Why do you get rectal tumor?

(1) Fat, cellulose and calories: Dietary factors play an extremely important role in the occurrence of colorectal cancer. At present, colorectal cancer ranks second in the world, second in western developed countries and eighth in some underdeveloped countries. Epidemiological observation and experimental research show that diet plays a decisive role in the occurrence of colorectal cancer, and the increase of fat consumption is parallel to the increase of incidence of colorectal cancer. The direct measurement of dietary fat content shows that people who eat a lot of fat have a high mortality rate of colorectal cancer. The study of immigrants from low-fat diet to high-fat diet found that the incidence of colorectal cancer was significantly higher than that in the original place. The mortality rate of colon cancer has increased significantly among immigrants from Japan to Hawaii, and immigrants from Poland to Australia have also shown this increase. Many case-control studies support the correlation between fat intake and colorectal cancer. However, other epidemiological data have not confirmed this correlation, especially in different parts of the same country, such as Utah. The incidence of colon cancer in the United States is far lower than the average incidence in the United States, and the fat consumption of each population is the same. The reason for this contradiction in epidemiological data is that the protective dietary factors for colon cancer are not considered. A study in northern Europe found that the incidence of colon cancer in Danes was significantly higher than that in Finland. Although the fat intake is the same, Finns consume more cellulose than Danes, which indicates that cellulose may have the carcinogenic effect of regulating fat. Recently, Willett and others once again confirmed that the occurrence of colon cancer is positively related to the consumption of animal fat. In addition, a recent epidemiological study analyzed the relationship between fat intake and various cancers, and found that fat intake was positively correlated with the occurrence of six cancers, including colorectal cancer.

Most epidemiological data show that colon cancer is related to total fat intake, not to special food fat. But there are also epidemiological studies to explain the relationship between fat types and colon cancer; Some studies believe that it is related to animal fat, while others support that plant fat has the greatest effect. In the experimental colon cancer induced by dimethylhydrazine (DMH), the animal with high concentration of vegetable oil and polyunsaturated fat has a higher incidence. On the contrary, highly polyunsaturated fish oil and monounsaturated olive oil have no enhancement effect on chemically induced animal colon cancer. Reddy et al. (199 1) reported that in a group of experiments of chemically induced colon cancer, it was found that fat type, fat consumption and time of fat consumption all had effects on the occurrence of colon cancer. There are two reports that monounsaturated fat has a protective effect on colon cancer. Anti et al. (1992) reported a double-blind controlled study, in which a patient with colon adenoma underwent biopsy after fish oil 12 weeks. The proliferation rate of the upper colon crypt slowed down within 2 weeks after fish oil supplementation. This deceleration is thought to inhibit the formation of adenoma.

The biochemical mechanism of dietary fat promoting colon cancer has not been confirmed, and it is speculated that there are several mechanisms: ① dietary fat causes the increase of steroid hormones in bile, which is harmful to colon epithelium and can cause excessive proliferation of colon epithelium; ② Free radicals produced in the process of lipid peroxidation can promote canceration; ③ Some fatty acids can promote their carcinogenicity by binding with the cell membrane, causing changes in the fluidity of the cell membrane and reacting with carcinogens; ④ Excessive linoleic acid can increase the synthesis of some prostaglandins, while the latter can promote cancer and stimulate cell proliferation; ⑤ Food fat determines the properties of intestinal bacteria and plays an important role in the metabolism of carcinogens; The carcinogenic effect of fat lies not in its special chemical composition, but in its heat density. Because fat has the highest calorie density, it is the most carcinogenic.

At present, it is not known to what extent food fat should be limited to reduce its carcinogenic effect on colon. In the United States and some western European countries, the average fat content accounts for about 40% of the total calories, which is in sharp contrast with the diet in third world countries, where fat only accounts for 10% ~ 25% of the total calories. Animal studies show that when the dietary fat increases from 10% to 40% of the total calories, there is a dose to induce colon tumors.

