Source: Journal of Affective Disorders
Read time: 2.5 minutes
 
This Happened
Complex PTSD was invented in 1992 on the premise that certain types of events were more damaging than single-event traumas by being repeated and prolonged (a dose-response theory) and interpersonal in nature. In the December 2024 issue, the Journal of Affective Disorders published a study claiming to show that being a civilian refugee with indirect exposure to war qualified as one of those extremely damaging types of events.
 
Who Did This?
Psychologist Karen-Inge Karstoft is an associate professor at the University of Copenhagen, and has published 15 first-author and approximately 36 secondary-author research articles, mostly on trauma or PTSD.
 
The Claim
Researchers sent requests to participate in their research study to all 18,389 adult Ukrainian refugees registered in Denmark. They received completed electronic surveys from 6,761 individuals. The types of experiences that counted as exposure to war included hometown was affected by war (with or without damage to their own homes), witnessed first-hand or just heard about combat, and lost a family member or close friend due to war.
Using ICD-11 diagnostic criteria, they found that 15.9% fulfilled criteria for PTSD but not complex PTSD, and 13.5% fulfilled criteria for both PTSD and complex PTSD.
 
They tested the dose-response premise by predicting that exposure to more war events would lead to more diagnoses of complex PTSD. This was not supported. Of the seven types of war exposure they measured, four significantly associated with PTSD, but only two significantly associated with complex PTSD.
 
The also tested the interpersonal premise by predicting that interpersonal trauma events prior to the war would lead to more diagnoses of complex PTSD. This was not supported. The authors claimed, however, this was supported with a misleading interpretation of their data: The odds ratio of interpersonal events with PTSD was 1.17, and for complex PTSD was 1.44, both of which were significant and similar in magnitude to each other.  The authors asserted that 1.44 was higher than 1.17, but they  did not conduct a significance test.
 
Analysis
There are multiple major flaws in this study. First, researchers did not gather information on whether events were repeated, prolonged, or interpersonal. These qualities seem to have been assumed.
Second, their assessment method did not determine the onset of any symptoms in relation to war exposure. They have no idea if PTSD symptoms, or the so-called complex PTSD symptoms, were present before or after war started.
​Third, they used self-report questionnaires which are prone to false positive diagnoses. The researchers nevertheless expressed zero reservations about the existence of complex PTSD in this sample. 

The absurdity of the evidence claimed by complex PTSD activists is described here and here. The proposed disorder was rejected by both DSM-IV and DSM-5 due to absence of evidence, but the ICD adopted it in 2019 for political reasons.
Despite the absence of validity, researchers frequently add new populations that allegedly have high rates of complex PTSD including prisoners in jail, gang members, violent criminals, prisoners of war, foster care children, soldiers, refugees without war exposure, domestic violence victims, police officers, North Korean defectors, and cardiac surgery patients.
 
As I wrote in my book, “The fundamental appeal of complex PTSD is moral, not scientific. To believe in complex PTSD is to believe in a mission to save weaker, disadvantaged people from being victims of stronger perpetrators. By supporting this mission, the believer is imbued with higher moral status. That is the true value of complex PTSD.” [1] The most enduring lesson of the complex PTSD scandal is that in the social sciences, where manipulation of soft data and misleading interpretations are chronic affronts, the most concerning aspect is that researchers seem to easily believe their own deceptions.

REFERENCES
[1] Scheeringa, M. S. The Trouble With Trauma: The Search to Discover How Beliefs Become Facts.  (Central Recovery Press, 2022).

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

Source: Journal of Psychiatric Research
Read time: 2.5 minutes
 
This Happened
In March 2024, a study was published using an eight-factor model of posttraumatic stress disorder (PTSD) symptoms. Previously, seven had been the highest number of factors considered to be the best model. In contrast, for more than three decades, PTSD had been diagnosed as just three clusters of symptoms.
 
Who Did This?
Psychologist Robert H. Pietrzak was the senior author on the study. He is a professor of Psychiatry and of Public Health at Yale University, and works at the U.S. Department of Veterans Affairs, National Center for PTSD. He has over 400 research publications, including at least twelve using factor analysis of PTSD symptoms.
 
The Premise
In this study, researchers collected data from 3,847 veterans on the twenty symptoms in the PTSD diagnostic criteria [1]. They created eight groupings of those symptoms to replicate an 8-factor model that recently had been created by the same research group [2]. Researchers found that three of the eight factors correlated with depression, four of the eight factors correlated with anxiety, and four of the eight factors correlated with suicidal ideation.
The authors concluded that these findings demonstrated validity of the 8-factor model. They suggested that this model may lead to better assessment, treatment, and prevention of PTSD.
The details of this study are summarized very briefly here because they are inconsequential. As the analysis below reveals, this study is emblematic of a larger problem in trauma research.
 
