**1. Introduction**

Cancer development is a result of interactions among environmental and hereditary factors (Kim, 2006). The majority of genetic abnormalities, which increase the risk of cancer are not hereditary, but a result of DNA damage occurring during lifetime. The causes of DNA damage include internal (nutrient metabolism, cell hormones) and/or external factors (diet, insufficient physical activity, tobacco use, exposure to chemical agents and radiation) (International Life Sciences Institute [ILSI], 2005; World Cancer Research Fund [WCRF], 2007; Kryston et al., 2011). Epidemiological studies have shown that diet and lifestyle are the most important external factors implicated in the development of malignant diseases (ILSI, 2005; WCRF & AICR, 2007; Go et al., 2003).

Why the same environmental factors cause different changes in human genome among individuals is a question for scientists searching unique combinations of factors leading to cancer (Brower, 2011). There is a growing body of evidence that many cancers are not caused by mutations in genes, but by chemical modifications that alter the way genes function. Chemical modifications of genes are called epigenetic changes. Epidemiological studies have shown that diet and lifestyle may cause such changes (Brower, 2011).

According to World Cancer Report (Boyle & Levin, 2008) 12.4 million new cases of cancer were reported in 2008. Malignant diseases accounted for 7.6% of all deaths during the same year and estimations are that in 2030, cancers will be responsible for 17.0% of deaths worldwide. The number of new cases is expected to rise, especially in developing countries (Boyle & Levin, 2008).

In total, malignancies account for 83 million disability-adjusted life years (DALYs). The estimated global economic loss from cancer is US\$ 895.2 billion, measured by the economic value of DALYs (American Cancer Society & Livestrong, 2010).

The aforementioned data, coupled with rising health care expenditures for cancer patients, led to cancer being seen not only as a health problem, but also as a political issue (WHO, 2011a, 2011b). Identification of cancers as the leading non-communicable diseases [NCDs], together with cardiovascular diseases, type 2 diabetes and chronic obstructive pulmonary diseases, was followed by an initiative to include NCDs among the global development goals that will succeed the Millennium Development Goals in 2015 (The NCD Alliance, 2011).

Lifestyle Changes May Prevent Cancer 153

phenotype (Thomas et al., 2011) and they are at greater risk of certain cancer localizations. TOFI is a pathological phenomenon, synonymous with "metabolically obese", whereas thin-on-the-outside, thin-on-the-inside [TOTI] is an acronym for healthy adipose tissue

TOFI phenotype may be used to explain the rising incidence of cancers in developing countries. Rapid economic growth and social transitions happening in these countries affect dietary and other lifestyle choices. Energy-dense foods become easily accessible to consumers, while the level of physical activity decreases, promoting overweight and obesity

Higher amount of IAAT or visceral adiposity is usually related to increased serum levels of insulin-like growth factor [IGF-1], insulin, leptin, sex hormones and adipocytokines (tumor necrosis factor-alpha [TNF-α], interleukin-6 [IL-6], C-reactive protein [CRP], adiponectin, resistin, visfatin, apelin), all known as cancer and type 2 diabetes risk factors (Donohoe et al., 2011; Bon, 2008; Redinger, 2008). Epidemiological studies show that type 2 diabetes patients are at higher risk for developing many types of cancer. There is an ongoing effort in research of shared risk factors for cancer and type 2 diabetes supported by the American Diabetes Association and the American Cancer Society. This research strives to find a biological link between cancer and type 2 diabetes, as well as to explain whether diabetes

Taller individuals are more likely to get cancer, due to cells being stimulated by IGF-1 and growth hormone continuously, increasing the possibility of DNA replication error, some of

Overweight and obesity are usually the result of external factors, and are therefore,

**Cancer site USA [%] UK [%] Brazil [%] China [%]**  Endometrium 70 56 52 34 Esophagus 69 75 60 44 Mouth, pharynx & larynx 63 67 63 44 Stomach 47 45 41 33 Colon 45 43 37 17 Pancreas 39 41 34 14 Breast 38 42 28 20 Lung 36 33 36 38 Kidney 24 19 13 8 Gallbladder 21 16 10 6 Liver 15 17 6 6 Prostate 11 20 n/a n/a

**combined** 34 39 30 27 **Total for all cancers** 24 26 19 20 Table 1. Estimated percentage of cancers that could be prevented by healthy diet, regular physical activity and healthy weight in selected countries based on the conclusions of the 2007 WCRF/AICR Diet and Cancer Report (n/a – exposure data not available). Adapted

preventable and treatable (WHO, 2005, 2008a) risk factors for some cancers (Table 1).

mellitus therapy affects the risk for cancer development (Giovannucci et al., 2010).

which may lead to malignant alterations (Hernandez et al., 2009).

distribution (Thomas et al., 2011).

**Total for these cancers** 

from AICR & WCRF, 2009.

(Popkin, 2001).

Scientists around the world declared war on cancer (Waldorp, 2011). Preventive medicine has been recognized as the most promising field in reducing the risk of malignant diseases development. As diet and lifestyle are believed to be the most important external factors implicated in cancer development, nutrition care process [NCP] (American Dietetic Association [ADA], 2006a, 2008) and medical nutrition prevention [MNP] are considered the most important tools in cancer risk management (Key et al., 2004; Béliveau & Gingras, 2007).

NCP and MNP can be used to reduce the potential of nutrition misinformation to increase the cancer risks in populations and individuals who are inadequately educated about healthy food and lifestyle choices (ADA, 2006b).

Registered dietitians are well aware of dietary reference values and safe upper limits for nutrients intake in different population groups, but these recommendations neglect genetic differences in population subgroups. Therefore, special scientific disciplines - nutrigenetics and nutrigenomics - study the effects of different foods and food constituents on gene expression (Fenech et al., 2011). There is a distinct difference between nutrigenetics and nutrigenomics. Nutrigenetics studies effects of genetic variations on body response to diet and nutrition, while nutrigenomics studies health effects of gene alterations influenced by food constituents (Milner, 2006a). Both disciplines aim to determine the optimal nutrient intake and nutrient combinations (called nutriom) in order to sustain the genome and support the physiological processes of gene expression, metabolism and cell functioning. These findings are expected to be used in cancer risk reduction in dietetic practice (Milner, 2006a).
