Archive for the ‘Obesity’ Category

Fat cells in abdomen fuel spread of ovarian cancer

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Posted 31 Oct 2011 — by James Street
Category Fasting, Obesity, Ovarian

Contact: John Easton
john.easton@uchospitals.edu
773-795-5225
University of Chicago Medical Center

Similar process may boost growth of other cancers

IMAGE: This is Ernst Lengyel, MD, PhD, professor of obstetrics & gynecology, the University of Chicago.

Click here for more information.

A large pad of fat cells that extends from the stomach and covers the intestines provides nutrients that promote the spread and growth of ovarian cancer, reports a research team based at the University of Chicago in the journal Nature Medicine, published online October 30th, 2011.

Ovarian cancer, the fifth leading cause of cancer deaths in women, tends to spread within the abdominal cavity as opposed to distant organs. In 80 percent of women, by the time ovarian cancer is diagnosed, it has spread to the pad of fat cells, called the omentum. Often, cancer growth in the omentum exceeds the growth of the original ovarian cancer.

“This fatty tissue, which is extraordinarily rich in energy-dense lipids, acts as a launching pad and energy source for the likely lethal spread of ovarian cancer,” said study author Ernst Lengyel, MD, PhD, professor of obstetrics and gynecology at the University of Chicago. “The cells that make up the omentum contain the biological equivalent of jet fuel. They feed the cancer cells, enabling them to multiply rapidly. Gaining a better understanding of this process could help us learn how to disrupt it.”

The researchers performed a series of experiments to identify the role of these fat cells as major mediators of ovarian cancer metastasis. The first step was to understand the biological signals that attract ovarian cancer cells to the omentum and use it for rapid growth.

The spread of ovarian cancer cells to the omentum can happen quickly. Ovarian cancer cells injected into the abdomen of healthy mice find their way to the omentum within 20 minutes. The researchers found that protein signals emitted by the omentum can attract the tumor cells. Inhibitors which disturbed these signals reduced this attraction by at least 50 percent.

Once ovarian cancer cells reach the omentum, they quickly develop the tools to devour the sustenance provided by this fatty tissue, reprogramming their metabolism to thrive on lipids acquired from fat cells. Ovarian cancer can rapidly convert the entire omentum, a soft fat pad, into a solid mass of cancer cells.

“This mechanism may not be limited to ovarian cancer cells,” the authors note. Fat metabolism may also contribute to cancer development in other environments where fat cells are abundant, such as breast cancer.

A protein known as fatty acid binding protein (FABP4), a fat carrier, may be crucial to this process and could be a target for treatment.

When the researchers compared primary ovarian cancer tissue with ovarian cancer tissue which had spread to the omentum, they found that tumor cells next to omental fat cells produced high levels of FABP4. Cancer cells distant from the fat cells did not produce FABP4.

When they inhibited FABP4, the transfer of nutrients from fat cells to cancer cells was drastically reduced. Inhibition of FABP4 also reduced tumor growth and the ability of tumors to generate new blood vessels.

“Therefore,” the authors wrote, “FABP4 emerges as an excellent target in the treatment of intra-abdominally disseminating tumors, which preferentially metastasize to adipose tissue such as ovarian, gastric, and colon cancers.”

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The research was supported by the National Institutes of Health, the Burroughs Wellcome Fund, the Committee on Cancer Biology at the University of Chicago and Bears Care, the charitable beneficiary of the Chicago Bears Football Club.

Additional authors include Kristin Nieman, Hilary Kenny, Carla Penicka, Andras Ladanyi, Marion Zillhardt, Iris Romero, Diane Yamada, Rebecca Buell-Gutbrod and Katja Gwin of the University of Chicago; Mark Carey and Gordon Mills of M.D. Anderson Cancer Center; Gökhan Hotamisligil of the Harvard School of Public Health, and Marcus Peter of Northwestern University.

Obesity and Breast Cancer

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Posted 19 Oct 2011 — by James Street
Category Breast Cancer, Obesity
By Jennifer Ligibel, MD1 | October 12, 2011
1Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts

 

ABSTRACT: Obesity is a growing health problem in the United States and, increasingly, around the world. Excess body weight has been linked to an increased risk of postmenopausal breast cancer, and growing evidence also suggests that obesity is associated with poor prognosis in women diagnosed with early-stage breast cancer. Dozens of studies demonstrate that women who are overweight or obese at the time of breast cancer diagnosis are at increased risk of cancer recurrence and death compared with leaner women, and some evidence suggests that women who gain weight after breast cancer diagnosis may also be at increased risk of poor outcomes. In this review, we describe the evidence linking obesity to breast cancer recurrence, discuss the potential biological mechanisms through which weight could impact breast cancer prognosis, and review the weight-loss intervention studies that have been performed in breast cancer populations to date.

Observational Studies Linking Weight to Prognosis in Early Breast Cancer

Weight at diagnosis

In 1976, Abe et al reported the first study investigating the relationship between body weight and breast cancer recurrence.[1] The study demonstrated that women who were overweight or obese had a 5-year survival rate of 55.6%, compared with a rate of 79.9% in leaner women. The study also showed that obese women were more likely to have larger tumors, with higher rates of lymphatic invasion and nodal involvement. Since this initial report, there have been more than 50 studies examining the relationship between body weight and breast cancer prognosis.[2] A recent meta-analysis of 45 studies reported prior to 2005 demonstrated that women who are obese at diagnosis have a 30% higher risk of breast cancer–related and overall mortality, compared with leaner women.[2] The authors also demonstrated that the relationship between obesity and poor prognosis was independent of menopausal status, type of study (observational vs treatment trial), year of study report (prior to or after 1995), and type of weight measurement (body mass index [BMI] vs weight).

Although these observational studies have consistently linked weight at diagnosis to breast cancer outcomes, there are still questions regarding the potential confounding of this relationship by treatment-related factors. In the past, obese patients were often treated with relatively lower doses of chemotherapy compared with leaner individuals. Common practices included dosing chemotherapy by ideal rather than actual body weight or capping the chemotherapy dosing at a body surface area (BSA) of 2 m2 in an effort to decrease toxicity. Treating obese patients with lower doses of chemotherapy was shown to be associated with an increased risk of cancer recurrence in Cancer and Leukemia Group B 8541, a randomized trial assessing the schedule and dose of adjuvant chemotherapy in women with lymph-node positive breast cancer.[3] In this study, 23% of obese patients (defined in the study as patients with a BMI of 27.3 kg/m2 or greater rather than the modern definition of obesity as a BMI of at least 30 kg/m2) received less than 95% of the expected weight-based doses of chemotherapy drugs for their first cycle of therapy. These women had an increased risk of cancer recurrence compared with obese women who received the full weight-based doses of chemotherapy drugs (adjusted risk ratio [ARR], 0.73; 95% confidence interval [CI], 0.53 to 1.00). Obese women who were treated with chemotherapy dosed according to actual body weight had a risk of recurrence similar to that of leaner women (ARR, 1.02; 95% CI, 0.83-1.26).

Given this potential confounding effect of treatment factors, it is important that several more recent reports have demonstrated an increased risk of cancer recurrence in obese women in the setting of adjuvant treatment trials. Because these data were collected in the setting of clinical trials, the effect of chemotherapy dosing practices could be taken into account, and all patients received the same treatment. Patients in these studies were also treated with modern chemotherapy regimens and hormonal agents, making the results more relevant to current clinical practice. In the Anastrozole(Drug information on anastrozole), Tamoxifen(Drug information on tamoxifen), Alone or in Combination (ATAC) trial, postmenopausal women with hormone receptor–positive, stage I to III breast cancer were randomized to 5 years of tamoxifen, anastrozole (Arimidex), or the combination. Women who had a BMI of 35 kg/m2 or higher had an increased risk of recurrence vs women with a BMI less than 23 kg/m2 (hazard ratio [HR], 1.39; 95% CI, 1.06-1.82).[4] The increased risk of recurrence in obese women was only seen among women treated with anastrozole and not those treated with tamoxifen; in all weight groups, however, the risk of recurrence was still greater in women treated with tamoxifen vs anastrozole.[4] Obese premenopausal women treated with ovarian ablation and anastrozole in the Austrian Breast Cancer Study Group 12 study also had a higher risk of recurrence (HR, 1.60; 95% CI, 1.06-2.41) and death (HR, 2.14; 95% CI, 1.17-3.92) compared with normal weight women.[5] Among overweight women in this study, the risk of cancer recurrence (HR, 1.49; 95% CI, 0.93-2.38) and death (HR, 3.03; 95% CI, 1.35-6.82) was higher in women treated with ovarian ablation and anastrozole, compared with those treated with ovarian ablation and tamoxifen, despite the fact that the two treatments were equivalent in the study population as a whole.

Obesity at diagnosis has also been linked to a higher risk of recurrence in recent adjuvant chemotherapy trials. In the Adjuvant Docetaxel(Drug information on docetaxel) vs Epirubicin(Drug information on epirubicin) Based Regimen (ADEBAR) study, a randomized trial that assessed the value of adding a taxane to anthracycline-based chemotherapy in patients with involved lymph nodes, obese women had a significantly higher risk of cancer recurrence vs women with a BMI less than 25 (P = .007).[6] A similar adjuvant study, the Eastern Cooperative Oncology Group (ECOG) 1199 trial, randomized women with lymph node–positive breast cancer to four different anthracycline- and taxane-containing adjuvant therapy regimens. Obese women with hormone receptor–positive tumors were found to have a higher risk of recurrence (HR, 1.23; 95% CI, 1.02-1.49) and death (HR, 1.46; 95% CI, 1.15-1.85), compared with leaner women.[7] There was no relationship between obesity at diagnosis and outcomes in patients with hormone receptor–negative or HER2-positive cancers. These results were verified in the ECOG 5188 study, which enrolled 1502 premenopausal women with estrogen receptor–positive, node-positive cancers. In this study, obese women were found to have a 40% increase in the risk of cancer recurrence and a 50% increase in the risk of death compared with leaner women.

