Intrapartum exposure to synthetic oxytocin, maternal BMI, and neurodevelopmental outcomes in children within the ECHO consortium.
ADHD
ASD
Autism
BMI
Neurodevelopment
Obesity
Synthetic oxytocin
Journal
Journal of neurodevelopmental disorders
ISSN: 1866-1955
Titre abrégé: J Neurodev Disord
Pays: England
ID NLM: 101483832
Informations de publication
Date de publication:
26 May 2024
26 May 2024
Historique:
received:
07
02
2023
accepted:
27
04
2024
medline:
26
5
2024
pubmed:
26
5
2024
entrez:
25
5
2024
Statut:
epublish
Résumé
Synthetic oxytocin (sOT) is frequently administered during parturition. Studies have raised concerns that fetal exposure to sOT may be associated with altered brain development and risk of neurodevelopmental disorders. In a large and diverse sample of children with data about intrapartum sOT exposure and subsequent diagnoses of two prevalent neurodevelopmental disorders, i.e., attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), we tested the following hypotheses: (1) Intrapartum sOT exposure is associated with increased odds of child ADHD or ASD; (2) associations differ across sex; (3) associations between intrapartum sOT exposure and ADHD or ASD are accentuated in offspring of mothers with pre-pregnancy obesity. The study sample comprised 12,503 participants from 44 cohort sites included in the Environmental Influences on Child Health Outcomes (ECHO) consortium. Mixed-effects logistic regression analyses were used to estimate the association between intrapartum sOT exposure and offspring ADHD or ASD (in separate models). Maternal obesity (pre-pregnancy BMI ≥ 30 kg/m Intrapartum sOT exposure was present in 48% of participants. sOT exposure was not associated with increased odds of ASD (adjusted odds ratio [aOR] 0.86; 95% confidence interval [CI], 0.71-1.03) or ADHD (aOR 0.89; 95% CI, 0.76-1.04). Associations did not differ by child sex. Among mothers with pre-pregnancy obesity, sOT exposure was associated with lower odds of offspring ADHD (aOR 0.72; 95% CI, 0.55-0.96). No association was found among mothers without obesity (aOR 0.97; 95% CI, 0.80-1.18). In a large, diverse sample, we found no evidence of an association between intrapartum exposure to sOT and odds of ADHD or ASD in either male or female offspring. Contrary to our hypothesis, among mothers with pre-pregnancy obesity, sOT exposure was associated with lower odds of child ADHD diagnosis.
Sections du résumé
BACKGROUND
BACKGROUND
Synthetic oxytocin (sOT) is frequently administered during parturition. Studies have raised concerns that fetal exposure to sOT may be associated with altered brain development and risk of neurodevelopmental disorders. In a large and diverse sample of children with data about intrapartum sOT exposure and subsequent diagnoses of two prevalent neurodevelopmental disorders, i.e., attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), we tested the following hypotheses: (1) Intrapartum sOT exposure is associated with increased odds of child ADHD or ASD; (2) associations differ across sex; (3) associations between intrapartum sOT exposure and ADHD or ASD are accentuated in offspring of mothers with pre-pregnancy obesity.
METHODS
METHODS
The study sample comprised 12,503 participants from 44 cohort sites included in the Environmental Influences on Child Health Outcomes (ECHO) consortium. Mixed-effects logistic regression analyses were used to estimate the association between intrapartum sOT exposure and offspring ADHD or ASD (in separate models). Maternal obesity (pre-pregnancy BMI ≥ 30 kg/m
RESULTS
RESULTS
Intrapartum sOT exposure was present in 48% of participants. sOT exposure was not associated with increased odds of ASD (adjusted odds ratio [aOR] 0.86; 95% confidence interval [CI], 0.71-1.03) or ADHD (aOR 0.89; 95% CI, 0.76-1.04). Associations did not differ by child sex. Among mothers with pre-pregnancy obesity, sOT exposure was associated with lower odds of offspring ADHD (aOR 0.72; 95% CI, 0.55-0.96). No association was found among mothers without obesity (aOR 0.97; 95% CI, 0.80-1.18).
CONCLUSIONS
CONCLUSIONS
In a large, diverse sample, we found no evidence of an association between intrapartum exposure to sOT and odds of ADHD or ASD in either male or female offspring. Contrary to our hypothesis, among mothers with pre-pregnancy obesity, sOT exposure was associated with lower odds of child ADHD diagnosis.
Identifiants
pubmed: 38796448
doi: 10.1186/s11689-024-09540-1
pii: 10.1186/s11689-024-09540-1
doi:
Substances chimiques
Oxytocin
50-56-6
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
26Subventions
Organisme : NIH Office of the Director
ID : U2COD023375
Organisme : NIH Office of the Director
ID : U24OD023382
Organisme : NIH Office of the Director
ID : U24OD023319
Organisme : NIH Office of the Director
ID : UH3OD023248
Organisme : NIH Office of the Director
ID : UH3OD023318
Organisme : NIH Office of the Director
ID : UH3OD023348
Organisme : NIH Office of the Director
ID : UH3OD023320
Organisme : NIH Office of the Director
ID : UH3OD023253
Organisme : NIH Office of the Director
ID : UH3OD023313
Organisme : NIH Office of the Director
ID : UH3OD023279
Organisme : NIH Office of the Director
ID : UH3OD023289
Organisme : NIH Office of the Director
ID : UH3OD023282
Organisme : NIH Office of the Director
ID : UH3OD023365
Organisme : NIH Office of the Director
ID : UH3OD023244
Organisme : NIH Office of the Director
ID : UH3OD023275
Organisme : NIH Office of the Director
ID : UH3OD023271
Organisme : NIH Office of the Director
ID : UH3OD023347
Organisme : NIH Office of the Director
ID : UH3OD023389
Organisme : NIH Office of the Director
ID : UH3OD023268
Organisme : NIH Office of the Director
ID : UH3OD023342
Organisme : NIH Office of the Director
ID : UH3OD023349
Organisme : NIH Office of the Director
ID : UH3OD023285
Organisme : NIH Office of the Director
ID : UH3OD023290
Organisme : NIH Office of the Director
ID : UH3OD023272
Organisme : NIH Office of the Director
ID : UH3OD023249
Organisme : NIH Office of the Director
ID : UH3OD023337
Organisme : NIH Office of the Director
ID : UH3OD023305
Informations de copyright
© 2024. The Author(s).
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