Dietary fibre Consumption and Colorectal Cancer

Dietary fiber consumption and colorectal cancer

Colorectal cancer is cancer of the colon and rectum. It is a major cause of mortality and morbidity accounting for 9% of all cancer deaths worldwide (Haggar and Boushey, 2009). It is the third most commonly diagnosed cancer in males and second in females (Jemal et al., 2011) with 1.2 million new cases diagnosed in 2008 worldwide (American Cancer Society, 2013). In the United States, African Americans are at the highest risk of developing and dying from colon cancer whose incidence is also higher than in Africans living in Africa (O'Keefe et al., 2009). Intakes dietary fiber rich foods, red and processed meats along with alcohol abuse are currently the major suspected and highly researched dietary factors that are related to colorectal cancer (Aune et al., 2011). Colorectal cancer can be inherited including hereditary non-polyposis colorectal cancer due to genetic instability, and familial adenomatous polyposis coli due to a mutation in the adenomatous polyposis coli gene. The second type is due to inflammation including Crohns’ disease and ulcerative colitis and thirdly, sporadic which is mainly caused by lifestyle (Kraus and Arber, 2009).

Dietary fiber, colon, rectal and colorectal cancers defined

Dietary fiber is the indigestible carbohydrate that is fermented by colonic bacteria yielding short chain fatty acids such as acetate, propionate and butyrate (Scharlau et al., 2009). There are different constituents of dietary fiber that are of particular interest which include arabinoxylan, inulin, B-glucan, pectin, bran and resistant starches (Lattimer and Haub, 2010). High fiber foods include whole grain products and cereals, vegetables, fruits and legumes especially the skins of vegetable and fruits, berries and bran layers of grains. Dietary fiber may further be defined by whether it’s soluble or insoluble.

Colorectal cancer is known as cancer of the colon and rectum. It is the second leading cause of cancer deaths in America when cases in both men and women are combined. The colon also referred to as the large intestine is the lower part of the digestive system, which processes food for energy and rids the body of solid waste. Rectal cancer occurs in the last six inches of the large intestine (the rectum), otherwise if it occurs in the other part of the large intestine it is referred to as colon cancer. Together, these cancers are referred to as colorectal cancers (American cancer society, 2013)

Risk factors for colorectal cancer

The American Cancer Society defines a risk factor as something that affects your chance of getting a disease and further explains that having a risk factor or several risk factors doesn’t mean that you will get the disease (American Cancer Society, 2010).  Risk factors for colorectal cancer are hence identified to be: old age, personal history of colorectal cancer or polyps, personal history of inflammatory bowel disease, family history of colorectal cancer, inherited syndromes, racial and ethnic background, type 2 diabetes, lifestyle, diets low in fruits and vegetables, physical inactivity, smoking and alcohol abuse (Haggar et al, 2009).

Studies have shown relationships between various risk factors and colorectal cancer. An increased risk of colorectal cancer was associated with alcohol consumption where 30-45g of alcohol per day (equivalent to two to three alcoholic drinks per day) increases the risk by 16% and greater than 45g of alcohol per day is associated with 41% increased risk of colorectal cancer (Swimson and Seymour, 2012). 

Results from analysis of different cohort studies using meta-analysis showed that diabetic patients had a 20% higher colorectal cancer risk than non-diabetic patients. Smokers had a 16% higher risk of developing colorectal cancer than nonsmokers. The same study showed a 20% increased risk of developing colorectal cancer in individuals who consumed red and processed meats while no positive relationship was observed with increased fruit and vegetable consumption. Heavy physical inactivity indicated a 20% lower risk of developing colorectal cancer while obese individuals had a 40% increased risk of developing colorectal cancer than normal individuals while (Huxley et al., 2009). The incidence of colorectal polyps increased with increasing weight gain and waist hip ratio while waist circumference, adult height and BMI at age 18 were not associated with colorectal cancer (Wise et al., 2012).

Ulcerative colitis is associated with an increased risk of developing colorectal cancer while a variety of drugs including non-steroidal anti-inflammatory analgesics and hormonal replacement therapy have been associated with a reduced risk of colorectal cancer. A familial risk can be identified in up to 30% of CRC cases where Familial Adenomatous Polyposis (FAP) and Lynch syndrome are the two major hereditary conditions (Swimson and Seymour, 2012)

Diet, race and colorectal cancer

African Americans have a higher colon cancer incidence than Africans living in Africa probably because African Americans consume more red meat and saturated animal fat than Africans in Africa (O'Keefe et al., 2009). With diets high in red meat, the undigested carbohydrate in the colon is chiefly metabolized by hydrogen-producing bacteria which are latter colonized by secondary bile producing bacteria. With diets low in red meat but high in vegetables and fruits as in the case of Africans living in Africa, the undigested carbohydrate is fermented by methane producing bacteria which are latter colonized by lactobacilli species that promote mucosal health as do butyrate-producing firmicute (Uccello et al., 2012). The lactic acid producing bacteria in the colon include lactobacillus rhamnosus GG (LGG), Bifidobacterium lactis, and streptococcus thermophiles (Thomas and Greer, 2010). Red meat is a rich source of sulfur containing amino acids (methionine and cysteine) which form sulfate ions in the colon and rectum. Sulfate is used as an oxidant by sulfur reducing bacteria to degrade organic matter forming an equivalent amount of hydrogen sulfide per mole of sulfate reduced. Hydrogen sulfide generates free radicals, impairs cytochrome oxidase, suppresses butyrate utilization and inhibits the synthesis of mucus; all factors lead to mucosal insult, inflammation and ultimately colorectal cancer (Andrea Azcárate-Peril et al., 2011).