Weight Gain

A few trials have also evaluated the association between weight gain after diagnosis and rates of recurrence, but the results have not been consistent. Four studies looked at recurrence and weight gain in small groups of patients treated with older chemotherapy regimens, which often incorporated significant doses of corticosteroids and therefore were associated with greater weight gain than is typically seen with modern chemotherapy regimens.[8-10] Three of these studies demonstrated an association between weight gain and increased risk of recurrence in at least a subset of patients, but many women in these studies gained 10 kg or more. Modern studies using shorter-course, often anthracycline-based chemotherapy, in which weight gain was less severe (often averaging less than 2 kg) have largely failed to identify a relationship between weight gain and poor prognosis. One notable exception is the Nurses’ Health Study (NHS), in which investigators showed that non-smoking women who gained 0.5 to 2 kg/m2 (median weight gain, 6 lbs) after the diagnosis of breast cancer, as well as women who gained more than 2 kg/m2 (median weight gain, 17 lbs), had a significantly increased risk of breast cancer death compared with women who maintained a stable weight (risk reduction [RR] for breast cancer death 1.35, 95% CI 0.93-1.95 for weight gain 0.5 to 2 kg/m2; and RR for death 1.64, 95% CI 1.07-2.51 for weight gain of > 2 kg/m2).[11] In contrast, Cann et al found no prognostic effect of obesity in women in the Life After Cancer Epidemiology (LACE) study cohort, even among those with extreme weight gain (greater than 10%).[12] Finally, recent data from several clinical trials also did not show a consistent relationship between weight gain after diagnosis and breast cancer outcomes, although some individual studies reported an increased risk of cancer recurrence in women who gained weight.[13] More work is needed to understand the relationship between post-diagnosis weight change and outcomes in women with early-stage breast cancer.

Weight Loss and Prognosis in Dietary Interventional Studies

Given that many women gain weight after breast cancer diagnosis, there are relatively few data from observational studies describing the relationship between weight loss after diagnosis and disease outcomes. There are also no studies examining the impact of purposeful weight loss on breast cancer prognosis. However, two randomized trials that assessed the impact of dietary modification on disease-free and overall survival in women with early stage breast cancer shed some light on this issue. The Women’s Interventional Nutrition Study (WINS) randomized 2400 women to a low-fat dietary intervention or a usual-care control group.[14] Patients assigned to the intervention group experienced a 6-lb weight loss and a 24% reduction in breast cancer recurrence vs control participants. In contrast, the Women’s Healthy Eating and Living (WHEL) study randomized 3088 women to a high fruit and vegetable, low-fat diet.[15] Participants in the intervention group did not lose weight, and there was no difference in rates of recurrence in the intervention and control groups. Although there were a number of other differences between the studies, the weight loss sustained by participants assigned to the dietary intervention in the WINS study has been suggested as one potential reason for the difference in the study outcomes. Further work is needed to test the impact of weight loss on the risk of recurrence in women with early breast cancer.

Observational Studies of Physical Activity and Prognosis in Early Breast Cancer

TABLE 1

Observational Studies of Exercise and Breast Cancer Outcomes

Observational data also suggest that physical activity, an important factor in maintaining a healthy weight, may yield beneficial effects on breast cancer outcomes. Several reports have demonstrated better breast cancer–specific and overall survival in individuals who are physically active after breast cancer diagnosis, compared with breast cancer survivors who were more sedentary, although the data are not entirely consistent (Table 1). For example, the NHS investigators looked at the relationship between physical activity after diagnosis and rates of breast cancer recurrence and death in a cohort of 2987 women diagnosed with stage I to IIIa breast cancer.[16] After a median follow-up of 96 months, patients who engaged in more than 9 MET (metabolic equivalent of task) hours per week of physical activity, equivalent to walking at an average pace for 3 hours per week, had a 50% lower risk of breast cancer recurrence, breast cancer death, and all-cause mortality than women who were inactive (engaging in less than an hour of moderate-intensity recreational activity per week). This finding adds to the growing evidence that obesity and related factors could affect breast cancer prognosis (Table 2).

Weight Loss Intervention Studies in Breast Cancer Populations

TABLE 2

Evidence Linking Obesity and Breast Cancer Prognosis

Despite the large number of observational studies demonstrating an association between increased weight at diagnosis and poor prognosis in patients with early breast cancer, there is no direct evidence that weight loss decreases risk of breast cancer recurrence. A growing number of small studies are investigating the feasibility of a variety of weight-loss interventions in breast cancer survivors. Most of these studies have enrolled fewer than 100 patients and have been conducted at a single institution. A few of these pilot studies have led to larger-scale trials, most of which are ongoing. A comprehensive review of these studies is beyond the scope of this article, but selected representative interventions, including those now being tested in larger populations, are described here.

Goodwin and colleagues performed a single-arm trial assessing the ability of a weight-management intervention, which incorporated support-group-provided diet-and-exercise counseling, to help patients lose weight or avoid weight gain during adjuvant chemotherapy.[17] The investigators reported that 70% of participants met the weight goals over the course of the study. In another report, Shaw and colleagues performed a randomized pilot study in 64 obese women with early-stage breast cancer and demonstrated that participants randomized to low-fat and low-calorie diets experienced significant weight loss and a reduction in body fat, compared with controls (P = .006 and .008, respectively).[18] Another small study randomized 48 obese breast cancer survivors to one of three dietary intervention arms (a Weight Watchers program, individualized dietary counseling, or both interventions combined), or to a control group.[19] Women assigned to the combination-intervention group lost significantly more weight than controls by 3 months and maintained this weight loss throughout the 12-month study. Women assigned to the individualized counseling group also lost a significant amount of weight by the end of the study, but the group assigned to Weight Watchers alone did not experience significant weight loss.

In one example of a pilot study leading to a larger weight-loss trial, Mefferd and colleagues performed a single-arm trial of a cognitive behavioral therapy (CBT) weight-loss intervention in 85 overweight breast cancer survivors and demonstrated significant reductions in body weight, body fat, and lipid levels following the 16-week intervention (P = .05).[20] The group then randomized 68 breast cancer survivors to the CBT weight-loss intervention or usual care control group and demonstrated that the CBT group lost significantly more weight at 16 weeks than the control group (5.7 kg vs 0.2 kg, P < .001).[21] This work led to development of the Exercise and Nutrition to Enhance Recovery and Good Health for You (ENERGY) trial (PI, Cheryl Rock, PhD, RD, School of Medicine, University of California at San Diego), in which the ability of a CBT weight-loss intervention to lead to weight loss and improvements in quality of life will be tested in 800 breast cancer survivors.

Thomson and colleagues have also recently launched a moderate-sized weight-loss trial that developed from a small weight-loss pilot study. In a 2010 report, these investigators demonstrated an average 6.1-kg weight loss among 40 breast cancer survivors taking part in two dietary weight-loss interventions, one focusing on a low-fat diet and the other on a low-carbohydrate diet.[22] Both intervention groups experienced a decrease in cholesterol and improvements in insulin sensitivity. The investigators are now conducting the CHOICE study, which will randomize approximately 370 long-term breast cancer survivors to low-fat and low-carbohydrate dietary interventions, to determine which approach has a greater impact on biomarkers linked to breast cancer prognosis.[23] These two ongoing studies will provide additional information about the feasibility of weight loss in large groups of breast cancer survivors, the impact of weight loss on quality of life, and the biological mechanisms through which weight loss could affect breast cancer outcomes.

The Lifestyle Intervention Study for Adjuvant Treatment of Early Breast Cancer (LISA)

In addition to the many small studies such as those described above demonstrating that weight-loss interventions are feasible in breast cancer populations, one study has demonstrated sustained weight loss in a larger group of survivors. The Lifestyle Intervention Study for Adjuvant Treatment of Early Breast Cancer (LISA), randomized 338 postmenopausal women with hormone receptor–positive breast cancer to an educational control group or to a 2-year, telephone-based weight-loss intervention, modeled on the Diabetes Prevention Project. The weight loss intervention focused on calorie restriction, a low-fat diet, and increased physical activity. Participants randomized to the intervention received 19 telephone calls, as well as mailings and a participant manual. Intervention participants lost approximately 4.5 kg more weight than the control group at 6, 12, and 18 months, and they reported a significant improvement in physical functioning scores compared with control participants.[24] Additional follow-up is ongoing.

Biologic Mechanisms Underlying the Relationship Between Obesity and Breast Cancer Outcomes

The biologic mechanisms underlying the relationship between lifestyle factors and breast cancer are not well understood. In post-menopausal women, obesity is associated with higher estrone and estradiol(Drug information on estradiol) levels due to increased peripheral aromatization of adrenal androgens in adipose tissue.[25] Obesity also leads to lower levels of sex-hormone-binding globulin, resulting in higher levels of free estradiol in circulation. In premenopausal women, however, pre-operative estradiol levels are not related to risk of breast cancer recurrence or death,[26] suggesting that obesity must affect prognosis through mechanisms other than estradiol levels in this population.

TABLE 3

Selected Studies of Insulin (and Related Factors) and Breast Cancer Prognosis

Studies have demonstrated that obesity, especially abdominal adiposity, is associated with higher levels of insulin and other metabolic hormones in both pre- and postmenopausal women.[27,28] Elevated insulin levels have been linked to an increased risk of breast cancer, and several recent reports have demonstrated that women with higher levels of insulin or related proteins at the time of breast cancer diagnosis are at increased risk of cancer recurrence and death (Table 3). For example, Goodwin and colleagues demonstrated a twofold increase in the risk of cancer recurrence and a threefold risk of death in patients with the highest vs the lowest quartile of fasting insulin levels,[29] and another recent study demonstrated that women with high levels of c-peptide, a breakdown product of insulin production, at the time of breast cancer diagnosis were found to have a higher risk of breast cancer–specific and overall death vs women with lower levels of c-peptide.[30]

Preclinical and epidemiologic studies also suggest that other metabolic hormones may play a role in the relationship between obesity and breast cancer recurrence. Observational studies show that premenopausal women with high levels of insulin-like growth factor-1 (IGF-1) are at increased risk of developing breast cancer,[31] and in vitro data also suggest that IGF-1 signaling plays a central role in the development and progression of breast cancer.[32,33] Epidemiologic studies also suggest that leptin and adiponectin, metabolic hormones produced by adipose cells that modulate insulin sensitivity, are associated with breast cancer risk.[34,35] Leptin and hepatocyte growth factor have been shown to stimulate growth of breast cancer cells lines in vitro,[36,37] providing support for the hypothesis that insulin and related metabolic hormones may mediate, at least in part, the relationship between obesity and breast cancer prognosis.

Recent data have also suggested that chronic inflammation, associated with obesity, diabetes, and several other disease states, may also play a role in breast cancer risk and prognosis.[38] It has long been known that chronic inflammation from conditions such as inflammatory bowel disease, infection with Heliobacter pylori, and hepatitis can lead to increased risk of cancer. Recent preclinical data also demonstrate that increased levels or genetic alterations in inflammatory biomarkers such as TNFα and IL-2 can lead to increased risk of breast cancer, and cohort studies have demonstrated that higher levels of inflammatory biomarkers such as c-reactive protein and IL-6 are associated with poor prognosis in early-stage breast cancer.[39]

Effect of weight loss and other lifestyle interventions on biomarkers linked to breast cancer prognosis

REFERENCE GUIDE

Therapeutic Agents
Mentioned in This Article

Anastrozole (Arimidex)
Docetaxel
Epirubicin
Tamoxifen

Brand names are listed in parentheses only if a drug is not available generically and is marketed as no more than two trademarked or registered products. More familiar alternative generic designations may also be included parenthetically.

