Dietary monounsaturated fat and cancer

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The great interest during the past several decades on the relationship between diet and cancer derives from the large variations on rates of specific cancer among countries, coupled with the dramatic changes in the incidence of these conditions among populations emigrating to regions with different rates. Mediterranean populations are known to be partially protected against coronary heart disease and certain types of cancers (Trichopoulou and Critselis, 2004; La Vecchia, 2004). Their dietary habits with low intake of saturated and polyunsaturated fats together with the high intake of oleic acid, n-3 fatty acids, fibre and natural antioxidants have been proposed to explain this protection (Bingham and Riboli, 2004).

Previous studies have shown that the switch from a diet high in MUFA to a diet containing a high proportion of SFA may have contributed to the rise in cancer incidences observed in different populations. There is evidence that MUFA have cancer chemoprotective effects. Recently, Bartsch et al. (2002) have suggested that molecular pathways to cancer involve multiple genetic changes, whereby extensive oxyradical damage causes mutations in cancer-related genes and leads to a cycle of cell death and regeneration. Besides direct oxidative DNA-damage, nitrogen species and reactive oxygen can induce etheno-DNA adducts mainly via trans-4-hydroxy-2-nonenal, generated as the major aldehyde by lipid peroxidation of PUFA. In contrast, previous studies with oleic acid show that the biomarkers for oxidative stress and lipid peroxidation are decreased compared with n-6 PUFA, suggesting a favourable effect in prevention and development of certain cancer types affected by diet. In concordance with this study, Hughes-Fulford et al. (2001) have found that the essential fatty acid, linoleic acid, and arachidonic acid stimulate tumour growth while eicosapentaenoic acid and oleic acid inhibit growth of PC-3 human prostate tumour cells in vitro.

Analytic epidemiological studies generally fail to detect a positive association of total fat intake with risk of colorectal cancer (Howe et al., 1997). On the other hand, recently, Llor et al. (2003) have observed that supplementation with olive oil results in an early down regulation of cox-2 followed by a decrease in Bcl-2 expression, important mediators of colorectal cancer development (Willett, 1997; Llor et al., 2003). Thus, olive oil is capable of influencing crucial processes responsible for colorectal cancer development. In concordance with this, Braga et al. (1998) have observed that there was some evidence that olive oil decreased the risk of colorectal carcinoma compared with other fat types. It has been suggested in at least three case-control studies conducted in Spain, Italy and Greece, that olive oil, which has a high MUFA content, may be associated with decreased risk of breast cancer (Willett, 1997). An analysis of data from a cohort in Sweden also suggested that MUFA may be associated with decreased risk of breast cancer, although interpretation of the results of this study is complicated by the fact that the major sources of MUFAs in the Swedish diet are also the main sources of SFAs (Wolk et al., 1998). Overall, these observations suggest that a high-MUFA diet may decrease the risk of breast cancer, although more work is necessary before such inferences can be made with confidence.

Emerging data suggest that the strong protective associations reported for olive oil intake in dietary studies may be due to some other protective components. A multinational study carried out by Simonsen et al. (1998) in five European centres shows that the protective effect reported for olive oil intake may be due to components contained in the unsaponificable fraction of the oil. Compelling data from in vitro and in vivo laboratory studies, epidemiological investigations and human clinical trials indicate that antioxidants present in the unsaponificable fraction of olive oil have important effects on cancer chemoprevention and therapy (Stark and Madar, 2002). These compounds may interfere in several of the steps that lead to the development of malignant tumours, including protecting DNA from oxidative damage, inhibiting carcinogen activation and activating carcinogen detoxifying systems. In addition, some studies have reported that antioxidants enhance the apoptosis induced by standard chemotherapeutic agents employed for the management of some cancers (Chinery et al., 1997; Pathak et al., 2002). In summary, this evidence shows that the amount and quality of dietary fat exert a clear influence on the aetiology of cancer.

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