• Tobias Pischon, Ute Nöthlings, and Heiner Boeing.
• Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, 14558 Nuthetal, Germany. pischon@dife.de
• P Nutr Soc. 2008 May 1;67(2):128-45.

AbstractThe prevalence of obesity, defined as a BMI of > or =30.0 kg/m2, has increased substantially over previous decades to about 20% in industrialized countries, and a further increase is expected in the future. Epidemiological studies have shown that obesity is a risk factor for: post-menopausal breast cancer; cancers of the endometrium, colon and kidney; malignant adenomas of the oesophagus. Obese subjects have an approximately 1.5-3.5-fold increased risk of developing these cancers compared with normal-weight subjects, and it has been estimated that between 15 and 45% of these cancers can be attributed to overweight (BMI 25.0-29.9 kg/m2) and obesity in Europe. More recent studies suggest that obesity may also increase the risk of other types of cancer, including pancreatic, hepatic and gallbladder cancer. The underlying mechanisms for the increased cancer risk as a result of obesity are unclear and may vary by cancer site and also depend on the distribution of body fat. Thus, abdominal obesity as defined by waist circumference or waist:hip ratio has been shown to be more strongly related to certain cancer types than obesity as defined by BMI. Possible mechanisms that relate obesity to cancer risk include insulin resistance and resultant chronic hyperinsulinaemia, increased production of insulin-like growth factors or increased bioavailability of steroid hormones. Recent research also suggests that adipose tissue-derived hormones and cytokines (adipokines), such as leptin, adiponectin and inflammatory markers, may reflect mechanisms linked to tumourigenesis.

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