A number of small studies in breast cancer and at-risk populations have demonstrated that lifestyle interventions can decrease visceral body fat, improve insulin sensitivity, and lead to alterations in other metabolic hormones. One study demonstrated that participation in a mixed strength and aerobic exercise intervention led to a 28% decrease in fasting insulin levels in a group of overweight breast cancer survivors,[40] and other reports demonstrate that participation in weight loss and physical activity interventions can impact other metabolic and inflammatory hormones linked to breast cancer risk and outcomes.[41-43] Data from large-scale lifestyle interventions are limited, however, and no clear intermediate markers of breast cancer prognosis have been established.

Conclusions

Obesity is a growing problem in the United States and may be especially problematic for breast cancer survivors. Dozens of studies have suggested that obesity at diagnosis is associated with poor outcomes in women with early-stage breast cancer. Recent observations confirm that this relationship persists in women treated with modern adjuvant therapy regimens. Data regarding the relationship between weight change after breast cancer diagnosis and prognosis are limited, but some reports suggest that women who gain significant amounts of weight after diagnosis could have a poor prognosis as well. The WINS study showed that women who were randomized to a low fat dietary intervention, and who lost an average of 6 lbs as a result of participation in the intervention, experienced a lower rate of breast cancer recurrence. However, no study has tested the impact of purposeful weight loss on disease outcomes in women with early breast cancer. A number of small weight-loss-intervention studies, as well as one larger-scale trial, have been performed in breast cancer populations. These trials demonstrate that weight loss is feasible after breast cancer diagnosis, and that women who lose weight experience improvements in quality of life and favorable alterations in serum biomarkers that are linked to breast cancer prognosis. More work is needed to determine whether weight loss after breast cancer diagnosis will lead to improvements in disease-free and overall-survival outcomes in women with early-stage disease.

Financial Disclosure: The author has no significant financial interest or other relationship with the manufacturers of any products or providers of any service mentioned in this article.

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47. Sternfeld B, Weltzien E, Quesenberry CP, Jr, et al. Physical activity and risk of recurrence and mortality in breast cancer survivors: findings from the LACE study. Cancer Epidemiol Biomarkers Prev. 2009;18:87-95.

48. Chen X, Lu W, Zheng W, et al. Exercise after diagnosis of breast cancer in association with survival. Cancer Prev Res (Phila). 2011;4:1409-18.

49. Pasanisi P, Berrino F, De Petris M, et al. Metabolic syndrome as a prognostic factor for breast cancer recurrences. Int J Cancer. 2006;119:236–8.

50. Duggan C, Irwin ML, Xiao L, et al. Associations of insulin resistance and adiponectin with mortality in women with breast cancer. J Clin Oncol. 2011;29:32-9.

National Cancer Institute, Obesity and Cancer: Questions and Answers

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Posted 29 Dec 2010 — by James Street
Category Obesity, Prevention

Key Points

* During the last two decades, the percentage of overweight and obese adults and children has been steadily increasing (see Question 2).
* Lack of physical activity is strongly associated with obesity (see Question 3).
* In addition to increasing the risk of coronary heart disease, stroke, high blood pressure, and diabetes, obesity increases the risk of cancers of the breast (postmenopausal), endometrium (the lining of the uterus), colon, kidney, and esophagus (see Questions 4, 6–10).
* Avoiding weight gain can lower the risk of cancers of the breast (postmenopausal), endometrium, colon, kidney, and esophagus (see Question 13).
* Regular physical activity lowers the risk of colon and breast cancers (see Question 15).

1. What is obesity?

People who are obese have an abnormally high and unhealthy proportion of body fat. To measure obesity, researchers commonly use a formula based on weight and height known as the body mass index (BMI). BMI is the ratio of weight (in kilograms) to height (in meters) squared. BMI provides a more accurate measure of obesity or being overweight than does weight alone.

Guidelines established by the National Institutes of Health (NIH) place adults age 20 and older into one of four categories based on their BMI (1):
<18.5
underweight
18.5 to 24.9
healthy
25.0 to 29.9
overweight
>30.0
obese

The following chart can be used to determine BMI category. (Find the height, and move across the chart to the appropriate weight.)

Body Mass Index Chart, Adults 20 and Over image

Compared with people in the healthy weight category, those who are overweight or obese are at greater risk for many diseases, including diabetes, high blood pressure, cardiovascular diseases, stroke, and certain cancers. Obesity lowers life expectancy.
2. How common is overweight or obesity?

Results from the 1999–2000 National Health and Nutrition Examination Survey (NHANES) show that an estimated 64 percent of U.S. adults are either overweight or obese (2). This represents an increase of 8 percentage points compared with the estimates from an earlier survey (NHANES III 1988–1994).

Nearly one-third of all adults are now classified as obese. This reflects an increase of 7.6 percentage points since 1994 (2). The data show that 31 percent of adults age 20 and older—nearly 59 million people—have a body mass index (BMI) of 30 or greater, compared with 23 percent in 1994.

In addition, the percentage of children who are overweight continues to increase. Among children and teens ages 6 to 19, 15 percent (almost 9 million) are overweight according to the 1999–2000 data, or triple what the proportion was in 1980 (3).
3. What causes obesity?

Experts have concluded that the chief causes of obesity are a sedentary lifestyle and overconsumption of high-calorie food (4):
* Sedentary lifestyle—Researchers have found a strong correlation between lack of physical activity and obesity (4, 5).

* Diet—A diet high in calories and/or fat appears to be an important factor in obesity (6).

4. What have scientists learned about the relationship between obesity and cancer?

In 2001, experts concluded that cancers of the colon, breast (postmenopausal), endometrium (the lining of the uterus), kidney, and esophagus are associated with obesity. Some studies have also reported links between obesity and cancers of the gallbladder, ovaries, and pancreas (4).

Obesity and physical inactivity may account for 25 to 30 percent of several major cancers—colon, breast (postmenopausal), endometrial, kidney, and cancer of the esophagus (4).

Preventing weight gain can reduce the risk of many cancers. Experts recommend that people establish habits of healthy eating and physical activity early in life to prevent overweight and obesity. Those who are already overweight or obese are advised to avoid additional weight gain, and to lose weight through a low-calorie diet and exercise. Even a weight loss of only 5 to 10 percent of total weight can provide health benefits (4).
5. How many people get cancer by being overweight or obese? How many die?

In 2002, about 41,000 new cases of cancer in the United States were estimated to be due to obesity. This means that about 3.2 percent of all new cancers are linked to obesity (7).

A recent report estimated that, in the United States, 14 percent of deaths from cancer in men and 20 percent of deaths in women were due to overweight and obesity (8).
6. Does obesity increase the risk of breast cancer?

The effect of obesity on breast cancer risk depends on a woman’s menopausal status. Before menopause, obese women have a lower risk of developing breast cancer than do women of a healthy weight (4, 9, 10, 11, 12). However, after menopause, obese women have 1.5 times the risk of women of a healthy weight (9, 10, 13, 14).

Obese women are also at increased risk of dying from breast cancer after menopause compared with lean women (4, 11, 15, 16). Scientists estimate that about 11,000 to 18,000 deaths per year from breast cancer in U.S. women over age 50 might be avoided if women could maintain a BMI under 25 throughout their adult lives (16).

Obesity seems to increase the risk of breast cancer only among postmenopausal women who do not use menopausal hormones. Among women who use menopausal hormones, there is no significant difference in breast cancer risk between obese women and women of a healthy weight (4, 9, 11, 17).

Both the increased risk of developing breast cancer and dying from it after menopause are believed to be due to increased levels of estrogen in obese women (18). Before menopause, the ovaries are the primary source of estrogen. However, estrogen is also produced in fat tissue and, after menopause, when the ovaries stop producing hormones, fat tissue becomes the most important estrogen source (14). Estrogen levels in postmenopausal women are 50 to 100 percent higher among heavy versus lean women (11). Estrogen-sensitive tissues are therefore exposed to more estrogen stimulation in heavy women, leading to a more rapid growth of estrogen-responsive breast tumors.

Another factor related to the higher breast cancer death rates in obese women is that breast cancer is more likely to be detected at a later stage in obese women than in lean women. This is because the detection of a breast tumor is more difficult in obese versus lean women (12).

Studies of obesity and breast cancer in minority women in the United States have been limited. There is some evidence that, among African American women, the risk associated with obesity may be absent or less than that of other populations (19, 20, 21). However, a recent report showed that African American women who have a high BMI are more likely to have an advanced stage of breast cancer at diagnosis (22). Another report showed that obese Hispanic white women were twice as likely to develop breast cancer as non-obese Hispanics, but the researchers did not detect a difference in risk for obese Hispanic women before and after menopause (23).

Weight gain during adulthood has been found to be the most consistent and strongest predictor of breast cancer risk in studies in which it has been examined (4, 10, 11, 24).

The distribution of body fat may also affect breast cancer risk. Women with a large amount of abdominal fat have a greater breast cancer risk than those whose fat is distributed over the hips, buttocks, and lower extremities (13, 25, 26). Results from studies on the effect of abdominal fat are much less consistent than studies on weight gain or BMI.
7. Does obesity increase the risk of cancer of the uterus?

Obesity has been consistently associated with uterine (endometrial) cancer. Obese women have two to four times greater risk of developing the disease than do women of a healthy weight, regardless of menopausal status (4, 27, 28, 29, 30). Increased risk has also been demonstrated among overweight women (28, 30). Obesity has been estimated to account for about 40 percent of endometrial cancer cases in affluent societies (31).

It is unclear why obesity is a risk factor for endometrial cancer; however, it has been suggested that lifetime exposure to hormones and high levels of estrogen and insulin in obese women may be contributing factors (4, 27, 28, 29, 32).
8. Does obesity increase the risk of colon cancer?

Colon cancer occurs more frequently in people who are obese than in those of a healthy weight (4, 33, 34, 35, 36, 37). An increased risk of colon cancer has been consistently reported for men with high BMIs (34, 37, 38). The relationship between BMI and risk in women, however, has been found to be weaker (4, 34, 38) or absent (39).

