Could vitamin D reduce obesity-associated inflammation? : observational and Mendelian randomization study
Palaniswamy, Saranya; Gill, Dipender; De Silva, N. Maneka; Lowry, Estelle; Jokelainen, Jari; Karhu, Toni; Mutt, Shivaprakash J.; Dehghan, Abbas; Sliz, Eeva; Chasman, Daniel I.; Timonen, Markku; Viinamäki, Heimo; Keinänen-Kiukaanniemi, Sirkka; Hyppönen, Elina; Herzig, Karl-Heinz; Sebert, Sylvain; Järvelin, Marjo-Riitta (2020-03-31)
Saranya Palaniswamy, Dipender Gill, N Maneka De Silva, Estelle Lowry, Jari Jokelainen, Toni Karhu, Shivaprakash J Mutt, Abbas Dehghan, Eeva Sliz, Daniel I Chasman, Markku Timonen, Heimo Viinamäki, Sirkka Keinänen-Kiukaanniemi, Elina Hyppönen, Karl-Heinz Herzig, Sylvain Sebert, Marjo-Riitta Järvelin, Could vitamin D reduce obesity-associated inflammation? Observational and Mendelian randomization study, The American Journal of Clinical Nutrition, Volume 111, Issue 5, May 2020, Pages 1036–1047, https://doi.org/10.1093/ajcn/nqaa056
© The Author(s) 2020. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
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https://urn.fi/URN:NBN:fi-fe2020070646938
Tiivistelmä
Abstract
Background: Obesity is associated with inflammation but the role of vitamin D in this process is not clear.
Objectives: We aimed to assess the associations between serum 25-hydroxyvitamin D [25(OH)D], BMI, and 16 inflammatory biomarkers, and to assess the role of vitamin D as a potential mediator in the association between higher BMI and inflammation.
Methods: Northern Finland Birth Cohort 1966 (NFBC1966) 31-y data on 3586 individuals were analyzed to examine the observational associations between BMI, 25(OH)D, and 16 inflammatory biomarkers. Multivariable regression analyses and 2-sample regression-based Mendelian randomization (MR) mediation analysis were performed to assess any role of vitamin D in mediating a causal effect of BMI on inflammatory biomarkers [soluble intercellular adhesion molecule 1 (sICAM-1), high sensitivity C-reactive protein (hs-CRP), and α1-acid glycoprotein (AGP)] for which observational associations were detected. For MR, genome-wide association study summary results ranging from 5163 to 806,834 individuals were used for biomarkers, 25(OH)D, and BMI. Findings were triangulated with a literature review of vitamin D supplementation trials.
Results: In NFBC1966, mean BMI (kg/m²) was 24.8 (95% CI: 24.7, 25.0) and mean 25(OH)D was 50.3 nmol/L (95% CI: 49.8, 50.7 nmol/L). Inflammatory biomarkers correlated as 4 independent clusters: interleukins, adhesion molecules, acute-phase proteins, and chemokines. BMI was positively associated with 9 inflammatory biomarkers and inversely with 25(OH)D (false discovery rate < 0.05). 25(OH)D was inversely associated with sICAM-1, hs-CRP, and AGP, which were positively associated with BMI. The MR analyses showed causal association of BMI on these 3 inflammatory biomarkers. There was no observational or MR evidence that circulating 25(OH)D concentrations mediated the association between BMI and these 3 inflammatory markers. Review of randomized controlled trials (RCTs) supported our findings showing no impact of vitamin D supplementation on inflammatory biomarkers.
Conclusions: The findings from our observational study and causal MR analyses, together with data from RCTs, do not support a beneficial role of vitamin D supplementation on obesity-related inflammation.
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