The Sugar-Cancer Link
At the world-famous Sloan-Kettering Cancer hospital in New York City, researchers found that tumors sucked up radioactively-labeled vitamin C like thirsty sponges because cancer cells thought they were getting their favorite fuel, glucose, which is nearly identical in chemical structure to vitamin C. Meanwhile, across the globe in a modern clinic in Germany, oncologists were injecting glucose into cancer patients to activate the cancer growth, then whack the cancer with intensive chemo, radiation, or hyperthermia. Their results have doubled 5-year survival for these patients undergoing Systemic Cancer Multistep Therapy. Researchers at Harvard University have developed a special Total Parenteral Nutrition formula for cancer patients that uses much less sugar (glucose) and more protein and fats. The net result of this “disease-specific” formula for starving cancer patients is to feed the immune system and not the cancer. In most major cancer hospitals around the world, oncologists use a $2 million device, called a PET scan (positron emission tomography), which detects cancer by finding hot spots of sugar feeding cells in the body. All of these world-class scientists are using the same principle: sugar feeds cancer. When we can lower blood glucose, we can slow cancer growth.
Tumors are primarily obligate glucose metabolizers, meaning “sugar feeders”.[i] The average American consumes 20% of calories from refined white sugar, which is more of a drug than a food. We also manifest poor glucose tolerance due to stress, obesity, low chromium and fiber intake, and sedentary lifestyles. Blood glucose is basically there to feed the brain and other glucose-dependent organs, while also supplying fuel for muscle movement. When we sit all day, the sugar in our blood is like a teenager with nothing to do–trouble is bound to happen. Elevated sugar levels in the blood will “tan” proteins (glycosylation), which makes immune cells and red blood cells less capable of doing their jobs. Elevated sugar in the blood has a number of ways in which it promotes cancer:
- 4 Rises in blood glucose generate corresponding rises of insulin, which then pushes prostaglandin production toward the immune-suppressing and stickiness-enhancing PGE-2. While fish oil (EPA) and borage oil (GLA) have a favorable impact on cancer, these potent fatty acids are neutralized when the blood glucose levels are kept high.
- 4 Cancer cells feed directly on blood glucose, like a fermenting yeast organism. Elevating blood glucose in a cancer patient is like throwing gasoline on a smoldering fire.
- 4 Elevating blood glucose levels suppresses the immune system
Cancer cells primarily use glucose for fuel, with lactic acid as an anaerobic by-product, thus generating a lower pH, fatigue (lactic acid buildup), and enlarged liver (where lactic acid is converted back to pyruvate in the Cori cycle). This inefficient pathway for energy metabolism yields only 5% of the ATP energy available in food, which is one of the reasons why 40% of cancer patients die from malnutrition or cachexia. Cancer therapies need to regulate blood glucose levels via diet, supplements, enteral and parenteral solutions for
cachectic patients, medication, exercise, gradual weight loss, stress reduction, etc. The role of glucose in the growth and metastasis of cancer cells can be utilized to help the cancer patient with such therapies as:
-diets designed with glycemic index in mind to regulate rises in blood glucose, hence selectively starving the cancer cells
-low glucose total parenteral nutrition (TPN) solution
-positron emission tomography (PET) assays of tumor progress
-hydrazine sulfate to inhibit gluconeogenesis in cancer cells
-avocado extract (mannoheptulose), which inhibits glucose uptake in cancer cells
-Systemic Cancer Multistep Therapy, which injects glucose into the cancer patient to initiate malignancy growth, then uses hyperthermia to selectively destroy tumor tissue.
Does Sugar (Glucose) Feed Cancer Cells?
Nobel laureate (1931 Medicine) Otto Warburg, PhD, first discovered that cancer cells have a fundamental difference in energy metabolism compared to healthy undifferentiated cells. Cancer cells ferment glucose anaerobically.[ii] Since Warburg’s pivotal study published in Science in 1956, many other researchers have corroborated his conclusions.
“A frequent characteristic of many malignant tumors is an increase in anaerobic glycolysis, that is the conversion of glucose to lactate, when compared to normal tissues.”