Unlike for breast and endometrial cancer, estrogen appears to be protective for colon cancer for women overall (40). However, obesity and estrogen status also interact in influencing colon cancer risk. Women with a high BMI who are either premenopausal or postmenopausal and taking estrogens have an increased risk of colon cancer similar to that found for men with a high BMI. In contrast, women with a high BMI who are postmenopausal and not taking estrogens do not have an increased risk of colon cancer (41).

There is some evidence that abdominal obesity may be more important in colon cancer risk (37, 38). In men, a high BMI tends to be associated with abdominal fat. In women, fat is more likely to be distributed in the hips, thighs, and buttocks. Thus, two measures of abdominal fat, waist-to-hip ratio or waist circumference, may be better predictors of colon cancer risk. Few studies have yet compared waist-to-hip ratios to colon cancer risk in women, however. One study that did find an increased risk of colon cancer among women with high waist-to-hip ratios found that the association was present only among inactive women, suggesting that high levels of physical activity may counteract the effects of increased abdominal fat (42).

A number of mechanisms have been proposed for the adverse effect of obesity on colon cancer risk. One of the major hypotheses is that high levels of insulin or insulin-related growth factors in obese people may promote tumor development (4, 43, 44).
9. Does obesity increase the risk of kidney cancer?

Studies have consistently found a link between a type of kidney cancer (renal cell carcinoma) and obesity in women (4, 30, 45, 46, 47, 48), with some studies finding risk among obese women to be two to four times the risk of women of a healthy weight.

Results of studies including men have been more variable, ranging from an association similar to that seen in women (30, 46, 49), to a weak association (48, 50, 51), to no association at all (45). A meta-analysis (where several studies are combined into a single report), which found an equal association of risk among men and women, estimated the kidney cancer risk to be 36 percent higher for an overweight person and 84 percent higher for an obese person compared to those with a healthy weight (52).

The mechanisms by which obesity may increase renal cell cancer risk are not well understood. An increased exposure to sex steroids, estrogen and androgen, is one possible mechanism (4).
10. Does obesity increase the risk of cancer of the esophagus or stomach?

Overweight and obese individuals are two times more likely than healthy weight people to develop a type of esophageal cancer called esophageal adenocarcinoma (4, 53, 54, 55, 56). A smaller increase in risk has been found for gastric cardia cancer, a type of stomach cancer that begins in the area of the stomach next to the esophagus (54, 55, 56, 57). Most studies have not observed increases in risk with obesity in another type of esophageal cancer, squamous cell cancer. An increased risk of esophageal adenocarcinoma has also been associated with weight gain, smoking, and being younger than age 59 (54, 57).

The mechanisms by which obesity increases risk of adenocarcinoma of the esophagus and gastric cardia are not well understood. One of the leading mechanisms proposed has been that increases in gastric reflux due to obesity may increase risk. However, in the few studies that have examined this issue, risk associated with BMI was similar for those with and without gastric reflux (56).
11. Does obesity increase the risk of prostate cancer?

Of the more than 35 studies on prostate cancer risk, most conclude that there is no association with obesity (4, 44, 58, 59, 60). Some report that obese men are at higher risk than men of healthy weight, particularly for more aggressive tumors (61, 62, 63). One study found an increased risk among men with high waist-to-hip ratios, suggesting that abdominal fat may be a more appropriate measure of body size in relation to prostate cancer (64).

Studies examining BMI and prostate cancer mortality have had conflicting results (8, 65, 66).

Despite the lack of association between obesity and prostate cancer incidence, a number of studies have examined potential biological factors that are related to obesity, such as insulin-related growth factors, leptin, and other hormones. Results of these studies are inconsistent, but generally, risk has been linked to men with higher levels of leptin (67), insulin (68), and IGF–1 (insulin-like growth factor-1) (69).
12. Is there any evidence that obesity is linked to cancer of the gallbladder, ovaries, or pancreas?

An increased risk of gallbladder cancer has been found to be associated with obesity, particularly among women (70, 71, 72). This may be due to the higher frequency of gallstones in obese individuals, as gallstones are considered a strong risk factor for gallbladder cancer. However, there is not enough evidence to draw firm conclusions.

It is unclear whether obesity affects ovarian cancer risk. Some studies report an increased risk among obese women (73, 74, 75), whereas others have found no association (76, 77). A recent report found an increased risk in women who were overweight or obese in adolescence or young adulthood; no increased risk was found in older obese women (78).

Studies evaluating the relationship between obesity and pancreatic cancer have been inconsistent (79, 80, 81, 82). One recent study found that obesity increases the risk of pancreatic cancer only among those who are not physically active (80). A recent meta-analysis reported that obese people may have a 19 percent higher risk of pancreatic cancer than those with a healthy BMI. The results, however, were not conclusive (83).
13. Does avoiding weight gain decrease the risk of cancer?

The most conclusive way to test if avoiding weight gain will decrease the risk of cancer is through a controlled clinical trial. At present, there have been no controlled clinical trials on the effect on cancer related to avoiding weight gain. However, many observational studies have shown that avoiding weight gain lowers the risk of cancers of the colon, breast (postmenopausal), endometrium, kidney, and esophagus. There is limited evidence for thyroid cancers, and no substantial evidence for all other cancers (4, 84).
14. Does losing weight lower the risk of cancer?

There is insufficient evidence that intentional weight loss will affect cancer risk for any cancer. A very limited number of observational studies have examined the effect of weight loss, and a few found some decreased risk for breast cancer among women who have lost weight. However, most of these studies have not been able to evaluate whether the weight loss was intentional or related to other health problems (4, 24, 25, 85).

One recent study that examined the effect of intentional weight loss found that women who experienced intentional weight loss of 20 or more pounds and were not currently overweight had cancer rates at the level of healthy women who never lost weight. However, unintentional weight loss episodes were not associated with decreased cancer risk (86).
15. Does regular physical activity lower the risk of cancer?

There have been no controlled clinical trials on the effect of regular physical activity on the risk of developing cancer. However, observational studies have examined the possible association between physical activity and a lower risk of developing colon or breast cancer:
* Colon cancer: In 2002, a major review of observational trials found that physical activity reduced colon cancer risk by 50 percent. This risk reduction occurred even with moderate levels of physical activity (4). For example, one study showed that even moderate exercise, such as brisk walking for 3 to 4 hours per week, can lower colon cancer risk (42).

A limited number of studies have examined the effect of physical activity on colon cancer risk for both lean and obese people. Most of these studies have found a protective effect of physical activity across all levels of BMI (4).
* Breast cancer: The pattern of the association between physical activity and breast cancer risk is somewhat different. Most studies on breast cancer have focused on postmenopausal women. A recent study from the Women’s Health Initiative found that physical activity among postmenopausal women at a level of walking about 30 minutes per day was associated with a 20 percent reduction in breast cancer risk. However, this reduction in risk was greatest among women who were of normal weight. For these women, physical activity was associated with a 37 percent decrease in risk. The protective effect of physical activity was not found among overweight or obese women (87).

16. What biological mechanisms are thought to be involved in explaining the link between obesity and cancer?

The biological mechanism that explains how obesity increases cancer risk may be different for different cancers. (See Questions 6–11.) The exact mechanisms are not known for any of the cancers. However, possible mechanisms include alterations in sex hormones (e.g., estrogen, progesterone, and androgens), and insulin and IGF–1 in obese people that may account for their increased risk for cancers of the breast, endometrium, and colon. Sex-hormone binding globulin, the major carrier protein for certain sex hormones in the plasma, may also be involved in the altered risk for these cancers in obese people (4, 32, 58, 88).
17. What are current research needs?

Although there has been extensive research with large populations looking at the possible link between obesity and cancer, few clinical trials have studied the effect of weight control, physical activity, and energy balance (the calories consumed compared with those burned) on cancer. For some cancers, such as colon and breast, it is not clear whether the increased cancer risk in obese people is due to the extra weight; a high-fat, high-calorie diet; a lack of physical activity; or a combination of these factors.

The 2002 International Agency for Research on Cancer (IARC) report on weight control, physical activity, and cancer (4) made several recommendations for future trials:
* Conduct long-term intervention studies on the effect of dietary changes on weight gain and cancer risk;

* Conduct long-term intervention studies on the effect of patterns of physical activity (the intensity, frequency, and duration of various sorts of physical activity) in relation to weight gain and cancer risk;

* Conduct long-term intervention studies on the combined effects of changes in diet and physical activity on obesity and cancer risk; and

* Conduct community intervention studies to prevent weight gain and promote physical activity.

Several international reports have concluded that controlling the obesity epidemic will require substantial investments by many segments of society. Efforts to increase physical activity and promote healthy eating are needed in families, day care centers, schools, and work sites. The efforts of community services such as health care and public education are needed, as well as transportation systems that encourage walking and the use of bicycles (4).
18. Is the National Cancer Institute (NCI) currently studying the possible link between obesity and cancer?

Several NCI-funded studies are investigating the relationship between obesity and cancer, including breast, ovarian, endometrial, prostate, colorectal, and esophageal cancers. Some of the studies with women include the following:
* The Four Corners Breast and Endometrial Cancer Study is focusing on the effects of obesity and weight changes on breast and endometrial cancer risk among Hispanic, Native American, and non-Hispanic white women (89).

* A study of white, African American, and Latina women is investigating whether phytoestrogen consumption can modify the risk of endometrial cancer associated with obesity (90).

* The Black Women’s Health Study is considering the effect of risk factors, including obesity, on breast cancer risk (91).

* The Health, Eating, Activity and Lifestyle (HEAL) Breast Cancer Prognosis Study is examining the interrelationships between diet, weight, physical activity, hormones, breast cancer prognosis, and quality of life in a multi-ethnic cohort of 1,200 breast cancer survivors (http://appliedresearch.cancer.gov/surveys/heal/).

The Division of Cancer Epidemiology and Genetics (DCEG), one of NCI’s intramural research divisions, is conducting a series of large-scale epidemiologic studies on the influence of obesity and physical inactivity on several major cancers. These include cohort studies within clinical trials, such as the Alpha-Tocopherol Beta-Carotene Study; the Prostate, Lung, Colorectal, and Ovarian Cancer study; and the Polyp Prevention Trial. In addition, DCEG is studying energy balance in cohort and case-control studies in Sweden, China, and the United States; these include the NIH-AARP (National Institutes of Health-American Association of Retired Persons) Diet and Health Study, a prospective cohort study of nutrition in relation to major cancers among over half a million American men and women, and the Cohort Consortium, a new effort that combines several prospective cohort studies from around the world, gathering information on energy balance-related factors from each cohort.