Another factor related to colorectal cancer in the diet is cellulose. Burkitt and Trowell first proposed that the diet of African blacks contains more cellulose, so the mortality rate of colorectal cancer is lower than that of whites, who consume little cellulose. However, the results of subsequent epidemiological studies are inconsistent. This inconsistency may be due to the fact that dietary fibres is not a special chemical entity, but a variety of compounds. The only similarity is that it comes from plants and is resistant to the action of human digestive enzymes. Different cellulose has different physiological and chemical characteristics, which can affect colon environment and colon mucosa in many ways. Some dietary fibers, such as bran, pass through the colon unchanged. Other cellulose gums are almost completely crushed by bacteria in colon, and most of them become short-chain fatty acids. These fatty acids regulate the pH value of colon and are used as the main energy source by colon cells.

Most epidemiological studies only analyzed the relationship between foods containing cellulose and colon cancer as a whole, but did not study special cellulose. However, in some studies, the risk of colorectal cancer is related to special fiber or foods containing special fiber. Kunes and others found that cruciferous vegetables such as broccoli, cabbage and soup have protective resistance to colon cancer. However, it is impossible to know whether its protective effect is due to cellulose in these vegetables or chemical preventive substances such as sulforaphane, which can stimulate enzymes to neutralize free radicals. Animal models show that special food cellulose bran and plant cellulose have protective effects on colon cancer caused by carcinogens, while pectin does not. However, some cellulose can cause changes in the colonic mucosa, which indicates that it can promote the canceration process. In experimental colon cancer, eating wheat bran and pectin can increase DNA synthesis, mucosal quality and cell migration, but oat bran can not change these changes. It must be emphasized that these influences may be inconsistent and may be related to race, gender or other factors. Considering that dietary fibres is composed of different physiological and chemical components, if it does have a protective effect, it seems that it may be unique to some celluloses.

The mechanism of cellulose in preventing colon cancer is not clear, but there are several possibilities: ① shortening the transmission time in colon, thus shortening the contact time between carcinogens in intestinal cavity and colon mucosa; ② Cellulose is combined with carcinogen in intestinal cavity and diluted, thus neutralizing its harmful effects; ③ Changes of colonic bacteria metabolizing bile acids; ④ After dietary fibres was metabolized into short-chain fatty acids in colon, the pH value in colon decreased. The decrease of pH value leads to ionization of free fatty acids and bile acids, which may be harmful. Recently, Cummings reported that the incidence of colon cancer in 20 people in 12 countries was negatively correlated with the amount of feces, and pointed out that when the intake of cellulose was >: 18g/d, the amount of feces was >: 150g/d, the occurrence of colon cancer could be prevented.

Animal studies and some epidemiological data show that excessive calorie intake and obesity will increase the incidence of various organ cancers. Tanaenbaum's early and recent studies have proved that limiting calorie intake and losing weight can inhibit chemically induced tumors, including colon cancer. International epidemiological studies and case-control studies show that increasing calorie consumption and weight gain will increase the risk of colon cancer. A study by the American Cancer Society found that the body mass index is positively correlated with the incidence of colon cancer. This phenomenon is also found among Japanese living in Hawaii. However, some epidemiological studies have not found the relationship between weight and colon cancer. At the recent seminar on "calorie and energy consumption in cancer occurrence", the conclusion was that "overnutrition is directly related to the high risk of cancer". However, it must be noted that there are complex relationships among calorie intake, energy consumption, weight and endocrine environment. Even if calorie intake does increase the occurrence of cancer, it is still necessary to judge whether the main factors are calorie intake, metabolic rate, direct effect of body weight or comprehensive effect.

According to the above situation, in recent years, the United States and other countries have recommended some dietary requirements to prevent cancer. The American Cancer Society (ACS) and the National Cancer Institute (NCI) recommend the following programs: ① Reduce fat intake to less than 30% of total calories. ② Increase the intake of cellulose to 20 ~ 30g/d, with a maximum of 35g/d ... ③ Including all kinds of fruits and vegetables. 4 prevent obesity. ⑤ moderate drinking. ⑥ Try to eat less salted and smoked food.

Reducing fat to 30% of total calories in NCI diet may be too little, but reducing fat to 20% ~ 25% of total calories may be more appropriate.

