© 2002 The American Society for Nutritional Sciences
J. Nutr. 132:3534S-3539S, November 2002
Supplement: International Research Conference on Food, Nutrition & Cancer
Oral Presentation Abstracts
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Energy Balance, Obesity and Cancer Risk—A Worldwide Epidemic. W.P.T. James. International Obesity Task Force, London, UK.
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Cancer has long been recognized as one of the principal causes of adult deaths in both the developed and developing world. Excess weight gain, however, was seen as only one of several contributors to the risk of a range of adult chronic diseases including diabetes, hypertension and other cardiovascular diseases. Now, however, the pattern of cancer incidence is changing and a clearer picture of the risk factors and pathophysiologic processes underlying carcinogenesis is emerging. Traditionally, cancers of the breast and endometrium were recognized to be more common in obese women, but only recently has the issue of excess weight gain per se been considered as an etiological factor. A recent systematic review concluded that overweight and obesity contributed to 8.6% of postmenopausal breast cancers, 
11% of colon cancers, 39% of endometrial cancers, 4.5% of prostate cancers and 25% to each of the much less common kidney and gallbladder cancers in the European Union. Thus overweight and obesity were associated with 72,000 new EU cases per year as a conservative estimate.
Most of these analyses depend on studies in only a small proportion of the world’s population (i.e., the United States and European Union), but the problem of excess weight is now a global epidemic—the largest unrecognized public health problem in the world, with >1 billion adults affected when a conservative cut-off point for body mass index (BMI) of 25 kg/m2 is used. In Asia, optimum health is seen in populations with an average BMI of 21 kg/m2 and the degree of fatness per unit body weight is greater with selective abdominal fat accumulation and probably a different sex steroid, adrenal and hypothalamic hormonal profile and responsiveness. All of these differences may contribute to enhancing the risk of cancer in Asia. Rapid childhood growth with early puberty and overweight comprise an additional major problem.
Distinguishing the different factors contributing to carcinogenesis in an overweight and obese population is challenging. Poor diets that are low in nonstarch polysaccharide-rich cereals, vegetables and fruit and physical inactivity likely contribute to both excessive weight gain and carcinogenesis. Distinguishing the differential roles of these potential confounders when analyzing the role of weight gain is a major clinical and epidemiologic issue that already involves functional genomic analyses and trials.
Although these etiological studies present a novel and exciting prospect, an even greater challenge is now presenting itself in public health terms. How do we counteract the currently overwhelming societal and probably primeval biological pressures to overeat and do as little as possible? Inadvertently, we have allowed the creativity of government, commerce and socially responsible sectors of society to design a convenient and supposedly egalitarian environment geared to individual responsibility and opportunity. In practice, this has led to our producing a harmful environment geared to persuading young children and families to eat inappropriately and do little. The affluent, confident, intelligent and self-motivated sectors of society flourish in this environment.
Our scientific approach to decision-making in medicine based on the needs for double-blind trials for new drugs has also now developed to the point at which it overwhelms the public health sector, which has become a rudimentary feature of policymaking in both the United States and the European Union. The World Cancer Research Fund produced a widely acclaimed new approach to the assessment of the role of diet in the development of cancer in its first report. Now we must consider how best to identify coherently and systematically the societal pressures that currently demand unusual behavior if overweight and the risk of cancer are to be limited. This is the next major intellectual and societal challenge for us all.
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Energy Restriction and Cancer. D. M. Klurfeld and D. Kritchevsky.* Wayne State University, Detroit, MI and *Wistar Institute, Philadelphia, PA.
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Over 20 years ago, we began reexploring the relationship between total energy intake and development of cancer in animal models. Previous work dated back to 1909, but nutritional requirements of rodents were not known then, and older diets lacked several essential nutrients. We showed that rats given carcinogens to induce mammary or colon cancer and fed high fat diets that were restricted in total energy were significantly less likely to develop tumors. The tumors that developed were much smaller, indicating growth inhibition of transformed cells. We went on to show that insulin and insulin-like growth factor-I levels were reduced by feeding low energy diets. Both of these hormones are growth factors for a variety of cancers, are elevated in overweight people and are associated with increased risk of cancer. Our work with rodents may explain the epidemiologic observations that dietary fat is associated with increased risk of breast or colon cancer but not after adjustment for total energy intake. In addition, an animal fed an unlimited amount of food should not be regarded as normal but as the equivalent of a morbidly obese human. Therefore, we are probably seeing the effects of obesity-associated sensitivity to carcinogenesis in control rats and a more normal response in those subjected to energy restriction. Recent results with DNA microarrays show that many previously unsuspected genes are affected by energy restriction. This technique may lead to genetic or pharmacologic interventions to inhibit or treat cancer.
