What is obesity?
Obesity is a condition in which a person has an unhealthy amount and/or distribution of body fat.
To measure obesity, researchers commonly use a scale known as the body mass index (BMI). BMI is calculated by dividing a person’s weight (in kilograms) by their height (in meters) squared (commonly expressed as kg/m2). (See our BMI calculator here.) BMI provides a more accurate measure of obesity than weight alone, and for most people it is a fairly good (although indirect) indicator of body fatness.
Other measurements that reflect the distribution of body fat—that is, whether more fat is carried around the hips or the abdomen—are increasingly being used along with BMI as indicators of obesity and disease risks. These measurements include waist circumference and the waist-to-hip ratio (the waist circumference divided by the hip circumference).
The standard weight categories based on BMI for adults age 20 years or older are
|BMI in kg/m2||Weight Category|
|18.5 to 24.9||Normal|
|25.0 to 29.9||Overweight|
|30.0 to 39.9||Obese|
|40.0 and higher||Severely Obese|
For children and adolescents (younger than 20 years of age), overweight and obesity are based on the Centers for Disease Control and Prevention’s (CDC’s) BMI-for-age growth charts, which are available at http://www.cdc.gov/growthcharts/clinical_charts.htm:
|BMI-for-age at or above sex-specific 85th percentile, but less than 95th percentile||Overweight|
|BMI-for-age at or above sex-specific 95th percentile||Obese|
The CDC has a BMI percentile calculator for children and teens at http://nccd.cdc.gov/dnpabmi/Calculator.aspx.
Compared with people of normal weight, those who are overweight or obese are at greater risk for many diseases, including diabetes, high blood pressure, cardiovascular disease, stroke, and many cancers. Extreme or severe obesity is also associated with an increased death rate; heart disease, cancer, and diabetes are responsible for most of the excess deaths (1, 2).
How common is overweight or obesity?
Results from the National Health and Nutrition Examination Survey (NHANES) showed that in 2011–2014, nearly 70% of U.S. adults age 20 years or older were overweight or obese and more than one-third (36.5%) were obese (3). In 1988–1994, by contrast, only 56% of adults aged 20 years or older were overweight or obese.
The percentage of children and adolescents who are overweight or obese has also increased (3). In 2011–2014, an estimated 9% of 2- to 5-year-olds, 17% of 6- to 11-year-olds, and 20% of 12- to 19-year-olds were overweight or obese. In 1988–1994, those figures were only 7%, 11%, and 10%, respectively. In 2011–2014, about 17% of U.S. youth ages 2 to 19 years old were obese. In 1988–1994, by contrast, only about 10% of 2 to 19-year old were obese (4).
According to the CDC, the prevalence of obesity in the United States differs among racial/ethnic groups. For example, in 2011–2012 among adults, non-Hispanic blacks had the highest prevalence of obesity (47.8%) followed by Hispanics (42.0%), non-Hispanic whites (33.4%), and non-Hispanic Asians (10.9%) (5). Among children and adolescents ages 2–19 years, the prevalence of obesity in 2011–2012 was 21.9% among Hispanics, 19.5% among non-Hispanic blacks, 14.7% among non-Hispanic whites, and 8.6% among non-Hispanic Asians.
The CDC has state-level estimates of obesity prevalence among U.S. adults available at http://www.cdc.gov/obesity/data/prevalence-maps.html.
What is known about the relationship between obesity and cancer?
Nearly all of the evidence linking obesity to cancer risk comes from large cohort studies, a type of observational study. However, data from observational studies can be difficult to interpret and cannot definitively establish that obesity causes cancer. That is because obese or overweight people may differ from lean people in ways other than their body fat, and it is possible that these other differences—rather than their body fat—are what explains their different cancer risk.
Despite the limitations of the study designs, there is consistent evidence that higher amounts of body fat are associated with increased risks of a number of cancers (6), including:
• Endometrial cancer: Obese and overweight women are two to about four times as likely as normal-weight women to develop endometrial cancer (cancer of the lining of the uterus), and extremely obese women are about seven times as likely to develop the more common of the two main types of this cancer (7). The risk of endometrial cancer increases with increasing weight gain in adulthood, particularly among women who have never used menopausal hormone therapy (8).