“The high rate of glucose consumption by malignant cells, their heavy dependence on the inefficient glycolytic mode for energy production, their increased energy expenditures, and the susceptibility to carbohydrate deprivation prompted several attempts to exploit the tumoricidal potential of manipulations interfering with carbohydrate and/or energy metabolism, hoping that such interventions could preferentially impair the malignant cells.”[iii]
“In normoglycemic hosts the in vivo consumption of glucose by neoplastic tissues was found to be very high. Cerebral tissue is reported to use from 0.23 to 0.57 gm of glucose per hour per 100 gm wet brain and rates as one of the highest consumers among the normal tissues. However, hepatomas and fibrosarcomas consumed roughly as much glucose as the brain does and carcinomas about twice as much.”[iv]
“The glucose utilization rate in neoplastic tissues, unlike in host tissues, is high. Glucose, in fact, is the preferred energy substrate, utilized mainly via the anaerobic glycolytic pathway. The large amount of lactate produced by this process is then transported to the liver where it is converted to glucose, thus contributing to further increase host’s energy wasting.”[v]
ELEVATED LACTATE LEVELS. “Our laboratory has been interested in the metabolic derangements of cancer, particularly lactate overproduction, in view of our work linking lactate overproduction in obesity to insulin resistance…Thus, in all four studies listed above, lactate levels were 27-83% higher in cancer patients than in related controls.”[vi]
LOWER PH THROUGH LACTIC ACID ACCUMULATION.
If cancer cells use glucose through anaerobic fermentation, then lactic acid must accumulate as the inefficient by-product of energy metabolism. Human tumors were implanted in rats, which were then given IV solutions of glucose. pH in the tumor tissue was reduced to an average of 6.43, given the logarithmic scale of hydrogen ions in pH measurement, “This pH value corresponds to a ten-fold increase in H+ ion activity in tumor tissue as compared to arterial blood.”[vii] By lowering pH in tumor cells, we can effectively create a selective systemic therapy which will kill cancer cells and not healthy tissue. “After IV glucose, tumor acidification occurred in 9 out of 10 patients…Larger tumors tended to exhibit a greater decrease in pH…We conclude that IV and IV + oral glucose administration are equally effective inducing tumor acute acidification.”[viii]
ELEVATED BLOOD GLUCOSE MAY SUPPRESS IMMUNE FUNCTIONS. Ten healthy human volunteers were assessed for fasting blood glucose levels and phagocytic index of neutrophils. “Oral 100 gm portions of carbohydrates from glucose, fructose, sucrose, honey, or orange juice all significantly decreased the capacity of neutrophils to engulf bacteria as measured by the slide technique. Starch ingestion did not have this effect.”[ix]
INSULIN-CANCER RELATIONSHIP. “Insulin is a major anabolic hormone in mammals and its involvement in malignancies is well documented.”[x]
EPIDEMIOLOGICAL EVIDENCE. “Risk associated with the intake of sugars, independent of other energy sources, is more than doubled [for biliary tract cancer]”.[xi] “In older women, a strong correlation was found between breast cancer mortality and sugar consumption…”[xii]
ACTION PLAN: STARVE CANCER CELLS
HYDRAZINE SULFATE. Since cancer cells derive most of their energy from anaerobic glycolysis, Joseph Gold, MD, developed hydrazine sulfate to inhibit the excessive gluconeogenesis that occurs in cancer patients. Hydrazine inhibits the enzyme phosphoenol pyruvate carboxykinase (PEP-CK), and in placebo-controlled clinical trials at UCLA, hydrazine was proven to slow and reverse cachexia in advanced cancer patients.[xiii] Unfortunately, this non-toxic and inexpensive substance has been banished by the FDA. Hydrazine for cancer cachexia is a troubling story of stupidity and greed preventing the American public from having easy access to a useful anti-cancer substance. Hydrazine sulfate may be available from: Life Support 209-529-4697, Life Energy 604-856-0171, Nutrilogics 800-618-1881, Biotech 800-345-1199.
