American Journal of Epidemiology Advance Access published online on September 27, 2006
American Journal of Epidemiology, doi:10.1093/aje/kwj330
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1 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Northern California Cancer Center, Fremont, CA; Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA
* To whom correspondence should be addressed. The mechanisms through which diet may influence the development of non-Hodgkin's lymphoma (NHL) are unclear but can be better understood by examining associations between nutrient consumption and NHL risk. Between 2000 and 2002, 591 NHL cases and 460 population-based controls in Sweden completed a semiquantitative food frequency questionnaire. Unconditional logistic regression was performed to estimate odds ratios and 95% confidence intervals for associations with nutrient intake; all statistical tests were two sided. Dietary intake of most macronutrients was not associated with risk of NHL or its common subtypes. Consumption of omega-3 or marine fatty acids was associated with decreased risk of NHL and chronic lymphocytic lymphoma, and dietary fiber was associated with lower risk of all subtypes examined. When the highest and the lowest quartiles of marine fat intake were compared, the odds ratio for NHL risk was 0.6 (95% confidence interval: 0.4, 0.9), ptrend = 0.03; for dietary fiber intake, the corresponding odds ratio was 0.5 (95% confidence interval: 0.3, 0.7), ptrend < 0.001. Dietary consumption of beta-carotene or alpha-tocopherol was associated with lower NHL risk, whereas intake of calcium or retinol was associated with increased NHL risk. Nutrients that affect inflammation, vitamin D activity, oxidative DNA damage, or DNA methylation may be associated with risk of NHL.
Received January 17, 2006
Accepted May 1, 2006
ORIGINAL CONTRIBUTIONS
Nutrient Intake and Risk of Non-Hodgkin's Lymphoma
Ellen T. Chang 1, Katarina M. Bälter 2, Anna Torrång 2, Karin Ekström Smedby 2, Mads Melbye 3, Christer Sundström 4, Bengt Glimelius 5, and Hans-Olov Adami 6 *
2 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
3 Department of Epidemiology Research, Danish Epidemiology Science Center, Statens Serum Institut, Copenhagen, Denmark
4 Department of Pathology, Akademiska Hospital, Uppsala, Sweden
5 Department of Oncology, Radiology and Clinical Immunology, University of Uppsala, Uppsala, Sweden; Department of Oncology and Pathology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden
6 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology, Harvard School of Public Health, Boston, MA
Hans-Olov Adami, E-mail: ellen{at}nccc.org
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