Diet and Cancer: Yet Another Connection
Incidence of obesity has reached an all-time high in the United States and continues to rise. In addition to the well known dangers of obesity—hypertension, heart disease, high cholesterol—obesity changes the body on the molecular level. These changes place overweight and obese people at an increased risk for a number of cancers including cancer of the esophagus, pancreas, colon, kidney, and gallbladder. Further, a disease intimately linked with obesity, type 2 diabetes, has been found to be associated with increased risk of tumors, especially those of the pancreas, liver, breast, endometrium, and bladder. A number of commonly used diabetes-control medications are suspected of also increasing the risk of tumor development, as recently described in a review by a Polish group (Wojciechowska et al 2016).
Adipose (fat) tissue releases adipokines, proteins whose numerous functions range from metabolic to immune-response. However, when someone has too much adipose tissue (and are termed “obese” or “overweight”), their levels of adipokines may become too high as excess adipose tissue produces more adipokines than the body can utilize. In response, the body releases adiponectin and leptin to help absorb the excess adipokines. Due to their function, the level of adiponectin and leptin are inversely related to the level of adipokines—as one goes up, the other goes down.
The release of adiponectin and leptin are helpful to reduce the levels of adipokines but they pose a significant risk to the body. Both adiponectin and leptin suppress apoptosis: the function by which superfluous or dangerous cells may be destroyed by the organism. Without this self-culling mechanism, cancerous cells can proliferate, leading to the development of tumors (Wojciechowska et al 2016). Some diabetes-management medications are thought to be harmful because they work by adjusting insulin levels, which in turn affects adiponectin and leptin levels and impairs the function of apoptosis (Wojciechowska et al 2016).
A diet high in fat and animal meat products and low in fiber and fresh produce—a recipe for obesity—can also increase one’s risk of cancer risk. A study from a group at Wake Forest Medical School (Soto-Pantoja et al., 2016) found that dietary fats actually limited the positive effects of thrombospondin-1 (TSP1), a protein that is inversely correlated with colon cancer. Contrary to leptin and adiponectin, TSP1 actually promotes cell regulation and apoptosis, reducing one’s risk of colon cancer. Soto-Pantoja and colleagues (Soto-Pantoja et al., 2016) followed mice with and without the TSP1 gene. Those without TSP1 develop tumors more frequently than their TSP1-positive counterparts. Additionally, mice with TSP1 developed tumors despite their genetic advantage when fed higher levels of dietary fat than their TSP1-positive, low-fat-diet peers. They demonstrated that the lack of the TSP1 gene leads to the increased risk of carcinogenesis. However, eating too much dietary fat even with the TSP1 gene present can also lead to the same risks as not having the TSP1 gene. Excessive dietary fat intake interferes with the body’s natural protections against tumors.
Another recent complementary report found similar results in human subjects (O’Keefe et al., 2015). The researchers compared the cancer risks of rural Africans and African Americans. The risk of developing colon cancer for a rural African adult is about 5:100,000. The risk for African Americans (that is, people with similar genetics but different environmental impacts and lifestyle) is 65:100,000. Scientists found that for Africans migrating to a Western country, like the US, their risk of colon cancer very quickly increased to match that of African Americans. For the first generation born in the US, their risk of colon cancer was the same as those of people whose families had lived in the US for many generations. This group studied the role of diet in altering these risks and found that in just two weeks of altered diets, biological markers of colon cancer risk were altered drastically. Rural Africans fed a high fat diet like those consumed in the US showed markedly higher “mucosal biomarkers of cancer risk and in aspect of the microbiota and metabolome know to affect cancer risk” (O’Keefe et al., 2015) while their American-dwelling counterparts were found to have markers of reduced risk of colon cancer compared to their assessment two weeks previously.
Obesity is an epidemic that affects nearly two-thirds of American adults and almost one fifth of children ages 11 to 15. This substantial portion of the Americans are at increased risk for a number of cancers and as cancer supersedes heart disease as the leading cause of death globally, we must consider the role of our diets and our gustatory environments in our risk of cancer. Emerging research on the link between obesity and cancer coupled with well established correlations with heart disease, diabetes, and hypertension makes obesity a national public health crisis we cannot afford to ignore any longer.
Soto-Pantoja DR, JM Sipes, G Martin-Manso, B Westwood, NL Morris, A Ghosh, NJ Emenaker, DD Roberts. (2016) Dietary Fat Overcomes the Protective Activity of Thrombospondin-1 Signaling in the ApcMin/ Model of Colon Cancer. Oncogenesis 5(5): doi:10.1038/oncsis.2016.37.
Wojciechowska J, W Krajewski, M Bolanowski, T Kręcicki, and T Zatoński. (2016) Diabetes and Cancer: A Review of Current Knowledge. Experimental and Clinical Endocrinology: Diabetes 124(05): 263-75. doi:10.1055/s-0042-100910.