Lowering Insulin Inhibits Cancer Growth

Sharon Dominick / Getty Images
Sharon Dominick / Getty Images. Sharon Dominick / Getty Images

It is generally understood that diabetes is a disease of insulin deficiency. Until now, it has not been widely recognized that insulin is high-octane fuel for cancer growth. The connection between high insulin blood levels and cancer growth was first brought to my attention by patients who adopted strict diets as a means for treating their cancer. Patients who began a macrobiotic regime would rapidly lose weight within a few months.

Over that same period, PSA levels would also drop, an encouraging sign that cancer might be held in check.

Macrobiotic diets are not new. In the 1920s, Yukikazu Sakurazawa came to Paris from Japan. He took the name “George Ohsawa,” calling his teaching “macrobiotics.” Ohsawa’s teaching was brought to the United States by Michio Kushi in 1949. The basis of this philosophy was a belief that returning to the diet common in agrarian cultures throughout most of human history could prevent and counteract disease.

There are many variations on the diet. The “healing version” of the diet is tailored specifically for cancer patients and is particularly restrictive, consisting mainly of whole grains and vegetables. Staples include Miso soup, brown rice, lentils, and “sea vegetables” like nori and kelp. Strictly forbidden are sugars, fats, meats, dairy, oils (with some allowance for cooking), and even most fruits.

Processed foods like breads and pasta are also rigorously avoided.

Clearly, this diet is not for the faint of heart. Moreover, proponents believe that the healing process is enhanced by each individual’s involvement in preparing their own food—the antithesis of our pre-packaged, microwave culture. The macrobiotic preference is always for food that is in season and locally grown.

The time for food gathering and preparation can be very demanding.

Medical support is growing for the use of diet to counteract prostate cancer. Dr. Dean Ornish, of cardiac diet fame, in the September 2005 issue of The Journal of Urology, published a study using an intensive dietary program consisting of a vegan diet (vegetarian, non-dairy). He also encouraged aerobic exercise and stress management techniques. He studied 93 men, half of whom were randomly allocated to the Ornish program. The remainder served as a non-treated comparison group. After 12 months, the treated men had achieved a statistically significant reduction in their PSA levels.

When Ornish did additional laboratory studies using the blood of his participants, the results were fairly dramatic. Blood serum from the men in both groups was “fed” to prostate cancer cells lines kept alive in Petri dishes. The cells that were fed serum from men who were not on the Ornish program grew 8 times faster than those cells receiving serum from men in the treatment group.

Ground breaking as these results are, Ornish’s article did not offer any theory as to why his program worked. A review of laboratory findings in patients in our medical practice, however, might provide a clue concerning the underlying mechanism that makes dietary intervention so effective. Men on macrobiotic diets run blood sugar levels in the 70’s, even though they had not been fasting. Blood sugars in most people, when checked after a meal, typically run in the 120 to 150 range. It is logical to conclude that there may be a connection between low blood sugar levels and retarded cancer growth. Cancer cells are particularly greedy for sugar. Sugar (glucose) is like gasoline, fueling all the cells.

All this would seem to indicate that blood sugar levels are the driving force in cancer growth. But it fails to explain the fact that diabetics--men with chronically high blood sugar—have less prostate cancer than normal men. Why?  Because diabetes is a disease of low insulin levels. We know that sugar in the blood is unable to enter the cells without the aid of insulin. Insulin is manufactured and stored in the pancreas until released into the blood in response to high glucose levels. As blood sugar levels rise, insulin release accelerates, and the cancer receives more of the energy it needs.

It may be that the connection between diet and cancer, therefore, hinges only indirectly on blood sugar levels. It is not high blood sugar per se, but rather the high level of insulin, triggered by high blood sugars, that simulates rapid cancer growth. There are several reasons why this makes sense. Insulin is one of the most potent growth hormones in the body. Several studies have already reported a connection between high insulin levels and prostate cancer. Two of these studies demonstrate that high insulin levels, or a high sugar diet (which causes high insulin levels), are connected with a higher incidence of prostate cancer. A third study has reported that increased insulin levels are associated with the development of more aggressive prostate cancer.

The real question then is how to best control and suppress insulin. Diet is certainly important. The dietary model for controlling insulin already exists, worked out many years ago for diabetics, in what is termed a low-glycemic index diet. A diabetic type of diet is likely to be beneficial. Studies have also shown anticancer effects with metformin, a generic medication that has been on the market for decades.

There are a number of studies confirming that being overweight and overeating contribute significantly to increased incidence and aggressiveness of prostate cancer. However, it appears that insulin may be a central driving force for cancer growth. Substantial research is being supported by pharmaceutical companies for further investigation into drugs that suppress insulin.

Sources

Kushi, Michio and Jack, Alex. The Cancer Prevention Diet:  Michio Kushi’s Macrobiotic Blueprint for the Prevention and Relief of Disease.  St. Martin’s Griffin, 1994.

Verne Varona Nature’s Cancer Fighting Foods: Prevent and Reverse the Most Common Forms of Cancer Using the Proven Power of Great Food and Easy Recipes. Reward Books, 2001.

Ornish, Dean et al: Intensive lifestyle changes may affect the progression of prostate cancerThe Journal of Urology Vol. 174:1065, 2005.

Rodriguez, Carmen et al: Diabetes and risk of prostate cancer in a prospective cohort of US men. American Journal of Epidemiology Vol. 161:147, 2005.

Hsing, Ann et al: Prostate cancer risk and serum levels of insulin and leptin: a population-based study.  Journal of the National Cancer Institute. Vol. 93:783, 2001.

Augustin, Livia et al: Glycemic index, glycemic load and risk of prostate cancer. Journal of Cancer Vol. 112:446, 2004.

Lehrer, S. et al: Serum insulin level, disease stage, prostate specific antigen (PSA) and Gleason score in prostate cancer. British Journal of Cancer Vol. 87:726, 2002. 

Freedland, Stephen et al: Body mass index as a predictor of prostate cancer: development versus detection on biopsyUrology Vol. 66:108, 2005.

Hsieh, Lillian et al: Association of energy intake with prostate cancer in a long-term aging study: Baltimore longitudinal study of aging (United States). Urology Vol. 61:297, 2003.

Freedland, Stephen et al: Obesity and risk of biochemical progression following radical prostatectomy at a tertiary care referral center. The Journal of Urology Vol. 174:919, 2005. 

Amling, Christopher et al: Pathologic variables and recurrence rates as related to obestity and race in men with prostate cancer undergoing radical prostatectomy. Journal of Clinical Oncology Vol. 22:439, 2004.

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