Cancer's Sweet Tooth

[Guest guest]

From The April 2000 Issue of Nutrition Science News Features

Cancer's Sweet Tooth by Patrick Quillin, PHD, RD, CNS

 

http://www.newhope.com/nutritionsciencenews/NSN_backs/Apr_00/cancer.cfm

 

During the last 10 years I have worked with more than 500 cancer patients as

director of nutrition for Cancer Treatment Centers of America in Tulsa, Okla. It

puzzles me why the simple concept " sugar feeds cancer " can be so dramatically

overlooked as part of a comprehensive cancer treatment plan.

Of the 4 million cancer patients being treated in America today, hardly any

are offered any scientifically guided nutrition therapy beyond being told to

" just eat good foods. " Most patients I work with arrive with a complete lack of

nutritional advice. I believe many cancer patients would have a major

improvement in their outcome if they controlled the supply of cancer's preferred

fuel, glucose. By slowing the cancer's growth, patients allow their immune

systems and medical debulking therapies—chemotherapy, radiation and surgery to

reduce the bulk of the tumor mass—to catch up to the disease. Controlling one's

blood-glucose levels through diet, supplements, exercise, meditation and

prescription drugs when necessary can be one of the most crucial components to a

cancer recovery program. The sound bite—sugar feeds cancer—is simple. The

explanation is a little more complex.

The 1931 Nobel laureate in medicine, German Otto Warburg, Ph.D., first

discovered that cancer cells have a fundamentally different energy metabolism

compared to healthy cells. The crux of his Nobel thesis was that malignant

tumors frequently exhibit an increase in anaerobic glycolysis—a process whereby

glucose is used as a fuel by cancer cells with lactic acid as an anaerobic

byproduct—compared to normal tissues.1 The large amount of lactic acid produced

by this fermentation of glucose from cancer cells is then transported to the

liver. This conversion of glucose to lactate generates a lower, more acidic pH

in cancerous tissues as well as overall physical fatigue from lactic acid

buildup.2,3 Thus, larger tumors tend to exhibit a more acidic pH.4

This inefficient pathway for energy metabolism yields only 2 moles of

adenosine triphosphate (ATP) energy per mole of glucose, compared to 38 moles of

ATP in the complete aerobic oxidation of glucose. By extracting only about 5

percent (2 vs. 38 moles of ATP) of the available energy in the food supply and

the body's calorie stores, the cancer is " wasting " energy, and the patient

becomes tired and undernourished. This vicious cycle increases body wasting.5 It

is one reason why 40 percent of cancer patients die from malnutrition, or

cachexia.6

Hence, cancer therapies should encompass regulating blood-glucose levels via

diet, supplements, non-oral solutions for cachectic patients who lose their

appetite, medication, exercise, gradual weight loss and stress reduction.

Professional guidance and patient self-discipline are crucial at this point in

the cancer process. The quest is not to eliminate sugars or carbohydrates from

the diet but rather to control blood glucose within a narrow range to help

starve the cancer and bolster immune function.

The glycemic index is a measure of how a given food affects blood-glucose

levels, with each food assigned a numbered rating. The lower the rating, the

slower the digestion and absorption process, which provides a healthier, more

gradual infusion of sugars into the bloodstream. Conversely, a high rating means

blood-glucose levels are increased quickly, which stimulates the pancreas to

secrete insulin to drop blood-sugar levels. This rapid fluctuation of

blood-sugar levels is unhealthy because of the stress it places on the body (see

glycemic index chart).

Sugar in the Body and Diet

Sugar is a generic term used to identify simple carbohydrates, which includes

monosaccharides such as fructose, glucose and galactose; and disaccharides such

as maltose and sucrose (white table sugar). Think of these sugars as

different-shaped bricks in a wall. When fructose is the primary monosaccharide

brick in the wall, the glycemic index registers as healthier, since this simple

sugar is slowly absorbed in the gut, then converted to glucose in the liver.

