A comparison of CRC rates in different countries shows great variation. And time trends within some countries are also notable. Dietary, lifestyle and environmental factors but not racial, ethnical or genetic factors seem to account for a great part of the differences in incidence. Some of the most striking, rapid and well documented changes in diet were seen in Japan . Consumption of meat and dairy products increased between the 1950s and 1990s and thus the rate of CRC . Changes in food habits have been shown in western countries , but also in developing countries such as China . Moreover, the observation that CRC in migrants from low-risk populations eventually rises to equal the rates of the new host population supports the hypothesis that exposure to environmental factors may be important in the aetiology of the disease.
Data on Japanese (with low incidence in native country) first-generation migrants to Hawaii confirmed a strong augmentation in colon cancer risk similar to whites living in Hawaii . Relevant incidence increases have been well documented for Puerto Ricans emigrating to the United States  and also for migrants from Poland to the United States and Australia .
Higher CRC rates in industrialised countries could be related to diets rich in animal products, red meat, animal fats and proteins, and refined sugar, and low in plant-based foods. On the other hand, low-risk diets in developing countries have been observed to be richer in vegetables (particularly cruciferous), protein from vegetable sources, fibre, whole grains and fruits . The protective effects of a plant-based diet could be due to some components like fibre, vitamins, mineral, antioxidants and phytochemicals.
The negative impact of an animal-based diet has been attributed to saturated fats, meat protein, excessive caloric intake and the scarce presence of protective foods . Low-risk diets include the traditional Mediterranean and Asian diets. It has been suggested that major developed countries could reduce their incidence of CRC by switching from a western diet to a Mediterranean diet . The effects of a presumed low-risk or high-risk diet may be stronger in females . There has been a weaker relationship between rectal cancer, more common in males, and diet with respect to colon cancer .
International comparison studies have shown an association between increased fat intake and CRC . However, some analytical studies do not support this finding , particularly for rectal cancer [105, 106]. It is possible that the total amount of fat and the intake from fat as well as the specific type and origin of consumed fats play a role. Several aetiolog-ical mechanisms have been postulated to explain how saturated fat could increase the risk of CRC. The concentration of bile acids in the large bowel may be augmente by a high-fat diet. This may lead to anaerobic bacterial flora (especially some Clostridia) metabolising primary bile acids, increasing the amount of secondary bile acids, which have been linked to increased risk of CRC [107,108]. The alkaline environment in the stool can increase the concentration of free bile acids .
Several studies [110, 111], but not all , suggest that a high intake of red meat could be associated with higher CRC risk. A number of mechanisms have been proposed regarding the contribution of meat to saturated fats intake, total caloric intake, iron intake , higher bile acids concentration in the bowel or exposure to nitrocompounds produced with food cooking . Compounds that can accumulate in the bowel and stool include pyrrolysis products such as benzopyrene, which result from broiling or frying of meat at high temperatures and mutagenic heterocyclic amines . Heterocyclic amines form in foods, especially meat, mostly with high temperature cooking, broiling, grilling, baking or pan-frying. However, a connection between meat processing, these compounds, and an increased risk of CRC is still not conclusive [116-118].
The role of fibre in determining low rates of CRCs stems from studies by Burkitt . Many mechanisms have been proposed to explain the protective effect on adenoma recurrence and CRC. Fibre can act by increasing faecal bulk, speeding up transit of stools, diluting gut content, reducing the faecal con centration of bile acids, binding them and inhibiting their production through reduction of pH in the lumen, modifications of bacterial activity and fermentation products . Studies on populations consuming diets similar in fat but differing in total fibre intake suggest a protective role for fibre [120, 121]; however, some randomised controlled trials found fibre to be useless in preventing colon cancer [122, 123]. It is still unclear if the protective effect could be due to fibre itself or to other chemicals present in high-fibre foods. Soluble fibre seems to have no protective effects, while insoluble constituents seem to be beneficial. Specific benefits of insoluble fibre have been shown for rectal cancer .
Some research, although not yet conclusive, supports a protective role for calcium and diets high in calcium . Among the purported biological mechanisms is the ability of calcium to bind with bile acids forming insoluble soaps  and vitamin D related action .
It has been speculated that a number of foods or diet nutrients have the potential effect of CRC risk reduction. The following foods, among others, have been investigated: milk, yoghurt, olive oil, soybeans, garlic, polyphenols, flavonoids, carotenoids, selenium, vitamins A, D, C, E and specialised plant compounds like resveratrol and curcumin.
High folate diets have been associated with CRC risk reduction . A factor that could increase the chances of developing CRC could be refined sugar , while resistant starches may prevent colon cancer . Omega-3 fatty acids, present in fish oil, could correlate inversely with CRC risk . Chlorinated water could increase the risk of rectal cancers , but the data is not conclusive . Water consumption  and methylxanthine-containing beverages such as green tea  and coffee may also exert some degree of protection .
Energy intake, metabolism, physical activity and various measures of body size or obesity are strictly related. According to several, but not all, studies , regular physical activity is associated with a lower risk of CRC while a sedentary lifestyle poses a risk factor . The protective effect on rectal cancer is not clear .
Being overweight or obese, particularly abdominal obesity , has been linked to an increased CRC risk, especially in men . The mechanism is complex and the effect of being overweight or obese reflects the negative consequences of high energy intake and metabolic changes. Hyperinsulinaemia  and high levels of insulin-like growth factor-1 (IGF-1)  could contribute to the CRC risk. However, while being overweight and having a higher Body Mass Index may be strongly related to colon cancer, the link appears to be weaker for rectal can cer . Animal studies show the benefits of reducing caloric intake alone, independently of diet composition, in preventing CRC [143, 144]. It is becoming quite evident that physical activity and appropriate energy balance can substantially decrease the risk of CRC , despite the fact that the association between CRC and calories is not conclusive.
There are other controllable lifestyle factors supposed to affect the risk of developing CRC. Several epidemiological research studies , but not all , have shown that alcohol consumption is associated with a moderate increase in the risk of CRC. Specifically, high alcohol intake, particularly of beer, has been implicated for both men and women in the development of rectal cancers [147,148].
According to some studies , but not all , a positive association exists between tobacco smoking and CRC. Also, occupational exposure to some chemicals (asbestos and some organic solvents) showed an increased risk . Recently, it has been suggested that cytomegalovirus infection may play a role in the development of CRC .
Hormonal use in postmenopausal women has been associated with a lower risk of colon cancer , but not clearly with rectal cancer . Several studies have shown that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) could reduce the incidence of colorectal polyps and the risk of CRC . The potential for the use of NSAIDs as primary prevention is under investigation, but more evidence is needed .
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