Frailty in older adults is a complex geriatric syndrome with multiple underlying causes. While some inflammatory markers have been linked to this condition, the exact mechanisms remain unclear. Our study aimed to explore the relationship between cytokine polymorphisms and frailty in older adults using an ordinal logistic regression model and principal component analysis (PCA).
We included a total of 908 older adults and analyzed the genotypes of IL-1 (rs1800587), IL-6 (rs1800796), TNF-ɑ (rs361525; rs1800629), IFNG rs2069705, and TGFB1 (rs1800470). The study groups were carefully characterized to identify factors contributing to the frailty syndrome. The best model was determined based on pseudo R2 and the percentage of coincidence between the predicted and observed values.
Our findings revealed an association between polymorphisms and frailty under different inheritance models. Specifically, we observed associations with IL-1-a (additive rs1800587), TNF-ɑ (rs361525), IL-6 (codominant rs1800796), IFNG (rs2069705), TNF-ɑ (recessive rs1800629), and TGFB1 (rs1800470). Additionally, we found that comorbidity, independence in activities of daily living, and general functional status were significant factors (adjusted R2 = 0.2015).
The model generated from our study suggests that older adults with advanced age, diabetes, greater dependency in daily activities, and decreased functional status are more prone to frailty. Furthermore, our findings indicate that genetic markers play a crucial role in increasing the risk of frailty.
This research provides valuable insights into the genetic association of proinflammatory cytokines in the pathogenesis of frailty syndrome. However, it is important to note that this is an unedited version of the manuscript, and further editing will be conducted before final publication. Please be aware that there may be errors present that affect the content, and all legal disclaimers apply.
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Controversy and Comment:
The relationship between inflammation and frailty is a complex and intriguing topic. While our study provides evidence of an association between proinflammatory cytokines and frailty, the exact causal mechanisms remain a subject of debate. Some researchers argue that inflammation is a primary driver of frailty, while others suggest it is a consequence or a secondary factor. What are your thoughts on this matter? Do you believe inflammation plays a central role in the development of frailty, or is it merely a symptom of underlying conditions? We invite you to share your opinions and engage in a thoughtful discussion in the comments section below.