Analysis
This study is one of approximately six hundred studies over the past four decades using the results of a statistical technique to discover or confirm factors of PTSD. The statistical technique is usually some variation of factor analysis.
Briefly, factor analysis works by calculating how frequently each symptom is present with every other symptom. The mathematics then reduces a large number of items into a handful of factors by grouping items that tend to co-occur with each other into a factor, and separating those that co-occur relatively less frequently into other factors.
The premise of factor analysis is that there exists a latent model of a construct that cannot be directly measured. This type of premise is unprovable with current technology. Whether the latent model exists is a theoretical question.
 
Why is this important? When criteria for psychiatric disorders were revised for the 2013 publication of DSM-5, a tragic decision was made that has gone barely noticed. The old three cluster algorithm of symptoms used to make a diagnosis was thrown out and replaced by a four-cluster algorithm. The sole reason for this momentous change was because many factor analysis studies had shown four factors was the best mathematical solution. For the first time in history, factor analysis research was used to change diagnostic criteria.
 
There have been at least seven important reviews of the massive factor analysis of PTSD literature. In the most recent review, I analyzed 206 studies on different metrics of whether factor analysis is a useful technique for designing diagnostic criteria [3]. There were too many interesting findings to summarize here, so, I’ll mention only two highlights.
1. In sixty-six confirmatory factor analysis studies with adults using DSM-5 criteria, researchers found twelve different best-fitting models that ranged from one to seven factors. A four-factor model was best-fitting most often, however, that was in only 59% of studies. With this variety of outcomes, factor analysis is closer to stamp collecting than a valid method of discovering human nature.
2. Results were contingent on which models researchers opted to study. Whenever four-factor models were tested against models with more than four factors (five, six, or seven factors), the four-factor model was best fitting in only 12.8%! Because factor analysis tries to find the model that accounts for the most mathematical variance, the model with a higher number of factors is almost always the best fitting. That is probably why the new 8-factor model was best-fitting in its inaugural test. When someone creates a 9-factor model, that will be best-fitting.
 
So, how many underlying factors really exist in a model of PTSD? Schmitt and colleagues probably have the answer. They conducted perhaps the most rigorous factor analysis possible, trying to avoid methodology pitfalls that have snared less careful researchers [4]. They concluded overall the “results provide greater evidence for a one-factor model.”
 

References 
[1] Stiltner B, Fischer IC, Duek O, Polimanti R, Harpaz-Rotem I, Pietrzak RH (2024). Functional correlates of a novel 8-factor model of PTSD in U.S. military veterans: Results from the National Health and Resilience in Veterans Study, Journal of Psychiatric Research 171:69-74. DOI: 10.1016/j.jpsychires.2024.01.017.
[2] Gross GM, Spiller TR, Duek O, Pietrzak RH, Harpaz-Rotem I (2023). Clinical significance of novel 8-factor model of DSM-5 PTSD in national VA PTSD residential treatment data: Internally- v. externally-cued intrusions, Journal of Affective Disorders, 328:255-260. DOI: 10.1016/j.jad.2023.02.046.
[3] Scheeringa MS (2024). Is factor analysis useful for revising diagnostic criteria for PTSD? A systematic review of five issues ten years after DSM-5. Journal of Psychiatric Research 176:98-107. DOI: 10.1016/j.jpsychires.2024.05.057.
[4] Schmitt T A, Sass DA, Chappelle W, Thompson W (2018). Selecting the "best" factor structure and moving measurement validation forward: An illustration. Journal of Personality Assessment, 100(4), 345-362. DOI: 10.1080/00223891.2018.1449116.

Source: WHQR public media
Read time: 2.2 minutes

This Happened
On August 22, 2024, a one-day summit was held in Wilmington, North Carolina to educate staff of youth-serving organizations about ways to minimize or cope with Adverse Childhood Experiences (ACE).
 
Who Did This?
Youth of North Carolina, a non-profit organization, sponsored the summit. Their executive director, James Allegretto, joined the organization in 2022.
 
The Premise
The Youth Resilience Summit was advertised as “an exciting and informative day to discover how you can better minimize adverse childhood experiences and build resilience for our children.” The keynote speaker was retired basketball star Kenny Anderson. Speakers included the chief judge of the local court district (Independent) and the local district attorney (Democrat), referring to themselves as Batman and Robin while fighting for justice together for over 25 years. Also among the fifteen speakers was the current Democrat nominee for governor Josh Stein.
Eleven presentations were offered on topics including:

• How Positive Childhood Experiences can counteract adverse childhood experiences
• How social media algorithms can lead to crimes and trauma which can impact biology and mental health
• The five protective factors to create trauma-informed and compassionate communities

The summit concluded with a screening of the 2016 documentary Resilience, a staple in ACE events, which follows the rise in research and advocacy for ACEs.
 
