Bertrand Kimberly A, Giovannucci Edward, Rosner Bernard A, Zhang Shumin M, Laden Francine, Birmann Brenda M
Slone Epidemiology Center, Boston University, Boston, MA;
Channing Division of Network Medicine and.
Am J Clin Nutr. 2017 Aug;106(2):650-656. doi: 10.3945/ajcn.117.155010. Epub 2017 Jun 28.
Dietary fat intake may contribute to non-Hodgkin lymphoma (NHL) pathogenesis by influencing carcinogen exposure or through immune modulation. We aimed to evaluate NHL risk associated with total and specific dietary fat intake. We evaluated associations within the Nurses' Health Study (NHS) ( = 88,598) and the Health Professionals Follow-Up Study (HPFS) ( = 47,531) using repeated validated dietary assessments. We confirmed 1802 incident NHL diagnoses through 2010. Using multivariable Cox proportional hazards models, we estimated hazard ratios (HRs) for all NHL and common subtypes associated with a 1-SD increase in cumulative mean intakes of total, animal, saturated, and vegetable fats and marine fatty acids. We pooled sex-specific HRs using random-effects meta-analysis. Over 24-30 y of follow-up, neither total nor specific dietary fats were significantly associated with NHL risk overall. Higher total, animal, and saturated fat intakes were positively associated with the risk of the chronic lymphocytic leukemia/small lymphocytic lymphoma subtype among women only (253 cases; -trend ≤ 0.05), driven by strong associations during 1980-1994. From baseline through 1994, among women and men combined, total fat intake was borderline-significantly positively associated with NHL overall (pooled HR per SD: 1.13; 95% CI: 0.99, 1.29) and was significantly associated with diffuse large B cell lymphoma (pooled HR per SD: 1.47; 95% CI: 1.06, 2.05), with similar trends for animal and saturated fat intake. For women only, fat was significantly positively associated with all NHL. In contrast, during 1994-2010, there was little evidence for associations of dietary fat intake with NHL overall or by subtype. Previous observations of an increased risk of NHL associated with intakes of total, animal, saturated, and fat with 14 y of follow-up did not persist with longer follow-up.
膳食脂肪摄入可能通过影响致癌物暴露或通过免疫调节作用,对非霍奇金淋巴瘤(NHL)的发病机制产生影响。我们旨在评估与总膳食脂肪摄入量和特定膳食脂肪摄入量相关的NHL风险。我们在护士健康研究(NHS)(n = 88,598)和卫生专业人员随访研究(HPFS)(n = 47,531)中,使用经过反复验证的膳食评估方法评估了两者之间的关联。截至2010年,我们确认了1802例NHL确诊病例。使用多变量Cox比例风险模型,我们估计了总脂肪、动物脂肪、饱和脂肪、反式脂肪和植物脂肪以及海洋脂肪酸累积平均摄入量每增加1个标准差与所有NHL及其常见亚型相关的风险比(HRs)。我们使用随机效应荟萃分析汇总了按性别分类的HRs。在24 - 30年的随访中,总体而言,总膳食脂肪或特定膳食脂肪与NHL风险均无显著关联。仅在女性中(253例),总脂肪、动物脂肪和饱和脂肪摄入量较高与慢性淋巴细胞白血病/小淋巴细胞淋巴瘤亚型的风险呈正相关(P趋势≤0.05),这是由1980 - 1994年期间的强关联驱动的。从基线到1994年,在男性和女性的综合分析中,总脂肪摄入量与总体NHL呈临界显著正相关(每标准差的汇总HR:1.13;95% CI:0.99,1.29),并且与弥漫性大B细胞淋巴瘤显著相关(每标准差的汇总HR:1.47;95% CI:1.06,2.05),动物脂肪和饱和脂肪摄入量也有类似趋势。仅对于女性,反式脂肪与所有NHL呈显著正相关。相比之下,在1994 - 2010年期间,几乎没有证据表明膳食脂肪摄入量与总体NHL或各亚型之间存在关联。先前观察到的随访14年时总脂肪、动物脂肪、饱和脂肪和反式脂肪摄入量与NHL风险增加之间的关联,在更长时间的随访中并未持续存在。