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Energy Balance and Postmenopausal Breast Cancer. T. A. Sellers. Mayo Clinic Cancer Center, Rochester, MN.
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The role of energy balance in the pathogenesis of postmenopausal breast cancer is of considerable medical and public health interest. This talk will summarize what has been learned on this topic from the Iowa Women’s Health Study. The cohort was established in 1986 through the recruitment of 41,836 women aged 55–69 y with a valid Iowa driver’s license. Data on physical activity, energy intake, anthropometrics and other risk factors at baseline were assessed through a mailed survey. Follow-up for cancer incidence was achieved through annual record linkage to the Iowa Cancer Registry and regular follow-ups by mail. Estimated energy intake at baseline is weakly associated with greater incidence. Regular physical activity appears to be weakly protective. The strongest evidence that energy imbalance is a risk factor comes from examination of the consequence, i.e., obesity. Adult body mass index, especially abdominal adiposity, is a consistent risk factor, primarily for tumors that express receptors for estrogen. Conversely, being overweight in adolescence is weakly protective, and the women at great risk are those who are thin early in life and gain the most weight as adults. Taken together, these results provide encouraging evidence that at least some fraction of postmenopausal breast cancer may be avoidable through maintenance of energy balance.
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Energy Intake, Cancer and Aging. R. Weindruch. Department of Medicine, University of Wisconsin-Madison and Geriatric Research Education and Clinical Center, Veterans Administration Hospital, Madison, WI.
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Energy restriction repeatedly and strongly increases maximum life span in rodent models while retarding the appearance of age-associated pathologic and biological changes. Three main questions concerning energy restriction and aging will be addressed: 1) By what mechanisms does energy restriction retard aging and disease processes in rodents? Mechanistic insight was gained by using oligonucleotide microarrays by which we described the gene expression profile of aging skeletal muscle (1) and brain (2) in mice and its alteration by energy restriction. 2) Will energy restriction exert similar actions in primates? Two ongoing studies in rhesus monkeys subjected to energy restriction as well as limited human epidemiologic data support the notion of human translatability. 3) Can substances be identified that mimic the beneficial actions of energy restriction? The search for such substances is rapidly becoming an active area of inquiry and may benefit from genomic- and proteomic-based approaches.
1. Lee, C. K., Klopp, R. G., Weindruch, R. & Prolla, T. A. (1999) (1999) Gene expression profile of aging and its retardation by caloric restriction. Science (Washington, DC) 285:1390-1393.[Abstract/Free Full Text]
2. Lee, C. K., Weindruch, R. & Prolla, T. A. (2000) Gene-expression profile of the ageing brain in mice. Nat. Genet. 25:294-297.[Medline]
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Enterolactone and Risk of Cancer. P. Pietinen and A. Kilkkinen.* World Health Organization, NCD Prevention and Health Promotion, Geneva, Switzerland and *National Public Health Institute, Helsinki, Finland.
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The strength of epidemiologic evidence indicating a protective effect of consumption of plant foods against several types of cancers has stimulated interest in secondary plant metabolites as potential chemopreventive agents. Of these, isoflavonoid and lignan phytoestrogens have received particular attention because of several of their biological properties. Isoflavonoids are found almost exclusively in soybean products, whereas mammalian lignan precursors are more widely distributed in plant foods and, therefore, are probably more important in most Western countries. The richest known source of lignans is flaxseed, with lesser amounts found in other seeds, nuts, whole grains, berries, fruits and vegetables. After consumption of lignan-containing foods, enzymatic metabolic conversions occur by gut microflora, resulting in the formation of mammalian lignans. The most abundant mammalian lignan is enterolactone.