The chief judge told a reporter that too many people cling to an old ‘tough-on-crime’ philosophy, whereas his aim is to identify the root causes of criminal behavior, which include adverse childhood experiences.
 
Analysis
No matter how you slice these types of events promoting ACEs, whether it’s negatively focused on the alleged harms or, like this one, positively focused on resilience, the foundational message is the same: Human minds are incredibly fragile to environmental psychological insults. The message is based on the belief that ACE research has established an incontrovertible fact that adverse experiences in childhood cause permanent harm in the forms of adult mental problems and physical illnesses.
The problem is that none of it is true. Adverse childhood experiences are associated with adult illnesses, but it is because bad things tend to travel together in life due to other shared factors. Childhood experiences do not cause these catastrophic outcomes.
 
While well-intentioned on humanitarian goals to help children, ACE programs are destined to fail. Trauma Dispatch documented some of the pushback against the ACE ideology and ACE screening here.
 
As the negative ACE message of catastrophic harms has grown a bit stale, the movement has been shifting to focus on resilience. Both messages are counterproductive for children. The harm message teaches children that they are incredibly fragile, and the resilience message teaches them that they are not naturally resilient. 

Why Is This Happening?
Allegretto was quoted as saying, “It almost feels like a movement, right? But the reality is that we discovered how adverse childhood experiences impact people two decades ago, and we're just now getting on board and making a difference.”
The movement is based on the moral foundation of progressive liberals that care for the disadvantaged trumps other moral concerns and that human nature is almost completely molded by life experiences. Events like this promoting ACEs have been happening for the past fifteen years around the United States every week in the form of conferences, workshops, and professional development trainings. Trauma Dispatch has documented some of their content here, here, and here. It’s an attractive ideology to believe in because researchers have used slippery language to conflate association with causation, and because it appeals to the compassionate impulse to help the disadvantaged.
 
 
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Source: Psychological Science journal
Read time: 2.5 minutes
 
This Happened
A new study published this month was the first to test whether psychotherapy that addresses trauma in very young children can potentially prevent serious disease later in life by slowing down the aging of the body’s cells [1]. This kind of extraordinary claim tends to generate media interest. It was reported by at least one local, one national media outlet, and highlighted by the National Institutes of Health program that funded the work.
 
Who Did This?
Alexandra Sullivan is a postdoctoral fellow at the Intergenerational Developmental Health Program at the University of California San Francisco. The director of the project was psychologist Nicole R. Bush, who has first- or co-authored over 200 papers. They are both trying to prove how stressful life experiences become biologically embedded in physiology and epigenetics and cause health problems.
 
The Claim
The outcome variable in this study used an epigenetic age clock, which is based on measuring the number of methyl groups attached to DNA strands. Methylation occurs at cytosine-guanine pairs, called CpG sites. Certain regions, which tend to regulate DNA expression, are unmethylated. It is believed that methylation at these sites can function like an off switch to stop DNA expression. Most vertebrate DNA regions, however, are not regulation sites, and they are methylated in the natural state.
 
Researchers realized that methyl groups are lost and added to DNA over time due to wear and tear. Steve Horvath figured out that this happened systematically with age, and, in 2013, developed the first epigenetic age clock based on 353 CpG sites (193 increase with age, 160 decrease with age) [2]. When the clock calculates a person’s epigenetic age older than their chronological age, this is called “age acceleration,” allowing researchers to speculate that premature aging may have been caused by stressful experiences, which has downhill effects of illness or early death.

In the current study, Sullivan and colleagues used an epigenetic clock designed for children based on 94 CpGs. Participants were mother-child dyads exposed to trauma or grief recruited from a clinic. Children were 3-6-years old. Two cheek swabs were taken from 45 children at the baseline start of therapy and again ten months later. A comparison group of 110 children of similar age was drawn from a different study that did not involve treatment.
The two groups did not differ on age acceleration at baseline. The groups differed at the second time point, as the comparison group showed some age acceleration while the treated group showed significantly less age acceleration.
 
The authors concluded, “Findings provide robust, quasi-experimental support that dyadic intervention is associated with trauma-related accelerated aging biomarkers, most likely in a direction beneficial for health and development.”
 
Analysis
This was the first study of this type in children. One similar prior study, in adult combat veterans, did not show a slowing down of age acceleration after receiving treatment [3].
 
There are multiple concerns about methylation studies as an index of bodily damage. While more than a dozen studies, mostly in adults, have shown that epigenetic age acceleration consistently predicts PTSD status, all were cross-sectional and have zero power to prove causation. In addition, age acceleration has been found (inconsistently) with anxiety, autism, depression, schizophrenia and other conditions, suggesting it’s a non-specific index of vulnerability, like baseline heart rate variability, and is not unique to stress or trauma.
 
