Essay on Food Habits and Cancer | Diseases | Biology

Here is an essay on ‘Food Habits and Cancer’ which states – How food habits may trigger the development of cancer.

Essay # 1. Food Contains Carcinogens as well as Anticarcinogens:

Besides tobacco and alcohol, where else do people encounter chemicals that may be carcinogenic? Of the thousands of chemicals we encounter each day, most of the chemicals that enter our bodies do so because we deliberately ingest them in the form of food. Although it is not often viewed that way, food is nothing more than a complex mixture of thousands of different chemicals. So it is obvious to ask whether any of these chemicals can cause cancer.

The narrow question of whether food contains any carcinogens is fairly easy to answer. Laboratory studies employing the Ames test to screen for chemicals that cause mutations, combined with animal testing to see if particular chemicals trigger tumor formation, have led to the identification of dozens of chemicals in food that can cause cancer.

Particular attention has been paid to artificial additives and pesticides, although the potential hazards from such substances are probably overempha­sized. It has been calculated, for example, that our daily diet is contaminated by about 0.05 to 0.10 milligrams of potentially carcinogenic synthetic pesticides.

To put this number in proper perspective, the same diet contains about 1500 milligrams of natural pesticides—that is, chemicals produced by plants (fruits and vegetables) to protect themselves against insect and animal predators. Thus, 99.99% of the pesticides we consume on a daily basis are natural components of fruits and vegetables.

When these natural pesticides are tested in animals, many turn out to be carcinogenic (Table 3). Such natural carcinogens are found in a wide variety of fruits and veg­etables, including apples, apricots, bananas, broccoli, Brussels sprouts, cabbage, cantaloupe, carrots, cauliflower, celery, cherries, grapefruit, grapes, honeydew, lentils, lettuce, mushrooms, mustard, oranges, parsley, peaches, pears, peas, pineapples, plums, potatoes, radishes, raspber­ries, and tomatoes, to name but a few!

In fact, probably every fruit and vegetable sold at the grocery store contains natural plant chemicals that can cause cancer in animals, and the overall concentration of these molecules is thou­sands of times higher than the concentration of the synthetic pesticides that are present as contaminants.

Despite the large number of natural carcinogens present in fruits and vegetables, dozens of epidemiological studies have shown that people who eat lots of fruits and vegetables actually have a decreased risk of developing cancer—especially stomach and colon cancers—rather than an increased risk! One possible explanation for the apparent paradox is that fruits and vegetables contain thousands of different chemicals, and while some have the potential to act as carcinogens, others may function as anticarcinogens that protect against the development of cancer.

So eating fruits and vegetables involves the consumption of a vast array of chemicals, and the potentially carcinogenic effects of some may be blocked by the protective effects of others. Lycopene in tomatoes, epigallocatechin gallate in green tea, resveratrol in the skin of red grapes, and sulfides in garlic are among the numerous natural substances currently being investigated for possible anticarcinogenic activity. These molecules exhibit a broad range of properties with potential cancer- fighting relevance, but the exact role they play, if any, in protecting against cancer is yet to be determined.

Given that eating fruits and vegetables tends to decrease rather than increase cancer risk, it seems unlikely that natural pesticides, or tiny residues of synthetic pesticides, represent much of a cancer hazard. However, at least one natural substance found in some foods—a molecule called aflatoxin—does pose a significant cancer risk.

Aflatoxin is a toxic chemical produced by the mold Aspergillus, which grows on grains and nuts stored under humid conditions. Contamination of food with aflatoxin is prevalent in certain areas of Africa and Asia, where its presence correlates with high rates of liver cancer. Laboratory tests have shown that aflatoxin is a strong mutagen and one of the most potent carcinogens ever studied.

A total dose of only 0.0001 gram of aflatoxin given to rats spread out over 16 months is sufficient to cause every single animal to develop liver cancer! Fortunately, aflatoxin contamination is only a minor problem in the United States. At least part of the reason can be traced to the widespread use of pesticides that kill the mold responsible for producing aflatoxin. In this particular case, using pesticides may actually be decreasing a carcinogenic hazard by preventing aflatoxin contamination of grains and nuts.

Food preservation techniques are another potential source of carcinogenic chemicals. It has been known for many years that high rates of stomach cancer are common in countries where large amounts of smoked, cured, and pickled foods are consumed. This may help explain why the incidence of stomach cancer in Japan is roughly ten times higher than in the United States.

The heavy use of salt, nitrates, and nitrites in preserved foods is thought to be at least partly responsible. Salt is not intrinsically car­cinogenic, but high salt intake can damage the stomach lining, stimulate cell proliferation, and trigger an inflam­matory response that makes the stomach lining more susceptible to other carcinogens.

Nitrate and nitrite are not very carcinogenic either, but they can be converted both in cured meats and in the stomach to N-nitroso compounds, which are potent carcinogens when tested in animals. However, the role played by such compounds in the etiology of human cancer is far from clear; especially since the data linking cancer risk to preserved foods may be confounded by other variables. For example, countries with a higher consumption of preserved foods also tend to have a lower consumption of fresh fruits and vegetables, which might contribute to the high rates of stomach cancer.

