The Body Fat Cancer List and the Overweight Diet – 


Are you on the list? The Body Fat Cancer list that is…. 

Over half of the population is counted on the list.

What list?

Individuals who are overweight are considered at risk for ten forms of cancer.  That list.

Why?  Because their body fat is located over the abdomen in the familiar “apple” body shape (Ballard-Barbash et al., 1990; Schapira et al., 1991; Swanson et al., 1993; Sellers et al., 1993). 

Indeed, there are ten cancers scientifically attributed to living a life with excessive, overweight body fat (Britton et al., 2013; Folsom, 1993).  If you are overweight, you are at risk of cancer of the pancreas, the thyroid, the kidney and the gallbladder (Obesity and Cancer Risk, 2012).  That’s four.4bodyfatrelatedcancerrisks

Add cancers of the colon, rectum, esophagus and ovaries caused by a high body fat or overweight lifestyle (Ovarian Cancer 2014 Report: Food, Nutrition, Physical Activity, and the Prevention of Ovarian Cancer, 2014; Obesity and Cancer Risk, 2012).  Now, that’s eight.

Round out the count… with endometrial cancer (uterine lining) and breast cancer after menopause due to high body fat and overweight conditions… and you have ten cancers (Obesity and Cancer Risk, 2012; Irwin et al., 2005; Morimoto et al., 2002; Austin, Austin, Partridge, Hatch & Shingleton, 1991).   

According to the National Cancer Institute each of the ten identified cancers considers a body mass index (BMI) of 25.0 kg/m2 as the “overweight” starting threshold for an individual (Obesity and Cancer Risk, 2012).    Obviously, to calculate BMI you must convert your height and weight to meters and kilograms and make sure to square the height by multiplying your height by the same number, again. 

Of course, you can get total body fat measurements instead of the BMI using a variety of techniques.  Lean body mass is used as the indirect measurement tool by collecting the potassium and water in the body and body density using underwater weight scales (Cohn, 1981). Then, there is a skinfold measurement. Total body nitrogen using something called, neutron activation, is another indirect measure (Cohn, 1981).

Distribution of overweight body fat and its effect on cancer risk are just like the real estate industry: location, location, location.  Body fat located around the belly, which creates the classic “apple” shape is the body fat location associated with these cancers (Canoy, et al., 2007).  Body fat located along the classic “pear” or curvy-patterned locations has the opposite effect; fat on the hips (below the abdomen or belly) provides a measure of protection for women, but only before menopause (Sonnenschein et al., 1999).

Researchers have followed this phenomenon to see why malignant tumors, especially breast cancer lesions, develop when body fat is located more in the “apple” and not in the “pear” distribution.  Schapira, Kumar & Lyman (1991) contrasted overweight from normal weight women and sorted them by body fat location and breast cancer status.  They then observed how the many female sex hormones affected each of these groups

Two hormones changed signficantly in the overweight group:  first, sex hormone-binding globulin (SHBG) levels decreased (SHBG is a transport protein to carry sex hormone through the body).  Second, testosterone levels rose substantially.  But, the SHBG level plummeted at a faster rate as women had more body fat in their abdomen location, instead of the hips (Schapira, Kumar & Lyman, 1991).  The pattern of sex hormone changes suggests that women with more body fat around the abdomen than fat around the hips are at increased risk of developing breast cancer.

Interestingly, the man’s prostate stands apart from “the list of ten” cancers because it is NOT linked to body fat for cancer risk.  Anderson et al. (1996) completed the seminal study that focused on the prostate cancer risk men-prostate-cancerwith dietary fat (saturated and monounsaturated) combined with vitamin A and C precursors, β-carotene and retinol (retinoic acid), respectively (Andersson et al., 1996). 

Earlier studies had suggested that taking vitamin A had a marginal benefit for decreasing the risk of prostate cancer (Ohno et al., 1988; Mettlin et al., 1989).  Others found significant improvement from vitamin C, which decreased the risk of prostate cancer (Hsing et al., 1990; West et al., 1991; Giovannucci et al., 1995).  But, it was Anderson et al. (1996) who discovered after researching 651 eligible males that fat had no effect on the prostate.

The Nurses’ Health Study, a highly acclaimed resource for data mining and solid, scientific research chimed in on the body weight distribution issue as it relates to insulin insensitivity, a known feature of overweight body cell membranes (Chamberlain, Rhinehart, Shaefer & Neuman, 2016).  There were almost 44,000 women in that study, each carefully measured for body mass index (BMI), waist-to-hip ratio (apple versus pear body shape differential), and waist circumference (Carey et al., 1997). The researchers removed from the study those factors that are known to be associated with diabetes because they would skew or bias the results.  Examples included: outlying age groups, a family history of diabetes, a history of smoking, excessive exercise patterns, and dietary contributors known to induce high blood sugar levels. 