Another concern is that researchers don’t know if “age acceleration” in PTSD is maladaptive, or, being a misnomer, is an adaptive response. Epigenetics changes were not linked to any functional significance in this study. An alternative theory is that methylation changes are simply the residue of a complex system and interaction of many parts, and may have little to no functional consequence.
 
Why Did This Happen?
The authors’ conclusion is consistent with many trauma researchers who believe societal impacts and life experiences determine most of one’s lack of success in life. Rather than being the Holy Grail that will finally find scientific proof for a belief system, epigenetics appears destined to go the way of brain imaging. While most researchers still fervently claim that trauma damages brains, pre-trauma prospective studies show that brain differences pre-exist trauma exposure [4]. Epigenetic differences are likely to pre-exist life experiences, too [5], and any shifts during psychotherapy may be noise.
 
​
REFERENCES
[1] Sullivan, A. D. W., Merrill, S. M., Konwar, C., Coccia, M., Rivera, L., MacIsaac, J. L., Lieberman, A. F., Kobor, M. S., & Bush, N. R. (2024). Intervening After Trauma: Child–Parent Psychotherapy Treatment Is Associated With Lower Pediatric Epigenetic Age Acceleration. Psychological Science, 35(9), 1062-1073. https://doi.org/10.1177/09567976241260247
[2] Horvath S. (2013). DNA methylation age of human tissues and cell types. Genome Biology 14(10):R115. doi: 10.1186/gb-2013-14-10-r115.
[3] Katrinli, S., King, A.P., Duval, E.R. et al.(2023).  DNA methylation GrimAge acceleration in US military veterans with PTSD. Neuropsychopharmacol. 48, 773–780. https://doi.org/10.1038/s41386-023-01537-z
[4] 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.
Andrea Danese et al. (2017). The origins of cognitive deficits in victimized children: Implications for neuroscientists and clinicians. American Journal of Psychiatry 174 (2017): 349-361.
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 (2020).
[5] Zannas AS, Linnstaedt SD, An X, et al. (2023). Epigenetic aging and PTSD outcomes in the immediate
aftermath of trauma. Psychological Medicine 53(15):7170-7179. doi:10.1017/S0033291723000636
 
 
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Source: International Society for Traumatic Stress Studies
Read time: 2.5 minutes

This Happened
The International Society for Traumatic Stress Studies (ISTSS) released the program schedule for its 2024 annual conference.
 
Who Did This
ISTSS is the world’s largest professional organization for researchers and clinicians interested in psychological trauma and stress. Over 1,000 attend its annual conference, which is where all the leading trauma researchers present their latest works.
 
The Premise
Being the premium gathering of trauma researchers, this conference influences the direction of research and clinical practice, and educates the next generation of professionals. It is the indispensable venue for networking and getting your work recognized.
 
Analysis
Over three days in November 2024, approximately 527 talks are scheduled. Of those, 170 (32%) will promote ideology of progressive leftist ideas. The breakdown of those 170 talks, is that 126 will be on oppression-based stress. Racial discrimination is the most common (44), followed by LGBTQ+/transgender discrimination (21), followed by immigrant discrimination, historical/intergenerational trauma, moral injury, and man-made climate change. These oppression experiences are controversial concepts for which no good evidence exists that they cause psychological disorders.
There will also be 28 talks on toxic stress and 16 on complex PTSD.
 
Lest one thinks these concepts will be presented in a neutral fashion that will stimulate productive debate of opposing views, that will not happen. I attended my first ISTSS conference in 2000 and presented my work for the next fifteen years. It was the conference I most looked forward to every year because PTSD research was a fresh field. Groundbreaking studies on important topics were being conducted. Gradually, the conference became overrun with controversial topics by activist researchers. I tried to generate debate from the audience, but this never went far. The presenters and audience members seemed to have no intellectual framework at the ready to understand how they might be mistaken. And, there were no other skeptics in the rooms to extend the discussions. I stopped going after 2017.
 
What should talks focus on? The types of questions that would provide real help to victims of trauma include improving access to treatment (13 talks), accurate assessment (0), prediction of responders and nonresponders (0), better retention in treatment (12), implementing evidence-based treatments (25), innovations in therapy techniques (18), and mastery of therapy techniques (0). These will account for only thirteen percent of the program.
 
Why Is This Happening?
Institutions of higher learning suffer from ideological capture in which professors in academia are overwhelmingly liberal. In psychology, the ratio of Democrat to Republican faculty members is 16.8:1. In sociology, it’s 43.8:1, and in anthropology it’s 56:0 [1].
 
David Horowitz documented the impact of this imbalance in his books The Professors (2006) and Indoctrination U: The Left’s War Against Academic Freedom (2007). He described activism within campuses as attempts to deconstruct the nation’s identity and divide its communities into victims and oppressors, all under the banner of social justice.
 
