Angela
Elite member
- Messages
- 21,823
- Reaction score
- 12,327
- Points
- 113
- Ethnic group
- Italian
See:
https://www.biorxiv.org/content/biorxiv/early/2017/12/19/234674.full.pdf
I'm not at all surprised...
"Background: Heritability of suicide risk is estimated at 43%, thus genetic risk likely plays an importantrole in completion of suicide. Previous genetic research has focused primarily on suicidal behavior orideation rather than actual completed suicide. And previous genome-wide association studies ofcompletion of suicide have been very small due to the difficulty in obtaining suicide sample data, andhave been unable to identify genome-wide significant variants, likely due to power limitations. This studypresents results from the first wave of a large Utah sample of completed suicides, and represent themost statistically powerful sample of completed suicide to date.Methods: Tissue samples from 1321 decedents were collected via partnership with the Utah Office ofthe Medical Examiner and genotyped using the Illumina Infinium PsychArray platform. Bioconductorpackage RaMWAS (A.S.) was used on post-QC hard call data (271,894 common variants) to conductGWAS. Because the sample is from Utah, the authors were able to conduct a relatively directcomparison with 1000 Genomes controls also from Utah (CEU), as well as European controls (EUR). Thefirst GWAS with Utah CEU controls (n of only 99) was followed by a second GWAS with EUR controls (n= 503) with and without CEU included in the control sample.Results: Analyses identified 8 SNPs in 6 genes associated with the completion of suicide. Six SNPs metgenome-wide significance. Two of these variant hits were replicated using EUR controls not includingthe CEU sample, though the case sample was the same in both analyses. Subsequent QC steps (linkagedisequilibrium analysis and EUR GWAS replication) further substantiated significant results implicatingcytochrome P450 genes.Conclusions: This GWAS and partial replication of findings across control samples, using hard callgenotype data, represents a significant step toward understanding the genetic architecture of suicide.These are late-breaking results, and in January this group will follow up with analyses using the full 2waves (N = 4800 cases), a larger control group, and imputed data to ~11 million variants. Analyses todate implicate cytochrome P450 sites involved in metabolism of arachidonic acid and relatedinflammatory mediators. Results implicate inflammation in suicide risk, and add to a growing body ofevidence that lung function may be tied to suicide."
https://www.biorxiv.org/content/biorxiv/early/2017/12/19/234674.full.pdf
I'm not at all surprised...
"Background: Heritability of suicide risk is estimated at 43%, thus genetic risk likely plays an importantrole in completion of suicide. Previous genetic research has focused primarily on suicidal behavior orideation rather than actual completed suicide. And previous genome-wide association studies ofcompletion of suicide have been very small due to the difficulty in obtaining suicide sample data, andhave been unable to identify genome-wide significant variants, likely due to power limitations. This studypresents results from the first wave of a large Utah sample of completed suicides, and represent themost statistically powerful sample of completed suicide to date.Methods: Tissue samples from 1321 decedents were collected via partnership with the Utah Office ofthe Medical Examiner and genotyped using the Illumina Infinium PsychArray platform. Bioconductorpackage RaMWAS (A.S.) was used on post-QC hard call data (271,894 common variants) to conductGWAS. Because the sample is from Utah, the authors were able to conduct a relatively directcomparison with 1000 Genomes controls also from Utah (CEU), as well as European controls (EUR). Thefirst GWAS with Utah CEU controls (n of only 99) was followed by a second GWAS with EUR controls (n= 503) with and without CEU included in the control sample.Results: Analyses identified 8 SNPs in 6 genes associated with the completion of suicide. Six SNPs metgenome-wide significance. Two of these variant hits were replicated using EUR controls not includingthe CEU sample, though the case sample was the same in both analyses. Subsequent QC steps (linkagedisequilibrium analysis and EUR GWAS replication) further substantiated significant results implicatingcytochrome P450 genes.Conclusions: This GWAS and partial replication of findings across control samples, using hard callgenotype data, represents a significant step toward understanding the genetic architecture of suicide.These are late-breaking results, and in January this group will follow up with analyses using the full 2waves (N = 4800 cases), a larger control group, and imputed data to ~11 million variants. Analyses todate implicate cytochrome P450 sites involved in metabolism of arachidonic acid and relatedinflammatory mediators. Results implicate inflammation in suicide risk, and add to a growing body ofevidence that lung function may be tied to suicide."