement, or Adequate Intake is set.
Although there is a positive dose-dependent relationship between the intake of dietary cholesterol with blood LDL cholesterol concentrations, the main dietary determinant of blood LDL cholesterol concentrations is saturated fat intake. ( *in other words, saturated fat increases LDL cholesterol)
Furthermore, most dietary cholesterol is obtained from foods which are also significant sources of dietary saturated fatty acids, e.g. dairy and meat products.
Therefore the Panel decided not to propose a reference on cholesterol intake beside its conclusion on the intake of saturated fatty acids
www.efsa.europa.eu/en/search/doc/1461.pdf
It's the European Food Safety on fats in the diet.
(Have you guessed what excess sugar makes yet?)