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Abstract

Background: Overweight and obesity are a global pandemic, contributing to death and disability-adjusted life-years. Obesity is a major factor in the onset of chronic inflammatory diseases (CIDs). Yet, several knowledge gaps remain: For several CIDs, inconsistent results have been reported, relating to their obesity-imposed risk, data on most rare CIDs remain unavailable, sex differences and racial disparities remain mostly unaddressed. Methods: A large-scale cohort study compared the risk of developing 46 CIDs in individuals with overweight/obesity (n=3,101,824) to an equal number of non-overweight/obese individuals. Propensity score matching optimized between-group comparability, and sensitivity analyses assessed study robustness. Results: The risk of developing any CID was 28.48% in overweight/obese individuals versus 17.55% in non-overweight/obese controls, with a hazard ratio (95%-confidence interval) of 1.52 (1.509-1.521, p<0.0001). This risk was consistent across all sensitivity, sex-, and race-stratified analyses. Overweight and obesity were associated with an increased risk for 24 of 46 CIDs in the primary analysis and all sensitivity analyses. For 12 diseases, increased risks were confirmed to one of the two sensitivity analyses, while for 10 diseases, results were discordant. No increased risk was observed for one disease. In sex-stratified analysis, overweight and obesity posed a more pronounced risk for four CIDs in female individuals. In race-stratified analysis, overweight and obesity were linked to a higher risk for seven CIDs in White individuals and to one CID in “Black or African American” individuals. Conclusion: Overweight and obesity increase the risk for the majority of CIDs in a sex- and race-specific manner.

OriginalspracheEnglisch
Aufsatznummer1516433
ZeitschriftFrontiers in Endocrinology
Jahrgang16
ISSN1664-2392
DOIs
PublikationsstatusVeröffentlicht - 2025

Fördermittel

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This research was funded by the Cluster of Excellence “Precision Medicine in Chronic Inflammation” (EXC 2167), the Collaborative Research Centre “Pathomechanisms of Antibody-mediated Autoimmunity” (SFB 1526), the Research Training Group “Autoimmune Pre-Disease” (GRK 2633), the Individual Research Grant DFG LU 877/25-1, all from the Deutsche Forschungsgemeinschaft, the Schleswig-Holstein Excellence-Chair Program from the State of Schleswig Holstein, Sinergia Unravel principles of self-organization in injured tissue (CRSII5_202301/1) from the Swiss National Science Foundation and the German Federal Ministry of Education and Research BMBF (2816ERA14E). This research was funded by the Cluster of Excellence “Precision Medicine in Chronic Inflammation” (EXC 2167), the Collaborative Research Centre “Pathomechanisms of Antibody-mediated Autoimmunity” (SFB 1526), the Research Training Group “Autoimmune Pre-Disease” (GRK 2633), the Individual Research Grant DFG LU 877/25-1, all from the Deutsche Forschungsgemeinschaft, the Schleswig-Holstein Excellence-Chair Program from the State of Schleswig Holstein, Sinergia Unravel principles of self-organization in injured tissue (CRSII5_202301/1) from the Swiss National Science Foundation and the German Federal Ministry of Education and Research BMBF (2816ERA14E). The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This research was funded by the Cluster of Excellence “Precision Medicine in Chronic Inflammation” (EXC 2167), the Collaborative Research Centre “Pathomechanisms of Antibody-mediated Autoimmunity” (SFB 1526), the Research Training Group “Autoimmune Pre-Disease” (GRK 2633), the Individual Research Grant DFG LU 877/25-1, all from the Deutsche Forschungsgemeinschaft, the Schleswig-Holstein Excellence-Chair Program from the State of Schleswig Holstein, Sinergia Unravel principles of self-organization in injured tissue (CRSII5_202301/1) from the Swiss National Science Foundation and the German Federal Ministry of Education and Research BMBF (2816ERA14E). Acknowledgments

TrägerTrägernummer
Deutsche Forschungsgemeinschaft
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
Bundesministerium für Bildung und Forschung2816ERA14E
State of Schleswig-Holstein*CRSII5_202301/1

    UN SDGs

    Dieser Output leistet einen Beitrag zu folgendem(n) Ziel(en) für nachhaltige Entwicklung

    1. SDG 3 – Gesundheit und Wohlergehen
      SDG 3 – Gesundheit und Wohlergehen

    Strategische Forschungsbereiche und Zentren

    • Forschungsschwerpunkt: Infektion und Entzündung - Zentrum für Infektions- und Entzündungsforschung Lübeck (ZIEL)

    DFG-Fachsystematik

    • 2.21-05 Immunologie
    • 2.22-18 Rheumatologie
    • 2.22-17 Endokrinologie, Diabetologie, Metabolismus

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