Enterolactone has been shown to possess several biological properties offering some potential mechanisms against cancers. On the basis of studies in human cell lines, enterolactone has antitumor, antiaromatase and antiangiogenetic effects. Further, a diet rich in lignans has been shown to protect against certain cancers in animal models. Results from epidemiologic studies are more contradictory. We are aware of eight studies to date that have explored the associations between risk of cancers and lignan exposure (Table 1
). On the basis of these studies, high urinary or serum enterolactone concentration may reduce the risk of breast cancer, whereas enterolactone exposure seems not to be associated with the risk of prostate cancer. In conclusion, experimental evidence supports the view that lignans and especially enterolactone may have substantial health benefits. However, epidemiologic evidence is scarce and inconclusive. Large gaps exist in our understanding of lignans and their effect on human health. At present, no recommendations can be made concerning the optimal intake of lignans for prevention of cancer.
1. Ingram, D., Sanders, K., Kolybaba, M. & Lopez, D. (1997) Case-control study of phyto-oestrogens and breast cancer. Lancet 350:990-994.[Medline]
2. den Tonkelaar, I., Keinan-Boker, L., Van’t Veer, P., Arts, C. J., Adlercreutz, H., Thijssen, J.H.H. & Peeters, P. (2001) Urinary phytoestrogens and postmenopausal breast cancer risk. Cancer Epidemiol. Biomark. Prev. 10:223-228.[Abstract/Free Full Text]
3. Pietinen, P., Stumpf, K., Männistö, S., Kataja, V., Uusitupa, M. & Adlercreutz, H. (2001) Serum enterolactone and risk of breast cancer: a case-control study in eastern Finland. Cancer Epidemiol. Biomark. Prev. 10:339-344.[Abstract/Free Full Text]
4. Horn-Ross, P. L., John, E. M., Lee, M., Stewart, S. L., Koo, J., Sakoda, L. C., Shiau, A. C., Goldstein, J., Davis, P. & Perez-Stable, E. J. (2001) Phytoestrogen consumption and breast cancer risk in a multiethnic population. Am. J. Epidemiol. 154:434-441.[Abstract/Free Full Text]
5. Strom, S. S., Yamamura, Y., Duphorne, C. M., Spitz, M. R., Babaian, R. J., Pillow, P. C. & Hursting, S. D. (1999) Phytoestrogen intake and prostate cancer: a case-control study using a new database. Nutr. Cancer 33:20-25.[Medline]
6. Stattin, P., Adlercreutz, H., Tenkanen, L., Jellum, E., Lumme, S., Hallmans, G., Harvei, S., Tepp, L., Stumpf, K., Luostarinen, T., Lehtinen, M., Dillner, J. & Hakama, M. (2002) Circulating enterolactone and prostate cancer risk: a Nordic nested case-control study. Int. J. Cancer 99:124-129.[Medline]
7. Horn-Ross, P. L., Hoggart, K. J. & Lee, M. M. (2002) Phytoestrogens and thyroid cancer risk: the San Francisco Bay Area Thyroid Cancer Study. Cancer Epidemiol Biomark. Prev. 11:43-49.[Abstract/Free Full Text]
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Linking Underserved Populations with Phytochemical-Rich Diets. A Menu for Program Design and Implementation. C. Engelking. Arlin Cancer Institute, Westchester Medical Center, Valhalla, NY.
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Underserved populations, including African-Americans, Hispanics and the elderly, experience higher prevalence rates for selected cancers; for a variety of reasons, they present later to receive medical attention and have higher overall cancer mortality rates. Although scientific data on nutritional literacy and lifestyle practices related to food selection, preparation and consumption as well as exercise in these populations are limited, it is thought that diet may explain some of the variation in cancer prevalence rates across race and ethnic groups. Studies of migrant populations suggest that environmental causes, such as diet, may be important determinants of cancer risk. It is also recognized that these underserved populations generally consume diets that do not comply with current nutritional recommendations for cancer prevention. For example, findings of the National Health and Nutrition Examination Survey epidemiologic follow-up study revealed that African-Americans have a significantly lower Healthy Eating Index score for consumption of fruits and vegetables, folate and total dietary fiber, all nutrients thought to be associated with lower cancer risk. Reaching these groups with healthy eating messages that result in sustainable behavioral change is challenging and requires a working knowledge of the unique characteristics of the group targeted for intervention. These characteristics include ethnic and cultural attributes, behavior-shaping experiences, values, attitudes and belief systems. Strategies for linking these populations with diets rich in cancer-preventing phytochemicals remain challenging but can be achieved. Such strategies encompass the use of partnership and coalition models (e.g., establishment of nutrition action teams and neighborhood networks), group-targeting using marketing applications (e.g., translation of national guidelines to group vernacular, use of churches and schools as vehicles), individual customization techniques (e.g., personalized print materials, audiovisual and computer messages), mobilization of social support and use of lay health advisors. Programs with demonstrated success should be highlighted to serve as models for action.
