Prenatal Vitamins and the Risk of Offspring Autism Spectrum Disorder: Systematic Review and Meta-Analysis.
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ABSTRACT:
SUBMITTER: Friel C
PROVIDER: S-EPMC8398897 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundAbnormal gestational weight gain (GWG) is a prenatal complication that may contribute to long-term behavioral and neurodevelopmental differences in offspring. This systematic review summarizes research on the association between maternal GWG and risk of autism spectrum disorder (ASD) in offspring.MethodsGoogle and electronic databases, including PubMed, SCOPUS, Embase, Cochrane Library and Google Scholar, were searched for original human studies published in English through June 2020. Articles that examined the association between GWG and risk of ASD in offspring were included. Duplicate and irrelevant studies were removed; and data were obtained through critical analysis.ResultsOf 96 articles searched, eight studies were included in the final review. All studies (n = 7) investigating the association of maternal excessive GWG with risk of ASD in offspring indicated that high GWG was independently associated with an increased risk of ASD. Of five studies investigating the association of inadequate GWG with the risk of ASD, four indicated that low GWG was not associated with an increased risk of ASD. Of seven studies examining the association of maternal pre-pregnancy BMI or weight with the risk of ASD, five reported that maternal pre-pregnancy BMI or weight did not appear to be independently associated with risk of ASD. The GWG-ASD association is independent of maternal BMI and child's intellectual disability, but offspring's genetic susceptibility connection to the GWG-ASD association remains a topic of debate.ConclusionsThe findings suggest that maternal excessive GWG may be associated with increased risk of ASD in offspring. However, insufficient GWG does not appear to have such association.
| S-EPMC7579946 | biostudies-literature
Project description:BackgroundThe effect of labor epidural anesthesia (LEA) on the risk of autism spectrum disorder (ASD) in offspring has been investigated recently, and available results are inconsistent.MethodsWe searched the PubMed and EMBASE databases for relevant studies and performed a systematic review and meta-analysis of the literature. Subgroup analyses were conducted to assess the sources of heterogeneity. Both fixed and random effects models were used was used to estimate overall relative risk.ResultsOur results showed that LEA was associated with an increased risk of ASD in offspring [HR = 1.3, 95% confidence interval (CI): 1.25-1.35; P < 0.001] after combining crude estimates from the included studies. This association was gradually reduced, but still statistically significant, when potential confounding factors were considered (HR 1.13, 95% CI 1.03-1.25, P = 0.014). However, there was no significant association when we combined data of siblings from other pregnancies (HR = 1.07, 95% CI: 0.99-1.16, P = 0.076), implying that the association was due to confounding factors.ConclusionThe statistically significant association between LEA and ASD in the offspring can be partially explained by unmeasured confounding.Systematic review registrationIdentifier CRD42022302892.
| S-EPMC9986298 | biostudies-literature
Project description:We performed a systematic literature search regarding maternal diabetes before and during pregnancy and the risk of autism spectrum disorders (ASD) in the offspring. Of the 178 potentially relevant articles, 12 articles including three cohort studies and nine case-control studies were included in the meta-analysis. Both the meta-analyses of cohort studies and case-control studies showed significant associations. The pooled relative risk and 95% confidence interval (CI) among cohort studies was 1.48 (1.25-1.75, p < 0.001). For case-control studies, the pooled odds ratio and 95% CI was 1.72 (1.24-2.41, p = 0.001). No indication of significant heterogeneity across studies or publication bias was observed. In conclusion, maternal diabetes was significantly associated with a greater risk of ASD in the offspring.
