Nicodemus KK, Jacobs Jr DR, Folsom AR (2001). Whole and refined grain intake and risk of incident postmenopausal breast cancer (United States). Cancer Causes Control 12, 917–925. Nicodemus KK, Sweeney C, Folsom AR (2004). Evaluation of dietary, medical and lifestyle risk factors for incident kidney cancer in postmenopausal women. Int J Cancer 108, 115–121. Nielsen TG, Olsen A, Christensen J, Overvad K, Tjonneland A (2005). Dietary carbohydrate intake is not associated with the breast cancer incidence rate ratio in postmenopausal Danish women. J Nutr 135, 124–128. Nomura AM, Hankin JH, Kolonel LN, Wilkens LR, Goodman MT, Stemmermann GN (2003). Case–control study of diet and other risk factors for gastric cancer in Hawaii (United States). Cancer Causes Control 14, 547–558. Otani T, Iwasaki M, Ishihara J, Sasazuki S, Inoue M, Tsugane S et al. (2006). Dietary fiber intake and subsequent risk of colorectal cancer: the Japan public health center-based prospective study. Int J Cancer 119, 1475–1480. Pandey M (2003). Risk factors for gallbladder cancer: a reappraisal. Eur J Cancer Prev 12, 15–24. Park Y, Hunter DJ, Spiegelman D, Bergkvist L, Berrino F, van den Brandt PA et al. (2005). Dietary fiber intake and risk of colorectal cancer: a pooled analysis of prospective cohort studies. JAMA 294, 2849–2857. Pelucchi C, Galeone C, Levi F, Negri E, Franceschi S, Talamini R et al. (2006). Dietary acrylamide and human cancer. Int J Cancer 118, 467–471. Pera M, Manterola C, Vidal O, Grande L (2005). Epidemiology of esophageal adenocarcinoma. J Surg Oncol 92, 151–159. Peters U, Sinha R, Chatterjee N, Subar AF, Ziegler RG, Kulldorff M et al. (2003). Dietary fibre and colorectal adenoma in a colorectal cancer early detection programme. Lancet 361, 1491–1495. Potischman N, Coates RJ, Swanson CA, Carroll RJ, Daling JR, Brogan DR et al. (2002). 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N Engl J Med 342, 1149–1155. Schernhammer ES, Hu FB, Giovannucci E, Michaud DS, Colditz GA, Stampfer MJ et al. (2005). Sugar-sweetened soft drink consumption and risk of pancreatic cancer in two prospective cohorts. Cancer Epidemiol Biomarkers Prev 14, 2098–2105. Schulz M, Lahmann PH, Riboli E, Boeing H (2004). Dietary determinants of epithelial ovarian cancer: a review of the epidemiologic literature. Nutr Cancer 50, 120–140. Silvera SA, Jain M, Howe GR, Miller AB, Rohan TE (2005b). Dietary carbohydrates and breast cancer risk: a prospective study of the Carbohydrates and cancer TJ Key and EA Spencer roles of overall glycemic index and glycemic load. Int J Cancer 114, 653–658. Silvera SA, Rohan TE, Jain M, Terry PD, Howe GR, Miller AB (2005a). Glycemic index, glycemic load, and pancreatic cancer risk (Canada). Cancer Causes Control 16, 431–436. Silvera SA, Rohan TE, Jain M, Terry PD, Howe GR, Miller AB (2005c). Glycaemic index, glycaemic load and risk of endometrial cancer: a prospective cohort study. Public Health Nutr 8, 912–919. Slattery ML, Benson J, Berry TD, Duncan D, Edwards SL, Caan BJ, Potter JD (1997). Dietary sugar and colon cancer. Cancer Epidemiol Biomarkers Prev 6, 677–685. Stolzenberg-Solomon RZ, Pietinen P, Taylor PR, Virtamo J, Albanes D (2002). Prospective study of diet and pancreatic cancer in male smokers. Am J Epidemiol 155, 783–792. Terry P, Jain M, Miller AB, Howe GR, Rohan TE (2002). No association among total dietary fiber, fiber fractions, and risk of breast cancer. Cancer Epidemiol Biomarkers Prev 11, 1507–1508. Terry P, Lagergren J, Ye W, Wolk A, Nyren O (2001). Inverse association between intake of cereal fiber and risk of gastric cardia cancer. Gastroenterology 120, 387–391. Terry PD, Jain M, Miller AB, Howe GR, Rohan TE (2003). Glycemic load, carbohydrate intake, and risk of colorectal cancer in women: a prospective cohort study. J Natl Cancer Inst 95, 914–916. van Dam RM, Seidell JC (2007). Carbohydrate intake and obesity. Eur J Clin Nutr 61 (Suppl 1), S75–S99. van den Brandt PA, Spiegelman D, Yaun SS, Adami HO, Beeson L, Folsom AR et al. (2000). Pooled analysis of prospective cohort studies on height, weight, and breast cancer risk. Am J Epidemiol 152, 514–527. Venn BJ, Green TJ (2007). Glycemic index and glycemic load: measurement issues and their effect on diet–disease relationships. Eur J Clin Nutr 61 (Suppl 1), S122–S131. Verhoeven DT, Assen N, Goldbohm RA, Dorant E, van ‘t Veer P, Sturmans F et al. (1997). Vitamins C and E, retinol, beta-carotene and dietary fibre in relation to breast cancer risk: a prospective cohort study. Br J Cancer 75, 149–155. Wilson KM, Rimm EB, Thompson KM, Mucci LA (2006). Dietary acrylamide and cancer risk in humans: a review. J Verbr Lebensm 1, 19–27. Wolk A, Lindblad P, Adami HO (1996). Nutrition and renal cell cancer. Cancer Causes Control 7, 5–18. 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S121 European Journal of Clinical Nutrition
REVIEW Glycemic index and glycemic load: measurement issues and their effect on diet–disease relationships BJ Venn and TJ Green Department of Human Nutrition, University of Otago, Dunedin, New Zealand Glycemic index (GI) describes the blood glucose response after consumption of a carbohydrate containing test food relative to a carbohydrate containing reference food, typically glucose or white bread. GI was originally designed for people with diabetes as a guide to food selection, advice being given to select foods with a low GI. The amount of food consumed is a major determinant of postprandial hyperglycemia, and the concept of glycemic load (GL) takes account of the GI of a food and the amount eaten. More recent recommendations regarding the potential of low GI and GL diets to reduce the risk of chronic diseases and to treat conditions other than diabetes, should be interpreted in the light of the individual variation in blood glucose levels and other methodological issues relating to measurement of GI and GL. Several factors explain the large inter- and intra-individual variation in glycemic response to foods. More reliable measurements of GI and GL of individual foods than are currently available can be obtained by studying, under standard conditions, a larger number of subjects than has typically been the case in the past. Meta-analyses suggest that foods with a low GI or GL may confer benefit in terms of glycemic control in diabetes and lipid management. However, low GI and GL foods can be energy dense and contain substantial amounts of sugars or undesirable fats that contribute to a diminished glycemic response. Therefore, functionality in terms of a low glycemic response alone does not necessarily