ABSTRACT
Cell Carcinoma Prevention .................................................................... 141 7.2.10 Liver Cancer ........................................................................................................... 141
7.2.10.1 Liver Cancer Background ...................................................................... 141 7.2.10.2 Glycemic Index, Glycemic Load, and Liver Cancer Prevention ........... 141
7.3 Limitations ............................................................................................................................ 142
Cancer is a leading cause of death, accounting for 8.2 million deaths globally in 2012 (Stewart and Wild 2014). Migration studies observed a 20-fold variation in cancer rates across geographical regions, suggesting that environmental causes are central to the etiology of cancer (King et al. 1985, Ziegler et al. 1993, Rastogi et al. 2008). Indeed, approximately one third of cancer deaths are due to the five leading behavioral and dietary risk factors: high body mass index (BMI), low fruit and vegetable intake, lack of physical activity, tobacco use, and alcohol use (Stewart and Wild 2014). It has been estimated that approximately 35% of cancer deaths could be avoided by dietary modifications alone (Doll and Peto 1981, Willett 1995, McCullough and Giovannucci 2004). Dietary factors associated with Western lifestyles, such as high intakes of refined carbohydrates, saturated fat, red meat, and excess energy, are linked to increased cancer rates and cancer mortality (Willett 1995, Santarelli et al. 2008, Kushi et al. 2012, Pan et al. 2012). Among dietary compounds, carbohydrates have been implicated in the etiology of cancer at various sites (Giovannucci 1995, Franceschi et al. 1997, Augustin et al. 2002). Specifically, it has been proposed that the extent of the rise in blood glucose produced by carbohydrates and captured by the glycemic index (GI) may play a differential role in cancer development (Augustin et al. 2002). The GI is a ranking of carbohydrate foods based on their ability to raise blood glucose concentration (Jenkins et al. 1981), and the glycemic load (GL) is the mathematical multiplication of the GI of a food by its available carbohydrate content (without fiber) (Salmeron et al. 1997b). Generally, the slower the rate of carbohydrate absorption, the lower the rise of blood glucose and insulin and the lower the GI value. Compared with low-GI foods, high-GI foods result in larger rises in blood glucose and insulin for the same amount of carbohydrate ingested (Jenkins et al. 1981), resulting in a further metabolic challenge, particularly in the presence of metabolic conditions such as impaired glucose tolerance (Hanefeld et al. 2003). Consuming high-compared with low-GI diets have been shown to increase the risk of developing type 2 diabetes (T2DM) (Salmeron et al. 1997a, 1997b, Barclay et al. 2008, Livesey et al. 2013), cardiovascular disease (CVD) (Liu et al. 2000, Kushi et al. 2012, Mirrahimi et al. 2012), CVD risk factors (Frost et al. 1999, Liu et al. 2001, 2002), and cancer (Augustin et al. 2001, Franceschi et al. 2001, Barclay et al. 2008, Turati et al. 2015a). Hyperglycemia and hyperinsulinemia have been involved in carcinogenesis, and several conditions linked to the disruption of glucose metabolism, including diabetes, obesity, hyperglycemia, hyperinsulinemia, and insulin resistance, may have relevant roles in cancer development (Kaaks and Lukanova 2001, Stocks et al. 2009, Campbell et al. 2012, Bosetti et al. 2012b, Boyle et al. 2013).
