European Code against Cancer 4th Edition:Obesity, body fatness and cancer

AbstractIt is estimated that over half the population of the European Union (EU) is overweight or obese due to an imbalance between energy expenditure and energy intake; this is related to an obesogenic environment of sociocultural, economic and marketing challenges to the control of body weight. Excess body fat is associated with nine cancer sites – oesophagus, colorectum, gall bladder, pancreas, postmenopausal breast, endometrium, ovary, kidney and prostate (advanced) – and 4–38% of these cancers (depending on site and gender) can be attributed to overweight/obesity status. Metabolic alterations which accompany excess body weight are accompanied by increased levels of inflammation, insulin, oestrogens and other hormonal factors. There are some indications that intentional weight loss is associated with reduced cancer incidence (notably in postmenopausal breast and endometrial cancers). Excess body weight is also a risk factor for several other diseases, including diabetes and heart disease, and is related to higher risk of premature death.In reviewing the current evidence related to excess body fat and cancer, the European Code against Cancer Nutrition Working Group has developed the following recommendation: ‘Take action to be a healthy body weight’

Adult weight gain and adiposity-related cancers: a dose-response meta-analysis of prospective observational studies

Backgrounds: Considerable evidence suggests that adiposity, measured by body mass index, is implicated in carcinogenesis. While adult weigh gain has diverse advantages over body mass index in measuring adiposity, systematic reviews on adult weight gain and risks of major cancers are lacking. Methods: PubMed and Embase were searched from the inception to May, 2014 to identify prospective observational studies investigating the relationship between adult weight gain and incident cancers of the breast, prostate, and colorectum. Dose-response meta-analyses were performed using a random-effects model to estimate summary relative risk (RR) and 95% confidence interval (CI) for each cancer type. Results: In the linear dose-response estimating cancer risk associated with 5kg increase in adult weight gain, a statistically significant direct association was found only for postmenopausal breast cancer and colon cancer. The summary RR was 1.11 (95% CI=1.08-1.13, I2=22%, seven studies with 4,570 cases, range=0-35kg) for postmenopausal breast cancer; 0.99 (95% CI=0.95-1.03, I2=36%, three studies with 2,409 cases, range=0-27.5kg) for premenopausal breast cancer. Etiologic heterogeneity by menopausal status at diagnosis was statistically significant (Pheterogeneity=0.001). The summary RR for colon cancer was 1.06 (95% CI=1.03-1.10, I2=0%, four studies with 2,909 cases, range=0-29kg). While there was no evidence of heterogeneity by sex (Pheterogeneity=0.17), the association was statistically significant only among men. No evidence of a linear association was indicated for prostate cancer (RR=0.98, 95% CI=0.94-1.02, four studies with 6,882 cases, range=0-25kg) and for its subtypes (localized: RR=0.96, 95% CI=0.92-1.00, I2=38%; advanced: RR=1.04, 95% CI=0.99-1.09, I2=0%). Conclusions: Avoiding adult weight gain itself may confer protection against postmenopausal breast cancer and colon cancer. As preventing weight gain is relatively more feasible than losing weight, clinicians and public health policies may prioritize weight maintenance throughout adulthood to reduce the burden of postmenopausal breast cancer and colon cancer

Renal cell cancer among African Americans: an epidemiologic review

<p>Abstract</p> <p>Incidence rates for renal cell cancer, which accounts for 85% of kidney cancers, have been rising more rapidly among blacks than whites, almost entirely accounted for by an excess of localized disease. This excess dates back to the 1970s, despite less access among blacks to imaging procedures in the past. In contrast, mortality rates for this cancer have been virtually identical among blacks and whites since the early 1990s, despite the fact that nephrectomy rates, regardless of stage, are lower among blacks than among whites. These observations suggest that renal cell cancer may be a less aggressive tumor in blacks. We have reviewed the epidemiology of renal cell cancer, with emphasis on factors which may potentially play a role in the observed differences in incidence and mortality patterns of renal cell cancer among blacks and whites. To date, the factors most consistently, albeit modestly, associated with increased renal cell cancer risk in epidemiologic studies among whites - obesity, hypertension, cigarette smoking - likely account for less than half of these cancers, and there is virtually no epidemiologic evidence in the literature pertaining to their association with renal cell cancer among blacks. There is a long overdue need for detailed etiologic cohort and case-control studies of renal cell cancer among blacks, as they now represent the population at highest risk in the United States. In particular, investigation of the influence on renal cell cancer development of hypertension and chronic kidney disease, both of which occur substantially more frequently among blacks, is warranted, as well as investigations into the biology and natural history of this cancer among blacks.</p