Cancer And Sugar: How Sweet It Isn’t

sugar-cubes-smTalk about linking sugar to cancer can be confusing. The “facts” are often presented in a misleading manner that can cause anxiety in those who have the disease. Yet, learning about the science behind the connection can help us make educated decisions about nutrition choices for better health. Sugar, or rather glucose, feeds every cell in the body. We need it to produce energy. Even if we eliminate sugar from our diets, our bodies will still make glucose from other sources, including proteins and fats. It’s a little more complicated than meets the eye. Eating lots of sugar forces the body to make more insulin, one of whose properties is to tell cells to grow. For healthy cells, this is good because all cells grow, divide, die and get replaced by new ones. However, cancer cells can be told to grow, too, when the body makes too much insulin (Goodwin, 2002) (Duggan, 2013). So, yes, there can be too much of a good thing. Knowing from the start that sugar in itself is not evil, we can proceed to the science.

A recent study at the University Rey Carlos in Madrid found a mechanism that links obesity and diabetes with cancer, based on gene activity that promotes the manufacture of insulin. Once sugar reaches the intestine a hormone called GIP is secreted. This enhances insulin release by the pancreas. GIP is controlled by a protein known as β-catenin, a suspected oncogene whose activity depends on sugar levels. Oncogenes are those that transform normal cells into cancerous ones, and mutations of the β-catenin gene are implicated in the incidence of colon and ovarian cancers, among others. Normal sugar levels do not induce accumulation of this protein in the nucleus, but diabetes and its characteristic elevated blood glucose levels does, and is associated with increased cancer risk (Chocarro-Calvo, 2012). The suspicion of a sugar-cancer link was investigated in Korea more than half a decade earlier, when physicians closed a ten-year study in which was recorded health parameters from the biennial physical exams of people receiving national health insurance. Adjusting for smoking and alcohol use, investigators found that those with the highest glucose levels had higher death rates from all cancers combined (Jee, 2005). Associations of sugar to cancer were strongest in pancreatic cancer for both genders. This was followed by esophagus, liver and colon cancers for men and by liver and cervix cancers for women. The bottom line is that cancer risk is elevated with increased fasting serum glucose (Ibid.).

For the last twenty years, diabetes rates have grown. Almost twenty-six million Americans are so diagnosed, but another seven million remain undiagnosed. The disease has been around since the Egyptians, whose ancient writings mention frequent urination as a disturbing problem. Not to be left out of the medical world, the Greeks coined the word diabetes two hundred years before Christ, and Indian physicians noted that diabetic urine would attract ants. In Type II diabetes, insulin resistance is the underlying pathology, accounting for most diagnoses.

The grading of obesity according to body mass index (BMI) aligns with disease specificity. The BMI of healthy people is 18.5-24.9. Between 25.0 and 29.9, a person is overweight. Grade I obesity runs from 30.0-34.0; Grade II from 35.0-39.9; and Grade III above 40.0. The sixty-six inch person who weighs four hundred pounds is off the charts. You can compute your BMI by multiplying your weight by 703, dividing by your height in inches, and then dividing by your height in inches once more.  A recent issue of the Journal of the AMA announced that obesity Grades II and III are associated with significantly higher all-cause mortality, and that simple overweight is associated with significantly lower all-cause death (Flegal, 2013). Imagine what a person with a BMI of 64.6 has to anticipate!

Of the cancer-awareness organizations, breast cancer support groups receive much attention, and rightly so because of this cancer’s ubiquity and horrid nature. It was realized years ago that a relationship between breast cancer and sugar intake exists, where insulin carries the onus of induction. Elevated sugar intake causes a rise in insulin. If the body’s regulatory mechanism is overtaxed, insulin levels get out of hand. Those with diabetes are especially susceptible (Seely, 1983). Just being overweight, in the absence of diabetes, is also a risk factor for breast disease (Lof, 2009). Men are not excused from soft tissue disease just by virtue of their gender. Dietary sugars, notably sucrose (table sugar), may present an ill-defined risk in males, but a risk nonetheless for pancreas, prostate, testis and even lung cancers (Burley, 1998) (DeStefani, 1998).

