Prenatal fever and autism risk.
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ABSTRACT:
SUBMITTER: Hornig M
PROVIDER: S-EPMC5822459 | biostudies-literature | 2018 Mar
REPOSITORIES: biostudies-literature
Publications
Prenatal fever and autism risk.
Hornig M M Bresnahan M A MA Che X X Schultz A F AF Ukaigwe J E JE Eddy M L ML Hirtz D D Gunnes N N Lie K K KK Magnus P P Mjaaland S S Reichborn-Kjennerud T T Schjølberg S S Øyen A-S AS Levin B B Susser E S ES Stoltenberg C C Lipkin W I WI
Molecular psychiatry 20170613 3
Some studies suggest that prenatal infection increases risk of autism spectrum disorders (ASDs). This study was undertaken in a prospective cohort in Norway to examine whether we could find evidence to support an association of the prenatal occurrence of fever, a common manifestation of infection, with ASD risk. Prospective questionnaires provided maternal exposure data; case status was established from clinical assessments and registry linkages. In a large, prospectively ascertained cohort of p ...[more]
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Project description:Autism spectrum disorder (ASD) is phenotypically and etiologically heterogeneous, with evidence for genetic and environmental contributions to disease risk. Research has focused on the prenatal period as a time where environmental exposures are likely to influence risk for ASD. Epidemiological studies have shown significant associations between prenatal exposure to maternal immune activation (MIA), caused by infections and fever, and ASD. However, due to differences in study design and exposure measurements no consistent patterns have emerged revealing specific times or type of MIA exposure that are most important to ASD risk. No prior studies have examined prenatal MIA exposure and ASD risk in an under-represented minority population of African ancestry. To overcome these limitations, we estimated the association between prenatal exposure to fever and maternal infections and ASD in a prospective birth cohort of an understudied minority population in a city in the United States. No association was found between prenatal exposure to genitourinary infections or flu and the risk of ASD in a nested sample of 116 ASD cases and 988 typically developing controls in crude or adjusted analyses. Prenatal exposure to fever was associated with increased ASD risk (aOR 2.02 [1.04-3.92]) after adjustment for educational attainment, marital status, race, child sex, maternal age, birth year, gestational age, and maternal smoking. This effect may be specific to fever during the third trimester (aOR 2.70 [1.00-7.29]). Our findings provide a focus for future research efforts and ASD prevention strategies across diverse populations. Autism Res 2017, 10: 1878-1890. © 2017 International Society for Autism Research, Wiley Periodicals, Inc.Lay summaryWe looked at whether activation of the immune system during pregnancy increases the chance a child will develop ASD. We examined 116 children with ASD and 988 children without ASD that came from a predominantly low income, urban, minority population. We found that having the flu or genitourinary tract infections during pregnancy is not related to the child being diagnosed with ASD. However, we did find children were at increased risk for ASD when their mothers had a fever during pregnancy.
| S-EPMC5685874 | biostudies-literature
Project description:BackgroundMaternal use of valproate during pregnancy has been associated with an increased risk of neurodevelopmental disorders in children. Although most studies of other antiseizure medications have not shown increased risks of these disorders, there are limited and conflicting data regarding the risk of autism spectrum disorder associated with maternal topiramate use.MethodsWe identified a population-based cohort of pregnant women and their children within two health care utilization databases in the United States, with data from 2000 through 2020. Exposure to specific antiseizure medications was defined on the basis of prescription fills from gestational week 19 until delivery. Children who had been exposed to topiramate during the second half of pregnancy were compared with those unexposed to any antiseizure medication during pregnancy with respect to the risk of autism spectrum disorder. Valproate was used as a positive control, and lamotrigine was used as a negative control.ResultsThe estimated cumulative incidence of autism spectrum disorder at 8 years of age was 1.9% for the full population of children who had not been exposed to antiseizure medication (4,199,796 children). With restriction to children born to mothers with epilepsy, the incidence was 4.2% with no exposure to antiseizure medication (8815 children), 6.2% with exposure to topiramate (1030 children), 10.5% with exposure to valproate (800 children), and 4.1% with exposure to lamotrigine (4205 children). Propensity score-adjusted hazard ratios in a comparison with no exposure to antiseizure medication were 0.96 (95% confidence interval [CI], 0.56 to 1.65) for exposure to topiramate, 2.67 (95% CI, 1.69 to 4.20) for exposure to valproate, and 1.00 (95% CI, 0.69 to 1.46) for exposure to lamotrigine.ConclusionsThe incidence of autism spectrum disorder was higher among children prenatally exposed to the studied antiseizure medications than in the general population. However, after adjustment for indication and other confounders, the association was substantially attenuated for topiramate and lamotrigine, whereas an increased risk remained for valproate. (Funded by the National Institute of Mental Health.).
