Neurological and Genetic Basis of PTSD in a Female Population

This report stems from a massive study conducted in 2009: “Protocol for investigating

genetic determinants of posttraumatic stress disorder in women from the nurses' health study II”

(Koenen, K. C, et al., 2009).

The motivation for the study is simple: with a somewhat high incidence rate and a known

hereditability factor for PTSD (cf. Carlson, 606-607), this research is concerned with specifying

the gene(s) responsible for PTSD specifically in a female population. The researchers note that 1

in 9 American women will be diagnosed with PTSD in their lifetime, citing the same caveat as

Carlson: even though men tend to be exposed to more traumatic events in their lifetime, women

are more likely to be diagnosed with PTSD. Further, PTSD is hereditable: monozygotic twins

(MZ) have a higher likelihood of diagnosis than dizygotic twins (DZ). The data from “twin

studies indicate genetic influences account for about one-third of the variance in PTSD risk”

(Koenen, 2).

I referred earlier to this study as massive—and for good reason. The method of this study

was based on the Nurses’ Health Study II, comprising 68,518 women. The researchers screened

the entire cohort for prior trauma exposure and PTSD. Then, of the 68,518 women, 3,000 were

selected for PTSD diagnostic interviews based on the initial screening. Finally, controlled studies

genotyped 1,000 women who were diagnosed with PTSD, and of course another 1,000 were

slated for the control group—women who experienced trauma, but were not diagnosed with

PTSD.

Summing up several pages of the study (several pages on their data collection, survey

methods, etc.), their research points to three specific systems “whose alterations are implicated in

PTSD etiology”: 1) Hypothalamic-pituitary-adrenal axis, 2) Locus coeruleus-noradrenergic

system and 3) Limbic-frontal neuro-circuitry (of fear). The association of those systems with

PTSD was not surprising. Carlson also notes the role of the MPC (Medial Prefrontal Cortex) and

the amygdala in control of emotional response.

Although highly interesting, the article is not without its limitations. The most poignant

limitation is the massive “N” used. The study noted in the beginning that one of their

motivational concerns was previous PTSD studies with little to no power and other equally

troubling statistical considerations. Yet, their study has an enormously high power (and thus a

high Cohen’s D) due simply to their sample size. There were two pages of statistical explanation

of power in the study. And while they included charts and graphs to justify their statistical

procedures, the possibility of a Type I error with such a high Cohen’s D is difficult to avoid.

Finally, the diagnosis for PTSD was conducted over the phone by a lay person, with no formal

psychological assessment training. This was clearly an issue. I wonder how many of the

participants would feel comfortable being assessed by a non-trained specialist.

In sum, although not without its limitations, the researchers nonetheless have made

significant headway to understanding the neurological basis for PTSD in a female population.

References

Carlson, Neil R. (2012). Physiology of Behavior. New York, NY: Allyn & Bacon.

Koenen, K. C., DeVivo, I., Rich-Edwards, J., Smoller, J. W., Wright, R. J., & Purcell, S. M. (2009). Protocol for investigating genetic determinants of posttraumatic stress disorder in women from the nurses' health study II. BMC Psychiatry, doi:10.1186/1471-244X-9-29.

Prepared by Phillip J. Kuna for John G. Kuna, PsyD and Associateshttp://johngkunapsydandassociates.com/https://www.facebook.com/JohnGKuna.PsyD.Associates(570)961-3361