The glycemic index (GI) is a measure of the effects of carbohydrates on blood glucose levels. Foods that break down quickly and release glucose rapidly have a high GI; those that break down slowly and release glucose gradually have a lower GI. Glucose is used as the reference point. In light of this, scrutiny has been given to an association of high-GI foods to colon cancer. Although no definitive conclusions were reached, there is enough evidence to suggest avoiding foods that are more energy-dense (read sugars and simple carbs) than nutrient-dense to prevent colon and other gastric disease (Galeone, 2012) (Tuyns, 1992) (Moerman, 1993).

Cancer cells thrive on sugar (Dell’Antone, 2012) (Sandulache, 2011), and glucose transport is misregulated in active disease.  Tumor cells have shown increased levels of glucose uptake, as seen in diagnostic images that use radio-labeled glucose analogs as identifiers (Adekola, 2012) (Jóźwiak, 2012). To compound the disorder, sugar increases angiogenesis, which is the growth of new blood vessels. That’s the last thing we want for a tumor—a feeding tube. Yes, angiogenesis is required for growth and development of an organism and for the healing of wounds, but it needs to stop there. Anti-angiogenic protocols are being studied as novel therapies (Merchan, 2010) (Brown, 1998) (Airley, 2007).

All sugars and carbohydrates need not be avoided. The healthy carbohydrates include vegetables, fruits, whole grains and legumes. There is debate about the value of grains in the diet, but we have to admit they are sources of fiber, phytochemicals, vitamins and minerals, and compounds yet to be identified. To keep insulin levels at bay, be sure to eat protein, fat and fiber. These work even in the presence of simpler carbs and sugars. Compared to the whole fruit with its fiber, fruit juices don’t make the cut. Limit desserts to a few times a week, dump sodas and other concentrated sugars, and focus on whole foods.

References

Adekola K, Rosen ST, Shanmugam M.
Glucose transporters in cancer metabolism.
Curr Opin Oncol. 2012 Nov;24(6):650-4.

Airley RE, Mobasheri A.
Hypoxic regulation of glucose transport, anaerobic metabolism and angiogenesis in cancer: novel pathways and targets for anticancer therapeutics.
Chemotherapy. 2007;53(4):233-56.

Baron JA, Weiderpass E, Newcomb PA, Stampfer M, Titus-Ernstoff L, Egan KM, Greenberg ER.
Metabolic disorders and breast cancer risk (United States).
Cancer Causes Control. 2001 Dec;12(10):875-80.

Brown NS, Bicknell R.
Thymidine phosphorylase, 2-deoxy-D-ribose and angiogenesis.
Biochem J. 1998 Aug 15;334 ( Pt 1):1-8.

Burley VJ.
Sugar consumption and human cancer in sites other than the digestive tract.
Eur J Cancer Prev. 1998 Aug;7(4):253-77.

Chocarro-Calvo A, García-Martínez JM, Ardila-González S, De la Vieja A, García-Jiménez C.
Glucose-Induced β-Catenin Acetylation Enhances Wnt Signaling in Cancer.
Mol Cell. 2012 Dec 26. pii: S1097-2765(12)00979-3.

Kathleen A. Cooney, MD; Stephen B. Gruber, MD, PhD, MPH
Hyperglycemia, Obesity, and Cancer Risks on the Horizon
JAMA. 2005;293(2):235-236.

Dell’ Antone P.
Energy metabolism in cancer cells: how to explain the Warburg and Crabtree effects?
Med Hypotheses. 2012 Sep;79(3):388-92.

De Stefani E, Deneo-Pellegrini H, Mendilaharsu M, Ronco A, Carzoglio JC.
Dietary sugar and lung cancer: a case-control study in Uruguay.
Nutr Cancer. 1998;31(2):132-7.

