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| 23. |
- Braem, Marieke G. M., et al.
(författare)
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Coffee and tea consumption and the risk of ovarian cancer : a prospective cohort study and updated meta-analysis
- 2012
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Ingår i: American Journal of Clinical Nutrition. - Bethesda : American Society for Nutrition. - 0002-9165 .- 1938-3207. ; 95:5, s. 1172-1181
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Tidskriftsartikel (refereegranskat)abstract
- Background: In 2007 the World Cancer Research Fund Report concluded that there was limited and inconsistent evidence for an effect of coffee and tea consumption on the risk of epithelial ovarian cancer (EOC). Objective: In the European Prospective Investigation into Cancer and Nutrition (EPIC), we aimed to investigate whether coffee intakes, tea intakes, or both are associated with the risk of EOC. Design: All women participating in the EPIC (n = 330,849) were included in this study. Data on coffee and tea consumption were collected through validated food-frequency questionnaires at baseline. HRs and 95% CIs were estimated by using Cox proportional hazards models. Furthermore, we performed an updated meta-analysis of all previous prospective studies until April 2011 by comparing the highest and lowest coffee- and tea-consumption categories as well as by using dose-response random-effects meta-regression analyses. Results: During a median follow-up of 11.7 y, 1244 women developed EOC. No association was observed between the risk of EOC and coffee consumption [HR: 1.05 (95% CI: 0.75, 1.46) for the top quintile compared with no intake] or tea consumption [HR: 1.07 (95% Cl: 0.78, 1.45) for the top quintile compared with no intake]. This lack of association between coffee and tea intake and EOC risk was confirmed by the results of our meta-analysis. Conclusion: Epidemiologic studies do not provide sufficient evidence to support an association between coffee and tea consumption and risk of ovarian cancer. Am J Clin Nutr 2012;95:1172-81.
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| 24. |
- Brunkwall, Louise, et al.
(författare)
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Sugar-sweetened beverage consumption and genetic predisposition to obesity in 2 Swedish cohorts
- 2016
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 104:3, s. 809-815
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Tidskriftsartikel (refereegranskat)abstract
- Background: The consumption of sugar-sweetened beverages (SSBs), which has increased substantially during the last decades, has been associated with obesity and weight gain.Objective: Common genetic susceptibility to obesity has been shown to modify the association between SSB intake and obesity risk in 3 prospective cohorts from the United States. We aimed to replicate these findings in 2 large Swedish cohorts.Design: Data were available for 21,824 healthy participants from the Malmö Diet and Cancer study and 4902 healthy participants from the Gene-Lifestyle Interactions and Complex Traits Involved in Elevated Disease Risk Study. Self-reported SSB intake was categorized into 4 levels (seldom, low, medium, and high). Unweighted and weighted genetic risk scores (GRSs) were constructed based on 30 body mass index [(BMI) in kg/m2]-associated loci, and effect modification was assessed in linear regression equations by modeling the product and marginal effects of the GRS and SSB intake adjusted for age-, sex-, and cohort-specific covariates, with BMI as the outcome. In a secondary analysis, models were additionally adjusted for putative confounders (total energy intake, alcohol consumption, smoking status, and physical activity).Results: In an inverse variance-weighted fixed-effects meta-analysis, each SSB intake category increment was associated with a 0.18 higher BMI (SE = 0.02; P = 1.7 × 10−20; n = 26,726). In the fully adjusted model, a nominal significant interaction between SSB intake category and the unweighted GRS was observed (P-interaction = 0.03). Comparing the participants within the top and bottom quartiles of the GRS to each increment in SSB intake was associated with 0.24 (SE = 0.04; P = 2.9 × 10−8; n = 6766) and 0.15 (SE = 0.04; P = 1.3 × 10−4; n = 6835) higher BMIs, respectively.Conclusions: The interaction observed in the Swedish cohorts is similar in magnitude to the previous analysis in US cohorts and indicates that the relation of SSB intake and BMI is stronger in people genetically predisposed to obesity.
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| 25. |
- Buckland, Genevieve, et al.
(författare)
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Adherence to a Mediterranean diet and risk of gastric adenocarcinoma within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort study
- 2010
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 91:2, s. 381-390
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The Mediterranean dietary pattern is believed to protect against cancer, although evidence from cohort studies that have examined particular cancer sites is limited. OBJECTIVE: We aimed to explore the association between adherence to a relative Mediterranean diet (rMED) and incident gastric adenocarcinoma (GC) within the European Prospective Investigation into Cancer and Nutrition study. DESIGN: The study included 485,044 subjects (144,577 men) aged 35-70 y from 10 European countries. At recruitment, dietary and lifestyle information was collected. An 18-unit rMED score, incorporating 9 key components of the Mediterranean diet, was used to estimate rMED adherence. The association between rMED and GC with respect to anatomic location (cardia and noncardia) and histologic types (diffuse and intestinal) was investigated. A calibration study in a subsample was used to control for dietary measurement error. RESULTS: After a mean follow-up of 8.9 y, 449 validated incident GC cases were identified and used in the analysis. After stratification by center and age and adjustment for recognized cancer risk factors, high compared with low rMED adherence was associated with a significant reduction in GC risk (hazard ratio: 0.67; 95% CI: 0.47, 0.94). A 1-unit increase in the rMED score was associated with a decreased risk of GC of 5% (95% CI: 0.91, 0.99). There was no evidence of heterogeneity between different anatomic locations or histologic types. The calibrated results showed similar trends (overall hazard ratio for GC: 0.93; 95% CI: 0.89, 0.99). CONCLUSION: Greater adherence to an rMED is associated with a significant reduction in the risk of incident GC.
