Obesity and cancer

Abstract

The prevalence of obesity, defined as a BMI of ‡ 30 . 0 kg/m 2 , 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: postmenopausal 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/m 2 ) 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. Obesity: Cancer risk: Cancer site: Body fat distributionThe prevalence of obesity has increased substantially over previous decades in most industrialized countries, and a further increase is expected in the future

Obesity hormone leptin induces growth and interferes with the cytotoxic effects of 5-fluorouracil in colorectal tumor stem cells

“…The risk of colorectal cancer development is increased in obese individuals, possibly due to elevated activity of biologically active substances produced by the fat tissue (Pischon et al 2008). The adipokine leptin has been implicated in colorectal cancer development and progression due to its mitogenic, anti-apoptotic, mitogenic, and pro-inflammatory activity (Garofalo & Surmacz 2006, Karagiannides & Pothoulakis 2007, Ratke et al 2010.…”

“…Indeed, adipocytes and preadipocytes can stimulate the growth of colon cancer cells (Amemori et al 2007). Furthermore, biologically active substances produced by adipocytes, such as cytokines (especially pro-inflammatory), growth factors, steroid hormones can exert oncogenic effects in the large bowel (Karagiannides & Pothoulakis 2007, Pischon et al 2008, Pais et al 2009.…”

Pleiotropic effects of obesity-susceptibility loci on metabolic traits: a meta-analysis of up to 37,874 individuals

“…Obesity is a key risk factor for a number of metabolic disorders, including type 2 diabetes, dyslipidaemia and cardiovascular disease, and has been associated with increased mortality [1][2][3][4][5][6]. Although the exact biological mechanisms linking obesity to these comorbidities are not fully understood, it has been shown that increased adiposity, especially abdominal fat accumulation, over time leads to a cluster of metabolic and cardiovascular abnormalities, including elevated blood glucose, insulin resistance, raised triacylglycerol, lower HDL-cholesterol and high BP [7,8].…”

Free will and the obesity epidemic

“…Most health experts agree that a BMI of 30?0 kg/m 2 represents the upper limit of a healthy weight (18) . A BMI of $ 30?0 kg/m 2 is associated with increases in the prevalence of CVD (19) , stroke (20) , atherosclerosis (21) , hypertension (22) , diabetes (23) , arthritis (24) and several cancers (25) . Just as with the food disappearance data, the obesity data can be divided into two linear components -one beginning in 1960 and ending around 1980 and the other continuing from 1980.…”