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PTSD: Traumatic Causation

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Unifying Causality and Psychology

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Abstract

The causality of abnormal or disordered behavior is referred to as etiology. The various versions of the DSM diagnostic manual are based on the medical model, which seeks clear, specific relationships among etiology, disorder category, and treatment. A major approach to understanding etiology involves the search for endophenotypes that lie between genes and disorders. This chapter reviews current conceptualization and research on PTSD, focusing on the biological markers of the disorder that might constitute endophenotypes. The search for candidate endophenotypes in PTSD must begin with determining its genetic bases, as well as the effects of epigenesis on their expression. However, establishing the endophenotype of PTSD is confounded by the uncertainty of which model best conceives it and the factor structure of its symptoms, let alone that both the number of its symptoms and their arrangement in clusters change from one version of the DSM to the next.

The chapter is heavily biological and is too dense to summarize in detail in this regard. Some of the candidate genes for the endophenotype for PTSD mentioned in the chapter include: SLC6A39 (dopamine transporter gene polymorphism, allele 9), FKBP5 (glucocorticoid receptor co-chaperone protein 5), COMT, RGS2 (regulator of G-protein signaling 2), 5-HTTLPR, BDNF, NR3C1, and DRD2 (dopamine receptor D2). Some of the brain areas involved in PTSD include: the hippocampus, the amygdala, the anterior cingulate, the insula, the orbitofrontal region, and the medial prefrontal cortex. As for neurotransmitters, they include: prefrontal cortex alpha 2c (PFC α 2c); alpha, noradrenergic (noradrenergic α); dopamine type 1 (DA1); serotonin type 2 receptor (5HT2R); dehydroepiandrosterone, or its sulfated derivative (DHEA (S)); cannabinoid type 1 receptor (CB1R); alpha 2c noradrenergic receptor polymorphism (α2cDel1322-325); gamma-aminobutyric acid (GABA); (allo)pregnanolone (ALLO); neuropeptide Y (NPY), catecholamines, serotonin, cortisol, corticotrophin-releasing factor (CRF), dehydroepiandrostorone, (allo)pregnalolone, and immune factors. The general message of the chapter is that progress is being made in determining the pathway to disorder for PTSD. However, as with the many disorders in the DSM, effort to establish the endophenotype of PTSD needs to consider the biopsychosocial model. A strict biological emphasis on the origins of PTSD will confound understanding of its causality (etiology).

Note. This contains material from Young, G. (2014). PTSD, endophenotypes, the RDoC, and the DSM-5. Psychological Injury and Law, 7, 75–91.

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Young, G. (2016). PTSD: Traumatic Causation. In: Unifying Causality and Psychology. Springer, Cham. https://doi.org/10.1007/978-3-319-24094-7_21

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