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Cancer's Sweet Tooth

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Desert Sky,

 

Thank you so much for this information. I have metastatic breast cancer and have

made great changes to my way of life since Easter last year. I have cut out

sugar, and it is incredibly heartening to receive fresh encouragement. I

sometimes feel quite alone as the changes I have made are more than anyone

either my McMillan nurse or my GP know of. It is easy to become disheartened

when noone else seems to be doing the same thing. It can cause a body to

question herself,, I can tell you ! I thank you for the information in this

article as it gives me the motivation to continue on a difficult , but

worthwhile course of action.

 

With gratitude,

 

 

Jill

 

 

 

 

 

From The April 2000 Issue of Nutrition Science News Features

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

 

http://www.newhope. com/nutritionsci encenews/ NSN_backs/ Apr_00/cancer. cfm

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please learn other ways to cure cancer such as baking soda cure water cure dr

hulda clark cancer cure grape cure dr max gerson cancer cure zeolite cancer

cure theres alot of ways to cure cancer start by useing a vit d supplement learn

about zappers very effective you dont have to die with cancer read the book step

out of the box not many cancer patients ever know that cancer is not really

hard to cure they are told there is no cure bolney dont be a victim of there

scam learn how not to die from cancer and live to tell others about your

victory over cancer learn how not to die from cancer pepperwatsonblue

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Classic article . . .

 

Cancer's Sweet Tooth

by Patrick Quillin, PHD, RD, CNS

 

From The April 2000 Issue of Nutrition Science News

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

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.

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