The findings proved that as a woman’s BMI increases to higher levels of the overweight range the centrally located body fat becomes more associated with insulin resistance, diabetes and ultimately cancer risks. What the researchers deduced was the location of the fat cells dictates the fat cell role, and central (apple) body fat creates insulin resistance, unlike hip (pear) body fat (Carey et al., 1997).   

How does diet make a difference? 

Most people know by now to change dietary fats from saturated butter to the more superior polyunsaturated margarine or monounsaturated olive oil from saturated butter. One of the sentinel articles was by Blankson et al. (2000) which published that conjugated linoleic acid (polyunsaturated fats) actually lowers the total body fat level in overweight individuals. 

But, what else makes a difference in lowering the risk from this “top ten” cancer list?  After all, we know that ten-cancerthe incidence of breast cancer varies directly with diet across the globe.  And the next generation offspring of those who move to a new country and adapt the local dietary lifestyle assume the breast cancer rates of that new country (Hunter & Willett, 1993).

So, modifying diet is essential to reducing the risk of cancer on this “top ten” cancer list.

Reduced overall calorie intake, especially avoiding sugary drinks and fast food restaurants is a start (Calle, EE & Kaaks, 2004).   Eat white meats such as fish, chicken, unsalted pork, and turkey instead of processed meats like bacon, hot dogs, ham, red meats and meats that are smoked, salted and cured (West et al., 1998).  The federal dietary guidelines just changed and included a 5-portion-a-day vegetable and fruit requirement that you can easily supplement by using flavorful smoothie recipes (Dietary Guidelines, 2015). 



Andersson, S. O., Wolk, A., Bergstroem, R., Giovannucci, E., Lindgren, C., Baron, J., & Adami, H. O. (1996). Energy, nutrient intake and prostate cancer risk: a population-based case-control study in Sweden. International journal of cancer, 68(6), 716-722. Retrieved March 23, 2016 from

Austin, H., Austin, J. M., Partridge, E. E., Hatch, K. D., & Shingleton, H. M. (1991). Endometrial cancer, obesity, and body fat distribution. Cancer research, 51(2), 568-572. Retrieved March 23, 2016 from

Ballard-Barbash, R., Schatzkin, A., Carter, C. L., Kannel, W. B., Kreger, B. E., D’Agostino, R. B., … & Helsel, W. E. (1990). Body fat distribution and breast cancer in the Framingham Study. Journal of the National Cancer Institute, 82(4), 286-290. doi: 10.1093/jnci/82.4.286

Blankson, H., Stakkestad, J. A., Fagertun, H., Thom, E., Wadstein, J., & Gudmundsen, O. (2000). Conjugated linoleic acid reduces body fat mass in overweight and obese humans. The Journal of nutrition, 130(12), 2943-2948. Retrieved March 23, 2016 from

Britton, K. A., Massaro, J. M., Murabito, J. M., Kreger, B. E., Hoffmann, U., & Fox, C. S. (2013). Body fat distribution, incident cardiovascular disease, cancer, and all-cause mortality. Journal of the American College of Cardiology, 62(10), 921-925.doi:10.1016/j.jacc.2013.06.027

Calle, EE & Kaaks, R. (2004). Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms. Nature Reviews Cancer. 4: 579-91. DOI:10.1038/nrc1408.

Canoy, D., Boekholdt, S. M., Wareham, N., Luben, R., Welch, A., Bingham, S., … & Khaw, K. T. (2007). Body Fat Distribution and Risk of Coronary Heart Disease in Men and Women in the European Prospective Investigation Into Cancer and Nutrition in Norfolk Cohort A Population-Based Prospective Study. Circulation, 116(25), 2933-2943. doi: 10.1161/CIRCULATIONAHA.106.673756

Carey, V. J., Walters, E. E., Colditz, G. A., Solomon, C. G., Willet, W. C., Rosner, B. A., … & Manson, J. E. (1997). Body fat distribution and risk of non-insulin-dependent diabetes mellitus in women the nurses’ health study. American journal of epidemiology, 145(7), 614-619. Retrieved March 23, 2016 from

Chamberlain JJ, Rhinehart AS, Shaefer CF & Neuman A. (2016). Diagnosis and Management of Diabetes: Synopsis of the 2016 American Diabetes Association Standards of Medical Care in Diabetes. Ann Intern Med. [Epub ahead of print 1 March 2016] doi:10.7326/M15-3016

Cohn, S. H., Ellis, K. J., Vartsky, D., Sawitsky, A., Gartenhaus, W., Yasumura, S., & Vaswani, A. N. (1981). Comparison of methods of estimating body fat in normal subjects and cancer patients. The American journal of clinical nutrition, 34(12), 2839-2847. Retrieved March 23, 2016 from

Dietary Guidelines. (2015). Scientific Report of the 2015 Dietary Guidelines Advisory Committee. Office of Disease Prevention and Health Promotion.  Retrieved March 23, 2016 from

