Sex differences and developmental stability in genetic and environmental influences on psychoactive substance consumption from early adolescence to young adulthood.
- Authors
- Baker, J H; Maes, H H; Larsson, H; Lichtenstein, P; Kendler, K S
- Year
- 2011
- Journal
- Psychological medicine
- PMID
- 21251345
- DOI
- 10.1017/S003329171000259X
- PMCID
- PMC3143251
BACKGROUND: Genetic and environmental factors are important in the etiology of substance use. However, little is known about the stability of these factors across development. We aimed to answer three crucial questions about this etiology that have never been addressed in a single study: (1) Is there a general vulnerability to substance consumption from early adolescence to young adulthood? (2) If so, do the genetic and environmental influences on this vulnerability change across development? (3) Do these developmental processes differ in males and females? METHOD: Subjects included 1480 twin pairs from the Swedish Twin Study of Child and Adolescent Development who have been followed since 1994. Prospective, self-reported regular smoking, alcohol intoxication and illicit drug use were assessed at ages 13-14, 16-17 and 19-20 years. Structural modeling was performed with the program Mx. RESULTS: An underlying common factor accounted for the association between smoking, alcohol and illicit drug consumption for the three age groups. Common genetic and shared environmental effects showed substantial continuity. In general, as participants aged, the influence of the shared environment decreased, and genetic effects became more substance specific in their effect. CONCLUSIONS: The current report answers three important questions in the etiology of substance use. The genetic and environmental risk for substance consumption is partly mediated through a common factor and is partly substance specific. Developmentally, evidence was strongest for stability of common genetic effects, with less evidence for genetic innovation. These processes seem to be the same in males and females.
Genetic components of the full model fitted to self-report measures of smoking (S), alcohol intoxication (E), and illicit drug consumption (D) at ages 13–14, 16–17 and 19–20 years. A1, A2 and A3, additive genetic effects for ages 13–14, 16–17 and 19–20 respectively; As1, Ae1 and Ad1, specific additive genetic effects for smoking, alcohol intoxication and illicit drug use respectively at age 13–14; As2, Ae2 and Ad2, specific additive genetic effects for smoking, alcohol intoxication and illicit drug use respectively at age 16–17; As3, Ae3 and Ad3, specific additive genetic effects for smoking, alcohol intoxication and illicit drug use respectively at age 19–20.
Proportion of total variance in substance consumption common factors accounted for by (a) genetic and (b) shared environmental effects at ages 13–14 (, Factor 1), 16–17 (, Factor 2) and 19–20 (■, Factor 3). The y axis represents the total phenotypic variance so the sum of all the factors equals total heritability.
| Name | Type |
|---|---|
| 10th graders USA local | cohort |
| 16- to 17-year-olds local | cohort |
| adolescents | cohort |
| age | phenotype |
| age 13–14 local | cohort |
| Age 13-14 local | cohort |
| Age 13–14 local | cohort |
| Age13-14 local | cohort |
| age 16–17 local | cohort |
| Age 16-17 local | cohort |
| Age 16–17 local | cohort |
| Age16-17 local | cohort |
| age >16.5 years local | cohort |
| age ≤16.5 years local | cohort |
| age 19–20 | cohort |
| Age 19-20 local | cohort |
| Age19-20 local | cohort |
| alcohol | phenotype |
| alcohol frequency of intoxication local | phenotype |
| alcohol frequency of use local | phenotype |
| Alcohol Initiation | phenotype |
| alcohol intoxication | phenotype |
| alcohol intoxication-specific shared environmental effects local | phenotype |
| alcohol problem use local | phenotype |
| amphetamine | drug |
| clinical study local | cohort |
| common factor | phenotype |
| Common factors local | phenotype |
| common genetic effects local | phenotype |
| common shared environmental effects local | phenotype |
| common substance consumption factor local | phenotype |
| common unique environmental effects local | phenotype |
| Common unique environmental effects local | phenotype |
| development local | cohort |
| ecstasy | drug |
| environmental factors | drug |
| environmental influences | phenotype |
| ESPAD local | cohort |
| externalizing disorders | phenotype |
| female–female dizygotic twin pairs local | cohort |
