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- Publisher Website: 10.1017/S0033291718001812
- Scopus: eid_2-s2.0-85052636943
- PMID: 30569882
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Article: Exploring shared genetic bases and causal relationships of schizophrenia and bipolar disorder with 28 cardiovascular and metabolic traits
Title | Exploring shared genetic bases and causal relationships of schizophrenia and bipolar disorder with 28 cardiovascular and metabolic traits |
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Authors | |
Keywords | Bipolar disorder cardiometabolic cardiovascular disease GWAS polygenic score |
Issue Date | 2019 |
Publisher | Cambridge University Press. The Journal's web site is located at http://journals.cambridge.org/action/displayJournal?jid=PSM |
Citation | Psychological Medicine, 2019, v. 49 n. 8, p. 1286-1298 How to Cite? |
Abstract | Background. Cardiovascular diseases represent a major health issue in patients with schizophrenia (SCZ) and bipolar disorder (BD), but the exact nature of cardiometabolic (CM) abnormalities involved and the underlying mechanisms remain unclear. Psychiatric medications are known risk factors, but it is unclear whether there is a connection between the disorders (SCZ/BD) themselves and CM abnormalities.
Methods. Using polygenic risk scores and linkage disequilibrium score regression, we investigated the shared genetic bases of SCZ and BD with 28 CM traits. We performed Mendelian randomization (MR) to elucidate causal relationships between the two groups of disorders. The analysis was based on large-scale meta-analyses of genome-wide association studies. We also identified the potential shared genetic variants and inferred the pathways involved.
Results. We found tentative polygenic associations of SCZ with glucose metabolism abnormalities, adverse adipokine profiles, increased waist-to-hip ratio and visceral adiposity (false discovery rate or FDR<0.05). However, there was an inverse association with body mass index. For BD, we observed several polygenic associations with favorable CM profiles at FDR<0.05. MR analysis showed that SCZ may be causally linked to raised triglyceride and that lower fasting glucose may be linked to BD. We also identified numerous single nucleotide polymorphisms and pathways shared between SCZ/BD with CM traits, some of which are related to inflammation or the immune system.
Conclusions. Our findings suggest that SCZ patients may be genetically predisposed to several CM abnormalities independent of medication side effects. On the other hand, CM abnormalities in BD may be more likely to be secondary. However, the findings require further validation. |
Persistent Identifier | http://hdl.handle.net/10722/274011 |
ISSN | 2023 Impact Factor: 5.9 2023 SCImago Journal Rankings: 2.768 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | So, HC | - |
dc.contributor.author | Chau, KL | - |
dc.contributor.author | Ao, FK | - |
dc.contributor.author | Mo, CH | - |
dc.contributor.author | Sham, PC | - |
dc.date.accessioned | 2019-08-18T14:53:15Z | - |
dc.date.available | 2019-08-18T14:53:15Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Psychological Medicine, 2019, v. 49 n. 8, p. 1286-1298 | - |
dc.identifier.issn | 0033-2917 | - |
dc.identifier.uri | http://hdl.handle.net/10722/274011 | - |
dc.description.abstract | Background. Cardiovascular diseases represent a major health issue in patients with schizophrenia (SCZ) and bipolar disorder (BD), but the exact nature of cardiometabolic (CM) abnormalities involved and the underlying mechanisms remain unclear. Psychiatric medications are known risk factors, but it is unclear whether there is a connection between the disorders (SCZ/BD) themselves and CM abnormalities. Methods. Using polygenic risk scores and linkage disequilibrium score regression, we investigated the shared genetic bases of SCZ and BD with 28 CM traits. We performed Mendelian randomization (MR) to elucidate causal relationships between the two groups of disorders. The analysis was based on large-scale meta-analyses of genome-wide association studies. We also identified the potential shared genetic variants and inferred the pathways involved. Results. We found tentative polygenic associations of SCZ with glucose metabolism abnormalities, adverse adipokine profiles, increased waist-to-hip ratio and visceral adiposity (false discovery rate or FDR<0.05). However, there was an inverse association with body mass index. For BD, we observed several polygenic associations with favorable CM profiles at FDR<0.05. MR analysis showed that SCZ may be causally linked to raised triglyceride and that lower fasting glucose may be linked to BD. We also identified numerous single nucleotide polymorphisms and pathways shared between SCZ/BD with CM traits, some of which are related to inflammation or the immune system. Conclusions. Our findings suggest that SCZ patients may be genetically predisposed to several CM abnormalities independent of medication side effects. On the other hand, CM abnormalities in BD may be more likely to be secondary. However, the findings require further validation. | - |
dc.language | eng | - |
dc.publisher | Cambridge University Press. The Journal's web site is located at http://journals.cambridge.org/action/displayJournal?jid=PSM | - |
dc.relation.ispartof | Psychological Medicine | - |
dc.rights | Psychological Medicine. Copyright © Cambridge University Press. | - |
dc.rights | This article has been published in a revised form in Psychological Medicine http://doi.org/10.1017/S0033291718001812. This version is free to view and download for private research and study only. Not for re-distribution, re-sale or use in derivative works. © copyright holder. | - |
dc.subject | Bipolar disorder | - |
dc.subject | cardiometabolic | - |
dc.subject | cardiovascular disease | - |
dc.subject | GWAS | - |
dc.subject | polygenic score | - |
dc.title | Exploring shared genetic bases and causal relationships of schizophrenia and bipolar disorder with 28 cardiovascular and metabolic traits | - |
dc.type | Article | - |
dc.identifier.email | Sham, PC: pcsham@hku.hk | - |
dc.identifier.authority | Sham, PC=rp00459 | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1017/S0033291718001812 | - |
dc.identifier.pmid | 30569882 | - |
dc.identifier.scopus | eid_2-s2.0-85052636943 | - |
dc.identifier.hkuros | 300975 | - |
dc.identifier.volume | 49 | - |
dc.identifier.issue | 8 | - |
dc.identifier.spage | 1286 | - |
dc.identifier.epage | 1298 | - |
dc.identifier.isi | WOS:000475956200006 | - |
dc.publisher.place | United Kingdom | - |
dc.identifier.issnl | 0033-2917 | - |