Unit of Oncology and Radiotherapy, Pereira Rossell Women's Hospital, Bvar. Artigas 1590, Montevideo 11600, Uruguay; School of Medicine, CLAEH University, Prado and Salt Lake, Maldonado 20100, Uruguay; Biomedical Sciences Center, University of Montevideo, Puntas de Santiago 1604, Montevideo 11500, Uruguay.
Epigenetics and Genomics Instability Laboratory and Biodosimetry Service, Instituto de Investigaciones Biológicas Clemente Estable, Av. Italia 3318, Montevideo 11600, Uruguay.
Cancer Treat Res Commun. 2021;28:100382. doi: 10.1016/j.ctarc.2021.100382. Epub 2021 Apr 25.
Dysregulation of the endogenous acid-base balance can contribute to inflammation and cancer development if metabolic acidosis is sustained. The epidemiologic evidence on the association between diet-dependent acid load and cancer risk is scarce and inconsistent. We aim to explore the possible role of dietary acid load in lung cancer (LC) risk.
A case-control study was performed on 843 LC cases and 1466 controls by using a multi-topic questionnaire, including a food frequency questionnaire. Controls were matched to cases by age-frequency, urban/rural residence, and region. Food-derived nutrients were calculated from available databases. The dietary acid load was calculated using validated measures as potential renal acid load (PRAL) score and net endogenous acid production (NEAP) score. Odds ratios (ORs) were estimated by logistic regression.
We found direct associations between dietary acid load and LC risk. The highest quartile of the NEAP score was significantly associated (OR=2.22, p<0.001). The PRAL score displayed similar associations in simpler regression models, but there was no association when a more complex one was used (OR=0.99, p =0.94). The NEAP score was associated with a significant risk increase in all cell types, except for small cell cancers, but the PRAL score did not show any association.
The NEAP scores, directly associated with meat intake and inversely associated with plant-based foods intake, suggest that a high acid load dietary style may increase LC risk. Studies focused on food groups, and nutritional patterns are in line with our findings. Although the data shown here represent the first one to be published on this issue, further studies are needed to confirm these findings.
如果代谢性酸中毒持续存在,内源性酸碱平衡的失调可能会导致炎症和癌症的发生。关于饮食相关酸负荷与癌症风险之间的关联的流行病学证据很少且不一致。我们旨在探索饮食酸负荷在肺癌(LC)风险中的可能作用。
通过使用多主题问卷(包括食物频率问卷)对 843 例 LC 病例和 1466 例对照进行病例对照研究。对照与病例按年龄频率、城乡居住和地区进行匹配。从可用数据库中计算食物来源的营养素。使用验证过的指标(潜在肾酸负荷(PRAL)评分和净内源性酸生成(NEAP)评分)来计算饮食酸负荷。使用逻辑回归估计比值比(OR)。
我们发现饮食酸负荷与 LC 风险之间存在直接关联。NEAP 评分的最高四分位数与 LC 风险显著相关(OR=2.22,p<0.001)。PRAL 评分在更简单的回归模型中显示出类似的关联,但当使用更复杂的模型时,没有关联(OR=0.99,p=0.94)。NEAP 评分与所有细胞类型的风险增加显著相关,除小细胞癌外,但 PRAL 评分与任何细胞类型均无关联。
与肉类摄入直接相关,与植物性食物摄入呈负相关的 NEAP 评分表明,高酸负荷的饮食方式可能会增加 LC 的风险。关注食物组和营养模式的研究与我们的研究结果一致。尽管这里显示的数据代表了第一个关于这个问题的出版物,但需要进一步的研究来证实这些发现。