(2) Vitamins and minerals: The incidence of colon cancer is influenced by the environment. Among environmental factors, epidemiological research focuses on eating habits and food choices. In addition to fat, cellulose and calories, micronutrients and minerals with antioxidant effects were also studied. Antioxidants can scavenge or neutralize some oxygen metabolites, which are called oxygen free radicals and singlet oxygen. These metabolites are formed in the routine biochemical process of the whole body, and they may be dangerous because they can damage DNA, lipid membrane and protein. This kind of molecular damage to cells, if not suppressed, will promote the formation of cancer. Several vitamins, minerals and trace elements have antioxidant effects. Therefore, scholars focus on observing whether colon cancer increases when micronutrients and VitA, c and e values are low.

The relationship between vitamin A and provitamin A substances such as β -carotene and cancer has been widely studied. Some retinoic acid (retinoic acid) has been found to help prevent skin cancer, lung cancer and bladder cancer. It is also used to treat leukemia, myelodysplastic syndrome and promyelocytic leukemia. Animal experiments show the role of vitamin A in preventing colon cancer, but human studies are not convincing. So I don't know how much vitamin A may affect colon cancer.

The research results of vitamin C are contradictory. Some studies show that tumors in animals lacking vitamin C will increase, but others do the opposite. Human epidemiological studies have shown that people with low vitamin C intake have an increased risk of rectal cancer, but other studies have failed to show this effect.

In some studies, low serum vitamin E is associated with an increased risk of colon cancer. The longitudinal study of serum vitamin E value also shows that the vitamin E value of some cancer patients tends to decrease. However, the true location of Vit E in colon cancer is still unknown.

Calcium is a mineral, which can reduce the excessive proliferation of colonic mucosal epithelial cells. It is speculated that this local effect may help to reduce the risk of colon, especially in high-risk groups. Epidemiological studies also believe that increasing calcium intake has a protective effect. In the intervention study of chemically induced colon cancer in experimental animals, it is also obvious that calcium supplementation can reduce the incidence of colon cancer.

Epidemiological data also show that the incidence of colon cancer is high in low selenium areas, and the blood selenium value of patients with colorectal cancer is obviously lower than normal. In the animal experiment of chemically induced colon cancer, it also shows that the incidence of cancer in low selenium diet is high, and additional selenium supplementation is helpful to prevent colon cancer, although the mechanism of selenium supplementation to prevent colon cancer is still unclear. Recent clinical studies show that selenium can significantly improve the cellular immune function of patients with colon cancer.

2. Genetic factors

Heredity is an important factor in colorectal adenomatous polyposis and colorectal cancer. There are two types of patients with prominent clinical genetic factors, one is familial adenomatous polyposis (FAP) and the other is hereditary nonpolyposis colorectal cancer (HNPCC), including site-specific colorectal cancer and cancer family syndrome. Except for these two types of patients, they are all called sporadic cases.

FAP is an autosomal dominant genetic disease with an penetrance of 95%, and the incidence of its children is 50%. If this disease is not treated, it will eventually become cancerous. The mutation of APC gene can be detected in 40% ~ 70% of patients, but it only accounts for about 1% in colorectal cancer.

HNPCC was originally called Cancer Family Syndrome (CFS), and recently it was called Lynch Syndrome Type I and Type II. The main feature of Lynch syndrome is that there are no multiple colonic polyps. But the gene transfer mode of Lynch syndrome is autosomal dominant inheritance. It accounts for about 6% of the total number of colorectal cancer. Unlike FAP, it has no premonitory phenotypic signs or biomarkers to help clinicians identify cases or families. Therefore, the only key to diagnose Lynch syndrome is family history. Lynch syndrome type I is characterized by site-specific colorectal cancer, which occurs at an early age, mostly in the right colon (up to 70%), and there are more simultaneous or metachronous multiple primary colon cancers. Lynch syndrome type ⅱ, that is, in addition to Lynch type ⅰ characteristics, endometrial cancer and ovarian cancer are common. In some Lynchⅱⅱ families, there are other malignant tumors such as ureteropelvic transitional cell carcinoma, gastric cancer, small intestine cancer, pancreatic cancer and so on.

As for the so-called sporadic colorectal cancer, it is now found that its familial risk increases. The risk of the first generation relatives of patients with colon cancer is increased by 2-3 times, and the relatives of patients with colorectal adenoma are also at risk of colorectal cancer. Colonoscopy data show that the first generation relatives of colon cancer patients are twice as likely to suffer from adenomatous polyp. If the age of colon cancer patients at diagnosis is

Studies on these relatives show that the increase in family risk is due to mild to moderate genetic susceptibility. This susceptibility exists in most patients with colorectal cancer and adenomatous polyp. Existing data show that genetic factors determine individual susceptibility to colorectal cancer, while environmental factors regulate this susceptibility.