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| 26. |
- Byberg, Liisa, et al.
(författare)
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Cancer death is related to high palmitoleic acid in serum and to polymorphisms in the SCD-1 gene in healthy Swedish men
- 2014
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 99:3, s. 551-558
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND:A high proportion of monounsaturated fatty acids (MUFAs) or a high ratio of MUFAs to saturated fatty acids in plasma, reflecting a high activity of the lipogenic enzyme stearoyl-CoA desaturase-1 (SCD-1), has been shown to be related to cancer death and incidence in some studies.OBJECTIVES:The objective was to study whether the serum cholesteryl ester proportion of palmitoleic acid [16:1n-7 (16:1ω-3)] and the ratio of palmitoleic to palmitic acid (16:1n-7/16:0), as an estimation of the activity of SCD-1, are related to cancer death and to investigate whether polymorphisms in the SCD-1 gene are related to cancer mortality.DESIGN:A community-based cohort of 50-y-old men was followed for a maximum of >40 y. Survival analysis was used to relate fatty acid composition in serum, analyzed at baseline by gas-liquid chromatography (n = 1981), and single nucleotide polymorphisms in the SCD-1 gene (n = 986) to cancer death. A 7-d dietary record was completed at age 70 y (n = 880).RESULTS:The proportions of 16:1n-7 and the ratio of 16:1n-7 to 16:0 were associated with cancer mortality during follow-up in a comparison of the highest with the lowest quartile of 16:1n-7 (adjusted HR: 1.37; 95% CI: 1.04, 1.82). Inherited variance of the SCD-1 gene seemed to be related to cancer death, especially among men with a low proportion of PUFA in the diet in a comparison of the highest with the lowest weighted genetic risk score (HR: 2.14; 95% CI: 1.13, 4.04).CONCLUSION:The findings are compatible with the hypothesis that there is an association between endogenously synthesized MUFAs and cancer death.
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| 27. |
- Byberg, Liisa, et al.
(författare)
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Reply to WB Grant
- 2017
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 106:2, s. 700-701
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 28. |
- Byberg, Liisa, et al.
(författare)
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Reply to Y Mao and H Yu.
- 2017
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Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 106:2, s. 698-699
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 29. |
- Bygdell, Maria, et al.
(författare)
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Childhood BMI is inversely associated with pubertal timing in normal-weight but not overweight boys.
- 2018
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Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 108:6, s. 1259-1263
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Tidskriftsartikel (refereegranskat)abstract
- An inverse association between childhood body mass index (BMI; in kg/m2) and pubertal timing is well established for girls. Among boys, studies are scarce and the results inconclusive.We aimed to determine the association between childhood BMI and age at peak height velocity (PHV) in boys.We collected height and weight measurements between 6.5 and 22 y of age for boys born 1945-1961 (original cohort; n=31,971; mean±SD childhood BMI: 15.74±1.41; age at PHV: 14.06±1.11 y) and 1981-1996 (replication cohort; n=1465; childhood BMI: 16.47±2.06; age at PHV: 13.71±1.08 y) attending schools in Gothenburg, Sweden, and examined at mandatory military conscription. Age at PHV was obtained from curve-fitting of measured heights with the use of a modified Infancy-Childhood-Puberty model.In the original cohort, childhood BMI was inversely associated with age at PHV (P<0.001) and a significant quadratic term for childhood BMI (P<0.001) indicated the nonlinearity of this association. Via piecewise linear regression, we identified a threshold for the association at a childhood BMI of 18.42. A significant inverse association was observed below (β:-0.17 y/BMI unit; 95% CI: -0.18, -0.16 y/BMI unit) but not above (β:0.02 y/BMI unit; 95% CI: -0.03, 0.06 y/BMI unit) this childhood BMI threshold. For every unit increase in childhood BMI, age at PHV was ∼2 mo earlier up to the childhood BMI threshold. Similar results were observed in the replication cohort, demonstrating a significant inverse association below (β:-0.16; 95% CI: -0.21, -0.11) but not above (β:-0.03; 95% CI: -0.11, 0.05) the childhood BMI threshold. The identified threshold was close to the cutoffs for overweight at 8 y of age, and childhood BMI was inversely associated with age at PHV below but not above the overweight cutoffs.The present findings establish an inverse association between childhood BMI and pubertal timing in normal-weight but not overweight boys.
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