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Late Effects in Survivors of Childhood Cancer. Opportunities for Intervention. C. A. Sklar. Department of Pediatrics, Memorial Sloan Kettering, New York.
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Survival rates for children and adolescents diagnosed with cancer have improved dramatically over the past 30 years. Currently, the overall 5-y survival rate for childhood cancer is in excess of 70%. It is estimated that 1 of every 900 young adults is a childhood cancer survivor and that >250,000 childhood cancer survivors are currently residing in the United States. These impressive survival rates are due, primarily, to improvements in cancer treatments. Contemporary therapy for childhood cancers generally includes the use of multimodality regimens (e.g., the combination of radiation and chemotherapy) and multiagent, highly intensive chemotherapy. Unfortunately, the long-term consequences of such exposures are considerable. Approximately two thirds of childhood cancer survivors will develop some type of medical complication or disability as a direct result of their earlier cancer therapy. We will focus on the late complications that may be amenable to nutritional interventions. These include second cancers, obesity, osteoporosis, premature coronary artery disease and hyperlipidemia.
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Carcinogens in Cooked Meats and Human Cancer. R. Sinha. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD.
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Diets containing substantial amounts of red meat may increase the risk of colorectal, pancreatic, breast, prostate and renal cancer. The association with red meat intake may be due to a combination of factors, such as content of fat, protein and iron and preparation methods (e.g., cooking, preserving). Laboratory results have shown that meats cooked at high temperatures contain heterocyclic amines (HCA) and polycyclic aromatic hydrocarbons (PAH), which are mutagenic and carcinogenic in animals. Many older epidemiologic studies of colon cancer using surrogates for HCA exposure from meat (e.g., doneness level, surface browning, frying, intake of gravy) produced suggestive but inconsistent results. These discrepancies may have resulted in part from having used dietary questionnaires that combined meat-cooking practices in ways that made the intake of HCA and PAH difficult to estimate. Thus, over the past decade we have taken a multidisciplinary approach to investigating whether the association with red meat intake can be explained by meat-cooking practices that produce mutagens and carcinogens. To estimate intake, two separate databases for HCA and PAH have been developed and used in conjunction with a validated meat-cooking food-frequency questionnaire (FFQ). To develop biological markers of internal exposure, a metabolic study was conducted in which subjects consumed controlled amounts of meat cooked at low and high temperatures. The roles of meat type, cooking methods, doneness levels and meat-cooking mutagens were examined in case-control studies of colorectal adenomas, lung cancers and breast cancers using both questionnaire information and biomarkers. In a case-control study of colorectal adenomas, an increased risk was associated with a high intake of red meat. Most of this risk was due to intake of red meat cooked until well or very well done or to high temperature cooking techniques such as grilling. Linking the FFQ information to the mutagen and carcinogen database enabled us to evaluate the effect on risk of mutagenic activity as well as exposure to several HCA and to 3,4-benzpyrene. An increased risk was associated with higher levels of meat-derived mutagenic activity, intake of 2-amino-3,8-dimethylimidazol[4,5-f]quinoxaline (MeIQx), possibly 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and 3,4-benzpyrene. Even though the results from these case-control studies lend support to a causative role for HCA in human cancer, other larger studies do not. Components of red meat, other than HCA, such as heme iron, fat, nitrite and nitrosamine and salt, must be explored further. This presentation examined the current epidemiologic knowledge in relation to meat cooking mutagens and evaluated the types of studies that may be required in the future to clarify the association of HCA in human cancers.
