Abstract
Background Biological markers of suicide risk have the potential to inform prevention and treatment efforts. It has recently been hypothesised that inflammation may influence mood and in turn suicide risk. We investigated the association between indicators of systemic inflammation and suicide in a large cohort of Taiwanese adults.
Methods White blood cell (WBC) count and levels of C-reactive protein (CRP) were
measured in 462,747 and 359,849 adults in the Taiwan MJ cohort, respectively. The associations between WBC, CRP and suicide risk were investigated using Cox
proportional hazards models adjusting for a range of potential confounding factors.
Results During a mean 15.1 and 15.8 years of follow-up, 687 and 605 suicides were identified in participants who had information on WBC and CRP respectively. There was an association of suicide with WBC count (adjusted hazard ratio [aHR] = 1.13 per 1 standard deviation increase of log-transformed WBC, 95% confidence interval [CI] 1.09, 1.77). The association was driven by the highest quintile of WBC count (aHR = 1.39, 95% CI 1.09, 1.77; reference: the lowest quintile). No association between CRP and suicide was found. Limitations Our cohort was from a privately-run health check-up programme and had a lower suicide rate than that in the general population.
Conclusions Individuals with the highest WBC counts may have increased risk of
suicide. Peripheral markers of inflammation are potential biomarkers of suicide risk; however, this seems to vary by population and the marker investigated and could be influenced by a range of confounding factors.
Methods White blood cell (WBC) count and levels of C-reactive protein (CRP) were
measured in 462,747 and 359,849 adults in the Taiwan MJ cohort, respectively. The associations between WBC, CRP and suicide risk were investigated using Cox
proportional hazards models adjusting for a range of potential confounding factors.
Results During a mean 15.1 and 15.8 years of follow-up, 687 and 605 suicides were identified in participants who had information on WBC and CRP respectively. There was an association of suicide with WBC count (adjusted hazard ratio [aHR] = 1.13 per 1 standard deviation increase of log-transformed WBC, 95% confidence interval [CI] 1.09, 1.77). The association was driven by the highest quintile of WBC count (aHR = 1.39, 95% CI 1.09, 1.77; reference: the lowest quintile). No association between CRP and suicide was found. Limitations Our cohort was from a privately-run health check-up programme and had a lower suicide rate than that in the general population.
Conclusions Individuals with the highest WBC counts may have increased risk of
suicide. Peripheral markers of inflammation are potential biomarkers of suicide risk; however, this seems to vary by population and the marker investigated and could be influenced by a range of confounding factors.
Original language | English |
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Pages (from-to) | 967-971 |
Number of pages | 5 |
Journal | Journal of Affective Disorders |
Volume | 281 |
Early online date | 29 Oct 2020 |
DOIs | |
Publication status | Published - 15 Feb 2021 |
Bibliographical note
Funding Information:None. The study was partly supported by grants awarded to S-SC from National Taiwan University (grant number NTU-CDP-105R7726, NTU-CDP-106R7726, NTU-CDP-107L7721, NTU-CDP-108L7708, NTU-CDP-109L7702) and grants awarded to CPW by Taiwan Ministry of Health and Welfare Clinical Trial Center (MOHW109-TDU-B-212-114004), Ministry of Science and Technology Clinical Trial Consortium for Stroke (MOST 109-2321-B-039-002), China Medical University Hospital (DMR-109-231), and Tseng-Lien Lin Foundation, Taichung, Taiwan. S-SC is supported by a grant from Taiwan Ministry of Science and Technology (grant number MOST 105-2628-B-002-039-MY4). BM and DG are supported by the NIHR Biomedical Research Centre at University Hospitals Bristol and Weston NHS Foundation Trust. AER was funded by the Medical Research Foundation and Medical Research Council (Grant ref: MR/R004889/1) Pathways to self-harm: Biological mechanisms and genetic contribution (PI: Dr Becky Mars). We thank Mr Min Kuang Tsai for his support on data analysis. Data used in this research were from MJ Health Resource Center (Authorization Code: MJHRFB2014001C). The MJ Health Resource Foundation is responsible for the data distribution. The views expressed in this brief report are those of the authors and not necessarily those of MJ Health Resource Center, the NIHR, UK, or the Department of Health and Social Care, UK.
Funding Information:
The study was partly supported by grants awarded to S-SC from National Taiwan University (grant number NTU-CDP-105R7726, NTU-CDP-106R7726, NTU-CDP-107L7721, NTU-CDP-108L7708, NTU-CDP-109L7702) and grants awarded to CPW by Taiwan Ministry of Health and Welfare Clinical Trial Center (MOHW109-TDU-B-212-114004), Ministry of Science and Technology Clinical Trial Consortium for Stroke (MOST 109-2321-B-039-002), China Medical University Hospital (DMR-109-231), and Tseng-Lien Lin Foundation, Taichung, Taiwan. S-SC is supported by a grant from Taiwan Ministry of Science and Technology (grant number MOST 105-2628-B-002-039-MY4). BM and DG are supported by the NIHR Biomedical Research Centre at University Hospitals Bristol and Weston NHS Foundation Trust. AER was funded by the Medical Research Foundation and Medical Research Council (Grant ref: MR/R004889/1) Pathways to self-harm: Biological mechanisms and genetic contribution (PI: Dr Becky Mars). We thank Mr Min Kuang Tsai for his support on data analysis. Data used in this research were from MJ Health Resource Center (Authorization Code: MJHRFB2014001C). The MJ Health Resource Foundation is responsible for the data distribution. The views expressed in this brief report are those of the authors and not necessarily those of MJ Health Resource Center, the NIHR, UK, or the Department of Health and Social Care, UK.
Publisher Copyright:
© 2020
Research Groups and Themes
- SASH
Keywords
- Inflammation
- suicide
- white blood cell count
- C-reactive protein
- Taiwan
- cohort
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Dr Becky Mars
- Bristol Medical School (PHS) - Associate Professor in Epidemiology
- Bristol Population Health Science Institute
- Bristol Neuroscience
Person: Academic , Member