Modeling complex genetic and environmental influences on comorbid bipolar disorder with tobacco use disorder
Open accessAbstract
BACKGROUND: Comorbidity of psychiatric and substance use disorders represents a significant complication in the clinical course of both disorders. Bipolar Disorder (BD) is a psychiatric disorder characterized by severe mood swings, ranging from mania to depression, and up to a 70% rate of comorbid Tobacco Use Disorder (TUD). We found epidemiological evidence consistent with a common underlying etiology for BD and TUD, as well as evidence of both genetic and environmental influences on BD and TUD. Therefore, we hypothesized a common underlying genetic etiology, interacting with nicotine exposure, influencing susceptibility to both BD and TUD. METHODS: Using meta-analysis, we compared TUD rates for BD patients and the general population. We identified candidate genes showing statistically significant, replicated, evidence of association with both BD and TUD. We assessed commonality among these candidate genes and hypothesized broader, multi-gene network influences on the comorbidity. Using Fisher Exact tests we tested our hypothesized genetic networks for association with the comorbidity, then compared the inferences drawn with those derived from the commonality assessment. Finally, we prioritized candidate SNPs for validation. RESULTS: We estimate risk for TUD among BD patients at 2.4 times that of the general population. We found three candidate genes associated with both BD and TUD (COMT, SLC6A3, and SLC6A4) and commonality analysis suggests that these genes interact in predisposing psychiatric and substance use disorders. We identified a 69 gene network that influences neurotransmitter signaling and shows significant over-representation of genes associated with BD and TUD, as well as genes differentially expressed with exposure to tobacco smoke. Twenty four of these genes are known drug targets. CONCLUSIONS: This work highlights novel bioinformatics resources and demonstrates the effectiveness of using an integrated bioinformatics approach to improve our understanding of complex disease etiology. We illustrate the development and testing of hypotheses for a comorbidity predisposed by both genetic and environmental influences. Consistent with our hypothesis, the selected network models multiple interacting genetic influences on comorbid BD with TUD, as well as the environmental influence of nicotine. This network nominates candidate genes for validation and drug testing, and we offer a panel of SNPs prioritized for follow-up.
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There is a significant genetic overlap between people with addictive disorders and people with bipolar disorder.
“There is a significant genetic overlap between people with addictive disorders and people with BD as demonstrated both by family studies (16) and shared polymorphisms of candidate genes involved in monoamine transport or metabolism (17, 18).”
From The detrimental effects of smoking on the course and outcome in adults with bipolar disorder—A narrative review (2023) · cites this paper as [18]
The Results (‘Overlapping candidate genes’; page not provided) identify three genes—COMT, SLC6A3 and SLC6A4—with replicated significant associations with both bipolar disorder and tobacco use disorder. This supports genetic overlap for tobacco use disorder, but the paper does not establish the same finding for addictive disorders generally or show that the same specific polymorphisms are shared. (LLM, conf=0.87)
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“There is a significant genetic overlap between people with addictive disorders and people with BD as demonstrated both by family studies (16) and shared polymorphisms of candidate genes involved in monoamine transport or metabolism (17, 18).”
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Identifying gene alterations required for the development of astrocytoma
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- Authors
- McEachin, R. C., Saccone, N. L., Saccone, S. F., Kleyman-Smith, Y. D., Kar, T., Kare, R. K., Ade, A. S., Sartor, M. A., Cavalcoli, J. D., & McInnis, M. G.
- Affiliations
- University of Michigan (US)
- Washington University in St. Louis (US)
- Eastern Michigan University (US)
- Corresponding author
- McEachin, Richard C
- Venue
- BMC Medical Genetics
- Published
- 2010-01-26
- Volume
- 11
- Issue
- 1
- Pages
- 14-14
- ISSN
- 1471-2350 (ISSN-L)
- PMC
- PMC2823619
- OpenAlex
- W2081091588
- Cited by
- 31
- References
- 96
- Citations by year
- 2024: 1 · 2023: 1 · 2021: 1 · 2020: 1 · 2017: 2 · 2016: 3 · 2015: 1 · 2014: 5 · 2013: 5 · 2012: 4
- FWCI
- 0.73
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- BMC Medical Genetics (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Deep Blue (University of Michigan) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Drug Abuse (K01DA024722, U54DA021519)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Bipolar Disorder and Treatment
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- bipolar disorder, tobacco use disorder, psychiatric comorbidity, substance use disorders, genetic comorbidity, nicotine exposure, candidate genes, catechol-O-methyltransferase, dopamine transporter, serotonin transporter, gene networks, neurotransmitter signaling, commonality analysis, single nucleotide polymorphisms, therapeutic target, etiology
- MeSH terms
- Bipolar Disorder, Catechol O-Methyltransferase, Environment, Humans, Models, Genetic, Risk Factors, Tobacco Use Disorder, Signal Transduction, Comorbidity, Neurotransmitter Agents, Computational Biology, Polymorphism, Single Nucleotide, Dopamine Plasma Membrane Transport Proteins, Serotonin Plasma Membrane Transport Proteins, Gene Regulatory Networks
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