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1. |
Trends in breast cancer mortality and diet in England and Wales from 1911 to 1980 |
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Nutrition and Cancer,
Volume 10,
Issue 1-2,
1987,
Page 1-9
KeyTimothyJ. A.,
DarbySarahC.,
PikeMalcolmC.,
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摘要:
AbstractA paper in a previous volume of this journal (Ingram, DM,Nutr Cancer 3, 75–80, 1981) reported that at the beginning of World War II there was a marked decrease in breast cancer mortality in England and Wales that coincided with a marked reduction in the consumption of sugar, meat, and fat, and a marked increase in the consumption of cereals and vegetables. Reexamination of the mortality data described in that paper shows that the apparent sudden decrease in breast cancer mortality at the beginning of World War II is an artefact caused by a changein the method of selecting the cause of death from jointly stated causes, which was intro‐duced in 1940. After adjusting for this change, trends in age‐specific mortality rates are described. Breast cancer mortality rates were greater in 1980 than in 1911 in the age group of 35–84 years, but this overall increase was interrupted by a period of decreasing mortality between the 1930s and the 1950s in the age group of 50–69 years. It is possible that some of this decrease was due to dietary changes; however, the evidence is poor and other factors that affect incidence and survival must be considered.
ISSN:0163-5581
DOI:10.1080/01635588709513935
出版商:Taylor&Francis Group
年代:1987
数据来源: Taylor
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2. |
GUT‐CNS peptide hormones, digestive dysfunction, and colon cancer |
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Nutrition and Cancer,
Volume 10,
Issue 1-2,
1987,
Page 11-22
HillP.,
GarbaczewskiL.,
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摘要:
AbstractDietary modification as protection against coronary heart disease and diet‐related cancers has been recommended, yet the central nervous system (CNS)‐neuroendocrine control of eating behavior and digestion is poorly understood. Maintenance of nutritional homeostasis (and therefore of an ideal body weight) requires a balance between appetite and satiety that currently appears to be related to CNS‐peptide hormones stimulating feeding counteracted by the release of gut satiety peptide hormones. This review stresses the importance of the composition of Iu‐minal nutrients on colonic motility and the release of peptide hormones; it also discusses the interaction of the CNS and environmental factors on colonic activity and the relationship to diet‐related diseases.
ISSN:0163-5581
DOI:10.1080/01635588709513936
出版商:Taylor&Francis Group
年代:1987
数据来源: Taylor
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3. |
Colonic carcinogenesis: The microbial feast or famine mechanism |
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Nutrition and Cancer,
Volume 10,
Issue 1-2,
1987,
Page 23-28
McBurneyMichaelI.,
Van SoestPeterJ.,
JeraciJosephL.,
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摘要:
AbstractA mechanism is presented which suggests that high‐fat, high‐protein, low‐fiber diets can cause an unfavorable microbial environment in the human colon which predisposes some individuals towards large bowel diseases. The digesta leaving the ileum on high‐fat, high‐protein, low‐fiber diets has a high proportion of mucins, malabsorbed carbohydrates and proteins, bile acids, and sloughed epithelial cells. The irregular (pulsatile) emptying of rapidly fermentable ileal digesta into the colon causes a massive surge in microbial activity. The sudden availability of rapidly fermentable substrate generates a large microbial population in the exponential growth phase that soon depletes its substrate. For microorganisms to perpetuate until the next high‐fat, high‐protein, low‐fiber meal propels ileal digesta into the colon, they must induce enzymes to ferment dying or dead microbes (cannibalism) in addition to colonic epithelial mucosa and mucins. As the carbohydrate‐to‐nitrogen ratio of the colonic contents decreases, the fermentation becomes more proteoly tic and subacute levels of fermentation products such as ammonia may be generated. Carcinogens are concentrated within a small colonic mass and the probability of precancerous lesions and polyps developing in the colonic mucosa is directly related to the severity, frequency, and duration of these microbial“feast or famine”situations in the colon.