Duggan C, Wang CY, Neuhouser ML, Xiao L, Smith AW, Reding KW, Baumgartner RN, Baumgartner KB, Bernstein L, Ballard-Barbash R, McTiernan A.
Associations of insulin-like growth factor and insulin-like growth factor binding protein-3 with mortality in women with breast cancer.
Int J Cancer. 2013 Mar 1;132(5):1191-200.

Katherine M. Flegal, PhD; Brian K. Kit, MD; Heather Orpana, PhD; Barry I. Graubard, PhD
Association of All-Cause Mortality With Overweight and Obesity Using Standard Body Mass Index CategoriesA Systematic Review and Meta-analysis
JAMA. 2013;309(1):71-82.

Galeone C, Pelucchi C, La Vecchia C.
Added sugar, glycemic index and load in colon cancer risk.
Curr Opin Clin Nutr Metab Care. 2012 Jul;15(4):368-73.

Goodwin PJ, Ennis M, Pritchard KI, Trudeau ME, Koo J, Madarnas Y, Hartwick W, Hoffman B, Hood N.
Fasting insulin and outcome in early-stage breast cancer: results of a prospective cohort study.
J Clin Oncol. 2002 Jan 1;20(1):42-51.

Sun Ha Jee, PhD, MHS; Heechoul Ohrr, MD, PhD; Jae Woong Sull, PhD, MHS; Ji Eun Yun, MPH; Min Ji, MPH; Jonathan M. Samet, MD, MS
Fasting Serum Glucose Level and Cancer Risk in Korean Men and Women
JAMA. 2005;293(2):194-202.

Jóźwiak P, Lipińska A.
The role of glucose transporter 1 (GLUT1) in the diagnosis and therapy of tumors
Postepy Hig Med Dosw (Online). 2012 Jan 4;66:165-74.

La Vecchia C.
Mediterranean diet and cancer.
Public Health Nutr. 2004 Oct;7(7):965-8.

Lof M, Weiderpass E
Impact of diet on breast cancer risk.
Curr Opin Obstet Gynecol. 2009 Feb;21(1):80-5.

Merchan JR, Kovács K, Railsback JW, Kurtoglu M, Jing Y, Piña Y, Gao N, Murray TG, Lehrman MA, Lampidis TJ.
Antiangiogenic activity of 2-deoxy-D-glucose.
PLoS One. 2010 Oct 27;5(10):e13699.

Moerman CJ, Bueno de Mesquita HB, Runia S.
Dietary sugar intake in the aetiology of biliary tract cancer.
Int J Epidemiol. 1993 Apr;22(2):207-14.

Sakanaka C, Sun TQ, Williams LT.
New steps in the Wnt/beta-catenin signal transduction pathway.
Recent Prog Horm Res. 2000;55:225-36.

Sandulache VC, Ow TJ, Pickering CR, Frederick MJ, Zhou G, Fokt I, Davis-Malesevich M, Priebe W, Myers JN.
Glucose, not glutamine, is the dominant energy source required for proliferation and survival of head and neck squamous carcinoma cells.
Cancer. 2011 Jul 1;117(13):2926-38.

Schernhammer ES, Hu FB, Giovannucci E, Michaud DS, Colditz GA, Stampfer MJ, Fuchs CS.
Sugar-sweetened soft drink consumption and risk of pancreatic cancer in two prospective cohorts.
Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2098-105.

Seely S, Horrobin DF.
Diet and breast cancer: the possible connection with sugar consumption.
Med Hypotheses. 1983 Jul;11(3):319-27.

Tuyns AJ, Kaaks R, Haelterman M, Riboli E.
Diet and gastric cancer. A case-control study in Belgium.
Int J Cancer. 1992 Apr 22;51(1):1-6.

Wang X, Goode EL, Fredericksen ZS, Vierkant RA, Pankratz VS, Liu-Mares W, Rider DN, Vachon CM, Cerhan JR, Olson JE, Couch FJ.
Association of genetic variation in genes implicated in the beta-catenin destruction complex with risk of breast cancer.

Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):2101-8.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Print Friendly, PDF & Email