Recent advances in the genetic epidemiology and molecular genetics of substance use disorders
Open accessAbstract
This article reviews current advances in the genetics of substance use disorders (SUDs). Both genetic and environmental sources of risk are required to develop a complete picture of SUD etiology. Genetic sources of risk for SUDs are not highly substance specific in their effects. Genetic and environmental risks for SUDs typically do not only add together but also interact with each other over development. Risk gene identification for SUDs has been difficult, with one recent success in identifying nicotinic receptor variants that affect risk for nicotine dependence. The impact of genetic variants on SUD risk will individually be small. Although genetic epidemiologic methods are giving us an increasingly accurate map of broad causal pathways to SUDs, gene discovery will be needed to identify the specific biological systems. Identifying these risk genes and understanding their action will require large clinical samples, and interaction between these studies and work in model organisms.
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Twin studies show that 40-60% of the variance for substance use disorder is accounted for by shared and non-shared environment.
“Twin studies have repeatedly demonstrated the magnitude of these effects, showing that somewhere between 40 and 60% of the variance for substance use disorder (SUD) is accounted for by shared and non-shared environment (Kendler et al., 2012).”
From Assessment of culture and environment in the Adolescent Brain and Cognitive Development Study: Rationale, description of measures, and early data (2018) · cites this paper as Kendler et al., 2012
The Introduction (page not available) reports that twin-study estimates attribute 40–70% of SUD risk variability to genetic differences, with estimates for most other substances in populations of European origin largely between 40% and 55%. This implies a substantial remaining non-genetic share, but the paper does not give the claimed 40–60% range for combined shared and non-shared environmental variance across SUDs. (LLM, conf=0.86)
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- Authors
- Kendler, K. S., Chen, X., Dick, D., Maes, H., Gillespie, N., Neale, M. C., & Riley, B.
- Affiliations
- Virginia Commonwealth University (US)
- Corresponding author
- Kendler, Kenneth S
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2012-01-26
- Volume
- 15
- Issue
- 2
- Pages
- 181-189
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC3297622
- OpenAlex
- W1994285916
- Cited by
- 179
- References
- 87
- Citations by year
- 2025: 5 · 2024: 5 · 2023: 8 · 2022: 15 · 2021: 4 · 2020: 34 · 2019: 13 · 2018: 11 · 2017: 18 · 2016: 20 · 2015: 19 · 2014: 12 · 2013: 8 · 2012: 5
- FWCI
- 8.48
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (K02AA018755, AA-011408, AA 15416, R37AA011408, P20AA017828, R01AA011408, R01AA015416, AA017828, AA018755)
- National Institute of Mental Health (MH084952)
- National Institute on Drug Abuse (R01DA024413, DA030005, R21DA027070, DA027070, R01DA030005, K01DA019498, R00DA023549, K99DA023549, U01DA024413, R01DA025109, DA-019498, DA025109, DA-18673, DA022989, DA024413, R01DA018673, DA023549, R37DA018673)
- 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
- substance use disorders, genetic epidemiology, molecular genetics, risk genes, gene-environment interaction, nicotine dependence, gene discovery
- MeSH terms
- Environment, Humans, Molecular Biology, Molecular Epidemiology, Risk Assessment, Substance-Related Disorders, Genetic Predisposition to Disease
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