ISSN:0163-5581
DOI:10.1080/01635588709513937
出版商:Taylor&Francis Group
年代:1987
数据来源: Taylor
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4. |
Vitamin A and other dietary factors in the etiology of esophageal cancer |
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Nutrition and Cancer,
Volume 10,
Issue 1-2,
1987,
Page 29-37
DecarliAdriano,
LiatiPaola,
NegriEva,
FranceschiSilvia,
La VecchiaCarlo,
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摘要:
AbstractThe risk of esophageal cancer, in relation to the frequency of consumption of selected dietary items, was evaluated in a hospital‐based case‐control study; this study was of 105 histologically confirmed cases and 348 control subjects with acute conditions unrelated to any of the established or potential risk factors for esophageal cancer. The frequency of consumption of carrots, green vegetables, or fresh fruits was lower in cases. Further, cases tended to eat meat and fish less frequently and eggs more frequently. The estimated multivariate relative risks were 0.6 for regular (more than once a week) carrot consumption and 0.6 and 0.3, respectively, for the highest levels of vegetable or fruit consumption (compared with the lowest ones). Consequently, a strong negative association emerged between estimatedβ‐carotene (but not retinol) intake and esophageal cancer risk. The risk of cancer of the esophagus was not significantly related to subjective scores of fat and whole‐meal food intake; however, a strong positive association did emerge with measures of alcohol consumption.Although the information collected does not allow precise definition of specific micro‐nutrient(s) causally related with esophageal cancer risk, the confirmation of marked differences in reported diet between esophageal cancer cases and controls is still of interest; this is mostly in consideration of the strength and persistence of the associations after allowing for alcohol and tobacco use in addition to indicators of socioeconomic status.
ISSN:0163-5581
DOI:10.1080/01635588709513938
出版商:Taylor&Francis Group
年代:1987
数据来源: Taylor
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5. |
Intestinal carcinogenesis and dietary fibers: The influence of cellulose or Fybogel chronically given after exposure to DMH |
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Nutrition and Cancer,
Volume 10,
Issue 1-2,
1987,
Page 39-51
WilpartM.,
RoberfroidM.,
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摘要:
AbstractThis study was initiated to analyze the effect of a) two characterized vegetal fibers [i.e., a polysaccharide (cellulose) and a mucilaginous substance (Fybogel)], which were b) added at two concentrations (5% and 15% wt/wt), c) as constituents of low (5% wt/wt) and high (20% wt/wt) fat isocaloric diets d) given chronically to rats one week after the administration of 1,2‐dimethylhydrazine (DMH) DMH had previously been injected once a week for 15 weeks to induce intestinal carcinogenesis.The dietary consumption, the body weight, and the fecal outflow showed a similar and regular evolution for the rats of all experimental groups; the exception was those receiving the 20 % lipids‐15 % Fybogel diet. That specific diet caused a decrease in body weight concomitant with an increase in dietary consumption and in fecal outflow.The variation in fecal outflow depended on fat and fiber concentrations. The mucilage was more degraded, in absolute and relative amount, than was cellulose when this polysaccharide was included at a 20% lipid diet. Concerning the effect of these two fibers on intestinal carcinogenesis, Fybogel showed an anticarcinogenic property, whereas cellulose did not. The inhibitory activity of Fybogel was on the incidence of intestinal and colonic tumors as well as on the colonic tumor yield. Moreover, it slowed down the rate of colonic formation.
