| 1. |
- Genkinger, J M, et al.
(författare)
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A pooled analysis of 12 cohort studies of dietary fat, cholesterol and egg intake and ovarian cancer
- 2006
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Ingår i: Cancer Causes and Control. - Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA USA. Harvard Univ, Sch Publ Hlth, Harvard Ctr Canc Prevent, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. Loma Linda Univ, Sch Med, Ctr Hlth Res, Loma Linda, CA USA. Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA. SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA. : SPRINGER. - 0957-5243 .- 1573-7225. ; 17:3, s. 273-285
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Tidskriftsartikel (refereegranskat)abstract
- Fat and cholesterol are theorized to promote ovarian carcinogenesis by increasing circulating estrogen levels. Although case-control studies have reported positive associations between total and saturated fat intake and ovarian cancer risk, two cohort studies have observed null associations. Dietary cholesterol and eggs have been positively associated with ovarian cancer risk. A pooled analysis was conducted on 12 cohort studies. Among 523,217 women, 2,132 incident epithelial ovarian cancer cases were identified. Study-specific relative risks (RR) and 95% confidence intervals (CI) were calculated by Cox proportional hazards models, and then pooled using a random effects model. Total fat intake was not associated with ovarian cancer risk (pooled multivariate RR = 1.08, 95% CI 0.86-1.34 comparing >= 45 to 30-< 35% of calories). No association was observed for monounsaturated, polyunsaturated, trans-unsaturated, animal and vegetable fat, cholesterol and egg intakes with ovarian cancer risk. A weakly positive, but non-linear association, was observed for saturated fat intake (pooled multivariate RR = 1.29, 95% CI: 1.01-1.66 comparing highest versus lowest decile). Results for histologic subtypes were similar. Overall, fat, cholesterol and egg intakes were not associated with ovarian cancer risk. The positive association for saturated fat intake at very high intakes merits further investigation.
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| 2. |
- Hunter, D J, et al.
(författare)
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Non-dietary factors as risk factors for breast cancer, and as effect modifiers of the association of fat intake and risk of breast cancer
- 1997
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Ingår i: Cancer Causes and Control. - : Springer Science and Business Media LLC. - 0957-5243 .- 1573-7225. ; 8:1, s. 49-56
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Tidskriftsartikel (refereegranskat)abstract
- To assess more precisely the relative risks associated with established risk factors for breast cancer, and whether the association between dietary fat and breast cancer risk varies according to levels of these risk factors, we pooled primary data from six prospective studies in North America and Western Europe in which individual estimates of dietary fat intake had been obtained by validated food-frequency questionnaires. Based on information from 322,647 women among whom 4,827 cases occurred during follow-up: the multivariate-adjusted risk of late menarche (age 15 years or more compared with under 12) was 0.72 (95 percent confidence interval [CI] = 0.62-0.82); of being postmenopausal was 0.82 (CI = 0.69-0.97); of high parity (three or more births compared with none) was 0.72 (CI = 0.61-0.86); of late age at first birth (over 30 years of age compared with 20 or under) was 1.46 (CI = 1.22-1.75); of benign breast disease was 1.53 (CI = 1.41-1.65); of maternal history of breast cancer was 1.38 (CI = 1.14-1.67); and history of a sister with breast cancer was 1.47 (CI = 1.27-1.70). Greater duration of schooling (more than high-school graduation compared with less than high-school graduation) was associated significantly with higher risk in age-adjusted analyses, but was attenuated after controlling for other risk factors. Total fat intake (adjusted for energy consumption) was not associated significantly with breast cancer risk in any strata of these non-dietary risk factors. We observed a marginally significant interaction between total fat intake and risk of breast cancer according to history of benign breast disease; with fat intake being associated nonsignificantly positively with risk among women with a previous history of benign breast disease; no other significant interactions were observed. Risks for reproductive factors were similar to those observed in case-control studies; relative risks for family history of breast cancer were lower. We found no clear evidence in any subgroups of a major relation between total energy-adjusted fat intake and breast cancer risk.
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| 3. |
- Mannisto, S, et al.
