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Inflammatory dietary pattern and risk of developing rheumatoid arthritis in women

  • Jeffrey A. Sparks
  • Medha Barbhaiya
  • Sara K. Tedeschi
  • Cianna L. Leatherwood
  • Fred K. Tabung
  • Cameron B. Speyer
  • Susan Malspeis
  • Karen H. Costenbader
  • Elizabeth W. Karlson
  • Bing Lu
Brief Report

Abstract

Our objective was to investigate whether a dietary pattern derived using inflammatory biomarkers is associated with rheumatoid arthritis (RA) risk. We prospectively followed 79,988 women in the Nurses’ Health Study (NHS, 1984–2014) and 93,572 women in the NHSII (1991–2013); incident RA was confirmed by medical records. Food frequency questionnaires (FFQ) were completed at baseline and approximately every 4 years. Inflammatory dietary pattern was assessed from FFQ data using the Empirical Dietary Inflammatory Pattern (EDIP), including 18 anti-/pro-inflammatory food/beverage groups weighted by correlations with plasma inflammatory biomarkers (interleukin-6, C-reactive protein, and tumor necrosis factor-α receptor 2). We investigated associations between EDIP and RA using Cox regression. We identified 1185 incident RA cases over 4,425,434 person-years. EDIP was not associated with overall RA risk (p trend = 0.21 across EDIP quartiles). Among women ≤ 55 years, increasing EDIP was associated with increased overall RA risk; HRs (95% CIs) across EDIP quartiles were 1.00 (reference), 1.14 (0.86–1.51), 1.35 (1.03–1.77), and 1.38 (1.05–1.83; p for trend = 0.01). Adjusting for BMI attenuated this association. Increasing EDIP was associated with increased seropositive RA risk among women ≤ 55 years (p for trend = 0.04). There was no association between EDIP and RA among women > 55 years (EDIP-age interaction, p = 0.03). An inflammatory dietary pattern was associated with increased seropositive RA risk with onset ≤ 55 years old, and this association may be partially mediated through BMI.

Keywords

Diet Epidemiology Inflammation Rheumatoid arthritis 

Notes

Acknowledgements

We thank the participants of the NHS and NHSII for their dedicated participation in this longitudinal study as well as the staff members at the Channing Division of Network Medicine (Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School).

Author contributions

All authors were involved in drafting the article or revising it critically for important intellectual contact, and all authors approved the final version to be published. Dr. Sparks had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Study conception and design: Sparks, Karlson, Lu

Acquisition of data: Sparks, Barbhaiya, Tedeschi, Leatherwood, Tabung, Costenbader, Karlson, Lu

Analysis and interpretation of data: Sparks, Barbhaiya, Tedeschi, Leatherwood, Tabung, Speyer, Malspeis, Costenbader, Karlson, Lu

Funding

This work was supported by the National Institutes of Health (grant numbers R01 AR061362, K24 AR052403, L30 AR066953, R01 AR049880, UM1 CA186107, UM1 CA176726, K99 CA207736, K23 AR069688, T32 AR007530, P30 AR070253, and P30 AR072577).

Compliance with ethical standards

Disclosures

None.

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Copyright information

© International League of Associations for Rheumatology (ILAR) 2018

Authors and Affiliations

  • Jeffrey A. Sparks
    • 1
    • 2
  • Medha Barbhaiya
    • 3
  • Sara K. Tedeschi
    • 1
    • 2
  • Cianna L. Leatherwood
    • 1
    • 2
  • Fred K. Tabung
    • 4
    • 5
  • Cameron B. Speyer
    • 1
  • Susan Malspeis
    • 1
  • Karen H. Costenbader
    • 1
    • 2
  • Elizabeth W. Karlson
    • 1
    • 2
  • Bing Lu
    • 1
    • 2
  1. 1.Department of Medicine, Division of Rheumatology, Immunology, and AllergyBrigham and Women’s HospitalBostonUSA
  2. 2.Harvard Medical SchoolBostonUSA
  3. 3.Hospital for Special SurgeryNew York CityUSA
  4. 4.Department of NutritionHarvard T.H. Chan School of Public HealthBostonUSA
  5. 5.Department of Internal Medicine, Division of Medical OncologyThe Ohio State University College of MedicineColumbusUSA

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