Dietary Pattern and Risk of Hodgkin Lymphoma
Classic Hodgkin lymphoma (cHL) has few known modifiable risk factors, and the relationship between diet and cHL risk is unclear. We performed the first investigation of an association between dietary pattern and cHL risk in 435 cHL cases and 563 population-based controls from Massachusetts and Connecticut (1997–2000) who completed baseline diet questionnaires. We identified 4 major dietary patterns ("vegetable," "high meat," "fruit/low-fat dairy," "desserts/sweets") using principal components analysis. We computed multivariable odds ratios and 95% confidence intervals for associations of dietary pattern score (quartiles) with younger-adult (age <50 years), older-adult (age ≥50 years), and overall cHL risk. Secondary analyses examined associations by histological subtype and tumor Epstein-Barr virus (EBV) status. A diet high in desserts/sweets was associated with younger-adult (odds ratio(quartile 4 vs. quartile 1) = 1.60, 95% confidence interval: 1.05, 2.45; Ptrend = 0.008) and EBV-negative, younger-adult (odds ratio = 2.11, 95% confidence interval: 1.31, 3.41; Ptrend = 0.007) cHL risk. A high meat diet was associated with older-adult (odds ratio = 3.34, 95% confidence interval: 1.02, 10.91; Ptrend = 0.04) and EBV-negative, older-adult (odds ratio = 4.64, 95% confidence interval: 1.03, 20.86; Ptrend = 0.04) cHL risk. Other dietary patterns were not clearly associated with cHL. We report the first evidence for a role of dietary pattern in cHL etiology. Diets featuring high intake of meat or desserts and sweets may increase cHL risk.
Classic Hodgkin lymphoma (cHL) is a relatively rare cancer with a poorly understood etiology. The epidemiology of cHL is noteworthy for a bimodal age incidence curve in developed countries, with incidence rates peaking in young adulthood (age 15–34 years) and in older adulthood (age ≥50 years). Known risk factors for cHL are largely unmodifiable and include age, sex, a family history of cHL or non-Hodgkin lymphoma, having a compromised immune system, and history of Epstein-Barr virus (EBV) infection. Personal history of infectious mononucleosis, which is often a manifestation of primary EBV infection, has been associated with an elevated risk of developing EBV-positive cHL, as have childhood social environment factors that influence age at first exposure to EBV, such as sibship size, birth order, and nursery school attendance. Serological studies suggest that severe/chronic EBV infection is associated with cHL risk, particularly with EBV-positive cHL independent of infectious mononucleosis. Observations that the distributions of EBV-positive tumors and cHL histological subtypes vary by age group suggest age-related heterogeneity in the role of EBV and other risk factors in cHL etiology.
A diagnosis of cHL is pathologically confirmed by the presence of malignant Reed-Sternberg cells in affected tissue. The microenvironment of Reed-Sternberg cells, which originate from B lymphocytes, is rich in reactive inflammatory cells and suggests that chronic inflammation may play a role in cHL pathogenesis, possibly in conjunction with EBV infection. Of note, numerous inflammatory mediators have been identified in Reed-Sternberg cells and Hodgkin lymphoma (HL)-derived cell lines and have been associated with HL risk in human populations. It is therefore plausible that modifiable factors that disrupt or modulate the immune system may be associated with cHL risk. Consistent with that hypothesis, we previously observed a 40% decreased risk of cHL in association with regular use of aspirin.
Of interest, specific dietary patterns have been associated with levels of inflammatory biomarkers. For example, diets rich in fruits, vegetables, and whole grains have been associated with lower levels of proinflammatory markers. In contrast, a "Western" style diet high in fat, refined grains, red and processed meats, and oils was associated with higher levels of inflammatory markers in the same populations and with inflammation-related chronic diseases.
Few previous studies have examined associations between dietary factors and cHL risk. These studies focused largely on individual food items or nutrients and reported inconsistent results. To our knowledge, no study has yet examined an association between dietary pattern and the risk of cHL. We undertook the present population-based case-control analysis to evaluate whether dietary patterns influence the risk of cHL in younger or older adults.