| S-EPMC4181720 | biostudies-literature
Project description:Although autism spectrum disorder (ASD) is known to be heritable, patterns of inheritance of subclinical autistic traits in nonclinical samples are poorly understood.To examine the familiality of Social Responsiveness Scale (SRS) scores of individuals with and without ASD.We performed a nested case-control study (pilot study: July 1, 2007, through June 30, 2009; full-scale study: September 15, 2008, through September 14, 2012) within a population-based longitudinal cohort. Participants were drawn from the Nurses' Health Study II, a cohort of 116,430 female nurses recruited in 1989. Case participants were index children with reported ASD; control participants were frequency matched by year of birth of case participants among those not reporting ASD. Of 3161 eligible participants, 2144 nurses (67.8%) returned SRS forms for a child and at least 1 parent and were included in these analyses.The SRS scores, as reported by nurse mothers and their spouses, were examined in association with risk of ASD using crude and adjusted logistic regression analyses. The SRS scores of the children were examined in association with SRS scores of the parents using crude and adjusted linear regression analyses stratified by case status.Autism spectrum disorder, assessed by maternal report, validated in a subgroup with the Autism Diagnostic Interview-Revised.A total of 1649 individuals were included in these analyses, including 256 ASD case participants, 1393 control participants, 1233 mothers, and 1614 fathers. Risk of ASD was increased by 85.0% among children whose parents had concordantly elevated SRS scores (odds ratio [OR],?1.85; 95% CI, 1.08-3.16) and by 52.0% when the score of either parent was elevated (OR, 1.52; 95% CI, 1.11-2.06). Elevated scores of the father significantly increased the risk of ASD in the child (OR,?1.94; 95% CI, 1.38-2.71), but no association was seen with elevated scores of the mother. Elevated parent scores significantly increased child scores in controls, corresponding to an increase in 23 points (P?<?.001).These findings support the role of additive genetic influences in concentrating inherited ASD susceptibility in successive generations and the potential role of preferential mating, and suggest that typical variation in parental social functioning can produce clinically significant differences in offspring social traits.
| S-EPMC4126195 | biostudies-literature
Project description:BackgroundDespite substantial similarities and overlaps in the pathophysiology of obsessive-compulsive disorders (OCD) and autism spectrum disorders, little is known about the clinical and etiologic cohesion of these two disorders. We therefore aimed to determine the patterns of comorbidity, longitudinal risks, and shared familial risks between these disorders.MethodsIn a prospective study design we explored the effect of a prior diagnosis of OCD in patients and parents on the susceptibility to autism spectrum disorders and vice versa. Analyses were adjusted for sex, age, calendar year, parental age and place at residence at time of birth. As measures of relative risk incidence rate ratios (IRR) and accompanying 95% confidence intervals (CIs) were employed.ResultsThe risk of a comorbid diagnosis of OCD in individuals with autism spectrum disorder and aggregation of autism spectrum disorders in offspring of parents with OCD were increased. Individuals first diagnosed with autism spectrum disorders had a 2-fold higher risk of a later diagnosis of OCD (IRR = 2.18, 95% CI = 1.91-2.48), whereas individuals diagnosed with OCD displayed a nearly 4-fold higher risk to be diagnosed with autism spectrum disorders (IRR = 3.91, 95% CI = 3.46-4.40) later in life. The observed associations were somewhat stronger for less severe types of autism spectrum disorders without a comorbid diagnosis of mental disabilities.ConclusionsThe high comorbidity, sequential risk, and shared familial risks between OCD and autism spectrum disorders are suggestive of partially shared etiological mechanisms. The results have implications for current gene-searching efforts and for clinical practice.
| S-EPMC4641696 | biostudies-literature
Project description:ObjectiveGlutamate plays an important role in brain development, neuronal migration, differentiation, survival and synaptogenesis. Recent studies have explored the relationship between blood glutamate levels and autism spectrum disorder (ASD). However, the findings are inconsistent. We undertook the first systematic review with a meta-analysis of studies examining blood glutamate levels in ASD compared with controls.MethodsA literature search was conducted using PubMed, Embase, and the Cochrane Library for studies published before March 2016. A random-effects model was used to calculate the pooled standardized mean difference (SMD) of the outcomes. Subgroup analyses were used to explore the potential sources of heterogeneity, and the publication bias was estimated using Egger's tests.ResultsTwelve studies involving 880 participants and 446 incident cases were included in this meta-analysis. The meta-analysis provided evidence for higher blood glutamate levels in ASD [SMD = 0.99, 95% confidence interval (95% CI) = 0.58-1.40; P < 0.001] with high heterogeneity (I2 = 86%, P < 0.001) across studies. The subgroup analyses revealed higher glutamate levels in ASD compared with controls in plasma [SMD = 1.04, 95% CI = 0.58-1.50; P < 0.001] but not true in serum [SMD = 0.79, 95% CI = -0.41-1.99; P = 0.20]. Studies employing high performance liquid chromatography (HPLC) or liquid chromatography-tandem mass spectrometry (LC-MS) assays also revealed higher blood glutamate levels in ASD. A sensitivity analysis found that the results were stable, and there was no evidence of publication bias.ConclusionsBlood glutamate levels might be a potential biomarker of ASD.