ISSN:0163-5581
DOI:10.1080/01635588709513939
出版商:Taylor&Francis Group
年代:1987
数据来源: Taylor
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6. |
Vitamin C intake and dietary sources by demographic characteristics |
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Nutrition and Cancer,
Volume 10,
Issue 1-2,
1987,
Page 53-65
BlockGladys,
SorensonAnn,
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摘要:
AbstractEvidence from several lines of research indicates a role for vitamin C in the prevention of some types of cancer in addition to a possible role in hypercholesterolemia and other conditions. It is not yet clear, however, whether observed relationships are due to ascorbic acid alone or in conjunction with other constituents present in the foods containing ascorbic acid. A knowledge of the particular food sources of vitamin C in different demographic groups thus becomes important to fully understand the etiology. This information will also aid in planning effective education or intervention programs.This paper identifies the dietary sources of vitamin C by age, sex, race, and poverty status, using data from the second National Health and Nutrition Examination Survey (NHANES II). Orange juice is the leading dietary source in all subgroups, but the importance of other sources varies markedly by subgroup. Fortified foods are major contributors among the young but not the old, and southern greens are very important sources among blacks but not among whites. The intake of vitamin C is substantially lower among the poor. Potential relationships with disease are also discussed.
ISSN:0163-5581
DOI:10.1080/01635588709513940
出版商:Taylor&Francis Group
年代:1987
数据来源: Taylor
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7. |
Reduced aflatoxicosis in livers of hamsters fed a manganese sulfate supplement |
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Nutrition and Cancer,
Volume 10,
Issue 1-2,
1987,
Page 67-77
HastingsCharlesE.,
LlewellynGeraldC.,
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摘要:
AbstractMale, weanling Syrian hamsters(Mesocricetus auratus)were given (for 10 weeks) diets supplemented with manganese sulfate, aflatoxin, or a combination of both. All animals were killed and a histopathologic evaluation was performed on each liver to assess the influence of a manganese‐supplemented diet on aflatoxicosis. Serum cholesterol and liver glycogen levels were also analyzed to further study the interaction of manganese and aflatoxin.Characteristic aflatoxin‐induced precancerous histopathologk changes were observed in animals receiving the toxin. These changes included bile duct cell hyperplasia, enlarged nuclei, nuclear inclusions, and meglahepatocytes. The dietary manganese addition to aflatoxin animals caused a slight reduction in the bile duct cell hyperplasia and significantly reduced the enlarged nuclei and nuclear inclusions. The latter indicates that the manganese may be influencing membrane chemistry.Animals receiving aflatoxin alone showed significantly increased serum cholesterol and liver glycogen. The cholesterol levels were significantly increased over the aflatoxin‐induced levels when manganese was given in combination with the aflatoxin. The manganese lowered the increased liver glycogen levels caused by the aflatoxin. Dietary manganese shows some potential in suppressing several, but not all, of the aspects of developing aflatoxicosis in the hamster. The specific mode and site of action of manganese requires additional study.
ISSN:0163-5581
DOI:10.1080/01635588709513941
出版商:Taylor&Francis Group
年代:1987
数据来源: Taylor
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8. |
Relationship of cytotoxic activity of natural killer cells to growth rates and serum zinc levels of female RIII mice fed zinc |
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Nutrition and Cancer,
Volume 10,
Issue 1-2,
1987,
Page 79-87
BunkMichaelJ.,
GalvinJamesE.,
YungYee‐Pang,
DnistrianAnnM.,
BlanerWilliamS.,
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摘要:
AbstractThis study examined a) the dietary zinc (Zn) requirement of RIII female weanling mice and b) the cytotoxicity of murine natural killer (NK) cells obtained from spleens of these mice fed varying levels of Zn. Zn was fed in a biotin‐enriched egg albumen diet in amounts ranging from 0.9 to 40.4μg/g diet. During a 28‐day growth assay, maximum carcass growth was obtained with a diet containing 5.4μg Zn/g diet. Maximal serum levels of Zn, however, were observed in mice fed diets containing 3.4μg Zn/g diet. The cytotoxic activity of NK cells obtained from spleens of selected treatment groups was maximal at 40.4μg Zn/g diet and was significantly higher (p≤0.05) than that observed in spleens from mice fed diets that maximized carcass growth rates and serum Zn concentrations. It is concluded that female RIII mice have a dietary Zn requirement for growth similar to that observed for other murine strains but considerably lower than that reported for the rat. Our findings also suggest that RIII NK cells are particularly sensitive to dietary Zn intake: the optimal functional activity of these cells may result from intake of Zn higher than that necessary to maximize carcass growth and serum Zn concentrations.
