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Breast and colon cancer Bougnoux et al (1994) made an important observation when they demonstrated an inverse relationship between ALA levels in breast tissue and risk of lymph node involvement and visceral metastases in breast cancer. This has been followed up with larger studies of similar design (Klein et al 2000, Maillard et al 2002) and one meta-analysis, all yielding comparable results (Saadatian-Elahi et al 2004). The data indicate that those women with the highest breast tissue concentrations of ALA have a relative risk of breast cancer between 0.36 and 0.39, while other FA levels fail to exhibit a statistically significant relationship. Interestingly, an epidemiological study has identified an association between low consumption of ALA in humans and increased cancer deaths in general (Dolecek 1992). Currently the only evidence from interventional studies using FSO as a chemoprotective agent is provided by animal trials, which demonstrate that dietary FSO is effective in preventing colon tumour development and malignant mammary tumours (Dwivedi et al 2005).

Prostate cancer There is much debate surrounding research into the hypothesised link between ALA and the risk of prostate cancer. Giovannucci, a prolific prostate cancer researcher, has contributed to numerous papers on this topic, deriving data

from large epidemiological or prospective cohort studies including The Health Professionals Follow-Up, The Physician's Health Study and the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (Gann et al 1994, Giovannucci et al 1993, Leitzmann et al 2004, Mannisto et al 2003). The conclusions oscillate between a positive independent association between increased ALA intake and prostate cancer risk (Gann et al 1994, Giovannucci et al 1993, Leitzmann et al 2004) to no significant association (Mannisto et al 2003). Further support of ALA as a risk factor has come from a large Norwegian epidemiological study (Harvei et al 1997), a review by Astorg and a meta-analysis by Brouwer et al in 2004. Although the majority of published data appear to implicate ALA as a prostate cancer risk factor, it is worthy of note that none of the trials were interventional and many rely exclusively on food frequency questionnaires rather than independent biochemical indices of ALA. Other researchers have also presented sound arguments against this theory, such as those articulated by de Lorgeril and Salen (2004), which query the quality of evidence being considered, the exclusion of trials that demonstrated minor risk reduction with increased ALA intake (Schuurman et al 1999) and other weaknesses of the study designs. Additional criticisms include the lack of distinction in the sources of dietary ALA, with red meat, an independent risk factor for prostate cancer, being a major dietary source of ALA in some studies (Brouwer et al 2004). Until interventional trials are conducted a resolution on the matter is not possible.

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