Chris Rufo diagnosed the genesis of this imbalance as the “long march through the institutions,” which he claims is the skeleton key for understanding the modern Left: it’s how they captured power, how they shape the narrative, and how they influence what you think about the world around you. It explains the invention of buzzwords and control of language that you hear but aren’t quite sure what they mean or where they came from.
 
Rufo marks the 1960s as the shift of Marxist intellectual strategy from popular revolt to the long march [2]. But the groundwork was set in the early 1900s when many of the social sciences—namely, psychology, sociology, and anthropology—were born. The vagueness of these sciences make them ideal for bending scientific methods to support ideology. Those who gravitated to these fields were often self-selected individuals with fevered dreams of social justice [3].
 
The Heterodox Academy was formed in 2015 by three scholars to try to combat this lack of ideological diversity through blog posts and hosting discussions on campuses. They are trying to ensure that universities are truth-seeking and provide constructive disagreement. While large in size, the effort has been deemed a failure, however, because the discussions are often liberal professors debating with liberal professors [4]. Apparently, there aren’t many conservative professors to go around.
 
 
REFERENCES
[1] Mitchell Langbert (2018). Homogenous: The Political Affiliations of Elite Liberal Arts College Faculty. Acad. Quest. (2018) 31:186–197. DOI 10.1007/s12129-018-9700-x
[2] Christopher F. Rufo (2021). Critical race theory: What it is and how to fight it. Imprimis. A Publication of Hillsdale College 50(3), March 2021:1-5
[3] Carl N. Degler (1991). In Search of Human Nature. The Decline and Revival of Darwinism in American Social Thought. New York: Oxford University Press
[4] Nathan Cofnas (2022). Four reasons why Heterodox Academy failed. Acad. Quest. 35(4):13-24, DOI: 10.51845.35.4.4
 
 
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Read time: 2.0 minutes

This Happened
Experts, agencies, activists, and politicians claim that climate change constitutes a severe psychological stress that causes mental health disorders.
 
Who Did This?
The theory of man-made climate change will create catastrophes has attracted serious scientific attention since the 1960s. This led to the Kyoto Protocol in 1997 in which 189 countries agreed in principle to reduce greenhouse gas emissions from burning fossil fuels. The theory received a burst of popular support in 2006 with Al Gore’s documentary An Inconvenient Truth.
 
The Claims
The man-made climate change theory hypothesizes that global temperature rise will cause melting of the polar ice caps, higher sea levels, more frequent and more severe hurricanes and tornados, floods, and droughts. Among the many dreadful outcomes was that without ice caps, polar bears would drown and become extinct. An emotional icon from An Inconvenient Truth was the animated image of a polar bear treading water in a nearly empty ocean.
 
Many government agencies and professional organizations embrace the theory that man-made climate change causes mental problems. For example, the Centers for Disease Control asserted there are two main paths:
(1) trauma from natural disasters that are becoming more frequent and more severe
(2) chronic stress from both reduced access to resources caused by disaster and anxiety about alleged current catastrophes and the possibility of future catastrophes.
 
Representatives of the World Health Organization published a review paper which concluded that climate change is “a most serious threat to the health and well-being of children and adolescents” [1]. They used the term eco-anxiety to describe the chronic stress from worrying about alleged catastrophes. Multiple peer-reviewed literature reviews about the concept of eco-anxiety have concluded that, without doubt, it causes lasting mental health problems for individuals [2].
 
Analysis
Are disasters becoming more frequent or more severe? Trauma from disasters, of course, causes posttraumatic stress disorder in some individuals, but a connection to climate change is only plausible if disasters are increasing.
This has been one of the easier claims to debunk because disasters can be counted. Evidence is clear that hurricanes have trended to decrease over the past 100 years [3], severe tornados are less frequent than fifty years ago, and heat waves have declined over the past eighty years [4].
 
Is eco-anxiety valid as a unique etiology of mental health problems? No. Eco-anxiety exists but so does excessive anxiety about driving over bridges, traffic accidents, body image, germs, and public embarrassment. All of these are common forms of anxiety that fall under a broader umbrella of generalized anxiety disorder. It is likely that if individuals with eco-anxiety did not have climate change to worry about, they would still have many other anxieties. Researchers have made no attempts yet to untangle eco-anxiety from other worries to determine if it is a unique syndrome. Even the literature reviews that embrace the notion of eco-anxiety have noted the flaws of existing studies as nearly all self-report, cross-sectional, and unsophisticated [1,2].
 
Why Is This Happening?
The emotional valence underpinning the need to act with the utmost urgency to reduce fossil fuel use has always been about individual morality. As Gore stated in his documentary, “This is not a political issue so much as a moral issue. If we allow that to happen it is deeply unethical.” This moral crisis provides the value proposition as a political tool, and, coupled with anticipatory fear of natural disasters, is largely what creates additional worries in a subset of individuals with pre-existing anxiety problems.