| female–female monozygotic twin pairs local | cohort |
| first genetic factor local | phenotype |
| general vulnerability local | phenotype |
| General Vulnerability local | phenotype |
| general vulnerability to substance use local | phenotype |
| Genetic factor local | variant |
| genetic factors | cohort |
| Genetic influence (age 13–14) local | phenotype |
| Genetic influence (age 16–17) local | phenotype |
| Genetic influence (age 19–20) local | phenotype |
| genetic risk | cohort |
| Han et al. 1999 local | cohort |
| heavy drinking | phenotype |
| heritability | phenotype |
| Hicks et al. 2007 local | cohort |
| illicit drug consumption local | phenotype |
| Illicit drug consumption local | phenotype |
| illicit drugs | phenotype |
| illicit drug use | phenotype |
| intoxication | phenotype |
| Karolinska Institutet local | cohort |
| Latent factor local | phenotype |
| Latent factors local | phenotype |
| male–male dizygotic twin pairs local | cohort |
| male–male monozygotic twin pairs local | cohort |
| marijuana | phenotype |
| McGue et al. 2000 local | cohort |
| Medical Birth Registry local | cohort |
| Never intoxicated local | phenotype |
| nicotine | drug |
| not a regular smoker local | phenotype |
| Often intoxicated local | phenotype |
| other drug use | phenotype |
| other substances | phenotype |
| participants | cohort |
| Poelen et al. 2008 local | cohort |
| Rhee et al. 2003 local | cohort |
| second genetic factor local | phenotype |
| sex | phenotype |
| sex effects local | phenotype |
| shared environmental influence | phenotype |
| smoke often local | phenotype |
| smoke sometimes local | phenotype |
| smoking | phenotype |
| smoking-specific genetic effects local | phenotype |
| Smoking-specific unique environmental effects local | phenotype |
| Sometimes intoxicated local | phenotype |
| specific substances local | drug |
| substance | phenotype |
| substance consumption factor local | phenotype |
| substances | phenotype |
| substance use | phenotype |
| substance use measure local | phenotype |
| Swedish birth cohort local | cohort |
| Swedish/European population local | cohort |
| Swedish Twin Study of Child and Adolescent Development | cohort |
| third genetic factor local | phenotype |
| tobacco dependence | phenotype |
| tobacco initiation | phenotype |
| tobacco problem use local | phenotype |
| tobacco use | phenotype |
| Twin cohort | cohort |
| Unique environmental effects local | phenotype |
| Viken et al. 1999 local | cohort |
| wave 2 | cohort |
| young adults | cohort |
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| Associations Between Alcohol Involvement and Drive for Thinness and Body Dissatisfaction in Adolescent Twins: A Bivariate Twin Study. | Baker JH et al. | — | 2018 | → |
| The gene-environmental architecture of the development of adolescent substance use. | Vitaro F et al. | — | 2018 | → |
| The genetic and environmental architecture of substance use development from early adolescence into young adulthood: a longitudinal twin study of comorbidity of alcohol, tobacco and illicit drug use. | Waaktaar T et al. | — | 2018 | → |
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| The genetic epidemiology of substance use disorder: A review. | Prom-Wormley EC et al. | — | 2017 | → |
| A Longitudinal Adoption Study of Substance Use Behavior in Adolescence. | Huibregtse BM et al. | — | 2016 | → |
| Sex differences in genetic and environmental contributions to alcohol consumption from early adolescence to young adulthood. | Seglem KB et al. | — | 2016 | → |
| Genetic relationship between the addiction diagnosis in adults and their childhood measure of addiction liability. | Vanyukov M et al. | — | 2015 | → |
| Maternal risk taking on the balloon analogue risk task as a prospective predictor of youth alcohol use escalation. | Banducci AN et al. | — | 2015 | → |
| Genetic and environmental influences on affiliation with deviant peers during adolescence and early adulthood. | Tarantino N et al. | — | 2014 | → |
| Gene × smoking interactions on human brain gene expression: finding common mechanisms in adolescents and adults. | Wolock SL et al. | — | 2013 | → |
| Genetic and neurophysiological correlates of the age of onset of alcohol use disorders in adolescents and young adults. | Chorlian DB et al. | — | 2013 | → |
| Shared environmental contributions to substance use. | Baker JH et al. | — | 2012 | → |
| The effects of childhood ADHD symptoms on early-onset substance use: a Swedish twin study. | Chang Z et al. | — | 2012 | → |