Obesity and Colon Cancer
Published on 8 August 2012 in Food, health and wellbeing
Introduction
There is now convincing scientific evidence linking obesity with increased risk of developing colon cancer. This knowledge is now coming to the attention of policy makers, but is not yet widely appreciated by the public.
Obesity is of course a growing concern as levels of obesity continue to rise in both adults and children. Obesity arises through a complex interplay of factors associated with diet (fat and sugar consumed), and lifestyle (sedentary versus physically active). Each individual’s genetic make-up also plays a role in development of both obesity and cancer. It is not known whether the increased risk of developing obesity related colon cancer is a consequence of the types of dietary fats consumed, high consumption of sugar rich foods that promote obesity, associated sedentary behaviour or do the resulting high levels of body fat lead to changes in the colon that predispose to cancer. A number of factors appear to protect the colon from cancer development such as fruit, vegetable and fibre consumption and increased physical activity.
The number of individuals at risk of obesity related cancer is increasing. Hence, it is important that we develop a better understanding of who is most at risk of obesity related colon cancer and determine the factors that link obesity and colon cancer. This is essential to offer properly informed advice on the benefits of maintaining a healthy lifestyle and body weight to reduce cancer risk. Additionally research will identify food products that may ameliorate cancer risk in individuals who are unable to maintain a healthy body weight.
Key Points
- Our research shows that consumption of high fat compared to low fat diets increase colon cancer risk.
- Obesity leads to altered regulation of fat derived hormones that can influence regulation of inflammatory signalling pathways linked to colon cancer
- Anti-inflammatory components in foods may be useful in ameliorating the detrimental impact of obesity on the colon.
Research Undertaken
Rising obesity levels in Scotland are predicted to increase the incidence of non-hereditary colon cancer as well as a number of other organ specific cancers. Since obesity and cancer are associated with increased inflammation the importance of dietary sources of anti-inflammatory compounds and reduced calorie consumption may be significant factors modulating the life-time risk of developing colon cancer.
Research at the University of Aberdeen, Rowett Institute of Nutrition and Health has led to development of research strategies to investigate links between obesity and colon cancer. The impact of high fat diets that promote obesity and inflammation are being illuminated using techniques to identify molecular changes in genes and proteins that are essential for maintaining a healthy colon. Changes in these genes and proteins may predispose the colon to an increased risk of cancer. Protective effects of anti-inflammatory products produced from consumption of fruit and vegetables are also being examined. The research has contributed to evidence of molecular mechanisms that link anti-inflammatory food components and diet-induced obesity with colon cancer. This has potential implications for other obesity related cancers.
Policy Implications
- Obesity can lead to an increased risk of colon cancer and should be reflected in health messages to the public.
- This research can provide health professionals with greater knowledge of cancer risks associated with overweight/obesity to assist in tailoring health advice to the general public.
- Health improvements to ameliorate the risks of obesity related cancers can be achieved with dietary advice tailored to increase consumption of foods that produce anti-inflammatory compounds in the body.
- The underlying mechanisms linking foods that lead to obesity and those that reduce inflammation will create opportunities for the food industry to generate new products that promote the health-enhancing properties of existing foods.
Author
Dr Janice Drew j.drew@abdn.ac.uk
