Fat and Cancer

On the other hand, within-population studies of a cross-sectional format have yielded conflicting results, but large prospective studies, which 

International comparitive studies show a strong correlation between per capitut disappearance of fat and rates of colon cancer (Willett, 2001a Kushi and Giovannucci, 2002). Early animal studies suggested that dietary fat plays an important role in the initiation and promotion of colon tumorigenesis. However, later evidence showed that total energy intake, rather than fat intake, was more likely to influence tumor development (Howe et al., 1997). 

Overall, epidemiological evidence from within-population studies does not support an independent role for dietary fat or fat subclasses in the risk of colon cancer. However, the evidence does not preclude the possibility that certain fatty acids, such as co-6s and co-3s, may exert opposing influences. 

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The relationship between diet and cancer risk is extremely complex (7). Factors that appear to enhance carcinogenesis under one set of conditions may have no effect or even inhibit carcinogenesis under different conditions (2). The link between dietary fat and cancer is complicated by many factors, in particular total calorie intake and fatty acid composition (2). Among the fatty acids that comprise lipid, only linoleic acid is clearly linked to the enhancement of carcinogenesis in rat manunary gland (5), pancreas (4) and colon (5). 

High intake of total fat is correlated with an increased incidence of breast cancer in international comparative studies. In addition to the usual factors that confound associations between dietary fat and cancer in this type of study, countries with a high fat intake also have a lower age at menarche, later age at first birth, lower parity and higher post-menopausal body weight, which are risk factors for breast cancer (Willett, 2001b Kushi and Giovannucci, 2002). 

In response to the U.S. food labeling regulations in 1994, the FDA has proposed to define nutrient-content claims such as fat free, low fat, and reduced fat. Products labeled fat free and low fat must contain less than 0.5 g of fat per serving and less than 3 g of fat per serving, respectively. Reduced or less fat may be used on the labels of products that contain 25% less fat than regular (fuU-fat) products. Products labeled percent fat free should be based on 100 g, when product meets the definition of low fat or a 100% fat free, claim can be made when products meet the definition of fat free (contains no added fat) (12). Proposals have also been published to permit health claims for a relationship between the level of dietary fats and cardiovascular disease, as well as for a relationship between the level of dietary fats and cancer. 

Health Claims. Approved health claims with potential applicability to margarines or spreads are the relationships between fat and cancer, saturated fat and cholesterol and risk of heart disease, and sodium and hypertension. A food that contains more than 13 g of fat, 4 g of saturated fat, 60 mg of cholesterol, or 480 mg of sodium per serving or per 50 g is disqualified from making any health claim. In addition the product must qualify as low fat for the cancer claim, low fat, low saturated fat, and low cholesterol for the coronary heart disease claim, and low sodium for the hypertension claim. The first two claims, therefore, would be limited to spreads containing 6% or less fat, and the hypertension claim would require the spread to contain less than 140 mg of sodium per 50 g (approximately 0.7% salt). 

Zock, P.L., Dietary fats and cancer, Curr. Opin. Lipidol, 12, 5-10,2001. 

Meera, J. (1988) Dairy Foods, Dairy Fats, and Cancer, a Review of Epidemiological Evidence, Nutr. Res. 18, 905-937. 

Pariza, M.W. (1988) Dietary fat and cancer risk evidence and research needs. Annu. Rev. Nutr. 8, 167-183. 

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