Pregnant women present during the September 11 World Trade Center collapse have passed on markers of Post Traumatic Stress Disorder (PTSD) to their unborn babies through transgenerational transmission. The findings strengthen the evidence for in utero or early life risk factors for the later development of adult mental or physical disorders. The study will be published online today in The Journal of Clinical Endocrinology & Metabolism, one of the four journals produced by The Endocrine Society.
Previous studies led researchers to believe that reduced cortisol levels observed in the adult children of Holocaust survivors could be attributed to mostly environmental factors, such as the stress of living with a parent who is depressed or anxious, or the experience of vicarious traumatization based on hearing stories of how parents suffered, rather than a ’transmitted’ biological trait. "In the current study, reduced stress hormone levels were observed in infants, suggesting a larger role for very early environmental, genetic, or genetic-environmental interactions than previously thought," explains Rachel Yehuda, Ph.D., principal investigator of the study.
Scientists at Mount Sinai School of Medicine and the University of Edinburgh studied the relationship between maternal posttraumatic stress syndrome disorder (PTSD) symptoms and salivary cortisol levels in 38 women and their infants. Mothers who experienced symptoms of PTSD in response to 9/11 had lower cortisol levels compared to mothers who did not develop this condition. Moreover, approximately one year after birth, the babies of mothers who had developed PTSD symptoms had significantly lower cortisol levels compared to that in babies of mothers who developed only minimal symptoms. This decrease in cortisol levels among the infants was similar to their mothers’ hormonal response to PTSD. Since lower cortisol levels in relation to maternal PTSD were most apparent in babies born to mothers who were in their third trimester on 9/11, the data implicate the possibility of in utero effects as contributors to a putative biological risk factor for PTSD.
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