• Esophageal adenocarcinoma: People who are overweight or obese are about twice as likely as normal-weight people to develop a type of esophageal cancer called esophageal adenocarcinoma, and people who are extremely obese are more than four times as likely (9).
• Gastric cardia cancer: People who are obese are nearly twice as likely as normal-weight people to develop cancer in the upper part of the stomach, that is, the part that is closest to the esophagus (10).
• Liver cancer: People who are overweight or obese are up to twice as likely as normal-weight people to develop liver cancer. The association between overweight/obesity and liver cancer is stronger in men than women (11, 12).
• Kidney cancer: People who are overweight or obese are nearly twice as likely as normal-weight people to develop renal cell cancer, the most common form of kidney cancer (13). The association of renal cell cancer with obesity is independent of its association with high blood pressure, a known risk factor for kidney cancer (14).
• Multiple myeloma: Compared with normal-weight individuals, overweight and obese individuals have a slight (10% to 20%) increase in the risk of developing multiple myeloma (15).
• Meningioma: The risk of this slow-growing brain tumor that arises in the membranes surrounding the brain and the spinal cord is increased by about 50% in people who are obese and about 20% in people who are overweight (16).
• Pancreatic cancer: People who are overweight or obese are about 1.5 times as likely to develop pancreatic cancer as normal-weight people (17).
• Colorectal cancer: People who are obese are slightly (about 30%) more likely to develop colorectal cancer than normal-weight people (18).
A higher BMI is associated with increased risks of colon and rectal cancers in both men and in women, but the increases are higher in men than in women (18).
• Gallbladder cancer: Compared with normal-weight people, people who are overweight have a slight (about 20%) increase in risk of gallbladder cancer, and people who are obese have a 60% increase in risk of gallbladder cancer (19, 20). The risk increase is greater in women than men.
• Breast cancer: Many studies have shown that, in postmenopausal women, a higher BMI is associated with a modest increase in risk of breast cancer. For example, a 5-unit increase in BMI is associated with a 12% increase in risk (21). Among postmenopausal women, those who are obese have a 20% to 40% increase in risk of developing breast cancer compared with normal-weight women (22). The higher risks are seen mainly in women who have never used menopausal hormone therapy and for tumors that express hormone receptors. Obesity is also a risk factor for breast cancer in men (23).
In premenopausal women, by contrast, overweight and obesity have been found to be associated with a 20% decreased risk of breast tumors that express hormone receptors (22).
• Ovarian cancer: Higher BMI is associated with a slight increase in the risk of ovarian cancer, particularly in women who have never used menopausal hormone therapy (24). For example, a 5-unit increase in BMI is associated with a 10% increase in risk among women who have never used menopausal hormone therapy (24).
• Thyroid cancer: Higher BMI (specifically, a 5-unit increase in BMI) is associated with a slight (10%) increase in the risk of thyroid cancer (25).
How might obesity increase the risk of cancer?
Several possible mechanisms have been suggested to explain how obesity might increase the risks of some cancers.
• Obese people often have chronic low-level inflammation, which can, over time, cause DNA damage that leads to cancer. Overweight and obese individuals are more likely than normal-weight individuals to have conditions or disorders that are linked to or that cause chronic local inflammation and that are risk factors for certain cancers (26). For example, chronic local inflammation induced by gastroesophageal reflux disease or Barrett esophagus is a likely cause of esophageal adenocarcinoma. Obesity is a risk factor for gallstones, a condition characterized by chronic gallbladder inflammation, and a history of gallstones is a strong risk factor for gallbladder cancer (27). Chronic ulcerative colitis (a chronic inflammatory condition) and hepatitis (a disease of the liver causing inflammation) are risk factors for different types of liver cancer (28).
• Fat tissue (also called adipose tissue) produces excess amounts of estrogen, high levels of which have been associated with increased risks of breast, endometrial, ovarian, and some other cancers.
• Obese people often have increased blood levels of insulin and insulin-like growth factor-1 (IGF-1). (This condition, known as hyperinsulinemia or insulin resistance, precedes the development of type 2 diabetes.) High levels of insulin and IGF-1 may promote the development of colon, kidney, prostate, and endometrial cancers (29).