NCI is also developing and supporting research initiatives to improve the measurement of diet and physical activity in the population, understand health professionals’ knowledge and practices about obesity treatment, and support the establishment of centers in nutrition, energetics, and physical activity and cancer outcomes. Some of these initiatives are cosponsored with other parts of the NIH (http://grants.nih.gov/grants/guide/pa-files/PA-01-017.html).

Other studies being conducted or funded by NCI use animal models to study obesity and cancer. One such study is examining the role of body fat mass on cancer progression in a mouse model of prostate cancer. The Center for Cancer Research, one of NCI’s intramural research divisions, is conducting studies examining mechanisms of energy modulation, specifically caloric restriction, fasting, physical activity, diet-induced obesity, and genetically induced obesity, frequently using animal models of cancer.

NCI is supporting the training of new scientists through programs such as the Nutrition and Obesity Training Program at the University of California, Los Angeles and grants to individual new scientists, who are studying topics such as Culturally Proficient Smoking and Weight Control Treatment, Exploration and Intervention in Weight Gain Associated With Adjuvant Chemotherapy for Breast Cancer, and Visceral Adipose Tissue and Colorectal Neoplasia.

Because the delivery of research results is important, NCI has ongoing programs to move obesity-related research into practice. For example, NCI’s Division of Cancer Control and Population Sciences is supporting the integration of diet and physical activity science into comprehensive cancer control planning. Cancer Control PLANET (Plan, Link, Act, Network With Evidence-Based Tools) provides access to data and resources that can help planners, program staff, and researchers design, implement, and evaluate science-based cancer control programs. The modules on Cancer Control PLANET include science-based information on interventions related to diet, physical activity, and NCI’s 5 A Day For Better Health Program (http://www.fruitsandveggiesmatter.gov/), which has incorporated messages on the importance of maintaining a healthy weight and a physically active lifestyle in its public awareness efforts. These messages are a key component of a recent NCI campaign, “9 A Day Campaign for African American Men,” to increase African American men’s consumption of fruits and vegetables. As the national health authority for 5 A Day, the NCI provides leadership through the implementation of a national media campaign, support of state 5 A Day programs, coordination of national partnership efforts and activities, and funding of nutrition behavior change research.

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51. Martel CL, Lara PN. Renal cell carcinoma: Current status and future directions. Critical Reviews in Oncology/Hematology 2003; 45(2):177–190.

52. Bergstrom A, Hsieh CC, Lindblad P, et al. Obesity and renal cell cancer—A quantitative review. British Journal of Cancer 2001; 85:984–990.

53. Brown LM, Swanson CA, Gridley G, et al. Adenocarcinoma of the esophagus: Role of obesity and diet. Journal of the National Cancer Institute 1995; 87(2):104–109.

54. Chow WH, Blot WJ, Vaughan TL, et al. Body mass index and risk of adenocarcinomas of the esophagus and gastric cardia. Journal of the National Cancer Institute 1998; 90(2):150–155.

55. Li SD, Mobarhan S. Association between body mass index and adenocarcinoma of the esophagus and gastric cardia. Nutrition Reviews 2000; 58(2 Pt 1):54–56.

56. Lagergren J, Bergström R, Nyrén O. Association between body mass and adenocarcinoma of the esophagus and gastric cardia. Annals of Internal Medicine 1999; 130(11):883–890.

57. Ji BT, Chow WH, Yang G, et al. Body mass index and the risk of cancers of the gastric cardia and distal stomach in Shanghai, China. Cancer Epidemiology, Biomarkers and Prevention 1997; 6(7):481–485.

58. Bianchini F, Kaaks R, Vainio H. Overweight, obesity, and cancer risk. The Lancet Oncology 2002; 3(9):565–574.

59. Nomura AM. Body size and prostate cancer. Epidemiology Review 2001; 23(1):126–131.

60. Lee IM, Sesso HD, Paffenbarger RS Jr. A prospective cohort study of physical activity and body size in relation to prostate cancer risk (United States). Cancer Causes and Control 2001; 12(2):187–193.

61. Cerhan JR, Torer JC, Lynch CF, et al. Association of smoking, body mass, and physical activity with risk of prostate cancer in the Iowa 65+ Rural Health Study (United States). Cancer Causes and Control 1997; 8(2):229–238.

62. Putnam, SD, Cerhan JR, Parker AS, et al. Lifestyle and anthropometric risk factors for prostate cancer in a cohort of Iowa men. Annals of Epidemiology 2000; 10(6):361–369.

63. Irani J, Lefebvre O, Murat F, Dahmani L, Dore B. Obesity in relation to prostate cancer risk; comparison with a population having benign prostatic hyperplasia. BJU International 2003; 91(6):482–484.

64. Hsing AW, Deng J, Sesterhenn IA, et al. Body size and prostate cancer: A population-based case-control study in China. Cancer Epidemiology, Biomarkers and Prevention 2000; 9(12):1335–1341.

65. Rodriguez C, Patel AV, Calle EE, et al. Body mass index, height, and prostate cancer mortality in two large cohorts of adult men in the United States. Cancer Epidemiology, Biomarkers and Prevention 2001; 10(4):345–353.

66. Daniell HW. A better prognosis for obese men with prostate cancer. Journal of Urology 1996; 155(1):220–225.

67. Stattin P, Soderberg S, Hallmans G, et al. Leptin is associated with increased prostate cancer risk: A nested case-referent study. Journal of Clinical Endocrinology and Metabolism 2001; 86(3):1341–1345.

68. Hsing AW, Gao YT, Chua S Jr, Deng J, Stanczyk FZ. Insulin resistance and prostate cancer risk. Journal of the National Cancer Institute 2003; 95(1):67–71.

69. Shaneyfelt T, Husein R, Bubley G, Mantzoros CS. Hormonal predictors of prostate cancer: A meta-analysis. Journal of Clinical Oncology 2000; 18(4):847–853.

70. Lowenfels AB, Maisonneuve P, Boyle P, Zatonski WA. Epidemiology of gallbladder cancer. Hepato-Gastroenterology 1999; 46(27):1529–1532.

71. Moerman CJ, Bueno-de-Mesquita HB. The epidemiology of gallbladder cancer: Lifestyle-related risk factors and limited surgical possibilities for prevention. Hepato-Gastroenterology 1999; 46(27):1533–1539.

72. Hartz AJ, Rupley DC, Rimm AA. The association of girth measurements with disease in 32,856 women. American Journal of Epidemiology 1984; 119(1):71–80.

73. Mori M, Nishida T, Sugiyama T, et al. Anthropometric and other risk factors for ovarian cancer in a case-control study. Japanese Journal of Cancer Research 1998; 89(3):246–253.

74. Mink PJ, Folsom AR, Sellers TA, Kushi LH. Physical activity, waist-to-hip ratio, and other risk factors for ovarian cancer: A follow-up study of older women. Epidemiology 1996; 7(1):38–45.

75. Farrow DC, Weiss NS, Lyon JL, Daling JR. Association of obesity and ovarian cancer in a case-control study. American Journal of Epidemiology 1989; 129(6):1300–1304.

76. Greggi S, Parazzini F, Paratore MP, et al. Risk factors for ovarian cancer in central Italy. Gynecologic Oncology 2000; 79(1):50–54.

77. Hartge P, Schiffman MH, Hoover R, et al. A case-control study of epithelial ovarian cancer. American Journal of Obstetrics and Gynecology 1989; 161(1):10–16.

78. Engeland A, Tretli S, Bjorge T. Height, body mass index, and ovarian cancer: A follow-up of 1.1 million Norwegian women. Journal of the National Cancer Institute 2003; 95(16):1244–1248.

79. Ji BT, Hatch MC, Chow WH, et al. Anthropometric and reproductive factors and the risk of pancreatic cancer: A case-control study in Shanghai, China. International Journal of Cancer 1996; 66(4):432–437.

80. Michaud DS, Giovannucci E, Willett WC, et al. Physical activity, obesity, height, and the risk of pancreatic cancer. Journal of the American Medical Association 2001; 286(8):921–929.

81. Silverman DT, Swanson CA, Dridley G, et al. Dietary and nutritional factors and pancreatic cancer: A case-control study based on direct interviews. Journal of the National Cancer Institute 1998; 90(22):1710–1719.

82. Silverman DT. Risk factors for pancreatic cancer: A case-control study based on direct interviews. Teratogenesis, Carcinogenesis, and Mutagenesis 2001; 21(1):7–25.

83. Berrington de Gonzalez A, Sweetland S, Spencer E. A meta-analysis of obesity and the risk of pancreatic cancer. British Journal of Cancer 2003; 89(3):519–523.

84. Vainio H, Kaaks R, Bianchini F. Weight control and physical activity in cancer prevention: International evaluation of the evidence. European Journal of Cancer Prevention 2002; 11 Suppl 2:S94–S100.

85. Ziegler RG, Hoover RN, Nomura AM, et al. Relative weight, weight change, height, and breast cancer risk in Asian American women. Journal of the National Cancer Institute 1996; 88(10):650–660.

86. Parker ED, Folsom AR. Intentional weight loss and incidence of obesity-related cancers: The Iowa Women’s Health Study. International Journal of Obesity and Related Metabolic Disorders 2003; 27(12):1447–1452.

87. McTiernan A, Kooperberg C, White E, et al. Recreational physical activity and the risk of breast cancer in postmenopausal women: The Women’s Health Initiative Cohort Study. Journal of the American Medical Association 2003; 290(10):1331–1336.

88. Key TG, Appleby PN, Reeves GK, et al. Body mass index, serum sex hormones, and breast cancer risk in postmenopausal women. Journal of the National Cancer Institute 2003; 95(16):1218–1226.

89. National Cancer Institute Cancer Research Portfolio, Project CA078762. The four corners breast and endometrial cancer study. Retrieved March 8, 2004, from: http://fundedresearch.cancer.gov/.

90. National Cancer Institute Cancer Research Portfolio, Project CA074877. Phytoestrogens, physical activity and endometrial cancer. Retrieved March 8, 2004, from: http://fundedresearch.cancer.gov/.

91. National Cancer Institute Cancer Research Portfolio, Project CA058420. Follow-up study for causes of illness in black women. Retrieved March 8, 2004, from: http://fundedresearch.cancer.gov/.

# # #

Related Resources

* The National Heart, Lung, and Blood Institute (NHLBI) Obesity Education Initiative seeks to reduce the risk of heart disease and overall morbidity and mortality from heart disease by reducing the prevalence of overweight and physical inactivity. The NHLBI Web site has information for health professionals as well as patients and the general public.