Folsom, A. R., Kaye, S. A., Sellers, T. A., Hong, C. P., Cerhan, J. R., Potter, J. D., & Prineas, R. J. (1993). Body fat distribution and 5-year risk of death in older women. Jama, 269(4), 483-487. Retrieved March 20, 2016 from doi:10.1001/jama.1993.03500040049035

Giovannucci, E., Ascherio, A., Rimm, E. B., Stampfer, M. J., Colditz, G. A., & Willett, W. C. (1995). Intake of carotenoids and retino in relation to risk of prostate cancer. Journal of the national cancer institute, 87(23), 1767-1776. doi: 10.1093/jnci/87.23.1767

Hsing, A. W., McLaughlin, J. K., Schuman, L. M., Bjelke, E., Gridley, G., Wacholder, S., … & Blot, W. J. (1990). Diet, tobacco use, and fatal prostate cancer: results from the Lutheran Brotherhood Cohort Study. Cancer Research, 50(21), 6836-6840. Retrieved March 23, 2016 from

Hunter, D. J., & Willett, W. C. (1993). Diet, body size, and breast cancer. Epidemiologic reviews, 15(1), 110-132.

Irwin, M. L., McTiernan, A., Baumgartner, R. N., Baumgartner, K. B., Bernstein, L., Gilliland, F. D., & Ballard-Barbash, R. (2005). Changes in body fat and weight after a breast cancer diagnosis: influence of demographic, prognostic, and lifestyle factors. Journal of Clinical Oncology, 23(4), 774-782. Retrieved March 23, 2016 from

Mettlin, C., Selenskas, S., Natarajan, N., & Huben, R. (1989). Beta‐carotene and animal fats and their relationship to prostate cancer risk. A case—control study. Cancer, 64(3), 605-612. DOI: 10.1002/1097-0142(19890801)64:3<605::AID-CNCR2820640307>3.0.CO;2-I

Morimoto, L. M., White, E., Chen, Z., Chlebowski, R. T., Hays, J., Kuller, L., … & Stefanick, M. L. (2002). Obesity, body size, and risk of postmenopausal breast cancer: the Women’s Health Initiative (United States). Cancer Causes & Control, 13(8), 741-751. Retrieved March 23, 2016 from’s_Health_Initiative_%28United_States%29/links/0046353cd7394af9a9000000.pdf

Obesity and Cancer Risk. (2012). National Cancer Institute at the National Institutes of Health. Retrieved March 23, 2016 from

Ohno, Y., Yoshida, O., Oishi, K., Okada, K., Yamabe, H., & Schroeder, F. H. (1988). Dietary β-carotene and cancer of the prostate: a case-control study in Kyoto, Japan. Cancer research, 48(5), 1331-1336. Retrieved March 23, 2016 from

Ovarian Cancer 2014 Report: Food, Nutrition, Physical Activity, and the Prevention of Ovarian Cancer (2014). The American Institute for Cancer Research and the World Cancer Research Fund. Retrieved March 23, 2016 from

Sellers, TA, Gapstur, SM, Potter, JD, Kushi, LH, Bostick, RM, and Folsom, AR. (1993). Association of Body Fat Distribution and Family Histories of Breast and Ovarian Cancer with Risk of Postmenopausal Breast Cancer. Am. J. Epidemiol, 138 (10), 799-803.

Schapira, D. V., Kumar, N. B., & Lyman, G. H. (1991). Obesity, body fat distribution, and sex hormones in breast cancer patients. Age (Yr), 25(40), 41-55. Retrieved March 23, 2016 from

Schapira, D. V., Kumar, N. B., Lyman, G. H., Cavanagh, D., Roberts, W. S., & LaPolla, J. (1991). Upper-body fat distribution and endometrial cancer risk. Jama, 266(13), 1808-1811. doi:10.1001/jama.1991.03470130088034

Sonnenschein, E., Toniolo, P., Terry, M. B., Bruning, P. F., Kato, I., Koenig, K. L., & Shore, R. E. (1999). Body fat distribution and obesity in pre-and postmenopausal breast cancer. International Journal of Epidemiology, 28(6), 1026-1031.doi: 10.1093/ije/28.6.1026

Swanson, C. A., Potischman, N., Wilbanks, G. D., Twiggs, L. B., Mortel, R., Berman, M. L., … & Brinton, L. A. (1993). Relation of endometrial cancer risk to past and contemporary body size and body fat distribution. Cancer Epidemiology Biomarkers & Prevention, 2(4), 321-327. Retrieved March 23, 2016 from

West, D. B., Delany, J. P., Camet, P. M., Blohm, F., Truett, A. A., & Scimeca, J. (1998). Effects of conjugated linoleic acid on body fat and energy metabolism in the mouse. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 275(3), R667-R672. Retrieved March 23, 2016 from

West, D. W., Slattery, M. L., Robison, L. M., French, T. K., & Mahoney, A. W. (1991). Adult dietary intake and prostate cancer risk in Utah: a case-control study with special emphasis on aggressive tumors. Cancer Causes & Control, 2(2), 85-94. DOI 10.1007/BF00053126