Unburdened by false humility, postmodern trauma activists claim to have understood for the first time what drives all of human suffering
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CATEGORY: CONTROL OF LANGUAGE AND IDEAS  Alexander "Sandy" McFarlane, MD Source: BMJ Military Health Read time: 2.5 minutes This Happened In the October 2024 issue, BMJ Military Health published a study that assessed inflammatory factors pre- and post-deployment in Australian soldiers to examine if trauma changes the biology of inflammation. Who Did This? The senior author was psychiatrist Alexander “Sandy” McFarlane, the Director of The University of Adelaide's Centre for Traumatic Stress Studies. He has received numerous awards and published over 250 articles and chapters and has co-edited three books. Dr. McFarlane’s work focused on the impact of disasters, longitudinal course, and cognitive deficits of PTSD. The first author was a young psychologist, Neanne Bennett, who appears to be a post-doc. She has two first-author publications. The Claim The hypothesis of the study was that exposure to combat trauma would cause both high levels of psychological symptoms and increased levels of inflammation, measured as C reactive protein (CRP) and interleukin 6 (IL-6). This represents another test of the so-called toxic stress theory that trauma permanently damages brains and alters neurobiology. Symptoms of PTSD and blood samples were gathered on personnel of the Australian military special forces one month prior to deployment to the Middle East. The deployment lasted for less than 6 months. They were able to collect the same measures on 63 of those personnel not more than 4 months post-deployment. All were male. Changes in CRP levels from pre- to post-deployment did not associate with severity of pre-deployment PTSD symptoms but did positively correlate with post-deployment PTSD symptoms. This seemed to agree with their main hypothesis (but see below for problems). Changes in IL-6 did not associate with severity of either pre- or post-deployment PTSD symptoms, contrary to their hypothesis. In a secondary analysis, they subdivided their modest size sample into four subgroups so that they could compare the least affected to the most affected individuals: (1) High Function (lower trauma symptoms, lower trauma exposure) n=35 (2) Resilient (lower trauma symptoms, higher trauma exposure) n=11 (3) Vulnerable (higher trauma symptoms, lower trauma exposure) n=9 (4) Risk (higher trauma symptoms, higher trauma exposure) n=7 The most affected (Risk) group showed a significantly greater decrease in CRP compared to the least affected (High Function) group. No difference was found for changes in IL-6. Both of these findings contradicted their hypothesis. Despite the contradictions between hypotheses and findings, the authors concluded that “sustained and repeated exposure to a range of occupational stressors throughout a military member’s period of service are likely to have a cumulative impact...,” consistent with the toxic stress theory. Analysis None of their hypotheses were satisfied. CRP levels did not increase in lockstep with increased symptoms. In their secondary analysis of tiny subgroups, CRP actually decreased in the most affected Risk group, which was opposite of their theory. IL-6 levels did not change in either direction with symptoms in any analysis. How did the authors reconcile their conclusion of supporting the toxic stress theory with the complete absence of findings for IL-6? They did what nearly every supporter of toxic stress does. They spun the interpretation. They claimed that the nonsignificant IL-6 “elevations may represent an attempt to re-establish a homeostatic state,” which is a way of saying that they might have been unlucky in measuring variables at the wrong time. It is noteworthy that they did not perform the test that should have been conducted. It would have been a much better test to create a change score in PTSD symptoms from pre- to post-, just like they created change scores for CRP and IL-6. Because the researchers tested pre-deployment PTSD symptoms and post-deployment PTSD symptoms separately, they did not know the direction of change in PTSD scores of individuals. Prior Studies When pre-trauma prospective studies are reviewed, they do not support the toxic stress theory [1, 2, 3]. Instead, they strongly support only the diathesis stress theory which posits that neurobiological differences found in individuals with PTSD exist prior to any trauma exposures, most likely due to genetic causes.
The Bennett et al. study represents another failure of the toxic stress theory, which has been vigorously promoted by Jack Shonkoff and his Harvard center (see here and here) and is the basis of the best-selling book The Body Keeps the Score (see here). REFERENCES [1] Julia A. DiGangi et al. (2013). Pretrauma risk factors for posttraumatic stress disorder: A systematic review of the literature. Clinical Psychology Review 33:728-744. [2] Andrea Danese et al. (2017). The origins of cognitive deficits in victimized children: Implications for neuroscientists and clinicians. American Journal of Psychiatry 174:349-361. [3] Michael S. Scheeringa (2020). Reexamination of diathesis stress and neurotoxic stress theories: A qualitative review of pre-trauma neurobiology in relation to posttraumatic stress symptoms. International Journal of Methods in Psychiatric Research 30:e1864. doi: 10.1002/mpr.1864 Comments are closed.
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