Neurobiology claims and the question of causality

One of the book’s most widely embraced ideas is that trauma inflicts direct, lasting damage on brain structures and neural networks involved in emotion regulation, memory and self-control. In addition, it is claimed to produce lasting damage to physical organs and systems, directly causing obesity, heart disease, autoimmune diseases and a wide range of other lethal conditions. Although neuroimaging studies have repeatedly documented structural and functional differences between individuals with and without PTSD, these were always cross-sectional designs – with no causal explanatory power – with findings that failed to replicate consistently. ^{Reference Siehl, Zohair, Guldner and Nees2} Further, these studies – extremely common in the peer-reviewed literature – rarely emphasise these ‘limitations’. When they are acknowledged, it is in cursory fashion with one or two sentences, while the central narratives portray confidence in trauma-inflicted damage.

There are three literature reviews of studies that measured neurobiological variables prior to trauma exposure and then followed the development of outcomes prospectively; all three concluded that differences likely precede trauma exposure. ^{Reference DiGangi, Gomez, Mendoza, Jason, Keys and Koenen3–Reference Scheeringa5} Even though prospective studies are more difficult to conduct than cross-sectional studies, the most recent of these reviews identified 25 such studies, ^{Reference Scheeringa5} and there have been half a dozen more since that publication. These reviews found little evidence for the book’s theory that trauma causes permanent brain damage. These findings are consistent with diathesis–stress models, which conceptualise such differences as vulnerability factors that increase the likelihood of developing PTSD following trauma.

The distinction between pre-existing vulnerabilities and trauma-induced damage is not a minor technicality – it has significant implications for how clinicians conceptualise resilience, prevention and treatment. Overemphasising damage models may unintentionally reinforce deterministic narratives, whereas recognising pre-existing vulnerabilities can encourage more targeted preventive strategies.

Treatment claims and comparative efficacy

Another major theme in the book is the claim that ten ‘body-based’ treatments (psychomotor therapy, sensorimotor psychotherapy, somatic experiencing therapy, neurofeedback, eye movement desensitisation and reprocessing (EMDR) therapy, art, music, dance, theatre and yoga) are uniquely effective for trauma. It is claimed that they are the only types of treatment that can successfully process trauma and rewire brains, because trauma is embedded in the body, with many victims not even cognisant of experiencing trauma. These, and other body-based treatments, are a burgeoning industry of clinician workshops and retreats. ^{Reference Carr6}

Although a few of these approaches have shown promise in preliminary studies, the available evidence does not demonstrate superiority over established, evidence-based interventions such as cognitive–behavioural therapy (CBT). Meta-analyses and large randomised controlled trials consistently indicate that structured, trauma-focused talking therapies yield the most robust and durable outcomes. ^{Reference Lewis, Roberts, Andrew, Starling and Bisson7} By contrast, studies of body-based interventions often face methodological limitations, including small sample sizes, lack of active control conditions and inconsistent follow-up data. ^{Reference Classen, Hughes, Clark, Mohammed, Woods and Beckett8} EMDR is an exception among these treatments, being one of the two main recommended treatments for trauma, along with CBT, but it has not shown superiority to CBT. This does not mean such treatments lack value, but rather that their promotion as superior to well-validated approaches is not currently justified by the weight of evidence.

Mechanisms of change and omitted evidence

If trauma damages the brain, identifying the mechanisms of such damage is essential. The book briefly mentions topics such as cortisol dysregulation and epigenetic changes, yet omits substantial discussion of the large – and largely inconclusive – literature on these topics. In the peer-reviewed literature, the early findings in stress-related cortisol research have proven difficult to replicate, ^{Reference Meewisse, Reitsma, De Vries, Gersons and Olff9} and the field of trauma-related epigenetics is still characterised by small effect sizes, unclear mechanisms and failures to replicate. ^{Reference Wellington, Boucas, Lagopoulos and Kuballa10}

By contrast, alternative explanatory models, such as diathesis–stress frameworks, integrate neurobiological findings with well-established developmental and genetic influences on risk and resilience. ^{Reference Scheeringa5} These models offer a broader, evidence-consistent account of why trauma exposure results in persistent distress for some individuals but not for others.

Why certain narratives prevail

The persistence and popularity of damage-focused neurobiological narratives cannot be understood solely in terms of selectively picked empirical support. Scholars have noted that neuroscience explanations often carry persuasive weight for both professionals and lay audiences – a phenomenon sometimes referred to as neurorealism, in which a theory possesses greater meaning because it is backed up by brain research. In the context of trauma, the idea that adversity leaves measurable ‘scars’ in the brain resonates with broader cultural movements towards validating lived experience, destigmatising mental illness and advocating for systemic change.

Although such aims are laudable, the uncritical acceptance of compelling but weakly supported narratives carries risks, including the potential to influence policy and clinical training in ways that are not supported by best available evidence. This underscores the need for continued scholarly engagement with widely disseminated mental health claims.

Implications for clinical practice and public communication

Given the reach of The Body Keeps the Score, its claims are not merely academic – they shape patient expectations, influence practitioner training and inform public discourse on trauma. For clinicians, aligning practice with robust evidence is critical to ensuring that patients receive the most effective care. For researchers, this case highlights the importance of public scholarship that engages with popular mental health narratives while maintaining fidelity to empirical standards.