IV GLUCOSE WITH HYPERTHERMIA. Since cancer growth can be accelerated with intravenous glucose solutions, researchers in Germany have developed a technique, Systemic Cancer Multistep Therapy (SCMT), in which the cancer patient is given injections of glucose to elevate blood glucose to around 400 mg%, which generates a substantial reduction in pH in all malignant tissues due to lactic acid formation, then the patient is given whole body hyperthermia (42°C core temp.). Patients may then be treated with chemotherapy and radiation, which are optional. Five year survival in these SCMT treated patients increased by 25-50%, and complete regression of tumor increased by 30-50%.[xiv]
LOW GLUCOSE TOTAL PARENTERAL NUTRITION (TPN) SOLUTION. When a cancer patient cannot eat enough food to prevent lean tissue wasting, nutrients may be injected into a port implanted in the sub-clavian artery. Since “tumors appear to be obligate glucose utilizers…”[xv], we can capitalize on the differences in energy metabolism between healthy and differentiated malignant cells by providing starving cancer patients with TPN solutions that are relatively low in glucose and higher in amino acids and lipids.[xvi] Many starving cancer patients are offered either no nutrition support or the standard TPN solution developed for intensive care units with 70% of kcal from glucose (dextrose). Disappointing results have been found when using standard high glucose TPN solutions for cachectic cancer patients.[xvii]
PET SCANS MAP TUMOR PROGRESS AND AGGRESSIVENESS. PET (positron emission tomography) scans use radioactively-labeled glucose (fluoro-2-deoxy-D-glucose, FDG) to tag areas of the body with unusually high levels of glycolysis. “Enhanced glucose utilization by tumor cells via glycolysis, identified by Warburg, is a characteristic exploited in cancer imaging using FDG-PET.”[xviii] “Specific parameters of the glucose consumption curves are predicted to be markedly different in normal and neoplastic tissues and critical to the tumor-host interaction. Tumor invasability and patient prognosis can be linked to these parameters.” PET scans can be used to plot the progress of cancer patients and decide if current protocols are effective, or if different protocols need to be employed.[xix]
TUMOR HYPOXIA AND TREATMENT RESISTANCE. “…tumor hypoxia is present in at least one third of cancers in the clinical setting.”[xx] “Tumors differ from normal tissues because there is not enough oxygen to meet demand, even under baseline conditions.”[xxi] Since solid tumors can develop pockets of hypoxic tissue that are particularly resistant to radiotherapy, a unique protocol using niacin (to improve aerobic energy metabolism) has been used by Jae Ho Kim, MD, PhD, at Ford Hospital in Detroit with noteworthy successes.
GLYCEMIC CONTROL OF CANCER PATIENT’S DIET.
Humans are not built to withstand the rigors of many aspects of modern life. We are going deaf at an alarming rate due to noise pollution. The same thing is happening with respect to sugar. Our bodies are not built to withstand the constant flood of simple sugars entering our bloodstream. If we were active and burning up the sugar in exercise, then the sugar would be of less consequence. But we sip and munch on sweet foods all day long while sitting at our desks or in front of the TV, then wonder why morbid obesity has increased by 300% since 1982.
Animals were injected with an aggressive strain of breast cancer, then fed diets that would provide either 1) hypoglycemia, 2) normoglycemia, or 3) hyperglycemia. There was a dose-dependent response in which the lower the blood glucose, the greater the survival percentage at 70 days.[xxii] In rats exposed to a carcinogen, then fed isocaloric intake levels of 49% of kcal as either sucrose or wheat starch, there was a doubling of the tumor incidence in the sugar-fed group (14 of 20 animals with tumors vs 7 out of 20).[xxiii] Educating the cancer patient on the importance of regulating glycemic index can become a key strategy in slowing tumor growth.
Glycemic index is a scientific approach to measuring the role of dietary carbohydrates in blood glucose levels and was developed in 1981 by Dr. David Jenkins. Though glycemic index does not take into consideration “nutrient density”, it is a useful means of helping people to select foods that will create a more favorable blood glucose level.
