摘要:

AbstractRegional age‐adjusted mortality rates of the Federal Republic of Germany from 1976 to 1980 were correlated with regional nutritional data from a national survey on income and consumption. This survey was conducted in 1973 and covered a sample of 50,000 households. The mortality rates due to carcinomas of the stomach, colon, rectum, liver, gallbladder, pancreas, breast, and prostate and the consumption data of 15 nutrients and other compounds are shown for the 11 Federal States. For alcohol, vitamin C and calcium variations range about 20%, whereas deviations in the consumption of protein, fat, and most carbohydrates appear of minor importance. Some of the 45 correlation coefficients significant at the 5% level (out of 210) may have etiologic importance. The associations that co incide in both sexes are alcohol and disaccharide consumption with stomach cancer and protein intake with pancreatic cancer.Because previous habits and consumption may have a stronger etiologic influence than do present ones in the induction of chronic diseases, the utilization of existing information from the 1930s (e.g., Atlas of Ethnic Studies) and the assessment of habits in previous decades by means of case‐control studies are emphasized.

ISSN:0163-5581    

DOI:10.1080/01635588509513847

出版商:Taylor&Francis Group    

年代:1985

数据来源: Taylor

摘要:

AbstractIn two surveys in The Peoples Republic of China, blood samples were collected for nutritional studies in two counties where the risks of esophageal cancer are very different. The first survey was done in May 1980 in Linxian County (Henan Province) where the risk of esophageal cancer is very high. Blood samples were obtained from 111 persons (58 men, 53 women) who were selected randomly from 528 subjects that underwent endoscopical examination. The second survey was done in May 1981 in Jiaoxian County (Shandong Province) where the risk of esophageal cancer is reported to be relatively low. Blood samples were obtained from 120 persons (66 men, 54 women) who were selected randomly from 252 subjects that had also had undergone endoscopy. The blood samples were used to measure the nutritional status of riboflavin (erythrocyte glutathione reductase activation coefficient), vitamin A (retinol and carotene concentrations), and zinc (plasma and hair zinc concentrations).Only riboflavin status was significantly different in the two communities. The distribution of erythrocyte glutathione reductase activation coefficient values suggested that riboflavin status was much better in the low‐risk community. Also in May 1981, a few more blood samples were obtained from some of the participants of the previous year's study in Linxian. A slight improvement in riboflavin and zinc status was detected. We considered the possibility that these changes may have been linked to the socioeconomic changes currently taking place in rural areas. Data were also collected from food allocation records in 15 production brigades in Linxian and 13 production brigades in Jiaoxian in the same years. The records used represented the food consumption of 3,491 and 2,552 persons, respectively, and were used to calculate daily food and nutrient intakes in the two communities. Dietary analyses highlighted the vegetarian nature of the diet, the low consumption of riboflavin, and the virtual dependence on carotene for vitamin A. Both communities consumed very little in the way of animal products or fruit, but intake of these items was higher in Jiaoxian.

ISSN:0163-5581    

DOI:10.1080/01635588509513848

出版商:Taylor&Francis Group    

年代:1985

数据来源: Taylor

摘要:

AbstractThe activities of an endogenous inhibitor and of a stimulator of cell proliferation were assayed in the livers of sham‐operated (SO) or partially hepatectomized (PH) adult rats; rats fed a choline‐supplemented (CS) or a choline‐devoid (CD) diet; the same diets followed by acute CCU intoxication; the same diets supplemented with phenobarbital (PHB) or a CD diet containing DL‐ethionine (ETH). The inhibitor and the stimulator were semipurified by fractional ethanol precipitation of a liver cytosolic fraction, and their activities were assessed by means of bioassays in vitro. The livers of SO rats and of rats fed the CS diet contained only inhibitor activity. Following PH, a CD diet, or CCU intoxication the inhibitor activity was suppressed, and there was a simultaneous appearance of a stimulator activity. Thus, PH, a CD diet, and CCU intoxication cause similar cellular (loss and regeneration) and humoral‐homeostatic changes in adult rat livers. We propose that these changes constitute a basic attribute of the mechanism whereby the three conditions affect similarly hepatocarcinogenesis in the rat, especially in the case of a CD diet, because the changes it induces are chronic rather than acute. PHB, another promoter of chemical hepatocarcinogenesis, affected neither the inhibitor nor the stimulator activity. Thus, PHB seems to be acting by a different mechanism than that of the other three agents. ETH did not modify the shift in the balance of the growth‐modulating factors induced by a plain CD diet. This shift may account for the marked stimulation of carcinogen‐induced oval cell proliferation exerted by a CD diet. The significance of these results is discussed in the context of known effects of a CD diet and of PHB on hepatocarcinogenesis in rats.

