Over 20 million people in the United States have type 2 diabetes, and that figure doesn’t even count the 6 million who have diabetes and don’t know it yet.  Type 2 diabetes has been called the most challenging health problem of the 21st century. The dangerously high prevalence of overweight and obesity is at the heart of this problem.  Diabetes is the 7th leading cause of death in the United States, is the leading cause of blindness and kidney failure in adults, and doubles the risk of heart attack and stroke.[1] 

Diabetes also increases the risk of several cancers, including colorectal cancer.

In a number of studies, diabetic patients have been shown to have an elevated risk of colorectal cancer and non-diabetics with elevated postprandial glucose levels also have a higher risk of colorectal cancer than individuals with normal glucose tolerance.[2]   A new review that analyzed data from several studies found that diabetic patients are 30% more likely to develop colorectal cancer, 20% more likely to develop breast cancer, and 82% more likely to develop pancreatic cancer.[3]  Diabetes not only increases the risk of being diagnosed with cancer, but also increases the risk of dying from cancer – specifically for colorectal cancer, mortality risk is 26% greater in diabetic patients.[4]

How could diabetes influence carcinogenesis?  The hyperglycemia and hyperinsulinemia associated with type 2 diabetes affect all tissues of the body.  It has been hypothesized that these factors contribute to cancer initiation and progression, and that diets high in simple sugars and white flour increase the risk of cancers because of their impact on these factors. 

Scientists believe that insulin therapy and elevated insulin levels contribute to the association between diabetes and colorectal cancer.  Insulin in high concentrations may bind to the receptor for a growth factor called insulin-like growth factor 1 (IGF-1) – this interaction has the potential to promote growth and division of cancer cells. Cancerous cells also often have elevated levels of insulin receptors, and when insulin binds these receptors it has growth-promoting effects.[4]

There is much evidence supporting the possibility that chronic exposure to diets rich in rapidly assimilated carbohydrates may act directly as a promoter of colorectal carcinogenesis.  Foods with a high glycemic load (GL) produce dangerous spikes in blood glucose, consequently resulting in hyperinsulinemia – these include white bread, sugar, and white potatoes.  Diets including large quantities of high GL foods increase the risk of several chronic diseases, including colorectal cancers.[5]  A recent meta-analysis found a 26% increase in colorectal cancer risk in people who consumed the most high glycemic load foods in their diets.[6] 

Obesity contributes to insulin resistance, amplifying the hyperglycemia and hyperinsulinemia brought on by high GL foods.  Obesity also promotes chronic inflammation, another factor that is implicated in the development of colorectal cancer.[7]
 
In my medical practice, we have documented with consective case histories that  superior nutrition and exercise can reverse diabetes in 90% of patients, and this aggressive nutritional approach is more effective and  much safer than conventional drug-centered care.  The best diet for preventing or reversing diabetes is also the best diet for cancer protection.  It is a diet with a high nutrient per calorie ratio – including lots of green and non-starchy vegetables, beans, raw nuts and seeds, and some fresh fruit; limiting animal products; and avoiding sweeteners, oils and white flour.

Following this diet-style allows diabetics to lose their excess weight quickly and eliminate their need for medications to regulate their blood glucose.  The high levels of dietary micronutrients fuel cell repair enhancing pancreatic function and gradually reduce and remove high blood pressure, lowering cholesterol and heart disease risk. Now we know that maintaining a healthy weight and avoiding the dangerous increases in blood glucose and insulin that go along with diabetes will also help to reduce the risk of colorectal cancer.

For more information on nutritional excellence visit Dr. Fuhrman’s website.

[1] American Diabetes Association: Diabetes statistics http://www.diabetes.org/diabetes-basics/diabetes-statistics/
[2] Scharlau D, Borowicki A, Habermann N, et al. Mechanisms of primary cancer prevention by butyrate and other products formed during gut flora-mediated fermentation of dietary fibre. Mutat Res. 2009 Jul-Aug;682(1):39-53.
Bordonaro M, Lazarova DL, Sartorelli AC. Butyrate and Wnt signaling: a
possible solution to the puzzle of dietary fiber and colon cancer risk? Cell
Cycle. 2008 May 1;7(9):1178-83.
Pisani P. Hyper-insulinaemia and cancer, meta-analyses of epidemiological
studies. Arch Physiol Biochem. 2008 Feb;114(1):63-70.
La Vecchia C, D"Avanzo B, Negri E, Franceschi S. History of selected diseases and the risk of colorectal cancer. Eur J Cancer 1991; 27: 582-6. Schoen RE, Tangen CM, Kuller LH, et al. Increased blood glucose and insulin, body size, and incident colorectal cancer. J Natl Cancer Inst 1999; 91: 1147-54.
[3] Eurekalert: Experts call for further research into the relationship between insulin therapy and cancer
http://www.eurekalert.org/pub_releases/2010-03/w-ecf030210.php
Pollak M, Russell-Jones D. Insulin analogues and cancer risk: cause for concern or cause célèbre? Int J Clin Pract. 2010 Feb 26. [Epub ahead of print]
[4] Vigneri P, Frasca F, Sciacca L, Pandini G, Vigneri R. Diabetes and cancer. Endocr Relat Cancer. 2009 Dec;16(4):1103-23.
[5] Barclay AW, Petocz P, McMillan-Price J, et al. Glycemic index, glycemic load, and chronic disease risk--a meta-analysis of observational studies. Am J Clin Nutr. 2008 Mar;87(3):627-37.
[6] Gnagnarella P, Gandini S, La Vecchia C, Maisonneuve P. Glycemic index, glycemic load, and cancer risk: a meta-analysis. Am J Clin Nutr. 2008 Jun;87(6):1793-801.
[7] Siegel EM, Ulrich CM, Poole EM, et al. The effects of obesity and obesity-related conditions on colorectal cancer prognosis. Cancer Control. 2010 Jan;17(1):52-7.