Clinical nutrition (Edinburgh, Scotland) · 2022
The inflammatory potential of the diet as a link between food processing and low-grade inflammation: An analysis on 21,315 participants to the Moli-sani study.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Mignogna Cristiana, Costanzo Simona, Di Castelnuovo Augusto, Ruggiero Emilia, Shivappa Nitin, Hebert James R, Esposito Simona, De Curtis Amalia, Persichillo Mariarosaria, Cerletti Chiara, Donati Maria Benedetta, de Gaetano Giovanni, Iacoviello Licia, Bonaccio Marialaura, Moli-sani Study Investigators
Аннотация
BACKGROUND & AIMS: Food processing may adversely affect human health through a variety of mechanisms, including the development of a chronic pro-inflammatory state. In this study we aimed to test the hypothesis that an increasing degree of food processing is directly associated with low-grade inflammation, and evaluate to what extent this association is mediated by the inflammatory potential of highly processed foods.
METHODS: Cross-sectional analysis on 21,315 subjects (mean age 55 ± 3 y) from the Moli-sani Study with complete dietary data collected by a validated 188-item food frequency questionnaire. The NOVA classification was used to categorize foods on the basis of industrial processing as: 1) unprocessed/minimally processed foods; 2) processed culinary ingredients; 3) processed foods; 4) ultra-processed foods (UPF). The inflammatory potential of the diet was evaluated through the Energy-adjusted Dietary Inflammatory Index (E-DII™). Low-grade inflammation was assessed by a composite INFLA-score including C-reactive protein, leukocyte and platelet counts and the granulocyte to lymphocyte ratio.
RESULTS: In multivariable-adjusted linear regression models, the INFLA-score was positively associated with E-DII (β = 0.15; 0.10, 0.19), processed foods (β = 0.04; 0.01, 0.08) and UPF (β = 0.13; 0.07, 0.19), but inversely associated with minimally processed foods (β = -0.09; -0.13, -0.06). The E-DII score was inversely associated with minimally processed food (β = -0.40; 95%CI -0.41, -0.39 for 5% increment in the weight ratio) but directly with either processed culinary ingredients (β = 0.18; 0.15, 0.21 for 1% increment), processed food (β = 0.28; 0.27, 0.29 for 5% increment) or UPF (β = 0.34; 0.32, 0.36 for 5% increment). The inclusion of the E-DII into the multivariable model explained 88.5% of the association of processed food with the INFLA-score (p < 0.0001) and mitigated by 32.6% (p < 0.0001) the association with UPF.
CONCLUSIONS: The association of UPF with low-grade inflammation is only partially explained by the high pro-inflammatory potential of these foods. Further studies are warranted to test whether the observed adverse relationship of UPF with low-grade inflammation could be triggered by mechanisms that are not directly related to the pro-inflammatory potential of highly processed food products.
METHODS: Cross-sectional analysis on 21,315 subjects (mean age 55 ± 3 y) from the Moli-sani Study with complete dietary data collected by a validated 188-item food frequency questionnaire. The NOVA classification was used to categorize foods on the basis of industrial processing as: 1) unprocessed/minimally processed foods; 2) processed culinary ingredients; 3) processed foods; 4) ultra-processed foods (UPF). The inflammatory potential of the diet was evaluated through the Energy-adjusted Dietary Inflammatory Index (E-DII™). Low-grade inflammation was assessed by a composite INFLA-score including C-reactive protein, leukocyte and platelet counts and the granulocyte to lymphocyte ratio.
RESULTS: In multivariable-adjusted linear regression models, the INFLA-score was positively associated with E-DII (β = 0.15; 0.10, 0.19), processed foods (β = 0.04; 0.01, 0.08) and UPF (β = 0.13; 0.07, 0.19), but inversely associated with minimally processed foods (β = -0.09; -0.13, -0.06). The E-DII score was inversely associated with minimally processed food (β = -0.40; 95%CI -0.41, -0.39 for 5% increment in the weight ratio) but directly with either processed culinary ingredients (β = 0.18; 0.15, 0.21 for 1% increment), processed food (β = 0.28; 0.27, 0.29 for 5% increment) or UPF (β = 0.34; 0.32, 0.36 for 5% increment). The inclusion of the E-DII into the multivariable model explained 88.5% of the association of processed food with the INFLA-score (p < 0.0001) and mitigated by 32.6% (p < 0.0001) the association with UPF.
CONCLUSIONS: The association of UPF with low-grade inflammation is only partially explained by the high pro-inflammatory potential of these foods. Further studies are warranted to test whether the observed adverse relationship of UPF with low-grade inflammation could be triggered by mechanisms that are not directly related to the pro-inflammatory potential of highly processed food products.