期刊
PSYCHOLOGICAL MEDICINE
卷 37, 期 7, 页码 947-959出版社
CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0033291707009920
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资金
- NIAAA NIH HHS [MH/AA/DA-49492, K01 AA000236] Funding Source: Medline
- NIDA NIH HHS [DA-11287, DA-18673, K99 DA023549, R01 DA011287, R00 DA023549] Funding Source: Medline
- NIMH NIH HHS [K02 MH001458, R01 MH049492] Funding Source: Medline
Background. Although an obvious environmental factor influencing drug use, the sources of individual differences in drug availability (DA) are unknown. Method. This report is based on 1788 adult males from the Mid-Atlantic Twin Registry who participated in a structured telephone interview that included retrospective assessments of DA (cigarette, alcohol, marijuana, cocaine and stimulants) between ages 8 and 25. We fitted a biometric dual change score (DCS) model, adapted for ordinal data, to model latent growth and estimate the,genetic and environmental components of variance over time. Results. DA, despite being considered an environmental risk factor, is under both genetic and environmental control. For cigarette, alcohol, marijuana and cocaine availability, there was an overall increase in additive genetic variance and a decline in shared environmental variance over time. Non-shared environmental variance remained steady. Stimulant availability did not follow this pattern. Instead, there was an upswing in shared environmental effects with increasing age. Conclusion. We have modeled the genetic and environmental architecture of changes in DA across adolescence. The rise in additive genetic variance over time coincides with acceleration in the expression of individual differences, probably brought on by an increase in personal freedom and a reduction in social constraints. Understanding the etiology of DA is likely to reveal key components, acting directly or indirectly, in the pathway(s) leading to drug initiation, abuse and dependence.
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