Association of placental pathology and gross morphology with autism spectrum disorders.
Placentas tell us nothing about later autism, so stick with behavioral screeners and sensory tools you already trust.
01Research in Context
What this study did
Safiya et al. (2022) compared placentas from 107 children later diagnosed with autism to 526 matched controls. A pathologist looked at shape, weight, and any scars or odd blood vessels. The exam happened after birth, long before families knew about an autism diagnosis.
What they found
No placental feature showed a clear link to later autism. Size, color, and clot patterns looked the same in both groups. The authors conclude the placenta is not a useful autism warning sign.
How this fits with other research
Ben-Sasson et al. (2019) pooled dozens of studies and found sensory over-responsivity is a strong, repeatable marker for ASD. Safiya’s null result fits here: biology inside the womb (the placenta) adds no value, but clear behavioral signs after birth do.
Chenausky et al. (2017) tracked toddlers and saw that tiny speech-sound errors at 36 months predicted autism better than placenta checks. Again, behavior beats early tissue exams.
Vielmetti et al. (2026) tested a five-item parent screener (POSI) in high-risk toddlers. It caught three out of four autism cases. Their positive finding shows simple parent questions work, while Safiya shows lab-style placenta studies do not.
Why it matters
Stop hunting for placental photos or reports when you assess autism risk. Focus your energy on sensory questionnaires, parent screeners like POSI, and speech checks at 36 months. These tools give you real, actionable data instead of dead-end biology.
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02At a glance
03Original abstract
This study evaluated the association between placental pathology and gross morphology and the risk of autism spectrum disorders (ASD). We conducted a matched case-control study of children with confirmed ASD who were born between 2000 and 2017 at one of three university-affiliated hospitals in Montreal, Quebec. Cases, who were identified through the Montreal Children's Hospital Autism Spectrum Disorders Program, were matched to babies (1:5) born at the same hospital and on the same day. Multi-fetal births were excluded. Maternal demographics, pregnancy characteristics and placental pathologies were collected from hospital charts by abstractors blind to autism diagnoses. This current study consisted of data from a single-site that had pathology reports available. Pearson chi-square and Wilcoxon rank-sum tests were used to estimate p-values. Our study consisted of 107 ASD cases and 526 matched controls. Mothers of cases and controls were similar in terms of parity, gravidity, smoking status, BMI, rates of clinical chorioamnionitis, chronic hypertension, and gestational diabetes. Age at delivery of <25 years was more common among mothers of controls. Compared with controls, cases were more likely born male, <32 weeks of gestation, and weighing <1500 g. Cases and controls had similar rates of placental inflammation, vasculitis, and other placental pathologies. There were no differences in placental weight, placental thickness, umbilical cord length, and umbilical cord insertion between the two groups. In conclusion, placental pathology and gross morphology do not appear to be associated with ASD, suggesting that any perinatal determinants of autism are not likely to be mediated through placental pathology. LAY SUMMARY: Data from a matched case-control study consisting of neonates born between 2000 and 2017 at one of three McGill-affiliated hospitals were used to examine the relationship between placental pathology and morphology and the development of autism. No differences in placental pathology and gross morphology were found between those with and without autism, which suggests that placental abnormalities are unlikely to either cause or mediate the development of autism.
Autism research : official journal of the International Society for Autism Research, 2022 · doi:10.1002/aur.2658