Obesity and Cancer with Emphasis on Bariatric Surgery

Fig. 1.

Mechanisms of decreased cancer risk by metabolic surgery. IGF-1 = Insulin-like Growth Factor 1, AMPK = 5′ adenosine monophosphate-activated protein kinase. (Figure adapted from Ashrafian, et al. [84] and reprinted by permission).

These authors suggest that bariatric (or metabolic) surgery “interrupts” the postulated mechanistic pathways that are thought to promote both obesity and subsequent cancer. As review authors, we predict that during the next few years, there will be a significant escalation in research related to the potential mechanisms postulated by Ashrafian et al., leading to a clearer understanding of the relationship of voluntary weight loss and cancer risk.

Conclusion

The link between increased adiposity (i.e., obesity) and greater risk for cancer has been well established. However, due to the difficulty in achieving meaningful and sustained weight loss in large population studies, whether or not voluntary weight loss reduced the risk of cancer incidence and cancer recurrence is not entirely clear. The opportunity to study cancer risk following voluntary weight loss is possible when bariatric surgical patients are followed over time. Although limited in number, studies have demonstrated a reduction in cancer mortality among post-bariatric patients compared with severely obese, nonoperated controls. In addition, one prospective study (SOS study) and a few observational studies have shown a lower risk for cancer incidence among patients who have undergone bariatric surgery compared with nonoperated, severely obese comparison groups. One study has suggested that the risk for obesity-related cancers following bariatric surgery is not reduced below cancer rates of the background population. Further, reported reductions in obesity-related cancer risk have been limited to females, perhaps due to the greater percentage of women who undergo weight loss surgery when compared with men. With reference to the various types of bariatric surgical procedures, there is limited evidence of how these procedures might differ in relation to their potential for reducing subsequent cancer risk. There is an increasing consensus that intentional weight loss may lead to lower cancer incidence [56]. Finally, recent national and international guidelines that have recommended weight loss for individuals (if clinically indicated), for the purpose of reducing cancer incidence risk, appear to be supported by the few weight loss and cancer studies that have been published, including those related to bariatric surgery.

Acknowledgments

We wish to thank Maureen Rice of the McMaster University Evidence-based Practice Center (MU-EPC), McMaster University, Hamilton, Ontario, for conducting a medical literature review. We also express appreciation to Kenneth Adams, Ph.D.; the late Eugenia Calle, Ph.D.; Paul Hopkins, M.D.; Richard Gress, M.S.; Nan Stroup, Ph.D.; Sherman Smith, M.D.; Steven Simper, M.D.; and Rodrick McKinlay, M.D.

T.D.A. receives partial funding through the Huntsman Fellowship—Advancing Community Cancer Prevention, Intermountain Research and Medical Foundation, Intermountain Healthcare Corporation, SLC, UT. T.D.A., S.C.H., and L.E.D. are supported by grant DK-55006 from the National Institutes of Health/the National Institute of Diabetes and Digestive and Kidney Diseases.

Review Questions and Answers

Question 1: Do pre-menopausal obese women have a greater risk for incidence of breast cancer compared to pre-menopausal normal weight women?

Answer 1:

No, population-based research suggests that pre-menopausal obese women are at lower risk for developing breast cancer compared to pre-menopausal normal weight women. However, post-menopausal obese women are at a greater risk for breast cancer compared to post-menopausal normal weight women.

Question 2: What are considered to be the primary mechanistic links between obesity and specific cancer types?

Answer 2:

Generally, three major categories have been identified as mechanisms associating obesity and obesity-related cancers. These include chronic inflammation, over-release of steroid-related hormones and tumor growth promotion (secondary to hyperinsulinemia.

Question 3: How strongly does the evidence support the recommendation that traditional weight loss reducesincident risk of cancer as well as cancer recurrence?

Answer 3:

The evidence relating weight loss from traditional therapies (i.e. diet, physical activity and behavioral modification) and reduced cancer risk are limited primarily because of the difficulty achieving significant and sustained weight loss among overweight and obese population groups.

Question 4: What is the evidence for reduced cancer incidence and cancer mortality among patients who have had bariatric surgery compared to obese, non-bariatric surgical subjects?

Answer 4:

Because patients who have undergone bariatric surgery generally lose a large amount of weight (i.e. greater than 20% of initial weight) and maintain significant weight loss for an extended period of time (i.e. years), these patients are ideal to study weight loss and subsequent cancer risk. There are multiple studies that have shown when bariatric cancer patients are compared to severely obese non-surgical subjects, the bariatric surgical patients demonstrate lower cancer mortality and cancer incidence when compared to severely obese non-operated controls.