3. Colitis disease

Among colitis diseases, three diseases are most closely related to colorectal cancer. Chronic ulcerative colitis is recognized as a disease with high canceration risk, but its canceration risk is related to the length of the course, the location and scope of the lesion. When the disease stage reaches 10 years, the risk increases, and the risk increases when the lesion is confined to the left colon, and the risk of cancer in patients with ulcerative proctitis and ulcerative colitis increases. Therefore, on the whole, the risk of colorectal cancer in patients with ulcerative colitis is 10 ~ 25 times that in patients without colitis, but a large group recently reported that the cumulative risk in 25 years is only 9%. However, only 1% of colorectal cancer patients have ulcerative colitis. The incidence of ulcerative colitis is relatively high in North America and Western Europe, and relatively rare in China, so it is even rarer in colorectal cancer.

Crohn's disease is another intestinal inflammatory disease that may be malignant. It is estimated that the risk of cancer is 4 to 20 times higher than that of the general population. The distribution of malignant transformation of Crohn's disease is 25% in small intestine, 70% in large intestine and 5% in other parts of gastrointestinal tract. Although the incidence of cancer in Crohn's disease is higher than that in ulcerative colitis (4%), most cancers occur in inflammatory intestinal segments, especially stenosis and long-term fistula. Both shunt small intestine and open colorectal cancer are easy to become cancerous. Fortunately, the bypass surgery has been abandoned now, so this kind of danger is rare, but the rectal stump outside the septum sometimes stays for a long time, so it is very dangerous.

Schistosomal colitis is also a disease with high canceration rate, which is very prominent in schistosomiasis endemic areas in China. For example, Jiashan and Haining in Zhejiang are both endemic areas of trematode and high incidence areas of colorectal cancer, and their morbidity and mortality are the highest in rural areas of China, accounting for 1/4 of malignant tumor deaths, which is 4 ~ 9 times higher than other provinces and cities. According to various reported clinical data, Zhou Xigeng and others reported that there were 266 cases of schistosomiasis in 1754 cases of colorectal cancer, accounting for 15. 17%. The Cancer Hospital affiliated to Shanghai Medical University reported 1 120 cases with schistosomiasis, accounting for 18. 1%. Hangzhou Cancer Hospital reported that among 507 cases of colorectal cancer, 27.4% were accompanied by schistosomiasis. Among the 3 14 cases of colorectal cancer reported by the First Hospital of Jiaxing, Zhejiang, 96. 1% were accompanied by schistosomiasis. These data fully reflect the close relationship between colorectal schistosomiasis and cancer. Due to the long-term deposition of Schistosoma eggs in colorectal mucosa, chronic inflammation, repeated ulcer formation and repair. It leads to the formation of mucosal granulation tissue and then canceration. Among 3678 patients with advanced schistosomiasis in the First Hospital of Jiaxing City, Zhejiang Province, 24 1 patient (6.55%) was accompanied by granuloma of colorectal schistosomiasis, of which 62.7% was accompanied by adenocarcinoma, which strongly indicated that schistosomiasis was an important factor in the occurrence of colorectal cancer.