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Chemoprevention of Colitis-Associated Colorectal Cancer. M. L. Clapper, H. S. Cooper, R. Coudry, M. A. Gary and W.-C.L. Chang. Division of Population Science, Fox Chase Cancer Center, Philadelphia, PA.
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The increased risk for colorectal malignancies in patients with inflammatory bowel disease, specifically ulcerative colitis, has been well established and increases with age at onset and extent and duration of disease. The cumulative risk of developing colorectal cancer in patients with long-standing pancolitis can reach as high as 33% after 2–3 decades of disease. Both the longevity of inflammatory bowel disease and the development of colitis-associated neoplasms through a dysplasia sequence provide a window of opportunity for chemopreventive intervention. Preclinical experimentation is underway to develop the first therapeutic regimen for the prevention of colitis-associated colorectal dysplasias and cancers using the dextran sulfate sodium (DSS) mouse model.
A detailed characterization of the pathology of DSS-induced colitis suggests that this is a reliable and relevant model for the future development of strategies for the chemoprevention of human colitis-associated colon cancer. In this model, acute (1 cycle) or chronic (2–4 cycles) inflammation is produced by administering DSS to Swiss Webster mice. Each cycle consists of 7 d of 4% DSS followed by 14 d of untreated water. By the end of the fourth cycle, 20% of the mice develop colonic dysplasias, cancers or both. Similar to humans with ulcerative colitis, DSS-treated mice experience periods of clinical activity and inactivity, possess various degrees of inflammation many months after DSS exposure and develop both flat and polypoid dysplasias and/or cancers that are morphologically identical to those of humans.
The ability of select chemopreventive agents to inhibit colitis-associated colorectal dysplasia and cancer is being evaluated in the DSS mouse model. Although 22% of the mice receiving 4 cycles of DSS developed colorectal neoplasms, the total number of colonic dysplasias and cancers was reduced significantly (P = 0.02) in mice receiving the prototypic chemopreventive agent and Phase II enzyme inducer, oltipraz. Furthermore, colorectal cancers were completely eliminated after oltipraz exposure. Oltipraz (250 mg/kg diet) was administered from 2 wk before DSS and throughout the experiment. Consistent with our data from a previous clinical trial, a higher dosage of oltipraz (500 mg/kg diet) was ineffective in reducing colon tumor incidence. The mechanism by which oltipraz inhibits colitis-associated colorectal cancer remains to be determined. Other chemopreventive agents under evaluation by this group include the bile acid, ursodeoxycholic acid, the nonsteroidal anti-inflammatory agent, celecoxib, and the antiproliferative agent, difluoromethylornithine. The primary endpoints of these in vivo investigations include the incidence and multiplicity of colonic dysplasias and cancers.
Unique knockout mouse strains have been developed by this group and represent a novel resource for assessing the contribution of genetic background to susceptibility for colitis-associated colorectal cancer. The role of the adenomatous polyposis coli (APC) gene in the development of colitis-associated neoplasms has been examined. Administration of DSS to a newly derived strain of multiple intestinal neoplasia (Min) mice carrying a germline mutation in this gene produced a 15-fold increase in the multiplicity of colonic adenomas, compared with age-matched untreated Min mice. A similar analysis of additional colon cancer genes is in progress. Data obtained from these genetically defined mouse strains, when combined with the results of the chemopreventive analyses, are anticipated to facilitate the development of an efficacious regimen for the prevention of colorectal cancer in patients with ulcerative colitis. [Supported by the Cancer Research Foundation of America and by National Institutes of Health NO1 CN05121.]
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Use of Fecal Water as a Biomarker in Dietary Intervention Studies. G. Rechkemmer, K. Schnaebele, A. Bub, S. Barth and K. Briviba. Institute of Nutritional Physiology, Federal Research Center for Nutrition, Karlsruhe, Germany.
