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Autism and Probable Prerequisites: Severe and Scheduled Prenatal Stresses at Spotlight.
Iranian Journal of Public Health 2018 September
Background: Due to the importance of prenatal maternal stress as environmental factor on autism, the influence of prenatal maternal psychological agitations was assessed in relation with the risk of autism.
Methods: In this case-control study, some mothers of autistic children in Isfahan, central Iran, in 2014, were retrospectively compared with control mothers in terms of quantity, quality, and schedule of exposure to 45 stressful events in a 15-month period. In addition, dividing the stressors into two groups of genome-dependent/independent events, their prevalence was separately scrutinized and compared among patient and control families.
Results: Although the child's risk of autism increases significantly with the increase of maternal stress during months 4-7 of pregnancy, the increased stress during months 2-3 of pregnancy can lead to a significant increase in the severity of autism affliction as well as a slight but significant increase in the possibility of LFA in afflicted children ( P <0.05). The overall prevalence of genome-dependent stressful events among two patient and control groups was significantly higher than that of genome-independent events ( P =0.000), but genome-dependent events led to more stress inpatient families.
Conclusion: Although the present study consistent with recent findings in the fields of epigenetics and gene-environment interactions can confirm the role of severe and scheduled prenatal stresses in causing autism, it does not deny the necessity of a perspective and wider study in Isfahan and Iran.
Methods: In this case-control study, some mothers of autistic children in Isfahan, central Iran, in 2014, were retrospectively compared with control mothers in terms of quantity, quality, and schedule of exposure to 45 stressful events in a 15-month period. In addition, dividing the stressors into two groups of genome-dependent/independent events, their prevalence was separately scrutinized and compared among patient and control families.
Results: Although the child's risk of autism increases significantly with the increase of maternal stress during months 4-7 of pregnancy, the increased stress during months 2-3 of pregnancy can lead to a significant increase in the severity of autism affliction as well as a slight but significant increase in the possibility of LFA in afflicted children ( P <0.05). The overall prevalence of genome-dependent stressful events among two patient and control groups was significantly higher than that of genome-independent events ( P =0.000), but genome-dependent events led to more stress inpatient families.
Conclusion: Although the present study consistent with recent findings in the fields of epigenetics and gene-environment interactions can confirm the role of severe and scheduled prenatal stresses in causing autism, it does not deny the necessity of a perspective and wider study in Isfahan and Iran.
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