The Relationship Between AD/HD and Perinatal (Oxytocin) Pitocin Induction: Risk for Developmental Adversity?
*Catherine Lisa Kurth, PhD and Robert Haussmann, PhD, Northcentral University

To date, the precise etiology of Attention Deficit Hyperactivity Disorder (AD/HD) remains a mystery. The steadily rising incidence of AD/HD and the coincidental increase of (Oxytocin) Pitocin use in labor/delivery underscored the rationale to investigate the relationship between these two factors. Specifically, it was proposed that perinatal exposure to obstetric Pitocin risks AD/HD onset in children. The specific mechanism of this impact was proposed as being neurobiological in nature.   

To test this theory, twenty-one variables were analyzed as potential AD/HD predictors: select obstetric complications, a confirmed AD/HD diagnosis and history of a first degree AD/HD relative. The medical labor and delivery records of a heterogeneous sample of 172 AD/HD and non-AD/HD children (ages 2-18) from throughout the U.S. and Canada were gathered from various agencies and independently reviewed for select obstetric markers and presence/non-presence of AD/HD.

A PLUM ordinal regression, chi-square, independent samples t-test and step-wise multiple regression comparatively analyzed and determined the predictive relationship(s) of obstetric factors to subsequent AD/HD onset.  In support of this hypothesis, results revealed Pitocin induction/augmentation (p<.001) was the chief AD/HD predictor (67.1%), while Pitocin exposure time (p<.001) and labor length (p<.002) also emerged as AD/HD predictors. Notable predictive trends included maternal epidurals, AROM (assisted rupture of membranes), post-birth oxygen supplementation, nuchal cord events, maternal gestation and newborn weight (LGA).  Familial AD/HD (i.e. first degree relative) predisposition played no predictive role.

These findings suggest a Pitocin-linked, interactive constellation of factors initiates a neuro-developmental cascade that disrupts cognitive executive functioning, kindling AD/HD.  These overlapping mechanisms may restrict fetal neural oxygen flow and insult soft neural tissue via prolonged, Pitocin-induced hypertonic uterine contractions. This pressure may impose neural convolutions or architectural imprints on the immature fetal brain, altering cortical topography, adversely affecting long-term neural development. Other contributing dynamics may include epigenetic triggering, neural chemical overstimulation (triggered by initial Pitocin exposure) and the down-regulation of fetal hormonal oxytocin via obstetric Pitocin infusion, triggering a switch in inhibitory neurotransmitter (GABA) signaling in the fetal brain, risking hypoxia and neuronal cell death. Immuno-suppression of brain tissue and brain inflammation may also play a role.

This study marks the first known attempt to identify a signature etiological mechanism in AD/HD.  It is concluded that Pitocin induced labor carries iatrogenic fetal risks. These findings beg the revision of obstetric practices toward more intelligent management of obstetric Pitocin to ensure neural toxinsulation for the unborn fetus.

As concerns of genesis peak around other neuro-developmental disorders (i.e. Autism spectrum disorders and Asperger’s Syndrome), these results provide for a fresh etiological conceptualization of these issues. Earlier detection of AD/HD via perinatal biomarkers and intervention in high-risk perinatal circumstances is implied. In viewing AD/HD as a disorder likened to neural insult, clinical protocols may effectively employ multi-modal treatment approaches of cognitive behavioral skills, appropriate pharmacotherapy and specific strategies aimed at strengthening and maximizing cognitive executive functioning in AD/HD.  

Pitocin use during labor may not be the sole litmus test for AD/HD onset, yet it likely plays a key role in its outcome. The risks of prolonged fetal exposure to obstetric Pitocin should be carefully explored, as should the precise neurobiological mechanism(s) and pathophysiology inherently involved.  Replication of this research via an expanded sample is urgently warranted to retest this hypothesis.  Grant application for this research purpose is currently underway in affiliation with Colorado State University, Department of Psychology.

**Author Contact Information
E-mail address: Alpinebtc@yahoo.com
Alpine Behavior Therapy Clinic, 1918 S. Lemay, Ste B., Fort Collins, Colorado 80525
Office (970) 482-7771 / Fax (970) 482-7776 

Disclaimer: The views in this article are of scientific nature only, with the sole intention to advance the progress of research in AD/HD.  No liability can be taken for any consequences potentially arising from claims made in or in relation to this article.

No grants have yet been accepted supporting this work.

*References

Ben-Amor, et al., (2005). Perinatal complications in children with attention-deficit hyperactivity disorder and their unaffected siblings. Journal of Psychiatry and Neuroscience, 30, 120-126.

Hilgetag, C. & Barbas, H. (2006). Role of mechanical factors in the morphology of the primate cerebral cortex. Computational Biology 2(3): e22. doi:10.1371/journal.pcbi.0020022.

Johanson, R., Newburn M. & Macfarlane, A. (2002). Has the medicalisation of childbirth gone too far?  British Medical Journal, 324, 892-895.

Kurth, C. L. & Haussmann, R. (2008). The Relationship between AD/HD and Perinatal (Oxytocin) Pitocin Induction: Risk for Developmental Adversity? Dissertation Abstracts International (UMI No. 3310167).

Nigg, J. (2005). What role might environmental contaminants play in ADHD? The ADHD Report, 13, 6-7. New York.

Wahl, R. (2004). Could oxytocin administration during labor contribute to autism and related behavioral disorders?-A look at the literature. Medical Hypotheses, 63, 456-460.

** A more comprehensive list of references is available upon request from the first author, Catherine Lisa Kurth, PhD at E-mail address: Alpinebtc@yahoo.com.  Dr. Kurth is Affiliate/ Associate faculty in the Department of Psychology, Colorado State University.