With that caveat in mind, let’s explain how the GI was developed and what it means to you. Human subjects, both healthy and diabetic, are fed 50 grams of carbohydrates from various foods. For instance, people are fed 200 grams of spaghetti in order to get 50 grams of carbohydrates, because spaghetti also contains some protein, fat, water, and fiber. Researchers then compare the size of the Oral Glucose Tolerance Test curve. If a food creates only half the rise in blood glucose compared to consuming a pure glucose drink, then the food gets a GI rating of 50, and so on.
The more that you process a food, the higher the GI becomes. Cooked whole wheat berries have a GI of 41, white bread has a GI of 70. The more the food is stripped of its fiber and ground into smaller particles, the higher the GI and the worse that food becomes for the diabetic.
You might say that ice cream has a better GI than whole wheat bread, so eat more ice cream? Actually, the sugar in ice cream may create havoc for the cancer patient. Use this glycemic index table[xxiv] as it was meant to be used: as a guideline to help people make the right food choices, not as
[i]. Rothkopf, M, Fuel utilization in neoplastic disease: implications for the use of nutritional support in cancer patients, Nutrition, supp, 6:4:14-16S, 1990
[ii] . Warburg, O., Science, vol.123, no.3191, p.309, Feb.1956
[iii] . Demetrakopoulos, GE, Cancer Research, vol.42, p.756S, Feb.1982
[iv] . Gullino, PM, Cancer Research, vol.27,p.1031, June 1967
[v] . Rossi-Fanelli, F., J.Parenteral Enteral Nutr., vol.15, p.680, 1991
[vi] .Digirolamo, M., in DIET AND CANCER: MARKERS, PREVENTION, AND TREATMENT, p.203, Plenum Press, NY, 1994
[vii] . Volk, T., Br.J.Cancer, vol.68, p.492, 1993
[viii] . Leeper, DB, Int.J.Hyperthermia, vol.14, no.3, p.257, 1998
[ix] . Sanchez, A., Amer.J.Clin.Nutr., vol.26, p.1180, Nov.1973
[x] . Yam, D., Medical Hypotheses, vol.38, p.111, 1992
[xi] . Moerman, CJ, Int.J.Epidemiology, vol.22, no.2, p.207, 1993
[xii] . Seeley,S.,, Med.Hypotheses, vol.11, p.319, 1983
[xiii] . Chlebowski, RT, J.Clin.Oncology, vol.8, no.1, p.9, Jan.1990; see also Chlebowski, RT, Cancer, vol.59, p.406, 1987; see also Gold, J., Nutrition & Cancer, vol.9, p.59, 1987
[xiv] . von Ardenne, M., Strahlentherapie und Onkologie, vol.170, p.581, 1994
[xv] . Rothkopf, M, Nutrition, vol.6, no.4, p.14S, July 1990 supp
[xvi] . Tuttle-Newhall, JE, Cancer & Nutrition, in ADJUVANT NUTRITION IN CANCER TREATMENT, Quillin, P (ed), p.145, Cancer Treatment Research Foundation, Arlington Heights, IL 1994
[xvii] . Sakurai, Y, Japanese J. Surgery, vol.28, p.247, 1998
[xviii] . Smith, TAD, Nuclear Med.Comm., vol.19, p.97, 1998
[xix] . Gatenby, RA, J.Nuclear Medicine, vol.36, p.893, 1995
[xx] . Vaupel, P., Int.J.Rad.OncologyBiol.Phys., vol.42, no.4, p.843, 1998
[xxi] . Gulledge, CJ, Anticancer Research, vol.16, p.741, 1996
[xxii] . Santisteban, GA, Biochem. & Biophys.Res.Comm., vol.132, no.3, p.1174, Nov.1985
[xxiii] . Hoehn, SK, Nutrition & Cancer, vol.1, no.3, p.27, 1982
[xxiv] . Brand-Miller, J., et al., THE GLUCOSE REVOLUTION, Marlowe, NYC, 1999