REFERENCES
[1] Proulx K; Daelmans B; Baltag V; Banati P. Climate change impacts on child and adolescent health and well-being: A narrative review. [Review] Journal of Global Health. 14:04061, 2024 May 24, doi: 10.7189/jogh.14.04061
[2] Coffey Y, Bhullar N, Durkin J, Islam MS, Usher K. Understanding eco-anxiety: A systematic scoping review of current lit­erature and identified knowledge gaps. J Clim Change Health. 2021;3:100047. doi:10.1016/j.joclim.2021.100047
Léger-Goodes T, Malboeuf-Hurtubise C, Mastine T, Généreux M, Paradis PO, Camden C. Eco-anxiety in children: A scoping review of the mental health impacts of the awareness of climate change. Front Psychol. 2022;13:872544. doi:10.3389/fpsyg.2022.872544
Martin G, Cosma A, Roswell T, Anderson M, Treble M, Leslie K, et al. Measuring negative emotional responses to climate change among young people in survey research: A systematic review. Soc Sci Med. 2023;329:116008. doi:10.1016/j.socscimed.2023.116008
[3] Nyberg J, Malmgren BA, Winter A, Jury MR, Kilbourne KH, Quinn TM. Low Atlantic hurricane activity in the 1970s and 1980s compared to the past 270 years. Nature. 2007 Jun 7;447(7145):698-701. doi: 10.1038/nature05895.
Vecchi GA, Landsea C, Zhang W, Villarini G, Knutson T. Changes in Atlantic major hurricane frequency since the late-19th century. Nat Commun. 2021 Jul 13;12(1):4054. doi: 10.1038/s41467-021-24268-5.
Yang W, Wallace E, Vecchi GA, Donnelly JP, Emile-Geay J, Hakim GJ, Horowitz LW, Sullivan RM, Tardif R, van Hengstum PJ, Winkler TS. Last millennium hurricane activity linked to endogenous climate variability. Nat Commun. 2024 Jan 27;15(1):816. doi: 10.1038/s41467-024-45112-6.
[4] Wrightstone G (2017). Inconvenient Facts: The Science That Al Gore Doesn’t Want You to Know. Silver Crown Productions, LLC: USA
 
 
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Source: Center on the Developing Child, Harvard University
Read time: 2.2 minutes
 
This Happened
On July 22, 2024, Jack Shonkoff, M.D., founder of the “toxic stress” movement, posted his aims for the next phase. In May 2024, he stepped down as director of the center he founded to assume a new role as Founding Director.
 
Who Did This?
Jack Shonkoff is a pediatrician who has run an advocacy center at Harvard University for the past two decades. He has done more than anyone to advance the hypothesis that trauma and stress permanently damage brains and bodies, and to leverage that vision to influence policy.
 
The Claim
Shonkoff’s post stated his new goals for advocacy would be directed by a trilogy of three working papers produced by his Harvard-based work group he calls the National Scientific Council on the Developing Child:

1. Working Paper 15 (2020) created a new emphasis that stress from poverty and systemic racism during early childhood can permanently damage brains and bodies.
2. Working Paper 16 (2023) laid out a new emphasis that the physical environment of where children live is a key source of toxic stress, and most importantly, the hazards in these environments are caused almost wholly by systemic racism.
3. Working Paper 17 (2024) acknowledged more clearly than any of Shonkoff’s prior writings the obvious role of genes as a source of how individuals respond differently to stress. Previously, his writings focused on life experiences to the exclusion of genes. Nevertheless, the main message was still that racial discrimination borne of systemic racism was a major source of toxic stress.

 
To emphasize the major nature of this shift, Shonkoff called the Center’s past agenda Early Childhood Development 1.0 (ECD 1.0), and christened the new agenda ECD 2.0.
 
Analysis
The validity of toxic stress is lacking because it is based on weak cross-sectional studies, lacks a feasible mechanism, and stronger prospective, pre-trauma studies consistently fail to support it. Likewise, there is no good evidence that the psychological stress of racial discrimination permanently damages brains or causes physical illnesses [See here and here]
 
Another concern is that Shonkoff blended into these papers an analysis that minorities tend to have more health problems because they tend to live in environments plagued by material hazards (e.g., air pollution and lead), and that this situation was due to discriminatory policies. This, however, is not consistent with the toxic stress theory, because the mechanism of stress is material toxins that would harm any racial group. This contrasts to the theory that racial discrimination is a mechanism of psychological toxin, consistent with the toxic stress theory. Shonkoff made no effort to clarify the difference in mechanisms. When claiming that all your work is “science-based,” confusing two completely different mechanisms is indefensible. The tortured language opens a whole new area of advocacy that has no connection to the original theory of psychological stress.
 