justify a health claim. Most studies, which have demonstrated health benefits of low GI or GL involved naturally occurring and minimally processed carbohydrate containing cereals, vegetables and fruit. These foods have qualities other than their immediate impact on postprandial glycemia as a basis to recommend their consumption. When the GI or GL concepts are used to guide food choice, this should be done in the context of other nutritional indicators and when values have been reliably measured in a large group of individuals. European Journal of Clinical Nutrition (2007) 61 (Suppl 1), S122–S131; doi:10.1038/sj.ejcn.1602942 Keywords: glycemic index; glycemic load; methodology; diet–disease relationships Introduction European Journal of Clinical Nutrition (2007) 61 (Suppl 1), S122–S131 & 2007 Nature Publishing Group All rights reserved 0954-3007/07 $30.00 www.nature.com/ejcn The glycemic index (GI) concept was introduced by Jenkins et al. (1981) in the early 1980s as a ranking system for carbohydrates based on their immediate impact on blood glucose levels. GI was originally designed for people with diabetes as a guide to food selection, advice being given to select foods with a low GI (Jenkins et al., 1983). Lower GI foods were considered to confer benefit as a result of the relatively low glycemic response following ingestion compared with high GI foods. The GI concept has been extended to also take into account the effect of the total amount of carbohydrate consumed. Thus glycemic load (GL), a product of GI and quantity of carbohydrate eaten provides an Correspondence: Dr B Venn, PO Box 56, Department of Human Nutrition, University of Otago, Dunedin, New Zealand. E-mail: bernard.venn@stonebow.otago.ac.nz indication of glucose available for energy or storage following a carbohydrate containing meal. Although GI is usually tested on individual foods, there are methods described whereby the GI and GL of meals and habitual diets can be estimated (Wolever and Jenkins, 1986; Salmeron et al., 1997a). In addition to a role in the treatment of diabetes, low GI and GL diets have more recently been widely recommended for the prevention of chronic diseases including diabetes, obesity, cancer and heart disease and in the treatment of cardiovascular risk factors, especially dyslipidaemia (Jenkins et al., 2002). The usefulness of GI and GL has been questioned on several counts: failure to consider the insulin response (Coulston et al., 1984), the high intra- and inter-subject variation in glucose response to a food (Pi-Sunyer, 2002), and a loss of discriminating power when foods are combined in a mixed meal (Flint et al., 2004). Furthermore, foods with a high sugar (sucrose) content and those containing both
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Comision Federal de la mejora regul
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Subject: MEXICO - Comments on PROY
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Item of PROY‐ NOM‐051 A.3.1 & A
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Annex 1.1: Ziesenitz, S.C.; 1996;
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Volume 61 Supplement 1 December 200
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Volume 61, Supplement 1, December 2
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S1 S5 S19 S40 S75 S100 S112 S122 S1
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FAO/WHO Scientific Update on carboh
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cardiovascular diseases and cancer)
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REVIEW Carbohydrate terminology and
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Table 2 Energy and macronutrient in
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are inulin and fructo oligosacchari
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Table 3 Principal physiological pro
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National Academy of Sciences in 200
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product contained X25% whole grain
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Henderson L, Gregory J, Swan G (200
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REVIEW Nutritional characterization
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Table 1 Nutritional characterizatio
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Table 2 Principles of carbohydrate
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Table 4 NSP in a selection of foods
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asked to consider both the ‘plant
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account for any supplemented materi
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eaction vessels, with successive tr
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similar to the situation with sugar
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company working on dietary carbohyd
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van Dam RM, Seidell JC (2007). Carb
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2003). In establishing the energy v
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combustible energy of the fermentab
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glucose, starch, NSP) there is also
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generated through bioenergetic inef
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Table 4 cE, ME and NME, and content
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ME (Atwater general system) (Merill
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(o0.8 kg in the adult), increase af
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B1.4 MJ from protein in men, did no
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esults may relate not only to the d
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ecologist, who is pre-occupied with
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Table 5 Effect of NSP (dietary fibr
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As already described, almost any ca
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in adolescents. Possible mechanisms
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unit, such as a grant or fellowship
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Annex 2.2: Roberfroid, M.B., 1999;
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1 Nutrition and Health Claims (CAC/
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3 Nutrition and Health Claims (CAC/
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