Essay # 2. Red Meat, Saturated Fat and Excess Calories Contribute to Cancer Risk:

One of the better-documented relationships between eating habits and cancer risk involves the connection between meat consumption and colon cancer. As shown in Figure 11, countries with high levels of meat consumption typically have higher colon cancer rates than countries where less meat is eaten. However, confounding variables might be responsible for the observed trend, so caution is needed in drawing any cause-and-effect conclu­sions.

For example, people who consume large amounts of meat might also eat fewer fruits and vegetables, in which cause the high rate of colon cancer could stem from eating too few fruits and vegetables rather than, or in addition to, eating too much meat.

The main usefulness of epidemiological data like those presented in Figure 11 is not in establishing cause and effect but in generating hypotheses about possible dietary risk factors that can be tested through additional epidemiological and experi­mental studies.

In the case of meat consumption and colon cancer, additional evidence has tended to support the idea that eating red meat (but not poultry or fish) contributes to colon cancer, perhaps through the large amount of saturated fat it contains. (The term saturated refers to a fat molecule in which all carbon atoms are bound to the maximum number of hydrogen atoms.)

Diets rich in saturated fat have frequently (although not always) been associated with increased rates of colon cancer in human epidemiological studies. Animal studies have confirmed that dietary fat is capable of increasing colon cancer rates, but the way in which fat increases cancer risk is not well understood and may involve indirect mechanisms.

For example, high-fat diets are known to cause the liver to secrete large amounts of bile acids into the intestines. One of these bile acids, lithocholic acid, can produce DNA damage and has been found to induce colon cancer when injected into animals.

Another possible indirect mechanism is related to the fact that fats contain more calories per gram than do proteins or carbohydrates. Animal studies have revealed that cancer rates go up as the number of calories in the diet is increased, so the elevated cancer rates seen in people who eat high-fat diets may be caused by the consumption of excess calories.

Support for such an inter­pretation has come from epidemiological data showing that people who are overweight exhibit an increased cancer risk. In fact, some studies suggest that up to one- third of all cancers of the colon, breast, kidney, and digestive tract are linked to obesity and lack of exercise.

In addition to the possible roles played by fat and calo­ries, cooking techniques may also influence the cancer risks associated with meat consumption. Grilling meat at high temperatures over an open flame causes fat droppings on the hot fire to create smoke containing polycyclic aromatic hydrocarbons, which are carcinogenic chemicals that adhere to the surface of the meat.

Carcinogenic aromatic amines are also produced under such conditions or even by regular cooking methods when meats are cooked at high tempera­tures or for a long time. The idea that cooking techniques can influence the production of carcinogens is supported by studies reporting elevated rates of colon cancer in people who prefer eating well-done meat with a darkly browned surface.

Essay # 3. Diet Appears as an Important Factor for Determining Cancer Risk (Dietary Risk Factor):

From this brief overview of dietary risk factors, it should be apparent that the human diet consists of a complex mixture of foods that are difficult to study in a systematic way. Consider how much easier it is to study smoking: Scientists simply collect data on people who smoke varying numbers of cigarettes per day and look for a dose- response relationship between smoking and lung cancer.

In contrast, it is difficult to find people whose diets differ in the quantity of only a single type of food and to study this difference systemically over many years. Moreover, the effect of any single food on cancer risk tends to be much smaller than the impact of cigarette smoke, making it more difficult to measure its influence reliably.

Dietary studies are also hampered by a lack of reliable methods for determining the kinds of foods that people eat. Consider, for example, the question of whether saturated fat in the diet increases the risk of breast cancer. A number of early retrospective studies suggested a link between fat consumption and breast cancer, but later prospective studies have generally failed to detect such a relationship.

One possible explanation for the conflicting data is related to the way in which fat intake is measured. The most commonly used approach is a food-frequency questionnaire that asks people to recall the kinds of foods they have been eating. A less widely used, but more accu­rate approach, is to ask participants to keep a food diary in which they record what they eat each day.

When the two approaches were compared in 25,000 participants involved in a long term study called the European Prospective Investigation into Cancer and Nutrition, the data showed that breast cancer risk was associated with saturated fat intake when measured using a food diary, but this connection was not detected in the same individuals when fat intake was measured using the food-frequency questionnaire. Such observations suggest that imprecise methods for assessing eating habits may be hampering our ability to identify dietary risk factors.

Given such obstacles, it is easy to understand why the history of dietary research has included many conflicting claims about the cancer hazards associated with particular foods. Of course, the difficulty in identifying the risks or benefits associated with individual foods does not mean that diet is unimportant.

To the contrary, the differences in cancer rates exhibited by populations with differing diets have led epidemiologists to estimate that diet plays a role in about 30% of all fatal cancers. This value, if correct, would make diet almost as important as tobacco smoke in determining a person’s overall risk of dying of cancer. However, assessments of dietary impact involve data that are much less precise than data related to tobacco use, making the 30% estimate no more than a rough approxi­mation.

The limited nature of our current understanding concerning the role played by diet, combined with its potential importance if the 30% estimate turns out to be correct, makes dietary studies a vital area for future research.