4. Colorectal adenoma

Colorectal adenoma is the most common polypoid lesion in clinic, and about two-thirds of colorectal polyps are adenomas. Histologically, adenomas are divided into three types: tubular, villous and tubular villous, among which tubular adenomas are the most common, and pure villous adenomas are rare, accounting for only 5% of all adenomas. This classification of adenoma is mainly based on the proportion of villi components, because the epithelial structure of adenoma is uneven in morphology. When the villous component accounts for 0% ~ 25%, it is called tubular adenoma, 25% ~ 75% is tubular villous adenoma, and 75% ~ 100% is called villous adenoma. From the naked eye, adenoma can be divided into three types: pedicled type, broad base type and flat type. Not all adenomas are polypoid, but only a slight lump on the mucosal surface, which is called flat polyp. Larger adenomas and villous adenomas are more prone to high variation. Epidemiological data show that the high incidence area of colorectal adenoma is the same as that of colorectal cancer. The frequent occurrence of highly anaplastic and locally invasive cancers can be seen in the pathological examination of a large group of polypectomy, which can explain that benign adenomas are often found near cancer resection specimens, which are manifested in hereditary colon cancer cases, including familial adenomatous polyposis (FAP) and hereditary nonpolyposis colon cancer (FNPCC) syndrome. Gilbertson reported a retrospective study. For 25 years, sigmoidoscopy 1 time has been performed every year for asymptomatic people over 45 years old to remove adenomas. As a result, the incidence of colorectal cancer was 85% lower than expected. Recently, Selby et al. also proved that in the past 10 years, the incidence of distal colon cancer decreased by 3 times among people screened by sigmoidoscopy. According to the preliminary analysis of NPS data, compared with the general population of the corresponding age, the incidence of colon cancer in people who entered the colonoscopy monitoring program decreased by more than 75%. These data suggest that blocking the growth of adenoma can prevent colon cancer, which is also the support of "adenoma-cancer" sequence. Of course, some people think that the occurrence of cancer is primary, that is, cancer (novo) from the beginning. Because there are some very small non-polypoid invasive adenocarcinoma and there are no adenomas nearby, no one can deny these phenomena. Both may exist, and even the smallest adenoma may be found to be malignant, which is the focus of debate. However, recent molecular gene discovery also supports the "adenoma-carcinoma" sequence. The final evidence and standard of this view is that there are markers of gene cloning in sporadic adenoma of progressive colon cancer.

5. Personal high risk factors

In the past, patients with colorectal cancer had a higher risk of developing colorectal cancer again than normal people. According to the data of St Marks Hospital, among 33,865,438+0 patients who underwent colorectal cancer resection, the incidence of metachronous colorectal cancer was 65,438+0.5%, and in the cases followed up for 25 years, the incidence was 5%. If the adenoma is resected at the same time, the incidence rate is 65,438 00%. Although most metachronous colorectal cancer occurred within 10 years after resection, it was reported that the incidence of metachronous colorectal cancer was 3.4%, and 67% occurred above 1 1 year after the first resection. It shows that the risk of metachronous colorectal cancer seems to be lifelong.

Among female patients with breast cancer, ovarian cancer or cervical cancer, the risk of colorectal cancer is significantly higher than that of those without the above medical history. According to the analysis of tumor registration data of Si Long Kettering Cancer Center, the risk of colorectal cancer in breast cancer patients is 1.2 and 1. 1 respectively, and the risk of colorectal cancer in the future is related to the age of breast cancer diagnosis.

The causal relationship between radiation and cancer stems from the epidemiological data of survivors after the atomic bomb explosion in Japan in World War II. Although the early data did not show any relationship, the long-term follow-up results showed that the mortality rate of colorectal cancer increased significantly. Slaughter reported the first group of cases of mucosal cancer after radiotherapy in 1957, including 2 cases of colon cancer and 1 case of anal canal cancer 1. Since then, there have been many case reports and animal experimental studies on this causal relationship. Case studies show that women who receive radiotherapy for cervical cancer have an increased risk of colorectal cancer. Of course, the real risk caused by this radiation is difficult to determine, because the risk of gynecological cancer in women has increased. However, the risk of colorectal cancer in ovarian patients who have received radiation after 5 years is indeed higher than that in patients who have not received radiation. Similarly, the risk of colorectal cancer increases after radiotherapy for benign diseases. Therefore, the occurrence of colorectal cancer should be closely monitored from 5 years after radiotherapy.

Second, vigilance: drinking unhealthy juice will get rectal cancer.

More and more doctors, scientists and public health officials believe that drinking more natural fruit juice may be harmful to health. Obesity caused by drinking natural fruit juice is no different from drinking soda such as cola and saccharin alcoholic drinks.

A glass of juice is mixed with the sugar of multiple portions of fruit. If calculated according to the same weight, juice contains more calories than soda.

You probably can't imagine that a cup of 240 ml pure fruit juice generally has about 100 calories, which is higher than the recognized "obesity drink" cola.

A cup of freshly squeezed orange juice contains 1 12 calories, apple juice contains 1 14 calories and grape juice contains 152 calories. The same amount of Coca-Cola contains 97 calories, while Pepsi contains 100 calories.

