A Nationwide Study on the Risk of Autism After Prenatal Stress Exposure to Maternal Bereavement
Danish Epidemiology Science Centre, Department of Epidemiology, Institute of Public Health, University of Aarhus, Aarhus, Denmark. PEDIATRICS
(Impact Factor: 5.47).
05/2009; 123(4):1102-7. DOI: 10.1542/peds.2008-1734
Prenatal stress has been linked to several adverse neurobehavioral outcomes, which may share a common pathophysiology with autism. We aimed to examine whether prenatal stress exposure after maternal bereavement is associated with an increased risk of autism later in life.
We conducted a nationwide population-based cohort study of all 1492709 singletons in Denmark born from 1978 to 2003. A total of 37275 children were born to women who lost a close relative during pregnancy or up to 1 year before pregnancy. These children were included in the exposed group, and the remaining children were in the unexposed group. All children were followed up from birth until their death, migration, onset of autism, or the end of 2006. Information on autism was obtained from the Danish Psychiatric Central Register. We used Cox regression models to estimate hazard ratios in the exposed group compared with those in the unexposed group.
Maternal bereavement during the prenatal period was not associated with an increased risk of autism in the offspring. The hazard ratios did not differ by the nature of the exposure (maternal relationship to the deceased or cause of death). The hazard ratios were comparable between the 5 prenatal exposure periods under study (7-12 months before pregnancy, 0-6 months before pregnancy, first trimester, second trimester, and third trimester).
This is the first population-based cohort study to examine the effect of prenatal stress on autism in childhood. Our data do not support any strong association between prenatal stress after maternal bereavement and the risk of autism.
Available from: David P Laplante
- "As hypothesized, and consistent with some prior literature evidencing that autism spectrum traits (Ronald et al., 2011) and autismprevalence rates (Kinney et al., 2008a) increased with exposure to increasingly severe stress exposure, the current study found both objective hardship and subjective distress were associated with more severe autism-like traits, although most children scored in the subclinical range. Findings are not, however, consistent with two recent population studies (Li et al., 2009; Rai et al., 2012). This discrepancy may be attributable to differences in nature of stress exposure (e.g., sudden-onset of uniform natural disaster versus variable stressors with more diffuse onset). "
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ABSTRACT: Research implicates prenatal maternal stress (PNMS) as a risk factor for neurodevelopmental disorders; however few studies report PNMS effects on autism risk in offspring. We examined, prospectively, the degree to which objective and subjective elements of PNMS explained variance in autism-like traits among offspring, and tested moderating effects of sex and PNMS timing in utero. Subjects were 89 (46F/43M) children who were in utero during the 1998 Quebec Ice Storm. Soon after the storm, mothers completed questionnaires on objective exposure and subjective distress, and completed the Autism Spectrum Screening Questionnaire (ASSQ) for their children at age 6½. ASSQ scores were higher among boys than girls. Greater objective and subjective PNMS predicted higher ASSQ independent of potential confounds. An objective-by-subjective interaction suggested that when subjective PNMS was high, objective PNMS had little effect; whereas when subjective PNMS was low, objective PNMS strongly affected ASSQ scores. A timing-by-objective stress interaction suggested objective stress significantly affected ASSQ in first-trimester exposed children, though less so with later exposure. The final regression explained 43% of variance in ASSQ scores; the main effect of sex and the sex-by-PNMS interactions were not significant. Findings may help elucidate neurodevelopmental origins of non-clinical autism-like traits from a dimensional perspective.
Available from: Vivette Glover
- "Other studies have shown a reduction in cognitive performance   associated with prenatal stress. Some studies have found an association between prenatal stress and increased risk of autism  , with exposure in mid-to late-gestation, although a large population study has failed to confirm the increased autism . Two studies have found an increased risk of schizophrenia in adults born to mothers who experienced stress during pregnancy. "
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ABSTRACT: Care for the emotional state of pregnant women remains a neglected aspect of obstetric medicine. Many prospective studies have shown that, if a mother is depressed, anxious, or stressed while pregnant, this increases the risk for her child having a wide range of adverse outcomes, including emotional problems, symptoms of attention deficit hyperactivity disorder, or impaired cognitive development. Although genetics and postnatal care clearly affect these outcomes, evidence for an additional prenatal causal component is substantial. Prenatal anxiety or depression may contribute 10-15% of the attributable load for emotional and behavioural outcomes. The Nurse Family Partnership remains the only intervention that starts in pregnancy and has been shown to have long-term benefits for the behaviour of the child. Several other interventions, however, are likely to be helpful. Depression, anxiety, and stress during pregnancy are frequently undetected by health professionals, and untreated. Programmes to help with this should eventually improve child outcome.
Available from: Susan L Prescott
- "For example, pregnancy stress results in the section of corticotrophin-releasing hormone (CRH) from the hypothalamus, and increased plasma levels of CRH have been linked to preterm labor (Hobel et al., 1999). While some evidence suggests that such maternal risk factors can contribute to the development of ASD (Rizzo et al., 1997; Croen et al., 2002, 2007; Hultman et al., 2002; Glasson et al., 2004; Beversdorf et al., 2005; Larsson et al., 2005; Lauritsen et al., 2005; Leonard et al., 2006; Reichenberg et al., 2006; Dionne et al., 2008; Durkin et al., 2008; Grant and Soles, 2009; Grether et al., 2009; King et al., 2009; Li et al., 2009a,b; Burstyn et al., 2010; James et al., 2010; Kalkbrenner et al., 2012; Meguid et al., 2010; Roza et al., 2010; Shelton et al., 2010; Dodds et al., 2011; Lee et al., 2012; Parner et al., 2012; Rai et al., 2012; Sandin et al., 2012; Schmidt et al., 2012), results remain largely mixed and are strongest for advanced maternal age. "
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ABSTRACT: Autism Spectrum Disorder (ASD) is the collective term for neurodevelopmental disorders characterized by qualitative impairments in social interaction, communication, and a restricted range of activities and interests. Many countries, including Australia, have reported a dramatic increase in the number of diagnoses over the past three decades, with current prevalence of ASD at 1 in every 110 individuals (~1%). The potential role for an immune-mediated mechanism in ASD has been implicated by several studies, and some evidence suggests a potential link between prenatal infection-driven inflammation and subsequent development of ASD. Furthermore, a modest number of contemporary studies have reported a markedly increased prevalence of ASD in children born preterm, who are at highest risk of exposure to perinatal inflammation. However, the mechanisms that underpin the susceptibility to infection-driven inflammation during pregnancy and risk of preterm birth, and how these intersect with the subsequent development of ASD in the offspring, is not understood. This review aims to summarize and discuss the potential mechanisms and evidence for the role of prenatal infection on the central nervous system, and how it may increase the susceptibility for ASD pathogenesis in children born preterm.
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