**1. Introduction**

Globally, colorectal cancer (CRC) is the third most commonly diagnosed malignancy and the fourth leading cause of cancer-related mortality, accounting for about 1.4 million new cases and almost 700,000 deaths in 2012 [1]. Its disease burden is expected to increase by 60%, resulting in over 2.2 million new cases and 1.1 million cancer deaths by 2030 [2]. The distribution of CRC burden varies widely across regions, as more than two-thirds of all cases and about 60% of all deaths occur in countries with a high or very high Human Development Index [1]. However, CRC is considered to be one of the strongest indicators of the global cancer transition, as countries undergoing rapid social and economic transition

are displaying rapid increases in the prevalence of cancers that are already more widespread in high-income countries [2]. Hence, CRC incidence and mortality rates are still rapidly increasing in many low-income and middle-income countries, while stabilizing or decreasing trends are being observed in highly developed countries where rates remain among the highest in the world [2]. As patterns and trends in CRC incidence and mortality are related to development levels, their incremental changes could be indicative of the adoption of a more Westernized lifestyle [2].

Targeted interventions tailored to available resources, including primary prevention, are necessary to decrease the global prevalence of CRC [2], as primary prevention dietary habits and other healthy lifestyle factors such as physical activity (PA) are viewed as the most effective and affordable strategy for curbing this global epidemic [3, 4]. In addition, genetic predisposition and environmental factors including diet and PA are considered to be the two main causes of CRC [3, 5].

Due to observed inconsistencies when appraising the effectivity of dietary and lifestyle-cancer relationships, this chapter will provide an overview of the current body of evidence regarding the role of diet, individual foods, alcoholic beverages, vitamins, body fatness, physical activity, and dietary supplements in terms of their classification as preventative or causative in the development of CRC. In addition, the strength of scientific evidence will be alluded to, as well as the modulating pathways responsible for reaping protective benefits or promoting carcinogenesis. Inconsistent findings across scientific literature related to dietary prevention of CRC include but are not limited to discrepancies in study design, dietary interventions assessed, baseline eating patterns, and populations sampled [6].
