It is More Important to Increase the Intake of Unsaturated Fats than to Decrease the Intake of Saturated Fats: Evidence from Clinical Trials Relating to Ischemic Heart Disease.
It is More Important to Increase the Intake of Unsaturated Fats than to Decrease the Intake of Saturated Fats: Evidence from Clinical Trials Relating to Ischemic Heart Disease.
Year: 1997
Authors: M P Oliver.
Publication Name: Am. J. Clin. Nutr.
Publication Details: Volume 66S; Page 9805.
Abstract:
Since the Seven Countries Study showing a positive correlation between the intake of dietary fat and ischemic heart disease (IHD), many epidemiologic surveys have confirmed this observation. As a result, it has been assumed that decreasing total fat, especially SFA, in the diet will lead to lowered risk of IHD. Oliver, however, suggests there is little evidence to support this assumption. In this review of several publications, the author states that the evidence from formal, controlled, long-term clinical trials which indicate that reducing total dietary fat intake decreases the incidence of IHD are scientifically not valid. Oliver presents the argument that those trials with a concurrent intervention, such as the reduction of cigarette smoking or those where dietary fat quality was altered (as opposed to reducing total fat or SFA) had any effect on IHD. Most of the trials were underpowered and in several of the studies, there was inadequate dietary control. Oliver describes the results of six published clinical trials of healthy individuals where diets were low in SFA and cholesterol and other risk factors were changed, yet no reduction was seen in the rate of IHD. The exception to this observation was the Oslo trial where IHD risk declined concomitant with a reduction in cigarette smoking by half. In five of six secondary prevention trials, diets low in SFA and high in PUFAs (supplied by soybean, corn, safflower and canola or increased fish intake) led to a reduction in IHD deaths. In the two studies done on dietary supplementation with n-3 fatty acids, striking reductions in IHD and all-cause mortality rates have been seen. The overall hypothesis presented by Oliver is that dietary supplementation with n-3 fatty acids may be preventive in those who have manifest IHD (i.e. thrombotic tendency) but may not be as protective in those who are healthy. In his summary, Oliver suggests that the evidence from formal, controlled, long-term clinical trials suggests that more emphasis should be given in national and international dietary recommendations to supplementation with MUFAs and PUFAs, especially oils rich in n-3 fatty acids, such as CO, rather than to diets low in SFA. Regardless of the arguments that Oliver presents, his conclusions support CO intake as the most effective source of dietary MUFAs as well as PUFAs, including ALA, in combination with the lowest SFA content of any vegetable oil on the market.
