Elsevier

The Lancet Oncology

Volume 3, Issue 9, September 2002, Pages 565-574
The Lancet Oncology

Review
Overweight, obesity, and cancer risk

https://doi.org/10.1016/S1470-2045(02)00849-5Get rights and content

Summary

Over the past few decades the proportion of people with excess body weight has been increasing in both developed and less developed countries. About 50% of men and 35% of women in Europe are currently estimated to be overweight or obese. In addition to an increase in the risk of cardiovascular disease and type II diabetes, the evidence summarised here shows that excess body weight is directly associated with risk of cancer at several organ sites, including colon, breast (in postmenopausal women), endometrium, oesophagus, and kidney. In part, these associations with cancer risk may be explained by alterations in the metabolism of endogenous hormones-including sex steroids, insulin, and insulin-like growth factors-which can lead to distortion of the normal balance between cell proliferation, differentiation, and apoptosis. Avoidance of weight gain thus seems to be an important factor for cancer prevention.

Section snippets

Methods for assessing obesity

An individual's BMI is defined as their weight in kilograms divided by the square of their height in metres; it is generally used as an indirect measure of adiposity in epidemiological studies. ‘Normal weight’ is classified as BMI between 18·5 and 25 kg/m2, ‘overweight’ is over 25 kg/m2, and ‘obesity’ is defined as a BMI of greater than 30 kg/m2.13 Although BMI does not distinguish directly between adipose tissue and lean body masses, there is a good correlation between BMI and the percentage

Adiposity and cancer risk

In this review, relative risks (RRs) are given for the highest versus the lowest categories of BMI (Figure 2, Figure 3, Figure 4, Figure 5). BMI ranges differed between cancer sites and between studies, but on average the ranges were:

  • <22 kg/m2 and >28·5 kg/m2 for colon and breast cancer,

  • <23·5 kg/m2 and >30 kg/m2 for endo-metrial cancer.

  • <22·5 kg/m2 and >27 kg/m2 for kidney and prostate cancer, and

  • <21·5 kg/m2 and >25 kg/m2 for oeso-phageal cancer.

Case-control and prospective cohort studies

Mechanisms of altered cancer risk

The relation between excess body weight and cancer risk suggests that excess energy is an important risk factor for development of cancer. This notion is supported by experimental observations that energy restriction can confer a strong protection against the development of several types of tumours in different species.40, 41, 42, 43 Furthermore, there is evidence that individuals who take regular physical activity are protected against cancers of the breast, colon, and possibly the endometrium.

Weight control and physical activity

Avoidance of weight gain should become one of the mainstays of chronic disease prevention in modern societies. Weight control can be achieved by changes in energy intake and by increased physical activity. About half of the adult population of industrialised countries are insufficiently active in their leisure time and one quarter to one third can be classified as totally inactive.38 Promotion of physical activity seems particularly effective for prevention of weight gain,79 but results are

Conclusions

There is sufficient evidence that adiposity can cause cancers of the colon, breast (in postmenopausal women), endometrium, kidney, oesophagus, and gastric cardia. Furthermore, plausible mechanistic explanations exist for most of these associations. Nevertheless, uncertainties remain about the extent of excess weight that constitutes an increase in cancer risk. For prevention of diabetes and cardiovascular disease, a BMI in the range 18·5–25 kg/m2 has been recommended. The breadth of this range

Search strategy and selection criteria

We did an exhaustive Medline search of scientific publications between 1966 and 2000, which formed the basis of a recent panel discussion by an international expert group convened by the International Agency for Research on Cancer, in Lyon, France.38 We selected studies on the basis of the number of cases included—at least 200 cases for breast and colorectal cancers; 100 cases for colon adenomas, endometrial, and prostate cancers; and 50 cases for cancers at other organ sites. Only those

References (79)

  • AM Hodge et al.

    Incidence, increasing prevalence, and predictors of change in obesity and fat distribution over 5 years in the rapidly developing population of Mauritius

    Int J Obes Relat Metab Disord

    (1996)
  • KM Flegal et al.

