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The New Zealand Medical Journal

 Journal of the New Zealand Medical Association, 09-August-2002, Vol 115 No 1159

Glucose and cancer
We agree with Dr Brian Scobie’s letter that New Zealand’s high cancer death rates call for prevention via dietary modification.1 He cites evidence impugning excessive consumption of animal products. Indeed, New Zealand’s intakes of animal fat and animal protein were reported to be highest in the world in a 37-country study on dietary factors in cancer by Carroll.2 The same study reported New Zealand’s sugar intake to be among the ten highest. In another survey, mortality due to breast cancer was reported to exhibit a positive correlation of 0.73 with per capita sugar intake independent of other variables in 41 countries.3 We seek to elucidate these dietary sugar associations.
Theory supported by human and animal studies, suggests the most common factor increasing tumour tolerance in the developed nations is the gross elevation of mean blood glucose.4,5 This resulted from a change in diet in the early 1900’s from an unrefined whole grain diet to one in which a major fraction of calories is derived from white flour and added sugar. In those countries where the unrefined diet still prevails, two-hour postprandial blood glucose values ranging from 2.8–5 mmol/L are reported.6
In prevention and successful treatment of cancer, the hexose monophosphate shunt (HMS) is needed to supply: 1) adequate H202 for effective phagocytosis; and 2) ribose for mitosis of lymphocytes to clone large numbers for competent attack against tumours or pathogens. The HMS runs at a rate proportional to intracellular ascorbic acid (AA) concentration.7 In even “modest” blood glucose elevations (ie ~7.2 mmol/L, commonly postprandial to Western diet meals), blood glucose molecules so outnumber AA that they competitively inhibit insulin-mediated active transport of AA into cells. This results in low intracellular AA levels,8,9 slow HMS,7 and cell dysfunction (ie leukocytes cannot multiply for effective response to tumours or pathogens, fetal cells divide too slowly, etc). When new tumours are sensed by the cytotoxic T-cells or other sentinels of immunity in humans on the Western diet, response to the neoplastic initiation frequently fails because mitosis is impaired by glucose elevation. Thus, cancer is a leading cause of death in the industrialised nations.
John T A Ely
Director
Cheryl A Krone
Senior Research Scientist
Applied Research Institute
Palmerston North

  1. Scobie B. Cancer flourishes. NZ Med J 2002;155:304.
  2. Carroll KK. Dietary factors in hormone-dependent cancers. Curr Concepts Nutr 1977;6:25–40.
  3. Hems G. The contributions of diet and childbearing to breast cancer rates. Br J Cancer 1978;37:974–82.
  4. Santisteban GA, Ely JTA, Hamel EE et al. Glycemic modulation of tumor tolerance in a mouse model of breast cancer. Biochem Biophys Res Commun 1985;132:1174–9.
  5. Hamel EE, Santisteban GA, Ely JTA, Read DH. Hyperglycemia and reproductive defects in non-diabetic gravidas: a mouse model test of a new theory. Life Sci 1986:39:1425–8.
  6. Chatterjee IB, Bannerjee A. Estimation of dehydroascorbic acid in blood of diabetic patients. Anal Biochem 1979;98:368–74.
  7. Cooper MR, McCall CE, DeChatelet LR. Stimulation of leukocyte hexose monophosphate shunt activity by ascorbic acid. Infect Immun 1971;3:851–3.
  8. Chen MS, Hutchinson ML, Pecoraro RE et al. Hyperglycemia-induced intracellular depletion of ascorbic acid in human mononuclear leukocytes. Diabetes 1983;32:1078–81.
  9. Hutchinson ML, Lee WYL, Chen MS et al. Effects of glucose and select pharmacologic agents on leukocyte ascorbic acid levels. Fed Proc 1983;42:930.

     
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