| S-EPMC11047762 | biostudies-literature
Project description:Causes of autism are unknown. Associations with maternal nutritional factors and their interactions with gene variants have not been reported.Northern California families were enrolled from 2003 to 2009 in the CHARGE (CHildhood Autism Risks from Genetics and Environment) population-based case-control study. Children aged 24-60 months were evaluated and confirmed to have autism (n = 288), autism spectrum disorder (n = 141), or typical development (n = 278) at the University of California-Davis Medical Investigation of Neurodevelopmental Disorders Institute using standardized clinical assessments. We calculated adjusted odds ratios (ORs) for associations between autism and retrospectively collected data on maternal vitamin intake before and during pregnancy. We explored interaction effects with functional genetic variants involved in one-carbon metabolism (MTHFR, COMT, MTRR, BHMT, FOLR2, CBS, and TCN2) as carried by the mother or child.Mothers of children with autism were less likely than those of typically developing children to report having taken prenatal vitamins during the 3 months before pregnancy or the first month of pregnancy (OR = 0.62 [95% confidence interval = 0.42-0.93]). Significant interaction effects were observed for maternal MTHFR 677 TT, CBS rs234715 GT + TT, and child COMT 472 AA genotypes, with greater risk for autism when mothers did not report taking prenatal vitamins periconceptionally (4.5 [1.4-14.6]; 2.6 [1.2-5.4]; and 7.2 [2.3-22.4], respectively). Greater risk was also observed for children whose mothers had other one-carbon metabolism pathway gene variants and reported no prenatal vitamin intake.Periconceptional use of prenatal vitamins may reduce the risk of having children with autism, especially for genetically susceptible mothers and children. Replication and mechanistic investigations are warranted.
| S-EPMC3116691 | biostudies-literature
Project description:The etiology of autism spectrum disorder (ASD) is multifactorial and complex and likely involves interactions among genetic, epigenetic and environmental factors. With respect to environmental influences, a growing literature implicates intrauterine experiences in the origin of this pervasive developmental disorder. In this prospective longitudinal design, we examine the hypothesis that fetal exposure to maternal cortisol may confer ASD risk. In addition, because ASD is four times more prevalent in males than females and because sexually dimorphic responses to intrauterine experiences are commonly observed, we examine whether or not any associations differ by fetal sex. Maternal plasma cortisol was measured at 15, 19, 25, 31, and 37 weeks' gestation in a sample of 84 pregnant women. ASD symptoms were assessed in their 5-year old children with the Social Communication Questionnaire (SCQ). Fetal exposure to lower levels of maternal cortisol was associated with higher levels of ASD symptoms among boys only. The observed hypocortisolemic profile exhibited by these mothers may indicate a risk factor that precedes the stress of caregiving for a child with ASD and may not be solely a consequence of the stress of caregiving as previously thought. Further, these findings confirm the value of examining prenatal hormone exposures as predictors of ASD risk and support the premise that altered prenatal steroid exposures may play a role in the etiology of ASD.
| S-EPMC7983844 | biostudies-literature
Project description:There is evidence that some maternal infections during the prenatal period are associated with neurodevelopmental disorders, such as childhood autism. However, the association between autism and Toxoplasma gondii (T. gondii), an intracellular parasite, remains unclear. The authors examined whether serologically confirmed maternal antibodies to T. gondii are associated with odds of childhood autism in offspring. The study is based on a nested case-control design of a large national birth cohort (N = 1.2 million) and the national psychiatric registries in Finland. There were 874 cases of childhood autism and controls matched 1:1 on date of birth, sex, birthplace and residence in Finland. Maternal sera were prospectively assayed from a national biobank for T. gondii IgM and IgG antibodies; IgG avidity analyses were also performed. High maternal T. gondii IgM antibody was associated with a significantly decreased odds of childhood autism. Low maternal T. gondii IgG antibody was associated with increased offspring odds of autism. In women with high T. gondii IgM antibodies, the IgG avidity was high for both cases and controls, with the exception of three controls. The findings suggest that the relationship between maternal T. gondii antibodies and odds of childhood autism may be related to the immune response to this pathogen or the overall activation of the immune system. Autism Res 2017, 10: 769-777. © 2016 International Society for Autism Research, Wiley Periodicals, Inc.
