The risk of offspring developing substance use disorders when exposed to one versus two parent(s) with alcohol use disorder: A nationwide, register-based cohort study
Introduction
Alcohol use disorders (AUD) are a serious and widespread public health problem in Europe. The mean prevalence of AUD in the general population is 7.5%, although large variations across countries have been noted (WHO, 2014). In Denmark, approximately 17% of the adult population is believed to have AUD (Hansen et al., 2011). As a consequence, the risk of growing up in a family where one or even two parent(s) suffer from AUD is elevated.
Parental AUD tends to aggregate in families, and may be transmitted to offspring through genetic and environmental influences (McGue, 1994, Merikangas, 1990, Verhulst et al., 2015). Both twin and adoption studies show that AUD has a heritability rate of 50% and that general environmental effects exert a modest influence (Verhulst et al., 2015). Despite this apparently modest environmental effect, there is evidence to suggest that direct exposure to alcoholic environments through parents (e.g. parental modeling of drinking, alcohol-specific parenting style) may represent a major risk factor for the development of AUD in offspring (Christoffersen and Soothill, 2003, Finan et al., 2015, Handley and Chassin, 2013, Hawkins et al., 1992, Latendresse et al., 2008, Stone et al., 2012). In addition to the twin- and adoption studies, as well as studies on specific environmental risk factors, several family studies report that offspring exposed to parental AUD are at risk of developing AUD, as well as other SUD’s (Christoffersen and Soothill, 2003, Hill et al., 2011, Marmorstein et al., 2009, Merikangas et al., 1998, Nurnberger et al., 2004, Sørensen et al., 2011). Hence, one would expect that exposure to double parental AUD should result in an additive effect of influences that further increase the risk of offspring developing addictive behaviour. However, little attention has been devoted to examining the specific associations between exposure to single vs. double parental AUD and the risk of offspring developing AUD. Furthermore, the few family studies found in this area focused solely on the transmission of AUD (Lieb et al., 2002, Yoon et al., 2013), and not SUD, which comprises several addictive disorders. Addictive disorders do not necessarily manifest themselves through the same drug of choice in offspring as they do in parents (Hill et al., 2011, Kendler et al., 2003, Krueger et al., 2002, Nurnberger et al., 2004, Tsuang et al., 2001, Young et al., 2006), whereby an extended association between parental AUD and SUD in offspring is possible. Indeed, AUD-AUD studies illustrate that offspring have an additive risk of developing AUD when exposed to either single or double parental AUD (Lieb et al., 2002, Yoon et al., 2013).
In considering the available evidence, we hypothesized that the number of AUD parents (one vs. two parents) is predictive of whether offspring have an additive risk of developing SUD. Given that SUD comprises several addictive disorders, and thus constitutes a broader outcome measure than AUD, we expect offspring to have an even greater additive risk of developing SUD.
The aim of this study was to investigate whether exposure to one vs. two parent(s) with AUD is associated with an increased risk of SUD developing in offspring.
Section snippets
Data and subjects
Danish national registries offer unique opportunities for researchers to conduct population-based studies on the effects of various exposures. The authors performed a cohort study using Danish, collected, longitudinal register data from the: Psychiatric Central Research Register (covering psychiatric hospitalisations) (Mors et al., 2011), Danish National Patient Registry (covering somatic hospitalisations) (Lynge et al., 2011), Fertility database (Blenstrup and Knudsen, 2011), Cause of Death
Descriptive analyses
As shown in Table 1, 398,881 offspring were included in the study. The cohort included 204,743 males and 194,138 females born between 1983 and 1989. Offspring were followed for an average of 23.89 years (SD = 5.08 years) until 2011. A total of 15,565 (3.9%) offspring were exposed to parental AUD.
SUD was diagnosed in 5019 (1.3%) adolescents and young adults. SUD’s were diagnosed approximately twice as often in offspring exposed to parental AUD, and AUD comprised one third of SUD diagnoses in
Discussion
To the best of our knowledge, this study is the first to examine the association between exposure to parental AUD and the risk of offspring developing SUD. We found that offspring exposed to single parental AUD had a 1.44-fold increased risk of developing SUD compared to non-exposed offspring. Offspring exposed to double parental AUD had an even higher risk of developing SUD. In this case, the increased risk was 2.29-fold. We found no differences in risk relating to either parental or offspring
Conclusion
Offspring exposed to parental AUD were found to have a higher risk of developing SUD compared to non-exposed offspring. An additive risk for developing SUD was found in offspring exposed to double parental AUD. Moreover, our findings revealed no specific risks relating to either parental or offspring gender.
Declaration of conflicting interests
The authors declared no conflicts of interest with respect to the authorship and/or publication of this article. The paper has not been submitted elsewhere.
Authors’ contributions
Mellentin, AI: drafted the article, participated in the data analysis and interpretation of data, and approved the final version.
Brink, M: participated in drafting of the article and in the data analysis and interpretation of data, and approved the final version.
Andersen, L: participated in drafting of the article and in the data analysis and interpretation of data, and approved the final version.
Erlangsen, A: participated in drafting of the article, data analysis and interpretation of data and
Funding
The authors received no financial support for the research and/or authorship of this article.
Acknowledgements
We would like to acknowledge Lotte Skøt for assistance with the proof reading of this article.
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