Pre-eclampsia, IUGR and Autism: Their association is expected due to the same etiology for all: FAILURE TO GENERATE MATERNAL IMMUNE TOLERANCE TO THE PREGNANCY

Autism has undoubtedly a genetic component but recent accumulation of evidences shows a clear association between autism and pregnancy complications, revealing that the prenatal period is a time of very high susceptibility to noxious factors in utero ; when compromised this leads to irreversible consequences on fetal health.

Pregnancy success relies on a tight regulation between the placenta and the maternal immune system. Pre-eclampsia (PE) is a complex disease that occurs in 3–5% of all pregnancies and contributes significantly to maternal and neonatal mortality and morbidity. Although the initial events that lead to pre-eclampsia occur during the first 12 weeks of pregnancy, i.e. inadequate trophoblast invasion and poor spiral artery remodeling that affect the delivery of blood to the placenta, the symptoms don’t manifest until at least 18 weeks of gestation and often not until the third trimester, many times leading to preterm delivery.
The cause of poor placental implantation is usually due to failed maternal tolerance for the paternal genetics and the risk factors for this are many. They are autoimmune disease in the mother, immunologic incompatibility between the parents, underlying inflammatory disease in the mother such as PCOS or endometriosis to name a few and these are the most common presentations to our center. The placental hypoxia caused by the poor implantation creates placental and vascular injuries (main cause of both pre-eclampsia and intra uterine growth restriction: IUGR) and induces the secretion of a number of circulating factors such as TNF-α, IL-6, IL-1 creating a systemic inflammatory environment.
Most importantly, it is crucial to note that these immune alterations are detectable and treatment may prevent the pregnancy complications that are a result of these inflammatory changes.
These early environmental damages may predispose subjects to autistic disorders by affecting fetal brain development apparently during the second trimester of the pregnancy. There is no evidence at this time that treatment for miscarriages will also prevent autism but as they seem to have the same root cause in cases of inflammation this is an area that must be investigated carefully.
The Childhood Autism Risks from Genetics and the Environment (CHARGE), a recent study recruited young children in California (24-60 months of age) who are autistic (n=517), who are developmental delayed (n=194) or healthy controls (n=350). The CHARGE study reported that autistic children were twice as likely to have been exposed to pre-eclampsia, while developmental delay was correlated to IUGR.
These results were confirmed with another study that linked the prevalence of autism in adolescent born preterm with a weight of less than 2kg.
In a Swedish study involving n=1216 autistic and n=6080 healthy controls children, pre-eclampsia was also associated with a 50% increased risk of having an autistic child. A strong correlation between a low Apgar score (common in preterm birth occurring frequently in pre-eclamptic women) and severe cases of autism has also been reported.

Altogether, these recent studies strongly suggest that an impaired embryo implantation and the subsequent obstetrical complications lead to a systemic inflammation and can cause dramatic effects on fetal neurodevelopment indicating that root causes of autism are likely to take place in utero.

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