Address:     Post Office Box 30105
Bethesda, MD 20824–0105
Telephone:     301–592–8573
Fax:     301–592–8563
Internet Web site:     http://www.nhlbi.nih.gov

* The Weight-control Information Network (WIN) is a national public information service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). WIN assembles and distributes information and publications about weight control, obesity, and nutritional disorders.

Address:     One Win Way
Bethesda, MD 20892–3665
Telephone:     1–877–946–4627
202–828–1025
Fax:     202–828–1028
Email:     win@info.niddk.nih.gov
Internet Web site:     http://win.niddk.nih.gov/index.htm

* The U.S. Preventive Services Task Force recommended that clinicians, using BMI, screen all adults for obesity and offer obese patients intensive counseling and behavioral interventions. For more information, visit the Agency for Healthcare Research and Quality Web site at http://www.ahrq.gov/clinic/3rduspstf/obesity/obesrr.htm on the Internet.

* The Centers for Disease Control and Prevention published the first Surgeon General’s report on physical activity and health, a comprehensive review of the research on physical activity and health. The report can be found at http://www.cdc.gov/nccdphp/sgr/index.htm on the Internet.

* BMI is calculated either as weight in pounds divided by height in inches squared multiplied by 703, or as weight in kilograms divided by height in meters squared. An online BMI calculator can be found at http://www.cdc.gov/healthyweight/assessing/bmi/index.html on the Internet.

* A major clinical trial, the Women’s Health Initiative Dietary Modification trial, is testing whether low-fat diet will lower breast cancer risk (http://www.nhlbi.nih.gov/whi/ctos.htm).

* The NCI Health, Eating, Activity, and Lifestyle (HEAL) Study is designed to look at the associations between physical activity, eating habits, weight patterns, diet, hormones, and prognostic factors for breast cancer among the early stage breast cancer participants. For more information, visit http://appliedresearch.cancer.gov/surveys/heal/ on the Internet.

# # #
Related NCI materials and Web pages:

* National Cancer Institute Fact Sheet 4.24, Physical Activity and Cancer
(http://www.cancer.gov/cancertopics/factsheet/prevention/physicalactivity)
* Energy Balance: Weight and Obesity, Physical Activity, Diet Home Page
(http://www.cancer.gov/cancertopics/energybalance)
* Prevention, Genetics, Causes Home Page
(http://www.cancer.gov/cancertopics/prevention-genetics-causes)

How can we help?

We offer comprehensive research-based information for patients and their families, health professionals, cancer researchers, advocates, and the public.

* Call NCI’s Cancer Information Service at 1–800–4–CANCER (1–800–422–6237)
* Visit us at http://www.cancer.gov or http://www.cancer.gov/espanol
* Chat using LiveHelp, NCI’s instant messaging service, at http://www.cancer.gov/livehelp
* E-mail us at cancergovstaff@mail.nih.gov
* Order publications at http://www.cancer.gov/publications or by calling 1–800–4–CANCER
* Get help with quitting smoking at 1–877–44U–QUIT (1–877–448–7848)

Obesity and Cancer: Questions and Answers

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Posted 29 Dec 2010 — by James Street
Category Obesity, Prevention

Key Points

* During the last two decades, the percentage of overweight and obese adults and children has been steadily increasing (see Question 2).
* Lack of physical activity is strongly associated with obesity (see Question 3).
* In addition to increasing the risk of coronary heart disease, stroke, high blood pressure, and diabetes, obesity increases the risk of cancers of the breast (postmenopausal), endometrium (the lining of the uterus), colon, kidney, and esophagus (see Questions 4, 6–10).
* Avoiding weight gain can lower the risk of cancers of the breast (postmenopausal), endometrium, colon, kidney, and esophagus (see Question 13).
* Regular physical activity lowers the risk of colon and breast cancers (see Question 15).

1. What is obesity?

People who are obese have an abnormally high and unhealthy proportion of body fat. To measure obesity, researchers commonly use a formula based on weight and height known as the body mass index (BMI). BMI is the ratio of weight (in kilograms) to height (in meters) squared. BMI provides a more accurate measure of obesity or being overweight than does weight alone.

Guidelines established by the National Institutes of Health (NIH) place adults age 20 and older into one of four categories based on their BMI (1):
<18.5
underweight
18.5 to 24.9
healthy
25.0 to 29.9
overweight
>30.0
obese

The following chart can be used to determine BMI category. (Find the height, and move across the chart to the appropriate weight.)

Body Mass Index Chart, Adults 20 and Over image

Compared with people in the healthy weight category, those who are overweight or obese are at greater risk for many diseases, including diabetes, high blood pressure, cardiovascular diseases, stroke, and certain cancers. Obesity lowers life expectancy.
2. How common is overweight or obesity?

Results from the 1999–2000 National Health and Nutrition Examination Survey (NHANES) show that an estimated 64 percent of U.S. adults are either overweight or obese (2). This represents an increase of 8 percentage points compared with the estimates from an earlier survey (NHANES III 1988–1994).

Nearly one-third of all adults are now classified as obese. This reflects an increase of 7.6 percentage points since 1994 (2). The data show that 31 percent of adults age 20 and older—nearly 59 million people—have a body mass index (BMI) of 30 or greater, compared with 23 percent in 1994.

In addition, the percentage of children who are overweight continues to increase. Among children and teens ages 6 to 19, 15 percent (almost 9 million) are overweight according to the 1999–2000 data, or triple what the proportion was in 1980 (3).
3. What causes obesity?

Experts have concluded that the chief causes of obesity are a sedentary lifestyle and overconsumption of high-calorie food (4):
* Sedentary lifestyle—Researchers have found a strong correlation between lack of physical activity and obesity (4, 5).

* Diet—A diet high in calories and/or fat appears to be an important factor in obesity (6).

4. What have scientists learned about the relationship between obesity and cancer?

In 2001, experts concluded that cancers of the colon, breast (postmenopausal), endometrium (the lining of the uterus), kidney, and esophagus are associated with obesity. Some studies have also reported links between obesity and cancers of the gallbladder, ovaries, and pancreas (4).

Obesity and physical inactivity may account for 25 to 30 percent of several major cancers—colon, breast (postmenopausal), endometrial, kidney, and cancer of the esophagus (4).

Preventing weight gain can reduce the risk of many cancers. Experts recommend that people establish habits of healthy eating and physical activity early in life to prevent overweight and obesity. Those who are already overweight or obese are advised to avoid additional weight gain, and to lose weight through a low-calorie diet and exercise. Even a weight loss of only 5 to 10 percent of total weight can provide health benefits (4).
5. How many people get cancer by being overweight or obese? How many die?

In 2002, about 41,000 new cases of cancer in the United States were estimated to be due to obesity. This means that about 3.2 percent of all new cancers are linked to obesity (7).

A recent report estimated that, in the United States, 14 percent of deaths from cancer in men and 20 percent of deaths in women were due to overweight and obesity (8).
6. Does obesity increase the risk of breast cancer?

The effect of obesity on breast cancer risk depends on a woman’s menopausal status. Before menopause, obese women have a lower risk of developing breast cancer than do women of a healthy weight (4, 9, 10, 11, 12). However, after menopause, obese women have 1.5 times the risk of women of a healthy weight (9, 10, 13, 14).

Obese women are also at increased risk of dying from breast cancer after menopause compared with lean women (4, 11, 15, 16). Scientists estimate that about 11,000 to 18,000 deaths per year from breast cancer in U.S. women over age 50 might be avoided if women could maintain a BMI under 25 throughout their adult lives (16).

Obesity seems to increase the risk of breast cancer only among postmenopausal women who do not use menopausal hormones. Among women who use menopausal hormones, there is no significant difference in breast cancer risk between obese women and women of a healthy weight (4, 9, 11, 17).

Both the increased risk of developing breast cancer and dying from it after menopause are believed to be due to increased levels of estrogen in obese women (18). Before menopause, the ovaries are the primary source of estrogen. However, estrogen is also produced in fat tissue and, after menopause, when the ovaries stop producing hormones, fat tissue becomes the most important estrogen source (14). Estrogen levels in postmenopausal women are 50 to 100 percent higher among heavy versus lean women (11). Estrogen-sensitive tissues are therefore exposed to more estrogen stimulation in heavy women, leading to a more rapid growth of estrogen-responsive breast tumors.

Another factor related to the higher breast cancer death rates in obese women is that breast cancer is more likely to be detected at a later stage in obese women than in lean women. This is because the detection of a breast tumor is more difficult in obese versus lean women (12).

Studies of obesity and breast cancer in minority women in the United States have been limited. There is some evidence that, among African American women, the risk associated with obesity may be absent or less than that of other populations (19, 20, 21). However, a recent report showed that African American women who have a high BMI are more likely to have an advanced stage of breast cancer at diagnosis (22). Another report showed that obese Hispanic white women were twice as likely to develop breast cancer as non-obese Hispanics, but the researchers did not detect a difference in risk for obese Hispanic women before and after menopause (23).

Weight gain during adulthood has been found to be the most consistent and strongest predictor of breast cancer risk in studies in which it has been examined (4, 10, 11, 24).

The distribution of body fat may also affect breast cancer risk. Women with a large amount of abdominal fat have a greater breast cancer risk than those whose fat is distributed over the hips, buttocks, and lower extremities (13, 25, 26). Results from studies on the effect of abdominal fat are much less consistent than studies on weight gain or BMI.
7. Does obesity increase the risk of cancer of the uterus?

Obesity has been consistently associated with uterine (endometrial) cancer. Obese women have two to four times greater risk of developing the disease than do women of a healthy weight, regardless of menopausal status (4, 27, 28, 29, 30). Increased risk has also been demonstrated among overweight women (28, 30). Obesity has been estimated to account for about 40 percent of endometrial cancer cases in affluent societies (31).

It is unclear why obesity is a risk factor for endometrial cancer; however, it has been suggested that lifetime exposure to hormones and high levels of estrogen and insulin in obese women may be contributing factors (4, 27, 28, 29, 32).
8. Does obesity increase the risk of colon cancer?

Colon cancer occurs more frequently in people who are obese than in those of a healthy weight (4, 33, 34, 35, 36, 37). An increased risk of colon cancer has been consistently reported for men with high BMIs (34, 37, 38). The relationship between BMI and risk in women, however, has been found to be weaker (4, 34, 38) or absent (39).

Unlike for breast and endometrial cancer, estrogen appears to be protective for colon cancer for women overall (40). However, obesity and estrogen status also interact in influencing colon cancer risk. Women with a high BMI who are either premenopausal or postmenopausal and taking estrogens have an increased risk of colon cancer similar to that found for men with a high BMI. In contrast, women with a high BMI who are postmenopausal and not taking estrogens do not have an increased risk of colon cancer (41).

