| Title: | In which common chronic conditions can (or cannot) obesity and lifestyle factors explain higher concentrations of C-reactive protein? |
| Journal: | Diabetes Obesity and Metabolism |
| Published: | 20 Sep 2024 |
| Pubmed: | https://pubmed.ncbi.nlm.nih.gov/39300958/ |
| DOI: | https://doi.org/10.1111/dom.15949 |
Publication 13460
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Abstract
AIM: Elevated C-reactive protein (CRP), a marker of inflammation, is common in many chronic conditions. We aimed to examine to what extent elevated CRP in chronic conditions could be explained by concurrent adiposity.</p>
MATERIALS AND METHODS: This cross-sectional study analysed UK Biobank data on 10 chronic conditions reported at baseline. Linear regression models explored the extent to which CRP concentrations were elevated in each condition, unadjusted; adjusted for sociodemographic confounders and lifestyle and body mass index (BMI) in a series of models; or adjusted for BMI and waist circumference together or for adiposity alone.</p>
RESULTS: After exclusion of participants with a potential acute infection at baseline, we tested the association in 292 772 UK Biobank participants. Linear regression showed that elevated CRP concentration was associated with all included conditions. After adjustment for sociodemographic confounders, lifestyle and BMI, chronic kidney disease, heart failure, liver disease, psoriasis, rheumatoid arthritis and chronic obstructive pulmonary disease were still associated with elevated CRP. In contrast, the association between prevalent diabetes, prior myocardial infarction (MI), hypertension and sleep apnoea and CRP could be mostly explained by adiposity alone. For example, the 42% higher CRP concentrations in diabetes compared to those without diabetes in the unadjusted model (lnCRP β: 0.35; 95% confidence interval [CI]: 0.32-0.37, p < 0.001) were completely attenuated after adjustment for BMI (lnCRP β: -0.07; 95% CI: -0.09-0.05, p < 0.001).</p>
CONCLUSIONS/INTERPRETATION: In diabetes, MI, hypertension and sleep apnoea and elevated CRP appears to be accounted for by the greater adiposity typically evident in these conditions. However, for the other conditions, systemic inflammation cannot be explained by excess adiposity alone.</p>
10 Authors
- Jana J. Anderson
- Salil V. Deo
- Paul Welsh
- Danny F. MacKay
- Frederick K. Ho
- Lyn D. Ferguson
- Carlos Celis-Morales
- Jason M. R. Gill
- Jill P. Pell
- Naveed Sattar
1 Application
| Application ID | Title |
|---|---|
| 71392 | Investigating complex relationships between genetics, exposures, biomarkers, endophenotypes and cardiometabolic, inflammatory, immune and brain-related health outcomes |
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