The relationship between dietary fat, fatty acids and cancers has been debated for a long time. The difficulty to disentangle the effects of specific nutrients, in a particular food or from a similar food pattern, from one another partly explains this. In addition, the complex interaction between nutrients at the different stages of carcinogenesis has contributed to the uncertainty of cause‐and‐effect. Finally, methodological considerations have also played a role in this debate. However, the knowledge and understanding of the role of dietary fat in cancer has progressed. Factors related to a high energy intake, such as obesity, are probable if not convincing risk factors for several cancers. Therefore, epidemiological findings tend to suggest that dietary fatty acids increase the risk of cancer. This is especially so for the least oxidisable, saturated and monounsaturated fatty acids. Polyunsaturatedn‐6 fatty acids and especially linoleic acid, which reproducibly enhances tumour incidence and growth in animal models, do not appear to have the same effects in humans. Interaction with other nutrients, such asn‐3 fatty acids and antioxidants, may explain this apparent contradiction. The major question yet unanswered and deserving more studies is the relation betweenn‐3 fatty acids (especially α‐linolenic acid) and prostate cancer. Progress in this area requires more complete food composition data and other experimental models of carcinogenesis.
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Gerber et al. (2005) studied this question.
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