(författare)
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Dietary patterns and breast cancer risk : results from three cohort studies in the DIETSCAN project
- 2005
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Ingår i: Cancer Causes and Control. - Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, FIN-00300 Helsinki, Finland. NYU, Dept Nutr Food Studies & Publ Hlth, New York, NY USA. TNO Nutr & Food Res, Dept Nutr Epidemiol, Zeist, Netherlands. Ist Nazl Studio & Cura Tumori, Epidemiol Unit, I-20133 Milan, Italy. Karolinska Inst, Inst Environm Epidemiol, Stockholm, Sweden. Maastricht Univ, Dept Epidemiol, Maastricht, Netherlands. NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA. Maastricht Univ, Dept Methodol & Stat, Maastricht, Netherlands. : SPRINGER. - 0957-5243 .- 1573-7225. ; 16:6, s. 725-733
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Only a few consistent findings on individual foods or nutrients that influence breast cancer risk have emerged thus far. Since people do not consume individual foods but certain combinations of them, the analysis of dietary patterns may offer an additional aspect for assessing associations between diet and diseases such as breast cancer. It is also important to examine whether the relationships between dietary patterns and breast cancer risk are consistent across populations. Methods: We examined the risk of breast cancer with two dietary patterns, identified as "Vegetables" (VEG) and "Pork, Processed Meat, Potatoes" (PPP), common to all cohorts of the DIETSCAN project. During 7 to 13 years of follow-up, three of the cohorts - the Netherlands Cohort Study on diet and cancer (NLCS), the Swedish Mammography Cohort (SMC), and the Ormoni e Dieta nella Eziologia dei Tumori (Italy-ORDET) - provided data on 3271 breast cancer cases with complete information on their baseline diet measured by a validated food frequency questionnaire. Results: After adjustment for potential confounders, VEG was not associated with the risk of breast cancer across all cohorts. PPP was also not associated with the risk of breast cancer in SMC and ORDET, but a high PPP score tended to be inversely associated with breast cancer in the NLCS study (RR = 0.69; 95% CI, 0.52-0.92, highest versus lowest quartile). PPP differed in one aspect between the cohorts: butter loaded positively on the pattern in all cohorts except NLCS, in which butter loaded negatively and appeared to be substituted by low-fat margarine loading positively. Conclusion: In general, the dietary patterns showed consistent results across the three cohorts except for the possible protective effect of PPP in the NLCS cohort, which could be explained by a difference in that pattern for NLCS. The results supported the suggestion derived from traditional epidemiology that relatively recent diet may not have an important role in the etiology of breast cancer.
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| 4. |
- Wolk, A., et al.
(författare)
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Nutrition and renal cell cancer
- 1996
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Ingår i: Cancer Causes and Control. - London, United Kingdom : Rapid Science Publisher. - 0957-5243 .- 1573-7225. ; 7:1, s. 5-18
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Forskningsöversikt (refereegranskat)abstract
- Epidemiologic evidence on the relation between nutrition and renal cell cancer is reviewed. Kidney cancer, comprising 1.7 percent of all malignant diseases diagnosed worldwide, shows about a 20-fold international variation in the incidence in men and 10-fold in women. This substantial variation indicates an important causal role of environmental factors. Renal cell (parenchymal) cancer (RCC) accounts for about 80 percent of all kidney cancers. While the etiology of RCC is incompletely understood, analytic epidemiologic studies provide consistent support for a positive association of obesity with risk of RCC; the dose-response observed supports a causal relationship. Only a few prospective studies, all of them limited in size, have been published, while ecologic and case-control studies suggest that diet may be important in the etiology of RCC. However, contradictory results and methodologic limitations in some case-control studies prevent definite conclusions concerning diet and RCC. A positive association of protein and fat intake, as well as their main food sources (meat, milk, fats), with risk of RCC-as suggested by ecologic studies-has no clear support in analytic epidemiologic studies. A protective effect of vegetables and fruits has been observed in most case-control studies, while the majority do not show an association between alcohol, coffee, and risk of RCC. Recent reports indicated an increased risk of RCC associated with consumption of fried/sauteed meat and low intakes of magnesium or vitamin E. An apparent positive association with total energy intake, perhaps due to bias, needs further investigation.
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