Subject: Cancer's Sweet Tooth

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Cancer's Sweet Tooth

 

 

From The April 2000 Issue of Nutrition Science News

http://www.chiro.org/nutrition/FULL/Cancers_Sweet_Tooth.html

by Patrick Quillin, PHD, RD, CNS

 

photo by Robert Morrissey/Dot for Dot

 

 

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, p. 166).

 

 

 

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; 111­125

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, p. 164).

 

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).

 

 

Sidebars:

 

Does Blood Sugar Affect Breast Cancer

 

Glycemic Index

 

References:

1. Warburg O. On the origin of cancer cells. Science 1956

Feb;123:309-14.

 

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.; 1999.

 

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.