ISSN:0163-5581    

DOI:10.1080/01635588509513849

出版商:Taylor&Francis Group    

年代:1985

数据来源: Taylor

摘要:

AbstractDiet and nutrition are increasingly recognized as likely to be major determinants of cancer, notably cancers of the gastrointestinal tract, breast, endometrium, ovary, and prostate. Dietary factors may collectively account for a greater proportion of all cancers that occur in contemporary Western society than does any other category of environmental exposure (1). With the development of knowledge of the protective properties of certain components of food, links with diet have been suggested for other cancer sites (2).The epidemiological evidence for the association of diet and cancer is, however, not uniformly convincing; also, the likely biological pathways are not always clear. In this paper, we comment on some current hypotheses in this area and examine the best epidemiological methods to test them.

ISSN:0163-5581    

DOI:10.1080/01635588509513850

出版商:Taylor&Francis Group    

年代:1985

数据来源: Taylor

摘要:

AbstractSyrian golden hamsters were fed a semipurified or commercial diet from weaning throughout life. Bis(2‐oxopropyl)nitrosamine (BOP) was administered at 8 weeks of age (10 mg/kg body wt, sc). Longevity was improved by 26% and 36% increases in the mean life‐spans of male and female hamsters, respectively, fed the semipurified diets. Carcinogen treatment did not alter survival. The age‐adjusted occurrence rates of pancreatic ductular proliferation, carcinomas, adenomas, and common duct polyps were higher in hamsters fed commercial diet; this indicates an earlier onset of these BOP‐induced lesions in hamsters fed this diet. However, their overall incidences were generally similar when the two diet groups were compared. Acinar cell nodules were observed only in hamsters fed semipurified diets and were elevated in BOP‐treated females. The onset of pancreatic ductular proliferation and adenomas, bile duct proliferation, parathyroid hyperplasia, and common duct papillary hyperplasia was earlier in females than in male hamsters, especially in groups fed commercial ration. Generalized vascular calcification was observed at an elevated rate and reached a higher overall incidence in hamsters fed commercial ration. The age‐adjusted rate of amyloidosis was high in female hamsters and elevated in groups that consumed the commercial ration. In addition, colitis and islet cell hyperplasia occurred more often and earlier in hamsters fed commercial ration, but gallbladder stones occurred most in animals fed semipurified diet. This paper discusses the possible association between these and other observed lesions and survival.

ISSN:0163-5581    

DOI:10.1080/01635588509513851

出版商:Taylor&Francis Group    

年代:1985

数据来源: Taylor

摘要:

AbstractThis paper summarizes recent developments linking methionine metabolism and S‐adenosylmethionine to DNA methylation and gene expression in relation to cancer. Methionine, obtained in the diet and synthesized by several reactions in the body, is the sole precursor of S‐adenosylmethionine, the primary methyl donor in the body. Disruptions in methionine metabolism and methylation reactions may be involved in cancer processes. S‐Adenosyl‐methionine is involved in, inter alia, the methylation of a small percentage of cytosine bases of DNA. Recent evidence suggests that enzymatic DNA methylation is an important component of gene control and may serve as a silencing mechanism for gene function. Some carcinogens interfere with enzymatic DNA methylation, and thus may allow oncogene activation. Demethy‐lation may be a necessary, but not always sufficient, condition for enhanced transcription. DNA hypomethylation has been observed in many cancer cells and tumors. The hypothesis that oncogenic transformation may be prevented or even reversed by a diet containing excess methionine and/or choline needs to be further investigated.

ISSN:0163-5581    

DOI:10.1080/01635588509513852

出版商:Taylor&Francis Group    

年代:1985

数据来源: Taylor

摘要:

Diet and Cancer, William A. Creasey, Lea and Febiger, Philadelphia, 478 pp., 1985

ISSN:0163-5581    

DOI:10.1080/01635588509513853

出版商:Taylor&Francis Group    

年代:1985

数据来源: Taylor

ISSN:0163-5581    

DOI:10.1080/01635588509513854

出版商:Taylor&Francis Group    

年代:1985

数据来源: Taylor