• Fat cells produce adipokines, hormones that may stimulate or inhibit cell growth. For example, the level of an adipokine called leptin, which seems to promote cell proliferation, in the blood increases with increasing body fat. And another adipokine, adiponectin—which is less abundant in obese people than in those of normal weight—may have antiproliferative effects.
• Fat cells may also have direct and indirect effects on other cell growth regulators, including mammalian target of rapamycin (mTOR) and AMP-activated protein kinase.
Other possible mechanisms by which obesity could affect cancer risk include changes in the mechanical properties of the scaffolding that surrounds breast cells (30) and altered immune responses, effects on the nuclear factor kappa beta system, and oxidative stress (31).
How many cancer cases may be due to obesity?
A population-based study using BMI and cancer incidence data from the GLOBOCAN project estimated that, in 2012 in the United States, about 28,000 new cases of cancer in men (3.5%) and 72,000 in women (9.5%) were due to overweight or obesity (32). The percentage of cases attributed to overweight or obesity varied widely for different cancer types but was as high as 54% for gallbladder cancer in women and 44% for esophageal adenocarcinoma in men.
A 2016 study summarizing worldwide estimates of the fractions of different cancers attributable to overweight/obesity reported that, compared with other countries, the United States had the highest fractions attributable to overweight/obesity for colorectal cancer, pancreatic cancer, and postmenopausal breast cancer (33).
Does avoiding weight gain or losing weight decrease the risk of cancer?
Most of the data about whether avoiding weight gain or losing weight reduces cancer risk comes from cohort and case-control studies. As with observational studies of obesity and cancer risk, these studies can be difficult to interpret because people who lose weight or avoid weight gain may differ in other ways from people who do not.
Nevertheless, when the evidence from multiple observational studies is consistent, the association is more likely to be real. Many observational studies have provided consistent evidence that people who have lower weight gain during adulthood have lower risks of colon cancer, kidney cancer, and—for postmenopausal women—breast, endometrial, and ovarian cancers (34).
Fewer studies have examined possible associations between weight loss and cancer risk. Some of these have found decreased risks of breast, endometrial, colon, and prostate cancers among people who have lost weight. However, most of these studies were not able to evaluate whether the weight loss was intentional or unintentional (and possibly related to underlying health problems).
Stronger evidence for a relationship between weight loss and cancer risk comes from studies of people who have undergone bariatric surgery (surgery performed on the stomach or intestines to induce weight loss). Obese people who have bariatric surgery appear to have lower risks of obesity-related cancers than obese people who do not have bariatric surgery (35).
Nevertheless, the follow-up study of weight and breast cancer in the Women’s Health Initiative (36) found that for women who were already overweight or obese at baseline, weight change (either gain or loss) was not associated with breast cancer risk during follow-up. However, for women who were of normal weight at baseline, gaining more than 5% of body weight was associated with increased breast cancer risk.
How does obesity affect cancer survivorship?
Most of the evidence about obesity in cancer survivors comes from people who were diagnosed with breast, prostate, or colorectal cancer. Research indicates that obesity may worsen several aspects of cancer survivorship, including quality of life, cancer recurrence, cancer progression, and prognosis (survival) (37, 38).
For example, obesity is associated with increased risks of treatment-related lymphedema in breast cancer survivors (39) and incontinence in prostate cancer survivors treated with radical prostatectomy (40). In a large clinical trial of patients with stage II and stage III rectal cancer, those with a higher baseline BMI (particularly men) had an increased risk of local recurrence (41). Death from multiple myeloma is 50% more likely for people at the highest levels of obesity compared with people at normal weight (42).
Several randomized clinical trials in breast cancer survivors have reported weight loss interventions that resulted in both weight loss and beneficial changes in biomarkers that have been linked to the association between obesity and prognosis (43, 44). However, there is little evidence about whether weight loss improves cancer recurrence or prognosis (45). The NCI-sponsored Breast Cancer WEight Loss (BWEL) Study, a randomized phase III trial that is currently recruiting participants, will compare recurrence rate in overweight and obese women who take part in a weight loss program after breast cancer diagnosis with that in women who do not take part in the weight loss program.
What research is being done on obesity and cancer?
