The incidence of obesity continues to rise to an alarming level in developed countries. It is also well documented that overweight and obese patients are at an increased risk of a number of cancers including cancer of the pancreas, colon, oesophagus, gallbladder and kidney. It has not been clear if these associations are causal, but addressing common factors could limit the risk factor of cancer and diabetes 

Type 2 diabetes, which is associated with obesity and insulin resistance is also associated with an increased risk of tumours, especially those of the pancreas, bladder, endometrium and breast.

A complex process

Obesity induces inflammation by stressing adipose tissues, a process that attracts immune cells and then produces inflammatory mediators like interleukin 6 and tumour necrosis factor (TNF). Both have been shown to be involved in tumour progression. 

Research evidence suggests the extension of cumulative and differential mechanisms influencing the relationship between these diseases. 

Adipose fat tissue releases adipokines, proteins that influence the immune and metabolic responses. Excess adipose tissue leads to excess adipokines. In response, the body releases adiponectin and leptin to absorb the excess adipokines. The level of adiponectin and leptin is inversely related to the level of adipokines. 

The release of adiponectin and leptin are helpful to reduce the level of adipokines but pose a significant risk to the body. Both molecules suppress apoptosis, the process by which dangerous cells may be destroyed by the organism. Henceforth cancer cells can proliferate, leading to the development of tumours.

It has been stated by some researchers that some diabetes medications may be harmful as they work by adjusting insulin levels which in turn affect adiponectin and insulin levels. A diet high in fat and animal products and low in fibre can also increase the risk of cancer. Dietary fats limit the positive effects of thrombospondin-1, a protein that is inversely related to colon cancer. This promotes cell regulation and apoptosis, reducing one’s risk of cancer. 

However, excess dietary fat interferes with the natural protectors against tumours. 

Research evidence

Soto-Pantoja et al¹ 2016 studied mice with and without the thrombospondin gene. Mice with this gene developed tumours despite their genetic advantage when fed higher levels of dietary fat than their low fat peers. They also demonstrated that lack of this gene leads to an increased risk of carcinogenesis. 

Rhodes mice without thrombospondin develop tumours more than their thrombospondin-positive counterparts. 

The risk of colon cancer for a rural African is about 5 in 100,000. The risk for African Americans is 65 in 100,000. Scientists found that for Africans migrating to a Western country, the risk of colon cancer quickly increased to that of the African Americans.²

The group studied the role of diet in altering these risks and found that in just two weeks of altered diet, biological markers of colon cancer were altered drastically. Rural Africans fed a high-fat diet like those consumed in the US showed higher mucosal biomarkers of cancer risk while their American counterparts on a high-fibre, low-fat diet were found to have markers of reduced risk of colon cancer compared to their assessment two weeks previously. 

We must continue to stem the tide of obesity. We are all living longer and obesity and the incidence of newly diagnosed cancers are rising in the western world. It is imperative that we consider the role of our diets and environments in our risk of cancer. Research on the links between obesity and cancer along with the well established correlations with heart disease and diabetes makes obesity and our diet a health crisis we must not ignore. 

Well controlled studies on the development of diabetes upon cancer treatment are necessary and should identify the underlying mechanisms responsible for these reciprocal interactions. 

References

1. Soto-Pantoja DR, Sipes JM, Martin-Manso G, et al. Dietary fat overcomes the protective activity of thrombospondin-1 signaling in the Apc(Min/+) model of colon cancer. Oncogenesis, 2016; 5 (5): e230 doi: 10.1038/oncsis.2016.37
2. O’Keefe S, LiJ, Lahti L, et al. Fat, fibre and cancer risk in African Americans and rural Africans. Nature Communications 6, Article number: 6342 (2015) doi:10.1038/ncomms7342