Abstract and Introduction
Abstract
Classic Hodgkin lymphoma (cHL) has few known modifiable risk factors, and the relationship between diet and cHL risk is unclear. We performed the first investigation of an association between dietary pattern and cHL risk in 435 cHL cases and 563 population-based controls from Massachusetts and Connecticut (1997–2000) who completed baseline diet questionnaires. We identified 4 major dietary patterns ("vegetable," "high meat," "fruit/low-fat dairy," "desserts/sweets") using principal components analysis. We computed multivariable odds ratios and 95% confidence intervals for associations of dietary pattern score (quartiles) with younger-adult (age <50 years), older-adult (age ≥50 years), and overall cHL risk. Secondary analyses examined associations by histological subtype and tumor Epstein-Barr virus (EBV) status. A diet high in desserts/sweets was associated with younger-adult (odds ratio(quartile 4 vs. quartile 1) = 1.60, 95% confidence interval: 1.05, 2.45; Ptrend = 0.008) and EBV-negative, younger-adult (odds ratio = 2.11, 95% confidence interval: 1.31, 3.41; Ptrend = 0.007) cHL risk. A high meat diet was associated with older-adult (odds ratio = 3.34, 95% confidence interval: 1.02, 10.91; Ptrend = 0.04) and EBV-negative, older-adult (odds ratio = 4.64, 95% confidence interval: 1.03, 20.86; Ptrend = 0.04) cHL risk. Other dietary patterns were not clearly associated with cHL. We report the first evidence for a role of dietary pattern in cHL etiology. Diets featuring high intake of meat or desserts and sweets may increase cHL risk.
Introduction
Classic Hodgkin lymphoma (cHL) is a relatively rare cancer with a poorly understood etiology. The epidemiology of cHL is noteworthy for a bimodal age incidence curve in developed countries, with incidence rates peaking in young adulthood (age 15–34 years) and in older adulthood (age ≥50 years). Known risk factors for cHL are largely unmodifiable and include age, sex, a family history of cHL or non-Hodgkin lymphoma, having a compromised immune system, and history of Epstein-Barr virus (EBV) infection. Personal history of infectious mononucleosis, which is often a manifestation of primary EBV infection, has been associated with an elevated risk of developing EBV-positive cHL, as have childhood social environment factors that influence age at first exposure to EBV, such as sibship size, birth order, and nursery school attendance. Serological studies suggest that severe/chronic EBV infection is associated with cHL risk, particularly with EBV-positive cHL independent of infectious mononucleosis. Observations that the distributions of EBV-positive tumors and cHL histological subtypes vary by age group suggest age-related heterogeneity in the role of EBV and other risk factors in cHL etiology.
A diagnosis of cHL is pathologically confirmed by the presence of malignant Reed-Sternberg cells in affected tissue. The microenvironment of Reed-Sternberg cells, which originate from B lymphocytes, is rich in reactive inflammatory cells and suggests that chronic inflammation may play a role in cHL pathogenesis, possibly in conjunction with EBV infection. Of note, numerous inflammatory mediators have been identified in Reed-Sternberg cells and Hodgkin lymphoma (HL)-derived cell lines and have been associated with HL risk in human populations. It is therefore plausible that modifiable factors that disrupt or modulate the immune system may be associated with cHL risk. Consistent with that hypothesis, we previously observed a 40% decreased risk of cHL in association with regular use of aspirin.
Of interest, specific dietary patterns have been associated with levels of inflammatory biomarkers. For example, diets rich in fruits, vegetables, and whole grains have been associated with lower levels of proinflammatory markers. In contrast, a "Western" style diet high in fat, refined grains, red and processed meats, and oils was associated with higher levels of inflammatory markers in the same populations and with inflammation-related chronic diseases.
Few previous studies have examined associations between dietary factors and cHL risk. These studies focused largely on individual food items or nutrients and reported inconsistent results. To our knowledge, no study has yet examined an association between dietary pattern and the risk of cHL. We undertook the present population-based case-control analysis to evaluate whether dietary patterns influence the risk of cHL in younger or older adults.
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