Several areas of research are exploring mechanisms that link obesity and cancer (29, 46). One research area involves understanding the role of the microbes that live in the human gastrointestinal tract (collectively called the gut microbiota, or microbiome) in both type 2 diabetes and obesity. Both conditions are associated with dysbiosis, an imbalance in the collection of these microbes. For example, the gut microbiomes of obese people are different from, and less diverse than, those of non-obese people. Imbalances in the gut microbiota are associated with inflammation, altered metabolism, and genotoxicity, which may in turn be related to cancer. Experiments in mice show that the microbiome may influence the efficacy of some types of cancer treatment, particular immunotherapy (47, 48). Researchers are beginning to think about ways to change the microbiota of cancer patients to improve their outcomes.
Another area of investigation is the role of insulin receptor signaling in cancer. Many cancer cells express elevated levels of IR-A, a form of the insulin receptor that has a high affinity for insulin and related growth factors. Researchers are investigating how these factors contribute to metabolic disease and cancer and which may be useful targets for therapeutic interventions to prevent obesity-related cancers.
Researchers are also trying to understand why the association between obesity and the risks of some cancers vary among racial/ethnic groups. For example, obesity has been found to be more strongly associated with an increased risk of prostate cancer among African American men than among white men (49). This observation might reflect a difference in the biological effects of obesity between these two groups, such as a difference in the effects of obesity on inflammation or insulin secretion.
NCI supports research on obesity and cancer risk through a variety of activities, including large cooperative initiatives, web and data resources, extramural and intramural epidemiologic studies, basic science, and dissemination and implementation resources. For example, the Transdisciplinary Research on Energetics and Cancer (TREC) initiative links four research centers and a coordination center to investigate how the combined effects of obesity, poor diet, and low levels of physical activity increase cancer risk.
The NCI Cohort Consortium is an extramural–intramural partnership within NCI’s Division of Cancer Control and Population Sciences that combines more than 50 prospective cohort studies from around the world with more than seven million participants. The studies are gathering information on energy balance–related factors from each cohort. The large size of the study will allow researchers to get a better sense of how obesity-related factors relate to less common cancers, such as cancers of the thyroid, gallbladder, head and neck, and kidney.
1. Flegal KM, Kit BK, Orpana H, Graubard BI. Association of all-cause mortality with overweight and obesity using standard body mass index categories: a systematic review and meta-analysis. JAMA 2013; 309(1):71-82.
2. Kitahara CM, Flint AJ, Berrington de Gonzalez A, et al. Association between class III obesity (BMI of 40-59 kg/m2) and mortality: a pooled analysis of 20 prospective studies. PLoS Medicine 2014; 11(7):e1001673.
3. National Center for Health Statistics. Health, United States, 2015: With Special Feature on Racial and Ethnic Health Disparities. Hyattsville, MD. 2016.
4. Ogden CL, Carroll MD, Lawman HG, et al. Trends in obesity prevalence among children and adolescentsin the United States, 1988-1994 through 2013-2014. JAMA 2016; 315(21):2292-2299.
5. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adult obesity in the United States, 2011-2012. JAMA 2014; 311(8):806-814.
6. Lauby-Secretan B, Scoccianti C, Loomis D, et al. Body Fatness and Cancer–Viewpoint of the IARC Working Group. New England Journal of Medicine 2016; 375(8):794-798. doi: 10.1056/NEJMsr1606602Exit Disclaimer.
7. Setiawan VW, Yang HP, Pike MC, et al. Type I and II endometrial cancers: have they different risk factors? Journal of Clinical Oncology 2013; 31(20):2607-2618.
8. Dougan MM, Hankinson SE, Vivo ID, et al. Prospective study of body size throughout the life-course and the incidence of endometrial cancer among premenopausal and postmenopausal women. International Journal of Cancer 2015; 137(3):625-37.
9. Hoyo C, Cook MB, Kamangar F, et al. Body mass index in relation to oesophageal and oesophagogastric junction adenocarcinomas: a pooled analysis from the International BEACON Consortium. International Journal of Epidemiology 2012; 41(6):1706-1718.
10. Chen Y, Liu L, Wang X, et al. Body mass index and risk of gastric cancer: a meta-analysis of a population with more than ten million from 24 prospective studies. Cancer Epidemiology, Biomarkers & Prevention2013; 22(8):1395-1408.
