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Articles by A Tjonneland
Total Records ( 4 ) for A Tjonneland
  B Buijsse , E. J Feskens , M. B Schulze , D Palli , G Tognon , J Halkjaer , A Tjonneland , M. U Jakobsen , D. L van der A , T. I Sorensen and H. Boeing
 

Background: High fruit and vegetable intakes may limit weight gain, particularly in susceptible persons, such as those who stop smoking.

Objective: The objective was to assess the association of fruit and vegetable intake with subsequent weight change in a large-scale prospective study.

Design: The data used were from 89,432 men and women from 5 countries participating in the European Prospective Investigation into Cancer and Nutrition (EPIC). The association between fruit and vegetable intake and weight change after a mean follow-up of 6.5 y was assessed by linear regression. Polytomous logistic regression was used to evaluate whether fruit and vegetable intake relates to weight gain, weight loss, or both.

Results: Per 100-g intake of fruit and vegetables, weight change was –14 g/y (95% CI: –19, –9 g/y). In those who stopped smoking during follow-up, this value was –37 g/y (95% CI: –58, –15 g/y; P for interaction < 0.0001). When weight gain and loss were analyzed separately per 100-g intake of fruit and vegetables in a combined model, the odds ratios (95% CIs) were 0.97 (0.95, 0.98) for weight gain ≥0.5 and <1 kg/y, 0.94 (0.92, 0.96) for weight gain ≥1 kg/y, and 0.97 (0.95, 0.99) for weight loss ≥0.5 kg/y. In those who stopped smoking during follow-up, the odds ratios (95% CIs) were 0.93 (0.88, 0.99), 0.87 (0.81, 0.92), and 0.97 (0.88, 1.07), respectively (P for interaction < 0.0001).

Conclusions: Fruit and vegetable intake relates significantly, albeit weakly inversely, to weight change. For persons who stop smoking, high fruit and vegetable intakes may be recommended to reduce the risk of weight gain.

  A. A Arslan , K. J Helzlsouer , C Kooperberg , X. O Shu , E Steplowski , H. B Bueno de Mesquita , C. S Fuchs , M. D Gross , E. J Jacobs , A. Z LaCroix , G. M Petersen , R. Z Stolzenberg Solomon , W Zheng , D Albanes , L Amundadottir , W. R Bamlet , A Barricarte , S. A Bingham , H Boeing , M. C Boutron Ruault , J. E Buring , S. J Chanock , S Clipp , J. M Gaziano , E. L Giovannucci , S. E Hankinson , P Hartge , R. N Hoover , D. J Hunter , A Hutchinson , K. B Jacobs , P Kraft , S. M Lynch , J Manjer , J. E Manson , A McTiernan , R. R McWilliams , J. B Mendelsohn , D. S Michaud , D Palli , T. E Rohan , N Slimani , G Thomas , A Tjonneland , G. S Tobias , D Trichopoulos , J Virtamo , B. M Wolpin , K Yu , A Zeleniuch Jacquotte and A. V. Patel
 

Background  Obesity has been proposed as a risk factor for pancreatic cancer.

Methods  Pooled data were analyzed from the National Cancer Institute Pancreatic Cancer Cohort Consortium (PanScan) to study the association between prediagnostic anthropometric measures and risk of pancreatic cancer. PanScan applied a nested case-control study design and included 2170 cases and 2209 control subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression for cohort-specific quartiles of body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]), weight, height, waist circumference, and waist to hip ratio as well as conventional BMI categories (underweight, <18.5; normal weight, 18.5-24.9; overweight, 25.0-29.9; obese, 30.0-34.9; and severely obese, ≥35.0). Models were adjusted for potential confounders.

Results  In all of the participants, a positive association between increasing BMI and risk of pancreatic cancer was observed (adjusted OR for the highest vs lowest BMI quartile, 1.33; 95% CI, 1.12-1.58; Ptrend < .001). In men, the adjusted OR for pancreatic cancer for the highest vs lowest quartile of BMI was 1.33 (95% CI, 1.04-1.69; Ptrend < .03), and in women it was 1.34 (95% CI, 1.05-1.70; Ptrend = .01). Increased waist to hip ratio was associated with increased risk of pancreatic cancer in women (adjusted OR for the highest vs lowest quartile, 1.87; 95% CI, 1.31-2.69; Ptrend = .003) but less so in men.

