Physical Activity, Dietary Fat and Colorectal Cancer

Abstract

Colorectal cancer (CRC) is one of the most commonly diagnosed cancers worldwide, with over 1.2 million new cases being recorded in 2008. Global cancer statistics show that there is great (10-fold) variation in the occurrence of CRC worldwide, with the highest incidence rates in economically developed countries and regions, such as Australia, New Zealand, Europe and North America. The latest report shows that CRC incidence rates are rapidly increasing in countries within Eastern Europe and Eastern Asia, which were formerly considered low-risk areas. In some countries, e.g., the Czech Repubic and Japan, the incidence of CRC has already exceeded the peak observed in the high-risk areas. Epidemiological studies have demonstrated that the increasing incidence of CRC in these developing countries is mostly due to a higher incidence of CRC in younger age groups, which readily adopt new lifestyle habits (Jemal et al., 2011). In addition, reports have shown that persons who were born in Asia and later migrated to the United States have a higher risk of CRC than their counterparts who have remained in Asia (Flood et al., 2000). Changes in worldwide variations in the incidence rates, together with the results of migrant studies, provide convincing evidence that the incidence rates depend largely on environmental (i.e., non-genetic) risk factors, including lifestyle. It is estimated that most cases of CRC occur sporadically (70-80%). Approximately 15% of CRC cases develop as a result of inherited factors and 5-10% of them result from known genetic syndroms, e.g., familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal carcinoma (HNPCC) (Souglakos, 2007). There are different approaches and strategies concerning how to reduce the incidence of and mortality due to CRC. Those directed toward the treatment of CRC, i.e., surgical and therapeutic measures, are mostly costly, painful and the prognosis is not promisig. Efforts have also recently been directed toward the identification and removal of precancerous lesions (visible polypoid adenomas) through screening programs, which is a promising approach and is an important step in reducing mortality due to CRC (Orlando et al., 2008). On the other hand, efforts invested into strategies directed toward public health promotion campaigns for the prevention or reduction of risk factors in populations at high risk of CRC have been few and obviously ineffective. Recent studies have shown that there is low level of awareness of the role that physical activity plays in preventing CRC among adults in the USA and Europe (Coups et al., 2008; Keighley et al., 2004).

Oxidative Stress in the Pathogenesis of Colorectal Cancer: Cause or Consequence?

“…Lipids and fatty acids obtained from dietary fats are metabolized and incorporated into the phospholipids of the cell membranes of many cell types and serve as precursors for many biologically active molecules, as well as being important for cell signalling or different intensity of inflammation response [59, 60]. A substantial increase in the PUFA content may overcome the protective action of the antioxidant system and increase susceptibility to lipid peroxidation [61].…”

Effect of high-fat mixed lipid diet and swimming on fibre types in skeletal muscles of rats with colon tumours

“…In recent years, high fat diet together with sedentary life style has been recognized as an important factor responsible for various diseases, such as obesity, diabetes, cardiovascular diseases, including colon cancer which is one of the most common cancers worldwide. 13 To investigate the underlying mechanisms through which various physiological and environmental factors interact with colon cancer development, various animal models have been used. One of the well-established models of the experimental multistep development of colon carcinogenesis with morphological and histological features similar to those seen in the human sporadic colon carcinogenesis ( i.e ., dysplastic crypts, adenomas, carcinomas) is the carcinogen 1,2 dimethyhydrazine (DMH) model.…”

“…Further, it was demonstrated that dietary fatty acids affect the lipid content of tissues, lipid peroxidation process, antioxidant status, arachidonic acid metabolism, immune function, cell signalling pathways, cell proliferation and apoptosis. 13 Nonetheless, the experimental studies in DMH rat model have shown that high fat diet, particularly high-fat mixed lipid (HFML) diet, which reflects the mixed lipid composition of the average Western-style diet and consists of a mixture of saturated, monosaturated and polyunsaturated fatty acids, has been strongly associated not only with an increased incidence of colon cancer but it compromised the antioxidant defence system in various tissues as well, including the skeletal muscle. 17-19 On the other hand, the endurance swimming reduced the development of colon tumours in DMH-treated rats on both HFML and low fat corn oil (LFCO) diet but affected the antioxidant defence system in the heart, liver and skeletal muscle only in rats on HFML diet.…”