| S-EPMC4938426 | biostudies-literature
Project description:IntroductionChildren and adolescents with autism spectrum disorder (ASD) appear to be at greater risk of excess weight gain. The aim of this systematic review and meta-analysis was to examine whether children with ASD have a greater prevalence of obesity and whether the prevalence of ASD is higher in children with obesity.MethodsWe conducted a systematic search on PubMed, Scopus, and PsychINFO until May 21, 2021. We used the meta package in the R in order to calculate the pooled prevalence and relative risk of obesity in children with ASD.ResultsWe found 20 eligible studies investigating the prevalence of obesity in children with ASD, with the prevalence ranging from 7.9 to 31.8% and from 1.4 to 23.6% among controls. All but three studies originated from the USA. The proportion of children with obesity in ASD populations was 17% (95% confidence interval [CI]: 13-22). The relative risk of obesity in children with ASD compared with control children was 1.58 (95% CI: 1.34-1.86). There were no controlled studies reporting on the prevalence of ASD in children with obesity.ConclusionChildren and adolescents with ASD have a higher prevalence of obesity than healthy controls. There is a need for further prevalence studies of obesity in children with ASD, especially outside the USA, since the few European studies carried out have failed to show a significant difference between obesity prevalence in children with and without ASD. There is no knowledge at all regarding the prevalence of ASD among children with obesity.
| S-EPMC9210004 | biostudies-literature
Project description:ImportanceMultiple studies have reported that people with autism spectrum disorder (ASD) are at a higher risk for self-injurious behavior and suicide. However, the magnitude of this association varies between studies.ObjectiveTo appraise the available epidemiologic studies on the risk of self-injurious behavior and suicidality among children and adults with ASD.Data sourcesPubMed, Embase, CINAHL, PsycINFO, and Web of Science were systematically searched for epidemiologic studies on the association between ASD and self-injurious behavior and suicidality. Databases were searched from year of inception to April through June 2020. No language, age, or date restrictions were applied.Study selectionThis systematic review and meta-analysis included studies with an observational design and compared self-injurious behavior (defined as nonaccidental behavior resulting in self-inflicted physical injury but without intent of suicide or sexual arousal) and/or suicidality (defined as suicidal ideation, suicide attempt, or suicide) in children (aged <20 years) or adults (aged ≥20 years) with ASD.Data extraction and synthesisInformation on study design, study population, ASD and self-harm definitions, and outcomes were extracted by independent investigators. Study quality was assessed using the Newcastle-Ottawa Scale. Overall summary odds ratios (ORs) and 95% CIs were estimated using DerSimonian-Laird random-effects models.Main outcomes and measuresThe ORs for the associations of ASD with self-injurious behavior and suicidality were calculated. Analyses were stratified by study setting and age groups as planned a priori.ResultsThe search identified 31 eligible studies, which were of moderate to high quality. Of these studies, 16 (52%) were conducted in children, 13 (42%) in adults, and 2 (6%) in both children and adults. Seventeen studies assessed the association between ASD and self-injurious behavior and reported ORs that ranged from 1.21 to 18.76, resulting in a pooled OR of 3.18 (95% CI, 2.45-4.12). Sixteen studies assessed the association between ASD and suicidality and reported ORs that ranged from 0.86 to 11.10, resulting in a pooled OR of 3.32 (95% CI, 2.60-4.24). In stratified analyses, results were consistent between clinical and nonclinical settings and between children and adults.Conclusions and relevanceThis study found that ASD was associated with a substantial increase in odds of self-injurious behavior and suicidality in children and adults. Further research is needed to examine the role of primary care screenings, increased access to preventive mental health services, and lethal means counseling in reducing self-harm in this population.
