A case-control study of diet and bladder cancer in men was conducted in five regions of Spain (117). Each of 432 case-patients was matched with one hospital and one community control. The average dietary pattern was typical for Mediterranean populations. Subjects in the highest quartile of intake of saturated fat were at significantly increased risk of bladder cancer. Smaller risks associated with high intake of monounsaturated fats and calcium and a protective effect of iron disappeared after correcting for saturated fat. Vitamin E remained slightly protective after correction for saturated fat. No association was seen for intake of retinol, vitamin C, total vitamin A, or carotene. Tobacco smoking and occupational exposures were major risk factors but failed to explain all cases of bladder cancer in this study. Smoking and occupational exposures were also the major risk factors for bladder cancer in a German study (118). A significant twofold increase in risk was associated with heavy coffee consumption in men and women and with beer and total fluid consumption in men. Chronic urinary infection and family history of bladder cancer were also risk factors. For men, frequent consumption of high fat meals was a significant risk factor. Frequent consumption of canned foods increased risk for   both   men and women. Dietary, smoking, family history, and medical history variables did not interact with risk attributable to occupational exposure.

OVERVIEW

The link between diet and cancer is firmly established in principle. Milner reviewed the information about nutrients and nonutrients whose effects on carcinogenesis have been verified, particularly those for which mechanisms of action can be explored (1). At same time he emphasized that the overall diet, not a single dietary component, is what can turn events toward or away from cancer. A corollary of this is that when cancer occurs, the dietary culprit is unlikely to be a contaminant or carcinogen taken out of the contest of  the total diet. This idea was underscored in a historical look at interest in the link between diet and cancer (2). According to traditional wisdom, malignancies arise from exposure to carcinogens, which were therefore the main target for research. But the list of chemical carcinogens grew so fast and so large that it became impossible to identify which ones pose a significant hazard, let alone to know what to do about it. Meanwhile, epidemiologists were proposing “life-style” hypotheses emphasizing dietary pattern. According to this line of thinking, the overall diet modulates the influence of a host of carcinogenic and anticarcinogenic  agents.

The proceedings of a conference on nutrition and cancer were published as a supplement to Cancer Research (3). Sessions at this conference were devoted to fats and energy, micronutrients and microconstituents, diet-associated carcinogens and mutagens, and mechanisms and risk assessment. In his keynote address, Doll spoke of the emergence of consensus among epidemiologists that diet might be responsible for 30-60% of cancers in developed countries-and that reduction of this effect would require decreasing consumption of fat, increasing require decreasing consumption of fat, increasing consumption of fruits, vegetables, fibers, and certain micronutrients, and perhaps improving methods of food preservation (4). He reviewed dietary trends and trends in cancer incidence and mortality, with examples for specific countries and cancer sites. His conclusions are encouraging : dietary changes that might reduce risk of fatal cancer by 20-60 % are practicable, and such changes have probably already contributed to recent reductions in the incidence of cancers of the stomach, colon, rectum, gallbladder, ovary, and endometrium. Participants in a panel discussion looked to future lines of inquiry that might be productive given the new perspective on diet and cancer (5).

A lively article highlighted some recent reviews of issues related o cancer and diet (6). The author rationalized the discrepant findings of a study linking meat consumption whit colon cancer in North American nurses and a case-control study in Japan that demonstrated an inverse relationship.  Other dietary and nondietary factors varied so greatly between studies that it was pointless to consider the results our of their context. Reviews of fiber,bcereals, sugar, and even hot peppers were touched on.

Another review discussed the mechanisms of neoplastic conversion and the subsequent growth and development of neplastic cells (7). Cancers of specific sites were considered in terms of mechanisms, geography, and nutritional traditions. One of a pair of complementary table summarized causes of cancer in North America: lifestyle (related to tobacco, diet, alcohol, sun, mycotoxin, and hepatitis B virus): transplacental chemicals; occupational; cryptogenic (viruses?); introgenic; multifactorial; and unspecified. The other listed specific actions that would promote health and lower risk of various chronic diseases.

In an important initative, the National Cancer Institute signed agreements with the Food and Drug Administration (FDA) and private companies and institutions to test foods for cancer prevention (8). The goal is to exploit the protective properties of natural phytochemicals by incorporating them into new fortified food products. The first studies will use fractions from citrus fruits, garlic, flaxseed, soybeans, and the parsley-carrot-celery family of vegetables. Later studies will be based on the most promising candidates from the initial groups plus cruciferous and solanaceous vegetables and combinations. Safety studies in animals will be followed by intervention trials in people at high risk for cancer. A positive outcome from these studies has been anticipated by several food companies that have already begun their own “designer food” projects. Meanwhile, epidemiologists from seven European countries have launched a prospective 5- year (or longer) dietary study in which more than 250,000 people will keep detailed food diaries and provide blood samples for analysis (9). In conjunction with this the effect of hormone replancement therapy will be studied in Great Britain.