| S-EPMC7256017 | biostudies-literature
Project description:Purpose of reviewEnvironmental chemicals and toxins have been associated with increased risk of impaired neurodevelopment and specific conditions like autism spectrum disorder (ASD). Prenatal diet is an individually modifiable factor that may alter associations with such environmental factors. The purpose of this review is to summarize studies examining prenatal dietary factors as potential modifiers of the relationship between environmental exposures and ASD or related neurodevelopmental outcomes.Recent findingsTwelve studies were identified; five examined ASD diagnosis or ASD-related traits as the outcome (age at assessment range: 2-5 years) while the remainder addressed associations with neurodevelopmental scores (age at assessment range: 6 months to 6 years). Most studies focused on folic acid, prenatal vitamins, or omega-3 fatty acids as potentially beneficial effect modifiers. Environmental risk factors examined included air pollutants, endocrine disrupting chemicals, pesticides, and heavy metals. Most studies took place in North America. In 10/12 studies, the prenatal dietary factor under study was identified as a significant modifier, generally attenuating the association between the environmental exposure and ASD or neurodevelopment. Prenatal diet may be a promising target to mitigate adverse effects of environmental exposures on neurodevelopmental outcomes. Further research focused on joint effects is needed that encompasses a broader variety of dietary factors, guided by our understanding of mechanisms linking environmental exposures with neurodevelopment. Future studies should also aim to include diverse populations, utilize advanced methods to optimize detection of novel joint effects, incorporate consideration of timing, and consider both synergistic and antagonistic potential of diet.
| S-EPMC9098668 | biostudies-literature
Project description:BackgroundPrenatal antibiotic exposure induces changes in infants' gut microbiota composition and is suggested as a possible contributor in the development of autism spectrum disorders (ASD). In this study, we examined the association between prenatal antibiotic exposure and the risk of ASD.MethodsThis was a population-based cohort study utilizing the Manitoba Population Research Data Repository. The cohort included 214 834 children born in Manitoba, Canada between April 1, 1998 and March 31, 2016. Exposure was defined as having filled one or more antibiotic prescription during pregnancy. The outcome was autism spectrum disorder diagnosis. Multivariable Cox proportional hazards regression was used to estimate the risk of developing ASD in the overall cohort and in a sibling cohort.ResultsOf all subjects, 80 750 (37.6%) were exposed to antibiotics prenatally. During follow-up, 2965 children received an ASD diagnosis. Compared to children who were not exposed to antibiotics prenatally, those who were exposed had a higher risk of ASD: (adjusted HR 1.10 [95% CI 1.01, 1.19]). The association was observed in those exposed to antibiotics in the second or third trimester (HR 1.11 [95% CI 1.01, 1.23] and 1.17 [95% CI 1.06, 1.30], respectively). In the siblings' cohort, ASD risk estimate remained unchanged (adjusted HR 1.08 [95% CI 0.90, 1.30], although it was not statistically significant.ConclusionsPrenatal antibiotic exposure is associated with a small increase in the risk of ASD. Given the potential of residual confounding beyond what it was controlled through our study design and because of possible confounding by indication, such a small risk increase in the population is not expected to be clinically significant.
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Project description:Prenatal nutrition is associated with offspring autism spectrum disorder (herein referred to as autism), yet, it remains unknown if the association is causal. Triangulation may improve causal inference by integrating the results of conventional multivariate regression with several alternative approaches that have unrelated sources of bias. We systematically reviewed the literature on the relationship between prenatal multivitamin supplements and offspring autism, and evidence for the causal approaches applied. Six databases were searched up to 8 June 2020, by which time we had screened 1309 titles/abstracts, and retained 12 articles. Quality assessment was guided using Newcastle-Ottawa in individual studies, and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) for the body of evidence. The effect estimates from multivariate regression were meta-analysed in a random effects model and causal approaches were narratively synthesised. The meta-analysis of prenatal multivitamin supplements involved 904,947 children (8159 cases), and in the overall analysis showed no robust association with offspring autism; however, a reduced risk was observed in the subgroup of high-quality observational studies (RR 0.77, 95% CI (0.62, 0.96), I2 = 62.4%), early pregnancy (RR 0.76, 95% CI (0.58; 0.99), I2 = 79.8%) and prospective studies (RR 0.69, 95% CI (0.48, 1.00), I2 = 95.9%). The quality of evidence was very low, and triangulation was of limited utility because alternative methods were used infrequently and often not robustly applied.
