So far we discussed the studies of resilience from a standpoint of sympathetic and vagal nerve function, but there are other biological mechanisms involved. Charney (2004) discuss this matter comprehensively. He mentions the notion of “allostasis” and explains that it is a process of achieving homeostasis through physiological changes including the regulation of the autonomic nervous system. He then introduces the notion of “allostatic load” as a state where the homeostasis is not fully recovered through allostatic response. He thus defines trauma as a condition where this allostasis finally fails.
Charney, D. (2004) Psychobiological Mechanisms of Resilience and Vulnerability: Implications for Successful Adaptation to Extreme Stress. Focus 2:368-391.
According to Charney, there are eleven neurochemical, neuropeptide, and hormonal mediators involved in allostasis. They are cortisol, DHEA, CRH, locus coeruleus, neuropeptide Y, galamin, dopamine, serotonin, benzodiazepine receptor, testosterone, and estrogen. These mediators are combined in a very intricate way to form allostasis, and above mentioned sympathetic and vagal system are integrated in this system.
Heredity, and Epigenetics
I would like to mention also the relationship between resilience and genetic factors. I stated above that initially resilience was considered to be mainly determined by one’s inborn nature and characteristics. It is true that some aspects of resilience are genetically programmed, but their genes themselves are subject to some ”epigenetic” changes. Epigenetics connotes a phenomenon in which manifestations of genes are changed through a mechanism different from the mutation of genomes themselves.
As for the genetic factors, morphological abnormalities in the brain related to PTSD have been pointed out by several researchers. There were studies concerning hippocampal atrophy and specific pattern of cerebral blood flow in individuals with PTSD (Rauch, Shin, et al, 1998） However, curious study followed: Gilbertson, et al. found that not only people with severe PTSD had a smaller hippocampus, and they also had trauma-unexposed twins with a smaller hippocampus. This means that smaller hippocampus might not a result of, but rather a risk factor for PTSD.
Rauch SL, Shin LM, Segal E, Pitman RK, Carson MA, McMullin K, Whalen PJ, Makris N. (2003) Selectively reduced regional cortical volumes in post-traumatic stress disorder. Neuroreport. 14:913-916.
Gilbertson, M.W., Shenton, M.E., Ciszewski, A., Kasai, K., Lasko, N.B., Orr, S.P., & Pitman, R.K. (2002). Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nature Neuroscience, 5, 1242-1247.
As the technology of brain imaging develops, studies of other location in the brain have also been found to be implicated. Kasai, et al. found that compared both with combat-unexposed twins and with combat-exposed twins without PTSD, combat-exposed twins with PTSD had significantly lower grey matter density of the pregenual ACC.
Kasai K, Yamasue H, Gilbertson MW, et al. (2008) Evidence for acquired pregenua anterior cingulate gray matter loss from a twin study of combat-related posttraumatic stress disorder. Biol Psychiatry. 63:550–556.
Another type of study focuses on some neurologic dysfunctions related to PTSD. A study with identical twins with PTSD found that not only combat-exposed veterans have neurological soft signs (NSSs) but also their combat-unexposed co-twins showed NSSs as well, indicating that subtle neurologic dysfunction in PTSD is not altogether acquired along with the trauma or PTSD but rather represents an antecedent vulnerability for developing PTSD.
Gurvits, T.V., Metzger, L.J., Lasko, N.B., Cannistraro, P.A., Tarhan, A.S., Gilbertson, M.W., Orr, SP., Charbonneau, A.M., Wedig, M.M., Pitman, R.K. (2006) Subtle Neurologic Compromise as a Vulnerability Factor for Combat-Related Posttraumatic Stress Disorder. Results of a Twin Study. Arch Gen Psychiatry. 63:571-576．
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