Can Diet Really Control Prostate Cancer?

Mark Scholz, MD and Ralph Blum
Reprinted from PCRI Insights February 2006 vol. 9, no. 1

In December 2001 Thomas Mueller, a Los Angeles attorney, learned he had prostate cancer (PC). Thomas’s disease was the contained variety of PC, but at age 45 and newly married, he was alarmed to learn that the common treatments, surgery and radiation, frequently cause impotence. “I couldn’t take that risk,” he said, “I had to find another way.”

Thomas Mueller is of medium height and slight build, with close-cropped, wavy blond hair. He is soft-spoken, yet intense, with a self deprecating, wry sense of humor. An intelligent, disciplined researcher, he quickly became knowledgeable about PC. There was another problem, however, a close call with melanoma when he was still in his 20s. Having had two cancers by age 45 convinced him that a change in lifestyle was necessary. With the guidance of his wife, he decided to embark on a rigorous program of diet and exercise as his principal mode of therapy.

Just three months after Thomas began his macrobiotic regime; his weight plummeted from 157 lbs., down to 122. At that point, he was beyond lean. He was also exercising intensely, including running a marathon. “At the end of that ordeal, he reported, “I was so hypoglycemic that I was hallucinating. I definitely don’t recommend marathons on such a stringent diet.” Over that same time period, his PSA dropped from 4.0 down to 1.5 ng/ml, an encouraging sign that his cancer was being held in check.

Reliance on a macrobiotic diet and lifestyle as a form of treatment is 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 Mishio Kushi in 1949.1,2 These teachings espoused a belief that returning to the diet used in agrarian cultures throughout most of human history could prevent and counteract disease.

Thomas’s “healing version” of the diet, tailored specifically for cancer patients, was 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 all 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 Thomas’s diet is not for the faint of heart. Moreover, he believes that the healing process is enhanced by preparing his own food – the antithesis of our pre-packaged, microwave culture. What’s more, the macrobiotic preference is always for food that is in season and locally grown. “The time for food gathering and preparation was so demanding,” he reports, “that I resigned from my law firm and committed all my energy to healing myself.”

There is now growing medical evidence for the effectiveness of diet in counteracting PC. Dr. Dean Ornish, of cardiac diet fame, has now moved boldly into the arena of diet therapy for treating PC. In the September 2005 issue of The Journal of Urology, Ornish published a study testing the effectiveness of an intensive dietary and lifestyle program. The program consisted of a vegan diet (vegetarian, non-dairy diet), supplemented with antioxidants (such as lycopene, selenium and vitamin E), moderate aerobic exercise, and stress management techniques. Ornish studied 93 men who, like Thomas Mueller, had chosen not to undergo conventional invasive treatment for their PC. Half these men were randomly allocated to the Ornish program, while the remainder served as a non-treated comparison group. After 12 months, the PSA of the treated group of men decreased an average of 0.25 ng/ml or 4%,and the PSA of the non-treated group of men increased an average of 0.38 ng/ml or 6%.3

Ornish did additional laboratory studies using the blood of his participants, with dramatic results. Extracting serum from the men in both groups, he fed it to PC cells lines kept alive in Petri dishes. The cells that were fed serum from men not on the Ornish program grew eight times faster than those cells receiving serum from men in the treatment group.

The Impact of Suppressed Blood Sugar Levels
Ground breaking as these results are, Ornish’s article did not offer any theory as to why his program is working. A review of Thomas Mueller’s medical history however, provided a clue concerning the underlying mechanism that may explain why dietary intervention works. Whenever Thomas came into our office, even if it was right after breakfast, his serum blood sugar was in the 70s, which is unusually low. Blood sugars in most patients, when checked after breakfast, can run as high as 120-150. It seems logical that there is a direct connection between low blood sugar levels and retarded cancer growth.

We should not be surprised that suppressed blood sugar levels could have a major impact on cancer growth. First, sugar (glucose) is like gasoline, fueling all the cells in the body. Cancer cells divide rapidly and therefore are greedy for sugar, because it is necessary for their growth. This fact is dramatically illustrated by Positron Emission Tomography, or PET scan. The PET scan uses radioactive sugar injected into the bloodstream to locate tumors throughout the body. PET can so effectively pinpoint growing, active groups of PC, that with a matter of minutes, the areas of high sugar uptake can be clearly seen in the scan images (see Figure 1.)

