Dietary fats and the risk of coronary heart disease 141 Epidemiological studies and clinical trials

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Cardiovascular diseases comprise many different disorders related to impaired blood flow, including disease of the heart (mostly coronary heart disease), the brain (ischaemic and haemorrhagic stroke) and peripheral blood vessels (e.g.

deep vein thrombosis). Effects of dietary fats on the risk of coronary heart disease have been most widely studied and are established by both epidemiological studies and randomised controlled clinical trials.

Of all cardiovascular diseases, a causal relationship with blood lipid levels is most clear for coronary heart disease. Although cholesterol lowering by drug treatment (HMG-CoA-reductase inhibitors, statins) lowers both the risk of coronary heart disease and that of stroke, the epidemiological data on dietary fats and stroke are very limited and show no clear associations with the amount or type of dietary fats (He et al., 2003). In contrast, for CHD there are several epidemiological studies that addressed the associations with dietary fats as well as randomised clinical trials that studied the effects of changing the intake of specific fatty acids (Hu & Willett, 2002) on disease outcome. This section therefore focuses on the relations between intake of saturated and trans fatty acids and the risk of coronary heart disease.

Epidemiological studies on associations with dietary fats A higher intake of fat and in particular of saturated fat is already long believed to contribute to the development of CHD. This belief originates in geographical and migration studies comparing the intake of fats and rates of CHD between countries (Keys, 1980) or in population groups moving from one country to another (Kato et al., 1973). In the Seven Countries Study (Keys, 1980), the percentage of energy as saturated fat in the diet was strongly correlated (r = 0.86) with coronary death rates across 16 different populations. Notably, the correlation between percentage energy from total fat and CHD rate was much weaker (r = 0.39). CHD rates were highest in Finland and lowest in Crete, but both regions had the same high amount of total fat intake (40% of energy). Because the high fat intake in Finland was mainly due to a high dairy fat intake (SAFA-rich diet) and that in Crete mainly due to high olive oil intake (MUFA-rich diet), Keys proposed that in particular the type of dietary fat is important. In a more recent analysis of the Seven Countries Study, Kromhout et al. (1995) found strong positive correlations between CHD death rates during 25-year of follow-up and initial intakes of SAFA (r > 0.80) and of TFA (r = 0.78).

Data from international comparisons and migration studies show the importance of diet, lifestyle and other environmental factors for developing CHD. However, such data do not provide strong evidence for the causal role of individual dietary components, because relations with CHD are easily confounded by other dietary aspects, physical activity, smoking habits, obesity and socio-economic status. Prospective cohort studies of individuals within a population, in which diet is assessed before the onset of disease and in which confounding factors can to a certain extent be controlled for, are considered as the strongest type of epidemiological evidence. Surprisingly, despite the long history of dietary fat and CHD research, the number of earlier cohort studies that have directly investigated associations between dietary fat intake and risk of CHD is relatively small and the results are not consistent. A statistically significant positive association between saturated fat intake and risk of CHD

was found in two studies (McGee et al., 1984; Kushi et al., 1985), but not in several others (e.g. Gordon, 1981; Shekelle et al., 1981; Ascherio et al., 1996). Possible explanations for these inconsistent findings are that most of these earlier studies were limited by small study size, inadequate dietary assessment, or insufficient adjustment for confounding factors.

The largest prospective epidemiological analysis of dietary fatty acids and risk of CHD is from the Nurses' Health Study cohort (Hu et al., 1997) in more than 80 000 women over 14 years of follow-up. This study found a weak relation between saturated fat intake and increased CHD risk; 5% of energy from saturated fatty acids as compared with the same amount of energy from carbohydrates was associated with a 17% higher risk of CHD. Trans fatty acid intake was much more strongly associated with CHD; it was estimated that 2% of energy as trans fatty acid as compared with carbohydrates was associated with a 93% higher CHD risk. Higher intakes of non-hydrogenated polyunsaturated fats and monounsaturated fat were associated with decreased risk. Total fat intake was not significantly related to risk, probably because of the opposing effects of different fat types.

In addition to the Nurses' Health Study (Hu et al., 1997), three other large prospective studies consistently found increased risks of CHD with higher intakes of trans fatty acids (Ascherio et al., 1996; Pietinen et al., 1997; Oomen et al., 2001). When the results of these four studies were combined (Oomen et al., 2001), the pooled relative risk of CHD with a difference of 2% of energy as trans fatty acids was 1.25 (a 25% increase in risk). Results from other types of epidemiological studies, such as case-control studies using biochemical markers of TFA intake, are less consistent (Ascherio et al., 1999). In a more recent case-control study, higher red-cell membrane levels of TFA were associated with significantly increased risk of primary cardiac arrest (Lemaitre et al., 2002). One study found no association between adipose tissue TFA and sudden death (Roberts et al., 1995), but another found a positive association between adipose TFA and myocardial infarction (Clifton et al., 2004). Because intake of SAFA is, unlike intake of TFA, not reliably reflected in body tissue, there are no epidemiological data on SAFA and heart disease using such biochemical markers of intake.

Randomised clinical trials of changes in dietary fats

The strongest type of evidence for a causal role of diet in the development of CHD is provided by long-term randomised trials on clinical end-points. If a randomised trial is successfully conducted with high compliance of subjects and few patients are lost to end-point ascertainment, then results can be fully ascribed to effects of the dietary intervention, without confounding by other lifestyle factors or the subjects' own choices. Important drawbacks of clinical trials are their practical limitations, required large sample sizes, long duration and high costs. Therefore, there are only a few trials that specifically tested the effects of changing dietary fat intake, without involving other treatments, such as blood pressure or plasma lipid lowering medication or combined lifestyle and

Table 1.2 Randomised clinical trials aimed at changing dietary (saturated) fat and CHD outcome (adapted from Hu & Willett, 2002)


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