ReviewPrenatal alcohol exposure and offspring subsequent alcohol use: A systematic review
Introduction
Alcohol use disorder is one of the leading modifiable causes of global disease burden and disability. Estimates from the Global Burden of Disease (GBD) study suggested that 2.8 million deaths and 6.0% of the total disability adjusted life years (DALYs) among men and 1.6% among women were attributable to alcohol use disorder (Griswold et al., 2018). Alcohol use disorder has been consistently linked to physical trauma and injury (Weil et al., 2018), unplanned and unwanted pregnancy (Connery et al., 2014), different types of criminal behaviours (Felson and Staff, 2010), prevalent sexual transmitted infections such as HIV, hepatitis C and others (Wilson et al., 2014, Scott-Sheldon et al., 2016), poor academic achievement (El Ansari et al., 2013, Tembo et al., 2017), several mental health problems (Kuria et al., 2012, Tembo et al., 2017) and even suicidal ideation and attempt (Darvishi et al., 2020), making it an alarming global public health concern. An early detection of the modifiable determinants of alcohol use disorder is therefore paramount to guide prevention and intervention efforts and better address this public health problem.
The precise causes of alcohol use disorder remain unclear. Epidemiological evidence from genetic sensitive examinations found an approximately three-to four-fold increased risk of alcohol use disorder in offspring of those with alcohol use disorder (Edenberg and Foroud, 2013). Similarly, a meta-analysis that synthesized the results of twelve twin and five adoption studies found that the heritability of alcohol use disorder was as high as 50%, suggesting the remaining proportion may be accounted by early-life environmental and developmental factors such as the prenatal environment (Verhulst et al., 2015). Maternal prenatal alcohol exposure is one such modifiable risk factor with an estimated prevalence of 9.8% globally, with the highest reported prevalence in Ireland, UK, Denmark, Belarus and Russia, which ranged from 60.4% to 36.5% (Popova et al., 2017).
Evidence from several longitudinal studies suggest that offspring exposed to prenatal alcohol use may have increased risk of harmful alcohol use (Duko et al., 2020), alcohol use disorder (Alati et al., 2006, O'Brien and Hill, 2014), alcohol use problems (Baer et al., 2003), persistence of alcohol drinking (Cornelius et al., 2016), alcohol use (Pfinder et al., 2014), increased levels of alcohol drinking (Goldschmidt et al., 2019) and alcohol sipping (Lees et al., 2020) in offspring compared to non-exposed. Nonetheless, additional studies presented inconsistent results (Goldschmidt et al., 2019, Zaso et al., 2021). A study of data from 608 mother-offspring pairs in the Maternal Health Practices and Child Development (MHPCD) project found that young adults exposed to prenatal alcohol use were more likely to report two or more symptoms of alcohol use disorder at 22 years of age, but not alcohol use disorder (Goldschmidt et al., 2019). Further, a study based on the Avon Longitudinal Study of Parents and Children (ALSPAC) found insufficient evidence for association between prenatal alcohol exposure and offspring alcohol initiation after adjusting for parental demographic covariates and confounders (Zaso et al., 2021).
Heterogeneity across studies in the ascertainment of prenatal alcohol exposure, offspring subsequent alcohol use and the level of control for potential confounders and covariates may underpin these conflicting results. To date, two theoretical and narrative reviews have been conducted to examine the effects of prenatal substance use on offspring subsequent substance consumption (Spear and Molina, 2005, Dodge et al., 2019). Of these reviews, the first review exclusively focuses on the in vivo studies whereas the second review gives the general overview of the effects of prenatal substance use on offspring subsequent substance use (Dodge et al., 2019). To our knowledge, however, there is no comprehensive systematic review on the subject. More specific, comprehensive and up to date systematic reviews are warranted as such reviews are based on the results of systematic literature searches, whereby minimize selection bias (Jahan et al., 2016). We, therefore, conducted this systematic review to examine the association between prenatal alcohol exposure and offspring subsequent alcohol use.
Section snippets
Study design
This systematic review followed the methodological framework suggested by the Preferred Reporting Items for Systematic review and Meta-Analysis guidelines (PRISMA) (Moher et al., 2015, Page et al., 2021). The literature search strategy, relevant study selection, data extraction and results were guided by a pre-defined study protocol, which was prospectively registered in the PROSPERO with the registration number-CRD42021279084 (https://www.crd.york.ac.uk/prospero/export_details_pdf.php).
Data sources and literature searches
Study selection
Our initial literature search retrieved a total of 3732 records. After removing duplicates, 2837 records were retained for titles and abstracts screening. A total of 2796 articles were excluded at titles and abstracts screening stage as they did not appear to be related to the topic. We conducted final review on 12 studies after excluding 29 full-text articles due to the following reasons: 25 studies did not report alcohol use as an outcome in the offspring; three studies were duplicates; and
Discussion
This systematic review was conducted to investigate the association between maternal prenatal alcohol exposure and offspring subsequent alcohol use, by appraising available literature on the topic and describing their findings. The findings of this review suggest that prenatal alcohol exposure was associated with an increased risk of offspring subsequent alcohol use. These associations were observed for different types of subsequent alcohol use by offspring. With exception of a study by Zaso et
CRediT authorship contribution statement
BD conceived the hypothesis, developed the methodology, identified all potential studies, extracted the data, assessed quality, conducted analysis, and wrote the first draft of the manuscript. AB assisted data extraction of the included studies. GP, RT, KB, JN and RA reviewed the protocol, data extraction, narrative data synthesis and contributed to subsequent drafts of the manuscript. All authors read and approved the final manuscript.
Author disclosures
None.
Role of funding
No external funding obtained for this systematic review.
Ethics approval
N/A.
Declaration of Competing Interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Acknowledgment
We are so grateful to the Curtin University for providing us a wide range of available online databases. Bereket Duko is a recipient of Curtin University International Postgraduate Research Scholarship (CIPRS) and the Raine Study PhD Top-Up Scholarship. Gavin Pereira was funded by NHMRC grants# 1099655 and 1173991, and the Research Council of Norway through Centre of Excellence grant #262700. The funders had no role in the data extraction, study design, the analysis, interpretations of the
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