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Gastrointestinal nutrition and cancer

Colorectal Cancer



Many theories have been put forward about the role of nutrition in the development of colon cancer. The human diet includes a large number of substances with mutagenic and carcinogenic properties, as well as antagonists and blockers of these compounds. Therefore, it is very difficult to determine which of them has a damaging effect. Carcinogens that damage the upper gastrointestinal tract are usually highly reactive compounds with a short half-life. In this regard, it is of great interest to study the pro-carcinogens and mucosal enzymes contained in the diet that activate them.

It is rather difficult to isolate the components of a regular diet, which are a risk factor for cancer. According to studies, the risk of developing colon cancer rises by 2.3% with every 100 calories consumed during the day. Moreover, the effect of the calorie diet on the risk of cancer is higher than the influence of its individual components. Data from epidemiological studies were obtained by studying the effects of consumption of fat, meat, fiber. A clear relationship has been established between the amount of fat and meat consumed and the incidence of colon cancer.

The mechanism by which a fat-rich diet facilitates the formation of colon tumors is associated with the action of bile acids on the intestinal mucosa (increased proliferation of intestinal epithelium). An increase in animal fat consumption from 62 to 152 g per day causes a significant increase in the content of bile and fatty acids in feces. At the same time, its volume, frequency of bowel movements, time of movement of feces in the intestines, content of? -Glucuronidase, the degree of degradation of steroids in it do not change. Intraintestinal administration of deoxycholic acid accelerates the proliferation of intestinal epithelium. This bile acid stimulates the formation of oxygen radicals, which in turn stimulate cell proliferation. This effect of deoxycholic acid can be eliminated by the introduction of agents capable of neutralizing the superoxide anion (for example, superoxide dismutase) or inhibiting the activity of lipoxygenase. Thus, free oxygen radicals, contributing to the formation of fatty acid oxidation products, stimulate the proliferation of colon epithelium. Oxidation of unsaturated fatty acids leads to proliferation stimulants. This explains the pronounced stimulating effect of unsaturated fatty acids on tumor growth in the experiment. Thus, bile acids and fat play a prominent role in the pathogenesis of transverse colon and rectal cancer.

Some fats can induce mitosis only in tumor epithelial cells, without affecting normal colon cells. Diglycerides containing stearic, palmitic, and myristic acids in the side chains are determined in feces at concentrations sufficient to stimulate the onset of mitosis (experiments were performed on cell cultures of human adenoma, carcinoma). Thus, a food rich in fat, even with a single intake, can stimulate the proliferation of intestinal epithelium. However, despite the significant effect of fats on the proliferation of both normal and transformed cells, the role of individual lipids in this process may depend on the stage of maturation of the epithelial cell.

Alimentary fiber. Foods consumed by residents of Western countries are poorer in dietary fiber than foods consumed by residents of other regions. This can play an important role in the pathogenesis of colon cancer. But the comparison is complicated by the fact that in countries of other regions, despite a smaller proportion of fat consumption, there is, at the same time, a shorter lifespan. If we summarize all the research data on this issue, most of them revealed a protective effect of fiber, although some did not show any effect. But not a single study found a stimulating effect of fiber on the development of colon cancer.

International studies have shown that stool volume directly depends on polysaccharide intake in the form of dietary fiber, and the incidence of colon cancer is inversely proportional to stool volume. Based on the fact that residents of Western countries, having a high risk of cancer, secrete approximately 80-120 g of feces per day, scientists suggested that an increase in fiber intake (more than 18 g per day) will lead to an increase in stool volume up to 150 g / day or more. This significantly reduces the risk of cancer. Studies have shown that adding 13.5 g / day of bran fiber to the diet significantly reduces proliferation of rectal epithelium in a group of patients with an increased risk of developing a disease who have previously undergone bowel resection for cancer.