There is some evidence that abdominal obesity may be more important in colon cancer risk (37, 38). In men, a high BMI tends to be associated with abdominal fat. In women, fat is more likely to be distributed in the hips, thighs, and buttocks. Thus, two measures of abdominal fat, waist-to-hip ratio or waist circumference, may be better predictors of colon cancer risk. Few studies have yet compared waist-to-hip ratios to colon cancer risk in women, however. One study that did find an increased risk of colon cancer among women with high waist-to-hip ratios found that the association was present only among inactive women, suggesting that high levels of physical activity may counteract the effects of increased abdominal fat (42).

A number of mechanisms have been proposed for the adverse effect of obesity on colon cancer risk. One of the major hypotheses is that high levels of insulin or insulin-related growth factors in obese people may promote tumor development (4, 43, 44).
9. Does obesity increase the risk of kidney cancer?

Studies have consistently found a link between a type of kidney cancer (renal cell carcinoma) and obesity in women (4, 30, 45, 46, 47, 48), with some studies finding risk among obese women to be two to four times the risk of women of a healthy weight.

Results of studies including men have been more variable, ranging from an association similar to that seen in women (30, 46, 49), to a weak association (48, 50, 51), to no association at all (45). A meta-analysis (where several studies are combined into a single report), which found an equal association of risk among men and women, estimated the kidney cancer risk to be 36 percent higher for an overweight person and 84 percent higher for an obese person compared to those with a healthy weight (52).

The mechanisms by which obesity may increase renal cell cancer risk are not well understood. An increased exposure to sex steroids, estrogen and androgen, is one possible mechanism (4).
10. Does obesity increase the risk of cancer of the esophagus or stomach?

Overweight and obese individuals are two times more likely than healthy weight people to develop a type of esophageal cancer called esophageal adenocarcinoma (4, 53, 54, 55, 56). A smaller increase in risk has been found for gastric cardia cancer, a type of stomach cancer that begins in the area of the stomach next to the esophagus (54, 55, 56, 57). Most studies have not observed increases in risk with obesity in another type of esophageal cancer, squamous cell cancer. An increased risk of esophageal adenocarcinoma has also been associated with weight gain, smoking, and being younger than age 59 (54, 57).

The mechanisms by which obesity increases risk of adenocarcinoma of the esophagus and gastric cardia are not well understood. One of the leading mechanisms proposed has been that increases in gastric reflux due to obesity may increase risk. However, in the few studies that have examined this issue, risk associated with BMI was similar for those with and without gastric reflux (56).
11. Does obesity increase the risk of prostate cancer?

Of the more than 35 studies on prostate cancer risk, most conclude that there is no association with obesity (4, 44, 58, 59, 60). Some report that obese men are at higher risk than men of healthy weight, particularly for more aggressive tumors (61, 62, 63). One study found an increased risk among men with high waist-to-hip ratios, suggesting that abdominal fat may be a more appropriate measure of body size in relation to prostate cancer (64).

Studies examining BMI and prostate cancer mortality have had conflicting results (8, 65, 66).

Despite the lack of association between obesity and prostate cancer incidence, a number of studies have examined potential biological factors that are related to obesity, such as insulin-related growth factors, leptin, and other hormones. Results of these studies are inconsistent, but generally, risk has been linked to men with higher levels of leptin (67), insulin (68), and IGF–1 (insulin-like growth factor-1) (69).
12. Is there any evidence that obesity is linked to cancer of the gallbladder, ovaries, or pancreas?

An increased risk of gallbladder cancer has been found to be associated with obesity, particularly among women (70, 71, 72). This may be due to the higher frequency of gallstones in obese individuals, as gallstones are considered a strong risk factor for gallbladder cancer. However, there is not enough evidence to draw firm conclusions.

It is unclear whether obesity affects ovarian cancer risk. Some studies report an increased risk among obese women (73, 74, 75), whereas others have found no association (76, 77). A recent report found an increased risk in women who were overweight or obese in adolescence or young adulthood; no increased risk was found in older obese women (78).

Studies evaluating the relationship between obesity and pancreatic cancer have been inconsistent (79, 80, 81, 82). One recent study found that obesity increases the risk of pancreatic cancer only among those who are not physically active (80). A recent meta-analysis reported that obese people may have a 19 percent higher risk of pancreatic cancer than those with a healthy BMI. The results, however, were not conclusive (83).
13. Does avoiding weight gain decrease the risk of cancer?

The most conclusive way to test if avoiding weight gain will decrease the risk of cancer is through a controlled clinical trial. At present, there have been no controlled clinical trials on the effect on cancer related to avoiding weight gain. However, many observational studies have shown that avoiding weight gain lowers the risk of cancers of the colon, breast (postmenopausal), endometrium, kidney, and esophagus. There is limited evidence for thyroid cancers, and no substantial evidence for all other cancers (4, 84).
14. Does losing weight lower the risk of cancer?

There is insufficient evidence that intentional weight loss will affect cancer risk for any cancer. A very limited number of observational studies have examined the effect of weight loss, and a few found some decreased risk for breast cancer among women who have lost weight. However, most of these studies have not been able to evaluate whether the weight loss was intentional or related to other health problems (4, 24, 25, 85).

One recent study that examined the effect of intentional weight loss found that women who experienced intentional weight loss of 20 or more pounds and were not currently overweight had cancer rates at the level of healthy women who never lost weight. However, unintentional weight loss episodes were not associated with decreased cancer risk (86).
15. Does regular physical activity lower the risk of cancer?

There have been no controlled clinical trials on the effect of regular physical activity on the risk of developing cancer. However, observational studies have examined the possible association between physical activity and a lower risk of developing colon or breast cancer:
* Colon cancer: In 2002, a major review of observational trials found that physical activity reduced colon cancer risk by 50 percent. This risk reduction occurred even with moderate levels of physical activity (4). For example, one study showed that even moderate exercise, such as brisk walking for 3 to 4 hours per week, can lower colon cancer risk (42).

A limited number of studies have examined the effect of physical activity on colon cancer risk for both lean and obese people. Most of these studies have found a protective effect of physical activity across all levels of BMI (4).
* Breast cancer: The pattern of the association between physical activity and breast cancer risk is somewhat different. Most studies on breast cancer have focused on postmenopausal women. A recent study from the Women’s Health Initiative found that physical activity among postmenopausal women at a level of walking about 30 minutes per day was associated with a 20 percent reduction in breast cancer risk. However, this reduction in risk was greatest among women who were of normal weight. For these women, physical activity was associated with a 37 percent decrease in risk. The protective effect of physical activity was not found among overweight or obese women (87).

16. What biological mechanisms are thought to be involved in explaining the link between obesity and cancer?

The biological mechanism that explains how obesity increases cancer risk may be different for different cancers. (See Questions 6–11.) The exact mechanisms are not known for any of the cancers. However, possible mechanisms include alterations in sex hormones (e.g., estrogen, progesterone, and androgens), and insulin and IGF–1 in obese people that may account for their increased risk for cancers of the breast, endometrium, and colon. Sex-hormone binding globulin, the major carrier protein for certain sex hormones in the plasma, may also be involved in the altered risk for these cancers in obese people (4, 32, 58, 88).
17. What are current research needs?

Although there has been extensive research with large populations looking at the possible link between obesity and cancer, few clinical trials have studied the effect of weight control, physical activity, and energy balance (the calories consumed compared with those burned) on cancer. For some cancers, such as colon and breast, it is not clear whether the increased cancer risk in obese people is due to the extra weight; a high-fat, high-calorie diet; a lack of physical activity; or a combination of these factors.

The 2002 International Agency for Research on Cancer (IARC) report on weight control, physical activity, and cancer (4) made several recommendations for future trials:
* Conduct long-term intervention studies on the effect of dietary changes on weight gain and cancer risk;

* Conduct long-term intervention studies on the effect of patterns of physical activity (the intensity, frequency, and duration of various sorts of physical activity) in relation to weight gain and cancer risk;

* Conduct long-term intervention studies on the combined effects of changes in diet and physical activity on obesity and cancer risk; and

* Conduct community intervention studies to prevent weight gain and promote physical activity.

Several international reports have concluded that controlling the obesity epidemic will require substantial investments by many segments of society. Efforts to increase physical activity and promote healthy eating are needed in families, day care centers, schools, and work sites. The efforts of community services such as health care and public education are needed, as well as transportation systems that encourage walking and the use of bicycles (4).
18. Is the National Cancer Institute (NCI) currently studying the possible link between obesity and cancer?

Several NCI-funded studies are investigating the relationship between obesity and cancer, including breast, ovarian, endometrial, prostate, colorectal, and esophageal cancers. Some of the studies with women include the following:
* The Four Corners Breast and Endometrial Cancer Study is focusing on the effects of obesity and weight changes on breast and endometrial cancer risk among Hispanic, Native American, and non-Hispanic white women (89).

* A study of white, African American, and Latina women is investigating whether phytoestrogen consumption can modify the risk of endometrial cancer associated with obesity (90).

* The Black Women’s Health Study is considering the effect of risk factors, including obesity, on breast cancer risk (91).

* The Health, Eating, Activity and Lifestyle (HEAL) Breast Cancer Prognosis Study is examining the interrelationships between diet, weight, physical activity, hormones, breast cancer prognosis, and quality of life in a multi-ethnic cohort of 1,200 breast cancer survivors (http://appliedresearch.cancer.gov/surveys/heal/).

The Division of Cancer Epidemiology and Genetics (DCEG), one of NCI’s intramural research divisions, is conducting a series of large-scale epidemiologic studies on the influence of obesity and physical inactivity on several major cancers. These include cohort studies within clinical trials, such as the Alpha-Tocopherol Beta-Carotene Study; the Prostate, Lung, Colorectal, and Ovarian Cancer study; and the Polyp Prevention Trial. In addition, DCEG is studying energy balance in cohort and case-control studies in Sweden, China, and the United States; these include the NIH-AARP (National Institutes of Health-American Association of Retired Persons) Diet and Health Study, a prospective cohort study of nutrition in relation to major cancers among over half a million American men and women, and the Cohort Consortium, a new effort that combines several prospective cohort studies from around the world, gathering information on energy balance-related factors from each cohort.

NCI is also developing and supporting research initiatives to improve the measurement of diet and physical activity in the population, understand health professionals’ knowledge and practices about obesity treatment, and support the establishment of centers in nutrition, energetics, and physical activity and cancer outcomes. Some of these initiatives are cosponsored with other parts of the NIH (http://grants.nih.gov/grants/guide/pa-files/PA-01-017.html).

