Trends in incidence rates for obesity-associated cancers in the US
Introduction
Increases in the age-adjusted estimated prevalence of self-reported diagnosed diabetes and obesity in the U.S have been referred to as “continuing epidemics” [1]. Using the body mass index (BMI) or ratio of measured weight (in kilograms) divided by measured height (in meters squared), the prevalence of obesity (BMI 30+) increased from 1976–1980 to 1988–1994 in all age groups in the US National Health and Nutrition Examination Survey (NHANES) of samples of non-institutionalized adults 20–74 years old [2]. Data from NHANES 1999–2000 indicate an age-adjusted obesity prevalence of 30.5% among US adults, compared to 22.9% in NHANES III (1988–1994) versus 15% in 1976–1980, 14.5% in 1971–1974 and 13.4% in 1960–1962 [3]. These temporal increases occurred in all age, sex and racial-ethnic groups [3].
It has been suggested that increases in incidence rates for cancers associated with obesity “may not be noticeable for the next few decades” in Europe, until young adults (with rising prevalence of obesity) reach older ages of higher risk (e.g., for breast cancer) [4]. However, the increases in obesity among middle-aged and older groups in the US (especially after the late 1970s) [3] already may have affected recent trends in US cancer incidence rates. For endometrial cancer, obesity at the time of cancer diagnosis (but not at younger ages) has been associated sociated with risk [5]. Thus, long time periods may not be required between the onset of obesity and the diagnosis of cancer. This may also hold for obesity and renal cancer, where promoters (estrogens) and/or cell proliferation due to renal damage may be involved [6], [7], and for postmenopausal breast cancer, where weight gain in adult life may be most important (presumably involving hormonal promotion of tumors) [8].
For this report, temporal trends in incidence rates were examined for cancers most clearly associated with obesity, and the numbers of cancers diagnosed in 2002 that may be potentially attributable to obesity were estimated.
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Materials and methods
Incidence data for selected cancers were obtained for the nine geographic areas (Atlanta GA, Connecticut, Detroit MI, Hawaii, Iowa, New Mexico, San Francisco-Oakland CA, Seattle, Utah) covered since 1973–1975 by the US National Cancer Institute’s Surveillance, Epidemiology and End Results (SEER) Program of high-quality population-based cancer registries, regarded as generally representative of (unknown) rates for the entire US [9].
Only those cancer sites or histologic groups for which risk has
Results
For all ages combined, ASIRs for adenocarcinoma of the uterine corpus/uterus unspecified declined to their lowest level in the late 1980s, followed by slight increases (Table 1). The decline in the 1970s–1980s, and the increase in the 1990s, were larger for all women and whites than for blacks (Table 1). The lowest ASIR was consistently reached in 1988–1990, except for blacks (for whom trends were more erratic). For all women and white women, the ASIRs increased slightly after 1988–1990 for
Discussion
Temporal increases in ASIRs were evident for kidney cancer and adenocarcinomas of the esophagus and gastric cardia, while during the 1990s the previous decline in ASIRs for adenocarcinoma of the uterine corpus was reversed and the ASIRs for breast cancer continued to increase for age 50+ years. These trends are generally consistent with a potential impact of rising obesity prevalence rates.
Study limitations include the use of SEER data as representative of the entire US, in the absence of
Acknowledgements
This work was supported in part by Contract NO1-CN-67005 between the National Cancer Institute and the Connecticut Department of Public Health.
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