It is important to know how the public perceive the role of dietary and other environmental factors in the causation and prevention of cancer, to maximize the impact of public health programs (10). A postal survey in South Australia revealed a relatively high degree of awareness and acceptance of lifestyle factors as determinants of cancer risk. This awareness extended with few differences to all sociodemographic groups. The roles of diet and  cigarettesmoking were widely recognized, but the importance of pollution of  the food supply was overestimated relative to nutrient imbalance. In this setting, the most effective public health efforts would most likely be ones directed at skill transfer and removal of barriers to change.

In discussing the future of nutrition research in cancer prevention, Greenwald first reviewed the role of specific dietary factors in cancer risk (11). He then described ongoing and proposed research programs, with emphasis on the extramural programs of the National Cancer Institute. Dietary guidelines developed by various organizations and government agencies were summarized. The author then identified gaps in knowledge, named some important areas for future research, and discussed changes in the food supply that have implications for health.

A volume in a series on nutrition dealt with the subject of vitamins and cancer prevention (12). The book is based on presentations at the Gladys Emerson Memorial symposium held at UCLA on 2-3 March 1989. Approaches range from basic laboratory research to clinical studies to preliminary studies of vitamin deficiency in cancer patients. Chapters address the role of specific vitamins in preventing or treating cancer and the mechanisms by which vitamins protect against  neoplasia. Of particular interest are discussions of folate, 1,25- dihydroxyvitamin D₃ and coenzyme Q₁₀ A conference at the National Institutes of Health, September 1990, was devoted to the biologic functions of ascorbic acid and its relation to cancer (13). Presentations considered vitamin C in relation to free radical scavenging, regulation of cellular and enzymatic function, the immune system, malignant transformation and growth of tumor cells, therapeutic applications, and dietary requirements.

Although a link between cancer and high consumption of red meat is frequently taken as proved, Kritchevsky’s review suggests that a cause – effect relationship is far from established (14). For example, in the USA between 1940 and 1970 per-capita meat consumption more than doubled, while cancer mortality was virtually unchanged. Further, risk of colon cancer did not show the socioeconomic gradient exhibited by meat consumption. Overall, 6 of 11 case – control studies of colon cancer found a positive association with meat consumption, 1 found a negative association, and 4 found none, Nor have epidemiologic studies of other types of cancer yielded convincing evidence that simply deleting beef (or meat) from the typical American diet would substantially reduce cancer risk. Having established this point, Kritchevskyreviewed animal and clinical studies of meat components specifically protein, fat, and cholesterol. Again, results are inconclusive and sometime surprising. Protein and fat may merely reflect the real culprit, affluence, which is manifested in excessive energy consumption and insufficient energy expenditure. Evidence for this is reviewed.

While evidence accumulates for a protective effect of wheat (15) and other fiber against cancer, the FDA has hesitated to allow health claims for fiber in nutrition labeling (16). Neverheless, they do endorse dietary guidelines recommending daily intake of 25 g of dietary fiber. While the distinction between health claims and dietary guidelines may be important in some circles, it should not obscure the message that fiber is a crucial constituent of a healthful diet.

A discussion of the “fat hypothesis” and cancer evaluated results of laboratory, clinical, and epidemiological studies (17). It concludes that although many lines of investigation converge upon fat as the main culprit in carcinogenesis, it is nearly impossible to control for the multitude of confounding factors. The authors believe that as the picture becomes more complex, more evidence points against the fat hypothesis than toward it. Further, they point out that after the key gene changes in carcinogenesis are known. Nutrition’s impact on the incidence and repair of DNA damage must still be understood.

Messina and Messina reviewed the use of soy foods and their potential role in cancer prevention (18). One of the sacred crops of ancient China, soybeans contain several substances with anticarcinogenic activity. Among these, protease inhibitors and phytic acid have traditionally been considered “antinutrients” but are beginning to be viewed in a positive light. Increasingly, the importance of nonnutrient phytochemicals is being recognized, and soybeans are rich in them.

A lead article in Science discusses possibilities for the primary prevention of cancer (19). We are at “the threshold of an era when many of the most prevalent human cancers can, to a significant extent, be prevented through lifestyle changes or medical interventions.” This bold statement is defended by a review of trends in incidence and mortality rates of major cancers and analysis of why these changes have occurred.