Dietary Fat and Protein in Relation to Risk of Non-Hodgkin's Lymphoma Among Women

Zhang, Shumin; Hunter, David J.; Rosner, Bernard; Colditz, Graham A.; Fuchs, Charlie; Speizer, Frank E.; Willett, Walter C.

doi:10.1093/jnci/91.20.1751

Cited by 134 publications

(157 citation statements)

References 26 publications

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“…15 In addition, an American cohort study following women for 14 years did not report any association between tobacco smoking and the development of NHL overall. 12 Nevertheless, our analyses for specific histological subtypes failed to confirm the association between smoking and follicular NHL recently reported by Interlymph 48 and also found in 3 cohort studies carried out in USA 7,10 and in Sweden. 5 The link between smoking and follicular NHL was biologically plausible, as the carcinogenic components of cigarette smoke should increase the frequency of the common translocation for follicular NHL, which leads to the persistent expression of the anti-apoptosis gene BCL2.…”

Section: Discussioncontrasting

confidence: 65%

Tobacco smoking, alcohol drinking and non‐Hodgkin's lymphoma: A European multicenter case‐control study (Epilymph)

Besson

Brennan

Becker

et al. 2006

Intl Journal of Cancer

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To study the role of tobacco smoking and alcohol drinking in the etiology of non-Hodgkin's lymphoma (NHL), we conducted a multicenter case-control study in Spain, France, Germany, Italy, Ireland and Czech Republic between 1998 and 2004, which included 1,742 cases of NHL and 2,465 controls matched on age, sex and recruitment area. Tobacco smoking was not associated with the risk of NHL overall or with risk of specific histological subtypes. Similarly, there was no association between alcohol drinking and the risk of NHL overall or across histological subtypes. However, a protective effect of alcohol drinking was observed among men (OR 5 0.76, 95% CI 5 0.62-0.93) and in non-Mediterranean countries (OR 5 0.73, 95% CI 5 0.61-0.86). There was no evidence of interaction between alcohol drinking and tobacco smoking in NHL etiology. The results of this large-scale European study did not support an association between tobacco and NHL and suggested a protective effect of alcohol on development of NHL for men and in non-Mediterranean countries. ' 2006 Wiley-Liss, Inc.Key words: lymphoma; non-Hodgkin's; tobacco; alcohol; EuropeThe incidence of non-Hodgkin's lymphoma (NHL) has increased considerably in the last few decades in all countries with reliable information. 1 In Europe, between the early and the late 1990s, the rise in mortality was 5% for men and 8% for women. 2 There is no clear explanation of this phenomenon. To date, the established risk factors for NHL are autoimmune diseases, 3 infection with human immunodeficiency virus and human T-cell leukemia/lymphoma virus, 4 but these factors explain only a small proportion of the etiology of NHL. The role of tobacco smoking and alcohol drinking in the development of NHL remains uncertain partly due to the small sample sizes of previous epidemiologic studies. Recently, the International Lymphoma Epidemiology Consortium (Interlymph) has reported results based on pooled data of studies from Europe, 32-34 USA 22,28,39,45 and Australia. 46 In this analysis based on 6,492 cases of NHL and 8,683 controls, a slight inverse association was found between alcohol intake and the development of NHL. 47 The analysis of the effect of tobacco smoking, based on 6,594 cases of NHL and 8,892 controls, reported a slightly increased risk of NHL overall and of B-cell follicular lymphoma in particular. 48 Thus, we have attempted to confirm the results of the pooled analysis using data from an independent European multicenter case-control study (Epilymph). Material and methodsOur investigation was conducted in 7 European countries (Czech Republic, Finland, France, Germany, Ireland, Italy, and Spain), but data from Finland were not included in this analysis because of methodological issues, in particular, controls were not matched to cases on age, sex and residence area, as done in other study centers, and the present study is based on data from 6 countries.Histologically or cytologically confirmed incident cases of lymphoma were recruited from 1998 to 2004 (Table I). Cases were classified ac...

