As I have said time and time again over the years.. more and more diseases will be linked to high blood glucose levels. The Western Diet is awash in high sugar and starchy carbs which raise blood glucose efficiently and rapidly. This is article refreshing because it takes the sights off of animal protein and animal fats for the first time in the onset and progression of colorectal cancer. Those who avoid animal proteins and fats think they are doing the right thing thanks to books like the China Study and balderdash movies like Forks Over Knives. More and more of these will be proven wrong assumptions and more linkages to chronic disease and unchecked blood sugar levels will become elucidated. I have a dream that one day animal protein will not be blamed for disease.. but instead.. embraced for its health benefits.. when it is derived from animals eating genetically correct natural diets.- Carl

BRONX, NY -- Elevated blood sugar levels are associated with an increased risk of colorectal cancer, according to a study led by researchers at Albert Einstein College of Medicine of Yeshiva University. The findings, observed in nearly 5,000 postmenopausal women, appear in the Nov. 29 online edition of the British Journal of Cancer.

According to the American Cancer Society, colorectal cancer is the third most commonly diagnosed cancer and the third leading cause of cancer death in both men and women in the U.S.

Statistics compiled by the U.S. Centers for Disease Control and Prevention for 2007 (the most recent year for which figures are available) show that 142,672 Americans were diagnosed with colorectal cancer, including 69,917 women; the 53,219 deaths from colorectal cancer that year were divided almost equally between men and women.

The Einstein study involved women who were enrolled in the National Institutes of Health's landmark Women's Health Initiative study. For these women, fasting blood sugar and insulin levels had been measured at baseline (i.e., the start of the study) and then several more times over the next 12 years.

By the end of the 12-year period, 81 of the women had developed colorectal cancer. The researchers found that elevated baseline glucose levels were associated with increased colorectal cancer risk—and that women in the highest third of baseline glucose levels were nearly twice as likely to have developed colorectal cancer as women in the lowest third of blood glucose levels. Results were similar when the scientists looked at repeated glucose measurements over time. No association was found between insulin levels and risk for colorectal cancer.

Obesity—usually accompanied by elevated blood levels of insulin and glucose—is a known risk factor for colorectal cancer. Researchers have long suspected that obesity's influence on colorectal cancer risk stems from the elevated insulin levels it causes. But the Einstein study suggests that obesity's impact on this cancer may be due to elevated glucose levels, or to some factor correlated with elevated glucose levels.

"The next challenge is to find the mechanism by which chronically elevated blood glucose levels may lead to colorectal cancer," said Geoffrey Kabat, Ph.D., a senior epidemiologist at Einstein and lead author of the paper. “It’s possible that elevated glucose levels are linked to increased blood levels of growth factors and inflammatory factors that spur the growth of intestinal polyps, some of which later develop into cancer.”

In many cases, tumors suppress a patient's immune system in a way that keeps the cancer safe from immune system attack. This is particularly true for patients with glioblastoma, a primary brain tumor that carries a prognosis of only 12-15 months survival after diagnosis.

A study at the University of Colorado Cancer Center, recently published as a featured article in the journal Clinical Cancer Research, shows that treatment with the over-the-counter amino acid arginine may reactivate cancer-fighting T-cells in patients with glioblastoma, thus potentially allowing the immune system to help cleanse the body of cancer.

T-cells are the primary agent responsible for anti-tumor immune responses.

"If you take T-cells from patients with glioblastoma and stimulate them in the lab, they aren't effective (in killing cancer cells)," says lead author Allen Waziri, MD, investigator at the CU Cancer Center, assistant professor of neurosurgery at the University of Colorado School of Medicine. "But when we add back arginine, we restore T-cell function."

In part, function is restored through the activity of neutrophils – an ancient and nonspecific type of white blood cell that kills invaders. After responding to inflammation, neutrophils stop the ongoing immune response. It's as if once they arrive, they consider the infection treated and so suppress any response that exceeds what is needed – a response that if left unchecked would lead to the destruction of healthy tissues.

Neutrophils stop the immune response by secreting an enzyme called arginase. And after they secrete arginase, commonly they die and are excreted by the body. However, in many glioblastoma patients, these neutrophils persist and continue to produce immune-suppressing arginase.

"Persistence of activated neutrophils and increased arginase in the circulation of glioblastoma patients is a fascinating phenomenon, particularly considering that under normal conditions, neutrophils are expected to have an average lifespan of just several hours after activation," he says.

Waziri's group has hypothesized that persistent arginase production from neutrophils suppresses the immune system and keeps cancers from becoming immune targets.

"From one perspective, it appears that glioblastoma is taking advantage of a simple, evolutionarily-ancient method for controlling out-of-control immunity to avoid the specific anti-tumor immune response," Waziri says.

However, there is a step between increased arginase and immune system suppression, and this is where Waziri and colleagues intervene – arginase, in fact, deletes the common amino acid arginine.

T-cells are critically dependent on arginine for activation and function. Therefore, it's not the increase in arginase per se that is responsible for blunting T-cell activity, but rather the resulting lack of arginine that suppresses the immune systems of glioblastoma patients, Waziri's group found.

Waziri and colleagues at the CU Cancer Center recently started a phase 0 clinical trial in newly diagnosed glioblastoma patients to explore whether a week-long, high-dose course of arginine before cancer surgery can allow an immune system that previously missed cancer cells to recognize and attack them. Waziri and his team will look at the effect of arginine on patients' immune systems as measured by T-cell function, immunological profile, and T-cell infiltration into resected tumor tissue.

"Our overall goal is to improve the efficacy of immunotherapy for glioblastoma," he says. "It's likely that this will require a two-stage approach, including stimulation of the immune system with something like a tumor vaccine while simultaneously targeting the suppressive effects of tumors on the immune system."

With positive results from this initial trial, Waziri hopes to further explore whether longer courses of arginine could help reduce the recurrence of glioblastoma and potentially offer a new strategy for patients with this otherwise incurable disease.

Waziri credits seed grants he has received from the AMC Cancer Fund (a fundraising arm of the CU Cancer Center), he Cancer League of Colorado, and an American Cancer Society Institutional Research Grant for contributing to the preclinical work that has led to this exciting clinical trial.