There are several mechanisms of the protective effect of fiber on the intestinal mucosa. Fiber helps increase the speed of movement of feces in the intestines, and also, due to its volume, reduces the concentration of other components of the stool. All this reduces the duration of contact of carcinogens with intestinal epithelium. Secondly, fiber polymers are able to bind toxic substances and prevent their contact with the intestinal epithelium. Thirdly, fiber is not digested and is not absorbed in the small intestine, but is fermented by colon bacteria. This lowers the pH of the feces, forming "volatile" short chain fatty acids. These fermentation fatty acids protect the intestinal wall from damage by deoxycholic acid. One of them - butyric acid - is found in large quantities in the lumen of the intestine. It is an important source of energy for the intestinal epithelium and can cause differentiation of epithelial cells in tissue culture.

The effect of non-steroidal anti-inflammatory drugs. According to epidemiologists, people taking aspirin are less likely to get cancer. As shown in experiments on animals with colon cancer, aspirin and other non-steroidal anti-inflammatory drugs inhibit tumor growth. Moreover, in patients with fibroadenomatous polyposis treated with sulindac, belonging to the group of NSAIDs (non-steroidal anti-inflammatory drugs), adenomas regression was observed.

In 1991, the ACS (American Cancer Society) conducted a large-scale study covering more than 660 thousand people. A significant decrease in the relative frequency of death from colon or rectal cancer who took aspirin (> 16 times per month) was found to be 0.60 in men and 0.58 in women. A decrease in the risk of developing cancer was observed even in people who took aspirin no more than 1 time per month. This gave rise to discussions about the mechanism of action.

NSAIDs and the required dose of the drug. The most significant result of these studies was the detection of an almost 40% reduction in mortality from cancer of the esophagus and stomach. Moreover, the maximum protective effect was observed with prolonged (more than 10 years) administration of NSAIDs, and there was practically no effect with the localization of cancer outside the gastrointestinal tract.

There are many assumptions about the mechanism of action of aspirin and other NSAIDs to prevent the development of tumors of the gastrointestinal tract. This effect cannot be completely explained by a change in the level of prostaglandin secretion in the gastrointestinal tract. It was shown that malignant cells of the gastric mucosa in an in vitro culture mainly produce leukotrienes (unlike normal gastrocytes that produce prostaglandins). Moreover, leukotrienes have a stimulating effect, and prostaglandins have an inhibitory effect on the growth of tumor cells.
Probably, during malignancy of a cell, its reaction to eicosanoids may change.



Stomach cancer

There are significant regional variations in the incidence of gastric cancer, depending on a whole range of factors. There is no single reason for the difference in the incidence of cancer, and there is no evidence that any product plays a significant role in carcinogenesis. The consumption of carbohydrate-rich foods is associated with an increased risk of developing stomach cancer, and the consumption of horse beans, potatoes, sour pancakes (a traditional food in the Shandong province of China) plays an important role in this. But not in all areas with a high risk of developing stomach cancer, these foods are found in the diet. Moreover, a carbohydrate-rich diet is often combined with increased salt intake, the use of pest-affected grains, and low consumption of fresh vegetables and fruits. In Japan, the risk factor is the high consumption of dried fish, soy sauce, marinades in combination with a reduced consumption of fruits and vegetables. Use for preservation of food marinades and drying is most common in areas with insufficient capacity for freezing food. It is believed that the advent of home refrigerators and the wider use of frozen food have led to a decrease in the incidence of gastrointestinal cancer in North America and Europe. However, there is no clear evidence of the positive effect of storing food in the refrigerator on a decrease in the incidence of cancer, nor on the effect of a decrease in the exposure of the gastric mucosa to mutagens or an increased consumption of anticarcinogens. In addition, these observations were carried out even before the discovery of Helicobacter pylori and its effect on the gastric mucosa.

Some foods can neutralize the effects of carcinogens. For example, garlic and onions have a protective effect on the gastric mucosa.

The effect of tobacco and alcohol. In the United States, increased alcohol consumption and tobacco smoking increase the risk of stomach cancer. But tobacco is unlikely to be the leading carcinogen in gastric cancer, because the frequency of this disease decreases despite the fact that tobacco consumption has increased sharply in the 20th century and the associated increase in the incidence of lung cancer. A 2.7-fold increase in the relative risk of developing stomach cancer in smokers was revealed, but it was not possible to determine the dose at which this carcinogenic effect begins. It is believed that alcohol and tobacco hide some other carcinogenesis factor. It can be a gram-negative microorganism Helicobacter pylori, which causes chronic gastritis. The epidemiology and role of Helicobacter pylori in carcinogenesis are discussed in detail in the section "The role of inflammation in the occurrence of gastric cancer."

