Sugar and Cancer
Contrary to rumors, sugar does not make cancer grow more quickly. All cells, including cancer cells, do depend on glucose for energy. Providing more sugar will not cause an increased rate of growth, and sugar deprivation will not slow the growth of cancer cells. Even if you abstain from eating carbohydrates, your body will make glucose from protein and fat. However, sugar can contribute excess calories to the diet, resulting in obesity. Obesity is linked to several types of cancer, so an indirect relationship may exist between excess sugar consumption and certain cancers.
Dietary sugar vs blood glucose
Researchers have had to use caution in making a distinction between dietary sugar and blood glucose when describing study results. Scientists at the Johns Hopkins Kimmel Cancer Center found that starving colon cancer cells of blood glucose may pave the way for possible treatment options in the future, but they caution that altering dietary intake of sugar is unlikely to have any impact.
Colorectal cancer cell lines that carry two of the most common cancer genes were studied, and it was discovered that one gene, glucose transporter type 1 (GLUT1), was consistently turned on at high levels in cells that had the common cancer genes. Proteins made by GLUT1, located on the surface of the cell, transport glucose inside of the cell. Increased expression of GLUT1 causes an increase in glucose ingestion. This led to the testing of an investigational drug, bromopyruvate, which inhibits glucose metabolism. The drug blocked cancer growth in mice with implant human tumors containing the two most common cancer genes and had no toxic side effects on the mice.
Glucose and glutamine
During both normal and cancerous cell growth, a cellular process takes place that involves both glucose (sugar) and glutamine (an amino acid). A study done at the Huntsman Cancer Institute found that by restricting glutamine availability, glucose utilization is halted. This means that, hypothetically, if you do not have glutamine, this will stop the growth of the tumor cell.
Researchers at Johns Hopkins have found that lymph gland cancer cells can use glutamine in the absence of glucose for cell replication and survival, especially in low-oxygen conditions. Low-oxygen conditions are common in tumors. This study showed that inhibiting glutaminase, a glutamine enzyme, can curb the growth of these lymph gland cancer cells. Use of the glutaminase inhibitor in petri dishes stopped the cancerous growth of the lymph gland cancer cells.
It is possible that impaired glucose metabolism might play a role in pancreatic cancer. A diet with a high glycemic load may increase risk in women who have insulin resistance. In a meta-analysis of epidemiological studies, diabetes that was diagnosed at least 5 years prior to cancer detection was associated with a twofold increase in risk of pancreatic cancer. Overweight is a well-known risk factor for pancreatic cancer. When researchers looked at eligible women from the Nurses’ Health Study, those with the highest dietary glycemic load had a 53% increase in pancreatic cancer risk, and those who had a high fructose intake had a 57% increase in risk.
However, these associations were not statistically significant. The associations were stronger among women who were overweight or sedentary.
No statistically significant correlation between dietary glycemic load, glycemic index, and fructose intake and the risk of pancreatic cancer was found among lean and physically active women. The study supported the hypothesis that abnormal glucose metabolism and states of relative hyperinsulinemia enhance pancreatic carcinogenesis, even though the overall association between glycemic load and pancreatic cancer risk failed to achieve statistical significance. The authors pointed out that fructose may relate to pancreatic cancer in other ways. Fructose was shown to contribute directly to oxidative stress in hamster islet tumor cells in another study.
Other epidemiological studies looking at carbohydrate consumption and pancreatic cancer have had mixed results. However, plenty of evidence shows that insulin and insulin resistance play a role in pancreatic cancer development in animals and humans. Metformin has inhibited pancreatic cancer in a hamster pancreatic adenocarcinoma model. In a study published in Cancer Epidemiology, Biomarkers & Prevention in September 2005, research found that consumption of sugar-sweetened soft drinks were associated with a modest, significant increase in risk of pancreatic cancer among women with underlying insulin resistance, but not among men.
A flawed study?
A study done in Sweden did show that both men and women with the highest blood glucose levels were more likely to have pancreatic cancer, urinary tract cancer, and malignant melanoma, compared to those with the lowest blood glucose levels. Nearly 64,600 people in northern Sweden participated in the study. All were nonsmokers without diabetes and were 40, 50, or 60 years old when they enrolled in the study. At the time of enrollment, the participants took a blood test after fasting and then took another after drinking a sugary drink.
At least 85% of the participants had normal blood glucose after fasting, and at least 92% had normal blood glucose after consuming the drink. The participants were followed for an average of 8 years. Women with the highest blood glucose levels when entering the study were more likely to receive a cancer diagnosis before the study was completed, and endometrial cancer was more common in women with the highest blood glucose levels, when compared to the women with the lowest blood glucose levels. Breast cancer was more common in women younger than 49 years who had high blood glucose. Other factors, such as weight and age, were considered. Diet, exercise, and family history were not considered, nor were blood glucose levels checked throughout the duration of the study.
References and recommended readings
Johns Hopkins Medicine Colorectal Cancer. Colon cancer may yield to cellular sugar starvation. Available at: http://www.hopkinscoloncancercenter.org/CMS/CMS_Page.aspx?CurrentUDV=59&CMS_Page_ID=C8DC0DE7-2E1D-4D23-A958-9D98C365F06A. Accessed April 9, 2012.
Kushi LH, Doyle C, McCullough M, et al; American Cancer Society 2010 Nutrition and Physical Activity Guidelines Advisory Committee. American Cancer Society Guidelines on nutrition and physical activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA Cancer J Clin [serial online]. 2012;62:30-67. Available at: http://onlinelibrary.wiley.com/doi/10.3322/caac.20140/full. Accessed April 9, 2012.
Mayo Clinic. Cancer causes: popular myths about the causes of cancer. Available at: http://www.mayoclinic.com/health/cancer-causes/CA00085. Accessed April 9, 2012.
Michaud DS, Liu S, Giovannucci E, Willett WC, Colditz GA, Fuchs CS. Dietary sugar, glycemic load, and pancreatic cancer risk in a prospective study. J Natl Cancer Inst [serial online]. 2002;94:1293-1300. Available at: http://jnci.oxfordjournals.org/content/94/17/1293.full. Accessed April 9, 2012.
Schernhammer ES, Hu FB, Giovannucci E, et al. Sugar-sweetened soft drink consumption and risk of pancreatic cancer in two prospective cohorts. Cancer Epidemiol Biomarkers Prev [serial online]. 2005;14:2098-2105. Available at: http://cebp.aacrjournals.org/content/14/9/2098.full. Accessed April 9, 2012.
ScienceDaily®. Cancer cells feed on sugar-free diet. Available at: http://www.sciencedaily.com/releases/2012/01/120110101824.htm. Accessed April 9, 2012.
ScienceDaily. Does sugar feed cancer? Available at: http://www.sciencedaily.com/releases/2009/08/090817184539.htm. Accessed March 11, 2012.
Review Date 4/12