We examined the hypothesis that pregnancy and delivery complications result in increased risk for the development of psychiatric disorders. The study sample included 1068 pregnancies classified as chronic fetal hypoxia, other complications, preterm birth, or normal pregnancy/delivery that had initially been studied prospectively from the prenatal period through age 7 years. Subjects were recontacted (ages 18 to 27 years) and lifetime psychiatric diagnoses made with the Diagnostic Interview Schedule. Preterm subjects had significantly higher rates of cognitive impairment. Subjects with chronic fetal hypoxia had higher rates of both cognitive impairment and psychotic disorders, although these differences failed to reach statistical significance due to the small number of cases. With these exceptions, the data did not support the hypothesis that rates of psychiatric disorders are higher among subjects born with complications of pregnancy and delivery than among normal controls born without complications.
"" The first major study (the " Providence 1000 " ) selected from the CPP 500 infants born with moderate perinatal complications, and 500 matched comparison subjects. Using standardized psychiatric assessments, the CPP team interviewed these children as adults at a mean age of 23 years [Buka et al., 1993]. The generally null results indicated no elevated risk for psychiatric disorder in relation to perinatal complications, with two exceptions. "
"The CPP used a single study design across all 12 sites. The sites participated in a systematic data collection from pregnancy to the fi rst 7 years to identify perinatal and early childhood factors that adversely affect subsequent child development (Buka et al., 1993). "
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to evaluate the association between maternal smoking during pregnancy (MSP) and lifetime risk for alcohol use disorder (AUD) and to explore possible mechanisms through which MSP may be related to neurobehavioral conditions during infancy and childhood, which could, in turn, lead to increased risk for AUD.
A sample of 1,625 individuals was followed from pregnancy for more than 40 years. Capitalizing on the long follow-up time, we used survival analysis to examine lifetime risks of AUD (diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition) in relation to levels of MSP (none, <20 cigarettes/day, and ≥20 cigarettes/day). We then used structural equation modeling to test hypotheses regarding potential mechanisms, including lower birth weight, neurological abnormalities, poorer academic functioning, and behavioral dysregulation.
Relative to unexposed offspring, offspring of mothers who smoked 20 cigarettes per day or more exhibited greater risks for AUD (hazard ratio = 1.31, 95% CI [1.08, 1.59]). However, no differences were observed among offspring exposed to fewer than 20 cigarettes per day. In structural equation models, MSP was associated with neurobehavioral problems during infancy and childhood, which, in turn, were associated with an increased risk for adult AUD.
MSP was associated with an increased lifetime risk for AUD. Adverse consequences were evident from birth to adulthood. A two-pronged remedial intervention targeted at both the mother (to reduce smoking during pregnancy) and child (to improve academic functioning) may reduce the risk for subsequent AUD.
Journal of studies on alcohol and drugs 03/2011; 72(2):199-209. DOI:10.15288/jsad.2011.72.199 · 2.76 Impact Factor
"The mechanism(s) by which low birth weight or preeclampsia increase risk for schizophrenia is not yet known. However, a current theory regarding preeclampsia hypothesizes that this condition gives rise to abnormal fetal blood flow that results in chronic fetal hypoxia or malnutrition  and both of these conditions are associated with schizophrenia [15, 16, 28–31, 102, 103]. Furthermore, preeclampsia involves a generalized inflammatory response in the mother as a result of the oxidatively stressed or hypoxic placenta , and inflammatory processes are hypothesized to damage the microvasular system of the brain   and increase risk of schizophrenia . "
[Show abstract][Hide abstract] ABSTRACT: Prenatal/obstetric complications are implicated in schizophrenia susceptibility. Some complications may arise from maternal-fetal genotype incompatibility, a term used to describe maternal-fetal genotype combinations that produce an adverse prenatal environment. A review of maternal-fetal genotype incompatibility studies suggests that schizophrenia susceptibility is increased by maternal-fetal genotype combinations at the RHD and HLA-B loci. Maternal-fetal genotype combinations at these loci are hypothesized to have an effect on the maternal immune system during pregnancy which can affect fetal neurodevelopment and increase schizophrenia susceptibility. This article reviews maternal-fetal genotype incompatibility studies and schizophrenia and discusses the hypothesized biological role of these ''incompatibility genes". It concludes that research is needed to further elucidate the role of RHD and HLA-B maternal-fetal genotype incompatibility in schizophrenia and to identify other genes that produce an adverse prenatal environment through a maternal-fetal genotype incompatibility mechanism. Efforts to develop more sophisticated study designs and data analysis techniques for modeling maternal-fetal genotype incompatibility effects are warranted.
BioMed Research International 04/2010; 2010(1110-7243):576318. DOI:10.1155/2010/576318 · 2.71 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.