ISSN:0163-5581
DOI:10.1080/01635588709513942
出版商:Taylor&Francis Group
年代:1987
数据来源: Taylor
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9. |
Weight change and peptide hormone responses in patients receiving interferon |
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Nutrition and Cancer,
Volume 10,
Issue 1-2,
1987,
Page 89-94
HurleyRobertaS.,
O'DorisioThomasM.,
BossettiBrendaM.,
RinehartJohnJ.,
RiceRobertR.,
NeidhartJamesA.,
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摘要:
AbstractThe purpose of this pilot study was to describe body weight status and peptide hormone responses in patients receiving interferon (IFN) therapy for renal cell carcinoma. Eighteen patients were on therapy for approximately two to three months. Mean weight loss of the patients was 2.2±0.9 kg (mean±SEM) or 4.9±0.9% of prestudy weight. Of the 18 patients, 6 were further evaluated for peptide hormone responses to meal stimulation before and after treatment (mean: 1.5 months). These subjects had a mean weight loss of 4.3±1.6 kg or 7.0±3.5% of prestudy weight. Blood was drawn from subjects before and six times after they had consumed a defined formula liquid meal to provoke enteroinsular peptide release. It was discovered that one‐half of this group (n = 3; Group A) had some glucose intolerance following IFN therapy, despite increased response of insulin, gastric inhibitory polypeptide (GIP), and pancreatic polypeptide (PP) to meal stimulation. Further, patients in Group A had a weight loss of—11.7±2.7% of prestudy weight, whereas the other three patients (Group B) experienced a mean loss of‐2.3±1.2% (p<0.04). The three subjects characterized by the smaller loss of prestudy weight (Group B) had decreased glucose response to meal stimulation, despite decreased responses of insulin and GIP. Response of PP was slightly increased with treatment in group B, but the increase was not as large as that in Group A. These data may suggest that extreme weigh t loss and altered peptide hormone response occur in a subset of cancer patients receiving interferon therapy.
ISSN:0163-5581
DOI:10.1080/01635588709513943
出版商:Taylor&Francis Group
年代:1987
数据来源: Taylor
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10. |
Disturbances in the formation of fad and covalently bound flavins in Novikoff hepatoma from riboflavin‐deficient rats |
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Nutrition and Cancer,
Volume 10,
Issue 1-2,
1987,
Page 95-102
PintoJohn,
HuangYeePing,
ChaudhuriRita,
RivlinRichardS.,
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摘要:
AbstractThe incorporation of radiolabeled riboflavin into flavin mononucleotide, flavin adenine dinucleotide, and flavin covalently bound to protein was determined in Novikoff hepatoma grown in both riboflavin‐deficient and normal chow‐fed rats. In Novikoff hepatoma, the incorporation of [14C]riboflavin into covalently bound flavins relative to that into FAD was substantially greater than that in host liver, and the turnover rate of riboflavin was also accelerated in tumor compared with the liver. The magnitude of incorporation of [14C]riboflavin into each of the various flavin fractions was substantially greater in tumors from riboflavin‐deficient animals than in tumors from control animals. These data support the hypothesis that in conditions of riboflavin deprivation, Novikoff hepatoma maintains the levels of the physiologically important flavin coenzymes at the expense of the free riboflavin fraction. The incorporation of riboflavin into covalently bound flavins relative to that into FAD is substantially greater in Novikoff hepatoma than in liver. Accordingly, covalently bound flavins are either present in greater amounts or regulated differently in tumor than in normal tissue. Because the flavin moiety cannot be reutilized, the covalently bound flavin fraction in Novikoff hepatoma theoretically should be able to sequester riboflavin and thereby deplete the body reserves of this vitamin when dietary intake is marginal.
ISSN:0163-5581
DOI:10.1080/01635588709513944
出版商:Taylor&Francis Group
年代:1987
数据来源: Taylor
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