    Overweight and obesity in the United States: prevalence and trends, 1960–1994.

    Int J Obes Relat Metab Disord

    (1998)
  • JC Seidell

    The epidemiology of obesity

  • CA Monteiro et al.

    Shifting obesity trends in Brazil.

    Eur J Clin Nutr

    (2000)
  • World Health Organisation Consultation on Obesity

    Global prevalence and secular trends in obesity

  • R Martorell et al.

    Obesity in women from developing countries.

    Eur J Clin Nutr

    (2000)
  • Seidell JC, Rissanen A. Prevalence of obesity in adults: the global epidemic. In: Bray GA, Bouchard C, (Eds). Handbook...
  • AH Mokdad et al.

    The continuing epidemics of obesity and diabetes in the United States.

    JAMA

    (2001)
  • JC Seidell et al.

    Prevalence and trends of obesity in the Netherlands 1987–1991.

    Int J Obes Relat Metab Disord

    (1995)
  • SA Bennett et al.

    Trends in cardiovascular risk factors in Australia: results from the National Heart Foundation's Risk Factor Prevalence Study, 1980–1989.

    Med J Aust

    (1994)
  • World Health Organisation

    WWW publications from the WHO MONICA project

  • National Task Force on the Prevention and Treatment of Obesity

    Overweight, obesity, and health risk

    Arch Intern Med

    (2000)
  • FAO/World Health Organisation/United Nations Organization

    Energy and protein requirements: report of a joint expert consultation

    WHO TR 724

    (1985)
  • P Deurenberg et al.

    Body-mass index as a measure of body fatness: age- and sex-specific prediction formulas.

    Br J Nutr

    (1991)
  • BJ Caan et al.

    Body size and the risk of colon cancer in a large case-control study.

    Int J Obes Relat Metab Disord

    (1998)
  • M Gerhardsson de Verdier et al.

    Diet, body mass and colorectal cancer: a case-referent study in Stockholm.

    Int J Cancer

    (1990)
  • ME Martinez et al.

    Leisure-time physical activity, body size, and colon cancer in women. Nurses' Health Study Research Group.

    J Natl Cancer Inst

    (1997)
  • AI Neugut et al.

    Obesity and colorectal adenomatous polyps.

    J Natl Cancer Inst

    (1991)
  • E Giovannucci et al.

    Physical activity, obesity, and risk of colorectal adenoma in women (United States).

    Cancer Causes Control

    (1996)
  • CL Bird et al.

    Obesity, weight gain, large weight changes, and adenomatous polyps of the left colon and rectum.

    Am J Epidemiol

    (1998)
  • L Le Marchand et al.

    Associations of sedentary lifestyle, obesity, smoking, alcohol use, and diabetes with the risk of colorectal cancer.

    Cancer Res

    (1997)
  • AT Dietz et al.

    The association of body size and large bowel cancer risk in Wisconsin (United States) women.

    Cancer Causes Control

    (1995)
  • S Kono et al.

    Obesity, weight gain and risk of colon adenomas in Japanese men.

    Jpn J Cancer Res

    (1999)
  • de WaardF et al.

    A prospective study in general practice on breast-cancer risk in postmenopausal women.

    Int J Cancer

    (1974)
  • DR Pathak et al.

    Combined effects of body size, parity, and menstrual events on breast cancer incidence in seven countries.

    Am J Epidemiol

    (1992)
  • DJ Hunter et al.

    Diet, body size, and breast cancer.

    Epidemiol Rev

    (1993)
  • Z Huang et al.

    Dual effects of weight and weight gain on breast cancer risk.

    JAMA

    (1997)
  • C Magnusson et al.

    Body size in different periods of life and breast cancer risk in post-menopausal women.

    Int J Cancer

    (1998)
  • Breast cancer and hormone replacement therapy: collaborative reanalysis of data from 51 epidemiological studies of 52 705 women with breast cancer and 108 411 women without breast cancer

    Lancet

    (1997)
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