Genetic Risk Variants Associated With Comorbid Alcohol Dependence and Major Depression
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Importance: Alcohol dependence (AD) and major depression (MD) are leading causes of disability that often co-occur. Genetic epidemiologic data have shown that AD and MD share a common possible genetic cause. The molecular nature of this shared genetic basis is poorly understood. Objectives: To detect genetic risk variants for comorbid AD and MD and to determine whether polygenic risk alleles are shared with neuropsychiatric traits or subcortical brain volumes. Design, Setting, and Participants: This genome-wide association study analyzed criterion counts of comorbid AD and MD in African American and European American data sets collected as part of the Yale-Penn study of the genetics of drug and alcohol dependence from February 14, 1999, to January 13, 2015. After excluding participants never exposed to alcohol or with missing information for any diagnostic criterion, genome-wide association studies were performed on 2 samples (the Yale-Penn 1 and Yale-Penn 2 samples) totaling 4653 African American participants and 3169 European American participants (analyzed separately). Tests were performed to determine whether polygenic risk scores derived from potentially related traits in European American participants could be used to estimate comorbid AD and MD. Main Outcomes and Measures: Comorbid criterion counts (ranging from 0 to 14) for AD (7 criteria) and MD (9 criteria, scaled to 7) as defined by the DSM-IV. Results: Of the 7822 participants (3342 women and 4480 men; mean [SD] age, 40.1 [10.7] years), the median comorbid criterion count was 6.2 (interquartile range, 2.3-10.9). Under the linear regression model, rs139438618 at the semaphorin 3A (SEMA3A [OMIM 603961]) locus was significantly associated with AD and MD comorbidity in African American participants in the Yale-Penn 1 sample (β = 0.89; 95% CI, 0.57-1.20; P = 2.76 × 10-8). In the independent Yale-Penn 2 sample, the association was also significant (β = 0.83; 95% CI, 0.39-1.28; P = 2.06 × 10-4). Meta-analysis of the 2 samples yielded a more robust association (β = 0.87; 95% CI, 0.61-1.12; P = 2.41 × 10-11). There was no significant association identified in European American participants. Analyses of polygenic risk scores showed that individuals with a higher risk of neuroticism (β = 1.01; 95% CI, 0.50-1.52) or depressive symptoms (β = 0.87; 95% CI, 0.32-1.42) and a lower level of subjective well-being (β = -0.94; 95% CI, -1.46 to -0.42) and educational attainment (β = -1.00, 95% CI, -1.57 to -0.44) had a higher level of AD and MD comorbidity, while larger intracranial (β = 1.07; 95% CI, 0.50 to 1.64) and smaller putamen volumes (β = -1.16; 95% CI, -1.86 to -0.46) were associated with higher risks of AD and MD comorbidity. Conclusions and Relevance: SEMA3A variation is significantly and replicably associated with comorbid AD and MD in African American participants. Analyses of polygenic risk scores identified pleiotropy with neuropsychiatric traits and brain volumes. Further studies are warranted to understand the biological and genetic mechanisms of this comorbidity, which could facilitate development of medications and other treatments for comorbid AD and MD.
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This genetic correlation is strongest for aspects of negative mood, including neuroticism and major depression, as also seen in twin studies and through recent specific molecular evidence for pleiotropy.
“This correlation is strongest for aspects of negative mood, including neuroticism and major depression, as also seen in twin studies35,36 and through recent specific molecular evidence for pleiotropy37,38.”
From Transancestral GWAS of alcohol dependence reveals common genetic underpinnings with psychiatric disorders (2018) · cites this paper as [38]
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- Authors
- Zhou, H., Polimanti, R., Yang, B.-Z., Wang, Q., Han, S., Sherva, R., Nuñez, Y. Z., Zhao, H., Farrer, L. A., Kranzler, H. R., & Gelernter, J.
- Affiliations
- Yale University (US)
- University of Iowa (US)
- Boston University (US)
- Philadelphia VA Medical Center (US)
- Corresponding author
- Gelernter, Joel
- ORCID
- Venue
- JAMA Psychiatry
- Publisher
- American Medical Association (AMA)
- Published
- 2017-12-01
- Volume
- 74
- Issue
- 12
- Pages
- 1234
- ISSN
- 2168-622X (ISSN-L)
- PMC
- PMC6331050
- OpenAlex
- W2766019160
- Cited by
- 94
- References
- 74
- Citations by year
- 2026: 2 · 2025: 13 · 2024: 9 · 2023: 15 · 2022: 8 · 2021: 12 · 2020: 10 · 2019: 14 · 2018: 10 · 2017: 1
- FWCI
- 6.35
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JAMA Psychiatry (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute on Drug Abuse (R01DA018432)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- alcoholism, major depressive disorder, comorbidities, genetic risk variants, semaphorin 3A, polygenic risk score, neuropsychiatric traits, subcortical volume, African Americans, European Americans, depression genetics, genetic overlap
- MeSH terms
- Adult, Alcoholism, Black or African American, Major Depressive Disorder, Depressive Disorder, Major, Female, Humans, Male, Middle Aged, Organ Size, Putamen, United States, Genetic Variation, Comorbidity, Genetic Predisposition to Disease, Multifactorial Inheritance, Diagnostic and Statistical Manual of Mental Disorders, Semaphorin-3A, White People
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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