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A developmental model for alcohol use disorders in Swedish men

Published online by Cambridge University Press:  22 July 2016

K. S. Kendler ,
H. Ohlsson ,
A. C. Edwards ,
J. Sundquist  and
K. Sundquist
K. S. Kendler*
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA, USA
H. Ohlsson
Affiliation:
Center for Primary Health Care Research, Lund University, Malmö, Sweden
A. C. Edwards
Affiliation:
Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA
J. Sundquist
Affiliation:
Center for Primary Health Care Research, Lund University, Malmö, Sweden
K. Sundquist
Affiliation:
Center for Primary Health Care Research, Lund University, Malmö, Sweden
*
*Address for correspondence: K. S. Kendler, M.D., Virginia Institute for Psychiatric and Behavioral Genetics of VCU, Box 980126, Richmond, VA 23298-0126, USA. (Email: Kenneth.Kendler@vcuhealth.org)
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Abstract

Background

Alcohol use disorder (AUD) is a classic multifactorial syndrome and it is critical to understand the diversity of the relevant risk factors and how they inter-relate over development.

Method

We examined 21 risk factors for AUD in four developmental tiers reflecting (i) birth, (ii) childhood and early adolescence, (iii) late adolescence, and (iv) early adulthood in 47 414 Swedish men of whom 3907 (8.2%) were registered for AUD at or after age 25 with a mean length of follow-up of 33.9 (6.6) years. Structural equational model fitting was performed using Mplus.

Results

The best-fitting model provided a good fit to the data and explained 23.4% of the variance in AUD. The five strongest predictors were: externalizing behaviors, criminal behavior, father's alcohol consumption, genetic risk, and low educational attainment. Two developmentally early familial/genetic risk factors had substantial direct paths to AUD: father's alcohol consumption and genetic liability. Other broad developmental pathways to risk for AUD were evident: externalizing, psychosocial and internalizing. Overall, the externalizing pathway to AUD was the strongest. However, these pathways were substantially interwoven over time such that risk factors from one domain were commonly predicted by and/or predicted risk factors from the other broad domains of risk.

Conclusion

AUD in men is an etiologically complex syndrome influenced by familial-genetic, psychosocial, internalizing, and especially externalizing risk factors that act and interact over development and have complicated mediational pathways.

Keywords

Alcohol use disorderdevelopmentenvironmentpersonalitypath models
Type
Original Articles
Information
Psychological Medicine , Volume 46 , Issue 13 , October 2016 , pp. 2759 - 2770
Copyright
Copyright © Cambridge University Press 2016 

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