This makes for " time-release foods, " which offer a more gradual rise and fall in

blood-glucose levels. If glucose is the primary monosaccharide brick in the

wall, the glycemic index will be higher and less healthy for the individual. As

the brick wall is torn apart in digestion, the glucose is pumped across the

intestinal wall directly into the bloodstream, rapidly raising blood-glucose

levels. In other words, there is a " window of efficacy " for glucose in the

blood: levels too low make one feel lethargic and can create

clinical hypoglycemia; levels too high start creating the rippling effect of

diabetic health problems.

The 1997 American Diabetes Association blood-glucose standards consider 126 mg

glucose/dL blood or greater to be diabetic; 111 & shy;125 mg/dL is impaired

glucose tolerance and less than 110 mg/dL is considered normal. Meanwhile, the

Paleolithic diet of our ancestors, which consisted of lean meats, vegetables and

small amounts of whole grains, nuts, seeds and fruits, is estimated to have

generated blood glucose levels between 60 and 90 mg/dL.7 Obviously, today's

high-sugar diets are having unhealthy effects as far as blood-sugar is

concerned. Excess blood glucose may initiate yeast overgrowth, blood vessel

deterioration, heart disease and other health conditions.8

Understanding and using the glycemic index is an important aspect of diet

modification for cancer patients. However, there is also evidence that sugars

may feed cancer more efficiently than starches (comprised of long chains of

simple sugars), making the index slightly misleading. A study of rats fed diets

with equal calories from sugars and starches, for example, found the animals on

the high-sugar diet developed more cases of breast cancer.9 The glycemic index

is a useful tool in guiding the cancer patient toward a healthier diet, but it

is not infallible. By using the glycemic index alone, one could be led to

thinking a cup of white sugar is healthier than a baked potato. This is because

the glycemic index rating of a sugary food may be lower than that of a starchy

food. To be safe, I recommend less fruit, more vegetables, and little to no

refined sugars in the diet of cancer patients.

What the Literature Says

A mouse model of human breast cancer demonstrated that tumors are sensitive to

blood-glucose levels. Sixty-eight mice were injected with an aggressive strain

of breast cancer, then fed diets to induce either high blood-sugar

(hyperglycemia), normoglycemia or low blood-sugar (hypoglycemia). There was a

dose-dependent response in which the lower the blood glucose, the greater the

survival rate. After 70 days, 8 of 24 hyperglycemic mice survived compared to 16

of 24 normoglycemic and 19 of 20 hypoglycemic.10 This suggests that regulating

sugar intake is key to slowing breast tumor growth (see chart).

In a human study, 10 healthy people were assessed for fasting blood-glucose

levels and the phagocytic index of neutrophils, which measures immune-cell

ability to envelop and destroy invaders such as cancer. Eating 100 g

carbohydrates from glucose, sucrose, honey and orange juice all significantly

decreased the capacity of neutrophils to engulf bacteria. Starch did not have

this effect.11

A four-year study at the National Institute of Public Health and Environmental

Protection in the Netherlands compared 111 biliary tract cancer patients with

480 controls. Cancer risk associated with the intake of sugars, independent of

other energy sources, more than doubled for the cancer patients.12 Furthermore,

an epidemiological study in 21 modern countries that keep track of morbidity and

mortality (Europe, North America, Japan and others) revealed that sugar intake

is a strong risk factor that contributes to higher breast cancer rates,

particularly in older women.13

Limiting sugar consumption may not be the only line of defense. In fact, an

interesting botanical extract from the avocado plant (Persea americana) is

showing promise as a new cancer adjunct. When a purified avocado extract called

mannoheptulose was added to a number of tumor cell lines tested in vitro by

researchers in the Department of Biochemistry at Oxford University in Britain,

they found it inhibited tumor cell glucose uptake by 25 to 75 percent, and it

inhibited the enzyme glucokinase responsible for glycolysis. It also inhibited

the growth rate of the cultured tumor cell lines. The same researchers gave lab

animals a 1.7 mg/g body weight dose of mannoheptulose for five days; it reduced

tumors by 65 to 79 percent.14 Based on these studies, there is good reason to

believe that avocado extract could help cancer patients by limiting glucose to

the tumor cells.

