Neurological and Genetic Basis of PTSD in a Female Population

Neurological and Genetic Basis of PTSD in a Female Population

                                                                                                    

  This post 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 Associates

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