Assessing the Independent and Joint Effects of Unmedicated Prenatal Depressive Symptoms and Alcohol Consumption in Pregnancy and Infant Neurodevelopmental Outcomes

• Type of Material: Article
• Authors: Gretchen Bandoli, University of California San Diego; Claire Coles, Emory University; Julie Kable, Emory University; Wladimir Wertelecki, University of California San Diego; Irina V. Granovska, Rivne Regional Medical Diagnostic Center; Alla O. Pashtepa, Khmelnytsky Perinatal Center; Christina D. Chambers, University of California San Diego
• Language: English
• Date: 2016-06-01
• Publisher: Wiley
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2016 Research Society on Alcoholism. This is the peer reviewed version of the following article, which has been published in final form. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.
• Final Published Version (URL): http://dx.doi.org/10.1111/acer.13081
• Title of Journal or Parent Work: Alcoholism: Clinical and Experimental Research
• ISSN: 0145-6008
• Volume: 40
• Issue: 6
• Start Page: 1304
• End Page: 1311
• Grant/Funding Information: Research described in this manuscript was supported by Contract #U01AA014835 funded by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) and the NIH Office of Dietary Supplements (ODS).; The project described was partially supported by the National Institutes of Health, Grant TL1TR001443.
• Keywords: SEROTONIN REUPTAKE INHIBITORS; Prenatal Alcohol Exposure; Substance Abuse; Prenatal Depression; DEVELOPMENTAL OUTCOMES; Life Sciences & Biomedicine; SEX-DIFFERENCES; Science & Technology; Infant Neurodevelopment; PITUITARY-ADRENAL-AXIS; IMPACT; SPECTRUM DISORDERS; CHILDREN; STRESS; EXPOSURE; MATERNAL DEPRESSION
• Research Categories: Psychology, Behavioral; Psychology, General

Abstract

Background: Prenatal alcohol exposure (PAE) is an established risk factor for neurodevelopmental deficits in the offspring. Prenatal depression has been associated with neurodevelopmental deficits in the offspring, although investigations into unmedicated prenatal depression have been inconsistent. We hypothesized that unmedicated prenatal depressive symptoms would independently and jointly with PAE predict neurodevelopmental outcomes in infant offspring. Methods: We studied 344 participants from a randomized clinical trial of multivitamin supplements in pregnant women in Ukraine. Women were recruited based upon periconceptional alcohol use and followed up to 12 months postpartum. Prenatal depressive symptoms were assessed at approximately 32 weeks of gestation using the Beck Depression Inventory score. Neurodevelopment was assessed with the Bayley Scales of Infant Development II Mental Development Index (MDI) and Psychomotor Development Index (PDI) at 6 and 12 months postpartum. Generalized linear regression models were constructed to assess the independent and joint effects of prenatal depressive symptoms and PAE in models adjusted for sociodemographic and pregnancy characteristics. Results: PAE was independently associated with deficits in neurodevelopmental outcomes at 6 and 12 months, however, level of prenatal depressive symptoms was not. We found marginal evidence of synergism of depressive symptoms and PAE, with larger deficits in those with both exposures observed for the PDI-6 months (p = 0.05) and MDI-12 months (p = 0.09). Additionally, there was a suggestion of sexual dimorphism; females had stronger deficits from joint exposures than males (depressive symptom [MDI-6 months] female: -8.28, 95% CI -13.06, -3.49; male: 0.68, 95% CI -4.58, 5.94; p for interaction 0.04). While not statistically significant for the MDI or PDI at 12 months, the trend persisted. Conclusions: Infants exposed to PAE and prenatal depression may be at an increased risk of neurodevelopmental deficits. Healthcare providers should be aware of this possible synergism in their efforts to mitigate the neurodevelopmental effects of these co-occurring exposures.