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New Meds That Heal |
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by
Patrick Quillin, PHD, RD, CNS |
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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. |
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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. |
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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 |
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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 |
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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. |
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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). |
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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 ?ugar). 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. |
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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. |
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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 |
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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. |
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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. |
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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.ll |
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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 |
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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.
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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 |
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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. |
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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 |
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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-1 study at the Von Ardenne
Institute of Applied Medical Research in Dresden,
Germany.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. |
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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. |
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A female patient in
her 505, 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. |
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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). |
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1. Warburg 0. On the origin of cancer cells. Science
1956 Feb;123:309-14 |
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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. |
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3. Digirolamo M. Diet and
cancer: markers, prevention and treatment. New York: Plenum
Press; 1994. p 203. |
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4. Leeper OB, 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. |
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5. Rossi-Fanelli
F, et al. Abnormal substrate metabolism and nutritional
strategies in cancer management. JPENJ Parenter Enteral Nutr
1991 Nov-Dec;15(6):680-3. |
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6. Grant JP.
Proper use and recognized role of TPN in the cancer patient.
Nutrition 1990 Jul-Aug;6( 4 5uppl):65-75,
105. |
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7. Brand-MillerJ, et al. The glucose revolution. Newpolt
(RI) Marlowe and Co.; 1999. |
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8. Mooradian AD,
et al. Glucotoxicity: potential mechanisms. Clin Geriatr Med
1999 May; 15(2) :255 |
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9. Hoehn, SK, et
al. Complex versus simple carbohydrates and mammary tumors in
mice. Nutr Cancer 1979;1(3):27. |
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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. |
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11. Sanchez
A, et al. Role of sugars in human neutrophilic phagocytosis.
Am J Clin Nutr 1973 Nov;26(11): 1180-4. |
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12. Moerman
0, et al. Dietary sugar intake in the aetiology of biliary
tract cancer. IntJ Epidemiol1993 Apr;22(2):207-14. |
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13. Seeley
S. Diet and breast cancer: the possible connection with
sugar consumption. Med Hypotheses 1983
Jul;11(3):319-27. |
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14. Board
/11, 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. |
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15. Chlebowski
RT, et al. Hydrazine sulfate in cancer patients with weight
loSS. A placebo-control'ed clinical experience. Cancer
1987 Feb 1;59(3):406-10. |
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16. Chlebowski
RT, et al. Hydrazine sulfate influence on nutritional status
and survival in non-small-cell lung cancer. J
Clin
Oncol1990 Jan;8(1):9-15. |
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17. American
College of Physicians. Parenteral nutrition in patients
receiving cancer chemotherapy. Ann Intern Med 1989
May;110(9):734. |
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18. Gatenby RA. Potential role of FDG-PET imaging in
understanding tumor-host interaction. J Nucl Med 1995
May;36(5):893-9. |
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19. von Ardenne
M. Principles and concept 1993 of the Systemic Cancer
Multistep Therapy (SCMT). Extreme whole-body hyperthermia
using the infrared-A technique IRA THERM 2000--selective
thermosensitisation by hyperglycemia--circulatory back-up by
adapted hyperoxemia. Strahlenther Onkol1994 Oct;170(10):581-9. |
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20. Steinhausen D, et al.
Evaluation of
systemic tolerance of42.0 degrees
C infrared-A whole-body
hyperthermia in combination with hyperglycemia and hyperoxemia.
A Phase-I study. Strahlenther |
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