References

Cowie CC, Rust KF, Ford ES, et al. Full accounting of diabetes and pre-diabetes in the U.S. population in 1988-1994 and 2005-2006. Diabetes Care. 2009;32(2):287–94.PubMedCentralPubMed

Freedman DS, Khan LK, Serdula MK, Galuska DA, Dietz WH. Trends and correlates of class 3 obesity in the United States from 1990 through 2000. JAMA. 2002;288(14):1758–61.PubMed

Sturm R. Increases in clinically severe obesity in the United States, 1986-2000. Arch Intern Med. 2003;163(18):2146–8.PubMed

Fox CS, Coady S, Sorlie PD, et al. Increasing cardiovascular disease burden due to diabetes mellitus: the Framingham Heart Study. Circulation. 2007;115(12):1544–50.PubMed

Preis SR, Hwang SJ, Coady S, et al. Trends in all-cause and cardiovascular disease mortality among women and men with and without diabetes mellitus in the Framingham Heart Study, 1950 to 2005. Circulation. 2009;119(13):1728–35.PubMedCentralPubMed

Olshansky SJ, Passaro DJ, Hershow RC, et al. A potential decline in life expectancy in the United States in the 21st century. N Engl J Med. 2005;352(11):1138–45.PubMed

Preston SH. Deadweight?–The influence of obesity on longevity. N Engl J Med. 2005;352(11):1135–7.PubMed

Food, Nutrition, Physical Activity, and the Prevention of Cancer: A Global Perspective. Washington, DC: AICR: World Cancer Research Fund/American Institute for Cancer Research;2007.

Patlak M, Nass SJ. The role of obesity in cancer survival and recurrence: Workshop summary. Washington, DC: Institute of Medicine of the National Academies; 2012.

10.

National Institutes of Health (NHLBI). Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: the evidence report. Obes Res. 1998;6(2):51S–209.

11.

National Task Force on the Prevention and Treatment of Obesity. Overweight, obesity, and health risk. Arch Intern Med. 2000;160:898–904.

12.

Calle E. Obesity and cancer (Chapter 10). In: Hu F, editor. Obesity Epidemiolog. Oxford: Oxford University Press; 2008. p. 196–215.

13.

Reeves G, Pirie K, Beral V, Green J, Spencer E, Bull D. Cancer incidence and mortality in relation to body mass index in the Million Woman Study: cohort study. Br Med J. 2007;335:1134–9.

14.

Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 2003;348(17):1625–38.PubMed

15.

Rapp K, Schroeder J, Klenk J, et al. Obesity and incidence of cancer: a large cohort study of over 145,000 adults in Austria. Br J Cancer. 2005;93(9):1062–7.PubMedCentralPubMed

16.

Samanic C, Chow WH, Gridley G, Jarvholm B, Fraumeni Jr JF. Relation of body mass index to cancer risk in 362,552 Swedish men. Cancer Causes Control. 2006;17(7):901–9.PubMed

17.

Renehan A, Tyson M, Egger M, Heller R, Zwahlen M. Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet. 2008;371(9612):569–78.PubMed

18.

Calle EE, Thun MJ. Obesity and cancer. Oncogene. 2004;23(38):6365–78.PubMed

19.

IARC. IRAC handbooks of cancer prevention weight control and physical activity. Lyon: International Agency for Research on Cancer; 2002.

20.

Schouten LJ, Goldbohm RA, van den Brandt PA. Anthropometry, physical activity, and endometrial cancer risk: results from the Netherlands Cohort Study. J Natl Cancer Inst. 2004;96(21):1635–8.PubMed

21.

Rodriguez C, Freedland SJ, Deka A, et al. Body mass index, weight change, and risk of prostate cancer in the Cancer Prevention Study II Nutrition Cohort. Cancer Epidemiol Biomarkers Prev. 2007;16(1):63–9.PubMed

22.

Xu WH, Xiang YB, Zheng W, et al. Weight history and risk of endometrial cancer among Chinese women. Int J Epidemiol. 2006;35(1):159–66.PubMed

23.

Aune D, Greenwood DC, Chan DS, et al. Body mass index, abdominal fatness and pancreatic cancer risk: a systematic review and non-linear dose-response meta-analysis of prospective studies. Ann Oncol. 2012;23(4):843–52.PubMed

24.

Calle EE. Obesity and cancer. BMJ. 2007;335(7630):1107–8.PubMedCentralPubMed

25.

Basen-Engquist K, Chang M. Obesity and cancer risk: recent review and evidence. Curr Oncol Rep. 2011;13(1):71–6.PubMedCentralPubMed

26.

Vainio H, Kaaks R, Bianchini F. Weight control and physical activity in cancer prevention: international evaluation of the evidence. Eur J Cancer Prev. 2002;11 Suppl 2:S94–100.PubMed

27.

Anderson AS, Caswell S. Obesity management–an opportunity for cancer prevention. Surgeon. 2009;7(5):282–5.PubMed

Only gold members can continue reading. Log In or Register to continue