Why Is This Happening?
The emphasis on racial discrimination is a sharp turn for the Council’s working paper series. The first fourteen papers, which spanned 2004-2018, never used the words race or racial to refer to stress.
The Council’s reason for this sudden shift was just “21st-century science,” as Working Paper 15 reminded readers five times, omitting to mention that studies on racial discrimination stress had existed since the 1980s [1]. It seems curious that Working Paper 15 appeared in the year of George Floyd and Black Lives Matter riots, when it became commonplace to frame nearly any problem in the U.S. as systemic racism.
 
Like all cultural revolutions that make progressive leftists feel exhilarated and truly alive [2] (e.g., Marxism, communism, the New Deal, the Great Society, man-made climate change, DEI, etc.), conflict, not outcomes, seems to be the point, and so they are eternal, and the revolutions need to be refreshed every now and then. Shonkoff, always a skilled wordsmith, expertly crafted the shift as being driven by new science, but, as usual, he gets the science wrong. If you’re a foot soldier for toxic stress, take note; you’re being handed a new party policy.
 
 
REFERENCES
[1] Barbarin, O. A. (1983). Coping with ecological transitions by Black families: A psychosocial model. Journal of Community Psychology, 11(4), 308–322. doi: 10.1002/1520-0629(198310)11:4<308::AID-JCOP2290110405>3.0.CO;2-Z
Jung, H. (1984). Indo-Chinese refugee services in metropolitan Boston: An impressionistic assessment. Asian American Psychological Association Journal, 16–18.
[2] Gornick, V (1977). The Romance of American Communism. Verso: London
 

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Source: Journal of Trauma and Dissociation
Read time: 1.9 minutes
 
This Happened
In July 2024, a study was published claiming to show that transgender-related experiences and the negative perceptions transgender people hold of themselves are fear-inducing enough to cause posttraumatic stress disorder (PTSD).
 
Who Did This?
Psychologist Sarah Valentine, PhD, conducted the study. Her program of research addresses care for PTSD among racial, ethnic, and sexual and gender minority populations.
 
The Claim
The study was conducted on 43 transgender and gender diverse (TGD) adults who responded to advertisements distributed at clinics and at a conference. They found that transgender-related stress experiences significantly associated with severity of PTSD symptoms.
The authors interpreted this to mean that transgender-related stress causes PTSD even though the stress is not the life-threatening type of stress that is known to cause PTSD. The revelation of this, according to the researchers, is that this conclusively explains why TGD people show PTSD at higher rates than the general population.
 
Analysis
The measure of transgender-related stress experiences was flawed at least three different ways. (1) Seventeen items measured events, such as “difficulty finding a bathroom to use,” and “heard negative statements about transgender” people, but no attempt was made to determine if these were experienced as positive or negative. The literature on stressful experiences has shown that it cannot be taken for granted how different individuals perceive events. (2) No attempt was made to date each event. The researchers did not know if reported events happened before or after development of PTSD symptoms. (3) Twenty-nine items measured perceptions (e.g., “People don’t understand me because they don’t see my gender as I do” and “When I think about my gender identity or expression, I feel unhappy”), which are not experiences. It's conceivable that participants imagined what others think about gender even if discrimination acts rarely happened to them.
These types of perceptions seem nearly identical to a character trait called neuroticism. Decades earlier, it was established that one of the best predictors of who develops psychiatric syndromes, including PTSD [1], was neuroticism, which describes excessive anger, anxiety, irritability, and emotional instability following minor frustrations, difficulty calming, and viewing situations as overwhelming [2].
An alternative explanation of the findings is that a large proportion of this self-selected TGD sample had high levels of neuroticism, and many, if not most, of the PTSD symptoms were false positives.
 
Why Is This Happening?
What’s the value to transgender people and their advocates of creating a narrative that existing as a transgender person puts them at higher risk for PTSD? It doesn’t help individuals manage distress or attain self-knowledge if it teaches them erroneously that society is the problem, behaviors are misdiagnosed, and they should not engage in introspection about their own weaknesses.
The value seems apparent when these types of flawed studies are placed in the context of historical ideologies for fighting social injustice that derive their appeal from oppression. We are witnessing an attempt to control language in academia by creating a category of “oppression-based stress” [3] that has special power to harm. The truth is that everyone faces stress, and there is no good evidence that oppression stress is any different from other stress in quantity or quality. The only difference is the valence that some advocates place on oppression as part of an ideology that fits their worldviews.
 