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Section: Discussioncontrasting

confidence: 65%

Tobacco smoking, alcohol drinking and non‐Hodgkin's lymphoma: A European multicenter case‐control study (Epilymph)

Besson

Brennan

Becker

et al. 2006

Intl Journal of Cancer

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“…If weight gain in early adulthood is not responsible, our results could instead suggest that obesity from childhood is a risk factor for NHL. It seems unlikely however that nutrition during childhood, linked to adult stature (Silventoinen, 2003), increases NHL risk, since generally little evidence of an association with height has been presented either here or elsewhere (Whittemore et al, 1985;La Vecchia et al, 1990;Zhang et al, 1999;Cerhan et al, 2002). Alternatively, it may be that an underlying genetic component of obesity is involved in the pathogenesis of NHL.…”

Section: Discussionmentioning

confidence: 81%

“…Accordingly, it has been suggested that anthropometric measures, reflecting the degree of adiposity, as well as polymorphisms in genes associated with energy homeostasis such as leptin (LEP), leptin receptor (LEPR) and adiponectin (APM1), may increase NHL risk. However, while positive associations have been reported between NHL and anthropometric characteristics (Holly et al, 1999;Calle et al, 2003;Bahl et al, 2004;Pan et al, 2004), others have not (Paffenbarger Jr et al, 1978;Whittemore et al, 1985;Franceschi et al, 1989;La Vecchia et al, 1990;Zhang et al, 1999;Cerhan et al, 2002;Chang et al, 2005). Furthermore, polymorphisms in the LEP (an A to G nucleotide (nt) change at position 19 in the 5 0 -untranslated region (Hager et al, 1998), and a G to A substitution at nt À2548 upstream of the ATG start site (Mammes et al, 1998)) and LEPR (an A to G transition at nt 668 from the start codon that converts glutamine to arginine at codon 223 (223Q4R) (Gotoda et al, 1997)) genes were recently shown to modulate NHL risk (Skibola et al, 2004).…”

mentioning

confidence: 98%

Non-Hodgkin's lymphoma, obesity and energy homeostasis polymorphisms

et al. 2005

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A population-based case -control study of lymphomas in England collected height and weight details from 699 non-Hodgkin's lymphoma (NHL) cases and 914 controls. Obesity, defined as a body mass index (BMI) over 30 kg m À2 at five years before diagnosis,, was associated with an increased risk of NHL (OR ¼ 1.5, 95% CI 1.1 -2.1). The excess was most pronounced for diffuse large B-cell lymphoma (OR ¼ 1.9, 95% CI 1.3 -2.8). Genetic variants in the leptin (LEP 19G4A, LEP À2548G4A) and leptin receptor genes (LEPR 223Q4R), previously shown to modulate NHL risk, as well as a polymorphism in the energy regulatory gene adiponectin (APM1 276G4T), were investigated. Findings varied with leptin genotype, the risks being decreased with LEP 19AA (OR ¼ 0.7, 95% CI 0.5 -1.0) and increased with LEP À2548GA (OR ¼ 1.3, 95% CI 1.0 -1.7) and À2548AA (OR ¼ 1.4, 95% CI 1.0 -1.9), particularly for follicular lymphoma. These genetic findings, which were independent of BMI, were stronger for men than women.

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“…Significant and nonsignificant positive associations, ranging between 1.1 and 1.76, for the highest versus lowest category of total fat intake have been reported in case-control and cohort studies. 384,385,[401][402][403] Findings by dietary fat subgroups have been heterogeneous; however, significant and nonsignificant elevated relative risks have been reported for saturated fats. 384,385,395,[401][402][403] Some studies have reported positive associations 385,402-404 and significant dose-response relationships 385 with animal protein, whereas other studies have not.…”

Section: Dietary Factorsmentioning

confidence: 99%

“…384,385,[401][402][403] Findings by dietary fat subgroups have been heterogeneous; however, significant and nonsignificant elevated relative risks have been reported for saturated fats. 384,385,395,[401][402][403] Some studies have reported positive associations 385,402-404 and significant dose-response relationships 385 with animal protein, whereas other studies have not. 384,405 In one casecontrol study, a significant inverse association was found with the highest compared with lowest quartile of protein from animal sources (OR 5 0.39, 95% CI: 0.22-0.70).…”

Section: Dietary Factorsmentioning

confidence: 99%

The non-Hodgkin lymphomas: A review of the epidemiologic literature

et al. 2007

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Dietary Fat and Protein in Relation to Risk of Non-Hodgkin's Lymphoma Among Women

Abstract: Greater dietary intake of certain meats and fats was associated with a higher risk of non-Hodgkin's lymphoma. These relationships and their potential mechanisms deserve further examination.

Cited by 134 publications

References 26 publications

Tobacco smoking, alcohol drinking and non‐Hodgkin's lymphoma: A European multicenter case‐control study (Epilymph)

Tobacco smoking, alcohol drinking and non‐Hodgkin's lymphoma: A European multicenter case‐control study (Epilymph)

Non-Hodgkin's lymphoma, obesity and energy homeostasis polymorphisms

The non-Hodgkin lymphomas: A review of the epidemiologic literature

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