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 href="http://ajp.psychiatryonline.org/cgi/content/full/157/8/1252">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.
transmission of cortisol and PTSD risk
Rachel Yehuda, and Linda M. Bierera
Progress in Brain Research
Volume 167, 2007, Pages 121-135
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.