Lisa Kurth1, Robert Haussmann. 1. Department of Psychology, Colorado State University, c/o Alpine Behavior Therapy Clinic, 1918 South Lemay, Suite B, Fort Collins, CO 80525, USA. Lisa.Kurth@ColoState.edu
Abstract
OBJECTIVE: To investigate a potential relationship between coincidental increases in perinatal Pitocin usage and subsequent childhood ADHD onset in an attempt to isolate a specific risk factor as an early biomarker of this neurodevelopmental disorder. METHOD: Maternal labor/delivery and corresponding childbirth records of 172 regionally diverse, heterogeneous children, ages 3 to 25, were examined with respect to 21 potential predictors of later ADHD onset, including 17 selected obstetric complications, familial ADHD incidence, and gender. ADHD diagnosis and history of perinatal Pitocin exposure distinguished groups for comparison. RESULTS: Results revealed a strong predictive relationship between perinatal Pitocin exposure and subsequent childhood ADHD onset (occurring in 67.1% of perinatal Pitocin cases vs. 35.6% in nonexposure cases, χ(2)=16.99, p<.001). Fetal exposure time, gestation length, and labor length also demonstrated predictive power, albeit significantly lower. CONCLUSION: The findings warrant further investigation into the potential link between perinatal Pitocin exposure and subsequent ADHD diagnosis.
OBJECTIVE: To investigate a potential relationship between coincidental increases in perinatal Pitocin usage and subsequent childhood ADHD onset in an attempt to isolate a specific risk factor as an early biomarker of this neurodevelopmental disorder. METHOD:Maternal labor/delivery and corresponding childbirth records of 172 regionally diverse, heterogeneous children, ages 3 to 25, were examined with respect to 21 potential predictors of later ADHD onset, including 17 selected obstetric complications, familial ADHD incidence, and gender. ADHD diagnosis and history of perinatal Pitocin exposure distinguished groups for comparison. RESULTS: Results revealed a strong predictive relationship between perinatal Pitocin exposure and subsequent childhood ADHD onset (occurring in 67.1% of perinatal Pitocin cases vs. 35.6% in nonexposure cases, χ(2)=16.99, p<.001). Fetal exposure time, gestation length, and labor length also demonstrated predictive power, albeit significantly lower. CONCLUSION: The findings warrant further investigation into the potential link between perinatal Pitocin exposure and subsequent ADHD diagnosis.
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