Diet, and especially its fat content, can have a varying influence upon cardiovascular risk factors and on mechanisms related to the onset and progression of atheroma plaques. The final aim of preventing and treating coronary arteriosclerosis is to reduce the risk of new heart attacks and mortality from them. In spite of this, research studies into the effects of dietary intervention on the clinical course of the disease are few in number and have only provided significant results in secondary prevention of the disease (Brousseau and Schaefer, 2000). Intervention studies researching the preventive effects of the traditional Mediterranean dietary model, i.e. a high concentration of total fat from MUFA, do not exist .
In a trial conducted on patients with coronary heart disease, the effect of a diet rich in n-3 alpha-linolenic acid, referred to as the Mediterranean diet, was studied (de Lorgeril et al., 1994). This diet was accompanied by a 70% reduction in cardiovascular risk, much higher than the reduction observed in previous studies with hypolipaemic drugs or other dietary models. However, the above-mentioned study does not establish the beneficial effects of the traditional Mediterranean diet, which is high in fat and MUFA, since the principal modification in the experimental group was not an increase in the concentration of MUFA but rather alpha-linolenic acid.
The most consistent epidemiological evidence in support of the benefits of consuming these fatty acids lies in observational studies, especially the Seven Countries Study (Keys et al., 1986) and the data from the Nurses Health Study (Hu et al., 1997). In the 15-year death rate in the Seven Countries Study comprising 11 579 men, all coronary heart disease death rates were low in cohorts consuming olive oil as the main fat. In the 14-year follow-up of the population included in the Nurses Health Study, a 5% increase in energy intake from MUFA, as compared with an equivalent energy intake from SFA, was associated with a relative risk of coronary disease of 0.81 (95% confidence interval, 0.65 to 1.00; p = 0.05). The greater protective effect of PUFA was also reported with a relative risk of 0.62 for every 5% increase in energy from PUFA (Hu et al., 1997). There are other controlled epidemiological studies with confounding factors that have confirmed the protective effect of MUFA in different populations (Artaud-Wild et al., 1993; Pietinen et al., 1997). However, this protective effect has not been confirmed by the data from the Framingham Heart Study or other studies (McGee et al., 1984; Posner et al., 1991). This may be due to the lack of control over confounding factors or because there exist other factors, associated with lifestyle or a higher consumption of other nutrients, in subjects and populations with a higher consumption of MUFA-enriched diets.
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