| S-EPMC8527356 | biostudies-literature
Project description:We examined associations between maternal smoking and autism spectrum disorder (ASD) in children in a statewide population-based cohort and sibling-comparison design using California birth records (n = 2,015,104) with information on maternal smoking, demographic factors, and pregnancy (2007-2010). ASD cases (n = 11,722) were identified through California Department of Developmental Services records with diagnoses based on the Diagnostic and Statistical Manual of Mental Disorders-IV-TR. We estimated odds ratios for ASD with and without intellectual disability in the full cohort using logistic regression and in a sibling comparison using conditional logistic regression. In the full cohort, the adjusted odds ratio for ASD and maternal smoking 3 months before/during pregnancy compared with nonsmoking was 1.15 (95% confidence interval (CI): 1.04, 1.26), and it was similar in cases with (odds ratio = 1.12, 95% CI: 0.84, 1.49) and without intellectual disability (odds ratio = 1.15, 95% CI: 1.04, 1.27). Heavy prenatal smoking (≥20 cigarettes/day in any trimester) was related to an odds ratio of 1.55 (95% CI: 1.21, 1.98). In the sibling comparison, the odds ratio for heavy smoking was similarly elevated but the confidence interval was wide. Our findings are consistent with an increased risk for ASD in offspring of mothers who smoked ≥20 cigarettes/day during pregnancy; associations with lighter smoking were weaker.
| S-EPMC8096427 | biostudies-literature
Project description:BackgroundExposure to ambient air pollution is widespread and may be detrimental to human brain development and a potential risk factor for Autism Spectrum Disorder (ASD). We conducted a systematic review of the human evidence on the relationship between ASD and exposure to all airborne pollutants, including particulate matter air pollutants and others (e.g. pesticides and metals).ObjectiveTo answer the question: "is developmental exposure to air pollution associated with ASD?"MethodsWe conducted a comprehensive search of the literature, identified relevant studies using inclusion/exclusion criteria pre-specified in our protocol (registered in PROSPERO, CRD # 42015017890), evaluated the potential risk of bias for each included study and identified an appropriate subset of studies to combine in a meta-analysis. We then rated the overall quality and strength of the evidence collectively across all air pollutants.ResultsOf 1,158 total references identified, 23 human studies met our inclusion criteria (17 case-control, 4 ecological, 2 cohort). Risk of bias was generally low across studies for most domains; study limitations were related to potential confounding and accuracy of exposure assessment methods. We rated the quality of the body of evidence across all air pollutants as "moderate." From our meta-analysis, we found statistically significant summary odds ratios (ORs) of 1.07 (95% CI: 1.06, 1.08) per 10-μg/m3 increase in PM10 exposure (n = 6 studies) and 2.32 (95% CI: 2.15, 2.51) per 10-μg/m3 increase in PM2.5 exposure (n = 3 studies). For pollutants not included in a meta-analysis, we collectively evaluated evidence from each study in rating the strength and quality of overall evidence considering factors such as inconsistency, imprecision, and evidence of dose-response. All included studies generally showed increased risk of ASD with increasing exposure to air pollution, although not consistently across all chemical components.ConclusionAfter considering strengths and limitations of the body of research, we concluded that there is "limited evidence of toxicity" for the association between early life exposure to air pollution as a whole and diagnosis of ASD. The strongest evidence was between prenatal exposure to particulate matter and ASD. However, the small number of studies in the meta-analysis and unexplained statistical heterogeneity across the individual study estimates means that the effect could be larger or smaller (including not significant) than these studies estimate. Our research supports the need for health protective public policy to reduce exposures to harmful airborne contaminants among pregnant women and children and suggests opportunities for optimizing future research.
| S-EPMC5031428 | biostudies-literature