While more and more clinicians appreciate the role of sugar in promoting insulin resistance, obesity, and heart disease, a much smaller number of these individuals would attribute any blame to its role in cancer.  Yet, epidemiological evidence suggests otherwise.  The data clearly indicates that dietary sugar and refined carbohydrates are significant risk factors for a variety of cancers (1-3.).

Under normal conditions, even with an abundance of glucose, healthy cells turn to glycolysis (the process of burning sugar for fuel) with at least somewhat limited contributions to internal energy needs.  Sometimes, when oxygen supply is limited, as in the case with high intensity or anaerobic exercise, the low oxygen limitations force healthy cells away from normal aerobic or mitochondrial respiration (which uses predominantly fat as fuel) to glycolysis.  However, in almost all types of cancer there is a unique glucose dependency for cellular growth and tumor development. Cancer cells have an incredible appetite.  While amino acids are both generated endogenously and consumed for various aspects of cancer cell metabolism, glucose is the primary fuel in a glycolytic pathway that never turns off.

This biochemical characteristic of cancer cells has led many of the leading cancer researchers to the assumption that cancer is more of a mitochondrial disease than a genetic mutation gone awry somewhere along the way. This concept is not new but has only recently been more appreciated.  Warburg first observed the unique sugar metabolism of cancer cells and so this glycolytic dominant source of energy was dubbed the Warburg Effect (4.). 

Subsequent studies demonstrated other unique abnormalities in the preference for sugar shuttling into cancer cells and for the enzymes that catalyze critical glycolytic pathways (5,6.).  Essentially, the wheels for sugar metabolism are more than greased in cancer cells, they are stacked so much in favor of consuming glucose that other fuel sources (fat and ketones) cannot be used.  This is one reason why research has consistently shown significant benefits to cancer patients when carbohydrate restriction has been applied (7.).

If an abundance of scientifically accepted investigations acknowledge that sugar consumption is both a risk factor for many forms of cancer and is also exclusively required metabolically, for the growth and metastasis of cancer, then why are we feeding it to cancer patients? Why would anyone recommend any sweetener or sweetened food for an individual with cancer?  While it may be likely that anything less than a full ketogenic diet will not completely stop a particular form of cancer from growing, it is equally likely that adding sugar to a cancer patient’s diet will only accelerate the cancer growth.  Less sugar imposes at least a partial limit on glycolysis in cancer cells and more sugar provides no limits.

Do you believe or have you been told that all sugars are the same? This could not be further from the truth and some sources of sugar may be worse than others when it comes to cancer metabolism.  One of the better interviews we can read is here:

Lewis C. Cantley PhD, Director of The Weill-Cornell Medical College’s Cancer Center, shares his career findings around fructose, altered sugar metabolism, and cancer cells.

A leading expert in cancer metabolism, Cantley’s work, in conjunction with that of others, has revealed the ability of fructose to accelerate the cancer cells use of sugar as a fuel (8.).

In summary, we are not talking about a cure for cancer but rather applying whatever metabolic restrictions we can through the use of more appropriate dietary recommendations or an enteral formula based on these principals. 

 ~ John Bagnulo MPH, PhD. - Director of Nutrition




1.Nothlings U et al. Dietary glycemic load, added sugars, and carbohydrates as risk factors for pancreatic cancer: the Multiethnic Cohort Study. Am J Clin Nutr November 2007 
vol. 86 no. 5 1495-1501

2.Lajous M et al. Carbohydrate intake, glycemic index, glycemic load, and risk of postmenopausal breast cancer in a prospective study of French women. Am J Clin Nutr. 2008 May;87(5):1384-91.

3. Hochwald JS and Zhang J Glucose Oncometabolism of Esophageal Cancer. Anticancer Agents Med Chem. 2016 Jun 26. [Epub ahead of print]

4. Atlante A et al. A disease with a sweet tooth: exploring the Warburg effect in Alzheimer's disease.Biogerontology. 2017 Jun;18(3):301-319. doi: 10.1007/s10522-017-9692-x. Epub 2017 Mar 17.

5. Patra KC, Hay N. The pentose phosphate pathway and cancer. Trends in biochemical sciences. 2014;39(8):347-354. doi:10.1016/j.tibs.2014.06.005.

6. Bobba A et al. Glycolytic enzyme upregulation and numbness of mitochondrial activity characterize the early phase of apoptosis in cerebellar granule cells. Apoptosis. 2015 Jan;20(1):10-28. doi: 10.1007/s10495-014-1049-1.

7. Khodadadi S, Sobhani N, Mirshekar S, et al. Tumor Cells Growth and Survival Time with the Ketogenic Diet in Animal Models: A Systematic Review. International Journal of Preventive Medicine. 2017;8:35. doi:10.4103/2008-7802.207035.

8. Cantley LC. The Phosphoinositide 3-Kinase Pathway Science  31 May 2002: Vol. 296, Issue 5573, pp. 1655-1657