Experts explained that people usually feel full when eating an apple, but four apples can only squeeze out a small amount of juice, even if they drink them all, they are not full. But even this cup of juice contains much more calories than an apple. This is especially true for juice drinks, and a considerable number of juice drinks have added sugar. At present, there are many studies on fruit juice and fruit juice drinks in the world, and many research results are aimed at protecting children from type 2 diabetes.

In addition, fruit juice contains a lot of fructose. Eating a lot of fructose will increase the risk of heart disease and type 2 diabetes, because fructose is more easily converted into fat by the liver than glucose.

Many research reports show that fruit juice is good for health and can lose weight. In 2008, a survey of 3,665,438+08 children aged 2 to 65,438+065,438+0 found that children who drink at least 6 ounces (about 65,438+077 ml) of fruit juice every day are lighter and have more vitamins and minerals than children who don't drink fruit juice at all. However, many experts believe that this data only reflects the correlation between fruit juice and healthy diet, not the causal relationship.

Children who drink more juice are more likely to eat breakfast, and children who eat breakfast are lighter than those who don't.

Eight days makes you dependent on sweet drinks.

In addition, some experts worry that children who drink a lot of sweet drinks will like sweets more when they grow up. A study in 2004 found that children aged 8 to 10 preferred sweet drinks after drinking sugary orange juice for eight consecutive days. They also drink more because they are used to the sweetness of orange juice.

Artificial pigments affect IQ.

Whether it is a fruit-flavored drink or a low-concentration juice drink, artificial colors will be used-bright colors will allow consumers to associate drinks with fruits in their perception. When the fruit juice content is too small to make the beverage have rich and colorful fruit colors, cheap artificial colors are the best choice.

The harm of artificial pigments to human body, especially children, has long been studied in modern nutrition.

Synthetic pigments will affect children's intellectual development. Children who often drink fruit juice and drink less water often have poor appetite, hyperactivity, bad temper and light weight.

Seven kinds of chemical additives such as lemon yellow and sunset yellow will reduce children's IQ by 5 points. Lemon yellow is a yellow food pigment contained in pea paste and cotton candy, and it is forbidden to be used in food and drink of children under 3 years old. On the other hand, quinoline yellow is an edible pigment often added to fruit juice drinks, soft drinks and cold capsules. Sodium benzoate, a preservative widely used in fruit juice drinks, is also harmful to health.

Too much pigment enters children's bodies and easily deposits on their immature digestive tract mucosa, causing loss of appetite and indigestion, interfering with the functions of various enzymes in the body and adversely affecting metabolism and physical development.

Obviously, a fruity beverage made of artificial colors, sweeteners, acidulants, spices and other food additives without any fruit juice has almost no nutritional value of any fruit.

Fruit juice will make you anemic?

In addition, fructose will also hinder the body's absorption of copper. The lack of copper will affect the production of hemoglobin, which will lead to anemia.

Domestic survey data show that the physical development of children addicted to juice drinks is polarized, either too thin or too fat. Because the sugar content of fruit juice drinks is too high, children can get a lot of heat energy from it after drinking, which affects eating dinner. This will inevitably lead to insufficient intake of protein, some vitamins, minerals and trace elements, which will affect physical and intellectual development.

Will make you more likely to get rectal cancer.

After squeezing and filtering, fruits and vegetables mainly throw away insoluble fibers. What effect does this insoluble fiber have on human body?

This fiber has no heat, is insoluble in water, and cannot be completely digested in the gastrointestinal tract. It contains vitamin B, can fill the gastrointestinal tract, and is a very effective and safe diet food.

After it enters the human body, it will enter the large intestine intact and become food for bacteria in the large intestine. The metabolism of bacteria will produce some ingredients that are beneficial to the human body. The biggest advantage of insoluble fiber is to promote the peristalsis of the large intestine, shorten the time of food staying in the large intestine, prevent constipation, and reduce the chance of bacteria in the large intestine turning food into toxic substances. It can also dilute the existing toxic substances in food, reduce the chance of injury to the large intestine, and prevent the occurrence of hemorrhoids and rectal cancer in the large intestine. When this fiber is lacking in food, the risk of colorectal cancer will increase.