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In epidemiologic studies investigating associations between nutritional factors and cancer, the observed study end point generally is the clinical diagnosis of tumor occurrence. In experimental studies, however, it is desirable to develop biomarkers linked to the early stages of carcinogenesis. In particular, such efforts have been made in colonic carcinogenesis in which the molecular details of the different stages are well characterized. The types of biomarkers necessary in dietary intervention studies are biomarkers of exposure, effect and susceptibility. The rapid advancement of genetic testing, determination of genetic polymorphisms and link of genetic disposition to dietary effects on carcinogenesis is of great scientific interest and importance. Biomarkers of exposure are usually measured in blood plasma, and dose-dependent changes in plasma concentration are studied to evaluate the bioavailability of dietary components. However, in colonic carcinogenesis, it is also important to determine the exposure biomarkers directly in the intestinal lumen or feces and the exposed epithelial cells. In dietary intervention studies with healthy volunteers, the effects of consuming carotenoid-containing foods (carrot and tomato juice) on the carotenoid concentration in fecal water was investigated. Carotenoid concentrations up to 50–60 µmol/L were measured. These values are at least 10 times higher than the maximal concentrations that would be achieved in the plasma after prolonged consumption of carotenoid-rich foods with high bioavailability or using dietary supplements. Investigating the biological effects of carotenoids at concentrations present in fecal water on human colon carcinoma cell lines (HT29) revealed that the high concentrations induced apoptosis in growing cells (50% inhibitory concentration: 15 µmol/L for ß-carotene). Fecal water itself not only induces apoptosis but also markedly reduces the proliferation of colon carcinoma cells. Fecal water (diluted 1:100) caused an inhibition of cell growth by 50%, indicating a pronounced antiproliferative potential. Intervention with carotenoid-rich foods did not significantly alter the antiproliferative effect of fecal water. In summary, the development and validation of suitable biomarkers is of great importance in dietary intervention studies investigating the link between dietary factors and various molecular and cellular processes of carcinogenesis.
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Diet and Cancer in a Country in Transition. The Case of Uruguay. P. Boffetta and E. De Stefani.* International Agency for Research on Cancer, Lyon, France and *National Cancer Registry, Montevideo, Uruguay.
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Cancer incidence rates in Uruguay are the highest in Latin America, and mortality rates exceed those of the United States. Breast, colon/rectum, lung and prostate are the most common sites; bladder and head and neck cancers also show a high incidence. High smoking rates, in particular of black tobacco cigarettes, explain part of the cancer pattern, and diet likely represents an additional important risk factor. Since the late 1980s, a series of case-control studies based on a validated food-frequency questionnaire have addressed the carcinogenic role of dietary factors in Uruguay. Mate drinking is a risk factor of esophageal cancer: high temperature is an important component of the carcinogenicity of mate, but an effect of the beverage per se cannot be excluded and may explain the observed association with cancer of other organs such as the bladder and kidney. High intake of salted or otherwise preserved meat is a risk factor of cancers of digestive and possibly respiratory organs. It is unclear whether high consumption of red meat per se is a risk factor. Low consumption of fruits and vegetables is prevalent in Uruguay and likely contributes to the high incidence of digestive and respiratory cancers. Dietary factors play an important role in shaping the cancer pattern in Uruguay; some aspects of the carcinogenicity of diet correspond to those identified in other countries, whereas other aspects are specific to this population. Results of studies from Uruguay stress the importance of studying the dietary factors of cancer in countries in economic and social transition.
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Diet and Cancer: An Evolving View. W. Willett. Department of Nutrition, Harvard School of Public Health, Boston, MA
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The large differences in cancer rates among countries, striking changes in these rates among migrating populations and rapid changes over time within countries indicate that some aspect of lifestyle or environment is largely responsible for the common cancers in Western countries. Dietary fat has been hypothesized to be the key factor because national consumption is correlated with the international differences, but these correlations are potentially confounded by other aspects of Western lifestyles. Detailed analyses in large prospective studies have not supported an important role of dietary fat. Instead, positive energy balance, reflected in early age at menarche and weight gain as an adult, is an important determinant of breast and colon cancers, consistent with numerous studies in animals. Physical inactivity has also been shown to be a risk factor for these diseases and in part accounts for the international differences in cancer rates. Although the percentage of calories from fat in the diet does not appear related to the risk of colon cancer, greater risks have been seen with higher consumption of red meat, suggesting that factors other than fat per se may be important. In many case-control studies, a high consumption of fruits and vegetables has been associated with reduced risks of numerous cancers, but recent prospective studies suggest that these associations may have been overstated. Among the factors in fruits and vegetables that have been examined in relation to cancer risk, present data most strongly support a benefit of higher folic acid consumption in reducing risks of colon and breast cancers. These findings have been bolstered by an association between incidence of colon cancer and a polymorphism in the gene for methlyenetetrahydrofolate reductase, an enzyme involved in folic acid metabolism. The benefits of folic acid appear strongest among persons who regularly consume alcohol, which itself is associated with risk of these cancers. Numerous other aspects of diet are hypothesized to influence the risks of cancers in Western countries, but for the moment the evidence is unclear. Two decades of effort in developing, evaluating and refining methods of dietary assessment have laid the groundwork for further insights into the role of diet in cancer etiology that will emerge from the >30 large prospective studies that are currently underway.
