Dietary inflammatory index and risk of multiple sclerosis: Findings from a large population-based incident case-control study.


Journal

Clinical nutrition (Edinburgh, Scotland)
ISSN: 1532-1983
Titre abrégé: Clin Nutr
Pays: England
ID NLM: 8309603

Informations de publication

Date de publication:
11 2020
Historique:
received: 14 07 2019
revised: 15 02 2020
accepted: 27 02 2020
pubmed: 22 3 2020
medline: 20 8 2021
entrez: 22 3 2020
Statut: ppublish

Résumé

For many decades diet, mainly its "pro-inflammatory" quality has been pondered as a possible risk factor for developing MS. However, the complexity of different dietary composition analysis provided controversial results. Recently a dietary inflammatory index (DII), a population-based score, was developed to objectify the inflammatory characteristics of a specific dietary intake. We investigated the potential association between DII (expressed as energy adjusted-DII (E-DII) and non-energy adjusted DII (DII)) assessed from a validated FFQ based on the participants' diet habits during adolescence and the risk for developing MS in a population-based incident case-control study. Multiple logistic regression was used to estimate the adjusted. We recruited 547 incident MS cases and 1057 general population controls from Tehran, Iran (August 2013-February 2015). A statistically significant higher risk of MS was found in analyses using E-DII scores as a continuous variable with an adjusted odds ratio (AOR) of 1.53 (95% confidence interval (CI): 1.42-1.65, P = 0.001), and as a categorical variable (4th quartile OR 7.01, 95% CI: 4.87-10.1, vs the first quartile), test for trend; OR 1.86 (95% CI: 1.67-2.07), P for trend <0.001. A similar pattern was demonstrated for DII score and risk for MS. We identified a pro-inflammatory diet characterized by higher E-DII and DII scores during adolescence as a strong risk factor for MS onset. Given the worldwide role of diet in general population health, improving nutritional pattern through educational programs is likely to reduce MS risk.

Sections du résumé

BACKGROUND & AIMS
For many decades diet, mainly its "pro-inflammatory" quality has been pondered as a possible risk factor for developing MS. However, the complexity of different dietary composition analysis provided controversial results. Recently a dietary inflammatory index (DII), a population-based score, was developed to objectify the inflammatory characteristics of a specific dietary intake.
METHODS
We investigated the potential association between DII (expressed as energy adjusted-DII (E-DII) and non-energy adjusted DII (DII)) assessed from a validated FFQ based on the participants' diet habits during adolescence and the risk for developing MS in a population-based incident case-control study. Multiple logistic regression was used to estimate the adjusted.
RESULTS
We recruited 547 incident MS cases and 1057 general population controls from Tehran, Iran (August 2013-February 2015). A statistically significant higher risk of MS was found in analyses using E-DII scores as a continuous variable with an adjusted odds ratio (AOR) of 1.53 (95% confidence interval (CI): 1.42-1.65, P = 0.001), and as a categorical variable (4th quartile OR 7.01, 95% CI: 4.87-10.1, vs the first quartile), test for trend; OR 1.86 (95% CI: 1.67-2.07), P for trend <0.001. A similar pattern was demonstrated for DII score and risk for MS.
CONCLUSIONS
We identified a pro-inflammatory diet characterized by higher E-DII and DII scores during adolescence as a strong risk factor for MS onset. Given the worldwide role of diet in general population health, improving nutritional pattern through educational programs is likely to reduce MS risk.

Identifiants

pubmed: 32197810
pii: S0261-5614(20)30097-2
doi: 10.1016/j.clnu.2020.02.033
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3402-3407

Informations de copyright

Copyright © 2020 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

Auteurs

Ibrahim Abdollahpour (I)

Department of Epidemiology, School of Public Health, Arak University of Medical Sciences, Arak, Iran; Isfahan Neurosciences Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Electronic address: ebrahemen@gmail.com.

Dejan Jakimovski (D)

Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA; Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.

Nitin Shivappa (N)

Cancer Prevention and Control Program, University of South Carolina, Columbia, SC 29208, USA; Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA; Connecting Health Innovations LLC, Columbia, SC 29201, USA.

James R Hébert (JR)

Cancer Prevention and Control Program, University of South Carolina, Columbia, SC 29208, USA; Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA; Connecting Health Innovations LLC, Columbia, SC 29201, USA.

Farhad Vahid (F)

Department of Nutritional Science, Nutrition and Food Research Institute, Shahid Beheshti University of Medical Science, Tehran, Iran. Electronic address: farhadvahid@outlook.com.

Saharnaz Nedjat (S)

Knowledge Utilization Research Center, Tehran University of Medical Science, Tehran, Iran; Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.

Mohammad Ali Mansournia (MA)

Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.

Bianca Weinstock-Guttman (B)

Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA.

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