ARCHIVED - Health Canada Scientific Summary on the U. S. Health Claim Regarding Dietary Fat, Saturated Fat, Cholesterol, Trans Fatty Acids and Coronary Heart Disease
Bureau of Nutritional Sciences
Food Directorate, Health Products and Food Branch
This report is a critical review and evaluation of the scientific literature from 1993-2000 inclusive on the relationship of the dietary level of total fat, saturated fat, cholesterol and trans fat on coronary heart disease (CHD), or plasma lipid risk factors for CHD. The cumulative evidence from these reports strongly indicates that the primary effect of dietary fat is related to saturated and trans fatty acids. Recent metabolic studies show that unless there is a concomitant reduction in saturated fat, a reduction in total fat will not lower plasma cholesterol or lipoprotein levels. A reduction in total fat does not have a beneficial effect on CHD, or CHD risk factors independent of its effect on lowering saturated fat.
The effectiveness of lowering dietary saturated fat in reducing plasma cholesterol, especially low-density lipoprotein (LDL)- cholesterol, the major risk factor for CHD, is well established. This position continued to be supported by the scientific findings over the past seven years and by meta-analyses of metabolic studies reported over the last 30 years. A reduction in saturated fat by replacement with either cis mono- or poly-unsaturated fatty acids, or a combination of both (i.e., modifying fat quality) rather than by increasing carbohydrate, produces more favourable effects. This judgement is based on the role of low plasma levels of high-density lipoprotein (HDL)-cholesterol and high plasma levels of triglyceride (TG) as risk factors for CHD and clinical trials showing a reduction of dietary fat along with an increase in carbohydrates decrease cardioprotective HDL-cholesterol and increase atherogenic TG.
Consumption of diets with higher levels of trans fatty acids results in increased plasma levels of LDL-cholesterol. In addition, trans fatty acids, in contrast to saturated fatty acids, lower plasma levels of HDL-cholesterol and raise the blood level of atherogenic lipoprotein (a), which suggests that trans fatty acids may be a greater risk factor for CHD than dietary saturated fatty acids.
Evidence has also accumulated over the period of 1993-1999 that indicates dietary cholesterol is not a major factor influencing plasma cholesterol and lipoprotein levels in the general population. It appears that the earlier predictions of the effect of each 100 mg of dietary cholesterol on plasma total cholesterol were too high; namely 1.75 mmol/L for each 100 mg/day dietary cholesterol. All the meta-analyses and carefully controlled studies reported since 1993 estimate that a decrease of 100 mg dietary cholesterol results in decrease of plasma cholesterol of 0.05 mmol/L. On a population basis this change is relatively insignificant considering that it represents approximately 1% of the average population plasma cholesterol concentration. Even though the magnitude of the effect of dietary cholesterol is very small for the general population, scientific literature continues to provide evidence that some individuals may be high responders to dietary cholesterol. However, the effect appears to be primarily on plasma total cholesterol; the effect of dietary cholesterol on plasma LDL varies among reports.
In conclusion, there is appreciable scientific support for the benefits of reducing the intakes of dietary saturated and trans fats in lowering the risk of CHD. The position is weaker for the benefits of reducing total fat and cholesterol. Guidelines for the prevention of CHD should therefore focus primarily on reducing the dietary intakes of saturated and trans fats. It is proposed that a health claim which states that diets low in saturated and trans fats "may" or "might" reduce the risk of heart disease is the most appropriate claim that may be made on the label or in the labelling of foods.1
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