11. Chen Y, Wang X, Wang J, Yan Z, Luo J. Excess body weight and the risk of primary liver cancer: an updated meta-analysis of prospective studies. European Journal of Cancer 2012; 48(14):2137-2145.
12. Campbell PT, Newton CC, Freedman ND, et al. Body mass index, waist circumference, diabetes, and risk of liver cancer for U.S. adults. Cancer Research 2016; 76(20):6076-6083.
13. Wang F, Xu Y. Body mass index and risk of renal cell cancer: a dose-response meta-analysis of published cohort studies. International Journal of Cancer 2014; 135(7):1673-86.
14. Sanfilippo KM, McTigue KM, Fidler CJ, et al. Hypertension and obesity and the risk of kidney cancer in 2 large cohorts of US men and women. Hypertension 2014; 63(5):934-41.
15. Wallin A, Larsson SC. Body mass index and risk of multiple myeloma: a meta-analysis of prospective studies. European Journal of Cancer 2011; 47(11):1606-1615.
16. Niedermaier T, Behrens G, Schmid D, et al. Body mass index, physical activity, and risk of adult meningioma and glioma: A meta-analysis. Neurology 2015; 85(15):1342-1350.
17. Genkinger JM, Spiegelman D, Anderson KE, et al. A pooled analysis of 14 cohort studies of anthropometric factors and pancreatic cancer risk. International Journal of Cancer 2011; 129(7):1708-1717.
18. Ma Y, Yang Y, Wang F, et al. Obesity and risk of colorectal cancer: a systematic review of prospective studies. PLoS One 2013; 8(1):e53916.
19. World Cancer Research Fund International/American Institute for Cancer Research. Continuous Update Project Report: Diet, Nutrition, Physical Activity and Gallbladder Cancer. 2015. Available at http://www.wcrf.org/sites/default/files/Gallbladder-Cancer-2015-Report.pdf.
20. Li L, Gan Y, Li W, Wu C, Lu Z. Overweight, obesity and the risk of gallbladder and extrahepatic bile duct cancers: A meta-analysis of observational studies. Obesity (Silver Spring) 2016; 24(8):1786-1802.
21. Renehan AG, Tyson M, Egger M, Heller RF, Zwahlen M. Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet 2008; 371(9612):569-578.
22. Munsell MF, Sprague BL, Berry DA, Chisholm G, Trentham-Dietz A. Body mass index and breast cancer risk according to postmenopausal estrogen-progestin use and hormone receptor status. Epidemiologic Reviews 2014; 36:114-136.
23. Brinton LA, Cook MB, McCormack V, et al. Anthropometric and hormonal risk factors for male breast cancer: male breast cancer pooling project results. Journal of the National Cancer Institute 2014; 106(3):djt465.
24. Collaborative Group on Epidemiological Studies of Ovarian Cancer. Ovarian cancer and body size: individual participant meta-analysis including 25,157 women with ovarian cancer from 47 epidemiological studies. PLoS Medicine 2012; 9(4):e1001200.
25. Kitahara CM, McCullough ML, Franceschi S, et al. Anthropometric factors and thyroid cancer risk by histological subtype: Pooled analysis of 22 prospective studies. Thyroid 2016; 26(2):306-318.
26. Gregor MF, Hotamisligil GS. Inflammatory mechanisms in obesity. Annual Review of Immunology 2011; 29:415-445.
27. Randi G, Franceschi S, La Vecchia C. Gallbladder cancer worldwide: geographical distribution and risk factors. International Journal of Cancer 2006; 118(7):1591-1602.
28. Bishayee A. The role of inflammation and liver cancer. Advances in Experimental Medicine and Biology2014; 816:401-435.
29. Gallagher EJ, LeRoith D. Obesity and diabetes: The increased risk of cancer and cancer-related mortality. Physiological Reviews 2015; 95(3):727-748.
30. Seo BR, Bhardwaj P, Choi S. Obesity-dependent changes in interstitial ECM mechanics promote breast tumorigenesis. Science Translational Medicine 2015; 7(301):301ra130.
