Low GL for Cancer Prevention
According to Dr Walter Willetts of the Harvard School of Public Health, being obese accounts for 14 per cent of cancer deaths in men and 20 per cent in women, compared with about 30 per cent each for smoking. However, one of the most significant new risk factors for breast cancer are indicators of blood sugar problems.
Dr. W.C. Willett, Symposium on Cancer Prevention, Annual meeting of the American Association for the Advancement of Science, March 2008
Eating foods with a high glycemic index (GI) and/or glycemic load (GL) have been linked to a higher risk of many cancers, including breast, colorectal, pancreatic, ovarian, thyroid, endometrial (womb), and gastric cancer. Conversely, low-GI and/or low-GL diets are associated with a reduced risk of breast, colorectal, ovarian and endometrial (womb) cancers. For example, researchers in Italy in 2005 found that regularly eating sweet foods, including biscuits, brioches, cakes, ice cream, honey and chocolate, increased the risk of breast cancer. As the authors point out, these foods also contain other nutrients that are potentially involved in causing breast cancer, including saturated fats.
A.W. Barclay, et al., ‘Glycemic index, glycemic load, and chronic disease risk: A meta-analysis of observational studies’’ American Journal of Clinical Nutrition, 2008 March, Vol 87(3): pp. 627–37
see also A. Tavani, et al., ‘Consumption of sweet foods and breast cancer risk in Italy’ Annals of Oncology, 2006 Feb, Vol 17(2): pp. 341–5
see also C.A. Krone and J.T. Ely, ‘Controlling hyperglycemia as an adjunct to cancer therapy’, Integrative Cancer Therapies, 2005 March, Vol 4(1): pp. 25–31
The reason why a high-GL diet is such bad news is that it increases levels of insulin-related growth factors, primarily IGF-1, which are major promoters of breast cancer. Insulin also stimulates hormones, including oestrogens, which are also associated with excess breast-cancer risk. Postmenopausal women with high insulin levels, for example, have been shown to have twice the risk of developing breast cancer. We explore this whole link between being hormonally overloaded and increased risk for a number of diseases in the January 10 newsletter.
G.C. Kabat, et al., ‘Repeated measures of serum glucose and insulin in relation to postmenopausal breast cancer’, International Journal of Cancer, June 2009
see also M.J. Gunter, et al., ‘Insulin, insulin-like growth factor-I, and risk of breast cancer in postmenopausal women’, Journal of the National Cancer Institute, 2009 Jan 7, Vol 101(1): pp. 48–60
According to a report in the Archives of Internal Medicine women who gain weight throughout adulthood rather than maintaining a stable weight may have an increased risk of breast cancer. Women who were not obese or overweight at age 18 but were at ages 35 and 50 were 40 per cent more likely to develop breast cancer than women who maintained a normal weight.
Obesity is known to be a risk factor for developing breast cancer after menopause. Oestrogens can accumulate in fat tissue, potentially initiating or promoting the growth of cancerous cells in the breast.
J. Ahn, et al., ‘Adiposity, adult weight change, and postmenopausal breast cancer risk’, Archives of Internal Medicine, 2007 Oct 22, Vol 167(19): pp. 2091–102
see also A.H. Eliassen, et al., ‘Adult weight change and risk of postmenopausal breast cancer’, Journal of the American Medical Association, 2006 July 12, Vol 296(2): pp. 193–201
Cancer risk has been found to be elevated in those with diabetes. A 2005 review of studies ranging from 1966 to 2005 found an 82 per cent increase in risk of pancreatic cancer. Two other reviews by Swedish Researchers reported a 30 per cent increase in risk of colorectal cancer and a 20 per cent increase in risk of breast cancer in those with diabetes.
R. Huxley, et al., ‘Type-II diabetes and pancreatic cancer: A meta-analysis of 36 studies’, British Journal of Cancer, 2005 June 6, Vol 92(11): pp. 2076–83
see also S.C. Larsson, et al., ‘Diabetes mellitus and risk of colorectal cancer: A meta-analysis’, Journal of the National Cancer Institute, 2005 Nov 16: Vol 97(22): pp. 1679–87<......
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