A projection of the future health and economic burden of obesity in 2030 estimated that continuation of existing trends in obesity will lead to about 500,000 additional cases (nearly a 15-fold increase) of cancer in the U.S. by 2030.1
For example, one study that used NCI Surveillance, Epidemiology and End Results (SEER) data estimated that, in 2007 in the U.S., nearly 34,000 new cases of cancer in men (4%) and 50,500 in women (7%) were due to obesity. The percentage of cases attributed to obesity was as high as 40% for some cancers, particularly endometrial cancer and esophageal adenocarcinoma.1
Deadly Consequences of High BMI
To measure obesity, researchers commonly use body mass index (BMI), which is calculated by dividing a person’s weight (in kilograms) by their height (in meters) squared. A value of 30 and higher is defined as obese. Obesity is associated with increased risks of these cancer types:
• Esophagus
• Endometrium (lining of the uterus)
• Pancreas
• Gallbladder
• Colon and rectum
• Thyroid
• Breast (after menopause)
• Kidney
SEE ALSO: Post-Operartive Care for Bariatric Surgery
Turkoz et al.5 followed 818 pre-menopausal women with non-metastatic breast cancer. These patients were classified into three groups according to BMI: 1) normal body weight (BMI: 18.5-24.9; 2) overweight (BMI: 25-29.9); and 3) obese (BMI:>30). Clinical and pathologic characteristics and survival rates were also analyzed for triple negative, HER-2 overexpressing and luminal subtypes.
Obese patients were older at diagnosis and more often had high-grade tumor and lymphovascular invasion. The median follow-up period after diagnosis was 29 months. According to the molecular subtypes, overall and disease-free survival were significantly shorter in obese patients with triple negative breast cancer. Obesity and lymphovascular invasion were found to be independent prognostic factors for triple negative breast cancer mortality.
The timing of weight gain might also affect cancer risk. Being overweight during childhood and young adulthood might be more of a risk factor than gaining weight later in life for some cancers. For example, some research suggests that women who are overweight as teenagers may be at higher risk for developing ovarian cancer before menopause.2
Excess body weight may affect cancer risk through a number of mechanisms, some of which might be specific to certain cancer types. Excess body fat might affect:
• Immune system function and inflammation.
• Levels of certain hormones, such as insulin and estrogen.
• Factors that regulate cell growth, such as insulin-like growth factor-1 (IGF-1).
• Proteins that influence how the body uses certain hormones, such as sex hormone-binding globulin.2,3
Best Odds Diet for Avoiding Cancer
Research on how losing weight might lower the risk of developing cancer is limited. However, there is growing evidence that weight loss might reduce the risk of breast cancer (after menopause), more aggressive forms of prostate cancer and possibly other cancers.2
A study of diet itself by T rraga-L¢pez found that excessive alcohol consumption and a cholesterol-rich diet are associated with a high risk of colon cancer. A diet poor in folic acid and vitamin B6 is also associated with a higher risk of developing colon cancer with an overexpression of p53. Eating less meat and consuming pulses at least three times a week lowers the risk of developing colon cancer by 33%, while eating brown rice at least once a week cuts the risk of CRC by 40%.
These associations suggest a dose-response effect. Frequently eating cooked green vegetables, nuts, dried fruit, pulses and brown rice has been associated with a lower risk of colorectal polyps. High calcium intake offers a protector effect against distal colon and rectal tumors as compared with the proximal colon. Higher intake of dairy products and calcium reduces the risk of colon cancer. Taking an aspirin (ASA) regularly after being diagnosed with colon cancer is associated with less risk of dying from this cancer, especially among people who have tumors with COX-2 overexpression. Given that they concluded that, “These data do not contradict the data obtained on a possible genetic predisposition, even in sporadic or non-hereditary colon cancer.”7
These findings don’t just apply to the adult population.
Estrada et al. pointed out that approximately 30% of US children have obesity-related comorbidities, such as hypertension, dyslipidemia, fatty liver disease, diabetes, polycystic ovary syndrome (PCOS), sleep apnea and psychosocial problems.8
David Plaut is a chemist and statistician in Plano, Texas.
References:
1. Obesity. NIH: National Cancer Institute. http://tinyurl.com/pu986j8
2. Obesity and Cancer. Cancer.net. http://tinyurl.com/gkt3e4v
3. Obesity and cancer progression: Is there a role of fatty acid metabolism? Balaban S, Lee LS, Schreuder M, et al. Biomed Res Int. 2015;2015:274585.
4. Turkoz FP, Solak M, Petekkaya I, et al. The prognostic impact of obesity on molecular subtypes of breast cancer in premenopausal women. Official Journal of Balkan Unit of Oncology. 2013 Apr-Jun;18(2):335-41.
5. T rraga L¢pez PJ, Albero JS, Rodr¡guez-Montes JA. Primary and secondary prevention of colorectal cancer. Clin Med Insights Gastroenterol. 2014 Jul 14;7:33-46. doi: 10.4137/CGast.S14039. eCollection 2014.
6. Estrada E, Eneli I, Hampl S. Children’s Hospital Association consensus statements for comorbidities of childhood obesity., et al. Child Obes. 2014 Aug;10(4):304-17.
7. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adult obesity in the United States, 2011-2012. Journal of the American Medical Association 2014;311(8):806-814. See also National Center for Health Statistics. Health, United States, 2011: With Special Features on Socioeconomic Status and Health. Hyattsville, MD; U.S. Department of Health and Human Services; 2012.
8. Sheng X, Mittelman S. The role of adipose tissue and obesity in causing treatment resistance of acute lymphoblastic leukemia. Front Pediatr. 2014, Jun 5.
