Abstract
BackgroundWe sought to identify and characterize predictors of poor fetal growth among variables extracted from perinatal medical records to gain insight into potential etiologic mechanisms. In this process we reevaluated a previously observed association between poor fetal growth and maternal psychiatric disease.MethodsWe evaluated 449 deliveries of >36 weeks gestation that occurred between 9/2008 and 9/2010 at the Women and Infants Hospital in Providence Rhode Island. This study group was oversampled for Small-for-Gestational-Age (SGA) infants and excluded Large-for-Gestational-Age (LGA) infants. We assessed the associations between recorded clinical variables and impaired fetal growth: SGA or Intrauterine Growth Restriction (IUGR) diagnosis. After validating the previously observed association between maternal psychiatric disease and impaired fetal growth we addressed weaknesses in the prior studies by explicitly considering antidepressant use and the timing of symptoms with respect to pregnancy. We then evaluated DNA methylation levels at 27 candidate loci in placenta from a subset of these deliveries (n = 197) to examine if epigenetic variation could provide insight into the mechanisms that cause this co-morbidity.ResultsInfants of mothers with prenatal psychiatric disease (Depression, Anxiety, OCD/Panic) had increased odds of poor fetal growth (ORadjusted = 3.36, 95%CI: 1.38-8.14). This relationship was similar among those who were treated with antidepressants (ORadjusted = 3.69, 95%CI: 1.31-10.45) and among those who were not (ORadjusted = 3.19, 95%CI: 1.30-7.83). Among those with a history of psychiatric disease but no active disease in pregnancy the ORadjusted was 0.45 (95%CI: 0.09-2.35). A locus near the transcription start site of the leptin receptor (cg21655790) had methylation levels that were decreased in the presence of: 1) SGA/IUGR, and 2) active but not resolved psychiatric disease (among mothers not on antidepressants).ConclusionsThese results validate and further characterize the association between maternal psychiatric disease and poor fetal growth. Because the association appears to depend on active psychiatric disease, this suggests a transient and potentially modifiable pathophysiology. The molecular findings in this study suggest that altered leptin signaling may be involved in the biological mechanisms that link prenatal maternal psychiatric symptoms and poor fetal growth.Electronic supplementary materialThe online version of this article (doi:10.1186/s12884-015-0627-8) contains supplementary material, which is available to authorized users.
Highlights
We sought to identify and characterize predictors of poor fetal growth among variables extracted from perinatal medical records to gain insight into potential etiologic mechanisms
An additional complication is that observational studies are limited in their ability to separate associations with psychiatric disease from associations with psychiatric medication. Despite these difficulties, evaluating associations with clinical psychiatric diagnoses is important because other psychosocial variables that have been associated with poor fetal growth [9,10,11] may not be available in medical records, and have limited potential to inform obstetrical care
We present an exploratory analysis of placental DNA methylation patterns to examine biological factors that may be involved in the pathophysiology linking maternal psychiatric symptoms to poor fetal growth
Summary
We sought to identify and characterize predictors of poor fetal growth among variables extracted from perinatal medical records to gain insight into potential etiologic mechanisms In this process we reevaluated a previously observed association between poor fetal growth and maternal psychiatric disease. As a group, the existing studies of maternal psychiatric disease and poor fetal growth are difficult to interpret because of ambiguous or non-comparable fetal growth outcomes (e.g. Low-Birth-Weight [LBW] vs Small-for-Gestational-Age [SGA]) and inconsistent findings. It is largely unclear if poor fetal growth is associated with the experience of psychiatric symptoms during pregnancy or other characteristics of mothers with psychiatric diagnoses whether they are symptomatic in pregnancy or not. Despite these difficulties, evaluating associations with clinical psychiatric diagnoses is important because other psychosocial variables that have been associated with poor fetal growth [9,10,11] may not be available in medical records, and have limited potential to inform obstetrical care
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