Assessing the Independent and Joint Effects of Unmedicated Prenatal Depressive Symptoms and Alcohol Consumption in Pregnancy and Infant Neurodevelopmental Outcomes. (30th April 2016)

• Record Type: Journal Article
• Authors: Bandoli, Gretchen; Coles, Claire D.; Kable, Julie A.; Wertelecki, Wladimir; Granovska, Irina V.; Pashtepa, Alla O.; Chambers, Christina D.
• Is Part Of: Alcoholism. Volume 40:Number 6(2016)
• Page Start: 1304
• Page End: 1311
• Publication Date: 2016-04-30
• Subjects: Prenatal Alcohol Exposure -- Prenatal Depression -- Infant Neurodevelopment; Alcoholism -- Periodicals; Alcoholism -- Periodicals; Alcoolisme; Electronic journals; Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 616.861005
• DOI: 10.1111/acer.13081
• Languages: English
• ISSNs: 0145-6008

Abstract

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. Abstract : From a sample of pregnant women in Ukraine recruited based upon periconceptional alcohol use, we found prenatal alcohol exposure (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 PAE and depressive symptoms in neurodevelopmental assessments. Healthcare providers should be aware of this possible synergism in their efforts to mitigate the neurodevelopmental effects of these co‐occurring exposures.