A great
deal of evidence has accumulated that there is a problem with
regulation of cortisol levels in persons with posttraumatic stress
disorder. Several years ago, it was
demonstrated that adult offspring of persons with PTSD had
lower circulating cortisol than others, and it appeared that the lower
cortisol was a risk factor for the development of PTSD.Now, it has been shown that, at least in some persons, lower cortisol levels can be seen in infant offspring of patients with PTSD.
Transgenerational transmission of cortisol and PTSD risk
Rachel Yehuda, and Linda M. Bierera
Progress in Brain Research
Volume 167, 2007, Pages 121-135
doi:10.1016/S0079-6123(07)67009-5
Abstract
Parental posttraumatic stress disorder (PTSD) appears to be a relevant risk factor for the development of PTSD, as evidenced by a greater prevalence of PTSD, but not trauma exposure, in adult offspring of Holocaust survivors with PTSD, compared to children of Holocaust-exposed parents without PTSD. This paper summarizes recent neuroendocrine studies in offspring of parents with PTSD. Offspring of trauma survivors with PTSD show significantly lower 24-h mean urinary cortisol excretion and salivary cortisol levels as well as enhanced plasma cortisol suppression in response to low dose dexamethasone administration than offspring of survivors without PTSD. In all cases, neuroendocrine measures were negatively correlated with severity of parental PTSD symptoms, even after controlling for PTSD and even other symptoms in offspring. Though the majority of our work has focused on adult offspring of Holocaust survivors, recent observations in infants born to mothers who were pregnant on 9/11 demonstrate that low cortisol in relation to parental PTSD appears to be present early in the course of development and may be influenced by in utero factors such as glucocorticoid programming. Since low cortisol levels are particularly associated with the presence of maternal PTSD the findings suggest the involvement of epigenetic mechanisms.
Mush of this research has been done in Holocaust survivors, clearly not a random sample. Likewise, the cohort of women who were pregnant on 9/11 is not random. These populations may not be representative of a broader population.
Even so, this research is important because it provides more complete picture of the relationship between cortisol abnormalities in PTSD, and because it opens another line of research.
Much of the early research on causes of mental illness was focused upon maternal behavior. This led to several decades of unfortunate blame-the-mother mentality. Perhaps the most egregious was the notion of the "schizophrenogenic mother."
The demonstration of epigenetic transmission of risk factors for mental illness would bring a new dimension to the nature vs. nurture debate in psychiatry. It would not resolve the debate; the whole issue is too heated for there to be a clean and simple outcome. However, it could bring our models into a closer approximation to the truth.
In order for this to happen, we would need to see a nice, reproducible dissection of the mechanism of this transmission. It seems obvious that this would be a lengthy and complex multidisciplinary undertaking. I am faintly hopeful that such an undertaking could lead to new opportunities for prevention and treatment.
Comments
Great post - epigenetics is a new interest of mine, so I enjoy learning about more ways it is affecting human health. Perhaps epigenetics can help us to understand larger-scale illness trends in society. In that vein, I predict we will see a new wave of changes in behavior and health over the next two decades as the children of the Iraq war veterans are born and grow up.
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