REFERENCES
[1] McFarlane AC (1989). The Aetiology of Post-traumatic Morbidity: Predisposing, Precipitating and Perpetuating Factors. British Journal of Psychiatry 154(2):221-228. doi:10.1192/bjp.154.2.221.
[2] Widiger TA, Oltmanns JR (2017). Neuroticism is a fundamental domain of personality with enormous public health implications. World Psychiatry 16(2):144-145. doi:10.1002/wps.20411. 
[3] Sarah Valentine and Kelly Harper (4/17/2023). Adaptation of evidence-based treatments for PTSD for sexual and gender minority youth. Grand rounds presentation for University of California, San Francisco Department of Psychiatry and Behavioral Sciences, Child and Adolescent Psychiatry. YouTube accessed 7/30/24.


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CATEGORY: CONTROL OF LANGUAGE AND IDEAS

Source: Journal of Trauma & Dissociation
Read time: 2.1 minutes
 
This Happened
On June 21, 2024, Julian Ford, editor of the Journal of Trauma & Dissociation, announced a call for submissions for a special issue on understanding and treating dissociation in the context of intersectional inequalities.
 
Who Did This?
Julian Ford has been a researcher on psychological trauma for over four decades. He has published over 250 articles, served on editorial boards of multiple journals, and was the president of the International Society for Traumatic Stress Studies in 2018-2019.
Like the strategy of Bessel van der Kolk and Judith Herman who attack the competency of those who disagree with them, he has embraced the notion that clinicians who do not follow his beliefs do harm to trauma victims by overlooking their true problems, misdiagnosing them, and giving them the wrong treatment. Ford was an early adopter of the controversial complex PTSD diagnosis, starting with a 1998 paper with his notion that traditional psychotherapy overwhelms and retraumatizes patients who have complex PTSD, causing them to dissociate. This notion has been debunked with evidence [1].
 
He may be best known for publishing a series of studies trying to promote a theory that interpersonal and multiple traumas, what he calls polyvictimization, has special, harmful effects that other traumas do not have. Using weak, cross-sectional studies with samples of convenience, he has not proven such extraordinary causal relations. Ford attributes the high severity of patients’ symptoms wholly to their experiences of polyvictimization and makes no mention of the possibility that other factors, such as genetics or nontrauma factors, could have caused their problems [2].
 
The Claim
Intersectionality was coined in 1989 by Kimberlé Crenshaw, an attorney and law school professor who was one of the founders of the systemic racism-based critical race theory. Intersectional theory posits that multiple, overlapping forms of discrimination combine to cause damaging social and political identities. Racial groups are defined not simply by additive inequalities of gender, class, sexuality, and immigration status, but by effects that are greater than the sum of those parts.
While widely supported on the Left, the claim has been criticized, mainly by conservatives, as ambiguous, ignorant of broader social problems, focuses too much on group identities instead of individual differences, and a form of identity politics.
​
The premise of Adverse Childhood Experiences—that the number of childhood experiences has a compounding effect—is the same premise as intersectionality, except in ACEs the predictors are any stress or trauma and the outcomes are mental and physical health.
In the field of mental health, supporters of intersectionality claim that unless providers take intersectionality into account, they will somehow be providing inadequate, harmful, or wrong types of interventions for victims.
 
Analysis
“Intersectionality” is a successful ideological branding borne of the strategy that you can’t see a problem if you can’t name a problem [3], regardless of whether it is true. In the trauma world, the branding names of ACEs, toxic stress, and complex PTSD have been successful, too.
The parallels between Ford’s theory of polyvictimization and intersectional theory are striking. It seems no coincidence that they arose concurrently during the phase of increasingly popular progressive leftist theories in academia, and not coincidentally the same time that the controversial and debunked theories of complex PTSD and toxic stress arose. It’s not clear whether they influenced each other in their early stages, but Ford’s editorial signals that these trauma theories have melded seamlessly with the racial- and class-based intersectional movement.
It is noteworthy that intersectional theory is a causal theory, i.e., that oppressive life experiences borne of societal inequalities cause extraordinary human suffering and failure to flourish. ACEs, toxic stress, and complex PTSD likewise are causal theories of a similar kin. Swap discriminations, stresses, and traumas with capitalism, and they are nearly the same as Marxism, the original, enduring intellectual manifesto that attributes degradation of the human self wholly to life experiences, and which shares a skewed view of human nature that genetic differences play no role in variations of behavior and humans are highly malleable.
 

REFERENCES
[1] De Jongh A, Resick PA, Zoellner LA, et al. Critical analysis of the current treatment guidelines for Complex PTSD in adults. Depression and Anxiety. 2016;33(5):359-369. doi:10.1002/da.22469
[2] Julian D. Ford, Tobias Wasser & Daniel Connor. "Identifying and determining the symptom severity associated with polyvictimization among psychiatrically impaired children in the outpatient setting," Child Maltreatment 16 (2011): 216-226.
[3] Kimberlé Crenshaw (December 7, 2016). The urgency of intersectionality. TED Talk, https://www.youtube.com/watch?v=akOe5-UsQ2o
 
 
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