Since cancer cells derive most of their energy from anaerobic glycolysis,

Joseph Gold, M.D., director of the Syracuse (N.Y.) Cancer Research Institute and

former U.S. Air Force research physician, surmised that a chemical called

hydrazine sulfate, used in rocket fuel, could inhibit the excessive

gluconeogenesis (making sugar from amino acids) that occurs in cachectic cancer

patients. Gold's work demonstrated hydrazine sulfate's ability to slow and

reverse cachexia in advanced cancer patients. A placebo-controlled trial

followed 101 cancer patients taking either 6 mg hydrazine sulfate three

times/day or placebo. After one month, 83 percent of hydrazine sulfate patients

increased their weight, compared to 53 percent on placebo.15 A similar study by

the same principal researchers, partly funded by the National Cancer Institute

in Bethesda, Md., followed 65 patients. Those who took hydrazine sulfate and

were in good physical condition before the study began lived an average

of 17 weeks longer.16

In 1990, I called the major cancer hospitals in the country looking for some

information on the crucial role of total parenteral nutrition (TPN) in cancer

patients. Some 40 percent of cancer patients die from cachexia.5 Yet many

starving cancer patients are offered either no nutritional support or the

standard TPN solution developed for intensive care units. The solution provides

70 percent of the calories going into the bloodstream in the form of glucose.

All too often, I believe, these high-glucose solutions for cachectic cancer

patients do not help as much as would TPN solutions with lower levels of glucose

and higher levels of amino acids and lipids. These solutions would allow the

patient to build strength and would not feed the tumor.17

The medical establishment may be missing the connection between sugar and its

role in tumorigenesis. Consider the million-dollar positive emission tomography

device, or PET scan, regarded as one of the ultimate cancer-detection tools. PET

scans use radioactively labeled glucose to detect sugar-hungry tumor cells. PET

scans are used to plot the progress of cancer patients and to assess whether

present protocols are effective.18

In Europe, the " sugar feeds cancer " concept is so well accepted that

oncologists, or cancer doctors, use the Systemic Cancer Multistep Therapy (SCMT)

protocol. Conceived by Manfred von Ardenne in Germany in 1965, SCMT entails

injecting patients with glucose to increase blood-glucose concentrations. This

lowers pH values in cancer tissues via lactic acid formation. In turn, this

intensifies the thermal sensitivity of the malignant tumors and also induces

rapid growth of the cancer. Patients are then given whole-body hyperthermia (42

C core temperature) to further stress the cancer cells, followed by chemotherapy

or radiation.19 SCMT was tested on 103 patients with metastasized cancer or

recurrent primary tumors in a clinical phase-I study at the Von Ardenne

Institute of Applied Medical Research in Dresden, Germany. Five-year survival

rates in SCMT-treated patients increased by 25 to 50 percent, and the complete

rate of tumor regression increased by 30 to 50 percent.20 The

protocol induces rapid growth of the cancer, then treats the tumor with toxic

therapies for a dramatic improvement in outcome.

The irrefutable role of glucose in the growth and metastasis of cancer cells

can enhance many therapies. Some of these include diets designed with the

glycemic index in mind to regulate increases in blood glucose, hence selectively

starving the cancer cells; low-glucose TPN solutions; avocado extract to inhibit

glucose uptake in cancer cells; hydrazine sulfate to inhibit gluconeogenesis in

cancer cells; and SCMT.

A female patient in her 50s, with lung cancer, came to our clinic, having been

given a death sentence by her Florida oncologist. She was cooperative and

understood the connection between nutrition and cancer. She changed her diet

considerably, leaving out 90 percent of the sugar she used to eat. She found

that wheat bread and oat cereal now had their own wild sweetness, even without

added sugar. With appropriately restrained medical therapy—including high-dose

radiation targeted to tumor sites and fractionated chemotherapy, a technique

that distributes the normal one large weekly chemo dose into a 60-hour infusion

lasting days—a good attitude and an optimal nutrition program, she beat her

terminal lung cancer. I saw her the other day, five years later and still

disease-free, probably looking better than the doctor who told her there was no

hope.

