ABSTRACT
Cancer is the second leading cause of death after heart disease in developed countries and the third in developing countries accounting for 7.6 million deaths or 20% of all deaths globally from noncommunicable diseases [1]. Considerable evidence suggests an involvement of environmental causes including diet in the etiology of cancer. A 20-fold variation in cancer rates has been observed across geographic regions for several cancer types, and migrant studies have shown an increase in the risk for cancer in migrants from low-risk areas that approximates that of the host population [2-4]. McKeown-Eyssen [5] and Giovannucci [6] independently suggested that hyperglycemia and hyperinsulinemia may be important factors in promoting malignant transformation and tumor growth. Clinical conditions related to impaired glucose tolerance and insulin resistance including type 2 diabetes, obesity, the metabolic syndrome, and polycystic ovarian syndrome have been associated with greater risk of cancer at various sites. These conditions share similar metabolic risk factors including hyperglycemia, hyperinsulinemia, higher inammatory markers, and unfavorable adipokine proles, which may also be shared by cancer [7-9]. Metformin, a diabetic medication that reduces hyperglycemia and improves insulin resistance, signicantly reduced total cancer incidence and mortality by 33% in people with type 2 diabetes [8] and cancer-related mortality in people with concomitant type 2 diabetes and cancer [10]. Carbohydrates are the dietary factors that primarily raise blood glucose and insulin levels, and they have been implicated in the etiology of cancer at various sites [6,11]. However, evidence suggests that different carbohydrates may impact cancer development differently, and hence, it has been proposed that the nature of the carbohydrates consumed, i.e., the glycemic index (GI), by virtue of differences in glycemic raising potential, may affect carcinogenesis differently [12].
