Cancer And The Food We Eat
( Originally Published Early 1960's )
Nutrition and cancer.
Life depends upon energy and building blocks that are derived from food. The main sources of energy are carbohydrates, such as starches, which are broken down to sugars, and fats, which are converted into fatty acids. Proteins are necessary not only as energy sources but as building blocks that are reconstructed with the amino acids derived from proteins. In addition to these major diet components, called macronutrients, the body requires minerals and salts, and a class of micronutrients called vitamins. These are similar to enzymes, since they are needed in certain essential metabolic reactions, but unlike them cannot be made by the body and have to be supplied from external sources.
Cancer, being a form of cellular growth, requires the same types of nutrients as the normal body. Despite intensive experimentation, no specific nutrient has been found that is essential for the development or growth of cancer and not needed by the host. However, changes in diet that produce effects on the animal, such as severe weight loss, also affect tumor growth. In general, the fully developed cancer is a very successful competitor for a limited food supply.
One of the more common manifestations of advanced cancer disease is loss of weight, to the extent of wasting, or cachexia. Even when the host has reached this stage, the cancer continues to grow. Some years ago scientists observed that by feeding cancer tissue to rats on which similar cancers were growing, this body weight loss could be partly prevented. The cancers, therefore, were competing favorably for the nutrients of the host, and acting as "nitrogen traps" by accumulating nitrogenous compounds needed for body function. Attempts to identify more specific factors that are replaced by feeding tumor tissue, however, have not been successful up to now, but the sodium ion appears to be important.
Nutrition, as a source of energy and of material for the synthesis of new tissue, plays a role not only during the growth phase but also during the development phase of cancers. Albert Tannenbaum of Chicago showed that by the simple expedient of cutting the food intake of mice by one-third, at which level the animals were quite healthy but not as fat, the occurrence of breast cancers was reduced by 50 percent or more. Restriction in the total caloric intake also reduced the occurrence, or slowed the time of appearance of several other types of tumors in mice. At the time that these laboratory experiments were being performed, tabulation of insurance policy holders by weight at their insurance examination also indicated a higher subsequent occurrence of cancers among those who were overweight. Alas, as too often happens, this interesting confirmation of laboratory work in man has not stood up under more rigid analysis. Overweight women with diabetes do develop somewhat more cancer of the body of the uterus and of the pancreas, but there is no general increase in cancer related to excess weight in man.
The development and growth of certain specific cancers in animals are also modified by the content of vitamins and other micronutrients. The early experiments on the production of liver cancers in rats fed on azo dyes that were reported from Japan could not be duplicated in the United States. Analysis of the discrepancy showed that the Japanese laboratory diet consisted mainly of polished rice, whereas in the United States it was supplemented for more optimal intake. Further studies revealed that riboflavin, one of the B vitamin complex, protected the animals, probably in the detoxification of the azo dyes. However, the role of these vitamins was not demonstrated in the occurrence of several other experimental tumor models, including the "spontaneous" hepatomas of mice.
There is some evidence that vitamin deficiency in man plays a role in the occurrence of cancers of the oral cavity and the esophagus. Chronic vitamin B complex deficiency, due to inadequate supply of vegetables, appears to be incriminated. However, reliable dietary histories over many years are notoriously hard to come by, and such deficiencies are probably a part of a number of necessary factors. Experimentally in animals, and also in human beings, deficiency of Vitamin A produces a thickening and piling up of the lining of the stomach, but these changes do not proceed to the development of actual cancers.
The mouth is one of our major routes of contact with our environment. The food we eat may contain preservatives and other, purposefully introduced additives; it may be the source of chemicals produced from the very food by heating and other processes; it may become contaminated by bacteria, fungi and other organisms that may produce metabolites such as the antibiotics. And, of course, we can introduce through the mouth an ever increasing number of chemicals for medicinal, cosmetic and pleasurable purposes. These exposures are not limited to the technically advanced populations. The diets of primitive peoples have similar opportunities for contamination, including the addition of herbs and other "natural" products that also may contain alkaloids and other chemicals.
We have already alluded to the possible roles of plant and mold products in the occurrence of liver cancers among the sub-Sahara peoples. Smoked fish, charred coffee, and burnt meat contain impressive amounts of identifiable 3, 4-benzyprene and have been suggested as factors in the occurrence of cancer. However, it should be pointed out that the actually burned portion of such produce is seldom ingested because it is unpalatable. The supposition that smoked fish is a causative factor in the high incidence of gastric cancer in Iceland must be considered only as a lead for further investigation. An equally high gastric cancer rate is found in Japan, where fish is not smoked but preserved in salt.
Cancer producing chemicals and other agents that gain access by the oral route may produce their effects at sites distant to the gastrointestinal tract. The end effects depend to a great extent upon the metabolic pathways and the route of excretion or deposition of such materials. When radium or radioactive strontium is ingested, the elements are deposited in bone, and bone sarcomas are induced. The azo dyes on ingestion produce the carcinogenic reaction in the liver. The fluorenes induce tumors of the breast and of the ear as well as in the liver of rats. Diethylstilbestrol and other compounds with estrogenic activity introduced by the oral route exert their carcinogenic potential in the breast and other distant target tissues, but not on the gastrointestinal tract. The polycyclic hydrocarbons on ingestion will produce intestinal cancers in mice, but also induce lung tumors, leukemia and breast cancer in susceptible strains of rats.
Volatile and particulate materials suspended in the air are not only inhaled, but usually ingested as well. The absorption of such materials is therefore not limited to the respiratory tract but also may proceed through the gastrointestinal tract. Important effects may be derived from a combined action of several cancer producing and cancer stimulating agents through different routes of entry. For example, mice given small doses of carbon tetrachloride by mouth become more liable to develop tumors following injection of polycyclic hydrocarbons. Perhaps a combination of oral alcohol and the inhalation of smoke may represent a similar situation in man, as in the occurrence of cancer of the esophagus in people who drink and smoke to excess.