Patrick Quillin, Ph.D., R.D., C.N.S., is director of nutrition for Cancer

Treatment Centers of America in Tulsa, Okla., and author of Beating Cancer With

Nutrition (Nutrition Times Press, 1998).

References

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2. Volk T, et al. pH in human tumor xenografts: effect of intravenous

administration of glucose. Br J Cancer 1993 Sep;68(3):492-500.

 

3.Digirolamo M. Diet and cancer: markers, prevention and treatment. New York:

Plenum Press; 1994. p 203.

 

4. Leeper DB, et al. Effect of i.v. glucose versus combined i.v. plus oral

glucose on human tumor extracellular pH for potential sensitization to

thermoradiotherapy. Int J Hyperthermia 1998 May-Jun;14(3):257-69.

 

5. Rossi-Fanelli F, et al. Abnormal substrate metabolism and nutritional

strategies in cancer management. JPEN J Parenter Enteral Nutr 1991

Nov-Dec;15(6):680-3.

 

6. Grant JP. Proper use and recognized role of TPN in the cancer patient.

Nutrition 1990 Jul-Aug;6(4 Suppl):6S-7S, 10S.

 

7. Brand-Miller J, et al. The glucose revolution. Newport (RI) Marlowe and Co.;

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8. Mooradian AD, et al. Glucotoxicity: potential mechanisms. Clin Geriatr Med

1999 May;15(2):255.

 

9. Hoehn, SK, et al. Complex versus simple carbohydrates and mammary tumors in

mice. Nutr Cancer 1979;1(3):27.

 

10. Santisteban GA, et al. Glycemic modulation of tumor tolerance in a mouse

model of breast cancer. Biochem Biophys Res Commun 1985 Nov 15;132(3):1174-9.

 

11. Sanchez A, et al. Role of sugars in human neutrophilic phagocytosis. Am J

Clin Nutr 1973 Nov;26(11):1180-4.

 

12. Moerman CJ, et al. Dietary sugar intake in the aetiology of biliary tract

cancer. Int J Epidemiol 1993 Apr;22(2):207-14.

 

13. Seeley S. Diet and breast cancer: the possible connection with sugar

consumption. Med Hypotheses 1983 Jul;11(3):319-27.

 

14. Board M, et al. High Km glucose-phosphorylating (glucokinase) activities in

a range of tumor cell lines and inhibition of rates of tumor growth by the

specific enzyme inhibitor mannoheptulose. Cancer Res 1995 Aug 1;55(15):3278-85.

 

15. Chlebowski RT, et al. Hydrazine sulfate in cancer patients with weight loss.

A placebo-controlled clinical experience. Cancer 1987 Feb 1;59(3):406-10.

 

16. Chlebowski RT, et al. Hydrazine sulfate influence on nutritional status and

survival in non-small-cell lung cancer. J Clin Oncol 1990 Jan;8(1):9-15.

 

17. American College of Physicians. Parenteral nutrition in patients receiving

cancer chemotherapy. Ann Intern Med 1989 May;110(9):734.

 

18. Gatenby RA. Potential role of FDG-PET imaging in understanding tumor-host

interaction. J Nucl Med 1995 May;36(5):893-9.

 

19. von Ardenne M. Principles and concept 1993 of the Systemic Cancer Multistep

Therapy (SCMT). Extreme whole-body hyperthermia using the infrared-A technique

IRATHERM 2000—selective thermosensitisation by hyperglycemia—circulatory back-up

by adapted hyperoxemia. Strahlenther Onkol 1994 Oct;170(10):581-9.

 

20. Steinhausen D, et al. Evaluation of systemic tolerance of 42.0 degrees C

infrared-A whole-body hyperthermia in combination with hyperglycemia and

hyperoxemia. A Phase-I study. Strahlenther Onkol 1994 Jun;170(6):322-34.

 

 

 

 

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