This chapter focuses on the effects of SAFA and TFA on CHD risk, because the evidence is most extensive and strong for this relationship. However, SAFA and TFA may also have other health effects. Next to CVD, the most important chronic diseases in Western societies for which a role of dietary fats has been suggested are obesity (and the resulting diabetes) and cancer.
There has long been and still is debate about the role of the total amount of fat in the diet in the aetiology of obesity (Katan et al., 1997). If the total amount of dietary fat would in the long term increase body weight (Astrup et al., 2000), this would increase CHD risk through adverse changes in blood lipids (Leenen et al., 1993) and higher risk of diabetes. However, data supporting a major role of dietary fat per se in determining body weight are not strong, with long-term clinical trials being scarce and conflicting (Willett & Lebel, 2002). This seems counter-intuitive given the high energy content of dietary fat, but it is often forgotten that dietary fat forms only part of the equation determining energy balance. In the United States, the prevalence of obesity has rapidly increased despite a decline in the relative amount of fat in the diet over the past decades (Willett & Lebel, 2002). Apparently, other factors play an important role in caloric overconsumption. Indeed, many foods high in carbohydrates are also energy-dense (e.g. refined foods, soft drinks), and energy expenditure (physical activity) is a major determinant of energy imbalance and weight gain.
It has also been suggested that the type of dietary fat, in particular reducing SAFA and TFA intake and increasing MUFA intake, could directly improve insulin sensitivity and reduce the risk of type 2 diabetes (Hu & Willett, 2002). This would be an additional mechanism to reduce CHD risk. However, most experts and food and health authorities agree that the predominant way in which dietary fat quality can reduce CHD risk is through improving blood lipids.
A high consumption of fat, and in particular of animal fat and saturated fatty acids, has been associated with higher risks of breast, colorectal and prostatic cancers (Zock, 2001). However, there is no convincing evidence for a role of dietary fats. The idea derives from geographical comparisons, showing that cancer is more frequent in countries where fat consumption is high. These findings were supported by animal studies, showing that saturated fats promoted growth of artificially induced tumours. However, comparisons between countries do not provide strong evidence for causal relationships, and for animal studies it remains uncertain to what extent results can be extrapolated to humans. Moreover, well-conducted, prospective cohort studies show no or only weak relations between cancer incidence and dietary fats (Zock, 2001). One recent meta-analysis of 23 case-control studies and 12 cohort studies on dietary fat and breast cancer risk found a summary relative risk for saturated fat of 1.19 (Boyd et al., 2003). Taken together, there is some evidence that intake of SAFA may somewhat increase the risk of cancer, but the evidence is not strong. There are no clear indications that TFA increases the risk of cancer.
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