Yunxia Lu1,2, Nitin Shivappa3,4, Yulan Lin5,6, Jesper Lagergren5,7, James R Hébert3,4. 1. Department of Molecular Medicine and Surgery, Karolinska Institutet, 171 76, Stockholm, Sweden. yunxia.lu@ki.se. 2. Department of Epidemiology and Biostatistics, Imperial College London, London, UK. yunxia.lu@ki.se. 3. Cancer Prevention and Control Program, University of South Carolina, Columbia, SC, USA. 4. Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. 5. Department of Molecular Medicine and Surgery, Karolinska Institutet, 171 76, Stockholm, Sweden. 6. European Palliative Care Research Centre, Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway. 7. Division of Cancer Studies, King's College London, London, UK.
Abstract
PURPOSE: This project sought to test the role of diet-related inflammation in modulating the risk of oesophageal cancer. METHODS: A nationwide population-based case-control study was conducted from 1 December 1994 through 31 December 1997 in Sweden. All newly diagnosed patients with adenocarcinoma of the oesophagus or gastroesophageal junction and a randomly selected half of patients with oesophageal squamous cell carcinoma were eligible as cases. Using the Swedish Registry of the Total Population, the control group was randomly selected from the entire Swedish population and frequency-matched on age (within 10 years) and sex. The literature-derived dietary inflammatory index (DII) was developed to describe the inflammatory potential of diet. DII scores were computed based on a food frequency questionnaire. Higher DII scores indicate more pro-inflammatory diets. Odds ratios and 95 % confidence intervals (CI) were computed to assess risk associated between DII scores and oesophageal cancer using logistic regression adjusted by potential confounders. RESULTS: In total, 189 oesophageal adenocarcinomas, 262 gastroesophageal junctional adenocarcinomas, 167 oesophageal squamous cell carcinomas, and 820 control subjects were recruited into the study. Significant associations with DII were observed for oesophageal squamous cell carcinoma (ORQuartile4vs1 4.35, 95 % CI 2.24, 8.43), oesophageal adenocarcinoma (ORQuartile4vs1 3.59, 95 % CI 1.87, 6.89), and gastroesophageal junctional adenocarcinoma (ORQuartile4vs1 2.04, 95 % CI 1.24, 3.36). Significant trends across quartiles of DII were observed for all subtypes of oesophageal cancer. CONCLUSIONS: Diet-related inflammation appears to be associated with an increased risk of oesophageal cancer, regardless of histological type.
PURPOSE: This project sought to test the role of diet-related inflammation in modulating the risk of oesophageal cancer. METHODS: A nationwide population-based case-control study was conducted from 1 December 1994 through 31 December 1997 in Sweden. All newly diagnosed patients with adenocarcinoma of the oesophagus or gastroesophageal junction and a randomly selected half of patients with oesophageal squamous cell carcinoma were eligible as cases. Using the Swedish Registry of the Total Population, the control group was randomly selected from the entire Swedish population and frequency-matched on age (within 10 years) and sex. The literature-derived dietary inflammatory index (DII) was developed to describe the inflammatory potential of diet. DII scores were computed based on a food frequency questionnaire. Higher DII scores indicate more pro-inflammatory diets. Odds ratios and 95 % confidence intervals (CI) were computed to assess risk associated between DII scores and oesophageal cancer using logistic regression adjusted by potential confounders. RESULTS: In total, 189 oesophageal adenocarcinomas, 262 gastroesophageal junctional adenocarcinomas, 167 oesophageal squamous cell carcinomas, and 820 control subjects were recruited into the study. Significant associations with DII were observed for oesophageal squamous cell carcinoma (ORQuartile4vs1 4.35, 95 % CI 2.24, 8.43), oesophageal adenocarcinoma (ORQuartile4vs1 3.59, 95 % CI 1.87, 6.89), and gastroesophageal junctional adenocarcinoma (ORQuartile4vs1 2.04, 95 % CI 1.24, 3.36). Significant trends across quartiles of DII were observed for all subtypes of oesophageal cancer. CONCLUSIONS: Diet-related inflammation appears to be associated with an increased risk of oesophageal cancer, regardless of histological type.
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