A population-based Swedish Twin and Sibling Study of cannabis, stimulant and sedative abuse in men.
- Authors
- Kendler, Kenneth S; Ohlsson, Henrik; Maes, Hermine H; Sundquist, Kristina; Lichtenstein, Paul; Sundquist, Jan
- Year
- 2015
- Journal
- Drug and alcohol dependence
- PMID
- 25660314
- DOI
- 10.1016/j.drugalcdep.2015.01.016
- PMCID
- PMC4431972
BACKGROUND: Prior studies, utilizing interview-based assessments, suggest that most of the genetic risk factors for drug abuse (DA) are non-specific with a minority acting specifically on risk for abuse of particular psychoactive substance classes. We seek to replicate these findings using objective national registry data. METHODS: We examined abuse of cannabis, stimulants (including cocaine) and sedatives ascertained from national Swedish registers in male-male monozygotic (1720 pairs) and dizygotic twins (1219 pairs) combined with near-age full siblings (76,457 pairs) to provide sufficient power. Modeling was performed using Mx. RESULTS: A common pathway model fitted better than an independent pathway model. The latent liability to DA was highly heritable but also influenced by shared environment. Cannabis, stimulant and sedative abuse all loaded strongly on the common factor. Estimates for the total heritability for the three forms of substance abuse ranged from 64 to 70%. Between 75 and 90% of that genetic risk was non-specific, coming from the common factor with the remainder deriving from substance specific genetic risk factors. By contrast, all of the shared environmental effects, which accounted for 18-20% of the variance in liability, were non-specific. CONCLUSIONS: In accord with prior studies based on personal interviews, the large preponderance of genetic risk factors for abuse of specific classes of psychoactive substance are non-specific. These results suggest that genetic variation in the primary sites of action of the psychoactive drugs, which differ widely across most drug classes, play a minor role in human individual differences in risk for DA.
Parameter estimates from the best-fitting common pathway model for cannabis, stimulant and sedative abuse in Swedish male–male twin and near-aged sibling pairs. (A, C and E) refer, respectively, to additive genetic, shared environmental, and unique environmental risk factors. The subscript “c” refers to risk factors on the common latent factor, here labeled “vulnerability to drug abuse.” The subscript “s” refers to risk factors specific to the abuse of individual substance classes. The paths from the common latent factor to the individual forms of drug abuse reflect the degree to which those forms of drug abuse index the liability to the latent factor.
LLM interpretation
This figure is a path diagram representing a common pathway model for cannabis, stimulant, and sedative abuse. It illustrates the influence of additive genetic ($A_c$), shared environmental ($C_c$), and unique environmental ($E_c$) risk factors on a latent "Vulnerability to Drug Abuse" factor, which in turn predicts the three specific types of abuse with path coefficients ranging from 0.89 to 0.94. Additionally, the model shows substance-specific risk factors ($A_s, C_s, E_s$) contributing directly to each form of abuse, with the highest specific genetic influence seen in cannabis abuse (0.41).
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|---|---|---|
| Genome-wide Association Study of Cannabis Dependence Severity, Novel Risk Variants, and Shared Genetic Risks. | 2016 | 27028160 |
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| Generalized genetic liability to substance use disorders. | Miller AP et al. | — | 2024 | → |
| The impact of schizophrenia genetic load and heavy cannabis use on the risk of psychotic disorder in the EU-GEI case-control and UK Biobank studies. | Austin-Zimmerman I et al. | — | 2024 | → |
| The Interrelationship of the Genetic Risks for Different Forms of Substance Use Disorder in a Swedish National Sample: A Top-Down Genetic Analysis. | Kendler KS et al. | — | 2023 | → |
| The moderation of the genetic risk for alcohol and drug use disorders in a Swedish national sample by the genetic aptitude for educational attainment. | Kendler KS et al. | — | 2023 | → |
| Understanding cannabis use in Singapore: profile of users and drug progression. | Chia DXY et al. | — | 2023 | → |
| Molecular genetics of cocaine use disorders in humans. | Fernàndez-Castillo N et al. | — | 2022 | → |
| Genomic and Personalized Medicine Approaches for Substance Use Disorders (SUDs) Looking at Genome-Wide Association Studies. | Cozzoli D et al. | — | 2021 | → |
| Genome-wide association study implicates CHRNA2 in cannabis use disorder. | Demontis D et al. | — | 2019 | → |
| Environmental, genetic and epigenetic contributions to cocaine addiction. | Pierce RC et al. | — | 2018 | → |
| Prediction of drug abuse recurrence: a Swedish National Study. | Kendler KS et al. | — | 2018 | → |
| Psychotic patients who used cannabis frequently before illness onset have higher genetic predisposition to schizophrenia than those who did not. | Aas M et al. | — | 2018 | → |
| A sibling based design to quantify genetic and shared environmental effects of venous thromboembolism in Sweden. | Zöller B et al. | — | 2017 | → |
| Genome-wide association study implicates<i>CHRNA2</i>in cannabis use disorder | Demontis D et al. | — | 2017 | — |
| Heritability of lifetime ecstasy use. | Verweij KJH et al. | — | 2017 | → |
| Annual Research Review: On the developmental neuropsychology of substance use disorders. | Conrod PJ et al. | — | 2016 | → |
| Genome-wide Association Study of Cannabis Dependence Severity, Novel Risk Variants, and Shared Genetic Risks. | Sherva R et al. | — | 2016 | → |
| Commentary on Kosty et al. (2015): Cannabis abuse from one generation to the next-a heightened vulnerability in women? | Melchior M | — | 2015 | → |