| S-EPMC8398897 | biostudies-literature
Project description:ImportancePrenatal diet may be causally related to autism; however, findings are inconsistent, with a limited body of research based on small sample sizes and retrospective study designs.ObjectiveTo investigate the associations of prenatal dietary patterns with autism diagnosis and autism-associated traits in 2 large prospective cohorts, the Norwegian Mother, Father, and Child Cohort Study (MoBa), and the Avon Longitudinal Study of Parents and Children (ALSPAC).Design, setting, and participantsThis cohort study used data from MoBa and ALSPAC birth cohort studies conducted across Norway and in the Southwest of England, respectively. Participants were people with singleton pregnancies with self-reported food frequency questionnaire responses. MoBa recruited between 2002 and 2008, and ALSPAC recruited between 1990 and 1992, and children were followed-up until age 8 years or older. Recruitment rates were 41% (95 200 of 277 702 eligible pregnancies) in MoBa and 72% (14 541 of 20 248 eligible pregnancies) in ALSPAC. Data analysis occurred February 1, 2022, to August 1, 2023.ExposureA healthy prenatal dietary pattern was derived using factor analysis and modeled as low, medium, and high adherence.Main outcomes and measuresIn MoBa, the offspring outcomes were autism diagnosis and elevated social communication questionnaire score at ages 3 years and 8 years, with further analysis of the social communication difficulties and restrictive and repetitive behaviors subdomains. In ALSPAC, offspring outcomes were elevated social communication difficulties checklist score at age 8 years. Odds ratios (ORs) were estimated using generalized nonlinear models.ResultsMoBa included 84 548 pregnancies (mean [SD] age, 30.2 [4.6] years; 43 277 [51.2%] male offspring) and ALSPAC had 11 760 pregnancies (mean [SD] age, 27.9 [4.7] years; 6034 [51.3%] male offspring). In the final adjusted models, high adherence to a healthy dietary pattern, compared with low adherence, was associated with reduced odds of autism diagnosis (OR, 0.78; 95% CI, 0.66-0.92) and social communication difficulties at age 3 years in MoBa (OR 0.76, 95% CI, 0.70-0.82) and age 8 years in ALSPAC (OR, 0.74; 95% CI, 0.55-0.98). There was no consistent evidence of association with the other outcomes.Conclusions and relevanceIn this cohort study of mother-child dyads, adherence to a healthy prenatal dietary pattern was associated with a lower odds of autism diagnosis and social communication difficulties but not restrictive and repetitive behaviors.
| S-EPMC11258593 | biostudies-literature
Project description:Importance:Maternal use of folic acid supplements has been inconsistently associated with reduced risk for autism spectrum disorder (ASD) in the child. No study to date has examined this association in the context of ASD recurrence in high-risk families. Objective:To examine the association between maternal prenatal vitamin use and ASD recurrence risk in younger siblings of children with ASD. Design, Setting, and Participants:This prospective cohort study analyzed data from a sample of children (n = 332) and their mothers (n = 305) enrolled in the MARBLES (Markers of Autism Risk in Babies: Learning Early Signs) study. Participants in the MARBLES study were recruited at the MIND Institute of the University of California, Davis and were primarily from families receiving services for children with ASD in the California Department of Developmental Services. In this sample, the younger siblings at high risk for ASD were born between December 1, 2006, and June 30, 2015, and completed a final clinical assessment within 6 months of their third birthday. Prenatal vitamin use during pregnancy was reported by mothers during telephone interviews. Data analysis for this study was conducted from January 1, 2017, to December 3, 2018. Main Outcomes and Measures:Autism spectrum disorder, other nontypical development (non-TD), and typical development (TD) were algorithmically defined according to Autism Diagnostic Observation Schedule and Mullen Scales of Early Learning subscale scores. Results:After exclusions, the final sample comprised 241 younger siblings, of which 140 (58.1%) were male and 101 (41.9%) were female, with a mean (SD) age of 36.5 (1.6) months. Most mothers (231 [95.9%]) reported taking prenatal vitamins during pregnancy, but only 87 mothers (36.1%) met the recommendations to take prenatal vitamins in the 6 months before pregnancy. The prevalence of ASD was 14.1% (18) in children whose mothers took prenatal vitamins in the first month of pregnancy compared with 32.7% (37) in children whose mothers did not take prenatal vitamins during that time. Children whose mothers reported taking prenatal vitamins during the first month of pregnancy were less likely to receive an ASD diagnosis (adjusted relative risk [RR], 0.50; 95% CI, 0.30-0.81) but not a non-TD 36-month outcome (adjusted RR, 1.14; 95% CI, 0.75-1.75) compared with children whose mothers reported not taking prenatal vitamins. Children in the former maternal prenatal vitamin group also had statistically significantly lower autism symptom severity (adjusted estimated difference, -0.60; 95% CI, -0.97 to -0.23) and higher cognitive scores (adjusted estimated difference, 7.1; 95% CI, 1.2-13.1). Conclusions and Relevance:Maternal prenatal vitamin intake during the first month of pregnancy may reduce ASD recurrence in siblings of children with ASD in high-risk families. Additional research is needed to confirm these results; to investigate dose thresholds, contributing nutrients, and biologic mechanisms of prenatal vitamins; and to inform public health recommendations for ASD prevention in affected families.
| S-EPMC6450282 | biostudies-literature