Consumption of water and nitrates. Stomach cancer has a high incidence in Colombia. In this South American country, areas with a high and low risk of gastrointestinal cancer have been identified, a detailed study of the differences in the diets traditional for these areas has been carried out. Groups of people with an increased risk of cancer consume water from reservoirs with a higher nitrate content than populations with a lower risk, and emit a correspondingly higher amount of nitrate in the urine. People with a high risk of cancer are more likely to have atrophic gastritis and intestinal metaplasia of the gastric epithelium. In areas with increased risk, about 75% of the population by age 45 have atrophic gastritis. In areas with an intermediate or low risk of cancer, atrophic gastritis is found in only half of the population. It is believed that a large number of other substances contained in water are involved in carcinogenesis, for example aflatoxins. They do not exclude a carcinogenic effect when consuming pepper, a deficiency of vitamins and minerals, and excessively “soft” water. But the clinical cases of cancer that has arisen under the influence of these factors have not yet been described.

It is believed that N-nitroso compounds (nitrosoamines) play an important role in carcinogenesis of the upper gastrointestinal tract. This is due to their spontaneous formation from food and the alkylating effect on nucleic acids. Nitrosoamines are formed in the stomach from nitrites and amines. Their formation does not require the presence of enzymes, but a low pH value is required. These are very unstable compounds, and they enter into various reactions at the site of their formation. In fact, the components of carcinogenesis in the stomach can be the products of various reactions, as well as carcinogens formed from precursors (carcinogens) under the action of enzymes of the gastric mucosa.

For the formation of nitrosoamines in the stomach, the presence of nitrites is necessary. Drinking water may contain varying amounts of nitrates, which are absorbed in the intestines and secreted into saliva. Nitrates are reduced to nitrites under the influence of microflora of the oral cavity and stomach. Typically, human saliva contains from 6 to 10 mg / l of nitrites and 15–35 mg / l of nitrates. The level of nitrite in the gastric juice is slightly lower, but it increases with increasing pH in the presence of nitrate-reducing bacteria. This picture is observed with atrophic gastritis, after an operation aimed at reducing acidity in the stomach. The concentration of salivary nitrates and nitrites increases significantly after an additional dose of nitrates is received. Their content is high in patients with stomach cancer.

The sources of nitrite intake into the stomach were studied using the example of a typical US diet. About 20% of nitrites are components of the daily diet. The largest amount of food nitrates comes from vegetables - more than 85%. About 25% of food nitrates are involved in the cycle between the intestines and saliva. About 20% of nitrates under the influence of microflora of the oral cavity are reduced to nitrites, which make up about 80% of all nitrites present in the contents of the stomach. The hypothesis about the role of amino compounds in the genesis of gastric cancer is based on their amount in food. The precursors of nitrosoamines are a large number of compounds, many of which occupy an important place in the diet of residents of areas with an increased risk of developing stomach cancer. Substances such as vitamins C and E inhibit the formation of nitrosoamines from amines and nitrites. Comparative measurements of the content of N-nitrose-containing substances were carried out in healthy people and patients with diseases of the stomach. With an increase in the pH of the stomach from 1 to 7, there was an increase in the content of N-nitroso compounds. The highest levels of these potential carcinogens were determined in patients with gastric carcinoma, with malignant anemia, as well as after partial gastrectomy. The theory that nitrosoamines are carcinogens explains the existence of areas with a high risk of stomach cancer. According to this theory, the occurrence of gastric cancer requires: food sources of nitrates, mechanisms for their recovery into nitrites, food sources of amines, as well as blocking or absence of antagonists of these mutagens.

Other factors. The era of industrialization in the 20th century brought plastics, solvents and other substances to our lives. This led to a change in diet, environmental factors, but, to the surprise of scientists, did not increase the number of diseases of stomach cancer. Moreover, the sharp increase in consumption in the United States over the past 30–40 years of grilled products did not affect the incidence of gastric cancer.
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Gastrointestinal nutrition and cancer

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