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Dissecting the causal association between inflammation and post-traumatic stress disorder: A bidirectional Mendelian
Chuanlong Zuo1, Zhenhuang Zhuang2, Ping Yang1
1School of Nursing, Peking University, Beijing 100191, China.
This study explored the causal link between inflammation and post-traumatic stress disorder (PTSD). While some inflammatory markers like IL-17 and RANTES showed suggestive associations with PTSD risk, overall evidence for a direct causal relationship was limited.
Area of Science:
- Investigates the complex interplay between immunology and mental health.
- Utilizes advanced genetic epidemiology techniques to explore disease etiology.
Background:
- A bidirectional association between post-traumatic stress disorder (PTSD) and inflammation is increasingly recognized.
- The causal nature of this relationship remains incompletely understood, necessitating further investigation.
Purpose of the Study:
- To evaluate the potential causal relationships between specific inflammatory cytokines and PTSD.
- Employs a two-sample bidirectional Mendelian randomization analysis to assess causality.
Main Methods:
- Utilized single nucleotide polymorphisms (SNPs) from genome-wide association studies (GWAS) for inflammatory cytokines and PTSD.
- Employed inverse variance weighting (IVW) for causal effect estimation.
- Conducted sensitivity analyses using weighted median, MR-Egger, and MR-PRESSO to ensure robustness.
Main Results:
- Suggestive associations were observed between genetically predicted interleukin-17 (IL-17) and RANTES (CCL5) levels and PTSD risk.
- Higher IL-17 levels were associated with a reduced risk of PTSD (OR=0.902), while higher RANTES levels were linked to an increased risk (OR=1.067).
- No definitive evidence of a causal association between PTSD and the selected inflammatory cytokines was found, with sensitivity analyses supporting primary findings.
Conclusions:
- Inflammation is suggestively causally linked to PTSD risk, though direct causal evidence for specific cytokines remains limited.
- Inflammatory cytokines did not demonstrate downstream effects on PTSD.
- Further research is required to elucidate the mechanisms of systemic and neuroinflammation in PTSD.
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