31. Roberts DL, Dive C, Renehan AG. Biological mechanisms linking obesity and cancer risk: new perspectives. Annual Review of Medicine 2010; 61:301–316.
32. Arnold M, Pandeya N, Byrnes G, et al. Global burden of cancer attributable to high body-mass index in 2012: a population-based study. Lancet Oncology 2015; 16(1):36-46.
33. Whiteman DC, Wilson LF. The fractions of cancer attributable to modifiable factors: A global review. Cancer Epidemiology 2016; 44:203-221.
34. Keum N, Greenwood DC, Lee DH, et al. Adult weight gain and adiposity-related cancers: a dose-response meta-analysis of prospective observational studies. Journal of the National Cancer Institute2015; 107(2). pii: djv088.
35. Tee MC, Cao Y, Warnock GL, Hu FB, Chavarro JE. Effect of bariatric surgery on oncologic outcomes: a systematic review and meta-analysis. Surgical Endoscopy 2013; 27(12):4449-4456.
36. Neuhouser ML, Aragaki AK, Prentice RL, et al. Overweight, obesity, and postmenopausal invasive breast cancer risk: A secondary analysis of the Women’s Health Initiative randomized clinical trials. JAMA Oncology 2015; 1(5):611-621.
37. Calle EE, Rodriguez C, Walker-Thurmond K, Thun MJ. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. New England Journal of Medicine 2003; 348(17):1625-1638.
38. Schmitz KH, Neuhouser ML, Agurs-Collins T, et al. Impact of obesity on cancer survivorship and the potential relevance of race and ethnicity. Journal of the National Cancer Institute 2013; 105(18):1344-1354.
39. Paskett ED, Dean JA, Oliveri JM, Harrop JP. Cancer-related lymphedema risk factors, diagnosis, treatment, and impact: a review. Journal of Clinical Oncology 2012; 30(30):3726-3733.
40. Gacci M, Sebastianelli A, Salvi M, et al. Role of abdominal obesity for functional outcomes and complications in men treated with radical prostatectomy for prostate cancer: results of the Multicenter Italian Report on Radical Prostatectomy (MIRROR) study. Scandinavian Journal of Urology 2014; 48(2):138-145.
41. Meyerhardt JA, Tepper JE, Niedzwiecki D, et al. Impact of body mass index on outcomes and treatment-related toxicity in patients with stage II and III rectal cancer: findings from Intergroup Trial 0114.Journal of Clinical Oncology 2004; 22(4):648-657.
42. Teras LR, Kitahara CM, Birmann BM, et al. Body size and multiple myeloma mortality: a pooled analysis of 20 prospective studies. British Journal of Haematology 2014; 166(5):667-676.
43. Goodwin PJ, Segal RJ, Vallis M, et al. Randomized trial of a telephone-based weight loss intervention in postmenopausal women with breast cancer receiving letrozole: the LISA trial. Journal of Clinical Oncology 2014; 32(21):2231-2239.
44. Harrigan M, Cartmel B, Loftfield E, et al. Randomized trial comparing telephone versus in-person weight loss counseling on body composition and circulating biomarkers in women treated for breast cancer: The Lifestyle, Exercise, and Nutrition (LEAN) Study. Journal of Clinical Oncology 2016; 34(7):669-676.
45. Goodwin PJ. Obesity and breast cancer outcomes: How much evidence is needed to change practice?Journal of Clinical Oncology 2016; 34(7):646-648. Epub 2015 Dec 28. doi: 10.1200/JCO.2015.64.7503
46. Sheflin AM, Whitney AK, Weir TL. Cancer-promoting effects of microbial dysbiosis. Current Oncology Reports 2014; 16(10):406.
47. Sivan A, Corrales L, Hubert N, et al. Commensal Bifidobacterium promotes antitumor immunity and facilitates anti-PD-L1 efficacy. Science 2015; 350(6264):1084-1089.
48. Vétizou M, Pitt JM, Daillère R, et al. Anticancer immunotherapy by CTLA-4 blockade relies on the gut microbiota. Science 2015; 350(6264):1079-1084.
49. Barrington WE, Schenk JM, Etzioni R, et al. Difference in association of obesity with prostate cancer risk between US African American and non-Hispanic white men in the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA Oncology 2015; 1(3):342-349.