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Nutrition and Cancer Throughout the Lifetime: From Womb to Chemotherapy. T. Byers. University of Colorado School of Medicine. Denver, CO.
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We are all nourished from the moment of conception until death. Across this broad timeline of life, nutritional factors can interact with the many genetic and environmental factors that affect health. The nutritional epidemiology of cancer has been based largely on studies relating measures of diet and nutritional status in adulthood to the risk of cancer incidence. In many instances, associations between diet and cancer risk have been much weaker in these studies than would have been predicted by the many hypotheses emanating from ecological studies correlating cancer risk to nutritional factors across populations. This paper reviews the evidence pointing to the importance of nutritional factors as determinants of cancer risk and prognosis across the entire span of life, from nutritional factors affecting the growing fetus to nutritional factors interacting with cancer therapy and the growth of advanced cancer. Although research on the effect of nutrition very early in life is scant, several observations suggest that nutritional factors can affect the growing fetus and the growing child in ways that increase the risk of cancer several decades later. In addition, although there is little research on nutrition and cancer prognosis, several observations indicate that nutritional change after cancer diagnosis may be an important adjunct to cancer therapy. In summary, nutritional factors seem to be affecting cancer risk at many different stages of life; thus, a full understanding of the role of diet in cancer will necessitate the consideration of diet across the lifespan.
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Update of the 1997 AICR/WCRF Expert Report. M. J. Wiseman. World Cancer Research Fund International, London, UK.
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It is now generally accepted that nutrition status, dietary patterns and other lifestyle factors are important determinants of the risk of a number of cancers. Doll and Peto in 1981 (1) estimated that 35% of cancers in the United States might be related to dietary exposures. By the early 1990s, despite substantial diversity in quality and study type, some patterns had emerged, such as the link between higher consumption of fruit and vegetables and lower risks of a number of cancers. By this time, there was a need for a further review of the evidence. The World Cancer Research Fund (WCRF) and the American Institute for Cancer Research expert report Food, Nutrition and the Prevention of Cancer: a Global Perspective, published in 1997 (2), changed the perception not only of the links among diet, nutrition and cancer but also of the potential for prevention through dietary and other lifestyle changes. Over the past few years, there have been developments in systematic reviews and meta-analysis, although relatively little attention has been given to applying these principles to questions surrounding the causation and prevention of disease as opposed to healthcare decisions. However, preventive policies must rely on the best evidence available as part of the approach to managing cancer. The question therefore arises concerning what constitutes the best evidence in relation to the development of chronic disease over decades. It is essential that observational data that are to be used to underpin important educational, policy and clinical decisions be analyzed in the most rigorous way. WCRF International has therefore started to update the report. A task force to address the question of how best to assimilate the evidence relating to the causation and development of cancer is the first step. On the basis of this evidence, a series of systematic reviews will be performed in academic centers of excellence. A separate panel will consider this evidence to form the foundation of a new report.
1. Doll, R. & Peto, R. (1981) The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J. Natl. Cancer Inst. 66:1191-1308.
2. World Cancer Research Fund & American Institute for Cancer Research (1997) Food, Nutrition and the Prevention of Cancer: a Global Perspective. American Institute for Cancer Research, Washington, DC.
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Energy Balance, Obesity and...
Energy Restriction and Cancer....