Conclusions  These findings provide strong support for a positive association between BMI and pancreatic cancer risk. In addition, centralized fat distribution may increase pancreatic cancer risk, especially in women.

  L Dossus , R Kaaks , F Canzian , D Albanes , S. I Berndt , H Boeing , J Buring , S. J Chanock , F Clavel Chapelon , H. S Feigelson , J. M Gaziano , E Giovannucci , C Gonzalez , C. A Haiman , G Hallmans , S. E Hankinson , R. B Hayes , B. E Henderson , R. N Hoover , D. J Hunter , K. T Khaw , L. N Kolonel , P Kraft , J Ma , L Le Marchand , E Lund , P. H.M Peeters , M Stampfer , D. O Stram , G Thomas , M. J Thun , A Tjonneland , D Trichopoulos , R Tumino , E Riboli , J Virtamo , S. J Weinstein , M Yeager , R. G Ziegler and D. G. Cox
 

Genes involved in the inflammation pathway have been associated with cancer risk. Genetic variants in the interleukin-6 (IL6) and prostaglandin-endoperoxide synthase-2 (PTGS2, encoding for the COX-2 enzyme) genes, in particular, have been related to several cancer types, including breast and prostate cancers. We conducted a study within the Breast and Prostate Cancer Cohort Consortium to examine the association between IL6 and PTGS2 polymorphisms and breast and prostate cancer risk. Twenty-seven polymorphisms, selected by pairwise tagging, were genotyped on 6292 breast cancer cases and 8135 matched controls and 8008 prostate cancer cases and 8604 matched controls. The large sample sizes and comprehensive single nucleotide polymorphism tagging in this study gave us excellent power to detect modest effects for common variants. After adjustment for multiple testing, none of the associations examined remained statistically significant at P = 0.01. In analyses not adjusted for multiple testing, one IL6 polymorphism (rs6949149) was marginally associated with breast cancer risk (TT versus GG, odds ratios (OR): 1.32; 99% confidence intervals (CI): 1.00–1.74, Ptrend = 0.003) and two were marginally associated with prostate cancer risk (rs6969502-AA versus rs6969502-GG, OR: 0.87, 99% CI: 0.75–1.02; Ptrend = 0.002 and rs7805828-AA versus rs7805828-GG, OR: 1.11, 99% CI: 0.99–1.26; Ptrend = 0.007). An increase in breast cancer risk was observed for the PTGS2 polymorphism rs7550380 (TT versus GG, OR: 1.38, 99% CI: 1.04–1.83). No association was observed between PTGS2 polymorphisms and prostate cancer risk. In conclusion, common genetic variation in these two genes might play at best a limited role in breast and prostate cancers.

  M. T Severinsen , S. R Kristensen , S. P Johnsen , C Dethlefsen , A Tjonneland and K. Overvad
 

Background— Obesity, measured as body mass index, is associated with venous thromboembolism (VTE). Body mass index is a marker of excess weight and correlates well with body fat content in adults; however, it fails to consider the distribution of body fat. We assessed the association between anthropometric variables and VTE.

Methods and Results— From 1993 to 1997, 27 178 men and 29 876 women 50 to 64 years of age were recruited into a Danish prospective study (Diet, Cancer, and Health). During 10 years of follow-up, the outcome of VTE events was identified in the Danish National Patient Registry and verified by review of medical records. Body weight, body mass index, waist circumference, hip circumference, and total body fat were measured at baseline. We used Cox proportional hazard models to assess the association between anthropometry and VTE. Age was used as a time axis, with further adjustment for smoking, physical activity, height, hypertension, diabetes mellitus, cholesterol, and, among women, use of hormone replacement therapy. We verified 641 incident VTE events and found monotonic dose-response relationships between VTE and all anthropometric measurements in both sexes. In mutually adjusted analyses of waist and hip circumference, we found that hip circumference was positively associated with VTE in women but not in men, whereas waist circumference was positively associated with VTE in men but not in women.

Conclusions— All measurements of obesity are predictors of the risk for VTE. Positive associations were found between VTE and body weight, body mass index, waist circumference, hip circumference, and total body fat mass.

 
 
 
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