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100 Biobehavioral Resilience to Stress

DHEA/cortisol ratio and dissociation (Morgan III et al., 2004); a negative
correlation between DHEA reactivity (in response to ACTH administra-
tion) and severity of PTSD symptoms (Rasmusson et al., 2004 ); and a pos-
itive correlation between DHEA/cortisol ratio and performance among
elite special forces soldiers during intensive survival training (Morgan III
et al., 2004).
Allopregnanolone, another neuroactive steroid, may play a role in deter-
mining vulnerability versus resilience to stress. Allopregnanolone has anxio-

lytic effects when it is released by the adrenal gland during stress. It is believed
that allopregnanolone exerts negative feedback inhibition to the HPA axis.
In a recent study of premenopausal women during the follicular phase of

their menstrual cycles, cerebrospinal fluid levels of allopregnanolone were

significantly lower in those diagnosed with PTSD compared with controls
(Rasmusson et al., 2006). It is possible that DHEA and allopregnanolone may
confer resilience to stress by helping to terminate and protect against the

damage effects of prolonged HPA axis activation.

Genetic Factors Associated with SNS and HPA
Responses to Stress

Genetic factors contribute to an individual’s capacity to cope with stressful
experiences by interacting with environmental factors. In the field of statisti-

cal genetics, heritability refers to the proportion of variation in a trait that
is directly explained by genetic factors. Responses to traumatic experiences

may be influenced by heritable factors linked to the variability of personal-
ity traits, trauma exposure history, and psychophysiological reactivity. For
example, in a study of 100 healthy twin female pairs, investigators showed
that heart rate, skin conductance, and blood pressure responses to socially
stressful films were moderately heritable (Lensvelt-Mulders & Hettema, 2001).

Several twin studies of Vietnam War veterans have also shown that genetic
factors play a signifi cant role in PTSD (see Baker, Risbrough & Schork, this
volume; True et al., 1993).
Of primary relevance here is the question of genetic infl uence upon ner-
vous system activity, in particular SNS and HPA responses involved in mod-
erating adaptation to stress. One recent example for a genetically mediated
variation in SNS activity was reported by Finley et al. (2004), who found that
a polymorphism in the alpha adrenergic-2 receptor gene was associated with
autonomic hyper-responsiveness in healthy subjects. Similarly, NPY levels
during stress exposure have been shown to be affected by polymorphism

in the gene that encodes the NPY molecule (Kallio et al., 2001). Th e rela-
tionship between life stress, noradrenergic systems, and depression appears
to be mediated, in part, by alpha-2 adrenergic receptor subtypes. Studies

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