Showing papers by "Jakob Linseisen published in 2002"

Polymorphisms in candidate obesity genes and their interaction with dietary intake of n-6 polyunsaturated fatty acids affect obesity risk in a sub-sample of the EPIC-Heidelberg cohort

Abstract: Background, aim: In several genes coding for molecules involved in the regulation of body weight (fat mass) and thermogenesis, polymorphisms have been reported which possibly modify human obesity risk. The aim of this study was a) to reproduce these observations with data and biological material from the Heidelberg cohort of EPIC, a large European prospective investigation into diet and cancer, and b) to investigate potential effects of interactions between dietary fatty acid intake and allelic variants on obesity risk. Subjects and methods: Within EPIC-Heidelberg, 154 subjects with a body mass index > 35 kg/m2 and 154 age- and sex-matched normal-weight controls were selected and genotypes determined for 11 candidate genes. Dietary intake was assessed by a validated food frequency questionnaire. Odds ratios (OR) were computed by means of unconditional logistic regression and different adjustment models. Genotyping was performed by PCR-RFLP and allele-specific PCR. Results: For most of the investigated genes (PPARA, PPARG2, UCP1, UCP2, UCP3, BAR-2, APM1, leptin, SORBS1, HSL, and TNFA) an indication for a minor effect on obesity risk was found. Indication of a risk-increasing effect was strongest for the homozygous form of leptin −2548AA with an adjusted OR of 3.53 (p < 0.009). Additionally, for the polymorphic sites of BAR-2 (Arg16Gly and Gln27Glu) a significant effect on obesity risk was seen. Importantly, the results of the analysis of gene-diet interactions suggest that the allelic variants of candidate genes (leptin, TNFA, PPARG2) might strongly affect diet-related obesity risk. Conclusions: The results support some but not all previous reports about a risk-modulating effect of polymorphisms in genes affecting obesity risk. The most important finding is an indication of substantial interaction between allelic variants of particular genes and fatty acid intake-related obesity risk. These observations suggest that future studies on polymorphisms in obesity genes should take data on dietary habits into account.

Nutrition and breast cancer risk by age 50: a population-based case-control study in Germany.

Abstract: Diet is recognized to play a role in the occurrence of breast cancer; however, the data are inconsistent. The goal of this study was to determine the influence of dietary factors on breast cancer risk among women up to 50 yr of age in a German population. A population-based case-control study was conducted including 706 cases and 1,381 controls. In addition to a risk factor questionnaire, a subgroup of 355 cases and 838 controls completed a food frequency questionnaire. Breast cancer risk was inversely associated with vegetable consumption (P for trend = 0.034). The odds ratio for the fourth quartile of vegetable intake compared with the first quartile was 0.64 (95% confidence interval = 0.43-0.96). Breast cancer risk increased with a higher consumption of red meat (P for trend = 0.016); women with the highest consumption level had an 85% elevated breast cancer risk compared with the lowest quartile (95% confidence interval = 1.23-2.78). When only premenopausal women were considered, the protective effect of vegetable intake and the positive association with meat intake were even stronger. These results are compatible with the international recommendations for a breast cancer preventive diet and suggest that the favorable effect of a diet high in vegetables and low in red meat, especially beef, may be stronger in premenopausal women.

Plasma 7beta-hydroxycholesterol as a possible predictor of lung cancer risk.

Abstract: Epidemiological data suggests a role of dietary cholesterol in the etiology of lung cancer without having a clear biological hypothesis. Although smoking as the outstanding risk factor for lung cancer may enhance lipid peroxidation reactions, this study was planned to assess smoking-independent associations between the extent of cholesterol oxidation and the risk for lung cancer. In the frame of a nested case-control study in European Prospective Investigation on Cancer-Heidelberg, six cholesterol oxidation products (COPs) were determined in plasma samples of 20 incident lung cancer patients obtained 1.9 +/- 0.6 years before diagnosis and in 40 matched (including smoking habits) controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by conditional logistic regression. Among all COP compounds tested, plasma 7beta-hydroxycholesterol was associated with lung cancer risk. The high crude risk estimate (OR approximately equals 5) became significant after adjustment for sports activity (OR = 6.83, CI = 1.08-43.01, 3rd versus 1st tertile). For the independent effect of 7beta-hydroxycholesterol, i.e., adjusted for other COP compounds, an OR of 8.08 (CI = 1.12-58.54, 3rd versus 1st tertile) was calculated (P = 0.04 for trend). Lung cancer risk adjusted for sports activity significantly increased by 26% (CI = 1.050-1.506, P = 0.01) per unit (1 nmol/mmol plasma cholesterol) of 7beta-hydroxycholesterol. No dietary factor had a significant effect in the regression model, but the dietary intake of meat, eggs, animal fat, cholesterol, and fruits (inversely) correlated with plasma COP concentrations. In this small study, plasma 7beta-hydroxycholesterol appeared to be a smoking-independent predictor of lung cancer risk and might therefore be used as a biomarker. Because of the rather high-risk estimate, research on possible intrinsic biological effects of this compound should be encouraged.