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Abstract
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.
Because nutrient intake influences immune system function (1, 2), exploring its potential effects is of particular interest in etiologic studies of non-Hodgkin's lymphoma (NHL). However, previous epidemiologic studies of associations between nutrient consumption and risk of NHL are inconclusive (3–14). We recently reported that high consumption of dairy products or fried red meat was associated with increased risk of NHL and several subtypes in men and women, whereas fruit and vegetable intake was inversely associated with risk of NHL in women (15). Building on these results, we next aimed to examine associations with a broad range of macro- and micronutrients to gain a better biologic understanding of how diet may affect NHL development.
Few findings have been replicated among previous dietary studies of NHL. Three studies detected a positive association between consumption of animal protein and/or fat, or saturated fat, and NHL risk (3, 6, 10), but three others did not (4,8, 13). An inverse association was observed between beta- or total carotene intake and risk of NHL in two studies (4, 7) but not in most others (6, 9, 10, 13,14). In contrast, two investigations found a positive association of retinol intake with NHL risk (7, 10), whereas another pair did not (9, 13). Finally, an inverse association has been observed between consumption of dietary fiber and NHL risk (9, 10), but two studies failed to detect an association (6, 13). Otherwise, reported associations have generally been null.
Importantly, most prior studies—with some exceptions (4, 10, 12–14)—grouped all NHL cases together, without examining whether associations differ by histopathologic subtype. Given that NHLs are a diverse set of malignancies (16), it is likely that etiologic associations vary by subtype. Therefore, in an effort to clarify the mechanisms by which diet may affect development of NHL subtypes, we extended our prior analysis of food items by identifying specific nutrients that may influence lymphomagenesis.
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