Oxytocin Dysfunction Seen in Both Depressed Moms and Kids

Megan Brooks

October 16, 2013

A dysfunctional oxytocin system may underpin the long-term harmful effects of maternal depression on child development, suggesting a potential for oxytocin-based interventions, researchers say.

"Infants of depressed mothers have long-lasting difficulties both in general and specifically in social and emotional outcomes, such as social engagement with others, the capacity for empathy, which underpin the capacity for intimacy," Ruth Feldman, PhD, psychology professor at Ban-Ilan University, Ramat Gan, Israel, who worked on the study, told Medscape Medical News.

"As we found that the oxytocin production of mothers and children is dysfunctional, interventions for infants that are known to induce oxytocin release may be implemented, such as touch therapies, massage, teaching mothers to engage in social-reciprocal interactions, the use of gaze synchrony, and how to answer the infant's social gaze, etc," she said.

But intervening early is "critical, as the oxytocin system is built during the first year of life on the basis of social experiences with the parent," she said.

The study is published in the October issue of the American Journal of Psychiatry.

Early Intervention Critical

For this analysis, the researchers recruited a group of women shortly after they gave birth. When their children reached the age of 6 years, the researchers evaluated the families of 46 chronically depressed mothers and 103 mothers reporting no depression since childbirth.

Among the children of the chronically depressed mothers, 61% displayed axis I disorders, consisting mainly of anxiety and oppositional defiant disorders, compared with 15% of the children of nondepressed mothers.

In the depressed mothers' families, salivary oxytocin levels were lower in the mothers, fathers, and children, and the children had lower empathy and social engagement levels.

In analyzing allelic variations on the oxytocin receptor gene (OXTR), the researchers found that the rs2254298 GG homozygous genotype was overrepresented in depressed mothers and their families and correlated with lower salivary oxytocin levels.

On the other hand, the presence of a single rs2254298 A allele (GA or AA) genotype in depressed mothers markedly decreased the risk for child psychopathology.

"It is thus possible that while the oxytocin system may be disrupted in depression, the OXTR rs2254298 A allele may chart greater resilience in the context of early and chronic exposure to maternal depression," the investigators say.

"Important" Research

"This work is important because chronic maternal depression negatively affects child social outcomes, and this is a large public health problem, affecting up to 15% of women in the developed world," Eric Hollander, MD, of the Albert Einstein College of Medicine and Montefiore Medical Center in New York City, writes in an accompanying editorial.

"These findings are the first to detail the involvement of genetic and peripheral biomarkers in the oxytocin system in families of depressed mothers. The role of oxytocin in moderating the effects of maternal depression on child psychopathology underscores the potential for oxytocin-based interventions," he concludes.

Dr. Feldman and colleagues note that oxytocin has been tested as a psychopharmacologic agent in disorders involving social dysfunction, including autism, schizophrenia, and social anxiety, "with mostly favorable results" and could be implemented in maternal depression.

They are currently conducting a clinical trial that involves oxytocin administration and parent-infant dyadic therapy that focuses on oxytocin-releasing behaviors.

Dr. Hollander notes, "While the oxytocin system in the infant brain is exquisitely influenced by parenting behavior, it is of interest that the system does not manifest a critical developmental window in regard to intervention and can be rescued at any stage of brain development."

"Ultimately the most promising approach may be to combine psychosocial interventions, tailored to teaching social skills and social decision making for the specific disorder, with the therapeutic use of agents that enhance oxytocin signaling. Such combination treatments might be most important for individuals with early-life vulnerability of this system and/or individuals with genetic vulnerability of this system," he concludes.

The study was supported by the Israel Science Foundation, the NARSAD Independent Investigator Award to Dr. Feldman, and the Katz Family Foundation. The authors have disclosed no relevant financial relationships. Dr. Hollander reports receiving research grants from the Simons Foundation, NARSAD, NIMH, NINDS, the Orphan Products Division of the FDA, Roche, Transcept, Coronado, and Forest; consulting for Roche, Coronado, and Transcept; and having intellectual property involving memantine, oxytocin, and fluoxetine in autism.

Am J Psychiatry. 2013;170:1086-1089,1161-1168. Abstract, Editorial


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