Figure 1. PET Scan image using FDG (18Fludeoxyglucose) of a 63-year-old male with hypo-laryngeal (neck) cancer on the left. FDG provides a signal that the PET scanner detects (gold colored mass in the neck) in tissues that are using large amounts of glucose. The uptake of glucose seen in the heart and brain are normal. Image used with permission: http://www.gehealthcare.com/ usen/index.html

Cancer cells require dramatically more glucose to survive and proliferate than normal cells. This is because cancer cells run on a primitive energy metabolism called anaerobic glycolysis that burns sugar without oxygen.

Oxygen metabolism (aerobic glycolysis) allows the healthy cells of the body to extract many more molecules of energy from glucose than with anaerobic glycolysis. In other words, the cancer cell’s demand for glucose is enormous.

Insulin: The Connection Between Diet and PC
All this would seem to indicate blood sugar levels are the driving force in cancer growth. But this does not explain the fact that diabetics – men with chronically high blood sugar – have less prostate cancer than normal men.4 How can we explain this? 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 (see Figure 2).

Figure 2. Regulation of glucose in Type 1 Diabetes. Medical Illustration Copyright © 2006 Nucleus Medical Art, All rights reserved.www.nucleusinc.com (Illustration used with permission.)

The connection between diet and PC, therefore, appears to hinge 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 PC growth. There are several reasons why this makes sense. Insulin is one of the most potent growth hormones in the body. Several studies have reported a connection between insulin and PC. Two of these studies show that high insulin levels, or a high sugar diet (which causes high insulin levels), are connected with a higher incidence of PC.5,6 A third study has reported that increased insulin levels are associated with more high grade PC.7 All this reinforces our conclusion that it is insulin, and not glucose, that is driving PC.

How to Suppress Insulin Levels
With such compelling evidence that insulin suppression is vital, the real question is how to best control and suppress insulin. Diet is the only effective method for manipulating insulin levels. The dietary model for controlling insulin already exists, worked out many years ago for diabetics, in what is termed a low-glycemic index diet. The glycemic index (GI) is a ranking of the carbohydrates in different foods on a scale from 0 to 100 according to the extent to which they raise blood sugar levels after eating (see Tables 1 and 2 for the GI range and value for selected foods).8 High-glycemic index food results in higher and more rapid increases in blood glucose levels than the consumption of low-glycemic index food. Rapid increases in blood glucose are potent signals to the beta-cells of the pancreas to increase insulin secretion.9 In contrast, the consumption of low-glycemic food results in lower blood glucose and lower insulin demands on pancreatic beta cells.10 Thus, it is basically a low-glycemic index or a diabetic’s diet that will most benefit men with prostate cancer.

Thomas’ choice of a macrobiotic diet has been remarkably effective. A repeat prostate biopsy in late 2004 showed less extensive disease than when he was originally diagnosed, and his PSA has remained low and stable. Periodically, he has undergone both high-resolution prostate scanning with spectrographic endorectal MRI and color Doppler ultrasound. There has been no evidence of cancer progression.
Thomas’s decision to forgo radiation or surgery at such a young age may seem reckless to members of the medical establishment. But he offers the following rationale: “The pace of advancing medical technology encourages me to wait as long as possible before undergoing any treatment with potentially irreversible consequences. I expect less toxic treatment alternatives will eventually become available. It’s only a matter of time. In the last few years, I have already seen substantial advances – in the area of prostate imaging, for example. I plan to use my diet as my primary therapy as long as my cancer remains stable.”

Conclusion
There are a number of studies confirming that being overweight and overeating contribute significantly to increased incidence and aggressiveness of PC.11, 12,13,14

However, it appears that insulin may be the real culprit, an idea that has been poorly understood and has not received the attention it deserves. This failure has resulted in diverse theories and conflicting medical recommendations about the impact and efficacy of diet for PC patients. If medical professionals can agree that insulin-stimulating foods are taboo, we can begin working together to educate patients, speaking with one voice. 

Editor’s Note: Both the PCRI and the authors stress that the treatment described in this article should only be used under the direction of a physician.

References
1. 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.

2. 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.

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

4. 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.

5. 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.

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

7. 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.

8. Foster-Powell, K et al. International table of glycemic index
and glycemic load values. Am J Clin Nutr.76 (1): 5-56, 2002.

9. Ludwig, DS. The glycemic index: physiological mechanisms
relating to obesity, diabetes, and cardiovascular disease.
JAMA.287 (18): 2414-2423, 2002.

10.Willett,WC.Eat,Drink, and be Healthy: The Harvard Medical
School Guide to Healthy Eating. New York: Simon &
Schuster; 2001.

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

12. 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.

13. 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.

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

 

Prostate Cancer Research Institute (PCRI)

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