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Dietary acid load and esophageal cancer risk: A case‐control study

BACKGROUND: A high dietary acid load (DAL) can produce metabolic acidosis, which is linked to cancer development through mechanisms of inflammation and cell transformation. There is limited epidemiological evidence linking DAL and cancer risk; however, none of the published studies focused on DAL an...

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Autores principales: Ronco, Alvaro Luis, Martínez‐López, Wilner, Calderón, Juan M., Storz, Maximilian Andreas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons Australia, Ltd 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9527162/
https://www.ncbi.nlm.nih.gov/pubmed/36054595
http://dx.doi.org/10.1111/1759-7714.14612
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author Ronco, Alvaro Luis
Martínez‐López, Wilner
Calderón, Juan M.
Storz, Maximilian Andreas
author_facet Ronco, Alvaro Luis
Martínez‐López, Wilner
Calderón, Juan M.
Storz, Maximilian Andreas
author_sort Ronco, Alvaro Luis
collection PubMed
description BACKGROUND: A high dietary acid load (DAL) can produce metabolic acidosis, which is linked to cancer development through mechanisms of inflammation and cell transformation. There is limited epidemiological evidence linking DAL and cancer risk; however, none of the published studies focused on DAL and esophageal cancer (EC) risk in particular. Therefore, we sought to explore this association in the present study. METHODS: A case‐control study was performed in 1295 male patients (185 squamous cell EC cases and 1110 age‐frequency and urban/rural residence matched controls) through a multitopic inquiry, including a food frequency questionnaire. Food‐derived nutrients were calculated from available databases. The DAL was calculated based on two validated measures: Potential renal acid load (PRAL) score and net endogenous acid production (NEAP) score. Odds ratios (OR) and their 95% confidence intervals (95% CI) were estimated by unconditional logistic regression, adjusting for confounders. RESULTS: We found direct, significant associations between dietary acid load and EC risk: (OR = 2.28, 95% CI: 1.44–3.61, ptrend <0.0001) and (OR = 2.17, 95% CI: 1.38–3.41, ptrend <0.0001) for highest PRAL and NEAP tertiles, respectively. Our data raise the possibility that a high DAL may contribute to EC development. Both acid load scores were directly associated with animal‐based foods (mainly meat) and inversely associated with the intake of plant‐based foods. CONCLUSION: To the best of our knowledge, this is the first epidemiological case–control study analyzing associations of DAL and squamous cell EC risk. Further research is warranted to confirm our findings.
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spelling pubmed-95271622022-10-06 Dietary acid load and esophageal cancer risk: A case‐control study Ronco, Alvaro Luis Martínez‐López, Wilner Calderón, Juan M. Storz, Maximilian Andreas Thorac Cancer Original Articles BACKGROUND: A high dietary acid load (DAL) can produce metabolic acidosis, which is linked to cancer development through mechanisms of inflammation and cell transformation. There is limited epidemiological evidence linking DAL and cancer risk; however, none of the published studies focused on DAL and esophageal cancer (EC) risk in particular. Therefore, we sought to explore this association in the present study. METHODS: A case‐control study was performed in 1295 male patients (185 squamous cell EC cases and 1110 age‐frequency and urban/rural residence matched controls) through a multitopic inquiry, including a food frequency questionnaire. Food‐derived nutrients were calculated from available databases. The DAL was calculated based on two validated measures: Potential renal acid load (PRAL) score and net endogenous acid production (NEAP) score. Odds ratios (OR) and their 95% confidence intervals (95% CI) were estimated by unconditional logistic regression, adjusting for confounders. RESULTS: We found direct, significant associations between dietary acid load and EC risk: (OR = 2.28, 95% CI: 1.44–3.61, ptrend <0.0001) and (OR = 2.17, 95% CI: 1.38–3.41, ptrend <0.0001) for highest PRAL and NEAP tertiles, respectively. Our data raise the possibility that a high DAL may contribute to EC development. Both acid load scores were directly associated with animal‐based foods (mainly meat) and inversely associated with the intake of plant‐based foods. CONCLUSION: To the best of our knowledge, this is the first epidemiological case–control study analyzing associations of DAL and squamous cell EC risk. Further research is warranted to confirm our findings. John Wiley & Sons Australia, Ltd 2022-08-21 2022-10 /pmc/articles/PMC9527162/ /pubmed/36054595 http://dx.doi.org/10.1111/1759-7714.14612 Text en © 2022 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Ronco, Alvaro Luis
Martínez‐López, Wilner
Calderón, Juan M.
Storz, Maximilian Andreas
Dietary acid load and esophageal cancer risk: A case‐control study
title Dietary acid load and esophageal cancer risk: A case‐control study
title_full Dietary acid load and esophageal cancer risk: A case‐control study
title_fullStr Dietary acid load and esophageal cancer risk: A case‐control study
title_full_unstemmed Dietary acid load and esophageal cancer risk: A case‐control study
title_short Dietary acid load and esophageal cancer risk: A case‐control study
title_sort dietary acid load and esophageal cancer risk: a case‐control study
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9527162/
https://www.ncbi.nlm.nih.gov/pubmed/36054595
http://dx.doi.org/10.1111/1759-7714.14612
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