Other studies being conducted or funded by NCI use animal models to study obesity and cancer. One such study is examining the role of body fat mass on cancer progression in a mouse model of prostate cancer. The Center for Cancer Research, one of NCI’s intramural research divisions, is conducting studies examining mechanisms of energy modulation, specifically caloric restriction, fasting, physical activity, diet-induced obesity, and genetically induced obesity, frequently using animal models of cancer.

NCI is supporting the training of new scientists through programs such as the Nutrition and Obesity Training Program at the University of California, Los Angeles and grants to individual new scientists, who are studying topics such as Culturally Proficient Smoking and Weight Control Treatment, Exploration and Intervention in Weight Gain Associated With Adjuvant Chemotherapy for Breast Cancer, and Visceral Adipose Tissue and Colorectal Neoplasia.

Because the delivery of research results is important, NCI has ongoing programs to move obesity-related research into practice. For example, NCI’s Division of Cancer Control and Population Sciences is supporting the integration of diet and physical activity science into comprehensive cancer control planning. Cancer Control PLANET (Plan, Link, Act, Network With Evidence-Based Tools) provides access to data and resources that can help planners, program staff, and researchers design, implement, and evaluate science-based cancer control programs. The modules on Cancer Control PLANET include science-based information on interventions related to diet, physical activity, and NCI’s 5 A Day For Better Health Program (http://www.fruitsandveggiesmatter.gov/), which has incorporated messages on the importance of maintaining a healthy weight and a physically active lifestyle in its public awareness efforts. These messages are a key component of a recent NCI campaign, “9 A Day Campaign for African American Men,” to increase African American men’s consumption of fruits and vegetables. As the national health authority for 5 A Day, the NCI provides leadership through the implementation of a national media campaign, support of state 5 A Day programs, coordination of national partnership efforts and activities, and funding of nutrition behavior change research.

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45. Chow WH, McLaughlin JK, Mandel JS, et al. Obesity and risk of renal cell cancer. Cancer Epidemiology, Biomarkers and Prevention 1996; 5(1):17–21.

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51. Martel CL, Lara PN. Renal cell carcinoma: Current status and future directions. Critical Reviews in Oncology/Hematology 2003; 45(2):177–190.

52. Bergstrom A, Hsieh CC, Lindblad P, et al. Obesity and renal cell cancer—A quantitative review. British Journal of Cancer 2001; 85:984–990.

53. Brown LM, Swanson CA, Gridley G, et al. Adenocarcinoma of the esophagus: Role of obesity and diet. Journal of the National Cancer Institute 1995; 87(2):104–109.

54. Chow WH, Blot WJ, Vaughan TL, et al. Body mass index and risk of adenocarcinomas of the esophagus and gastric cardia. Journal of the National Cancer Institute 1998; 90(2):150–155.

55. Li SD, Mobarhan S. Association between body mass index and adenocarcinoma of the esophagus and gastric cardia. Nutrition Reviews 2000; 58(2 Pt 1):54–56.

56. Lagergren J, Bergström R, Nyrén O. Association between body mass and adenocarcinoma of the esophagus and gastric cardia. Annals of Internal Medicine 1999; 130(11):883–890.

57. Ji BT, Chow WH, Yang G, et al. Body mass index and the risk of cancers of the gastric cardia and distal stomach in Shanghai, China. Cancer Epidemiology, Biomarkers and Prevention 1997; 6(7):481–485.

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59. Nomura AM. Body size and prostate cancer. Epidemiology Review 2001; 23(1):126–131.

60. Lee IM, Sesso HD, Paffenbarger RS Jr. A prospective cohort study of physical activity and body size in relation to prostate cancer risk (United States). Cancer Causes and Control 2001; 12(2):187–193.

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62. Putnam, SD, Cerhan JR, Parker AS, et al. Lifestyle and anthropometric risk factors for prostate cancer in a cohort of Iowa men. Annals of Epidemiology 2000; 10(6):361–369.

63. Irani J, Lefebvre O, Murat F, Dahmani L, Dore B. Obesity in relation to prostate cancer risk; comparison with a population having benign prostatic hyperplasia. BJU International 2003; 91(6):482–484.

64. Hsing AW, Deng J, Sesterhenn IA, et al. Body size and prostate cancer: A population-based case-control study in China. Cancer Epidemiology, Biomarkers and Prevention 2000; 9(12):1335–1341.

65. Rodriguez C, Patel AV, Calle EE, et al. Body mass index, height, and prostate cancer mortality in two large cohorts of adult men in the United States. Cancer Epidemiology, Biomarkers and Prevention 2001; 10(4):345–353.

66. Daniell HW. A better prognosis for obese men with prostate cancer. Journal of Urology 1996; 155(1):220–225.

67. Stattin P, Soderberg S, Hallmans G, et al. Leptin is associated with increased prostate cancer risk: A nested case-referent study. Journal of Clinical Endocrinology and Metabolism 2001; 86(3):1341–1345.

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# # #

Related Resources

* The National Heart, Lung, and Blood Institute (NHLBI) Obesity Education Initiative seeks to reduce the risk of heart disease and overall morbidity and mortality from heart disease by reducing the prevalence of overweight and physical inactivity. The NHLBI Web site has information for health professionals as well as patients and the general public.

Address:     Post Office Box 30105
Bethesda, MD 20824–0105
Telephone:     301–592–8573
Fax:     301–592–8563
Internet Web site:     http://www.nhlbi.nih.gov

* The Weight-control Information Network (WIN) is a national public information service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). WIN assembles and distributes information and publications about weight control, obesity, and nutritional disorders.

Address:     One Win Way
Bethesda, MD 20892–3665
Telephone:     1–877–946–4627
202–828–1025
Fax:     202–828–1028
Email:     win@info.niddk.nih.gov
Internet Web site:     http://win.niddk.nih.gov/index.htm

* The U.S. Preventive Services Task Force recommended that clinicians, using BMI, screen all adults for obesity and offer obese patients intensive counseling and behavioral interventions. For more information, visit the Agency for Healthcare Research and Quality Web site at http://www.ahrq.gov/clinic/3rduspstf/obesity/obesrr.htm on the Internet.

* The Centers for Disease Control and Prevention published the first Surgeon General’s report on physical activity and health, a comprehensive review of the research on physical activity and health. The report can be found at http://www.cdc.gov/nccdphp/sgr/index.htm on the Internet.

* BMI is calculated either as weight in pounds divided by height in inches squared multiplied by 703, or as weight in kilograms divided by height in meters squared. An online BMI calculator can be found at http://www.cdc.gov/healthyweight/assessing/bmi/index.html on the Internet.

* A major clinical trial, the Women’s Health Initiative Dietary Modification trial, is testing whether low-fat diet will lower breast cancer risk (http://www.nhlbi.nih.gov/whi/ctos.htm).

* The NCI Health, Eating, Activity, and Lifestyle (HEAL) Study is designed to look at the associations between physical activity, eating habits, weight patterns, diet, hormones, and prognostic factors for breast cancer among the early stage breast cancer participants. For more information, visit http://appliedresearch.cancer.gov/surveys/heal/ on the Internet.

# # #
Related NCI materials and Web pages:

* National Cancer Institute Fact Sheet 4.24, Physical Activity and Cancer
(http://www.cancer.gov/cancertopics/factsheet/prevention/physicalactivity)
* Energy Balance: Weight and Obesity, Physical Activity, Diet Home Page
(http://www.cancer.gov/cancertopics/energybalance)
* Prevention, Genetics, Causes Home Page
(http://www.cancer.gov/cancertopics/prevention-genetics-causes)

How can we help?

We offer comprehensive research-based information for patients and their families, health professionals, cancer researchers, advocates, and the public.

* Call NCI’s Cancer Information Service at 1–800–4–CANCER (1–800–422–6237)
* Visit us at http://www.cancer.gov or http://www.cancer.gov/espanol
* Chat using LiveHelp, NCI’s instant messaging service, at http://www.cancer.gov/livehelp
* E-mail us at cancergovstaff@mail.nih.gov
* Order publications at http://www.cancer.gov/publications or by calling 1–800–4–CANCER
* Get help with quitting smoking at 1–877–44U–QUIT (1–877–448–7848)

Obesity soon to outscore smoking as cancer risk, professor warns

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Posted 29 Dec 2010 — by James Street
Category Obesity, Prevention

Dec 29, 2010, 11:58 GMT

Heidelberg, Germany – Obesity will soon outscore smoking as the principal risk factor in Germany for cancer, the head of the country’s main cancer-research laboratory said Wednesday.

The reason was the growth in Germany’s obesity rate. Overweight people are at greater risk of oesophageal, bowel, kidney, pancreatic and breast cancer, although the precise mechanisms involved have still not yet been fully explained.

‘That’s an important topic in the next stage of our research,’ said Otmar Wiestler, head of the German Cancer Research Centre, or DKFZ, told the German Press Agency dpa in Heidelberg.

He said the overall number of cancer cases was bound to rise as the average person’s life expectancy grew in Germany.

‘Cancers are diseases that mainly show up in old age,’ he explained.

Professor Wiestler said that of 450,000 people who come down with cancer in Germany every year, about half could expect to be cured and many others could expect therapy that kept the cancer in check.

New drugs and the trend to carefully tailor therapies to the individual promised to increase the rate of cures, he said.

DKFZ in Heidelberg says it is the largest biomedical research institute in Germany with more than 2,200 staff.

‘Cure rates will improve,’ he forecast, adding that scientists ‘now have a fairly good for the majority of cancers’ which genetic mutations and which cellular changes are involved.

‘That makes it possible to devise drugs that block such changes. There are more and more drugs that can be prescribed individually, depending on the characteristics of the patient,’ he said. Single forms of cancer can be of many types, needing different drugs.

Obesity worstens prostate cancer

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Posted 26 Dec 2010 — by James Street
Category Obesity, Prostate Cancer

A recent study published last Wednesday is suggesting that the size of a tumor in prostate cancer is directly proportional to the weight of the concerned individual; therefore, someone who has a bigger prostate cancer tumor is likely obese. Alternatively, a bigger tumor means it is more aggressive and it is likely to spread in the body.

Lead author Dr. Nilesh Patil of the Henry Ford Hospital based in Detroit, Michigan validates, “As the patients’ body mass index increased, the tumor volume increased synchronously. He also adds, “Based on our results, we believe having a larger percentage of tumor volume may be contributing to the aggressive nature of the disease in men with a higher BMI.”

The said study looked at the existing cases of 6,327 individuals who had tumors removed via a robotic procedure with the participants categorized into six groups based on their recorded BMI.

The prostate cancer sufferers’ tumor were also weighed and then classified in an existing database of prostate weight.