Colorectal cancer treatment, drug-nutrient interactions

In the United States, annual updates about occurrence and trends regarding cancer are provided by a collaborative effort from the National Cancer Institute (NCI), the Centers for Disease Control and Prevention (CDC), the North American Association of Central Cancer Registries (NAACCR) and the American Cancer Society (Edwards et al., 2010). According to the American Cancer Society, (2013) the main treatments for cancer include surgery, radiation therapy, chemotherapy and targeted therapy.

Chemotherapy for colorectal cancer

The American cancer society identifies the common chemotherapy drugs that are known to relieve colorectal cancer as Irinotecan (Campstosar), 5-Fluorouracil, Capecitabine (Xeloda) and Oxaliplatin (Eloxatin). These may be applied singly or as a combination depending on the cancer stage (American Cancer Society, 2013).  Research shows that less than 25% of colon cancer patients who undergo chemotherapy are responsive despite the prevalence and availability of early detection mechanisms (Meckling, 2006).

Drug-nutrient interactions for colorectal cancer

5-Fluorouracil (5-FU), is often given with the vitamin-like drug leucovorin (also called folinic acid), which makes it work better. Fluorouracil is an antimetabolite of the pyrimidine analog type. In the form of its active metabolite 5-FU inhibits the conversion of thiamine to TPP and inhibits DNA and RNA synthesis. The cofactor of transketolase, TPP promotes nucleic acid ribose synthesis and tumor cell proliferation through the non-oxidative transketolase (TK) pathway (Stargrove et al., 2008).

Studies supporting dietary fiber and colorectal cancer

Intakes of dietary fiber were significantly inversely associated with the risks of colorectal cancer when 4 to 7-day food diaries of participants were analyzed (Dahm et al., 2010). In a follow up study for 11 years based on total cereal, fruit, vegetable and fiber intakes as estimated from dietary questionnaires at baseline, total dietary fiber was inversely associated with colorectal cancer. This study employed multivariable adjustments for all other factors known to affect cancer initiation and progression leaving only dietary fiber as a treatment where an increase of 10g/day in dietary fiber intake was effected (Murphy et al., 2012). In reference to what particular sources of dietary fiber reduce carcinogenesis, studies showed that since dietary fibers differ in composition, they also differ in degree of protection against colorectal cancer for example wheat bran was effective in stimulating bacterial fermentation, oat bran had little effect and corn bran had no effect (Berg, 2001).

Mechanisms: dietary fiber rich foods in prevention of colorectal cancer

Prebiotics are non-digestible food ingredients that benefits the host by selectively stimulating the favorable growth and/or activity of one or more indigenous probiotic bacteria (Thomas and Greer, 2010). Currently all known prebiotics are oligosaccharides (carbohydrate compounds) known to resist digestion in the human small intestine and so reach the colon, where they are fermented by gut microflora. Oligosaccharides of interest include inulin, oligofructose, lactulose and resistant starch. Inulin and oligofructose are found in a variety of foods including chicory, onions, leeks, garlic, asparagus, bananas and articichokes. The bonds that connect the fructose subunits in both oligosaccharides cannot be cleaved by enzymes in the human intestines (Clark et al., 2012).

Dietary fiber (prebiotics) is fermented in the colon by gram-positive bacteria producing short chain fatty acids (SCFA) which are 2-carbon to 5-carbon weak acids, including acetate (C2), propionate (C3), butyrate (C4), and 5-carbon valerate (Canani et al., 2011). Butyrate is highly recognized for the potential to act on secondary chemoprevention by slowing growth and activating apoptosis in colon cancer cells. Additionally, SCFA can also act on primary prevention by activation of different drug metabolizing enzymes. This can reduce the burden of carcinogens and, therefore, decrease the number of mutations, reducing cancer risk (Scharlau et al., 2009). Dietary fiber increases stool bulk and stimulates intestinal transit thus reducing epithelial exposure to intraluminal carcinogens (Hawk and Mishra, 2012). Increased fiber increases water holding capacity and stool volume and dilutes any carcinogens or other toxicants that may be present in the colon. The larger, softer more fluid stool is easier to pass and is less abrasive. The faster transit time means that there is less time to interact with the colon wall or to produce secondary bile acids and other potential carcinogens (Salovaara et al., 2007).

Future directions in new research

Almost all the available information from prospective studies is based on less than 10 years of follow-up; some researchers believe that further evaluation of the effects of diet earlier in life and at longer intervals of observation is needed. A lot of literature relates intake of dietary fiber to reduction in colorectal cancer but still there are many studies that prove no relationship between the two. All the same, someone who is interested in reducing the risk of colorectal cancer should minimize intake of animal foods and increase intake of fruits and vegetables. Though fruits and vegetables may prove not to reverse the colorectal cancer, a higher fiber, low fat diet is likely to be beneficial not only protective.

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